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Agentic and Language Techniques Research

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Methotrexate osteopathy in rheumatic disease. OBJECTIVE: To determine whether two adults with stress fractures receiving low weekly doses of methotrexate had methotrexate osteopathy. CASE REPORTS: Two adult patients developed features consistent with methotrexate osteopathy while receiving low weekly doses of methotrexate. METHODS: Iliac crest biopsy samples were taken and bone histomorphometry carried out. RESULTS: Symptoms resolved when the methotrexate was discontinued. Bone histology showed changes consistent with osteoblast inhibition by methotrexate. CONCLUSIONS: When given in low doses for prolonged periods, methotrexate may have adverse effects on bone, particularly in post-menopausal women.

[Iliac crest biopsy samples <Multi-tissue_structure>] [bone <Tissue>] [Bone <Tissue>] [osteoblast <Cell>] [bone <Organ>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Spacing effects on the memory for faces. 25 undergraduate women studied 12 stimulus pictures of female faces successively presented in spaced or massed conditions and made affective judgments for the pictures along a dimension of like to dislike. One week after the exposure (study) period, subjects were given an identification test comprised of photographs of the same female faces with different expressions. Analysis showed that the pictures presented in the spaced condition were more frequently and accurately identified than those presented under the massed condition and that affective judgment was unrelated to conditions of presentation.

[faces <Organism_subdivision>] [faces <Organism_subdivision>] [faces <Organism_subdivision>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Relative phage haplotype frequencies in PAO1 samples, (A) planktonic, (B) biofilm 4 days, (C) biofilm 11 days.

[biofilm <Cell>] [biofilm <Cell>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Background Opioid analgesics are generally used to combat the pain associated with cancerous conditions. These agents not only inhibit respiratory function and cause constipation, but also induce other significant side effects such as addiction and tolerance, all of which further contribute to a reduced quality of life for cancer patients. Thus, in the present study, the effects of electro-acupuncture treatment (EA) on mechanical allodynia were examined in a cancer pain mouse model.

[cancerous <Pathological_formation>] [respiratory <Anatomical_system>] [cancer <Pathological_formation>] [cancer <Pathological_formation>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Absence of microbiota (germ-free conditions) accelerates the atherosclerosis in ApoE-deficient mice fed standard low cholesterol diet. AIM: The aim of our work was to determine the influence of intestinal bacteria on the development of atherosclerotic lesions using apolipoprotein E (ApoE)-deficient knockout mice. METHODS: The experiments were performed on ApoE-/--deficient mouse strain C57BL/6, bred under germ-free (GF) conditions for two generations or under conventional conditions with defined microflora (CV). The mice were fed a standard low cholesterol diet or cholesterol-rich diet for 3-4 months. We studied the development of advanced lesions in the thoracic and abdominal aorta by histological, morphometric and immunohistological methods. RESULTS: Conventionally reared ApoE-/- mice (containing no pathogenic intestinal microbiota) and fed a standard low cholesterol diet in contrast to a high cholesterol diet did not develop atherosclerotic aortic plaques. In contrast, ApoE-/- mice reared under germfree conditions for 2 generations and fed a low cholesterol diet exhibited atherosclerotic plaques in the aorta. Characteristic lipid deposition with foam cells and macrophages was found in their arterial walls. CONCLUSION: In contrast to the absence of atherosclerotic plaques in conventionally reared ApoE-deficient mice, germ-free ApoE-/- mice consuming the same low cholesterol standard diet developed atherosclerotic plaques in the aorta. Differences in atherosclerotic plaques between GF and CV ApoE-/- mice are not so apparent when mice are fed a high cholesterol diet. Our findings thus document the protective effect of microbiota (commensal bacteria) on atherosclerosis development.

[intestinal <Multi-tissue_structure>] [atherosclerotic lesions <Pathological_formation>] [lesions <Pathological_formation>] [thoracic <Multi-tissue_structure>] [abdominal aorta <Multi-tissue_structure>] [intestinal <Multi-tissue_structure>] [atherosclerotic aortic plaques <Pathological_formation>] [atherosclerotic plaques <Pathological_formation>] [aorta <Multi-tissue_structure>] [cells <Cell>] [macrophages <Cell>] [arterial walls <Multi-tissue_structure>] [atherosclerotic plaques <Pathological_formation>] [atherosclerotic plaques <Pathological_formation>] [aorta <Multi-tissue_structure>] [atherosclerotic plaques <Pathological_formation>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

A potential role for the Src-like adapter protein SLAP-2 in signaling by the colony stimulating factor-1 receptor. The development of macrophages from myeloid progenitor cells is primarily controlled by the growth factor colony stimulating factor-1 (CSF-1) and its cognate receptor, a transmembrane tyrosine kinase encoded by the c-Fms proto-oncogene. The CSF-1 receptor exerts its biological effects on cells via a range of signaling proteins including Erk1/2 and Akt. Here we have investigated the potential involvement of the Src-like adapter protein (SLAP-2) in signaling by the CSF-1 receptor in mouse bone marrow-derived macrophages. RT-PCR analysis revealed constitutive expression of the SLAP-2 gene in bone marrow macrophages. Surprisingly, co-immunoprecipitation and GST binding experiments demonstrated that the CSF-1 receptor could bind to SLAP-2 in a ligand-independent manner. Furthermore, the binding of SLAP-2 to the CSF-1 receptor involved multiple domains of SLAP-2. SLAP-2 also bound c-Cbl, with the interaction being mediated, at least in part, by the unique C-terminal domain of SLAP-2. Overexpression of SLAP-2 in bone marrow macrophages partially suppressed the CSF-1-induced tyrosine phosphorylation and/or expression level of a approximately 80 kDa protein without affecting CSF-1-induced global tyrosine phosphorylation, or activation of Akt or Erk1/2. Significantly, CSF-1 stimulation induced serine phosphorylation of SLAP-2. Pharmacologic inhibition of specific protein kinases revealed that CSF-1-induced phosphorylation of SLAP-2 was dependent on JNK activity. Taken together, our results suggest that SLAP-2 could potentially be involved in signaling by the CSF-1 receptor.

[macrophages <Cell>] [myeloid progenitor cells <Cell>] [transmembrane <Cellular_component>] [cells <Cell>] [bone marrow <Multi-tissue_structure>] [macrophages <Cell>] [bone marrow macrophages <Cell>] [bone marrow macrophages <Cell>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

In vitro cytotoxic potential and mechanism of action of selected coumarins, using human renal cell lines. This study determined the selective cytotoxicity of eight coumarin compounds to human renal carcinoma cells, relative to non-carcinoma proximal tubular cells. Selectivity cytotoxicity was observed following exposure to 6-nitro-7-hydroxycoumarin (6-NO(2)-7-OHC) and 7,8-dihydroxycoumarin (7,8-OHC). 6-NO(2)-7-OHC induced cytotoxicity was irreversible in both cell lines, unlike 7,8-OHC, which was reversible in the carcinoma cells only. Mobility shift and BrdU incorporation assays showed that both compounds did not intercalate DNA but had a concentration-dependent inhibitory effect on its synthesis. All coumarins studied were found to be non-mutagenic using the standard Ames test. These results would suggest that 6-NO(2)-7-OHC and 7,8-OHC might have a therapeutic role to play in the treatment of renal cell carcinoma.

