gebhart/patrepeval huggingface dataset:
The multi-media medical monitoring, diagnosis, and consultation project (2002)

The authors have designed and are implementing a multi-media medical monitoring, diagnosis and consultation system. It combines computer, video, and voice data in a medical environment in support of both clinical care and basic research. They build on a distributed computer network (NeuroNet), which currently includes 80 computer nodes installed in six hospitals and multiple research laboratories throughout the University of Pittsburgh. The communications backbone of the current network is an Ethernet local area network to which are attached sub-networks defined by the functional requirements of clinical and research problems. In the existing system, all nodes on the network can access real time displays of data being acquired anywhere on the network. Thus physicians at remote locations can consult and collaborate with their colleagues on the interpretation of complex data. In the new system, they are integrating video, voice and computer data enabling multiple persons at multiple sites to consult using this shared data.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
CHRONIC REJECTION—AN UNDEFINED CONUNDRUM (1991)

TILNEY, NICHOLAS L.; WHITLEY, W. DAVID; DIAMOND, JONATHAN R.; KUPIEC-WEGLINSKI, JERZEY W.; ADAMS, DAVID H. Author Information
A pathway for disulfide bond formation in vivo. (1993)

Protein disulfide bond formation in Escherichia coli requires the periplasmic protein DsbA. We describe here mutations in the gene for a second protein, DsbB, which is also necessary for disulfide bond formation. Evidence suggests that DsbB may act by reoxidizing DsbA, thereby regenerating its ability to donate its disulfide bond to target proteins. We propose that DsbB, an integral membrane protein, may be involved in transducing redox potential across the cytoplasmic membrane.
AHR Activation Is Protective against Colitis Driven by T Cells in Humanized Mice (2016)

Existing therapies for inflammatory bowel disease that are based on broad suppression of inflammation result in variable clinical benefit and unwanted side effects. A potential therapeutic approach for promoting immune tolerance is the in vivo induction of regulatory T cells (Tregs). Here we report that activation of the aryl hydrocarbon receptor using the non-toxic agonist 2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) induces human Tregs in vitro that suppress effector T cells through a mechanism mediated by CD39 and Granzyme B. We then developed a humanized murine system whereby human CD4<sup>+</sup> T cells drive colitis upon exposure to 2,4,6-trinitrobenzenesulfonic acid and assessed ITE as a potential therapeutic. ITE administration ameliorated colitis in humanized mice with increased CD39, Granzyme B, and IL10-secreting human Tregs. These results develop an experimental model to investigate human CD4<sup>+</sup> T responses in vivo and identify the non-toxic AHR agonist ITE as a potential therapy for promoting immune tolerance in the intestine.
The stimulation of paracrine and autocrine mitogenic pathways by the platelet-derived growth factor receptor (1987)

Platelet-derived growth factor (PDGF) and PDGF-like polypeptides stimulate cell proliferation through paracrine and autocrine pathways. Each of these pathways is mediated by the PDGF receptor. Recently, cDNA clones for the receptor have been isolated and sequenced. The receptor gene on chromosome 5 is transcribed into a single 5.2 kb mRNA. The translated product, which is processed through at least one identifiable precursor, is expressed at the cell surface and is rapidly degraded. When activated by PDGF, the receptor mediates a group of diverse intracellular reactions. The receptor domains that mediate tyrosine kinase activity can be identified in the amino acid sequence of the receptor. However, the domains that mediate other PDGF-stimulated responses, such as turnover of phosphatidylinositol and enhanced expression of the c-myc and c-fos genes, have not been determined. Recently, a full-length receptor cDNA clone has been expressed in cells that normally lack PDGF receptors. This expression system should provide an approach to studies of the function of specific receptor domains and should help determine the relationship among the intracellular reactions stimulated by PDGF.
A Tn 7 -Like Transposon Is Present in the glmUS Region of the Obligately Chemoautolithotrophic Bacterium Thiobacillus ferrooxidans (1998)

