tbuckley/cabot-search huggingface dataset:
Interpretation and physiological significance of diastolic coronary artery pressure-flow relationships in the canine coronary bed.
Authors: W P Dole, G M Alexander, A B Campbell, E L Hixson, V S Bishop
Journal: Circulation Research (1984)

We analyzed the relationship between diastolic coronary artery pressure and flow in the canine coronary bed, using an electrical analog model of the coronary circulation based on the theory of critical closure. The model contains a voltage-dependent nonlinear resistance and capacitance. The behavior of the resistive element was described using experimental diastolic pressure-flow curves obtained in the absence of compliance effects. Compliance free zero flow pressure intercepts (Pf0) exceeded coronary venous pressure (Pv) by 2- to 5-fold and were related to initial diastolic coronary artery pressure Pa(0) and flow F(0), and Pv by: Pf0 = 14.3 [(Pa(0) - Pv)/F(0)] + Pv + 4.0 (r = 0.93). When coronary artery pressure was suddenly lowered to values less than or equal to the compliance-free Pf0, diastolic flow abruptly decreased and, after a transient reversal, remained at zero for up to 8 seconds. In the model, zero flow pressure represents critical closing pressure and the resistance regulating flow is the difference between coronary artery and venous pressure divided by flow. Theoretically predicted pressure-flow curves were in good agreement with existing experimental data, including the effects of elevating coronary venous pressure on zero flow pressure. Differences between compliance-free pressure-flow curves and those obtained with pressure gradually decreasing were explained by a coronary arterial compliance whose magnitude varies inversely with pressure and is dependent on vasomotor tone. In conclusion, the results of this study demonstrate the existence of a diastolic pressure gradient across the canine coronary bed at zero flow which is dependent on coronary vasomotor tone. A theoretical model of the coronary circulation based on the concept of critical closure describes the observed relationship between diastolic coronary artery pressure and flow during various experimental conditions.
Proliferative and cytotoxic T-cell clones recognize endogenously synthesized HBcAG in an asymptomatic HBsAg carrier
Authors: Pei-Yun Shu, Chungming Chang, Lih-Hwa Hwan, Cheng-Po Hu
Journal: Hepatology (1993)

The characterization of immune responses to hepatitis B virus is crucial for the understanding of hepatitis B virus-caused liver disease. However, lack of a suitable autologous effector-target cell system makes a precise study of the pathogenesis of hepatitis B difficult. In this study we established a model system by using autologous HBcAg-expressing Epstein-Barr virus-immortalized lymphoblastoid cell lines as stimulator/target cells. T-cell cultures were established by repetitive stimulation with recombinant HBcAg or autologous HBcAg-expressing lymphoblastoid cell lines. Both proliferative and cytotoxic T-cell clones were obtained from the peripheral blood of an asymptomatic HBsAg carrier. Clones T12 (CD8+) and T2B (CD4+) were cytotoxic clones specific against autologous lymphoblastoid cell lines expressing endogenously synthesized HBcAg, whereas five CD4+ T-cell clones proliferated in response to lymphoblastoid cell lines incubated with exogenous recombinant HBcAg and autologous HBcAg-expressing lymphoblastoid cell lines. These results indicate that autologous HBcAg-expressing lymphoblastoid cell lines are appropriate stimulator/target cells for the study of HBcAg-specific T lymphocytes. By using this approach, we have demonstrated that both proliferative and cytotoxic T lymphocytes recognizing endogenously synthesized HBcAg are induced during chronic hepatitis B virus infection.
Gastric emptying and release of incretin hormones after glucose ingestion in humans.
Authors: J Schirra, M Katschinski, C Weidmann, T Schäfer, U Wank, R Arnold, B Göke
Journal: Journal of Clinical Investigation (1996)

