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what is adrenaline biology

Adrenaline is a hormone, and is secreted from the adrenal glands-which are situated just above the kidneys.Whenever you are nervous or excited, your body will secrete this hormone; because your brain sends messages along nerves to the adrenal glands, which tells them to secrete adrenaline into the blood stream.The function of adrenaline is to prepare the body for something (whatever is making you nervous).henever you are nervous or excited, your body will secrete this hormone; because your brain sends messages along nerves to the adrenal glands, which tells them to secrete adrenaline into the blood stream. The function of adrenaline is to prepare the body for something (whatever is making you nervous).

Adrenaline is a hormone produced by the adrenal gland in the body. When it is produced it stimulates the heart-rate, dilates blood vessels and air passages, and has a number of more minor effects.

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which hormone cause women moody

Hormones and the Brain. That's not to say estrogen isn't a major player in regulating moods. Estrogen acts everywhere in the body, including the parts of the brain that control emotion. Some of estrogen's effects include: 1 Increasing serotonin, and the number of serotonin receptors in the brain.

Here’s how to escape the horror hormones cause. Hormones! From PMS to menopause, these messengers of womanhood can affect your mood, your weight, your food cravings - even your desire for sex. For many women, it's smooth sailing, but for others, it's a shipwreck at every turn of the hormonal bend.

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regulation of the secretion of a hormone may be stimulated by __________.

Hormone secretion can be stimulated and inhibited by: 1 Other hormones (stimulating- or releasing -hormones) 2 Plasma concentrations of ions or nutrients, as well as binding globulins. 3 Neurons and mental activity. Environmental changes, e.g., of light or temperature.

Neural Regulation of Hormone Release. Neural regulation of hormone release is when neuronal input to an endocrine cell increases or decreases hormonal secretion. We will consider three different examples: the autonomic innervation of the pancreas, the adrenal medulla, and neurosecretory cells of the hypothalamus.n this case, epinephrine and norepinephrine are considered hormones because they are released to the circulation. However they both bind to adrenergic receptors, and thus have much the same physiological effects as sympathetic neural stimulation.

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functions of prostaglandins

Prostaglandins function to activate an inflammatory response, which is the body’s way of neutralizing an infection caused by internal or external stimuli (burns, toxins, frostbite, radiation and splinters). Typical inflammatory responses include fever, the sensation of pain and swelling.

Prostaglandin E2: One of the prostaglandins, a group of hormone-like substances that participate in a wide range of body functions such as the contraction and relaxation of smooth muscle, the dilation and constriction of blood vessels, control of blood pressure, and modulation of inflammation.

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where are your glands located

Your Adrenal Glands. The adrenal glands are orange-colored endocrine glands which are located on the top of both kidneys. The adrenal glands are triangular shaped and measure about one-half inch in height and 3 inches in length. Each gland consists of a medulla (the center of the gland) which is surrounded by the cortex.

Apocrine Glands. This type of gland is found in hairy places on the body, such as the armpits and between the legs. Near the skin’s surface, inside the hair follicle, apocrine glands secrete: “A milky fluid that most commonly [occurs] when you’re under emotional stress. This fluid is odorless . . . .”.

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does stress affect the immune system

Too Much Stress. The way stress affects the immune system is complicated but explained well by Harrison Wein, Ph. D, in the National Institutes of Health newsletter, Word on Health.. In the article, Stress and Disease: New Perspectives, Dr. Wein states that stress produces a hormone in the body called cortisol. report in the November 1990 edition of Psychological Bulletin, states that stress suppresses immune system function and that, over time, the immune system does not adapt but instead continues to wear away. What was intended to protect the body, begins to harm it when unregulated.

Stress also can overactivate the immune system, resulting in an increased risk of autoimmune diseases such as arthritis and multiple sclerosis. Skin conditions such as psoriasis, eczema, hives and acne also may worsen, and stress can trigger asthma attacks. The mechanisms behind this are complex and still only partially understood, but what we do know is that our reactions to life events can have far-reaching effects on our health.

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the difference between pressure and stress

Originally Answered: What is the difference between pressure and stress? Pressure is often used with fluids (gases or liquids), whereas stress is more often used with solids. One major difference is that pressure only acts perpendicular to a surface, whereas stress can also be parallel to a surface as well as perpendicular to it.

Stress comes from the pressures we feel in life, as we are pushed by work or any other task that puts undue pressure on our minds and body, adrenaline is released, extended stay of the hormone causes depression, a rise in the blood pressure and other negative changes and effects.

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cortisol is

Cortisol & Adrenal Function. Cortisol is a life sustaining adrenal hormone essential to the maintenance of homeostasis. Called “the stress hormone,” cortisol influences, regulates or modulates many of the changes that occur in the body in response to stress including, but not limited to: 1 Blood sugar (glucose) levels. 2 Fat, protein and carbohydrate metabolism to maintain blood glucose (gluconeogenesis). 3 Immune responses.

cortisol. a hormone from the adrenal cortex; the principal glucocorticoid. Called also 17-hydroxycorticosterone and, pharmaceutically, hydrocortisone. A synthetic preparation is used for its anti-inflammatory actions.

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what are some examples of conditions that are maintained constant in the body

This is because it takes time for protein synthesis to commence, the hormone to diffuse into the blood-steam, and for it to circulate around the body and take effect. Temperature Homeostasis (thermoregulation) One of the most important examples of homeostasis is the regulation of body temperature.

It is important that the internal environment of the body is controlled. Maintaining a constant internal environment is called homeostasis. The nervous system and hormones hormones: Chemical messengers produced in glands and carried by the blood to specific organs in the body are responsible for this. These are some of the internal conditions that are controlled.

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what is allostasis

Allostasis is the process of achieving stability, or homeostasis, through physiological or behavioral change. This can be carried out by means of alteration in HPA axis hormones, the autonomic nervous system, cytokines, or a number of other systems, and is generally adaptive in the short term (McEwen & Wingfield 2003).

In 1988, Peter Sterling and Joseph Eyer of the University of Pennsylvania named the homeostatic process allostasis in the Handbook of Life Stress, Cognition, and Health. Allostasis is the mind/brain and body’s ability to achieve stability through and despite change.

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what is argireline peptide

Acetyl hexapeptide-3 or acetyl hexapeptide-8 (sources differ) is a synthetic anti-wrinkle cosmetics ingredient. It is a peptide which is a fragment of SNAP-25, a substrate of Botulinum toxin (Botox). Acetyl hexapeptide-8 is marketed as Argireline by the Barcelona-based research laboratory Lipotec.

Vasopressin, also known as arginine vasopressin (AVP), antidiuretic hormone (ADH), or argipressin, is a neurohypophysial hormone found in most mammals. Its two primary functions are to retain water in the body and to constrict blood vessels.asopressin is a peptide hormone that increases water permeability of the kidney's collecting duct and distal convoluted tubule by inducing translocation of aquaporin-CD water channels in the plasma membrane of collecting duct cells.

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aldosterone is secreted by the

Aldosterone is the main mineralocorticoid secreted by the adrenal cortex. When low blood pressure is detected by the kidneys, we see the start of the renin-angiotensin system, which is a hormonal cascade that leads to the production of angiotensin II. Angiotensin II is a powerful stimulator of aldosterone release.

Aldosterone is secreted by the adrenal cortex in the adrenal gland - more specifically, in the zona glomerulosa. The adrenal gland is located right above your kidneys. It'…s normally depicted in most images by a yellow triangular shaped object that sits atop both the left and right kidneys. Epinephrine or adrenaline is secreted by adrenal medula. 3 people found this useful.

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can taurine raise blood pressure

Taurine Offsets Multiple Stressors of High Blood Sugar. Update Required To play the media you will need to either update your browser to a recent version or update your Flash plugin. When your fasting blood sugar rises above 90 your body enters into a state of stress trying to deal with extra sugar. This is true long before blood sugar rises to the level of type 2 diabetes. The extra sugar in your circulation is a challenge for the health of your arteries, heart, liver, pancreas, kidneys, and eyes. A number of new studies show that supplemental taurine can help combat the stress of high blood sugar and act as a tool to assist in normalizing your blood sugar regulating systems.

In the blood vessels, it triggers vasoconstriction (narrowing of blood vessels), which increases blood pressure. Blood pressure is further raised by norepinephrine as a result of its effects on the heart muscle, which increase the output of blood from the heart. Norepinephrine also acts to increase blood glucose levels and levels of circulating free fatty acids. The substance has also been shown to modulate the function of certain types of immune cells (e.g., T cells).

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what is the function of the sympathetic nervous system

The sympathetic branch of your autonomic nervous system originates in the spinal cord. It goes into action to prepare the body for physical or mental activity. In response to a stressor, the sympathetic nervous system orchestrates what you familiarly call the fight-or-flight response.

Sympathetic nervous system. The sympathetic nervous system (SNS) is part of the autonomic nervous system (ANS), which also includes the parasympathetic nervous system (PNS). The sympathetic nervous system activates what is often termed the fight or flight response.

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what does the adrenal gland do for the body

The main purpose of your adrenals is to enable your body to deal with stress from every possible source, ranging from injury and disease to work and relationship problems. They largely determine the energy of your body’s responses to every change in your internal and external environment.

Adrenal Gland Functions. Your adrenal glands work to regulate certain hormones, primarily cortisol, adrenaline and aldotesterone. These are all related to stress and affect your blood sugar, blood pressure, energy and appetite.

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stress stimulates what part of the brain the reptilian brain

If the situation is judged as being stressful, the HYPOTHALAMUS (at the base of the brain) is activated. The hypothalamus in the brain is in charge of the stress response. When a stress response is triggered, it sends signals to two other structures: the pituitary gland, and the adrenal medulla. These short term responses are produced by The Fight or Flight Response via the Sympathomedullary Pathway (SAM).

But, in the sleep-deprived brain, the amygdala seemed to be rewired, coupling instead with a brain stem area called the locus coeruleus, which secretes norepinephrine, a precursor of the hormone adrenaline that triggers fight-or-flight type reactions.

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what is the epilator used for

For the device intended to permanently remove one hair at a time, see Electric tweezers. Closeup of the head of an epilator. An epilator is an electrical device used to remove hair by mechanically grasping multiple hairs simultaneously and pulling them out. The way in which epilators pull out hair is similar to waxing, although unlike waxing, they do not remove cells from the epithelium of the epidermis. Aside from the spring in early spring-type epilators, there are no parts in epilators that require regular replacement.

