tbuckley/cabot-search huggingface dataset:
Distribution and release of human pancreatic polypeptide.
Authors: T E Adrian, S R Bloom, M G Bryant, J M Polak, P H Heitz, A J Barnes
Journal: Gut (1976)

A simple and reliable radioimmunoassay has been developed for a new gut hormone, HPP. In the primate 93% of the total PP was found in the pancreas with a small amount throughout the remaining gastrointestinal tract. HPP has been shown to be produced by a number of pancreatic apudomas and their metastases. The immunoreactive PP from these tumours and from normal pancreas was chromatographically indistinguishable from the pure peptide. The plasma PP concentration rose rapidly after a meal in normal subjects and was still raised six hours later. Fasting plasma PP levels in patients with PP cell containing pancreatic endocrine tumours were higher than even the postprandial level in normal subjects. PP measurements is thus useful in diagnosis of pancreatic endocrine tumours.
Circulating Leukocyte Counts, Activation, and Degranulation in Dahl Hypertensive Rats
Authors: K. Shen, F. A. DeLano, B. W. Zweifach, G. W. Schmid-Schönbein
Journal: Circulation Research (1995)

Previous evidence has shown that rats with spontaneous hypertension have on average about twice as many circulating leukocytes in comparison with their normotensive counterparts, the Wistar-Kyoto rats. Since such high levels of leukocytes may increase the risk for vascular complications for hypertensive animals, it is useful to ascertain whether a comparable derangement is present in other forms of hypertension. The present study deals with the properties of the circulating leukocytes in rats exhibiting another form of experimental hypertension; Dahl salt-sensitive (Dahl-S) hypertensive rats were compared with Dahl salt-resistant (Dahl-R) control rats. Measurements were performed to determine the following: circulating hematocrit levels, leukocyte counts, differential counts, number of activated leukocytes (by means of nitro blue tetrazolium [NBT] reduction), leukocyte adhesion in vitro and neutrophil CD-18 expression, alkaline phosphatase activity in individual neutrophils and in the plasma, and myeloperoxidase activity in neutrophils. The experimental cohort consisted of Dahl-S and Dahl-R rats maintained for a 6-week period on a 6% NaCl diet. The results show a highly significant elevation in the number of total leukocytes, neutrophil and monocyte counts, and NBT-positive neutrophils and monocytes in Dahl-S but not Dahl-R rats. There was a significant loss of alkaline phosphatase and myeloperoxidase activity in the neutrophils of the salt-treated Dahl-S rats but not in the neutrophils of the untreated Dahl-S or Dahl-R rats. No significant differences were found in neutrophil adhesion under in vitro test conditions between the two strains maintained on the salt diet.(ABSTRACT TRUNCATED AT 250 WORDS)
A neural interface provides long-term stable natural touch perception
Authors: Daniel W. Tan, Matthew A. Schiefer, Michael W. Keith, James Robert Anderson, Joyce Tyler, Dustin J. Tyler
Journal: Science Translational Medicine (2014)

Electrical stimulation, using patterned intensity, applied through cuff-type peripheral nerve interfaces provided stable touch perceptions in the fingers, thumb, and hand of two subjects with upper limb loss for 16 to 24 months.
Lipids and Glucose in Type 2 Diabetes
Authors: Guenther Boden, Markku Laakso
Journal: Diabetes Care (2004)

Historically, type 2 diabetes was considered to revolve around a glucose-insulin axis. The foundations for this thinking were probably laid down by two momentous discoveries in diabetes research. According to popular legend, Oskar Minkowski noticed that urine from his pancreatectomized dogs attracted an inordinate number of flies. He is then alleged to have tasted the urine and noted its sweetness. From this observation came the supposition that the pancreas produced a substance that controlled sugar concentration, and diabetes occurred in the absence of this substance. The second landmark was the discovery by Frederick Banting that insulin was the active element from the pancreas. As a consequence of these two discoveries, the concept that the glucose-insulin relationship was the central element of fuel metabolism gained a firm hold. Diabetes has since been considered to be a disorder primarily associated with abnormal glucose metabolism. This notion is given credence by the considerable amount of data indicating that the chronic elevation of plasma glucose causes many of the microvascular complications of diabetes.

