tbuckley/cabot-search huggingface dataset:
THE VIRUS-NEUTRALIZING ACTION OF SERUM FROM MICE INFECTED WITH POLIOMYELITIS VIRUS
Authors: Gordon C. Brown, Thomas Francis
Journal: The Journal of Experimental Medicine (1945)

Evidence is presented that the serum of mice paralyzed with the Lansing strain of poliomyelitis virus possesses the capacity to protect normal mice against the same virus when mixtures of virus and serum are inoculated intracerebrally. The virus-neutralizing action was present mainly in mice paralyzed between the 3rd and 6th days following inoculation and was rarely demonstrable in the serum of mice developing paralysis more than 10 days after inoculation. Serum from non-paralyzed mice had approximately the same neutralizing capacity when obtained during the same period following inoculation in which serum from paralyzed mice showed the greatest effect. Neutralization of the virus was not obtained with serum from normal mice or from mice inoculated with normal nervous tissue. Further investigation of the phenomenon is in progress.
Anti–Tumor Necrosis Factor-Alpha Improves Myocardial Recovery After Ischemia and Reperfusion
Authors: Jacob Gurevitch, Inna Frolkis, Yael Yuhas, Beatriz Lifschitz-Mercer, Esther Berger, Yosef Paz, Menachem Matsa, Amir Kramer, Rephael Mohr
Journal: Journal of the American College of Cardiology (1997)
Multiple side effects of penicillamine therapy in one patient with rheumatoid arthritis.
Authors: W.K Essigman
Journal: Annals of the Rheumatic Diseases (1982)

Skin rashes, proteinuria, systemic lupus erythematosus, polymyositis and myasthenia gravis have all been recorded as complications of penicillamine therapy in patients with rheumatoid arthritis. A patient who had developed all 5 is now described. The skin lesion resembled elastosis perforans serpiginosa, which has been reported as a rare side effect in patients with Wilson's disease but not in patients with rheumatoid arthritis treated with penicillamine.
Role of adenosine in mediating the coronary vasodilative response to acute hypoxia
Authors: H. GEWIRTZ, R. A OLSSON, A. S MOST
Journal: Cardiovascular Research (1987)

To test the hypothesis that adenosine is required to mediate the coronary vasodilative response to acute hypoxia haemodynamic indices, regional myocardial blood flow, and oxygen and lactate metabolism were measured in nine closed chest anaesthetised domestic swine at control, after 3–5 min of 100% nitrogen inhalation, at second control, and after 3–5 min of 100% nitrogen inhalation plus adenosine deaminase infusion in the left anterior descending coronary artery. Cardiac lymph adenosine deaminase concentration was also measured in a separate group of four animals previously reported on. Heart rate was held constant by atrial pacing during the study. Aortic mean pressure did not change. Changes in arterial and anterior interventricular vein pH, PO2, Pco2, and oxygen content were similar for each intervention. Transmural left anterior descending artery zone flow increased significantly (p <0.01) compared with control (1.22(0.23) ml·min−1·g−1; mean(SD)) in response to hypoxia (2.73(0.92)). Intracoronary adenosine deaminase infusion (167 nmol·s−1), however, failed to blunt the flow response to hypoxia (1.33(0.30) to 2.79(1.32); second control to hypoxia plus adenosine deaminase respectively, p <0.01). Mean adenosine deaminase activity (nmol·s−1) in cardiac lymph was 105(85) at the end of 10 min of intracoronary infusion (167 nmol·s−1) and 203 (148) nmol·s−1 at the end of 15 min. Even at considerably accelerated rates of myocardial adenosine production (for example, 2 μmol·min−1·litre−1 interstitial fluid), interstitial fluid adenosine deaminase activity of 105 nmol·s−1 resulted in steady state adenosine concentrations at least 10-fold lower than generally accepted base values (0.1–0.2 μmol·litre−1). Accordingly, the data indicate that coronary vasodilatation in response to acute hypoxia is not uniquely dependent on adenosine.
Survivors — Dialysis, Immigration, and U.S. Law
Authors: Rajeev Raghavan, Ricardo Nuila
Journal: New England Journal of Medicine (2011)

Santiago, one of 6000 undocumented U.S. residents with end-stage renal disease, is in the ER again. He sits among 20 patients, all waiting for one result: the potassium. Will it be high enough today to earn him one of the 12 chairs in the dialysis unit?
Letter: Pyridoxine and oestrogen-induced glucose intolerance.
Authors: E J Cornish, W Tesoriero
Journal: BMJ (1975)