[renal cell lines <Cell>] [renal carcinoma cells <Cell>] [non-carcinoma proximal tubular cells <Cell>] [cell lines <Cell>] [carcinoma cells <Cell>] [renal cell carcinoma <Pathological_formation>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

ERK signaling is involved in decreasing BDNF-induced gene activity via Eph receptors Data provided so far suggest that ephrin-A5 might counteract BDNF-mediated gene expression and growth cone responses via decreasing ERK activity and nuclear localization (Figs. 2 and 3). To test this hypothesis more directly, we analyzed whether Eph forward signaling can still suppress BDNF-stimulated IEG induction and growth cone collapse when ERK kinase activity was experimentally raised. For this, ERK activity was elevated by expressing constitutively-active MEK1 (CA-MEK1), an ERK upstream activator, in cortical neurons (Fig. S3). Subsequently, neurons were subjected to either an ephrin-A5 mediated growth cone collapse assay (Fig. 5) or stimulated with guidance cues for 20 minutes and IEG mRNA levels were quantified via qRT-PCR (Fig. 6). 10.1371/journal.pone.0026089.g005 Figure 5 Constitutively-active MEK1 blocks ephrin-A5 mediated growth cone collapse. Wild-type neurons were electroporated with vectors expressing GFP (control; A, C, E) or expressing a FLAG-tagged constitutively-active MEK1 (CA-MEK1; B, D, F). Neurons were treated with ephrin-A5-Fc for 30 min followed by visualization of GFP (A, C, E) or CA-MEK-1 (green in B, D, F), F-actin and betaIII tubulin. (A, B) Overexpression of CA-MEK1 (B) reduces mean neurite length compared to a control GFP-expressing neuron (A). (C-F) A control growth cone without ephrin-A5 application (C) typically protrudes multiple filopodia (arrow). CA-MEK-1 expressing growth cones (D) were indistinguishable from a GFP-expressing growth cone. Note that CA-MEK1 was expressed in a dot-like pattern in the growth cone (arrowheads in D and F). Upon ephrin-A5 application, a control growth cone (E) collapsed resulting in only few filopodia. In contrast, a CA-MEK1 expressing growth cone (F) was only partially collapsed and many filopodia structures were preserved after ephrin-A5 induction. (G) Quantification of average neurite length. (H, I) Quantification of growth cone area (H) and filopodia number/growth cone (I) in the four conditions. Ephrin-A5 induces a growth cone collapse, resulting in reduced growth cone area and filopodia number in GFP but not CA-MEK1 expressing neurons. Scale-bar (A, B) = 10 microm; (C-F) = 2 microm. 10.1371/journal.pone.0026089.g006 Figure 6 Ephrin-A5 suppresses BDNF-induced IEG responses via MAP kinase signaling. Wild-type cortical neurons, mock-electroporated (black bars) or with a vector expressing constitutively-active MEK1 (white bars), were treated with guidance cues for 20 minutes as depicted, followed by mRNA quantification. In mock-electroporated neurons, BDNF induced an IEG response of c-fos (A), Egr1 (B), Egr2 (C) and Arc (D). Co-application of ephrin-A5 and BDNF reduced mRNA levels of all four IEGs in mock-electroporated neurons (A-D). In contrast, expression of constitutively-active MEK1 prevented Eph forward signaling from suppressing BDNF-evoked IEG responses. This was most evident for the IEGs Egr1 (B) and Egr2 (C). First of all, we analyzed the impact of CA-MEK1 on neurite outgrowth and ephrin-A5 mediated growth cone responses (Fig. 5). The average neurite length of neurons overexpressing CA-MEK1 (Fig. 5B) was clearly reduced compared to control GFP expressing neurons (Fig. 5A; see quantification in (G)). Growth cones of GFP (C) and CA-MEK1 expressing neurons were similar and protruded many filopodia (arrows in Fig. 5C-F). CA-MEK1 expression in growth cones was confined to individual dot-like structures (arrowheads in Fig. 5D, F). Ephrin-A5 application on a GFP expressing control growth cone (Fig. 5E) resulted in a growth cone collapse as revealed by reduced overall growth cone area and filopodia number (quantified in Fig. 5H, I). In contrast, in neurons overexpressing CA-MEK1 (Fig. 5F), ephrin-A5 induced only a partial growth cone collapse. Thus, growth cone area and filopodia number were not reduced (see Fig. 5H, I). This result suggests that an ephrin-A5 induced signaling cascade targets MAP kinase signaling to exert a full growth cone collapse. This result is in contrast to a recent report [46] which excluded ERK signaling downstream of an ephrin-A5 mediated growth cone collapse. Next, we tested whether ephrin-A5 signaling suppresses ERK kinase signaling also to interfere with BDNF-mediated gene expression (Fig. 6). In agreement with previous results (Fig. 4), in mock-electroporated neurons, ephrin-A5 incubation reduced the BDNF-mediated up-regulation of c-fos (Fig. 6A), Egr1 (Fig. 6B), Egr2 (Fig. 6C) and Arc (Fig. 6D) mRNA. In contrast, in neurons over-expressing CA-MEK1, ephrin-A5 could not suppress BDNF-induced IEG responses to the same degree. Particularly Egr1 (Fig. 6B) and Egr2 (Fig. 6C) mRNA levels were almost identical when comparing neurons treated with BDNF alone and neurons with BDNF and ephrin-A5 together. Thus, ephrin-A5 represses gene activity elicited by BDNF at least in part via MAP kinases. Besides IEGs, we inspected the influence of both guidance cues on cytoskeletal genes, whose gene products might modulate cytoskeletal dynamics evoked by ephrin-As and/or neurotrophins (Fig. S4). Therefore, the filamentous actin (F-actin) stabilizing tropomyosins (Tpm1 and Tpm2), the F-actin cross-linker alpha-actinin 1 (Actn1) and the motor protein dynein light chain 1 (Dnal1) were analyzed. mRNA levels of other cytoskeletal genes were not altered by any of the guidance cues (i.e. cofilin, filamin A, mena, vinculin and smooth muscle actin; data not shown). Short-term stimulation with guidance cues did not result in major alterations of cytoskeletal mRNA levels except for upregulation of Tpm1 by ephrin-A5 (Fig. S4A). At 16h of incubation, both tropomyosin genes were induced by BDNF and ephrin-A5 alone and both together (Fig. S4B, D). Actn1 levels were induced by individual application of ephrin-A5 and BDNF and by co-application of both (Fig. S4F). A similar profile was observed for the dynein light chain (Fig. S4H). Taken together, cytoskeletal gene expression was modulated by ephrin-A5 and BDNF. In contrast to the antagonistic impact on the IEG gene response (Figs. 4 and 6), ephrin-A5 and BDNF resulted in rather synergistic action on cytoskeletal gene expression. This difference might be due to short-term (i.e. 20 minutes) vs. long-term (i.e. 16h) exposure of both guidance cues in the IEG and cytoskeletal gene response, respectively.