In 1992, McGarry (1) asked what would have happened if Minkowski had lacked a sense of taste but had a good nose. If that had been the case, he may have smelled acetone, and this may have led him to the conclusion that removal of the pancreas affects fatty acid metabolism. If this had happened, our understanding of the pathogenesis of type 2 diabetes may have developed along a different route and led us more quickly to our current awareness that obesity, or more accurately, the products of excess adipose tissue, precede the perturbations of glucose metabolism.

It is now apparent that elevation of plasma free fatty acids (FFAs) plays a pivotal role in the development of type 2 diabetes by causing insulin resistance. Type 2 diabetes develops because pancreatic β-cells …
Primary T wave abnormalities caused by uniform and regional shortening of ventricular monophasic action potential in dog.
Authors: G Autenrieth, B Surawicz, C S Kuo, M Arita
Journal: Circulation (1975)

We correlated primary T wave changes with the changes of monophasic action potentials (MAP) recorded with suction electrodes from the ventricular surface of the dog heart following systemic or intracoronary infusions of small doses of isoproterenol (ISP). The portions of the heart perfused with ISP were excised and weighed to determine the mass of perfused tissue. ISP shortened the ventricular MAP by an average of 12-18 msec in the entire ventricular mass following systemic administration, in 34 plus or minus 6 per cent of the ventricular mass after injection into the left circumflex coronary artery (LCA), in 8.5 plus or minus 2.6% of the ventricular mass after injection into a branch of LCA and in 17 plus or minus 8 per cent of the ventricular mass after injection into the right CA. The MAP changes induced by ISP were similar to the transmembrane action potential changes recorded with microelectrodes from papillary muscles excised from the same dogs. The most important results of this study showed that: 1) the early and the late effects of ISP administration produced opposite effects on the T wave polarity. The early T wave change was associated with nonhomogeneous and the late change with homogeneous MAP shortening; 2) the T wave change was greater after infusion into LCA than after systemic administration, 3) the T wave change was greater after infusion into LCA than after infusion into LCA branch apparently because of greater mass of the ISP-perfused myocardium; 4) the T wave change was greater after infusion into LCA branch than after infusion into RCA, apparently due to the unequal regional repolarization contribution to the T wave; 5) the ventricular gradient did not always reflect the magnitude of the primary T wave change. Our study helps to identify factors contributing to high sensitivity and low specificity of T wave abnormalities.
Reduced Thalamic Volume in Patients With Chronic Schizophrenia After Switching From Typical Antipsychotic Medications to Olanzapine
Authors: Babak Khorram, Donna J Lang, Lili C Kopala, Robert A Vandorpe, Qing Rui, Vina M Goghari, Geoffrey N Smith, William G Honer
Journal: American Journal of Psychiatry (2006)

Objective: The authors performed a longitudinal study of the effects on thalamic volume of switching from typical to atypical antipsychotic medications. Method: Magnetic resonance imaging scans were acquired from 10 subjects with chronic schizophrenia taking typical antipsychotics and 20 healthy volunteers. Subjects with schizophrenia were switched to olanzapine; both groups were rescanned. Results: At baseline, thalamic volumes in subjects with chronic schizophrenia were 5.8% greater than those of healthy volunteers. At follow-up, there was no significant difference between groups. Additional analysis revealed a significant positive correlation between baseline thalamic volume and dosage of typical antipsychotic medication. Higher dosages at baseline were correlated with larger reductions in volume after the switch to olanzapine. Conclusions: Antipsychotic medication effects may be a factor in the wide range of thalamic volume differences reported between subjects with schizophrenia and healthy volunteers.
Selling Bone Marrow —<i>Flynn v. Holder</i>
Authors: I. Glenn Cohen
Journal: New England Journal of Medicine (2011)

On December 1, 2011, in Flynn v. Holder, the U.S. Ninth Circuit Court of Appeals held that the ban on selling "bone marrow" that is part of the National Organ Transplantation Act of 1984 does not encompass "peripheral blood stem cells" obtained through apheresis.
New strategies for treatment of pulmonary fibrosis.
Authors: S H Phan
Journal: Thorax (1995)