This study investigated in eight healthy male volunteers (a) the gastric emptying pattern of 50 and 100 grams of glucose; (b) its relation to the phase of interdigestive motility (phase I or II) existing when glucose was ingested; and (c) the interplay between gastric emptying or duodenal perfusion of glucose (1.1 and 2.2 kcal/min; identical total glucose loads as orally given) and release of glucose-dependent insulinotropic peptide (GIP), glucagon-like peptide-1(7-36)amide (GLP-1), C-peptide, insulin, and plasma glucose. The phase of interdigestive motility existing at the time of glucose ingestion did not affect gastric emptying or any metabolic parameter. Gastric emptying of glucose displayed a power exponential pattern with a short initial lag period. Duodenal delivery of glucose was not constant but exponentially declined over time. Increasing the glucose load reduced the rate of gastric emptying by 27.5% (P < 0.05) but increased the fractional duodenal delivery of glucose. Both glucose loads induced a fed motor pattern which was terminated by an antral phase III when approximately 95% of the meal had emptied. Plasma GLP-1 rose from basal levels of approximately 1 pmol/liter of peaks of 3.2 +/- 0.6 pmol/liter with 50 grams of glucose and of 7.2 +/- 1.6 pmol/liter with 100 grams of glucose. These peaks occurred 20 min after glucose intake irrespective of the load. A duodenal delivery of glucose exceeding 1.4 kcal/min was required to maintain GLP-1 release in contrast to ongoing GIP release with negligibly low emptying of glucose. Oral administration of glucose yielded higher GLP-1 and insulin releases but an equal GIP release compared with the isocaloric duodenal perfusion. We conclude that (a) gastric emptying of glucose displays a power exponential pattern with duodenal delivery exponentially declining over time and (b) a threshold rate of gastric emptying of glucose must be exceeded to release GLP-1, whereas GIP release is not controlled by gastric emptying.
UFT Plus Vinorelbine in Advanced Non-small Cell Lung Cancer: A Phase I and an Elderly Patient-Directed Phase II Study
Authors: Tadashi Igishi, Yasushi Shigeoka, Kazuhito Yasuda, Hisashi Suyama, Satoru Katayama, Akinori Sugitani, Shingo Matsumoto, Mitsunobu Yamamoto, Yasuto Ueda, Kenichi Takeda, Takashi Sumikawa, Takanori Sako, Masahiro Kodani, Yutaka Hitsuda, Eiji Shimizu
Journal: Journal of Thoracic Oncology (2009)
Changes in glomerular epithelial cells induced by FGF2 and FGF2 neutralizing antibody in puromycin aminonucleoside nephropathy
Authors: Tamaki Sasaki, Yoshiyuki Jyo, Nobuya Tanda, Yasuhiko Kawakami, Tsutomu Nohno, Hitoshi Tamai, Gengo Osawa
Journal: Kidney International (1997)
Changes of Hepatic Fatty Acid Metabolism Produced by Chronic Thioacetamide Administration in Rats
Authors: Fumihiro Nozu, Naoshi Takeyama, Takaya Tanaka
Journal: Hepatology (1992)

Hepatic mitochondrial functions related to fatty acid metabolism, including the respiratory control ratio, fatty acid oxidative capacity and carnitine palmitoyltransferase I activity, were studied in vitro with mitochondria isolated from rats treated with thioacetamide for up to 12 wk. The levels of ketone bodies, carnitine, carnitine esters and malonyl-coenzyme A were also determined in liver extracts. Polarography of mitochondrial respiration from succinate or glutamate plus malate showed a lower respiratory control ratio in thioacetamide–treated rats, whereas uncoupled oxygen consumption was not altered. This suggests that the mitochondrial respiratory chain capacity remained intact in the thioacetamide–treated rats. The oxygen consumption associated with palmitoyl-coenzyme A and palmitoyl–L–carnitine oxidation by isolated liver mitochondria was increased by thioacetamide treatment on both a per-mitochondrial protein and a per-total liver basis. The carnitine palmitoyl–transferase I activity; the tissue levels of ketone bodies, carnitine and carnitine esters; and the β–hydroxybutyrate/acetoacetate ratio were all higher in the livers of thioacetamide–treated animals than in control livers, whereas the hepatic malonyl-coenzyme A level was decreased by thioacetamide. These results indicate the increased diversion of cytosolic longchain acyl–coenzyme As into the mitochondria for β–oxidation rather than their esterification and use in lipogenesis. These intrahepatic metabolic changes induced by chronic thioacetamide administration may reflect the whole–body catabolic state and can be seen as adaptive for maintaining energy homeostasis under conditions of impaired glucose tolerance. (Hepatology 1992;15:1099-1106).
No going back
Authors: I. Iheanacho
Journal: BMJ (2009)

Forget the future; that’s all in the past now. Referring to it just makes you look like a dinosaur and so out of touch that you’re unaware how the world has moved on. Smart people wouldn’t dream of using this F word, not when they can talk instead of “going forward.”