[growth cone <Cellular_component>] [nuclear <Cellular_component>] [growth cone <Cellular_component>] [cortical neurons <Cell>] [neurons <Cell>] [growth cone <Cellular_component>] [growth cone <Cellular_component>] [neurons <Cell>] [Neurons <Cell>] [neurite <Cellular_component>] [neuron <Cell>] [growth cone <Cellular_component>] [filopodia <Cellular_component>] [growth cones <Cellular_component>] [growth cone <Cellular_component>] [growth cone <Cellular_component>] [growth cone <Cellular_component>] [filopodia <Cellular_component>] [growth cone <Cellular_component>] [filopodia <Cellular_component>] [neurite <Cellular_component>] [growth cone <Cellular_component>] [filopodia <Cellular_component>] [growth cone <Cellular_component>] [growth cone <Cellular_component>] [growth cone <Cellular_component>] [filopodia <Cellular_component>] [neurons <Cell>] [cortical neurons <Cell>] [neurons <Cell>] [neurons <Cell>] [neurite <Cellular_component>] [growth cone <Cellular_component>] [neurite <Cellular_component>] [neurons <Cell>] [neurons <Cell>] [Growth cones <Cellular_component>] [neurons <Cell>] [filopodia <Cellular_component>] [growth cones <Cellular_component>] [growth cone <Cellular_component>] [growth cone <Cellular_component>] [growth cone <Cellular_component>] [filopodia <Cellular_component>] [neurons <Cell>] [growth cone <Cellular_component>] [growth cone <Cellular_component>] [filopodia <Cellular_component>] [growth cone <Cellular_component>] [growth cone <Cellular_component>] [neurons <Cell>] [neurons <Cell>] [neurons <Cell>] [neurons <Cell>] [cytoskeletal <Cellular_component>] [cytoskeletal <Cellular_component>] [filamentous <Cellular_component>] [cytoskeletal <Cellular_component>] [smooth muscle <Tissue>] [cytoskeletal <Cellular_component>] [cytoskeletal <Cellular_component>] [cytoskeletal <Cellular_component>] [cytoskeletal <Cellular_component>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Stimulation of the sodium pump by azide and high internal sodium: changes in the number of pumping sites and turnover rate. 1. The effects of 5 mM azide on [3H]ouabain uptake and 22Na efflux were determined. Both glycoside uptake and 22Na efflux were enhanced by azide. 2. Azide stimulated the Na pump in muscles whose pumping sites had been inhibited by ouabain and then transferred to a glycoside-free solution. This stimulation was observed before detecting any recovery of the initial pumping activity. 3. When both the resting and the azide-stimulated 22Na efflux had been blocked by ouabain, an additional exposure to azide, in a ouabain-free solution, had no further effects on 22Na efflux. 4. It is concluded that the increase in Na pumping caused by azide is due in part to an increase in the number of pumping sites. 5. [3H]ouabain binding was measured in muscles with different intracellular alkali cation concentrations. Variations in [Na]i from 15 up to 50 mM did not significantly affect the amount of glycoside bound. A substantial increase in binding occurred when [Na]i reached 70 mM. 6. It is proposed that the increase in Na extrusion that occurs during the recovery of Na loaded muscles mostly results from an increased turnover rate of the pump rather than from an increase in number of pumping sites.

[muscles <Tissue>] [muscles <Tissue>] [intracellular <Immaterial_anatomical_entity>] [muscles <Tissue>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Lactotransferrin binding to its platelet receptor inhibits platelet aggregation. A fluorescent lactotransferrin probe was prepared by coupling 5-(([2-(carbhydrazino)methyl]-thio)acetyl)amino fluorescein to aldehyde groups that were produced by a mild periodic-acid oxidation of the glycan moieties of lactotransferrin. In this manner, the receptor-binding site of the lactotransferrin remains active in contrast to the binding site of the lactotransferrin derivatized with fluorescein isothiocyanate. The fluorescent probe allowed us to characterize, by flow cytometry, the binding of lactotransferrin to non-activated human platelets. The putative lactotransferrin platelet receptor was purified and its immunological and physico-chemical properties were found to be very similar to those of the receptor previously isolated from activated human lymphocytes. Lactotransferrin inhibits ADP-induced platelet aggregation at concentrations down to 5 nM, which can be reached in the plasma after leukocyte degranulation. Inhibition of platelet aggregation was also observed with the N-terminal fragment of lactotransferrin (residues 3-281; 50% inhibition = 2 microM) and with CFQWQRNMRKVRGPPVSC synthetic octodecapeptide (residues 20-37; 50% inhibition = 20 microM) corresponding to one of the two external loops (residues 28-34 and 39-42) where we recently located the receptor-binding site. The activity (50% inhibition = 500 microM) of the tetrapeptide KRDS (residues 39-42), which has already been described, was at least 25-times and 16000-times lower than the activity of the octodecapeptide and of the lactotransferrin molecules, respectively. Finally, the inhibition was demonstrated to be mediated by a mechanism which requires the binding of lactotransferrin to its putative receptor and not to platelet glycoprotein IIb-IIIa.

[platelet <Cell>] [platelet <Cell>] [platelets <Cell>] [platelet <Cell>] [lymphocytes <Cell>] [platelet <Cell>] [plasma <Organism_substance>] [leukocyte <Cell>] [platelet <Cell>] [platelet <Cell>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Effects of hypertension and sympathetic denervation on cerebral blood flow in newborn pigs. To investigate the potential role of sympathetic nerves in preventing pronounced increases in cerebral blood flow, we evaluated the effects of abrupt hypertension on the cerebral circulation of newborn pigs with intact cerebral sympathetic innervation and after cerebral sympathetic denervation. Epinephrine infusion was used to induce abrupt increases in mean (+/- SEM) arterial pressure (innervated pigs, 62 +/- 3 mm of Hg to 115 +/- 3 mm of Hg; denervated pigs, 71 +/- 4 mm of Hg to 132 +/- 4 mm of Hg) that remained increased for the 3 minutes of the study. Abrupt hypertension increased blood flow to all brain regions. In denervated pigs, the increased flow to the cerebrum was prolonged, compared with that in pigs with intact sympathetic innervation. Differences between pigs of the innervated and denervated groups were not apparent, with respect to blood flow to any other region (caudate region, brain stem, cerebellum). In newborn pigs, sympathetic nerves may attenuate hypertension-induced increases in blood flow to the cerebrum, but do not appear to affect flow to the rest of the brain.