A Lifesaving Drug. Epinephrine pens, or EpiPens, can be lifesaving tools. The epinephrine (also called adrenaline) is a cardiac stimulant and is used for severe allergic reactions of all types, including food, drug, insect bites, and stings.Prescribed to those for whom the risk of anaphylactic shock due to allergic reaction is very high, it comes in the form of an auto-injector or “pen”.he epinephrine (also called adrenaline) is a cardiac stimulant and is used for severe allergic reactions of all types, including food, drug, insect bites, and stings. Prescribed to those for whom the risk of anaphylactic shock due to allergic reaction is very high, it comes in the form of an auto-injector or “pen”.

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what is adrenergic function

Adrenergic is a term used to describe proteins and drugs that interact with adrenaline or noradrenaline, also known as epinephrine and norepinephrine, respectively.

These adrenergic nerves release the neurotransmitter norepinephrine (NE), which binds to specific receptors in the target tissue to produce their physiological responses. Neurotransmitter binding to receptors activates signal transduction pathways that cause the observed changes in cardiac function.Adrenergic receptors (adrenoceptors) are receptors that bind adrenergic agonists such as the sympathetic neurotransmitter NE and the circulating hormone epinephrine (EPI).The most important adrenoceptor in the heart (not including coronary vascular adrenoceptors) is the β1-adrenoceptor.irculating catecholamines (epinephrine) released by the adrenal medulla also bind to these same alpha and beta adrenoceptors in the heart. In addition to sympathetic adrenergic nerves, the heart is innervated by parasympathetic cholinergic nerves derived from the vagus nerves.

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what do androgens do

The AR gene provides instructions for making a protein called an androgen receptor. Androgens are hormones (such as testosterone) that are important for normal male sexual development before birth and during puberty.Androgen receptors allow the body to respond appropriately to these hormones.The receptors are present in many of the body's tissues, where they attach (bind) to androgens. The resulting androgen-receptor complex then binds to DNA and regulates the activity of androgen-responsive genes.ndrogen receptors allow the body to respond appropriately to these hormones. The receptors are present in many of the body's tissues, where they attach (bind) to androgens. The resulting androgen-receptor complex then binds to DNA and regulates the activity of androgen-responsive genes.

What do testosterone and estrogen do? Testosterone is an androgen, or steroid hormone; in men, androgens trigger the development of reproductive organs — the penis, testes, prostate, etc. Testosterone promotes muscle and bone mass, hair growth, sperm production and sex drive.

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what hormones are produced in the adrenal medulla?

The two most important hormones of the adrenal medulla are the catecholamines. epinephrine and norepinephrine (Figure 1). The synthesis pathway for. norepinephrine is identical to that used by adrenergic neurons. However, the. adrenal medulla expresses an additional enzyme, phenylethanolamine-N-methyl-.

Epinephrine and Norepinephrine. hormone produced in the adrenal medulla; increases alertness, metabolizes high-energy foods, and creates/preserves glucose; inhibits digestion/urination and insulin secretion.

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is adrenaline and epinephrine the same

Epinephrine (also known as adrenaline) is released by the adrenaline glands and is responsible for the regulation of body’s “fight or flight” response. It regulates the transfer of nerve signals between neurons and the body cells and increases the rate and strength of cardiac contraction.

Adrenaline, or epinephrine, and cortisol, or hydrocortisone, are stress hormones secreted from the adrenal glands, which sit above the kidneys. Though both chemicals are stress hormones, adrenaline and cortisol play different biochemical roles. Adrenaline primarily binds to receptors on the heart and heart vessels. This increases heart rate, force of muscle contraction and respiration. Cortisol binds to receptors on the fat cells, liver and pancreas, which increases glucose levels available for muscles to use. It also temporarily inhibits other systems of the body, including digestion, growth, reproduction and the immune system. Video of the Day

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can a person live without adrenal glands

To emphasize how important this gland is, consider that the gonads (testicles or ovaries) of a man or woman could be removed and without any further medication that person would live. Without critical medical care, a patient would die shortly after the removal of the adrenal glands.

This is false information, the adrenal glands do NOT need support, the adrenal glands are what CAUSE depression because they excrete TOO MUCH ADRENALIN. To start curing yourself, you must remove the STRESS that CAUSED your adrenal glands to pump out a constant flow of Adrenalin. That is the key to success.

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what function does your adrenal gland control

1 The adrenal cortex—the outer part of the gland—produces hormones that are vital to life, such as cortisol (which helps regulate metabolism and helps your body respond to stress) and aldosterone (which helps control blood pressure).ormones of the Adrenal Glands. The adrenal cortex and the adrenal medulla have very different functions. One of the main distinctions between them is that the hormones released by the adrenal cortex are necessary for life; those secreted by the adrenal medulla are not.

The Adrenal Medulla is the inner part of the adrenal gland. The hormones secreted effect the structures in the body that are under the control of the sympathetic nervous system, aiding the body to deal with stressful situations such as fright, attack or pursuit.he Endocrine system regulates the activities of the body by secreting complex chemical substances (hormones) into the blood stream. These secretions come from a variety of glands which control various organs of the body. The key functions are: 1 To regulate the metabolic functions of the body.

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what are pain receptors

Top 10 amazing movie makeup transformations. A pain receptor is a type of nerve cell that is primarily responsible for receiving and then transmitting stimulation signals from various nerve endings to the brain, which will typically interpret then as pain.f a drug inhibits the release of second messengers, then the pain receptors will not be activated, the pain impulse will not reach the brain, and the person will not perceive pain from the damaged tissue. The same thing happens if the brain’s response is delayed or neutralized.

The adrenergic receptors are a class of G protein-coupled receptors that are targets of the catecholamines, especially norepinephrine and epinephrine. Many cells possess these receptors, and the binding of a catecholamine to the receptor will generally stimulate the sympathetic nervous system. The sympathetic nervous system is responsible for the fight-or-flight response, which includes dilating the pupil, increasing heart rate, mobilizing energy, and diverting blood flow from non-essential orga

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which part of the nervous system controls smooth muscle, cardiac muscle, glands, and adipose tissue subconsciously?

The autonomic nervous system (ANS) is to a large extent responsible for automatically and subconsciously regulating the cardiovascular, renal, gastrointestinal, thermoregulatory, and other systems, in order to enable the body to meet the continual and ever-changing stresses to which it is exposed.

The autonomic nervous system is the part of the nervous system that controls muscles of internal organs (such as the heart, blood vessels, lungs, stomach, and intestines) and glands (such as salivary glands and sweat glands).

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a histamine reaction to pressure

slide 1 of 6. Histamine is a chemical in the body tissues that is produced by the breakdown of histidine. It is released in allergic reactions and causes widening of capillaries, decreased blood pressure, increased release of gastric juice and tightening of the muscles of the bronchial tubes and the uterus.

Histamine is an important mediator of immediate hypersensitivity reactions acting locally and causing smooth muscle contraction, vasodilation, increased vascular permeability, edema and inflammation. Histamine acts through specific cellular receptors which have been categorized into four types, H1 through H4.

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effects of ghrelin hormone

According to the BBC, the researchers said there have been suggestions that blocking the body’s response to the hormone could be a possible weight-loss treatment. This new study however, found that it may also produce “unintended effects on mood”. The researchers are quoted in the article as saying that although signs of depression and anxiety decrease as ghrelin levels increase, “an unfortunate side effect…is increased food intake and body weight”. The researchers now want to look at the antidepressant effect of ghrelin in conditions such as anorexia.

Ghrelin (pronounced /ˈɡrɛlɪn/), the hunger hormone, also known as lenomorelin (INN), is a peptide hormone produced by ghrelinergic cells in the gastrointestinal tract which functions as a neuropeptide in the central nervous system.

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where is epinephrine produced

Epinephrine: Also known as adrenaline. A substance produced by the medulla inside of the adrenal gland. The name epinephrine was coined in 1898 by the American pharmacologist and physiologic biochemist John Jacob Abel who isolated it from the adrenal gland which is located above (epi-) the kidney nephros in Greek). substance produced by the medulla inside of the adrenal gland. The name epinephrine was coined in 1898 by the American pharmacologist and physiologic biochemist John Jacob Abel who isolated it from the adrenal gland which is located above (epi-) the kidney nephros in Greek).

Epinephrine is synthesized in the medulla of the adrenal gland in an enzymatic pathway that converts the amino acid tyrosine into a series of intermediates and, ultimately, epinephrine. Tyrosine is first oxidized to L-DOPA, which is subsequently decarboxylated to give dopamine.

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what supports the adrenal glands

Benefits of Support Adrenals. Therapeutic support for the Adrenal Glands. Assists in the body's ability to fend off chronic stress. Helps with mental function and fatigue. Does not hyper stimulate compromised organ function. Assists in the reduction of inflammation. High in necessary B Vitamins to help with energy and chronic fatigue or stress.

The adrenal glands are small glands located on top of each kidney. They produce hormones that you can't live without, including sex hormones and cortisol. Cortisol helps you respond to stress and has many other important functions. With adrenal gland disorders, your glands make too much or not enough hormones. In Cushing's syndrome, there's too much cortisol, while with Addison's disease, there is too little. Some people are born unable to make enough cortisol.

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what is a stressor

A Stressor is anything (physical or psychological) that produces stress (negative or positive) is considered a stressor.

Physiologists define stress as how the body reacts to a stressor, real or imagined, a stimulus that causes stress. Acute stressors affect an organism in the short term; chronic stressors over the longer term. Alarm is the first stage, which is divided into two phases: the shock phase and the antishock phase. Shock phase: During this phase, the body can endure changes such as hypovolemia, hypoosmolarity, hyponatremia, hypochloremia, hypoglycemia—the stressor effect.

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what do sympathetic postganglionic neurons release

The postganglionic neurons of sweat glands release acetylcholine for the activation of muscarinic receptors. The chromaffin cells of the adrenal medulla are analogous to post-ganglionic neurons—the adrenal medulla develops in tandem with the sympathetic nervous system and acts as a modified sympathetic ganglion.

Upper motor neurons release a neurotransmitter, acetylcholine, from their axon terminal knobs, which are received by nicotinic receptors of the alpha motor neurons. In turn, alpha motor neurons relay the stimulus. From there, acetylcholine is released from the axon terminal knobs of alpha motor neurons and received by postsynaptic receptors (Nicotinic acetylcholine receptors) of muscles, thereby relaying the stimulus to contract muscle fibers.

