tbuckley/cabot-search huggingface dataset:
DEPRESSION BY ANTIBODY OF THE IMMUNE RESPONSE TO HOMOGRAFTS AND ITS ROLE IN IMMUNOLOGICAL ENHANCEMENT
Authors: George D. Snell, Henry J. Winn, Jack H. Stimpfling, Stephen J. Parker
Journal: The Journal of Experimental Medicine (1960)

This paper reports tests of two hypotheses that have been proposed to account for the enhanced growth of tumor homografts in the presence of antiserum reactive with the graft (immunological enhancement). According to the first hypothesis, enhancement is due to some "physiological" alteration in the tumor, induced by its contact with antiserum, which insures its survival despite the hostile response of the host. According to the second hypothesis, antiserum alters the response of the host. By blocking the development of the cellular type of immunity, which is the main agent in graft destruction, it permits the graft to survive. To test hypothesis 1, strain A tumor SaI was passed from A's, and from enhanced B10.D2's, into untreated B10.D2's. The per cent of deaths was essentially the same in both groups (48 and 44 per cent, respectively); there was no evidence that passage through enhanced B10.D2's altered the capacity of the tumor to grow in the foreign strain. Several other groups of mice included in the experiment all confirmed this conclusion. The experiment failed to confirm hypothesis 1. In the tests of hypothesis 2, the effect of isoantiserum on immune responses of both the humoral and cellular type was measured. When antiserum was given together with foreign strain lymphoid cells (antigen), almost no additional antibody was manufactured; in contrast with this, controls receiving foreign cells only produced red cell agglutinating antibody in high titer. The effect of antiserum on the development of immunity of the cellular type was tested by the method of Winn. In this assay, presumptively immune node cells, in various dilutions, are mixed with tumor cells and injected into appropriate mice. Immunity is indicated by inhibited tumor growth. Antiserum given at the same time as a tumor homograft greatly depressed the immunity of the cells expressed from the draining nodes. At 6 days after the graft, the level of immunity of cells from treated mice was 1/24th to 1/32nd that of cells from controls receiving tumor alone. The same sort of depressing effect was noted when the immunizing tissue was foreign thymus or embryo. Antiserum given 1 or more days after the immunizing tissue also resulted in a lower level of cellular immunity (but the assay used in this case was a less critical one). These results provide an adequate explanation of the phenomenon of immunological enhancement, at least as it occurs in the particular test system used in these experiments. Since it is cellular immunity rather than humoral antibody that inhibits the growth of most grafts (transplantable leukemias are an exception), the depression of this immunity by antibody is favorable to the growth of a homograft.
Sustained intra-articular release of celecoxib from in situ forming gels made of acetyl-capped PCLA-PEG-PCLA triblock copolymers in horses
Authors: Audrey Petit, Everaldo M. Redout, Chris H. van de Lest, Janny C. de Grauw, Benno Müller, Ronald Meyboom, Paul van Midwoud, Tina Vermonden, Wim E. Hennink, P. René van Weeren
Journal: Biomaterials (2015)
Dissolution Rate of Cholesterol in Monooctanoin
Authors: Joseph B. Bogardus
Journal: Hepatology (1984)

Monooctanoin is used clinically for dissolution of common bile duct cholesterol gallstones. A number of factors influencing the dissolution rate of cholesterol monohydrate in this solvent were investigated. Water increased cholesterol dissolution rate in a manner inconsistent with previous solubility measurements. Dissolution rate increased approximately 50% in the presence of 10 to 15% water in monooctanoin. Further studies on viscosity, the effect of polymers and temperature showed that the solvent viscosity had a dominating influence on dissolution rate. This was thought to be caused by the interaction of cholesterol with the solvent in the dissolving surface layer which caused a decrease in the diffusion coefficient (and dissolution rate) of cholesterol. Reducing viscosity and increasing temperature were identified as possible approaches for increasing cholesterol gallstone dissolution rate in monooctanoin.
Mechanisms of a clonidine-induced decrease in portal pressure in normal and cirrhotic conscious rats
Authors: Dominique Roulot, Alain Braillon, Christophe Gaudin, Yves Ozier, Catherine Girod, Didier Lebrec
Journal: Hepatology (1989)