[cerebral <Organ>] [blood <Organism_substance>] [nerves <Multi-tissue_structure>] [cerebral <Organ>] [blood <Organism_substance>] [cerebral <Organ>] [cerebral <Organ>] [cerebral <Organ>] [arterial <Multi-tissue_structure>] [blood <Organism_substance>] [brain <Organ>] [cerebrum <Multi-tissue_structure>] [blood <Organism_substance>] [brain stem <Multi-tissue_structure>] [cerebellum <Multi-tissue_structure>] [nerves <Multi-tissue_structure>] [blood <Organism_substance>] [cerebrum <Multi-tissue_structure>] [brain <Organ>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Introduction Yeast infections cause significant mortality in critically ill and immunocompromised patients. In particular, Candida species are the 4th most common cause of nosocomial bloodstream infections in the United States, and Cryptococcus neoformans, the commonest cause of fungal meningitis worldwide [1], [2]. Whilst Candida albicans remains the leading pathogenic yeast, infections due to non-C. albicans species such as Candida glabrata, as well as previously rare opportunists such as Trichosporon and Geotrichum species, are increasingly reported [1], [3]-[6]. Novel pathogenic Candida species such as Candida nivariensis and Candida bracarensis have also been described [7]. Since many non-C. albicans Candida and non-Candida yeasts are resistant or less susceptible to antifungal agents, rapid accurate species identification is central to timely, effective antifungal therapy [3]-[6], [8], [9]. Conventional phenotypic-based methods for yeast identification, however, are slow (24-72 h), insensitive and often unable to identify more unusual species. Various molecular techniques including real-time PCR, DNA sequence analysis, microarray analysis, and fluorescence in-situ hybridization provide accurate identification [10], [11] but are expensive, require substantial specimen processing time (hours to a day) and are not easily implemented as routine techniques in the clinical laboratory. Matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) has emerged as a powerful and rapid tool for the identification of bacterial and yeast pathogens [12]-[17]. Using MALDI-TOF MS, the protein spectral "fingerprint" of an isolate is compared to a reference spectral database for identification [18]. Previous studies have reported species identification rates of 92-99% amongst collections of yeasts and yeast-like organisms [14]-[17], [19], [20]. However, taken collectively, the results may not be directly comparable since these studies have used different approaches to assign species - from comparing spectra from test organisms to reference spectra in MALDI-TOF MS databases [16], [20], to enhancing these databases, and in some instances developing study-specific databases, with "in-house" spectral signatures [14], [15]. There also is a continuing need to extend the repository of reference spectra in MALDI-TOF MS databases. We therefore undertook the present study to evaluate the utility of the MALDI Biotyper 2.0 Microflex LT spectrometer (Bruker Daltonik GmbH; Bremen, Germany) with its current spectral database in comparison with phenotypic-based methods for the identification of a broad range of yeasts in a diagnostic laboratory. The first part of the study comprised testing of reference and clinical strains from our culture collection. The second was a blinded prospective analysis of freshly-collected yeast isolates recovered during routine laboratory work flow; discrepant results between MALDI TOF MS and phenotypic methods were resolved using sequence analysis of the fungal internal transcribed spacer (ITS) regions [21], [22]. Results obtained by preparation of yeasts by extraction of fungal proteins and by direct application of yeast colonies onto the MALDI TOF MS plate were also compared.

[blood <Organism_substance>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

No evidence for an influence of the human platelet antigen-1 polymorphism on the antiplatelet effects of glycoprotein IIb/IIIa inhibitors. This study investigated the hypothesis that the human platelet antigen-1 (HPA-1) polymorphism may influence the antiplatelet effects of glycoprotein (GP)IIb/IIIa inhibitors. Adenosine diphosphate (30 micro mol)-induced fibrinogen binding was measured by flow cytometry. Abciximab (0.03-3 micro g/ml), tirofiban (0.3-30 nmol/l) or eptifibatide (0.01-1 micro g/ml) were incubated for 15 min with the samples prior to stimulation. IC(50) values for the inhibition of fibrinogen binding were determined from each experiment. All subjects were genotyped by GALIOS and automated fluorescence correlation spectroscopy. Although a marked variability in the inhibitory effects of all three GPIIb/IIIa inhibitors was confirmed, there were no significant differences between the genotypes with respect to the inhibition of fibrinogen binding. Thus, the present study does not provide evidence for an effect of HPA-1 polymorphism on the inter-individual variability in the platelet inhibitory effects of the three GPIIb/IIIa inhibitors approved for clinical use.

[platelet <Cell>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Outcomes The primary outcomes of this study are smoking abstinence rates post release as well as number of days to first cigarette after release. Seven day point-prevalence abstinence will be determined by combining self-reported tobacco use over the prior seven days and urine cotinine assays (below 200 ng/ml versus 200 or above). Participants with self-reported abstinence and cotinine levels below the cut-off will be classified as abstinent. Participants lost to follow-up will be considered non-abstinent. A secondary analysis will examine the effect of length of forced abstinence on quit rates.

[urine <Organism_substance>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

[Suppurated acute obstructive cholangitis. Anatomoclinical and therapeutic aspects]. A total of 134 cases are discussed, with suppurated acute obstructive angiocholitis, that underwent surgical treatment over a period of 10 years, representing 12,8% of the total number of organic obstructions of the hepato-choledocus. From the standpoint of the etiopathogenic mechanisms the angiocholitis was determined by biliary lithiasis in 59 cases, by sclerosis of the Oddi sphincter in 5 cases, by postoperative cicatriceal stenosis of the main biliary pathway in 2 cases, by hepatic hydatitosis in 16 cases, by Vater ampuloma in 10 cases by cancers of the main biliary pathway in 40 cases and by the congenital cyst of the choledocus in one case. The high frequency was noted, of the severe forms of ictero-uremigenic angiocholitis (representing 68 cases, or 50,7% of the total, with a death rate of 34%). Medico-surgical treatment should be performed as early as possible, and it must be intensive, complex, and adapted to the anatomo-clinical forms. The authors performed evacuation choledocotomy with external draining in 22 cases (3 deaths), and choledoco-duodenal anastomosis in 46 cases (10 deaths), choledoco-jejunostomia in 3 cases, Oddi sphincterotomia in 12 cases (2 deaths) ampulectomia in 5 cases (2 deaths). Peripheral bilio-hepatodigestive anastomoses were performed in 40 cases with 5 deaths.

[hepato-choledocus <Multi-tissue_structure>] [Oddi sphincter <Tissue>] [hepatic <Organ>] [cancers <Pathological_formation>] [cyst <Pathological_formation>] [choledocus <Multi-tissue_structure>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Treatment effects on nigrostriatal projection integrity in partial 6-OHDA lesions: comparison of L-DOPA and pramipexole. There is controversy over potential effects of dopaminergic replacement therapies on the partially lesioned nigrostriatal dopaminergic projection. We evaluated indirect (levodopa, L-DOPA) versus direct (pramipexole, PRA) dopaminergic treatment effects on nigrostriatal lesion severity as measured with vesicular monoamine transporter type-2 (VMAT2) binding. Prior studies have shown that striatal VMAT2 density provides an objective estimate of dopaminergic neuronal integrity, without confounding effects of compensatory regulation. Partial unilateral median forebrain bundle lesions were made by injection of 6-hydroxydopamine in adult male Sprague-Dawley rats. Lesion severity was estimated using rotational behavior after injections of apomorphine and amphetamine. Rats were ranked and matched in pairs by rotation and assigned to receive either PRA (1 mg/kg/day) or L-DOPA/benserazide (100/25 mg/kg/day) ip via osmotic pump. After 4 weeks of drug treatment, in vitro autoradiography was performed with [(3)H]methoxytetrabenazine to measure striatal VMAT2 binding density. Lesion-to-intact VMAT2 density correlated with rotation in both treatment groups. There was no treatment effect on VMAT2 expression in the partially lesioned striatum and thus no differential effect of indirect versus direct dopamimetic treatment on nigrostriatal integrity.

[nigrostriatal <Multi-tissue_structure>] [lesions <Pathological_formation>] [lesioned nigrostriatal <Multi-tissue_structure>] [nigrostriatal lesion <Pathological_formation>] [striatal <Multi-tissue_structure>] [neuronal <Cell>] [unilateral median forebrain bundle lesions <Multi-tissue_structure>] [Lesion <Pathological_formation>] [striatal <Multi-tissue_structure>] [Lesion <Pathological_formation>] [lesioned striatum <Multi-tissue_structure>] [nigrostriatal <Multi-tissue_structure>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Mineralization (red) of the aorta is prevented by local (left), but not global (right), Mgp expression.

