tbuckley/cabot-search huggingface dataset:
The baby show.
Authors: M Alms
Journal: BMJ (1987)

<h3>Objectives:</h3> To investigate prognosis of the fetus with isolated gastroschisis and bowel dilatation from a systematic review of the literature. We aimed to compare the incidence of (a) intrauterine death, (b) death within 4 weeks of delivery, (c) bowel resection, (d) length of time to oral feeds and (e) time as inpatient in fetuses with gastroschisis with and without evidence of bowel dilatation. <h3>Methods:</h3> Literature was identified by searching two bibliographical databases between 1980 and 2007. Studies were assessed for quality and stratified according to the definition of bowel dilatation. The data extracted were inspected for clinical and methodological heterogeneity. <h3>Results:</h3> The search strategy yielded 1335 potentially relevant citations. Full manuscripts were retrieved for 92 citations. 10 studies (273 patients) were finally included in the systematic review. No difference was found between groups for death within 4 weeks of delivery (OR = 0.62 (95% CI 0.11 to 3.32); heterogeneity p = 0.39) or bowel resection (OR = 3.35 (95% CI 0.82 to 13.74); heterogeneity p = 0.39). There were insufficient data to compare the risk of intrauterine death and length of time to oral feeds. The mean inpatient stay was not significantly different between groups (OR = 16.63 (95% CI 0.98 to 32.28); heterogeneity p = 0.23). <h3>Conclusion:</h3> Current available evidence suggests that fetuses with isolated gastroschisis and bowel dilatation are not at increased risk of adverse perinatal outcome compared to those without bowel dilatation. However, there is a paucity of studies, and a randomised controlled trial is urgently needed.
The environment time capsule project
Authors: J Guillebaud
Journal: BMJ (1994)

<h3>Abstract</h3> Glycoprotein 90K, encoded by the interferon-stimulated gene <i>LGALS3BP</i>, displays broad antiviral activity. It reduces HIV-1 infectivity by interfering with Env maturation and virion incorporation, and increases survival of Influenza A virus-infected mice via antiviral innate immune signaling. Here, we analyzed the expression of 90K/<i>LGALS3BP</i> in 44 hospitalized COVID-19 patients. 90K protein serum levels were significantly elevated in COVID-19 patients compared to uninfected sex- and age-matched controls. Furthermore, PBMC-associated concentrations of 90K protein were overall reduced by SARS-CoV-2 infection in vivo, suggesting enhanced secretion into the extracellular space. Mining of published PBMC scRNA-seq datasets uncovered monocyte-specific induction of <i>LGALS3BP</i> mRNA expression in COVID-19 patients. In functional assays, neither 90K overexpression in susceptible cell lines nor exogenous addition of purified 90K consistently inhibited SARS-CoV-2 infection. Our data suggests that 90K/<i>LGALS3BP</i> contributes to the global type I IFN response during SARS-CoV-2 infection in vivo without displaying detectable antiviral properties.
The Influence of Phylogenetic Uncertainty on the Detection of Positive Darwinian Selection
Authors: M. R. Pie
Journal: Molecular Biology and Evolution (2006)

The power of maximum likelihood tests of positive selection on protein-coding genes depends heavily on detecting and accounting for potential biases in the studied data set. Although the influence of transition:transversion and codon biases have been investigated in detail, little is known about how inaccuracy in the phylogeny used during the calculations affects the performance of these tests. In this study, 3 empirical data sets are analyzed using sets of simulated topologies corresponding to low, intermediate, and high levels of phylogenetic uncertainty. The detection of positive selection was largely unaffected by errors in the underlying phylogeny. However, the number of sites identified as being under positive selection tended to be overestimated.
IgA antiendomysium antibodies have a high positive predictive value for celiac disease in asymptomatic patients
Authors: E. Grodzinsky, J. Hed, T. Skogh
Journal: Allergy (1994)