This pesky phrase is everywhere, and its appeal is obvious. No longer is it the preserve of people who converse entirely in marketing speak and who believe, for example, that thinking can’t …
The fate of Staphylococcal exfoliatin in newborn and adult mice*
Authors: PETER FRITSCH, PETER ELIAS, JANOS VARGA
Journal: British Journal of Dermatology (1976)

The distribution and excretion of the staphylococcal exfoliatin was investigated following in vivo administration of highly purified 125I-labelled exfoliatin fractions to adult and newborn mice. Adult mice excrete approximately one-third of a test dose by 3 hours as compared to a fifteenth of a test dose excreted by newborn mice. Accordingly, blood tracer radioactivity reaches a relatively higher peak and shows a slower decline in newborns than in adults. The urine of adult mice contains considerable biologically active exfoliating material. Both nephrectomized and carbon tetrachloride-poisoned adult mice injected with exfoliatin develop generalized exfoliation whereas comparable doses in untreated controls have no effect. On the other hand, subtotal hepatectomy, followed by injection of exfoliatin, does not lead to exfoliation. We conclude that renal immaturity is a critical factor responsible for the susceptibility of neonates to generalized staphylococcal scalded skin syndrome.
A Young Boy With a Novel, Autosomal-Dominant Signal Transducer and Activator Of Transcription 1 (STAT1) Hypermorphic Mutation Presenting With Pneumocystis Jirovecii Pneumonia (PJP), Chronic Mucocutaneous Candidiasis (CMC), and Combined Immunodeficiency
Authors: Matthew C. Altman, David Hagin, David Buchbinder, Suzanne Skoda-Smith, Hans D. Ochs, Troy R. Torgerson
Journal: Journal of Allergy and Clinical Immunology (2014)
Arrest of Development of Both Bones of the Leg
Authors: J. N. Stevens
Journal: BMJ (1849)

TO THE EDITOR OF THE PROVINCIAL MEDICAL AND SURGICAL JOURNAL. SIR, Should you consider the following simple narrative *of facts referring to a case which occurred in my practice, and which are sent in a true spirit of pro fessional communication, of sufficient interest for insertion in your valuable Journal, they are quite at your service. I remain, Sir, your obedient servant, J. N. STEVENS. 11, Princess Square, Plymouth, May 16, 1849,
The polycystin-1 C-terminal fragment triggers branching morphogenesis and migration of tubular kidney epithelial cells
Authors: Christian Nickel, Thomas Benzing, Lorenz Sellin, Peter Gerke, Anil Karihaloo, Zhen-Xiang Liu, Lloyd G. Cantley, Gerd Walz
Journal: Journal of Clinical Investigation (2002)

Mutations of either PKD1 or PKD2 cause autosomal dominant polycystic kidney disease, a syndrome characterized by extensive formation of renal cysts and progressive renal failure. Homozygous deletion of Pkd1 or Pkd2, the genes encoding polycystin-1 and polycystin-2, disrupt normal renal tubular differentiation in mice but do not affect the early steps of renal development. Here, we show that expression of the C-terminal 112 amino acids of human polycystin-1 triggers branching morphogenesis and migration of inner medullary collecting duct (IMCD) cells, and support in vitro tubule formation. The integrity of the polycystin-2–binding region is necessary but not sufficient to induce branching of IMCD cells. The C-terminal domain of polycystin-1 stimulated protein kinase C-α (PKC-α), but not the extracellular signal–regulated kinases ERK1 or ERK2. Accordingly, inhibition of PKC, but not ERK, prevented polycystin-1–mediated IMCD cell morphogenesis. In contrast, HGF-mediated morphogenesis required ERK activation but was not dependent on PKC. Our findings demonstrate that the C-terminal domain of polycystin-1, acting in a ligand-independent fashion, triggers unique signaling pathways for morphogenesis, and likely plays a central role in polycystin-1 function.
Cigarette Smoking and Dysplasia and Carcinoma In Situ of the Uterine Cervix
Authors: Edwin Trevathan
Journal: JAMA (1983)