[aorta <Multi-tissue_structure>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

The effects of oxidative stress on in vivo brain GSH turnover in young and mature mice. Glutathione (GSH) synthetase activities and GSH turnover rates were examined during severe oxidative stress in the mouse brain as induced by t-butylhydroperoxide (t-BuOOH). Brain GSH synthetase activities in 8-mo-old mice in the cortex, striatum, thalamus, hippocampus, midbrain, and cerebellum were found to increase following t-BuOOH treatment. The effect of GSH synthesis on brain GSH turnover rates for 2- and 8-mo-old mice were determined after intracerebroventricular (icv) injection of [35S]cysteine. Rate constants for GSH turnover were determined by least-squares iterative minimization from the specific activity data from 20 min to 108 h after [35S]cysteine administration. GSH and glutathione disulfide (GSSG) specific activities were determined after separation by high-pressure liquid chromatography (HPLC). The half-life of GSH in the 2-mo-old mouse was 59.5 h and in the 8-mo-old mouse was 79.1 h. In summary, defense mechanisms against oxidative stress in the brain differ with age. Young mice can increase the cellular availability of GSH, whereas mature mice can increase GSH synthetase activity during oxidative stress. These differences make mature mice more susceptible to brain oxidative damage.

[brain <Organ>] [brain <Organ>] [Brain <Organ>] [cortex <Multi-tissue_structure>] [striatum <Multi-tissue_structure>] [thalamus <Multi-tissue_structure>] [hippocampus <Multi-tissue_structure>] [midbrain <Multi-tissue_structure>] [cerebellum <Multi-tissue_structure>] [brain <Organ>] [brain <Organ>] [cellular <Cell>] [brain <Organ>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

The effect of early diagnosis and treatment in cystic fibrosis: a seven-year study of 16 sibling pairs. Data on 16 sibling pairs with cystic fibrosis were analyzed to test the hypothesis that early treatment of this condition improves prognosis. Younger siblings' conditions were diagnosed before 1 year of age, usually before the onset of pulmonary disease. Older siblings' conditions were diagnosed after 1 year of age and after the onset of pulmonary disease. Although the sibling pairs received similar treatment, comparison at 7 years of age showed that the younger siblings had significantly better chest roentgenogram scores, total clinical scores, residual lung volumes, and ratios of residual volume to total lung volume. Younger siblings also required fewer hospital admissions to control their lung disease. The results suggest that, in general, early initiation of therapy is beneficial for patients with cystic fibrosis.

[pulmonary <Organ>] [pulmonary <Organ>] [chest <Organism_subdivision>] [lung <Organ>] [lung <Organ>] [lung <Organ>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Range of motion limitation after rotator cuff repair. HYPOTHESIS: This study was conducted to identify preoperative factors correlating with limited motion after rotator cuff repair (RCR) and to evaluate the affect of loss of motion on outcome. We hypothesized that patients with preoperative ROM loss, diabetes, and workman's compensation claims would exhibit postoperative ROM loss at 3 months. MATERIAL AND METHODS: Preoperative and postoperative evaluations, including outcomes assessment and physical examination parameters, were reviewed for 345 patients who underwent RCR. Correlations between demographic, physical examination, and surgical variables and postoperative limitation of motion and need for capsular release were determined. RESULTS: At 3-month follow-up, mean active forward elevation (AFE), active external rotation (AER), and passive internal rotation (PIR) were 90%, 78%, and 80% of the contralateral side. Limitation of preoperative motion correlated with limitation of postoperative AFE, AER, and PIR (P < .001). Forty-seven patients considered clinically stiff were followed at 1 year postoperatively. Three patients required arthroscopic capsular release for persistent range of motion loss. CONCLUSION: Early postoperative limitation of motion after RCR is associated with restricted preoperative motion. Other factors, including diabetes mellitus and worker's compensation claim, are also associated with range of motion loss. Most shoulders with early motion loss recover motion and rarely require capsular release.

[rotator cuff <Organ>] [rotator cuff <Organ>] [shoulders <Organism_subdivision>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

TxA2, generated from arachidonic acid by cyclooxygenase 1 (COX-1) and Tx synthase, further amplifies platelet activation. COX-1 converts arachidonic acid into prostaglandin endoperoxides PGG2 and PGH2, the latter being, in turn, transformed by Tx synthase into TxA2, a potent amplifier of platelet aggregation with vasoconstrictive properties. At the site of the atheroma rupture, platelet-released TxA2 leads to downstream micro-vessel contraction and thrombus propagation (7). In addition to its role in coagulation, thrombin at extremely low concentrations is one of the major platelet activators (8). Human platelets express two cell surface G-protein-coupled protease-activated receptors (PARs) for thrombin: PAR-1 and PAR-4. By binding the hirudin-like extracellular amino terminal domain (the so-called thrombin receptor), thrombin activates platelets and smooth muscle cells, thus promoting platelet pro-coagulant activity, shape change, secretion and release of agonists (ADP and TxA2), expression of P-selectin, activation of the alphaIIbbeta3 integrin receptor, and aggregation. Thrombin also binds to GpIbalpha on the surface of platelets, thought to act as a co-factor that localizes the enzyme on the platelet surface and accelerates the hydrolysis of PAR-1 (9). PAR-1 and P2Y12 cross-react in platelet activation, and Galphaq and Galphai-coupled receptors are involved in this process. Thrombin-dependent platelet aggregation is mediated in part by secreted ADP, acting on the Galphai-linked ADP receptor. By blocking Galphaq via PAR-1 and Gbetai via P2Y12, combined inhibition of thrombin and P2Y12 receptors leads to a synergistic inhibitory effect on thrombin-induced platelet aggregation (10). 5-HT is a vasoconstrictor agent that binds to 5HT-2A receptors and amplifies the platelet response by stimulating shape change and enhancing platelet recruitment at sites of injury (3). It may also play a pro-coagulant role by promoting the retention of fibrinogen and thrombospondin on the platelet surface. Intraplatelet 5-HT stores are implicated in shear-induced platelet aggregation and thrombus propagation (3).

[platelet <Cell>] [platelet <Cell>] [atheroma <Pathological_formation>] [platelet <Cell>] [micro-vessel <Tissue>] [thrombus <Organism_substance>] [platelet <Cell>] [platelets <Cell>] [cell surface <Cellular_component>] [extracellular <Immaterial_anatomical_entity>] [platelets <Cell>] [smooth muscle cells <Cell>] [platelet <Cell>] [platelets <Cell>] [platelet surface <Cellular_component>] [platelet <Cell>] [platelet <Cell>] [platelet <Cell>] [platelet <Cell>] [platelet <Cell>] [platelet surface <Cellular_component>] [Intraplatelet <Cell>] [platelet <Cell>] [thrombus <Organism_substance>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

The presence of nitrite during UVA irradiation protects from apoptosis. Nitrite occurs ubiquitously in biological fluids such as blood and sweat, representing an oxidation product of nitric oxide. Nitrite has been associated with a variety of adverse effects such as mutagenicity, carcinogenesis, and toxicity. In contrast, here we demonstrate that the presence of nitrite, but not nitrate, during irradiation of endothelial cells in culture exerts a potent and concentration-dependent protection against UVA-induced apoptotic cell death. Protection is half-maximal at a concentration of 3 mM, and complete rescue is observed at 10 mM. Nitrite-mediated protection is mediated via inhibition of lipid peroxidation in a similar manner as seen with butylated hydroxytoluene, a known inhibitor of lipid peroxidation. Interestingly, nitrite-mediated protection is completely abolished by coincubation with the NO scavenger cPTIO. Using electron paramagnetic resonance (EPR) spectroscopy or Faraday modulation spectroscopy, we directly prove UVA-induced NO formation in solutions containing nitrite. In conclusion, evidence is presented that nitrite represents a protective agent against UVA-induced apoptosis due to photodecomposition of nitrite and subsequent formation of NO.