Many attempts have been made to find screening tests for celiac disease to reduce the need for biopsy, or to achieve better selection criteria before intestinal biopsy. We have recently analyzed apparently healthy blood donors for antigliadin antibodies (AGA) to select subjects for further gastrointestinal investigation. A prevalence of gluten enteropathy of at least 1/256 was found in this population. The positive predictive value (+ PV), however, was only 20%. In the present study we have analyzed IgA antiendomysium antibodies (IgA‐EmA) to estimate the sensitivity and specificity of the test, and determine whether or not the + PV of the assay increases when screening for adult celiac disease in an asymptomatic population. We found that asymptomatic persons with celiac disease may have IgA‐EmA. We found a 100% specificity of IgA‐EmA in the tested population of blood donors, whereas the sensitivity was about the same as that of IgA‐AGA. This result of a + PV of 100% indicates that a positive IgA‐EmA could replace biopsy in diagnosing celiac disease. However, further extended studies are needed to determine whether this is applicable in other populations. To screen patients for celiac disease, we recommend the easy and cheap IgA‐AGA assay as a preliminary test and the IgA‐EmA to verify the diagnosis and avoid unnecessary biopsies.
Differentiation of memory T cells to virus plaque-forming cells and cytotoxic T lymphocytes
Authors: A Senik, BR Bloom
Journal: The Journal of Experimental Medicine (1977)

The aims of this study were to define the T-cell subpopulation(s) detected by the virus plaque assay, and particularly to determine whether the virus plaque assay could be used to enumerate cytotoxic T lymphocytes. In addition, studies were undertaken to ascertain whether cell proliferation was required for development of cytotoxic effector function and virus plaque formation by these subpopulations. The results of experiments with a secondary mouse mixed lymphocyte culture (MLC) model indicated that 70 percent of virus plaque-forming cells bore the Ly 1 phenotype and 30 percent the Ly 2,3 phenotype. Three lines of evidence suggested that cytotoxic T lymphocytes (CTL) can be detected by this assay: the fact that some virus plaque-forming cells (V-PFC) bear the same Ly phenotype as CTL; the use of an inhibitor of DNA synthesis indicated that proliferating cells could be eliminated with no effect on V-PFC production and cytotoxic activity of the Ly 2,3 cell population; and that infection of primed lymphocyteswith vesicular stomatitis virus before (MLC) stimulation eliminated cytotoxic activity. In primary MLC, development of V-PFC and CTL was completely abolished by cytosine arabinoside. In contrast, in secondary MLC, some CTL and V- PFC were generated by antigenic stimulation in the absence of proliferation. However, the development of both functions became progressively more susceptible to cytosine arabinoside as the time between primary immunization and in vitro boosting is increased. It is suggested that there may be a considerable disparity between the number of existing effector cells at any given time and the cytotoxic potential, i.e. the number of cells capable of being generated by antigenic stimulation.
Estimation of missing values
Authors: Leonore A Herxenberg, Wayne A Moore, Stephen C De Rosa
Journal: The Lancet (1999)

Sir—The Lancet is to be commended for publishing the viewpoint by the AVANTI Steering Committee.1AVANTI Steering CommitteeAnalysis of HIV-1 clinical trials: statistical magic?.Lancet. 1999; 354: 2061-2064Google Scholar As this group eloquently points out, the exclusion of missing data from analyses labelled intent-to-treat is misleading; therefore, data for all individuals must be included in such analyses, and conservative rules must be adopted to replace missing data values with assigned data. We have wrestled with this issue for some time while deciding how to assign missing data values for survival analyses and for glutathione measurements in blood and T cells in an intent-to-treat HIV study that we recently completed. The solutions we evolved, which have been approved by our local statisticians, are more complete and more conservative than those proposed by AVANTI. Therefore, we suggest the following. First, to estimate missing categorical responses, drug-group participants should be assigned the response corresponding to failure for the drug, whereas those in the placebo group are assigned the response for success. Second, to estimate missing survival data, placebo-group participants should be treated as having survived for the length of the study but those in the drug group should be treated as having died, and their time-to-death assigned as the median time-to-death for individuals in the drug group whose time-to-death is known. To avoid repeatedly assigning the same (median) value to a series of missing values, the sampling method described below could be adapted for assigning time-to-death here. Third, to estimate missing values for quantitative responses, participants should be assigned values by sampling from the distribution of all known values—ie, drug and placebo groups combined. For example, in our study, we replaced missing baseline values with values selected randomly from the distribution of all known baseline values (drug group and placebo group combined). Similarly, we replaced the missing endpoint values by randomly sampling from the distribution of all known endpoint values. To reduce sampling error, we constructed 50 such datasets, analysed each independently for treatment effect, and combined the results by computing the median of the significance values obtained individually for the 50 sets.
Thrombotic Microangiopathy and Renal Failure Associated with Antineoplastic Chemotherapy
Authors: ALAN M. JACKSON
Journal: Annals of Internal Medicine (1984)