Clinical examination of the possibility that xanthurenic acid is the cause of oral contraceptive (OC) induced glucose tolerance and gestational diabetes has been carried out. The reduction by pyridoxine of excessive xanthurenic acid excretion following a tryptophan load has been associated with an improvement in glucose tolerance, yet it is not believed that the 2 are causally related. Instead, the beneficial effects of pyridoxine are possibly because of normalization of other tryptophan metabolites. Some women suffer from estrogen-induced glucose intolerance independent of any abnormalities in xanthurenic acid excretion. It has been found that the administration of xanthurenic acid 120 mg/kg intraperitoneally in ammoniated saline failed to alter blood glucose in male Sprague Dawley or Wistar rats. The experiments were repeated using the special high fat diet which had been used in the original studies on the diabetogenic effects of xanthurenic acid, and xanthurenic acid was found to be inactive. Xanthurenic acid did not impair glucose tolerance when given 1 hour before an oral glucose load in further experiments. The failure to demonstrate any diabetogenic effect of xanthurenic acid could not be because of contamination with the 8-methyl ether of xanthurenic acid, which has been reported to be antidiabetogenic, since the sample of xanthurenic acid used was found to be free from this contaminant.
186 Is fatigue as a symptom of hepatic encephalopathy (HE) induced by early changes of cerebral adenosin A1 receptors? Investigations with F-18-CPFPX and pet techniques in cirrhotics with manifest and non-manifest HE
Authors: C. Boy, G. Kircheis, P. Meyer, H. Herzog, M. Holschbach, J. Hemker, A. Bauer, H.H. Coenen, D. Haussinger, K.J. Zilles
Journal: Journal of Hepatology (2004)
Cost effectiveness of home based population screening for <i>Chlamydia trachomatis</i> in the UK: economic evaluation of chlamydia screening studies (ClaSS) project
Authors: Tracy E Roberts, Suzanne Robinson, Pelham M Barton, Stirling Bryan, Anne McCarthy, John Macleod, Matthias Egger, Nicola Low
Journal: BMJ (2007)

<b>Objective</b> To investigate the cost effectiveness of screening for <i>Chlamydia trachomatis</i> compared with a policy of no organised screening in the United Kingdom. <b>Design</b> Economic evaluation using a transmission dynamic mathematical model. <b>Setting</b> Central and southwest England. <b>Participants</b> Hypothetical population of 50 000 men and women, in which all those aged 16-24 years were invited to be screened each year. <b>Main outcome measures</b> Cost effectiveness based on major outcomes averted, defined as pelvic inflammatory disease, ectopic pregnancy, infertility, or neonatal complications. <b>Results</b> The incremental cost per major outcome averted for a programme of screening women only (assuming eight years of screening) was £22 300 (€33 000; $45 000) compared with no organised screening. For a programme screening both men and women, the incremental cost effectiveness ratio was approximately £28 900. Pelvic inflammatory disease leading to hospital admission was the most frequently averted major outcome. The model was highly sensitive to the incidence of major outcomes and to uptake of screening. When both were increased the cost effectiveness ratio fell to £6200 per major outcome averted for screening women only. <b>Conclusions</b> Proactive register based screening for chlamydia is not cost effective if the uptake of screening and incidence of complications are based on contemporary empirical studies, which show lower rates than commonly assumed. These data are relevant to discussions about the cost effectiveness of the opportunistic model of chlamydia screening being introduced in England.
Does the emphasis on risk in psychiatry serve the interests of patients or the public? Yes
Authors: J. F. Morgan
Journal: BMJ (2013)

Identifying patients who are likely to harm themselves or others has become central to psychiatry. <b>John Morgan</b> argues that though the methods are flawed, identifying risk is essential, but <b>Matthew Large </b>(doi:10.1136/bmj.f857) thinks we should focus on the wider harms that patients may experience
Altered expression of E-cadherin in hepatocellular carcinoma: Correlations with genetic alterations, β-catenin expression, and clinical features
Authors: Yu Wei, Jeanne Tran Van Nhieu, Sylvie Prigent, Petcharin Srivatanakul, Pierre Tiollais, Marie-Annick Buendia
Journal: Hepatology (2002)