[biological fluids <Organism_substance>] [blood <Organism_substance>] [sweat <Organism_substance>] [endothelial cells <Cell>] [cell <Cell>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Colorimetrical rate assay for urinary dipeptidyl peptidase IV (DPPIV) activity using a new substrate. We synthesized a new substrate glycyl-L-proline 3,5-dibromo-4-hydroxyanilide (Gly-Pro-DBAP), for dipeptidyl peptidase IV (DPPIV). Its hydrolysis by DPPIV resulted in the formation of a chromophore, 2,6-dibromophenol-indo-p-xylenol, and its maximal absorption wavelength (600 nm) was longer than that of p-nitroaniline (415 nm) released from conventional substrate, glycyl-L-proline p-nitroanilide (Gly-Pro-pNA). We also established the rate assay for urinary DPPIV activity using Gly-Pro-DBAP. The optimum pH was between 8.5 and 9.0. The apparent Km was 1.1 mmol/1. The detectable range was 2.5-350 U/l. No changes in blank values occurred throughout the enzyme reaction in the optimum pH. Its value was also much lower than Gly-Pro-pNA. CVs for within-run and between-run were 1.1% (n = 10) and 3.0% (n = 10), respectively. Among tested peptidases, only DPPIV could hydrolyze Gly-Pro-DBAP. Among the protease inhibitors, only two, diprotin-A and phenylmethylsulfonyl fluoride (PMSA), could inhibit DPPIV activity. The present method did not interfere with urinary ingredients such as hemoglobin. The correlation between the present (y) and conventional (x) methods is presented by the equation y = 1.121x + 0.096 (r = 0.993). Thus the present method provides practical advantages over the conventional method for routine laboratory use.

[urinary <Organism_substance>] [urinary <Organism_substance>] [urinary <Organism_substance>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Tropical splenomegaly syndrome in Zambia: further observations and effects of cycloguanil and proguanil. Nineteen Zambian patients with the tropical splenomegaly syndrome and sinusoidal lymphocytosis on liver biopsy were studied. The association of macrobulinaemia with the tropical splenomegaly syndrome has again been confirmed. Sixteen patients were treated with antimalarials-12 with cycloguanil pamoate alone, 3 with cycloguanil and proguanil, and 1 with proguanil alone. Twelve patients were observed for periods of sufficient length for the drug effect to be assessed, and in 11 there was a good response in terms of decrease in spleen size.Cycloguanil pamoate may be of value both for prophylaxis and treatment in areas where tropical splenomegaly syndrome is endemic.

[sinusoidal <Tissue>] [liver <Organ>] [spleen <Organ>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

The most highly represented gene ontology themes in the neurosphere vs. differentiated cells comparison (F-G).

[neurosphere <Cell>] [differentiated cells <Cell>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Newly recognized syndrome with heminasal aplasia and ocular anomalies or wider spectrum of heminasal aplasia/atypical clefting syndrome? We report on five unrelated Brazilian patients with heminasal aplasia associated with diverses anomalies, including lateral proboscis, and anomalies of the eye and first branchial arch. We suggest that these patients represent different conditions within the spectrum of the heminasal aplasia malformation. Clinical, genetic, and differential diagnosis are discussed.

[ocular <Organ>] [eye <Organ>] [branchial arch <Multi-tissue_structure>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Neurohypophyseal granulomatous germinoma invading the right cavernous sinus: case report and review of the literature. We encountered a rare case of neurohypophyseal germinoma with a prominent granulomatous reaction, which invaded the right cavernous sinus. The neuroimaging and histopathology features in this case were unique, distinguishing it from other types of suprasellar lesions. A 13-year-old boy presented with loss of appetite and polyuria; both symptoms were present for 1 year, and headache, general fatigue and blurred vision present for the prior 2 months. On admission, neurological examination indicated bitemporal hemianopsia and optic atrophy. Endocrinological exam showed panhypopituitarism. Tumor markers such as alpha-fetoprotein, human growth hormone, carcinoembryonic antigen, and placental alkaline phosphatase were negative. Brain CT revealed a suprasellar tumor with calcification. MR T(1)-weighted and T(2)-weighted images showed the tumor to be isointense to normal brain parenchyma and to be enhanced densely. The tumor also involved the right cavernous sinus, so that a biopsy was performed by the transsphenoidal approach. On pathologic examination of the specimen, typical large tumor cells with lymphocytic cell infiltration and prominent granulomatous reaction were observed. Neurohypophyseal granulomatous germinoma was diagnosed. Radiotherapy was performed with a total dose of 51 Gy and the tumor shrank remarkably. The patient returned to school under hormone replacement therapy.

[Neurohypophyseal granulomatous germinoma <Pathological_formation>] [right cavernous sinus <Immaterial_anatomical_entity>] [neurohypophyseal germinoma <Pathological_formation>] [right cavernous sinus <Immaterial_anatomical_entity>] [suprasellar lesions <Pathological_formation>] [Tumor <Pathological_formation>] [placental <Organ>] [Brain <Organ>] [suprasellar tumor <Pathological_formation>] [tumor <Pathological_formation>] [brain <Organ>] [tumor <Pathological_formation>] [right cavernous sinus <Immaterial_anatomical_entity>] [transsphenoidal <Multi-tissue_structure>] [tumor cells <Cell>] [lymphocytic cell <Cell>] [Neurohypophyseal granulomatous germinoma <Pathological_formation>] [tumor <Pathological_formation>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

The impact of tracheal intubation on host defenses and risks for nosocomial pneumonia. Nosocomial pneumonia remains a common complication in patients treated with endotracheal intubation and mechanical ventilation and continues to have a significant impact on the mortality rate of these patients. Epidemiologic studies have shown that the risk of pneumonia increases with the duration of intubation but that the period of highest risk is the first 2 weeks of therapy. Gram-negative bacteria account for most nosocomial pneumonias in intubated patients, but Staphylococcus aureus may also play a role in what may be a polymicrobial infection. In the most seriously ill individuals, and in those treated with long-term mechanical ventilation, Pseudomonas aeruginosa is a common pathogen. Endotracheal intubation and mechanical ventilation predispose to pneumonia for a variety of reasons (see Fig. 1). The endotracheal tube can have direct effects on the airway that result in a reduction in local host defenses. Thus, mucosal injury can reduce mucociliary function, while upper airway defenses are bypassed and the effectiveness of cough is reduced. Indirectly, intubation can result in an enhanced capacity of tracheobronchial cells to bind gram-negative bacteria, an effect that favors airway colonization and pneumonia. The injury to the airway can create binding sites for bacteria in the basement membrane of the bronchial tree and the stimulation of the secretion of mucus, which then stagnates and can create potential sites for bacterial adherence. The endotracheal tube also enhances bacterial entry to the lung by serving as a reservoir for bacteria to remain sequestered, safe from host defenses. Respiratory therapy devices can allow bacteria to proliferate and can then introduce them into the patient if not handled properly. Finally, patients who are ill enough to require intubation also have disease-associated impairments in systemic host defense, which add to the impairments caused by the use of an artificial airway. The host defense impairments that occur in mechanically ventilated patients can lead to respiratory tract infection in the form of either febrile tracheobronchitis or pneumonia. The diagnosis of pneumonia in intubated patients is difficult and controversial. It can be made by either clinical criteria or microbiologic criteria, the latter by using a bronchoscopically directed protected specimen brush. Therapy of pneumonia in mechanically ventilated patients is not always successful, and systemic antibiotics may need to be supplemented by topical antimicrobials. No clearly effective prophylactic strategy currently exists, but our understanding of pneumonia pathogenesis has led to some promising directions. As more data are collected, inhaled antibiotics, selective digestive decontamination, and enhancement of host defenses by cytokines and pre-formed antibodies may emerge as useful approaches.