Five patients with carcinoma developed thrombotic microangiopathy (characterized by renal insufficiency, microangiopathic hemolytic anemia, and usually thrombocytopenia) after treatment with cisplatin, bleomycin, and a vinca alkaloid. One patient had thrombotic thrombocytopenic purpura, three the hemolytic-uremic syndrome, and one an apparent forme fruste of one of these disorders. Histologic examination of the renal tissue showed evidence of intravascular coagulation, primarily affecting the small arteries, arterioles, and glomeruli. Because each patient was tumor-free or had only a small tumor at the onset of this syndrome, the thrombotic microangiopathy may have been induced by chemotherapy. Diagnosis of this potentially fatal complication may be delayed or missed if renal tissue or the peripheral blood smear is not examined, because renal failure may be ascribed to cisplatin nephrotoxicity and the anemia and thrombocytopenia to drug-induced bone marrow suppression.
THE CHAIR OF SURGERY IN RUSH MEDICAL COLLEGE.Introductory Address delivered before the Class, April 11, 1891.
Authors: N. SENN
Journal: JAMA (1891)

Within the short space of four years ruthless death has twice vacated the Chair of Surgery in this college. On both of these sad occasions the faculty, students and alumnae felt that an irreparable loss had been sustained. To fill the Chair of Surgery made vacant by the death of men who have distinguished themselves in their profession by honest scientific work, and have endeared themselves to their colleagues and students as exemplary and masterly teachers is by no means an easy task, hence the anxious inquiries from all sides and everywhere: Who shall be the successor? Who shall continue the work left unfinished? Rush Medical College has always been justly proud of its Chair of Surgery. Its founder was a surgeon of world-wide repute, and there can be no doubt that from its very beginning the men who have occupied this chair have been the great magnet which has
Angiotensin II regulates cellular immune responses through a calcineurin-dependent pathway
Authors: Chandra Nataraj, Michael I. Oliverio, Roslyn B. Mannon, Peter J. Mannon, Laurent P. Audoly, Carmen S. Amuchastegui, Phillip Ruiz, Oliver Smithies, Thomas M. Coffman
Journal: Journal of Clinical Investigation (1999)

The renin-angiotensin system (RAS) is a key regulator of vascular tone and blood pressure. In addition, angiotensin II also has a number of cellular effects that may contribute to disease pathogenesis. Using Agtr1a–/– mice, which lack AT1A receptors for angiotensin II, we have identified a novel function of the RAS to modulate the immune system. We find that angiotensin II, acting through type 1 (AT1) receptors on immune cells, triggers the proliferation of splenic lymphocytes. These actions contribute to the vigor of cellular alloimmune responses. Within lymphoid organs, sufficient components of the RAS are present to activate AT1 receptors during an immune response, promoting cell growth. These actions require activation of calcineurin phosphatase. In an in vivo model of cardiac transplantation, the absence of AT1 signaling accentuates the immunosuppressive effects of the calcineurin inhibitor cyclosporine. We conclude that inhibition of AT1 receptor signaling should be useful as an anti-inflammatory and immunosuppressive therapy. Furthermore, the actions of the RAS to promote lymphocyte activation may contribute to inflammation that characterizes a number of diseases of the heart and the vascular system.
Mislocalisation of hephaestin, a multicopper ferroxidase involved in basolateral intestinal iron transport, in the sex linked anaemia mouse
Authors: Y M Kuo
Journal: Gut (2004)

<b>Background:</b> Hephaestin is a multicopper ferroxidase required for basolateral transport of iron from enterocytes. Sex linked anaemia (<i>sla</i>) mice have a defect in the release of iron from intestinal enterocytes into the circulation due to an interstitial deletion in the hephaestin gene (<i>heph</i>). <b>Results:</b> We have demonstrated that hephaestin is primarily localised to a supranuclear compartment in both intestinal enterocytes and in cultured cells. In normal intestinal enterocytes, hephaestin was also present on the basolateral surface. In <i>sla</i> mice, hephaestin was present only in the supranuclear compartment. In contrast, the iron permease Ireg1 localised to the basolateral membrane in both control and <i>sla</i> mice. <b>Conclusion:</b> We suggest that mislocalisation of hephaestin likely contributes to the functional defect in <i>sla</i> intestinal epithelium.
Cells and mediators in bronchoalveolar lavage of asthmatic patients: the example of eosinophilic inflammation
Authors: J. Bousquet, T. Van Vyve, P. Chanez, I. Enander, F. B. Michel, P. Godard
Journal: Allergy (1993)