The region downstream of the Thiobacillus ferrooxidans ATCC 33020 atp operon was examined, and the genes encoding N-acetylglucosamine-1-uridyltransferase (glmU) and glucosamine synthetase (glmS) were found. This atpEFHAGDC-glmUS gene order is identical to that of Escherichia coli. The T. ferrooxidans glmS gene was shown to complement E. coli glmS mutants for growth on minimal medium lacking glucosamine. A Tn7-like transposon, Tn5468, was found inserted into the region immediately downstream of the glmS gene in a manner similar to the site-specific insertion of transposon Tn7 within the termination region of the E. coli glmS gene. Tn5468 was sequenced, and Tn7-like terminal repeat sequences as well as several open reading frames which are related to the Tn7 transposition genes tnsA, tnsB, tnsC, and tnsD were found. Tn5468 is the closest relative of Tn7 to have been characterized to date. Southern blot hybridization indicated that a similar or identical transposon was present in three T. ferrooxidans strains isolated from different parts of the world but not in two Thiobacillus thiooxidans strains or a Leptospirillum ferrooxidans strain. Since T. ferrooxidans is an obligately acidophilic autotroph and E. coli is a heterotroph, ancestors of the Tn7-like transposons must have been active in a variety of physiologically different bacteria so that their descendants are now found in bacteria that occupy very different ecological niches.
Distribution and characterization of plasmalemma vesicle protein-1 in rat endocrine glands (2002)

Plasmalemma vesicle protein-1 (PV-1) is an integral membrane protein associated with endothelial cell caveolae and fenestrae. Since endocrine glands are enriched with fenestrated endothelium, we examined the distribution of PV-1 mRNA and protein in endocrine glands and determined its cellular localization. A single transcript was detected by RT-PCR in all endocrine glands examined. A synthetic peptide was used to generate antibodies for Western blotting and immunohistochemistry (IHC). Western blotting of membrane fractions from lung, pituitary, adrenal, testis and PV-1-transfected Cos-1 cells revealed a major 65 kDa protein. This protein binds to heparin with high affinity. Using IHC, PV-1 was localized to both endothelial cells of the adrenal zona reticularis and chromaffin cells of the medulla. In the pancreas, PV-1 expression was restricted to a few cells in the islets of Langerhans that partially overlap with somatostatin-positive delta-cells. In both neonatal and adult pituitaries, strong PV-1 immunoreactivity was detected in neural lobe pituicytes in a pattern similar to that of glial fibrillary acidic protein (GFAP). PV-1 and GFAP expression was seen in the adult, but not neonatal, intermediate lobe. Endothelial cells throughout the neonatal anterior lobe were PV-1 positive, but PV-1 in the adult was restricted to some endothelial and endocrine cells localized near the margins of lobe. In the adult testis, strong PV-1 expression was seen in germ cells within the seminiferous tubules that varied with the stage of spermatogenesis. In contrast, PV-1 in the neonatal testis was localized to the interstitial cells but not seminiferous tubules. In the ovary, PV-1 was expressed in stromal endothelial cells as well as the thecal layer of developing follicles. Over half the corpus luteal cells were positive for PV-1. Our data have shown that PV-1 is not restricted to endothelial cells but is localized in many types of endocrine and non-endocrine cells. Furthermore, PV-1 expression in the pituitary and testis is developmentally regulated.
코발트 ( Co-60 ) 치료를 받은 자궁경암의 임상적 고찰 (1981)

1974년 1월부터 1981년 3월까지 만 7년 2개월동안 본 병원에서 자궁경부암으로 Co-60 방사선 치료를 받은 환자 156명을 대상으로 조사하였으며, 이중 72명은 1979년 1월부터 1981년 3월 까지 최소 1회 이상 산부인과 외래에서 follow up check를 받았다. 이들에 대한 임상적 고찰 을 해 본 결과 다음과 같은 결론을 얻었다. 1. 연도별 자궁경부암 발생빈도에서 매년 환자 수가 증가되는 추세를 보이고 있었다. 2. 자궁경부암의 발생연령은 41-50세군이 66명(42.4%)으로 제일 많았으며 이들의 평균연령은 50.1세이었다. 3. 자궁경부암 환자에서 배우자가 잇는 경우는 134명(85.9%)이엇고, 배우자가 없는 경우는 18 명(11.6%)이었다. 4. 자궁경부암 환자에서 분만경험이 3-4회인 군이 44명(28.2%)으로 제일 많았으며 분만 무경험 자도 2명(1.3%)이 있었으나, 이들은 최소 1회 이상의 유산경험은 있었으며 이들의 평균 분만횟 수는 4.99회이었다. 5. 자궁경부암 환자에서 폐경이 초래된 연령은 46-48세군이 17명(25.8%)으로 제일 많았으며 이 들의 평균 연령은 46.5세이었다. 6. 초진시 성기 점상출혈을 제일 많이 호소하였으며(41.7%) 대하(23.1%), 성기 다량출혈 (21.2%)의 순으로 나타났다. 7. 추적조사기간이 1년 미만인 자궁경부암 환자가 101명(64.8%)으로 제일 많았으며 1년에서 5 년 미만이 53명(33.9%)이었으며, 1년에서 5년 미만이 53명(33.9%)이었으며 5년이상인 경우는 단지 2명(1.3%)뿐이었다. 8. 조직학적으로 편평세포암이 106명(93.8%)으로 제일 많았다.
Purification and cDNA cloning of a second apoptosis-related cysteine protease that cleaves and activates sterol regulatory element binding proteins. (1996)