We conducted a case-control study of cigarette smoking and dysplasia and carcinoma in situ of the uterine cervix. Cases were black women 17 to 55 years of age who were attending a dysplasia clinic and had biopsy-confirmed cervical pathologic conditions. Controls were women who were attending the family planning clinic at the same hospital and who had at least two normal Papanicolaou smears. Results were adjusted for age, number of sexual partners, age at first intercourse, socioeconomic status, and oral contraceptive use. Cigarette smoking was significantly associated with carcinoma in situ, severe dysplasia, and mild-moderate dysplasia (relative risks, 3.6, 3.3, and 2.4, respectively). Cumulative exposure to cigarette smoking (as measured by pack-years smoked) was strongly related to the risk of these conditions; women with 12 or more pack-years of exposure had relative risks of 12.7, 10.2, and 4.3, respectively, for the three conditions. There was some evidence that the risk was greatest in women who began smoking in their early teenage years. A reduction in the risk of cervical cancer appears to be another inducement for young women not to smoke.
Dissociation of HLA heavy chain and light chain (β2 microglobulin) expression on the cell surface of cutaneous malignancies
Authors: G. MAUDUIT, M. TURBITT, RONA M. MacKIE
Journal: British Journal of Dermatology (1983)

Biopsies from twenty-nine malignant skin tumours and four benign dermatoses and fourteen samples of normal skin were stained for cell surface membrane or cytoplasmic expression of HLA heavy chain and light chain (beta 2 microglobulin) by use of the immunoperoxidase technique on frozen sections using monoclonal antibodies. Results showed a loss of beta 2 microglobulin from the surface of malignant cells in twenty-four out of twenty-nine cutaneous malignancies and the presence of HLA heavy chain in all twenty-nine primary and secondary tumours. Expression of both heavy and light chains was observed in the four benign lesions and in normal epidermis in all samples examined. This would appear to be the first report of dissociation of heavy and light HLA chain expression in various forms of cutaneous malignancy.
Association Between Use of Interferon Beta and Progression of Disability in Patients With Relapsing-Remitting Multiple Sclerosis
Authors: Afsaneh Shirani, Yinshan Zhao, Mohammad Ehsanul Karim, Charity Evans, Elaine Kingwell, Mia L. van der Kop, Joel Oger, Paul Gustafson, John Petkau, Helen Tremlett
Journal: JAMA (2012)

Interferon beta is widely prescribed to treat multiple sclerosis (MS); however, its relationship with disability progression has yet to be established.To investigate the association between interferon beta exposure and disability progression in patients with relapsing-remitting MS.Retrospective cohort study based on prospectively collected data (1985-2008) from British Columbia, Canada. Patients with relapsing-remitting MS treated with interferon beta (n = 868) were compared with untreated contemporary (n = 829) and historical (n = 959) cohorts.The main outcome measure was time from interferon beta treatment eligibility (baseline) to a confirmed and sustained score of 6 (requiring a cane to walk 100 m; confirmed at >150 days with no measurable improvement) on the Expanded Disability Status Scale (EDSS) (range, 0-10, with higher scores indicating higher disability). A multivariable Cox regression model with interferon beta treatment included as a time-varying covariate was used to assess the hazard of disease progression associated with interferon beta treatment. Analyses also included propensity score adjustment to address confounding by indication.The median active follow-up times (first to last EDSS measurement) were as follows: for the interferon beta-treated cohort, 5.1 years (interquartile range [IQR], 3.0-7.0 years); for the contemporary control cohort, 4.0 years (IQR, 2.1-6.4 years); and for the historical control cohort, 10.8 years (IQR, 6.3-14.7 years). The observed outcome rates for reaching a sustained EDSS score of 6 were 10.8%, 5.3%, and 23.1% in the 3 cohorts, respectively. After adjustment for potential baseline confounders (sex, age, disease duration, and EDSS score), exposure to interferon beta was not associated with a statistically significant difference in the hazard of reaching an EDSS score of 6 when either the contemporary control cohort (hazard ratio, 1.30; 95% CI, 0.92-1.83; P = .14) or the historical control cohort (hazard ratio, 0.77; 95% CI, 0.58-1.02; P = .07) were considered. Further adjustment for comorbidities and socioeconomic status, where possible, did not change interpretations, and propensity score adjustment did not substantially change the results.Among patients with relapsing-remitting MS, administration of interferon beta was not associated with a reduction in progression of disability.
Endoscopic Transgastric Necrosectomy for Infected Necrotizing Pancreatitis
Authors: O. Joe Hines, Graham W. Donald
Journal: JAMA (2012)