The effects of clonidine on portal pressure and splanchnic blood flow were studied in conscious rats with sinusoidal portal hypertension due to cirrhosis induced by bile duct ligation. In cirrhotic and sham-operated rats, clonidine (20 micrograms per kg body weight, intravenously) significantly reduced portal, pressure from 19.0 +/- 0.6 to 14.5 +/- 1.0 mmHg and from 9.8 +/- 0.9 to 7.3 +/- 0.5 mmHg, respectively. No significant change in systemic hemodynamics was observed. In cirrhotic rats, clonidine reduced portal pressure, probably by producing a significant increase in portal tributary vascular resistance leading to a 25% decrease in portal tributary blood flow (radioactive microsphere method). In sham-operated rats, clonidine reduced portal pressure presumably by decreasing hepatic portal vascular resistance, since no significant change in portal tributary blood flow was observed. In both groups, clonidine administration significantly decreased plasma noradrenaline concentration. Placebo administration produced neither significant hemodynamic nor significant plasma noradrenaline concentration change. These findings indicate that the sympathetic regulation of the splanchnic circulation is impaired in cirrhotic rats.
The Penikese Hospital
Authors: Thomas D. Sabin
Journal: New England Journal of Medicine (1981)

The first official record of Hansen's disease (HD)* in Massachusetts appeared in 1882. A man in Salem was said to have the tubercular form of the disease.1 He was isolated at the Salem almshouse, and he died there in March 1883. The disease was also occasionally diagnosed among seamen in the thriving port of Boston during that era. These patients could be held in the quarantine hospital on Gallup's Island in Boston Harbor and were often deported.However, in 1904 the Massachusetts Board of Charity received word that a resident of Harwich on Cape Cod had been diagnosed as having . . .
Serum screening for Down's syndrome: Authors' reply
Authors: N. J Wald, H. S Cuckle, J. W Densem, K. Nanchahal, P. Royston, T. Chard, J. E Haddow, G. J Knight, G. E Palomaki, J. A Canick
Journal: BMJ (1989)

Breach of this standard is ipso facto malpractice.Furthermore, responsibility for professional acts rests with the actUal treatihg physician and may not be trahsferted to leiployers, government pro- gramnmes, hospital officials or commnittees, chiefs of service, comftiiWs §onets, atid the like.We have no professional dMty to any such party; our obligatlon is solely t6 out patienits.
Surgeons' performance data to be available from July
Authors: K. Chinthapalli
Journal: BMJ (2013)

Data on performance of individual surgeons in nine specialties will be published from the beginning of July, the Royal College of Surgeons announced on 10 June.

Norman Williams, the college’s president and a colorectal surgeon, said at a press briefing, “We really do see this as a watershed moment for the profession, and it is all about transparency. I think it is most appropriate, particularly after the Francis report [on failings at Mid Staffordshire NHS Foundation Trust] . . . and what we want to do is drive up standards to get everybody up to a really excellent standard.”

The move comes after NHS England’s commitment to publish outcomes for individual surgeons in December 2012.1 For the first time, publication of data will cover all NHS operations of named consultant surgeons in bariatric surgery, colorectal surgery, head and neck …
Specific Genetic Predictors of Chemotherapeutic Response and Survival in Patients With Anaplastic Oligodendrogliomas
Authors: J. Gregory Cairncross, Keisuke Ueki, Magdelena C. Zlatescu, David K. Lisle, Dianne M. Finkelstein, Robert R. Hammond, Jonathan S. Silver, Paul C. Stark, David R. Macdonald, Yasushi Ino, David A. Ramsay, David N. Louis
Journal: JNCI Journal of the National Cancer Institute (1998)

Gliomas are common malignant neoplasms of the central nervous system. Among the major subtypes of gliomas, oligodendrogliomas are distinguished by their remarkable sensitivity to chemotherapy, with approximately two thirds of anaplastic (malignant) oligodendrogliomas responding dramatically to combination treatment with procarbazine, lomustine, and vincristine (termed PCV). Unfortunately, no clinical or pathologic feature of these tumors allows accurate prediction of their response to chemotherapy. Anaplastic oligodendrogliomas also are distinguished by a unique constellation of molecular genetic alterations, including coincident loss of chromosomal arms 1p and 19q in 50%-70% of tumors. We have hypothesized that these or other specific genetic changes might predict the response to chemotherapy and prognosis in patients with anaplastic oligodendrogliomas. Therefore, we have analyzed molecular genetic alterations involving chromosomes 1p, 10q, and 19q and the TP53 (on chromosome 17p) and CDKN2A (on chromosome 9p) genes, in addition to clinicopathologic features in 39 patients with anaplastic oligodendrogliomas for whom chemotherapeutic response and survival could be assessed.Allelic loss (or loss of heterozygosity) of chromosome 1p is a statistically significant predictor of chemosensitivity, and combined loss involving chromosomes 1p and 19q is statistically significantly associated with both chemosensitivity and longer recurrence-free survival after chemotherapy. Moreover, in both univariate and multivariate analyses, losses involving both chromosomes 1p and 19q were strongly associated with longer overall survival, whereas CDKN2A gene deletions and ring enhancement (i.e., contrast enhancement forming a rim around the tumor) on neuroimaging were associated with a significantly worse prognosis. The inverse relationship between CDKN2A gene deletions and losses of chromosomes 1p and 19q further implies that these differential clinical behaviors reflect two independent genetic subtypes of anaplastic oligodendroglioma. These results suggest that molecular genetic analysis may aid therapeutic decisions and predict outcome in patients with anaplastic oligodendrogliomas.
Nucleotide-Binding Oligomerization Domain 2 Receptor Is Expressed in Platelets and Enhances Platelet Activation and Thrombosis
Authors: Si Zhang, Shenghui Zhang, Liang Hu, Lili Zhai, Ruyi Xue, Jianqin Ye, Leilei Chen, Guanjun Cheng, Jozef Mruk, Satya P. Kunapuli, Zhongren Ding
Journal: Circulation (2015)