We have purified from hamster liver a second cysteine protease that cleaves and activates sterol regulatory element binding proteins (SREBPs). cDNA cloning revealed that this enzyme is the hamster equivalent of Mch3, a human enzyme that is related to the interleukin 1beta converting enzyme. We call this enzyme Mch3/SCA-2. It is 54% identical to hamster CPP32/SCA-1, a cysteine protease that was earlier shown to cleave SREBPs at a conserved Asp between the basic helix-loop-helix leucine zipper domain and the membrane attachment domain. This cleavage liberates an NH2-terminal fragment of approximately 460 amino acids that activates transcription of genes encoding the low density lipoprotein receptor and enzymes of cholesterol synthesis. Mch3/SCA-2 and CPP32/SCA-I are synthesized as inactive 30-35 kDa precursors that are thought to be cleaved during apoptosis to generate active fragments of approximately 20 and approximately 10 kDa. The current data lend further support to the notion that SREBPs are cleaved and activated as part of the program in programmed cell death.
Cancer and the Immortal Strand Hypothesis (2006)

THE main causes of mortality in the Western world are largely a matter of somatic genetics. As we age, our cells accumulate more and more mutations. Eventually one of them acquires a set of changes in phenotype that allows it to generate an expanding clone of descendants, causing an atheromatous plaque in an artery or an invasive cancer. These changes are the result of a cumulative process extending throughout our life, as is demonstrated in the relation between smoking and lung cancer and between pregnancy and breast cancer. Someone who started smoking at the age of 15 will, when 65, have a higher risk of lung cancer than someone who started at 20, showing that lungs can store for half a century the damage acquired in your teenage years (Doll and Peto 1981). Conversely, because pregnancy protects somewhat against the subsequent risk of breast cancer, a woman who first became pregnant when 13 will, when 70, have a lower risk of breast cancer than a woman whose first pregnancy was in her 20s, showing that the latter was accumulating risk as a teenager (MacMahon et al. 1973).

Long-lived animals protect themselves from the physical and chemical dangers of their environment by continuous replacement of the cells on their external surfaces and it is in these sites of continuous cell division that most human cancers arise. An adult human contains ∼1012 rapidly multiplying cells. During a life span of ∼30,000 days, each of us makes and discards from skin, gut, and certain internal organs such as lymph glands and bone marrow about one-third of these cells each day (Potten and Morris 1988). If all these 1012 cells divide every third day, the cells remaining after 80 years would each have had ∼10,000 successive divisions in their ancestry. So by the age of 80, given a mutation rate of ∼10−6/gene/replication (Drake 1999), 1 in 100 of the copies of each gene would be mutant. In a collection of 1012 cells, 1010 would have a mutant copy of any particular gene, 108 would have mutations in any pair of genes, and a million would have mutations in any trio of genes. Nevertheless, despite there being many combinations of mutant genes that can trigger cancer (Hahn and Weinberg 2002), most people never develop cancer. So there must be some feature of multicellular systems that slows the rate of accumulation of replication errors.
The influence of catabolic reactions on polyamine excretion (1985)