E-cadherin is a key cell adhesion protein implicated as a tumor/invasion suppressor in human carcinomas and a binding partner of β-catenin, which plays a critical role in Wnt signaling and in tumorigenesis. Here we report genetic and expression studies of E-cadherin and β-catenin in hepatocellular carcinoma (HCC). Immunohistochemical analysis of E-cadherin expression in 37 HCCs and adjacent nontumor tissues revealed important variations among tumor samples, ranging from complete or heterogeneous down-regulation in 35% of cases to marked overexpression in 40% of tumors. Loss of E-cadherin expression was closely associated with loss of heterozygosity (LOH) at the E-cadherin locus and methylation of CpG islands in the promoter region ( P &lt; .002), predominantly in hepatitis B virus (HBV)-related tumors ( P &lt; .005). No mutation of the E-cadherin gene could be detected in the tumors examined, suggesting the requirement for reversible mechanisms of E-cadherin down-regulation. In most HCCs, including E-cadherin-positive and -negative cases, β-catenin was strongly expressed at the cell membrane and nuclear accumulation of the protein was correlated with the presence of mutations in the β-catenin gene itself, but not with E-cadherin loss. At difference with a number of epithelial cancers, vascular invasion was frequently noted in HCCs showing enforced expression of the membranous E-cadherin/β-catenin complex. In conclusion, these data support the notion that E-cadherin might play diverse and seemingly paradoxic roles in HCC, reflecting specific requirements for tumor growth and spread in the liver environment.
Abstract 1096: Loss of miR-200 family of microRNAs confers resistance to tamoxifen in human breast cancer cells
Authors: Tissa T. Manavalan, Carolyn M. Klinge
Journal: Cancer Research (2012)

Abstract MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level. MiR-200 family includes two clusters i.e. miR-200 a/200b/ 429 and miR-200c/141 encoded on chromosome 1 and chromosome 12, respectively. Previous studies have demonstrated that miR-200 family targets ZEB1, a transcription factor that promotes epithelial-to-mesenchymal transition (EMT). Previous reports demonstrated a loss of miR-200a, b and c in MDA-MB-231 breast cancer cells resulted in EMT. These studies also showed a concomitant increase in ZEB1 protein. We observed lower miR-200a, b and c expression in estrogen-independent LCC1 and endocrine-resistant LCC2, LCC9, and LY2 compared to the parental, endocrine-sensitive MCF-7 human breast cancer cell line. We found that ZEB1 protein is expressed in tamoxifen-resistant LY2 cells but not in tamoxifen-sensitive MCF-7 cells. LY2 cells did not express E-cadherin, a ZEB1 target which is also a marker for epithelial phenotype. This is the first demonstration that LY2 cells have undergone EMT as part of their endocrine-resistant phenotype. These studies indicate that loss of miR-200 and a corresponding increase in ZEB1 protein is an indicator of tamoxifen-resistance in breast cancer cells. Further, in concordance with higher miR-221/222, there was decreased expression of estrogen receptor alpha (ERα) mRNA and protein in LY2 cells when compared to MCF-7 cells. We hypothesize that ERα expression is decreased in cells that have undergone EMT and this subsequently leads to endocrine-resistance and an invasive phenotype. Future studies will determine whether re-expression of ERα or knockdown of ZEB1 restores TAM-sensitivity in LY2 cells. By evaluating the expression of E-cadherin, it will be possible to determine whether restoration of ERα or knockdown of ZEB1 can revert cells from a mesenchymal to an epithelial phenotype. If validated, loss of miR-200 could be used as a marker of poor prognosis in TAM-resistant breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1096. doi:1538-7445.AM2012-1096
924 CLASSIFICATION OF ACUTE LIVER FAILURE OF INDETERMINATE ETIOLOGY: USEFULNESS OF CLUSTERING ANALYSIS USING A SELF-ORGANIZING MAP (SOM)
Authors: N. Nakayama, M. Oketani, Y. Kawamura, M. Inao, S. Nagoshi, K. Fujiwara, H. Tsubouchi, S. Mochida
Journal: Journal of Hepatology (2011)
Age and acute myeloid leukemia: real world data on decision to treat and outcomes from the Swedish Acute Leukemia Registry
Authors: Gunnar Juliusson, Petar Antunovic, Åsa Derolf, Sören Lehmann, Lars Möllgård, Dick Stockelberg, Ulf Tidefelt, Anders Wahlin, Martin Höglund
Journal: Blood (2008)
Outcomes of Adrenalectomy for Isolated Synchronous Versus Metachronous Adrenal Metastases in Non–Small-Cell Lung Cancer: A Systematic Review and Pooled Analysis
Authors: Tawee Tanvetyanon, Lary A. Robinson, Michael J. Schell, Vivian E. Strong, Rachna Kapoor, Daniel G. Coit, Gerold Bepler
Journal: Journal of Clinical Oncology (2008)