Background— Pattern recognition receptor nucleotide-binding oligomerization domain 2 (NOD2) is well investigated in immunity, but its expression and function in platelets has never been explored. Method and Results— Using reverse transcription polymerase chain reaction and Western blot, we show that both human and mouse platelets express NOD2, and its agonist muramyl dipeptide induced NOD2 activation as evidenced by receptor dimerization. NOD2 activation potentiates platelet aggregation and secretion induced by low concentrations of thrombin or collagen, and clot retraction, as well. These potentiating effects of muramyl dipeptide were not seen in platelets from NOD2-deficient mice. Plasma from septic patients also potentiates platelet aggregation induced by thrombin or collagen NOD2 dependently. Using intravital microscopy, we found that muramyl dipeptide administration accelerated in vivo thrombosis in a FeCl 3 -injured mesenteric arteriole thrombosis mouse model. Platelet depletion and transfusion experiments confirmed that NOD2 from platelets contributes to the in vivo thrombosis in mice. NOD2 activation also accelerates platelet-dependent hemostasis. We further found that platelets express receptor-interacting protein 2, and provided evidence suggesting that mitogen activated-protein kinase and nitric oxide/soluble guanylyl cyclase/cGMP/protein kinase G pathways downstream of receptor-interacting protein mediate the role of NOD2 in platelets. Finally, muramyl dipeptide stimulates proinflammatory cytokine interleukin-1β maturation and accumulation in human and mouse platelets NOD2 dependently. Conclusions— NOD2 is expressed in platelets and functions in platelet activation and arterial thrombosis, possibly during infection. To our knowledge, this is the first study on NOD-like receptors in platelets that link thrombotic events to inflammation.
South American pemphigus foliaceus: Study of an epidemic in El Bagre and Nechi, Colombia 1982 to 1986
Authors: MARY ANN ROBLEDO, C. STEMA PRADA, DIEGO JARAMILLO, W. LEON
Journal: British Journal of Dermatology (1988)

Between 1982 and 1986 we have had the chance to study 21 patients with pemphigus foliaceus of the 'fogo selvagem' type. The patients came from El Bagre and Nechi, rural areas of Colombia with some gold mining. This is the first outbreak of South American pemphigus foliaceus reported in Colombia. The majority of the patients were mestizo men, who worked as farmers or miners or both, with an average age of 44. Five patients were relatives. Eleven patients (52%) had mild disease, three (14%) moderate disease and seven (33%) severe disease. During hospitalization, three patients died due to complications or as a result of immunosuppressive treatment. Of the remaining 18 patients, 10 were in remission with treatment, one was in remission without treatment, while no information was available on the remaining seven.
THE SPECIFICITY OF EARLY CHANGES IN THE SKIN DURING CARCINOGENESIS
Authors: M.C. Bibby
Journal: British Journal of Dermatology (1981)

Journal Article THE SPECIFICITY OF EARLY CHANGES IN THE SKIN DURING CARCINOGENESIS Get access M.C. Bibby M.C. Bibby Postgraduate School of Studies in Medical & Surgical Sciences, University of Bradford, Bradford BD7 1DP Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 104, Issue 4, 1 April 1981, Pages 485–488, https://doi.org/10.1111/j.1365-2133.1981.tb15324.x Published: 01 April 1981
Development and in vitro/in vivo evaluation of controlled release provesicles of a nateglinide–maltodextrin complex
Authors: Ranjan Ku. Sahoo, Nikhil Biswas, Arijit Guha, Nityananda Sahoo, Ketousetuo Kuotsu
Journal: Acta Pharmaceutica Sinica B (2014)