Complete inhibition of polyamine catabolism is possible by combined administration of two compounds. Aminoguanidine (25 mg/kg body wt., intraperitoneally) inhibits all reactions that are catalysed by copper-containing amine oxidases (CuAO). The products of the CuAO-catalysed reactions cannot be reconverted into polyamines (terminal catabolism) and therefore usually escape observation. N1-Methyl-N2-(buta-2,3-dienyl)butane-1,4-diamine (MDL 72521) is a new inhibitor of polyamine oxidase. It inhibits completely the degradation of N1-acetylspermidine and N1-acetylspermine. The enhanced excretion of N1-acetylspermidine in urine after administration of 20 mg of MDL 72521/day per kg body wt. is a measure of the rate of spermidine degradation in vivo to putrescine, and thus of the quantitative significance of the interconversion pathway. From the enhancement of total polyamine excretion by aminoguanidine-treated rats, one can calculate that only about 40% of the polyamines that are destined for elimination are usually observed in the urine, the other 60% being catabolized along the CuAO-catalysed pathways. The normally observed urinary polyamine pattern gives, therefore, an unsatisfactory picture of the actual polyamine elimination. Although aminoguanidine alone is sufficient to block terminal polyamine catabolism, rats that were treated with a combination of aminoguanidine and MDL 72521 excrete more polyamines than those that received aminoguanidine alone. The reason is that a certain proportion of putrescine, which is formed by degradation of spermidine, is normally reutilized for polyamine biosynthesis. In MDL 72521-treated animals this proportion appears in the urine in the form of N1-acetylspermidine. Thus it is possible to determine polyamine interconversion and re-utilization in vivo and to establish a polyamine balance in intact rats by using specific inhibitors of the CuAO and of polyamine oxidase.
Regulation of lymphocyte proliferation after influenza virus infection of human mononuclear leukocytes (1989)

Previous studies demonstrated that in vitro infection with influenza A viruses altered several functions of human monocytes-macrophages but did not detectably alter functions of human lymphocytes. However, both types of cells were infected, as determined by production and surface expression of viral antigens. In the current studies, human mononuclear leukocytes were infected in vitro and assayed for both influenza virus-induced proliferation and mitogen (phytohemagglutinin [PHAl)-induced proliferation, as well as for ability to stimulate proliferative responses by normal autologous leukocytes. The leukocytes showed proliferation in response to the infectious virus, but concomitant depressed proliferative responses to PHA. Coculture experiments suggested suppression of PHA-induced responses by the virus-infected cells. However, upon coculture with fresh autologous leukocytes (without PHA stimulation), both virus-infected macrophages and virus-infected lymphocytes induced autologous lymphocyte proliferative responses. Altered proliferative responses to mitogen stimulation after exposure to the virus were not due to diminished interleukin-1 production or diminished expression of HLA-DR by monocytes-macrophages. The expression of influenza virus antigens and resulting induction of autologous proliferative responses, combined with depressed mitogen-induced proliferation, may be important in human antiviral defense.
The murine Hox-2 genes display dynamic dorsoventral patterns of expression during central nervous system development (1991)

This report demonstrates that the genes in the murine Hox-2 cluster display spatially and temporally dynamic patterns of expression in the transverse plane of the developing CNS. All of the Hox-2 genes exhibit changing patterns of expression that reflect events during the ontogeny of the CNS. The observed expression correlates with the timing and location of the birth of major classes of neurons in the spinal cord. Therefore, it is suggested that the Hox-2 genes act to confer rostrocaudal positional information on each successive class of newly born neurons. This analysis has also revealed a striking dorsal restriction in the patterns of Hox-2 expression in the spinal cord between 12.5 and 14.5 days of gestation, which does not appear to correlate with any morphological structure. The cellular retinol binding protein (CRBP) shows a complementary ventral staining pattern, suggesting that a number of genes are dorsoventrally restricted during the development of the CNS. The expression of Hox-2 genes has also been compared with the Hox-3.1 gene, which exhibits a markedly different dorsoventral pattern of expression. This suggests that, while genes in the different murine Hox clusters may have similar A-P domains of expression, they are responding to different dorsoventral patterning signals in the developing spinal cord.
Dose-escalation trial of M195 labeled with iodine 131 for cytoreduction and marrow ablation in relapsed or refractory myeloid leukemias. (1993)

These data suggest that safe leukemic cytoreduction can be achieved with 131I-M195 even in multiply relapsed or chemotherapy-refractory leukemias. This agent may be useful as part of a preparative regimen for BMT.
Diversity of Alpha-Fetoprotein Gene Expression in Mice Is Generated by a Combination of Separate Enhancer Elements (1987)

The 5' flanking region of the mouse alpha-fetoprotein (AFP) gene contains a tissue-specific promoter and three upstream regulatory elements that behave as classical enhancers. At least one of these enhancers is now shown to be required for the tissue-specific expression of the AFP gene when it is introduced into the mouse genome by microinjection of cloned DNA fragments into fertilized eggs. Each enhancer can direct expression in the appropriate tissues, the visceral endoderm of the yolk sac, the fetal liver, and the gastrointestinal tract, but each exerts different influence in these three tissues. These differences may explain the tissue-specific diversity in the levels of expression characteristic of the AFP gene. The postnatal repression of transcription of the AFP gene in both liver and gut, as well as the reinitiation of its transcription during liver regeneration, is mimicked by the introduced gene when it is linked to the enhancer domains together or singly. Thus, the DNA sequence elements responsible for directing the activation of AFP transcription, its repression, and reinduction are contained in a limited segment of DNA within or 5' to the gene (or both) and are operative in the absence of the closely linked albumin gene.
Room-temperature ultraviolet laser emission from self-assembled ZnO microcrystallite thin films (1998)