For decades, treatment of severe acute pancreatitis and pancreatic necrosis incorporated aggressive pancreatic debridement via an open necrosectomy. 1The indications for surgical intervention included confirmed or suspected nonviable pancreatic parenchyma, infection within that necrotic collection, or both.This approach often resulted in poor outcomes due to precipitation of a systemic inflammatory response with subsequent organ failure as a result of gross disturbance of an infected necrotic collection. 2 In the 1990s, it became apparent that this approach was not required for most patients with sterile pancreatic necrosis. 3However, patients presenting to the hospital with infected pancreatic necrosis-as evidenced by a positive culture from a pancreatic aspirate or gas in the pancreatic phlegmon identified by CT scan-often were promptly taken to the operating room because of the perception that delay in operative intervention with drainage would result in an extremely high mortality rate.Despite advances in critical care, open necrosectomy has both substantial complication rates and mortality rates, in some series as high as 92% and 58%, respectively. 4,
Effect on suicide rate of having reduced unemployment is uncertain
Authors: I. H. Makinen
Journal: BMJ (1999)

EDITOR—Lewis and Sloggett recommend policies to reduce unemployment in order to prevent suicide.1 They show that those unemployed in 1981 were overrepresented among suicides 2-11 years later. This seems to imply that the suicides are caused by the unemployment. Their exclusion of cases up to two years after registration to “reduce selection effects” shows that they think that the consequences are long term. Selection problems can hardly be avoided or reduced here by exclusion of the cases nearest in time to registration; it just blurs the hypothesis by excluding …
Can aldose reductase inhibition ameliorate diabetic neuropathy?
Authors: Elizabeth Rasche González
Journal: JAMA (1981)

Aldose reductase, the enzyme "highest up" on the polyol pathway, may play a crucial role in the development of diabetic neuropathy. At the recent meeting of the American Diabetes Association in Cincinnati, a team of investigators headed by Roman Judzewitsch, MD, reported that pharmacologic inhibition of that enzyme significantly increased motor nerve conduction velocity in a group of 36 diabetic patients. Some of the patients were evaluated at the University of Chicago-Pritzker School of Medicine and others at the University of Washington School of Medicine in Seattle. The agent used to accomplish the inhibition was sorbinil, an experimental drug manufactured by Pfizer Laboratories. In an interview with<i>JAMA</i>MEDICAL NEWS, Judzewitsch's co-worker, Daniel Porte, Jr, MD, director of the Diabetes Research Center and professor of medicine at the University of Washington, explained that at the initiation of the study all patients were hyperglycemic on stable diabetic treatment regimens. No patient
Diarrhea Deaths in Children
Authors: Joan Stephenson
Journal: JAMA (2009)

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Abstract 15644: A Fully Human Monoclonal IgG Phosphorylcholine Antibody Prevents Accelerated Atherosclerosis in Mice
Authors: Knut Pettersson, Mark M Ewing, Margreet R de Vries, Rajai Atout, Mariette Nordzell, Daniel J Sexton, Frederic Charlotte, Wouter Jukema, Ewa Ninio, Sonia Karabina, Paul Quax
Journal: Circulation (2011)

Background: Serum contains natural IgM antibodies against the phosphorylcholine headgroup of phosphatidylcholine (anti-PC). Low levels are associated with an increased risk for cardiovascular disea...