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what is stressor

A stressor is a chemical or biological agent, environmental condition, external stimulus or an event that causes stress to an organism.[1]

Stress is the internal resistance, or counterforce, of a material to the distorting effects of an external force or load. These counterforces tend to return the atoms to their normal positions. The total resistance developed is equal to the external load. This resistance is known as stress.

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definition of repressor in biology

In molecular genetics, a repressor is a DNA-or RNA-binding protein that inhibits the expression of one or more genes by binding to the operator or associated silencers.

repression. 1. the act of restraining, inhibiting, or suppressing. 2. in molecular genetics, inhibition of gene transcription by a repressor. 3. in psychiatry, a defense mechanism by which a person unconsciously banishes unacceptable ideas, feelings or impulses from consciousness. A person using repression to obtain relief from mental conflict is unaware of “forgetting” unpleasant situations as a way of avoiding them.

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what human body system does erythropoietin regulate

Hormone, erythropoietin: Erythropoietin is a substance produced by the kidney that leads to the formation of red blood cells in the bone marrow. Abbreviated: EPO.The kidney cells that make EPO are specialized and are sensitive to low oxygen levels in the blood coming into the kidney.hese cells release erythropoietin when the oxygen level is low in the kidney. Erythropoietin stimulates the bone marrow to produce more red blood cells which in turn increases the oxygen-carrying capacity of the blood.

Erythropoietin is produced and released into the blood by the kidneys in response to low blood oxygen levels (hypoxemia). EPO is carried to the bone marrow, where it stimulates production of red blood cells. The hormone is active for a short period of time and then eliminated from the body in the urine.

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effects of sympathetic nervous system

As the SNS continues to trigger physical reactions, it causes a wear-and-tear on the body. It's not so much what chronic stress does to the nervous system, but what continuous activation of the nervous system does to other bodily systems that become problematic.

1 With the exception of the sweat glands (enervated by the sympathetic nervous system), the peripheral nervous system effects (on the cardiac conduction system, exocrine glands, and smooth muscle) mediated by muscarinic receptors are parasympathetic. With the exception of the sweat glands (enervated by the sympathetic nervous system), the peripheral nervous system effects (on the cardiac conduction system, exocrine glands, and smooth muscle) mediated by muscarinic receptors are parasympathetic.

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what part of the body is affected by stress

Stress can affect every part of your body. muscle aches, head aches, how your hair grows, the texture of your skin, it can affect your menstrual cycle.

Stress can affect all aspects of your life, including your emotions, behaviors, thinking ability, and physical health. No part of the body is immune. But, because people handle stress differently, symptoms of stress can vary.

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what is addison disease

In Addison's disease, the adrenal glands don't make enough of a hormone called cortisol, or less often, a related hormone called aldosterone. That's why doctors sometimes call the illness ''chronic adrenal insufficiency,'' or hypocortisolism.

11.08.12 l Leave a Comment. Addison’s disease, also known as primary adrenal insufficiency, is an endocrine condition involving destruction of parts of the adrenal gland (which sits atop the kidney), resulting in a deficiency of the steroid hormones produced by this gland, including cortisol and aldosterone.

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which gland releases epinephrine and norepinephrine

Adrenal medulla. The inner part of the adrenal gland. The adrenal medulla produces the hormones epinephrine (adrenaline), which stimulates the heart, tightens blood vessels, and relaxes some smooth muscles; and norepinephrine, which has similar effects. Mentioned in: Adrenal Gland Scan, Pheochromocytoma, Vasodilators.

A hormone that is secreted by the adrenal gland in response to physical or mental stress, as from fear, and is regulated by the autonomic nervous system. The release of epinephrine causes an increase in heart rate, blood pressure, and respiratory rate. Epinephrine also raises glucose levels in the blood for use as fuel when more alertness or greater physical effort is needed.

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what is cortisol pm

A cortisol test measures the level of the hormone cortisol in a 24-hour sample of urine. The cortisol level may show problems with the adrenal glands or the pituitary gland. Cortisol is made by the adrenal glands.

Cortisol is a steroid hormone released from the adrenal gland in response to ACTH, a hormone from the pituitary gland in the brain. Cortisol affects many different body systems. It plays a role in: 1 Bone.

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definition indolamines

Indolamines are a class of monoamines, and consist of the neurotransmitter serotonin. Epinephrine, which is released from the adrenal glands, stimulates the sympathetic nervous system. Monoamines are neuromodulators, which means they are able to stimulate many neurons located far away from each other.

Mesalamine is a medication that is licensed for the treatment of ulcerative colitis in adults. It helps to reduce symptoms of the condition by inhibiting the production of the chemicals that cause inflammation in the lining of the colon.

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what is normetanephrine

Normetanephrine is a metabolite of norepinephrine created by action of catechol-O-methyl transferase on norepinephrine.It is excreted in the urine and found in certain tissues. It is a marker for catecholamine-secreting tumors such as pheochromocytoma.ormetanephrine is a metabolite of norepinephrine created by action of catechol-O-methyl transferase on norepinephrine.

Norepinephrine (INN) (abbreviated norepi or NE) or noradrenaline (BAN) (abbreviated NA or NAd) is a. catecholamine with multiple roles including as a hormone and a neurotransmitter.[5] As a stress hormone, norepinephrine affects parts of the brain where attention and responding actions are controlled.

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which is not a catecholamine

Is GABA a catecholamine? No GABA is not a catecholamine. The catecholamine family is made up of epinephrine (Called adrenaline in the United Kingdom), norepinephrine (Called noradrenaline in the Unite … d Kingdom) and dopamine. These neurotransmitters are derived from tyrosine and phenylalanine, while GABA is derived from glutamate.

As members of both the neurotransmitter and hormone families, catecholamines are made by nerve tissue, the brain, and the adrenal glands located on top of your kidneys. The name catecholamine comes from the chemical structures of a benzene ring (termed catechol) and a nitrogen-containing group (amine).

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definition, stresses

Stress: In a medical or biological context stress is a physical, mental, or emotional factor that causes bodily or mental tension. Stresses can be external (from the environment, psychological, or social situations) or internal (illness, or from a medical procedure). Stress can initiate the fight or flight response, a complex reaction of neurologic and endocrinologic systems. Catecholamine hormones, such as adrenaline or noradrenaline, facilitate immediate physical reactions associated with a preparation for violent muscular action.

Definition. Stress is defined as an organism's total response to environmental demands or pressures. When stress was first studied in the 1950s, the term was used to denote both the causes and the experienced effects of these pressures. More recently, however, the word stressor has been used for the stimulus that provokes a stress response.

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does muscle inflammation cause cortisol

Cortisol is a powerful anti-inflammatory hormone, so you might think that high levels of it would protect us from inflammatory diseases like arthritis and heart disease. Unfortunately, it doesn't. Cortisol and cortisol-like medicines suppress inflammation by suppressing parts of the immune system. That makes us more susceptible to new infections, and sooner or later we will get them. The new infections will raise our inflammation and cortisol levels, making us susceptible to still more infections. And so on.

When cortisol is secreted, it causes a breakdown of muscle protein, leading to release of amino acids into the bloodstream. These amino acids are then used by the liver to synthesize glucose for energy, in a process called gluconeogenesis.

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what is autonomic reactivity

1. the extent or level to which an organism responds physiologically to a stimulus, such as a stressor in the environment. 2. a pattern of autonomic nervous system responses that become characteristic of an individual throughout life.

role of the autonomic nervous system in modulating the release of ANF remains controversial. Finally, there is growing evidence to suggest that there is a reciprocal interplay between ANF and the sympathetic nervous sys- tem in peripheral target tissues which may have important pathophysiological significance. Key words: Atrial natriuretic factor, Autonomic nervous system, Sympathetic nervous system, Blood pressure, Renal function Interactions between atrial natriuretic factor and the autonomic nervous system

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what is the main chemical stimulus autoregulation

Autoregulation is a process within many biological systems, resulting from an internal adaptive mechanism that works to adjust (or mitigate) that system's response to stimuli. While most systems of the body show some degree of autoregulation, it is most clearly observed in the kidney, the heart, and the brain. Perfusion of these organs is essential for life, and through autoregulation the body can divert blood (and thus, oxygen) where it is most needed. 1 Cerebral autoregulation.

The secretion of endogenous insulin is a response of the beta cells to a stimulus. The primary stimulus is glucose; others are amino acids, particularly leucine, and the 'gut hormones', such as secretin, pancreozymin and gastrin.he secretion of endogenous insulin is a response of the beta cells to a stimulus. The primary stimulus is glucose; others are amino acids, particularly leucine, and the 'gut hormones', such as secretin, pancreozymin and gastrin.

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what is cortisol am

Cortisol is the major adrenal steroid hormone and is controlled by the pituitary gland and the hypothalamus. The body’s stress response increases cortisol in order to mobilize energy to manage and resolve the stressor.

What is Cortisol? Cortisol is an important hormone produced by the adrenal glands, small endocrine glands that sit on top of our kidneys. Cortisol is secreted by the body in response to stress, and is one of the hormones our bodies secrete in what is known as the fight or flight response.. Cortisol, in turn, plays an important role in everything from how our bodies use glucose (sugar), to our blood pressure, to the function of our immune systems.

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difference between aldosterone and adh

1. ADH is synthesized in the hypothalamus while aldosterone is made in the adrenal cortex. 2. ADH conserves water directly through its reabsorption while aldosterone conserves water indirectly through the reabsorption of sodium.hese processes can be carried out by these two hormones. ADH is completely known as the antidiuretic hormone. It is also identified as AVP or arginine vasopressin or simply vasopressin. Basically, the difference between the two is regarding the mechanism of action.

Difference Between ADH and Aldosterone. Basic learners of Biology and the concept of the urinary system may somehow have difficulty in separating the roles of ADH and aldosterone. Fortunately for those who have taken advanced courses involving these concepts, the two terms are just like their everyday word.

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what is the stress hormone

Stress hormones are produced by your body in situations that might be perceived as potentially dangerous. Daily activities, physical and emotional, that cause increased anxiety may cause your body to release some of these hormones and may cause you to feel more stressed about a routine situation.hese hormones include glucagon, epinephrine (adrenaline), norepinephrine, cortisol, and growth hormone. They cause the liver to release glucose and the cells to release fatty acids for extra energy. If there’s not enough insulin present in the body, these extra fuels can build up and lead to hyperglycemia.