The aim of this study was to characterize the provesicle formulation of nateglinide (NTG) to facilitate the development of a novel controlled release system of NTG with improved efficacy and oral bioavailability compared to the currently marketed NTG formulation (Glinate™ 60). NTG provesicles were prepared by a slurry method using the non-ionic surfactant, Span 60 (SP), and cholesterol (CH) as vesicle forming agents and maltodextrin as a coated carrier. Multilamellar niosomes with narrow size distribution were shown to be successfully prepared by means of dynamic laser scattering (DLS) and field emission scanning electron microscopy (FESEM). The absence of drug-excipient interactions was confirmed by Fourier transform infrared spectroscopy (FT-IR), differential scanning calorimetry (DSC) and X-ray diffraction (XRD) studies. In vitro release of NTG in different dissolution media was improved compared to pure drug. A goat intestinal permeation study revealed that the provesicular formulation (F4) with an SP:CH ratio of 5:5 gave higher cumulative amount of drug permeated at 48 h compared to Glinate™ 60 and control. A pharmacodynamic study in streptozotocin-induced diabetic rats confirmed that formulation F4 significantly (P<0.05) reduced blood glucose levels in comparison to Glinate 60. Overall the results show that controlled release NTG provesicles offer a useful and promising oral delivery system for the treatment of type II diabetes.
L-Arginine reverses low coronary reflow and enhances postischaemic recovery of cardiac mechanical function
Authors: M. Amrani, A.H. Chester, J. Jayakumar, C.J. Schyns, M.H. Yacoub
Journal: Cardiovascular Research (1995)

To evaluate the effect of L-arginine, the physiological substrate of nitric oxide (NO), upon coronary flow (CF) and mechanical function during reperfusion following cardioplegic arrest.Two groups of isolated rat hearts were subjected to cardioplegic arrest for 4 h at 4 degrees C. In group 1 (n = 10) cardioplegic arrest was followed by 4 consecutive periods of reperfusion with Krebs buffer (control), Krebs plus L-lysine (1 mmol/1), Krebs plus L-arginine (1 mmol/1) and Krebs plus L-NGmonomethylarginine (L-NMMA), a specific inhibitor of NO synthesis, (0.5 mmol/1). In group 2, hearts (n = 8) were perfused by Krebs, then L-NMMA, during both pre- and postischaemic periods. In group 3, hearts (n = 8) were perfused by Krebs, then L-arginine (1, 2 and 4 mmol/1). In group 4 (n = 5), NO released into the perfusate was measured before ischaemia and during reperfusion.In group 1, L-arginine enhanced the postischaemic CF (ml/min +/- s.e.m.) from 15.0 +/- 0.4 to 17.2 +/-0.4. This was reduced by L-NMMA to 11.3 +/- 0.3. Postischaemic cardiac output (% of preischaemic value +/- s.e.m.) was increased from 55.8 +/- 2.4 to 80.1 +/- 2.5 by L-arginine and dropped to 54.3 +/- 2.3 with L-NMMA. In group 2, the pre- and postischaemic loss of coronary flow (CF) by L-NMMA was 51% and 31% respectively. In group 3, L-arginine did not modify CF. In group 4 the preischaemic level of NO (in nmol/ml/min) in the coronary effluent, measured by chemiluminescence, was 14.84 +/- 0.83 and dropped significantly (P < 0.05) to levels ranging from 3.80 +/- 0.56 to 4.75 +/- 0.51 during the postischaemic period.Exogenous administration of L-arginine improves low coronary reflow and postischaemic mechanical function.
A mouse model of ethanol dependent pancreatic fibrosis
Authors: G Perides
Journal: Gut (2005)

The majority of patients with chronic pancreatitis are alcoholics. Our goal was to develop a mouse model of alcohol dependent chronic pancreatitis.Mice were fed either the non-alcohol containing Lieber-DeCarli diet or the Lieber-DeCarli diet containing 24% of calories as ethanol. After eight weeks and while on their respective diets, mice were subjected to repeated episodes of acute pancreatitis elicited by administration of caerulein. They were sacrificed 1, 3, and 5 weeks after the last dose of caerulein. Pancreatic morphology and collagen deposition were evaluated in samples stained with haematoxylin-eosin and Sirius red. Collagen content was quantitated by measuring OH-proline. Gene expression was determined by quantitative polymerase chain reaction.Both groups of mice gained weight at the same rate. Those receiving the alcohol containing diet had serum alcohol levels of approximately 100 mM. No histological or gene expression differences were found in mice that were not subjected to acute pancreatitis, regardless of their diet. Necrosis, Sirius red staining, OH-proline content, and expression of alpha-1 collagen I, alpha-smooth muscle actin, transforming growth factor beta1, and tissue inhibitor of metalloproteinase 1 were all increased in mice fed the alcohol containing diet and given caerulein compared with those fed the control diet and given caerulein. Matrix metalloproteinase 9 expression was transiently decreased in mice fed ethanol and given caerulein compared with the group given caerulein but not fed ethanol.We have developed a mouse model of alcohol dependent chronic pancreatic fibrosis. This mouse model may be useful in studies examining the effects of genetic manipulation on chronic pancreatitis.
Role of metformin in treatment of diabetes mellitus
Authors: Riccardo Vigneri, Ira D Goldfine
Journal: Diabetes Care (1987)