Purpose Several small studies have reported that an adrenalectomy for isolated adrenal metastasis in non–small-cell lung cancer (NSCLC), along with a surgical resection for the primary lung cancer, can be curative. However, some suggest that the survival outcome among patients with a synchronous metastasis is poor. It remains unclear whether this treatment approach is warranted among those with synchronous metastasis. Methods A search for publications on adrenalectomy for NSCLC was performed via the MEDLINE database. Studies reporting on survival outcomes and containing at least four analyzable patients who had surgery for primary lung cancer were included. Those not allowing separation of outcomes between synchronous and metachronous metastases were excluded. Synchronous metastasis was defined as a disease-free interval (DFI) of 6 months or less. Results There were 10 publications contributing 114 patients; 42% of patients had synchronous metastases and 58% had metachronous metastases. The median DFIs were 0 and 12 months, respectively. Patients in the synchronous group were younger than those in the metachronous group (median age 54 v 68 years). Complications from adrenalectomy were infrequent. Median overall survival was shorter for patients with synchronous metastasis than those with metachronous metastasis (12 months v 31 months, generalized Wilcoxon P value = .02). However, the 5-year survival estimates were equivalent at 26% and 25%, respectively. Conclusion For an isolated adrenal metastasis from NSCLC, patients with a synchronous metastasis who underwent adrenalectomy had a shorter median overall survival than those with a metachronous metastasis. However, a durable long-term survival is achieved in approximately 25% in both groups.
FOXO1 impairs whereas statin protects endothelial function in diabetes through reciprocal regulation of Krüppel-like factor 2
Authors: Hae-Young Lee, Seock-Won Youn, Hyun-Jai Cho, Yoo-Wook Kwon, Sae-Won Lee, Sung-Jin Kim, Young-Bae Park, Byung-Hee Oh, Hyo-Soo Kim
Journal: Cardiovascular Research (2012)

Krüppel-like factor 2 (KLF2) is implicated as a key molecule maintaining endothelial function. This study was designed to evaluate the reciprocal regulation of KLF2 by the forkhead transcription factor FOXO1, and the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor atorvastatin, in hyperglycaemic conditions.Exposure of human umbilical vein endothelial cells to 30 mM glucose activated FOXO1 and suppressed KLF2. These effects were reversed by FOXO1 small interfering RNA. Adenoviral transfection of constitutively active FOXO1 suppressed KLF2 expression. Interestingly, atorvastatin inhibited FOXO1 by increasing phosphorylation and also by inhibiting nuclear localization and replenished KLF2 in high-glucose conditions. This effect of atorvastatin was attenuated by mevalonate. Chromatin immunoprecipitation analysis demonstrated that glucose increased whereas atorvastatin decreased FOXO1 binding to the promoter region of the KLF2 gene. In the vessels of Otsuka Long-Evans Tokushima Fatty rats, animal models of type 2 diabetes, FOXO1 was activated and KLF2 was suppressed, and this was reversed by atorvastatin treatment. The arteries from Otsuka Long-Evans Tokushima Fatty rats showed impairment of endothelium-dependent vasodilatation, and both atorvastatin and KLF2 gene therapies restored it.Suppression of KLF2 by FOXO1 may be a plausible mechanism of diabetic endothelial dysfunction. High-glucose-induced, FOXO1-mediated KLF2 suppression was reversed by atorvastatin, suggesting that intensive statin treatment could be a therapeutic option in diabetic vascular dysfunction.
Topical imiquimod eradicates skin metastases of malignant melanoma but fails to prevent rapid lymphogenous metastatic spread
Authors: S. Ugurel, A. Wagner, C. Pfohler, W. Tilgen, U. Reinhold
Journal: British Journal of Dermatology (2002)