What Some Research Shows About Stress and Low T. Over the years, some studies have suggested that the stress hormone cortisol and the sex hormone testosterone work against each other. This has led to the theory that stress may cause infertility and loss of libido in men by inhibiting testosterone.

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which autonomic nervous system rules day to day life

Transmission of Autonomic Stimuli. Like other nerves, those of the autonomic nervous system convey their messages to the appropriate end organs (blood vessels, viscera, etc.) by releasing transmitter substances to which the receptors of the target cells are responsive.

The autonomic nervous system (ANS) is a part of the central nervous system, which controls visceral functions of the human body, e.g. blood pressure, gut motility, emptying the urinary bladder, regulation of body temperature, etc. These regulations occur promptly.

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what is adrenaline edu

To understand its effect on the body, one first must understand what adrenaline, or epinephrine, is. Epinephrine is a hormone released by the adrenal medulla located within the adrenal glands, atop the kidneys (Reece, et al. 528).

Epinephrine, also known as adrenaline, is a hormone secreted by the medulla (inner part) of the adrenal glands, located on the kidneys. The adrenal glands are one of the body's endocrine glands (glands producing substances that are distributed by way of the bloodstream).t is also the chemical agent that is responsible for transmission of nerve impulses in the sympathetic nervous system. When a person has certain tumors of the adrenal glands, large amounts of epinephrine and norepinephrine are produced, causing a great increase in blood pressure.

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what does the adrenal medulla secrete

It is the innermost part of the adrenal gland, consisting of cells that secrete epinephrine (adrenaline), norepinephrine (noradrenaline), and a small amount of dopamine in response to stimulation by sympathetic preganglionic neurons.he adrenal medulla consists of irregularly shaped cells grouped around blood vessels. These cells are intimately connected with the sympathetic division of the autonomic nervous system (ANS).

The smaller, inner region-the adrenal medulla-is part of the sympathetic nervous system and is the body's ... Click to read more below. The supraneal, or adrenal, glands are a pair of glands that secrete hormones directly into the bloodstream. Each gland can be divided into two distinct organs. The outer region, the adrenal cortex, secretes hormones which have important effects on the way in which energy is stored and food is used, on chemicals in the blood, and on characteristics such as hairiness and body shape.

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what are effectors biology

Effector. Definition. noun, plural: effectors. (biochemistry) A molecule that binds to a protein and affects the function of that protein. (physiology) An organ, a gland, or a muscle that can respond and becomes active in response to a stimulus (e.g. nerve impulse).upplement. In biochemistry, an effector is that molecule that binds to a specific protein, and regulates the latter's biological activity. An effector molecule acts as a ligand that is capable of increasing or decreasing the activity of that protein.

Used Occasionally. effector is one of the 30000 most commonly used words in the Collins dictionary

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what does our autonomic system control

Your autonomic nervous system is the part of your nervous system that controls involuntary actions, such as the beating of your heart and the widening or narrowing of your blood vessels. When something goes wrong in this system, it can cause serious problems, including. Blood pressure problems.

The autonomic nervous system is the part of the nervous system that automatically controls breathing, heart rate, blood pressure, sweating, and digestive function. Autonomic symptoms include shortness of breath, dizziness, fainting, rapid or slow heart rate, irregular heartbeats (palpitations), flushing, sweating, and nausea.

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Obestatin attenuated doxorubicin-induced cardiomyopathy via enhancing long noncoding Mhrt RNA expression.

Long non-coding RNAs in the failing heart and vasculature

Mitochondrial Dysfunction and Oxidative Damage inparkin-deficient Mice

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Raf/MAPK and rapamycin-sensitive pathways mediate the anti-apoptotic function of p21Ras in IL-3-dependent hematopoietic cells

E4BP4 is a cardiac survival factor and essential for embryonic heart development

High-affinity glucose uptake in Saccharomyces cerevisiae is not dependent on the presence of glucose-phosphorylating enzymes

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Time Course and Cellular Distribution of Hsp27 and Hsp72 Stress Protein Expression in a Quantitative Gerbil Model of Ischemic Injury and Tolerance: Thresholds for Hsp72 Induction and Hilar Lesioning in the Context of Ischemic Preconditioning

The Two Patterns of Reactive Astrocytosis in Postischemic Rat Brain

Porin channels in intact cells of Escherichia coli are not affected by Donnan potentials across the outer membrane.

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Studies on the substrate interactions with P-450 in drug hydroxylation by liver microsomes.

Short-term ethanol administration impairs the elimination of chlordiazepoxide (Librium®) in man

A new CYP21A2 nonsense mutation causing severe 21-hydroxylase deficiency

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An Immunocytochemical Approach to Detection of Mitochondrial Disorders

High-Content Screening for Compounds That Affect mtDNA-Encoded Protein Levels in Eukaryotic Cells

Inability of the Submaximal Treadmill Stress Test to Predict the Location of Coronary Disease

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Nuclear localization of the hypoxia-regulated pro-apoptotic protein BNIP3 after global brain ischemia in the rat hippocampus

In vivo Contributions of BH3-Only Proteins to Neuronal Death Following Seizures, Ischemia, and Traumatic Brain Injury

High-speed running performance is largely unaffected by hypoxic reductions in aerobic power

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Oxidized low-density lipoprotein (ox-LDL) accumulation is one of the critical determinants in endothelial dysfunction in many cardiovascular diseases such as atherosclerosis. C1q/TNF-related protein 9 (CTRP9) is identified to be an adipocytokine with cardioprotective properties. However, the potential roles of CTRP9 in endothelial function remain largely elusive. In the present study, the effects of CTRP9 on the proliferation, apoptosis, migration, angiogenesis, nitric oxide (NO) production and oxidative stress in human umbilical vein endothelial cells (HUVECs) exposed to ox-LDL were investigated. We observed that treatment with ox-LDL inhibited the proliferation, migration, angiogenesis and the generation of NO, while stimulated the apoptosis and reactive oxygen species (ROS) production in HUVECs. Incubation of HUVECs with CTRP9 rescued ox-LDL-induced endothelial injury. CTRP9 treatment reversed ox-LDL-evoked decreases in antioxidant enzymes including heme oxygenase-1 (HO-1), nicotinamide adenine dinucleotide phosphate (NAD(P)H) dehydrogenase quinone 1, and glutamate-cysteine ligase (GCL), as well as endothelial nitric oxide synthase (eNOS). Furthermore, CTRP9 induced activation of peroxisome proliferator-activated receptor γ co-activator 1α (PGC1-α) and phosphorylation of adenosine monophosphate-activated protein kinase (AMPK). Of interest, AMPK inhibition or PGC1-α silencing abolished CTRP9-mediated antioxidant enzymes levels, eNOS expressions, and endothelial protective effects. Collectively, we provided the first evidence that CTRP9 attenuated ox-LDL-induced endothelial injury by antioxidant enzyme inductions dependent on PGC-1α/AMPK activation.

The beating heart consumes more ATP per weight than any other organ. The machineries required for this are many and complex. Fuel and oxygen must be transported via the vasculature, absorbed by cardiomyocytes, broken down, and regulated to match cellular demands. Much of this occurs in mitochondria, which comprise fully one third of cardiac mass. The PGC-1 proteins are transcriptional coactivators that have emerged as powerful orchestrators of these numerous processes, ensuring their proper coregulation in response to intracellular and extracellular cues. An important role for PGC-1s in cardiac function has been revealed over the past few years, and more recently interest in their role in the vasculature has been burgeoning. We review this literature, focusing on recent developments.

The reduction of proline by Clostridium sporogenes NCIB8053 is coupled to transmembrane proton translocation in an uncoupler-sensitive fashion (and might therefore conserve free energy). This finding serves to explain the increase in the growth yield of this organism when proline is added to a defined growth medium containing glucose as the catabolic substrate.

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Multiple factors have been hypothesized over the years to be contributory and or causative for Parkinson’s disease (PD). Hereditary factors, although originally discounted, have recently emerged in the focus of PD research. The study of a large Italian family with PD using a genome scan approach led to the mapping of a PD susceptibility gene to the 4q21-q23 genomic region, where the gene for α-synuclein was previously mapped. Mutation analysis of the α-synuclein in four unrelated families with PD revealed a missense mutation segregating with the illness. α-Synuclein is an abundant presynaptic protein of the human brain of unknown function. It is conceivable that the mutation identified in the PD families may result in self-aggregation and or decreased degradation of the protein, leading to the development of intracytoplasmic inclusion bodies and eventually to neuronal cell death. Moreover, the discovery of a mutation in the synuclein gene may offer us new insights into the understanding of the pathways that lead to neuronal degeneration.

Parkinson’s disease is a common age-related neurodegenerative disease characterized pathologically by a loss of dopaminergic neurons in the substantia nigra with resultant depletion of striatal dopamine and presence of Lewy bodies in the remaining neurons. The Lewy body contains numerous functional and structural proteins, including α-synuclein and ubiquitin; aggregation of α-synuclein is thought to be important in Lewy body formation as well as neurodegeneration, although the detailed mechanisms remain to be defined. Increasing evidence has suggested that mitochondrial dysfunction, increased oxidative stress, and dysfunction of the ubiquitin-proteasome system may be involved in α-synuclein aggregation, Lewy body formation, and neurodegeneration. However, how these processes are related to each other is not fully understood, given that there are Parkinsonian animal models as well as human diseases with significant nigral neurodegeneration regardless of whether Lewy bodies form or not. This review summarizes the current related research fields and proposes a proteomic approach to investigate the mechanisms that may dictate α-synuclein aggregation, Lewy body formation, and neurodegeneration.

We prove that groups acting geometrically on delta-quasiconvex spaces contain no essential Baumslag-Solitar quotients as subgroups. This implies that they are translation discrete, meaning that the translation numbers of their nontorsion elements are bounded away from zero.

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The Role of Oxidative Stress in Myocardial Ischemia and Reperfusion Injury and Remodeling: Revisited

Xanthine oxidase inhibitor allopurinol attenuates the development of diabetic cardiomyopathy

Ischemia-reperfusion injury causes oxidative stress and apoptosis of Schwann cell in acute and chronic experimental diabetic neuropathy.

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Cerebroprotective effect of resveratrol through antioxidant and anti-inflammatory effects in diabetic rats

Ischemia-reperfusion injury causes oxidative stress and apoptosis of Schwann cell in acute and chronic experimental diabetic neuropathy.