Metformin, a biguanide antidiabetic agent that can be administered either alone or in combination with sulfonylureas, has been extensively used in Europe and Canada. The mechanism of action of metformin and other biguanides is not completely understood, but recent in vitro and in vivo studies suggest that metformin may act in part by both increasing the binding of insulin to its receptor and potentiating insulin action. Metformin, because of its chemical structure, does not interact with the liver and has a short half-life. Consequently, lactic acidosis, which is a rare complication of metformin, has not been associated with the proper use of this drug. In addition to its antidiabetic actions, metformin causes weight loss in obese diabetic patients and may be useful in managing associated lipid disorders.
Evaluation of reperfusion strategy for the globally ischaemic rat heart. Recovery of function and energy metabolism
Authors: N. H st, K. Peuhkurinen, S. Hauns , I. Hassinen
Journal: Cardiovascular Research (1992)

The sequelae of myocardial ischaemia can in principle be alleviated by repeated reperfusion, but the accumulation of adenosine monophosphate (AMP) and the loss of interstitial adenosine may lead to adenylate depletion. Repeated oxidative stress could predispose the heart to reperfusion injury. The aim of this study was to investigate the effect of intermittent reperfusion on myocardial energetics and postischaemic function.Isolated retrogradely perfused rat hearts were subjected to 20 min ischaemia, this being continuous in group I while the hearts in group II were reperfused for three 2 min periods at 5 min intervals. Function and energy metabolism were evaluated during the postischaemic reperfusion.Considerable efflux of adenosine compounds was seen during the final reperfusion, this being greater in group I than in group II, at 6.6(SEM 0.9) v 2.0(0.4) mumol.g-1 dry weight (p < 0.01). Tissue AMP, inorganic phosphate, and adenosine catabolites were higher in group I than in II after the ischaemic insult (p < 0.02), and ATP was higher in group II at the end of the final reperfusion (p < 0.05). All the hearts recovered; however, in group I the rate-pressure product was lower than in group II.Repetitive reperfusion, although short in duration, is beneficial in ischaemia in terms of lower adenylate loss and better postischaemic recovery. This should be taken into consideration when designing clinical reperfusion interventions.
Effect of Elevated Basal Insulin on Cancer Incidence and Mortality in Cancer Incident Patients
Authors: Rachel Dankner, Michael H. Shanik, Lital Keinan-Boker, Cindy Cohen, Angela Chetrit
Journal: Diabetes Care (2012)

Diabetes is associated with many forms of cancer. Recent evidence has suggested that some treatments for diabetes are associated with an increased cancer risk. Less is known about the association between endogenous insulin in the prediabetes state and cancer risk.We investigated cumulative cancer incidence and cancer incidence density over 29 years, according to basal insulin, in a cohort of 1,695 nondiabetic men and women of four ethnic origins, aged 51.8 ± 8.0 years at baseline. Total mortality among the 317 subjects (18.7%) who developed cancer at least 2 years after baseline was assessed.In a Cox proportional hazards model, the all-site hazard ratio of cancer incidence comparing the highest insulin quartile with the other three quartiles was 1.09 (95% CI 0.85-1.40), adjusted for age, sex, and ethnicity. BMI, smoking, and fasting blood glucose were not statistically significant in this model. Basal insulin level was not significantly associated with cancer of specific sites (breast, prostate, colon/rectum, or bladder). Fasting insulin in the upper quartile conferred a 37% increased risk for total mortality among cancer patients, adjusting for age, sex, and ethnic origin (95% CI 0.94-2.00, P = 0.097) compared with that of the lower quartiles. Male sex, older age, and North African origins were associated with a greater risk of mortality during follow-up time.This long-term cohort study may suggest a role for basal elevated insulin levels, mainly as a negative predictor in cancer prognosis.