Sir, Imiquimod [1‐(2‐methylpropyl)‐1H‐imidazo[4,5c]quinolin‐4‐amine] is a new immunomodulating agent that has been shown to possess both antiviral and antitumoral activity.1, 2 These effects are at least partially based on its role as an inducer of cytokines such as interferon‐α, tumour necrosis factor‐α, interleukin (IL)‐6 and IL‐8.3 Imiquimod has been described as an efficient topical agent in the treatment of virally induced genital and anal warts.4 Recent observations suggest imiquimod to be a new and promising agent for the topical treatment of different types of skin cancers such as basal cell carcinoma,5 squamous cell carcinoma6 and even melanoma.7, 8 The exact mechanisms of action in vivo and particularly, the range of its systemic effects after topical application, are still unclear. We report an 81‐year‐old man with melanoma, whose skin satellite metastases were successfully treated with topical imiquimod, but who was nevertheless subsequently diagnosed as having rapidly growing metastatic spread in the regional lymph node area despite ongoing therapy. The patient was first diagnosed as having malignant melanoma of the upper right arm in June 2000. Six months after complete resection of the primary lesion, he developed multiple satellite metastases surrounding the primary excision site (Fig. 1a). As he refused further surgery, topical treatment with imiquimod was initiated. Imiquimod 12·5 mg (Aldara® cream; 3M Medica, Borken, Germany) was applied daily under occlusion (OpSite transparent film; Smith & Nephew, Hull, U.K.) to the visible metastatic area of 6 cm diameter as well as to a 2‐cm margin of surrounding skin. During 12 weeks of treatment, the patient was monitored at weekly intervals on an out‐patient basis; tests included haemograms and blood chemistry. In addition, ultrasound imaging of the regional lymph nodes was performed at 4‐week intervals. Two weeks after onset of therapy, the metastatic skin area showed intense erythema, induration and small erosive patches (Fig. 1b). After 4 weeks of treatment, the erythematous area enlarged to cover the entire area undergoing topical application of imiquimod (Fig. 1c). Furthermore, the erosive patches increased in size while visible tumour nodes decreased. Thereafter, the treatment schedule was changed from daily to alternate daily application of topical imiquimod. After a total of 6 weeks of treatment the clinical signs of inflammation decreased (Fig. 1d). Ten weeks after onset of therapy the tumour residues appeared clinically undetectable, with only moderate signs of inflammation visible at the treatment site (Fig. 1e).
The Book of Job and the Modern View of Depression
Authors: Morton Allan Kapusta, Solomon Frank
Journal: Annals of Internal Medicine (1977)

The Biblical Book of Job is a wisdom book. Wisdom, in this context, refers to the intellectual discipline taught by the sages of ancient Israel to provide professionals with a realistic approach to the problems of life. Chapter 30 of the Book of Job is a key-index of ideas that, if followed through the book, discloses a modern scientifically accurate description of a depression that, at times, was life-threatening. There are practical clinical clues to distinguish between normal mourning and depression, as well as aids to the differential diagnosis of somatic symptoms that may arise from depression. A timeless model of the scope and limitations of the professional relation between patient and comforter is also presented. Part of the wisdom of the Book of Job is to use depression as an example of a life-threatening illness to provide an unexcelled standard of clinical observation and medical intervention.
Expression of tumor-associated carbohydrate antigen Tn in cancer cells is stimulated by cytokine secreted from cancer cells
Authors: Alex Lin, Chiao-en Chen, Jaulang Hwang
Journal: Journal for ImmunoTherapy of Cancer (2014)

Meeting abstracts Tumour-associated carbohydrate antigen (TACA) Tn is always observed on the cell surface of malignant tumour cells. Tn is presented as mucin-type carbohydrate. It has been reported to be associated with cancer progression, but the regulation on Tn expression in cancer cells is not
MP criticises government response on open access publishing
Authors: Lynn Eaton
Journal: BMJ (2004)

A leading Labour MP has criticised the government's response to proposals for an overhaul in the way scientific journals are funded, claiming that the Department of Trade and Industry (DTI) has “kowtowed to the powerful publishing lobby.”

Ian Gibson, chairman of the House of Commons Science and Technology Committee, told the BMJ that the government's response to his committee's report was “abominable” and went on to criticise the apparent dilution of comments from one of the main supporters of the “open access, author pays” publishing model.

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The “author pays” model of open access, online publishing, as exemplified by the new journal PLoS Medicine , could potentially threaten subscription based journals, such as the BMJ and the Lancet 

Dr Gibson is a strong proponent of the “author pays” model of open access, online publishing, as exemplified by the Public Library …

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Discordant Cortisol Response to Exogenous ACTH and Insulin-Induced Hypoglycemia in Patients with Pituitary Disease
Authors: George C. Borst, H. Jakob Michenfelder, John T. O'Brian
Journal: New England Journal of Medicine (1982)

AN assessment of hypothalamic-pituitary-adrcnocortical (HPA) function in patients with pituitary or hypothalamic disease is often necessary for estimating the risk that acute adrenal insufficiency will occur in response to severe stress, such as trauma, surgery, or infection. Several investigators have suggested that the adrenal response to an intravenous bolus dose of ACTH accurately predicts the integrity of the HPA axis, without causing the side effects attendant on insulin-induced hypoglycemia or administration of metyrapone or pyrogen.1 2 3 However, ACTH stimulation does not directly measure hypothalamic or pituitary responsiveness, and thus it carries the theoretical risk of diagnostic error in patients with pituitary . . .