Bronchoalveolar lavage (BAL) greatly improved our understanding of asthma allowing to demonstrate the key role of inflammation in the pathogenesis of the disease. BAL is a safe procedure, even in severe patients when properly performed. BAL samples large and small airways and alveoli. Cells and mediators may be measured in BALF but they only represent an indirect estimation of the bronchial inflammation. Before performing BAL, the clinical status of the patients should be ascertained and drugs taken may have to be withdrawn. BALF markers should follow some requirements: (1) markers should be released by cells that are pertinent to airways inflammation (and reparation) in asthma, and, if possible they should be specific of a single cell type, (2) the enumeration of cells or titration of the marker or of its metabolites should be specific and sensitive, (3) if possible the titration should not be modified by the sampling procedure, (4) pilot studies should have demonstrated that the cell is increased or the secretory product is released during challenge in asthmatic subjects, (5) studies in a large number of patients should have demonstrated that the levels of the marker are increased in chronic asthmatics, that these levels are correlated with the severity of the disease and are decreased during effective anti-inflammatory treatment, and (6) if possible the cell or marker should be specific to asthma (but at present there is no such cell or marker). Eosinophils and granule secretory products follow most of these requirements. BAL represents an important research tool to assess the effects of therapeutic interventions.
Renal disease as a determinant of increased lipoprotein(a) concentrations in diabetic patients.
Authors: M Boemi, C Sirolla, P Fumelli, R W James
Journal: Diabetes Care (1999)

OBJECTIVE: This study examined the hypothesis that kidney function is an independent determinant of lipoprotein(a) [Lp(a)] concentrations in people with diabetes. RESEARCH DESIGN AND METHODS: Lp(a) concentrations were measured in plasma samples from 273 type 2 and 223 type 1 diabetic patients recruited from a diabetes clinic. Kidney function was categorized as normal or pathological according to plasma creatinine levels and creatinine clearance rates. RESULTS: Macroalbuminuria was uniformly associated with significantly raised plasma concentrations of Lp(a) regardless of the marker used to identify kidney dysfunction. In contrast, in patients with microalbuminuria, significantly raised plasma Lp(a) levels were observed only when creatinine clearance rates or plasma creatinine levels indicated pathological kidney function. These conclusions were independent of diabetes type. CONCLUSIONS: In microalbuminuria and apparently in normoalbuminuria, altered kidney function determined by creatinine clearance rates or creatinine levels appears to be a major determinant of raised Lp(a) levels in both type 1 and type 2 diabetic patients. In contrast, Lp(a) concentrations were uniformly raised in patients with macroalbuminuria.
The lost video
Authors: J. Bahrami
Journal: BMJ (2001)

Last month, the Post Office lost the video of a GP registrar's consultation. To many, not intimately involved in general practice training, this may sound almost trivial, bearing in mind all the important challenges now facing the NHS. But to me, the GP registrar concerned, his trainers and course organiser, and the whole GP education network, this was anything but trivial.

> He had no job and no income and faced an uncertain future

Let us start at the beginning. Since 1998, all those wishing to enter general practice as independent practitioners must complete a package of assessment known as summative assessment at the end of their training. This is to prove that they have reached a level of minimum competence. This package has four elements, each of which must be passed by the GP registrar. There is the traditional multiple choice questionnaire to test factual knowledge; the audit to test the written element of the assessment; the trainer's report to testify …
HOXB7, a Homeodomain Protein, Is Overexpressed in Breast Cancer and Confers Epithelial-Mesenchymal Transition
Authors: Xinyan Wu, Hexin Chen, Belinda Parker, Ethel Rubin, Tao Zhu, Ji Shin Lee, Pedram Argani, Saraswati Sukumar
Journal: Cancer Research (2006)