MiR-146a negatively regulates TLR2-induced inflammatory responses in keratinocytes.

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The effects of age and resveratrol on the hypoxic preconditioning protection against hypoxia–reperfusion injury: studies in rat hearts and human cardiomyocytes

Inhibition of SIRT1 Impairs the Accumulation and Transcriptional Activity of HIF-1α Protein under Hypoxic Conditions

High-speed running performance is largely unaffected by hypoxic reductions in aerobic power

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Genetic studies reveal the role of the endocrine and metabolic systems in aging.

Activation-Induced Autophagy Is Preserved in CD4+ T-Cells in Familial Longevity

Exogenous growth factors do not affect the development of individually cultured murine embryos

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Exercise Training Stimulates Ischemia-Induced Neovascularization via Phosphatidylinositol 3-Kinase/Akt-Dependent Hypoxia-Induced Factor-1 Reactivation in Mice of Advanced Age

Angiotensin type 1 receptor blocker reduces intimal neovascularization and plaque growth in apolipoprotein E-deficient mice.

Inactivation of the NHEJ Activity of DNA-PKcs Prevents Fanconi Anemia Pre-Leukemic HSC Expansion

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Lack of glucose recycling between endoplasmic reticulum and cytoplasm underlies cellular dysfunction in glucose-6-phosphatase-beta-deficient neutrophils in a congenital neutropenia syndrome.

A Novel Homozygous Mutation in G6PC3 Presenting as Cyclic Neutropenia and Severe Congenital Neutropenia in the Same Family

A straightforward route to enantiopure 2-substituted-3,4-dehydro-β-proline via ring closing metathesis

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This article mainly presents a control method for an underactuated tractor-trailer vehicle, subject to the nonholonomic constraint, uncertain disturbance and various physical limits, which is aimed at receiving a good tracking performance. All in all, linear quadratic regulator (LQR) and model predictive control (MPC) are used to design the posture controller to make the midpoint of two parallel plating wheels for the underactuated trailer follow an arbitrary reference trajectory given by earth-fixed frame, and sliding mode control (SMC) is introduced to design the dynamic controller for the tracking of the desired velocities produced by the posture controller. The simulation results validate the control strategy consisting of the MPC-based kinematic controller and the SMC-based dynamic controller is rather effective and efficient for the underactuated tractor-trailer vehicle, thereby demonstrating the effectiveness and feasibility of the proposed controllers.

One of the most critical tasks in tractor operation is the accurate steering during field operations, e.g., accurate trajectory following during mechanical weeding or spraying, to avoid damaging the crop or planting when there is no crop yet. To automate the trajectory following problem of an autonomous tractor-trailer system and also increase its steering accuracy, a nonlinear model predictive control approach has been proposed in this paper. For the state and parameter estimation, moving horizon estimation has been chosen since it considers the state and the parameter estimation within the same problem and also constraints both on inputs and states can be incorporated. The experimental results show the accuracy and the efficiency of the proposed control scheme in which the mean values of the Euclidean error for the tractor and the trailer, respectively, are 6.44 and 3.61 cm for a straight line trajectory and 49.78 and 41.52 cm for a curved line trajectory.

Differentiation and dedifferentiation of vascular smooth muscle cells (VSMCs) are essential processes of vascular development. VSMC have biosynthetic, proliferative, and contractile roles in the vessel wall. Alterations in the differentiated state of the VSMC play a critical role in the pathogenesis of a variety of cardiovascular diseases, including atherosclerosis, hypertension, and vascular stenosis. This review provides an overview of the current state of knowledge of molecular mechanisms involved in the control of VSMC proliferation, with particular focus on mitochondrial metabolism. Mitochondrial activity can be controlled by regulating mitochondrial dynamics, i.e., mitochondrial fusion and fission, and by regulating mitochondrial calcium handling through the interaction with the endoplasmic reticulum (ER). Alterations in both VSMC proliferation and mitochondrial function can be triggered by dysregulation of mitofusin-2, a small GTPase associated with mitochondrial fusion and mitochondrial-ER interaction. Several lines of evidence highlight the relevance of mitochondrial metabolism in the control of VSMC proliferation, indicating a new area to be explored in the treatment of vascular diseases.

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Autophagy, an intralysosomal degradation of cells' own constituents that includes macro-, micro-, and chaperone-mediated autophagy, plays an important role in the renewal of cardiac myocytes. This cell type is represented by long-lived postmitotic cells with very poor (if any) replacement through differentiation of stem cells. Macroautophagy, the most universal form of autophagy, is responsible for the degradation of various macromolecules and organelles including mitochondria and is activated in response to stress, promoting cell survival. This process is also involved in programmed cell death when injury is irreversible. Even under normal conditions, autophagy is somewhat imperfect, underlying gradual accumulation of defective mitochondria and lipofuscin granules within aging cardiac myocytes. Autophagy is involved in the most important cardiac pathologies including myocardial hypertrophy, cardiomyopathies, and ischemic heart disease, a fact that has led to increasing attention to this process.

The ocean quahog Arctica islandica is one of the longest-living and slowest growing marine bivalves. The oldest specimens obtained for the present study approached 200 yr. To achieve such a long lifespan, accumulation of oxidative damage markers in tissues must ideally be main- tained at low levels over time, because the accumulating debris disturbs cellular functions. We inves- tigated shell growth and cellular aging in an Icelandic population of A. islandica. Specifically, we analyzed protein carbonyl concentration as a marker for the oxidative deterioration of tissue proteins, and the accumulation of the fluorescent age pigment lipofuscin over quahog lifetime in gill, mantle and adductor muscle. The very slow growth rates of A. islandica correlate with very efficient mainte- nance of body proteins compared to other, faster aging bivalves. Lipofuscin granules accumulated mainly in connective tissues of gill and mantle. Lowest lipofuscin accumulation was found in the adductor muscle, and there, only outside the myofibrils. Consistent with the pleiotropic theory of aging, A. islandica seems to trade slow growth and late onset of reproduction for a very efficient autophagic potential that mitigates oxidative damage accumulation and supports long lifetime and presumably reproduction in very old ocean quahog.

Autophagy is a catabolic mechanism, allowing the degradation of cytoplasmic content via lysosomal activity. Several forms of autophagy are described in mammals. Macroautophagy leads to integration of cytoplasmic portions into vesicles named autophagosomes that ultimately fuse with lysosomes. Chaperone-mediated autophagy is in contrast the direct translocation of protein in lysosomes. Macroautophagy is central to lymphocyte homeostasis. Although its role is controversial in lymphocyte development and in naive cell survival, it seems particularly involved in the maintenance of certain lymphocyte subtypes. Its importance in memory B and T cells biology has recently emerged. Moreover, some effector cells like plasma cells rely on autophagy for survival. Autophagy is central to glucose and lipid metabolism, and to the maintenance of organelles like mitochondria and endoplasmic reticulum. In addition macroautophagy, or individual components of its machinery, are also actors in antigen presentation by B cells, a crucial step to receive help from T cells, this crosstalk favoring their final differentiation into memory or plasma cells. Autophagy is deregulated in several autoimmune or autoinflammatory diseases like systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, and Crohn's disease. Some treatments used in these pathologies impact autophagic activity, even if the causal link between autophagy regulation and the efficiency of the treatments has not yet been clearly established. In this review, we will first discuss the mechanisms linking autophagy to lymphocyte subtype survival and the signaling pathways involved. Finally, potential impacts of autophagy modulation in lymphocytes on the course of these diseases will be approached.

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ABSTRACTMitochondria are essential organelles that produce ATP and regulate cell growth, proliferation, and cell death. To maintain homeostasis, fusion and fission of mitochondria must be strictly regulated. Even though oligomerization of ATP synthase could affect the mitochondrial morphology, the exact mechanism is not clear. We confirmed that structure and function of ATP5B, which is a major component of the catalytic center of ATP synthase complexes, are closely connected to the mitochondrial morphology. ATP5B itself can enhance elongation of mitochondria. Moreover, mutations of the threonine residue at β-barrel domain, and the serine residue at nucleotide-binding domain of ATP5B, produce the opposite effect on the fission and fusion of mitochondrial networks. Here, we demonstrate that ATP5B is clearly involved in the mechanism of regulation for mitochondrial fusion and fission in mammalian cells.

Human induced pluripotent stem cells (iPSCs) can be differentiated in vitro into bona fide cardiomyocytes for disease modelling and personalized medicine. Mitochondrial morphology and metabolism change dramatically as iPSCs differentiate into mesodermal cardiac lineages. Inhibiting mitochondrial fission has been shown to promote cardiac differentiation of iPSCs. However, the effect of hydrazone M1, a small molecule that promotes mitochondrial fusion, on cardiac mesodermal commitment of human iPSCs is unknown. Here, we demonstrate that treatment with M1 promoted mitochondrial fusion in human iPSCs. Treatment of iPSCs with M1 during embryoid body formation significantly increased the percentage of beating embryoid bodies and expression of cardiac-specific genes. The pro-fusion and pro-cardiogenic effects of M1 were not associated with changes in expression of the α and β subunits of adenosine triphosphate (ATP) synthase. Our findings demonstrate for the first time that hydrazone M1 is capable of promoting cardiac differentiation of human iPSCs, highlighting the important role of mitochondrial dynamics in cardiac mesoderm lineage specification and cardiac development. M1 and other mitochondrial fusion promoters emerge as promising molecular targets to generate lineages of the heart from human iPSCs for patient-specific regenerative medicine.

We prove that groups acting geometrically on delta-quasiconvex spaces contain no essential Baumslag-Solitar quotients as subgroups. This implies that they are translation discrete, meaning that the translation numbers of their nontorsion elements are bounded away from zero.