[tracheal <Multi-tissue_structure>] [endotracheal tube <Multi-tissue_structure>] [airway <Multi-tissue_structure>] [mucosal <Multi-tissue_structure>] [mucociliary <Tissue>] [airway <Multi-tissue_structure>] [tracheobronchial cells <Cell>] [airway <Multi-tissue_structure>] [airway <Multi-tissue_structure>] [basement membrane <Multi-tissue_structure>] [bronchial tree <Multi-tissue_structure>] [mucus <Organism_substance>] [endotracheal tube <Multi-tissue_structure>] [lung <Organ>] [airway <Multi-tissue_structure>] [respiratory tract <Multi-tissue_structure>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Absence of antisperm antibodies in anejaculatory men. Antisperm antibodies were assessed in the serum samples of 73 men unable to ejaculate naturally and on the sperm cells of 13 of these men. None of the serum samples were found to be positive by sperm agglutination or sperm immobilization methods and antibodies were detected by an immunobead assay on the sperm cells of one of the 13 men examined.

[serum samples <Organism_substance>] [sperm cells <Cell>] [serum samples <Organism_substance>] [sperm <Cell>] [sperm <Cell>] [sperm cells <Cell>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Crystal data C15H12ClN3O2S2 F(000) = 752 Mr = 365.85 Dx = 1.507 Mg m-3 Monoclinic, P21/n Mo Kalpha radiation, lambda = 0.71073 A Hall symbol: -P 2yn Cell parameters from 25 reflections a = 10.175 (2) A theta = 9-12degrees b = 8.4958 (17) A micro = 0.51 mm-1 c = 19.318 (4) A T = 293 K beta = 105.01 (3)degrees Block, yellow V = 1613.0 (6) A3 0.25 x 0.15 x 0.15 mm Z = 4

[Cell <Cell>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Role of interleukin 1 in antigen-specific T cell proliferation. The role of interleukin 1 (IL 1) in human antigen-specific T cell proliferation was examined. Nylon wool-purified T cells proliferated in the presence of autologous monocytes (Mo.) pulsed for 18 h with tetanus toxoid (TT) antigen (Mo.TT). Irradiation of Mo.TT with ultraviolet (UV) light (72 J/m2) abolished their capacity to support T cell proliferation and drastically reduced their capacity to secrete IL 1 after stimulation with Staphylococcus albus. The defect in antigen presentation induced by UV irradiation of Mo.TT was reversed in a dose-dependent manner by the addition of two different preparations containing human interleukin 1 (IL 1). The first preparation consisted of supernatants of Mo. stimulated with Con A for 18 hr and in which Con A activity was blocked by alpha-D-methyl-mannoside (Mo.-Con A-Sup). The second preparation consisted of human IL 1 partially purified from supernatants of human peripheral blood mononuclear cells stimulated with S. albus. This IL 1 copurified with human leukocyte pyrogen (LP) and was termed IL 1/LP. Both IL 1-containing preparations enhanced the response of C57BL/6 mouse thymocytes to phytohemagglutinin. A rabbit antibody to human IL 1/LP inhibited the capacity of T cells to proliferate in response to Mo.TT and inhibited the capacity of Mo.-Con A-Sup to reconstitute the T cell response to UV-irradiated Mo.TT. IL 1/LP was not necessary for T cells to recognize the immunogenic moiety presented by Mo., because monolayers of UV-irradiated Mo.TT were equivalent to monolayers of unirradiated MO.TT in their capacity to adsorb TT-reactive T cells specifically. Furthermore, the addition of rabbit antibody to IL 1/LP did not interfere with the capacity of UV-irradiated Mo.TT to adsorb TT-reactive T cells. The results obtained in this study indicate that IL 1 is involved in optimal antigen-driven proliferation of human T lymphocytes.

[T cell <Cell>] [T cell <Cell>] [T cells <Cell>] [autologous monocytes <Cell>] [Mo <Cell>] [Mo <Cell>] [Mo <Cell>] [T cell <Cell>] [Mo <Cell>] [Mo <Cell>] [Mo <Cell>] [peripheral blood mononuclear cells <Cell>] [leukocyte <Cell>] [thymocytes <Cell>] [T cells <Cell>] [Mo <Cell>] [Mo <Cell>] [T cell <Cell>] [Mo <Cell>] [T cells <Cell>] [Mo <Cell>] [Mo <Cell>] [MO <Cell>] [T cells <Cell>] [Mo <Cell>] [T cells <Cell>] [T lymphocytes <Cell>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

1. Introduction Phase I clinical trials of new anticancer agents have been commonly conducted using the method of modified Fibonacci [1]. In brief, 3 patients are treated at a starting dose which is typically one tenth of the dose that is lethal to 10% of animals defined in preclinical studies. If none of the 3 patients experiences DLT, then the next 3 patients will be treated at the next higher dose. If DLT is observed, additional patients will be treated at the same or lower dose level to determine MTD according to a predetermined schema. The MTD is defined as the highest dose reached for which the incidence of DLT occurs in less than 33% of the subjects. Typically, intrapatient dose escalation is not allowed. There are several shortcomings associated with the modified-Fibonacci design. It has long been recognized that a substantial number of patients are likely to be treated at subtherapeutic doses [2, 3]. This is particularly true for drugs with potential anticancer activity. Since the primary purpose of phase I trials is to determine DLT and MTD, the efficacy of the drug may not be evident for certain tumor types as there are only a small number of patients enrolled into the trial. Furthermore, the modified-Fibonacci design does not take into account individual variations in therapeutic and toxicologic responses due to genomic polymorphisms [4, 5]. In addition, since there is a limit of 3 subjects allowed for each cohort, a waiting period of up to four weeks is commonly required before enrollment of the next cohort of subjects. This latter requirement creates anxiety of waiting for eligible patients. Several alternative phase I designs have been proposed which limit the number of patients accrued at each dose level and accelerate the dose escalation process [1, 6]. There has also been an increase in the number of clinical trials that include a component of intrapatient dose escalation although no formal validation with the modified-Fibonacci approach has been reported [7-9]. We have pioneered a population-based design to maximize therapeutic efficacy, to provide preliminary efficacy information and to allow derivation of a pMTD for subsequent phase II trials. Irinotecan and cisplatin have been shown to have promising efficacy in patients with small-cell lung cancer in phase III trial where irinotecan was given on a weekly schedule [10]. We wished to perform a population-based phase I trial of irinotecan, given every 3 weeks, and carboplatin, a platinated anticancer drug which is generally better tolerated than its cisplatin analog.