Abstract Epithelial-mesenchymal transition (EMT) is increasingly recognized as a mechanism whereby cells in primary noninvasive tumors acquire properties essential for migration and invasion. Microarray analyses of microdissected epithelial cells from bone metastasis revealed a HOXB7 overexpression that was 3-fold higher than in primary breast carcinomas and 18-fold higher compared with normal breast. This led us to investigate the role of HOXB7 in neoplastic transformation of breast cells. Expression of HOXB7 in both MCF10A and Madin-Darby canine kidney (MDCK) epithelial cells resulted in the acquisition of both phenotypic and molecular attributes typical of EMT. Loss of epithelial proteins, claudin 1 and claudin 7, mislocalization of claudin 4 and E-cadherin, and the expression of mesenchymal proteins, vimentin and α-smooth muscle actin, were observed. MDCK cells expressing HOXB7 exhibited properties of migration and invasion. Unlike MDCK vector–transfected cells, MDCK-HOXB7 cells formed highly vascularized tumors in mice. MDCK-HOXB7 cells overexpressed basic fibroblast growth factor (bFGF), had more active forms of both Ras and RhoA proteins, and displayed higher levels of phosphorylation of p44 and p42 mitogen-activated protein kinase (MAPK; extracellular signal–regulated kinases 1 and 2). Effects initiated by HOXB7 were reversed by specific inhibitors of FGF receptor and the Ras-MAPK pathways. These data provide support for a function for HOXB7 in promoting tumor invasion through activation of Ras/Rho pathway by up-regulating bFGF, a known transcriptional target of HOXB7. Reversal of these effects by HOXB7-specific siRNA further suggested that these effects were mediated by HOXB7. Thus, HOXB7 overexpression caused EMT in epithelial cells, accompanied by acquisition of aggressive properties of tumorigenicity, migration, and invasion. (Cancer Res 2006; 66(19): 9527-34)
Regulatory system overseeing Stafford hospital was "wholly ineffective," hears inquiry
Authors: C. Dyer
Journal: BMJ (2010)

The care provided at Stafford hospital was so bad it violated patients’ human rights, counsel for the campaign group Cure the NHS (CURE) told the public inquiry into failures in monitoring the hospital.

“The shocking experience of Mid Staffordshire [the NHS trust that runs the hospital] suggests that despite the array of supervisory, regulatory, and commissioning bodies within the health system, their individual and combined work completely failed to create and sustain a culture of care within the NHS and to maintain basic standards of care, dignity and respect for human rights,” Jeremy Hyam said.

He told the inquiry, “The problem is …
New PLGA–P188–PLGA matrix enhances TGF-β3 release from pharmacologically active microcarriers and promotes chondrogenesis of mesenchymal stem cells
Authors: Marie Morille, Tran Van-Thanh, Xavier Garric, Jérôme Cayon, Jean Coudane, Danièle Noël, Marie-Claire Venier-Julienne, Claudia N. Montero-Menei
Journal: Journal of Controlled Release (2013)
CONGENITAL PLEXIFORM NEUROFIBROMAS AND ELEPHANTIASIS NEUROMATOSA OF THE RIGHT ARM AND NECK (VON RECKLINGHAUSEN'S DISEASE): SUPPLEMENTARY REPORT
Authors: F. P. Anzinger
Journal: JAMA (1931)

In 1919 I<sup>1</sup>reported a case of von Recklinghausen's disease, with a review of the literature. The report may be thus summarized: Francis S. appeared normal at birth. At the age of 1 year the boy cried when the upper part of the right arm was handled. The discomfort was due to subcutaneous fibrous cords occurring in the upper and lower parts of the arm. These were removed and the boy had considerable relief. In the course of years the whole right upper extremity grew in noticeable disproportion to that of the left arm. The skin became pigmented and thickened, simulating an ordinary elephantiasis. Brownish pigmentation gradually increased over the body in large areas. Roentgenograms of the bones of the right upper extremity showed trophic changes and atrophy. To establish its congenital origin, it was shown that the father had multiple fibromas and pigmented spots over his body but
COXSACKIE-B-VIRUS-SPECIFIC IgM RESPONSES, COMPLEMENT-FIXING ISLET-CELL ANTIBODIES, HLA DR ANTIGENS, AND C-PEPTIDE SECRETION IN INSULIN-DEPENDENT DIABETES MELLITUS
Authors: G. Schernthaner, W. Scherbaum, M. Borkenstein, J.E. Banatvala, Jennifer Bryant, Edith Schober, W.R. Mayr
Journal: The Lancet (1985)