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This study was designed to characterize changes in the expression of mitofusin-1 (Mfn1) and fission-1 (Fis1), as well as in mitochondrial morphology in the kidney of rats subjected to chronic fluorosis and to elucidate whether any mitochondrial injury observed is associated with increased oxidative stress. Sixty Sprague-Dawley (SD) rats were divided randomly into 3 groups of 20 each, i.e., the untreated control group (natural drinking water containing

To investigate the effect of excessive fluoride on the mitochondrial function of cardiomyocytes, 20 healthy male mice were randomly divided into 2 groups of 10, as follows: control group (animals were provided with distilled water) and fluoride group (animals were provided with 150 mg/L F- drinking water). Ultrastructure and pathological morphological changes of myocardial tissue were observed under the transmission electron and light microscopes, respectively. The content of hydrolysis ATP enzyme was observed by ATP enzyme staining. The expression levels of ATP5J and ATP5H were measured by Western blot and quantitative real-time PCR. The morphology and ultrastructure of cardiomyocytes mitochondrial were seriously damaged by fluoride, including the following: concentration of cardiomyocytes and inflammatory infiltration, vague myofilaments, and mitochondrial ridge. The damage of mitochondrial structure was accompanied by the significant decrease in the content of ATP enzyme for ATP hydrolysis in the fluoride group. ATP5J and ATP5H expressions were significantly increased in the fluoride group. Thus, fluoride induced the mitochondrial dysfunction in cardiomyocytes by damaging the structure of mitochondrial and interfering with the synthesis of ATP. The proactive ATP5J and ATP5H expression levels were a good response to the mitochondrial dysfunction in cardiomyocytes.

Oxidative stress (OS) is thought to play an important role in the pharmacological and toxic effects of various drugs of abuse. Herein we review the literature on the mechanisms responsible for the cardiovascular and hepatic toxicity of cocaine with special focus on OS-related mechanisms. We also review the preclinical and clinical literature concerning the putative therapeutic effects of OS modulators (such as N-acetylcysteine, superoxide dismutase mimetics, nitroxides and nitrones, NADPH oxidase inhibitors, xanthine oxidase inhibitors, and mitochondriotropic antioxidants) for the treatment of cocaine toxicity. We conclude that available OS modulators do not appear to have clinical efficacy.

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Sphingosine-1-phosphate (S1P) plays important roles in cardiovascular development and immunity. S1P is abundant in plasma because erythrocytes-the major source of S1P-lack any S1P-degrading activity; however, much remains unclear about the source of the plasma S1P precursor, sphingosine (SPH), derived mainly from the hydrolysis of ceramides by the action of ceramidases that are encoded by 5 distinct genes, acid ceramidase 1 ( ASAH1)/ Asah1, ASAH2/ Asah2, alkaline ceramidase 1 ( ACER1)/ Acer1, ACER2/ Acer2, and ACER3/ Acer3, in humans/mice. Previous studies have reported that knocking out Asah1 or Asah2 failed to reduce plasma SPH and S1P levels in mice. In this study, we show that knocking out Acer1 or Acer3 also failed to reduce the blood levels of SPH or S1P in mice. In contrast, knocking out Acer2 from either whole-body or the hematopoietic lineage markedly decreased the blood levels of SPH and S1P in mice. Of interest, knocking out Acer2 from whole-body or the hematopoietic lineage also markedly decreased the levels of dihydrosphingosine (dhSPH) and dihydrosphingosine-1-phosphate (dhS1P) in blood. Taken together, these results suggest that ACER2 plays a key role in the maintenance of high plasma levels of sphingoid base-1-phosphates-S1P and dhS1P-by controlling the generation of sphingoid bases-SPH and dhSPH-in hematopoietic cells.-Li, F., Xu, R., Low, B. E., Lin, C.-L., Garcia-Barros, M., Schrandt, J., Mileva, I., Snider, A., Luo, C. K., Jiang, X.-C., Li, M.-S., Hannun, Y. A., Obeid, L. M., Wiles, M. V., Mao, C. Alkaline ceramidase 2 is essential for the homeostasis of plasma sphingoid bases and their phosphates.

Sphingolipid metabolism starts with the biosynthesis of ceramide, a bioactive lipid and the backbone for the biosynthesis of complex sphingolipids such as sphingomyelin and glycosphingolipids. These are degraded back to ceramide and then to sphingosine, which enters the ceramide–sphingosine-1-phosphate signaling pathway or is further degraded. Several enzymes with multiple catalytic properties and subcellular localizations are thus involved in such metabolism. Hereditary defects of lysosomal hydrolases have been known for several years to be the cause of lysosomal storage diseases such as gangliosidoses, Gaucher disease, Niemann–Pick disease, Krabbe disease, Fabry disease, and Farber disease. More recently, many other inborn errors of sphingolipid metabolism have been recognized, involving enzymes responsible for the biosynthesis of ceramide, sphingomyelin, and glycosphingolipids. Concurrently, epidemiologic and biochemical evidence has established a link between Gaucher disease and Parkinson’s disease, showing that glucocerebrosidase variants predispose individuals to α-synuclein accumulation and neurodegeneration even in the heterozygous status. This appears to be due not only to lysosomal overload of non-degraded glucosylceramide, but to the derangement of vesicle traffic and autophagy, including mitochondrial autophagy, triggered by both sphingolipid intermediates and misfolded proteins. In this review, old and novel disorders of sphingolipid metabolism, in particular those of ganglioside biosynthesis, are evaluated in light of recent investigations of the link between Gaucher disease and Parkinson’s disease, with the aim of better understanding their pathogenic mechanisms and addressing new potential therapeutic strategies.

The antithesis of Specker's theorem states that every sequence eventually hounded away from each point of [0,1] is eventually bounded away from [0,1]. We show constructively (that is, with intuitionistic logic) that this is equivalent to a version of the fan theorem.

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Epigenetic control of gene expression is a consistent feature of differentiated mammalian cell types. Epigenetic expression patterns are mitotically heritable and are stably maintained in adult cells. However, unlike somatic DNA mutation, little is known about the occurrence of epigenetic change, or epimutation, during normal adult life. We have monitored the age-associated maintenance of two epigenetic systems--X inactivation and genomic imprinting--using the genes Atp7a and Igf2, respectively. Quantitative measurements of RNA transcripts from the inactive and active alleles were performed in mice from 2 to 24 months of age. For both genes, older animal cohorts showed reproducible increases in transcripts expressed from the silenced alleles. Loss of X chromosome silencing showed cohort mean increases of up to 2.2%, while imprinted-gene activation increased up to 6.7%. The results support the hypothesis that epigenetic loss of gene repression occurs in normal tissues and may be a contributing factor in progressive physiological dysfunction seen during mammalian aging. Quantitatively, the loss of epigenetic control may be one to two orders of magnitude greater than previously determined somatic DNA mutation.

Autophagy is a major cellular recycling process that delivers cellular material and entire organelles to lysosomes for degradation, in a selective or non-selective manner. This process is essential for the maintenance of cellular energy levels, components and metabolites, as well as the elimination of cellular molecular damage, thereby playing an important role in numerous cellular activities. An important function of autophagy is to enable survival under starvation conditions and other stresses. The majority of factors implicated in ageing are modifiable through the process of autophagy, including the accumulation of oxidative damage and loss of proteostasis, genomic instability and epigenomic alteration. These primary causes of damage could lead to mitochondrial dysfunction, deregulation of nutrient sensing pathways and cellular senescence, finally causing a variety of ageing phenotypes. Remarkably, advances in the biology of ageing have revealed that ageing is a malleable process: a mild decrease in signalling through nutrient-sensing pathways can improve health and extend lifespan in all model organisms tested. Consequently, autophagy is implicated in both ageing and age-related disease. Enhancement of the autophagy process is a common characteristic of all principal, evolutionary conserved anti-ageing interventions, including dietary restriction, as well as inhibition of target of rapamycin (TOR) and insulin/IGF-1 signalling (IIS). As an emerging and critical process in ageing, this review will highlight how autophagy can be modulated for health improvement.

Blunt trauma abdomen rarely leads to gastrointestinal injury in children and isolated gastric rupture is even rarer presentation. We are reporting a case of isolated gastric rupture after fall from height in a three year old male child.

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Neuroprotective effects of Rhizoma Dioscoreae polysaccharides against neuronal apoptosis induced by in vitro hypoxia

Mitochondrial Inner Membrane Electrophysiology Assessed by Rhodamine-123 Transport and Fluorescence

High-speed running performance is largely unaffected by hypoxic reductions in aerobic power

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Cytochrome Oxidase Repair during Treatment of Copper Deficiency: Relation to Mitochondrial Turnover*

SPECTROPHOTOMETRIC STUDIES XI. THE DIRECT MICRO SPECTROPHOTOMETRIC DETERMINATION OF CYTOCHROME C

Mitochondrial Dysfunction and Oxidative Damage inparkin-deficient Mice

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Dynamic Changes in the Nigrostriatal Pathway in the MPTP Mouse Model of Parkinson's Disease

Microglia derive from progenitors, originating from the yolk sac, and which proliferate in the brain

Cardiac sympathetic denervation is not related to nigrostriatal degeneration in Parkinson’s disease

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Mitochondrial permeability and ATPase activity.

Functional remodeling of heart mitochondria in acute diabetes: interrelationships between damage, endogenous protection and adaptation.

Targeting TAO kinases using a new inhibitor compound delays mitosis and induces mitotic cell death in centrosome amplified breast cancer cells.

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A randomized clinical trial of coenzyme Q10 and GPI-1485 in early Parkinson disease

The Sources of Reactive Oxygen Species and Its Possible Role in the Pathogenesis of Parkinson's Disease

High-affinity glucose uptake in Saccharomyces cerevisiae is not dependent on the presence of glucose-phosphorylating enzymes

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Caenorhabditis elegans Aurora A kinase AIR-1 is required for postembryonic cell divisions and germline development

Aurora/Ipl1p-related kinases, a new oncogenic family of mitotic serine-threonine kinases.

Artificial incubation does not affect the post-hatch development, health, or survival of the Lance-tailed Manakin (Chiroxiphia lanceolata), a tropical passerine

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A concept of biological aging: The role of compensatory processes

Review of cell aging in Drosophila and mouse

An instrumental variable approach finds no associated harm or benefit from early dialysis initiation in the United States

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Cytokines Inhibit p 53-Mediated Apoptosis but Not p 53-Mediated G 1 Arrest

Oncogenic ras and p53 cooperate to induce cellular senescence

Proinflammatory Cytokines Are Soluble Mediators Linked with Ventricular Arrhythmias and Contractile Dysfunction in a Rat Model of Metabolic Syndrome

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Phosphorus Magnetic Resonance Spectroscopy Studies of the Role of Mitochondria in the Disease Process

Exogenous ethyl pyruvate versus pyruvate during metabolic recovery after oxidative stress in neonatal rat cerebrocortical slices.

Exogenous growth factors do not affect the development of individually cultured murine embryos

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Cell loss in retinal dystrophies by apoptosis--death by informed consent!

Inducible apoptosis-promoting activity in retinal cell-conditioned medium.