Room-temperature ultraviolet (UV) laser emission of ZnO microcrystallite thin films is reported. The hexagonal ZnO microcrystallites are grown by laser molecular beam epitaxy. They are self-assembled and parallelly arrayed on sapphire substrates. The facets of the hexagons form natural Fabry–Pérot lasing cavities. The optical gain for the room-temperature UV stimulated emission is of an excitonic nature and has a peak value an order of magnitude larger than that of bulk ZnO crystal. The observation of room-temperature UV lasing from the ordered, nano-sized ZnO crystals represents an important step towards the development of nanometer photoelectronics.
Biotransformation of 4'-ethynl-2-fluorobiphenyl in the rat. In vitro and in vivo studies. (1979)

The absorption, metabolism, and plasma pharmacokinetics of a novel anti-inflammatory agent, 4'-ethynyl-2-fluorobiphenyl, was studied in the rat. 4'-[1-14C]Ethynyl-2-fluorobiphenyl was quantitatively absorbed from the gastrointestinal tract. Excretion of radiocarbon into urine was greater than excretion into bile. Appreciate amounts of radiocarbon remained in the carcass 24 hr after dosing. The only metabolite in plasma was (2-fluoro-4'-biphenylyl)acetic acid, which also possessed anti-inflammatory activity. Unchanged 4'-ethynyl-2-fluorobiphenyl was present after administration of higher doses. Peak plasma concentrations of (5-fluoro-4'-biphenylyl)acetic acid were observed within 1 hr of administration. The apparent plasma half-life of this acidic metabolite was 4 hr. The major eliminated metabolite was (4-hydroxy-2-fluoro-4'-biphenylyl)acetic acid. In vivo and in vitro metabolism studies suggest that the major metabolic pathway involves microsomal hydroxylation of the C-H bond of the ethynyl moiety to yield, after rearrangement, a highly reactive intermediate metabolite, 2-fluoro-4'-biphenylylketene.
Genetic and biochemical pathways of β‐cell failure in type 2 diabetes (2009)

We review mechanisms of beta-cell failure in type 2 diabetes. A wealth of information indicates that it is caused by impaired insulin secretion and decreased beta-cell mass. Interestingly, there appears to be a link between these two mechanisms. The earliest reaction to peripheral insulin resistance is an increase in insulin production, owing primarily to increased secretion, and to a lesser extent to decreased clearance. Experimental animal models indicate that hyperinsulinaemia promotes an increase in beta-cell mass, largely via increased beta-cell replication. In contrast, following the onset of overt diabetes, there is a slowly progressive loss of beta-cell function and mass, both in animal models and in diabetic humans. It is of great interest that most diabetes-associated genes identified in genome-wide association studies appear to be enriched in the beta-cell and to have the potential to regulate mass and/or function. Here, we review evidence derived from experimental animal models to unravel the mechanisms underlying beta-cell dysfunction. We focus primarily on signalling pathways, as opposed to nutrient sensing, and specifically on the notion that insulin and growth factor signalling via Foxo1 in pancreatic beta-cells links insulin secretion with cellular proliferation and survival.
Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl4 induced oxidative stress and cellular degeneration in rat liver (2010)

In conclusion, our study demonstrated the protective effect of natansnin against CCl4 induced oxidative stress and cellular degeneration in rat liver tissue. This protective effect of natansnin can be correlated to its direct antioxidant effect.
Regulation of Fasted Blood Glucose by Resistin (2004)

The association between obesity and diabetes supports an endocrine role for the adipocyte in maintaining glucose homeostasis. Here we report that mice lacking the adipocyte hormone resistin exhibit low blood glucose levels after fasting, due to reduced hepatic glucose production. This is partly mediated by activation of adenosine monophosphate–activated protein kinase and decreased expression of gluconeogenic enzymes in the liver. The data thus support a physiological function for resistin in the maintenance of blood glucose during fasting. Remarkably, lack of resistin diminishes the increase in post-fast blood glucose normally associated with increased weight, suggesting a role for resistin in mediating hyperglycemia associated with obesity.