[tumor <Pathological_formation>] [small-cell lung cancer <Pathological_formation>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Luciferase Assay For Fig. 1, 10 ng of TORC1, 5 ng of TORC2, and 15 ng of PKAalpha expression plasmids were transfected into HEK293 cells. For Fig. 2, 800 ng of total DNA consisted of 200 ng of the pMLHoxb1ARE luciferase reporter and 100 ng of each expression plasmid. A lacZ reporter was co-transfected to normalize transfection efficiency. For Fig. 3A, the amounts of pENTR T2i shRNA (TORC2 shRNA) are given within the panel. For Fig. 3B, 25,000 cells per well were plated in 48-well plates and transfected using Lipofectamine 2000 with the following vectors: 40 ng of pML5xUAS, 40 ng of pGAL-DBD or pGAL-MEIS1A(335-390), 40 ng of pRSV-PBS or pRSV-PKA, 40 ng of pENTR U6 (control shRNA) or pENTR T2i shRNA (TORC2 shRNA), and 100 ng of pRSV-beta-galactosidase. At 48 h post-transfection, cell lysates were prepared using 100 mul per well of lysis buffer (1% Triton X-100, 1 mm dithiothreitol, 92.8 mm K2HPO4, pH 7.8, 9.2 mm KH2PO4, pH 7.8) and centrifuged for 5 min at 4 degreesC. A 20-mul aliquot of the supernatant was added to 12.5 mul of assay buffer (20 mm ATP, 40 mm MgCl2, 0.4 m Tris-Cl, pH 7.8). The mixture was immediately quantified for luciferase activity using a Lumat LB 9507 luminometer (EG&G Berthold) that dispensed 100 mul per reaction of luciferin solution, which contains 1 mm d-(-)-luciferin (catalogue number 11626353001, Roche) and 0.1 m Tris-Cl, pH 7.8.

[plasmids <Cellular_component>] [HEK293 cells <Cell>] [cells <Cell>] [cell lysates <Organism_substance>] [supernatant <Organism_substance>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Postpartum rubella immunization: association with development of prolonged arthritis, neurological sequelae, and chronic rubella viremia. Six women developed chronic long-term arthropathy after postpartum immunization against rubella. All individuals developed acute polyarticular arthritis within 12 days to three weeks postimmunization and have had continuing chronic or recurrent arthralgia or arthritis for two to seven years after vaccination. Acute neurological manifestations, consisting of carpal tunnel syndrome or multiple paresthesiae, developed postvaccination in three women. Two have developed continuing active or chronic recurrent episodes of blurred vision, paresthesiae, and painful limb syndromes together with recurrent joint symptoms. Chronic rubella viremia has been detected in peripheral blood mononuclear cell (MNC) populations in five of the six women up to six years after vaccination. In addition rubella virus was isolated from breast milk MNCs in one individual at nine months postvaccination and from peripheral blood MNCs in two of four breast-fed infants studied at 12-18 months of age. Immune responses to rubella virus studied at sequential intervals after vaccination correlated with development of rheumatologic and neurological manifestations.

[neurological <Anatomical_system>] [neurological <Anatomical_system>] [limb <Organism_subdivision>] [peripheral blood mononuclear cell <Cell>] [MNC <Cell>] [breast milk MNCs <Cell>] [peripheral blood MNCs <Cell>] [breast <Organism_subdivision>] [neurological <Anatomical_system>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

In situ alkylation of cysteine residues in a hydrophobic membrane protein immobilized on polyvinylidene difluoride membranes by electroblotting prior to microsequence and amino acid analysis. For identification of cysteine residues on microsequence analysis it is crucial to derivatize the sulfhydryl groups. This reaction requires a desalting step which often represents a major obstacle, especially if the sample consists of limited amounts of a hydrophobic membrane protein. An alkylation procedure is described, allowing efficient derivatization (greater than 90%) of cysteines and cystines even in low microgram quantities, as revealed by test analyses with lysozyme and a hydrophobic membrane protein. The modified protein is recovered in high yields in a form suitable for both microsequence analysis and amino acid analysis. The method involves electrophoretic desalting by miniaturized Tricine-sodium dodecyl sulfate-polyacrylamide gel electrophoresis and in situ alkylation after electro-transfer onto polyvinylidene difluoride membranes. Precautions against NH2-terminal blocking during sample preparations are provided. The general applicability of the method is illustrated by the structural characterization of the low abundance membrane receptor for human urokinase plasminogen activator.

[membrane <Cellular_component>] [membrane <Cellular_component>] [membrane <Cellular_component>] [membrane <Cellular_component>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Measurement of serum glycosylated proteins and glycosylated low density lipoprotein fraction in diabetes mellitus. A simple method was developed for estimating serum glycosylated protein levels using gel filtration with Bio-Gel P6 by determining the protein and sugar content in the void volume fraction. The glycosylated protein levels (GSP) correlated well with fasting blood sugar levels and glycosylated albumin level (G-ALB) determined by affinity chromatography with Blue Sepharose CL6B. The glycosylation level of heparin-citrate precipitable fraction of serum which predominantly contained low density lipoprotein (G-LDL) also correlated well with GSP and LDL-cholesterol levels. Significantly different values were obtained for GSP, G-ALB, and G-LDL between normals and diabetics.

[serum <Organism_substance>] [serum <Organism_substance>] [blood <Organism_substance>] [serum <Organism_substance>]

You are provided with a text. Your objective is to identify, extract and classify all anatomical entities mentioned in the text, maintaining the order in which they appear. Types are [Pathological_formation, Organ, Tissue, Multi-tissue_structure, Developing_anatomical_structure, Cell, Anatomical_system, Organism_subdivision, Organism_substance, Cellular_component, Immaterial_anatomical_entity]. The entities should be presented in the following format: [entity <type>].

Cardiac gap junction configuration after an uncoupling treatment as a function of time. Rabbit ventricle either was fixed in glutaraldehyde without injury (control) or was injured before fixation, presumably causing electrical uncoupling of the gap junctions. All tissue was then processed for freeze-fracture. Replicas of control gap junctions exhibited irregular packing of the P-face particles and E-face pits. Average center-to-center spacing of the particles was 10.5 nm. Tissue fixed 1-5 min after injury showed clumping of gap junctional particles and pits. Within the clumps, the particles and pits were hexagonally packed and the center-to-center spacing of the particles averaged 9.5 nm. In tissue fixed 15-30 min after injury, the clumps of gap junctional particles had coalesced into a homogeneous structure in most junctions. The packing of the particles and pits was hexagonal and the spacing of the particles averaged 9.5 nm. A few pieces of rabbit atrium were frozen without prior fixation or cryoprotection to try to assess the effect of glutarldehyde fixation on gap junction structure. In this tissue the gap junctional particles were irregularly packed and their spacing averaged 10.0 nm.

[Cardiac <Organ>] [ventricle <Multi-tissue_structure>] [tissue <Tissue>] [Tissue <Tissue>] [tissue <Tissue>] [atrium <Multi-tissue_structure>] [tissue <Tissue>]