Cardiac sympathetic denervation is not related to nigrostriatal degeneration in Parkinson’s disease

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Neuronal Protective Role of PBEF in a Mouse Model of Cerebral Ischemia

Brain Injury Does Not Alter the Intrinsic Differentiation Potential of Adult Neuroblasts

High-affinity glucose uptake in Saccharomyces cerevisiae is not dependent on the presence of glucose-phosphorylating enzymes

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Matrine Exerts Hepatotoxic Effects via the ROS-Dependent Mitochondrial Apoptosis Pathway and Inhibition of Nrf2-Mediated Antioxidant Response

The role of Ca+2 on rhein-induced apoptosis in human cervical cancer Ca Ski cells.

High-speed running performance is largely unaffected by hypoxic reductions in aerobic power

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Label-Free Proteomic Analysis of Molecular Effects of 2-Methoxy-1,4-naphthoquinone on Penicillium italicum

The circadian protein CLOCK regulates cell metabolism via the mitochondrial carrier SLC25A10.

Gap junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo

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Protective effects of XBP1 against oxygen and glucose deprivation/reoxygenation injury in rat primary hippocampal neurons

Deficiency of SUMO-specific protease 1 induces arsenic trioxide-mediated apoptosis by regulating XBP1 activity in human acute promyelocytic leukemia

High-speed running performance is largely unaffected by hypoxic reductions in aerobic power

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Apnea produces excitotoxic hippocampal synapses and neuronal apoptosis

Title Sex-specific hippocampus volume changes in obstructive sleep apnea

High-affinity glucose uptake in Saccharomyces cerevisiae is not dependent on the presence of glucose-phosphorylating enzymes

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The destruction of organic model substances by indirect electrooxidation was investigated. The oxidation agent Co(II1) was used because of the high redox potential of the Co(III)/Co(II) redox couple (E0 = 1.808 V). Experiments were performed in a batch and in a continuous electrolytic cell by using various model substances (especially phenol and different chlorophenols). Intermediate and final products of the oxidation were identified and quantified. Organic carbon is ultimately transformed to CO2 and to small amounts of CO. The residual carbon in the process solution was determined by TOC measurement to be about 20 ppm. Organic chlorine is oxidized via chlorate to perchlorate. The remaining amount of adsorbahle organic halogens (AOX) was less than 3 ppm. Based on these results, a pilot plant was constructed and is presently in operation.

With the development of human society, discharge of toxic organics in industrial waste water increased sharply. It is difficult to treat these types of waste water efficiently by traditional bio-process to meet the more critical discharge standard. Advanced oxidation processes (AOPs) attracted more and more attention as efficient methods to remove the toxic organics from waste water. Compared with other AOPs, electrochemical oxidation process was considered as an effective and environmental friendly process due to its simplicity in operation, robustness in system configuration, strong oxidizing ability, reliable performance for a wide variety of toxic organics and chemical reagents free.

Aging is an agglomerate of biological long-lasting processes that result being inevitable. Main actors in this scenario are both long-term inflammation and oxidative stress. It has been proved that oxidative stress induce alteration in proteins and this fact itself is critically important in the pathophysiological mechanisms leading to diseases typical of aging. Among reactive species, chlorine ones such as hypochlorous acid (HOCl) are cytotoxic oxidants produced by activated neutrophils during chronic inflammation processes. HOCl can also cause damages by reacting with biological molecules. HOCl is generated by myeloperoxidase (MPO) and augmented serum levels of MPO have been described in acute and chronic inflammatory conditions in cardiovascular patients and has been implicated in many inflammatory diseases such as atherosclerosis, neurodegenerative conditions, and some cancers. Due to these data, we decided to conduct an up-to-date review evaluating chlorinative stress effects on every age-related disease linked; potential anti-oxidant countermeasures were also assessed. Results obtained associated HOCl generation to the aging processes and confirmed its connection with diseases like neurodegenerative and cardiovascular pathologies, atherosclerosis and cancer; chlorination was mainly linked to diseases where molecular (protein) alteration constitute the major suspected cause: i.e. inflammation, tissue lesions, DNA damages, apoptosis and oxidative stress itself. According data collected, a healthy lifestyle together with some dietary suggestion and/or the administration of nutracetical antioxidant integrators could balance the effects of chlorinative stress and, in some cases, slow down or prevent the onset of age-releated diseases.

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Use of the conventional cancer chemotherapy (i.e. vincristine) is limited in tumor cells exhibiting pre-existing or acquired resistance. Here, we found that C6 ceramide (C6) dramatically sensitized vincristine's activity. In vitro, C6 and vincristine coadministration induced substantial necrosis and apoptosis in multiple human cancer cell lines, which were accompanied by a profound AMP-activated protein kinase (AMPK) activation, subsequent p53 activation, mTORC1 inactivation and Bcl-2/HIF-1α downregulation. Such synergistic effects were attenuated by AMPK inactivation through genetic mutation or short hairpin RNA silencing. Coadministration-activated p53 translocated to mitochondria, and formed a complex with cyclophilin-D, leading to mitochondrial permeability transition pore opening and cell necrosis. Disrupting p53-Cyp-D complexation through pharmacological or genetic means reduced costimulation-induced cytotoxicity. In vivo, a liposomal C6 was synthesized, which dramatically enhanced the antiproliferative activity of vincristine on HCT-116 or A2780 xenografts. Together, C6 sensitizes vincristine-induced anticancer activity in vivo and in vitro, involving activating AMPK-p53 signaling.

Autophagy is essential for optimal cell function and survival, and the entire process accompanies membrane dynamics. Ceramides are produced by different enzymes at different cellular membrane sites and mediate differential signaling. However, it remains unclear which ceramide-producing pathways/enzymes participate in autophagy regulation under physiological conditions such as nutrient starvation, and what the underlying mechanisms are. In this study, we demonstrate that among ceramide-producing enzymes, neutral sphingomyelinase 2 (nSMase2) plays a key role in autophagy during nutrient starvation. nSMase2 was rapidly and stably activated upon starvation, and the enzymatic reaction in the Golgi apparatus facilitated autophagy through the activation of p38 MAPK and inhibition of mTOR. Moreover, nSMase2 played a protective role against cellular damage depending on autophagy. These findings suggest that nSMase2 is a novel regulator of autophagy and provide evidence that Golgi-localized ceramides participate in cytoprotective autophagy against starvation.

ABSTRACTUNC-45A is an ubiquitously expressed protein highly conserved throughout evolution. Most of what we currently know about UNC-45A pertains to its role as a regulator of the actomyosin system...

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Oxidative stress in astrocytes has been observed in a number of pathological conditions, however the effect of nitric oxide on oxidatively stressed astrocytes remains unclear. The goal of this research was to determine how nitric oxide influences the mechanism of peroxide-induced oxidative stress in astrocytes. We used enriched mouse-astrocyte cultures and tertiary-butyl hydroperoxide to study astrocyte oxidative stress. Cellular integrity was measured at the ultrastructural level by electron microscopy and plasma membrane integrity measured by lactate dehydrogenase release. Mitochondrial swelling and disruption of cristae were observed by electron microscopy in the absence of damage to other organelles. Astrocytes exposed to peroxide eventually succumbed to necrotic loss of plasma membrane integrity. However, when astrocytes were subjected to oxidative stress in the presence of nitric oxide, mitochondrial integrity was preserved and cell death delayed. This protection of nitric oxide resembled that of iron chelation and nitric oxide reduced susceptibility usually associated with iron-loaded astrocytes exposed to oxidative stress. Taken together, these data suggest that nitric oxide can act as a powerful antioxidant for astrocytes preserving mitochondrial and cellular integrity during oxidative stress.

Melatonin protects the electron transport chain (ETC) in multiple ways. It reduces levels of ·NO by downregulating inducible and inhibiting neuronal nitric oxide synthases (iNOS, nNOS), thereby preventing excessive levels of peroxynitrite. Both ·NO and peroxynitrite-derived free radicals, such as ·NO2, hydroxyl (·OH) and carbonate radicals (CO3·-) cause blockades or bottlenecks in the ETC, by ·NO binding to irons, protein nitrosation, nitration and oxidation, changes that lead to electron overflow or even backflow and, thus, increased formation of superoxide anions (O2·-). Melatonin improves the intramitochondrial antioxidative defense by enhancing reduced glutathione levels and inducing glutathione peroxidase and Mn-superoxide dismutase (Mn-SOD) in the matrix and Cu,Zn-SOD in the intermembrane space. An additional action concerns the inhibition of cardiolipin peroxidation. This oxidative change in the membrane does not only initiate apoptosis or mitophagy, as usually considered, but also seems to occur at low rate, e.g., in aging, and impairs the structural integrity of Complexes III and IV. Moreover, elevated levels of melatonin inhibit the opening of the mitochondrial permeability transition pore and shorten its duration. Additionally, high-affinity binding sites in mitochondria have been described. The assumption of direct binding to the amphipathic ramp of Complex I would require further substantiation. The mitochondrial presence of the melatonin receptor MT1 offers the possibility that melatonin acts via an inhibitory G protein, soluble adenylyl cyclase, decreased cAMP and lowered protein kinase A activity, a signaling pathway shown to reduce Complex I activity in the case of a mitochondrial cannabinoid receptor.

Blunt trauma abdomen rarely leads to gastrointestinal injury in children and isolated gastric rupture is even rarer presentation. We are reporting a case of isolated gastric rupture after fall from height in a three year old male child.

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Using highly purified recombinant mitochondrial aconitase, we determined the kinetics and mechanisms of inactivation mediated by nitric oxide (NO), nitrosoglutathione (GSNO), and peroxynitrite (ONOO–). High NO concentrations are required to inhibit resting aconitase. Brief NO exposures led to a reversible inhibition competitive with isocitrate (KI = 35 μM). Subsequently, an irreversible inactivation (0.65 M− 1 s− 1) was observed. Irreversible inactivation was mediated by GSNO also, both in the absence and in the presence of substrates (0.23 M− 1 s− 1). Peroxynitrite reacted with the [4Fe-4S] cluster, yielding the inactive [3Fe-4S] enzyme (1.1 × 105 M− 1 s− 1). Carbon dioxide enhanced ONOO–-dependent inactivation via reaction of CO3− with the [4Fe-4S] cluster (3 × 108 M− 1 s− 1). Peroxynitrite also induced m-aconitase tyrosine nitration but this reaction did not contribute to enzyme inactivation. Computational modeling of aconitase inactivation by O2− and NO revealed that, when NO is produced and readily consumed, measuring the amount of active aconitase remains a sensitive method to detect variations in O2− production in cells but, when cells are exposed to high concentrations of NO, aconitase inactivation does not exclusively reflect changes in rates of O2− production. In the latter case, extents of aconitase inactivation reflect the formation of secondary reactive species, specifically ONOO− and CO3−, which also mediate m-aconitase tyrosine nitration, a footprint of reactive NO-derived species.

Diabetes mellitus (DM) is characterized by chronic hyperglycemia resulting from defects in the secretion and/or action of insulin. Diabetic nephropathy (DN) develops in diabetic patients and is characterized by a progressive deterioration of renal function. The mitochondrial electron transport chain (ETC) produces most of the reactive oxygen species (ROS) that are involved in diabetic nephropathy. Due to the high incidence of DM in the elderly, the aim of this study was to evaluate oxidative and nitrosative stress in kidney mitochondria from aged rats. We evaluated lipid peroxidation (LPO), nitric oxide (NO(•)) production, S-nitrosylation profiles, glutathione levels, and glutathione reductase and aconitase activities under streptozotocin (STZ)-induced experimental diabetes in kidney mitochondria from aged rats. The results showed an increase in LPO, NO(•) production, and S-nitrosylated proteins in rats with STZ-induced diabetes. A decrease in glutathione (GSH) levels and glutathione reductase (GR) and aconitase activities in the rats that received the STZ-induced diabetes treatment was also observed, when compared with the age-related controls. The data suggest that oxidative and nitrosative stresses promote mitochondrial oxidative dysfunction in the more advanced age rat kidney in STZ-induced diabetes.

The effect of hyperoxia on activity of the superoxide-sensitive citric acid cycle enzyme aconitase was measured in cultured human epithelial-like A549 cells and in rat lungs. Rapid and progressive loss of > 80% of the aconitase activity in A549 cells was seen during a 24-hr exposure to a PO2 of 600 mmHg (1 mmHg = 133 Pa). Inhibition of mitochondrial respiratory capacity correlated with loss of aconitase activity in A549 cells exposed to hyperoxia, and this effect could be mimicked by fluoroacetate (or fluorocitrate), a metabolic poison of aconitase. Exposure of rats to an atmospheric PO2 of 760 mmHg or 635 mmHg for 24 hr caused respective 73% and 61% decreases in total lung aconitase activity. We propose that early inactivation of aconitase and inhibition of the energy-producing and biosynthetic reactions of the citric acid cycle contribute to the sequelae of lung damage and edema seen during exposure to hyperoxia.

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Moringin Pretreatment Inhibits the Expression of Genes Involved in Mitophagy in the Stem Cell of the Human Periodontal Ligament

Mitofusins Mfn1 and Mfn2 coordinately regulate mitochondrial fusion and are essential for embryonic development

Lectins as mitosis stimulating factors: Briefly reviewed

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Neurotoxicity from glutathione depletion is mediated by Cu-dependent p53 activation.

Ribosomal protein S3 gene expression of Chironomus riparius under cadmium, copper and lead stress

High-affinity glucose uptake in Saccharomyces cerevisiae is not dependent on the presence of glucose-phosphorylating enzymes

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Sirt6 mRNA-incorporated endothelial microparticles (EMPs) attenuates DM patient-derived EMP-induced endothelial dysfunction

Sirt6-induced autophagy restricted TREM-1-mediated pyroptosis in ox-LDL-treated endothelial cells: relevance to prognostication of patients with acute myocardial infarction

The Mediatorless Electroanalytical Sensing of Sulfide Utilizing Unmodified Graphitic Electrode Materials

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Explicit construction of characteristic classes

Spring 5-15-2018 Regulators on Higher Chow Groups

Cardiac sympathetic denervation is not related to nigrostriatal degeneration in Parkinson’s disease

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Abstract 3379: cGMP Specific Phosphodiesterase Type 5A Activity is Regulated by S-nitrosylation at Cys 181

S-Nitrosylation in Cardiovascular Signaling

Phosphorylation of S409/410 of TDP-43 is a consistent feature in all sporadic and familial forms of TDP-43 proteinopathies

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Mitochondria represent approximately one-third of the mass of the heart and play a critical role in maintaining cellular function-however, they are also a potent source of free radicals and pro-apoptotic factors. As such, maintaining mitochondrial homeostasis is essential to cell survival. As the dominant source of ATP, continuous quality control is mandatory to ensure their ongoing optimal function. Mitochondrial quality control is accomplished by the dynamic interplay of fusion, fission, autophagy, and mitochondrial biogenesis. This review examines these processes in the heart and considers their role in the context of ischemia-reperfusion injury. Interventions that modulate mitochondrial turnover, including pharmacologic agents, exercise, and caloric restriction are discussed as a means to improve mitochondrial quality control, ameliorate cardiovascular dysfunction, and enhance longevity.

The maintenance of the proteome is essential to preserve cell functionality and the ability to respond and adapt to the changing environment. This is regulated by the proteostasis network, a dedicated set of molecular components comprised of molecular chaperones and protein clearance mechanisms, regulated by cell stress signaling pathways, that prevents the toxicity associated with protein misfolding and accumulation of toxic aggregates in different subcellular compartments and tissues. The efficiency of the proteostasis network declines with age and this failure in protein homeostasis has been proposed to underlie the basis of common age-related human disorders. The current advances in the understanding of the mechanisms and regulation of proteostasis and of the different types of digressions in this process in aging have turned the attention toward the therapeutic opportunities offered by the restoration of proteostasis in age-associated degenerative diseases. Here, we discuss some of the unresolved questions on proteostasis that need to be addressed to enhance healthspan and to diminish the pathology associated with persistent protein damage.

The ability to change the degree of hybridization of a donor electron state between the coulombic potential of its donor atom and that of a nearby quantum well in a silicon transistor has now been achieved. This is a promising step in the development of atomic-scale quantum control.

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Previous studies have shown that the bcl-2 gene encodes a mitochondrial protein that contributes to neoplastic cell expansion primarily by promoting cell survival through interference with "programmed cell death" (PCD), also termed "apoptosis." Because many chemotherapeutic drugs are capable of initiating pathways leading to apoptosis, we determined whether deregulated bcl-2 expression could render cells resistant to several drugs commonly used in the treatment of non-Hodgkin's lymphomas, including dexamethasone (DEX), methotrexate (MTX), 1-beta-D-arabinofuranosyl-cytosine (Ara-C), etoposide (VP-16), vincristine (VC), cisplatin (CP), and hydroperoxycyclophosphamide (4-HC). For these experiments, we achieved high levels of p26-Bcl-2 protein production in a human pre-B-cell leukemia line 697 by stable infection with a recombinant bcl-2-containing retrovirus and then compared these cells with control virus-infected 697 cells. Control 697 cells were induced to undergo apoptosis by all drugs tested as defined by DNA degradation into oligonucleosomal-length fragments, cell shrinkage, and subsequent cell death. In contrast, 697 cells with elevated Bcl-2 protein levels exhibited strikingly prolonged cell survival and markedly reduced DNA fragmentation when cultured in the presence of these antineoplastic agents. Although high levels of Bcl-2 protein protected 697 cells from the acute cytotoxic effects of DEX and the other drugs tested, Bcl-2 did not prevent these drugs from suppressing the proliferation of 697 cells. However, when 697 cells were treated with DEX or MTX for 3 days, then washed and cultured in semisolid media without drugs, bcl-2-virus-infected cells gave rise to colonies at much higher frequencies than 697 cells stably infected with control virus. These results indicate that by protecting 697 leukemic cells from the acute cytotoxicity of DEX and some other chemotherapeutic drugs, high levels of p26-Bcl-2 can create the opportunity for re-initiation of cell growth when drugs are withdrawn. The findings may be relevant to clinical correlative studies of non-Hodgkin's lymphoma patients that have found an association between worse prognosis and bcl-2 gene rearrangements or t[14;18] translocations.

We tested the effects of theophylline, a phosphodiesterase inhibitor inducing intracellular accumulation of cyclic adenosine monophosphate (cAMP), on malignant B cells from 15 patients with B-chronic lymphocytic leukemia (B-CLL). We observed a large increase in apoptotic cell numbers (mean, 90% v 20% in medium alone) in the presence of theophylline (100 micrograms/mL) or chlorambucil (10 mumol/L) after 72 hours of incubation. Maximal apoptosis (90%) was reached after 36 hours when the two drugs were used together at fourfold lower concentrations, indicating a synergistic effect; no effect was observed with normal B cells, suggesting that the combination might have therapeutic interest. Chlorambucil induced intracellular Ca+2 influx, pointing to the involvement of two signaling pathways that might explain its synergy with theophylline through their effects on oncogenes. The expression of bcl-2 protein, a proto-oncogene inhibiting apoptosis, decreased after incubation with the drugs, while c-myc, recently described as having a potent role in apoptosis, was overexpressed. For p53 we observed an overexpression in the presence of chlorambucil or both theophylline-chlorambucil and a decrease after theophylline incubation. Chlorambucil- and theophylline-induced apoptosis was partially inhibited by interleukin-4 (IL-4), which also abrogated the effects on oncogene expression. These results provide insight into the mechanisms underlying B-CLL apoptosis and suggest that the theophylline-chlorambucil combination may be of therapeutic value in this setting.

Accepted features of neurodegenerative disease include mitochondrial and protein folding dysfunction and activation of pro-death factors. Neurons that experience high metabolic demand or those found in organisms with genetic mutations in proteins that control cell stress may be more susceptible to aging and neurodegenerative disease. In neurons, events that normally promote growth, synapse formation and plasticity are also often deployed to control neurotoxicity. Such protective strategies are coordinated by master stress-fighting proteins. One such specialized protein is the anti-cell death Bcl-2 family member Bcl-xL, whose myriad death-protecting functions include enhancement of bioenergetic efficiency, prevention of mitochondrial permeability transition channel activity, protection from mitochondrial outer membrane permeabilization to pro-apoptotic factors, and improvement in the rate of vesicular trafficking. Synapse formation and normal neuronal activity provide protection from neuronal death. Therefore Bcl-xL brings about synapse formation as a neuroprotective strategy. In this review we will consider how this multi-functional master regulator protein uses many strategies to enhance synaptic and neuronal function and thus counteracts neurodegenerative stimuli.

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