New strategies for treatment of pulmonary fibrosisSem H Phan Fibrosis is a common response to various in- sults or injuries to the lung.As such, it com- prises a heterogeneous group of diseases whose initiating factors may be quite different, but whose terminal stages have a common theme -namely, the progressive accumulation of connective tissue replacing normal functional par- enchyma.Recent progress in the understanding of the mechanisms which mediate lung injury and fibrosis should produce more rational and specific therapeutic strategies.However, a con- sequence of this progress is the increasing re- cognition of the complexity of the targets which could be susceptible to new therapeutic agents.In this review the pathogenetic mechanisms relevant to pulmonary fibrosis will be summarised and highlighted, with more detailed discussion reserved for the possible points of therapeutic attack.More detailed reviews of mechanisms and aetiological factors have been presented previously.
Breaking Up Prolonged Sitting Reduces Postprandial Glucose and Insulin Responses
Authors: David W. Dunstan, Bronwyn A. Kingwell, Robyn Larsen, Genevieve N. Healy, Ester Cerin, Marc T. Hamilton, Jonathan E. Shaw, David A. Bertovic, Paul Z. Zimmet, Jo Salmon, Neville Owen
Journal: Diabetes Care (2012)

Observational studies show breaking up prolonged sitting has beneficial associations with cardiometabolic risk markers, but intervention studies are required to investigate causality. We examined the acute effects on postprandial glucose and insulin levels of uninterrupted sitting compared with sitting interrupted by brief bouts of light- or moderate-intensity walking.Overweight/obese adults (n = 19), aged 45-65 years, were recruited for a randomized three-period, three-treatment acute crossover trial: 1) uninterrupted sitting; 2) seated with 2-min bouts of light-intensity walking every 20 min; and 3) seated with 2-min bouts of moderate-intensity walking every 20 min. A standardized test drink was provided after an initial 2-h period of uninterrupted sitting. The positive incremental area under curves (iAUC) for glucose and insulin (mean [95% CI]) for the 5 h after the test drink (75 g glucose, 50 g fat) were calculated for the respective treatments.The glucose iAUC (mmol/L) · h after both activity-break conditions was reduced (light: 5.2 [4.1-6.6]; moderate: 4.9 [3.8-6.1]; both P < 0.01) compared with uninterrupted sitting (6.9 [5.5-8.7]). Insulin iAUC (pmol/L) · h was also reduced with both activity-break conditions (light: 633.6 [552.4-727.1]; moderate: 637.6 [555.5-731.9], P < 0.0001) compared with uninterrupted sitting (828.6 [722.0-950.9]).Interrupting sitting time with short bouts of light- or moderate-intensity walking lowers postprandial glucose and insulin levels in overweight/obese adults. This may improve glucose metabolism and potentially be an important public health and clinical intervention strategy for reducing cardiovascular risk.
Celiprolol, A Vasodilatory β-Blocker, Inhibits Pressure Overload–Induced Cardiac Hypertrophy and Prevents the Transition to Heart Failure via Nitric Oxide–Dependent Mechanisms in Mice
Authors: Yulin Liao, Masanori Asakura, Seiji Takashima, Akiko Ogai, Yoshihiro Asano, Yasunori Shintani, Tetsuo Minamino, Hiroshi Asanuma, Shoji Sanada, Jiyoong Kim, Soichiro Kitamura, Hitonobu Tomoike, Masatsugu Hori, Masafumi Kitakaze
Journal: Circulation (2004)

The blockade of beta-adrenergic receptors reduces both mortality and morbidity in patients with chronic heart failure, but the cellular mechanism remains unclear. Celiprolol, a selective beta(1)-blocker, was reported to stimulate the expression of endothelial NO synthase (eNOS) in the heart, and NO levels have been demonstrated to be related to myocardial hypertrophy and heart failure. Thus, we aimed to clarify whether celiprolol attenuates both myocardial hypertrophy and heart failure via the NO-signal pathway.In rat neonatal cardiac myocytes, celiprolol inhibited protein synthesis stimulated by either isoproterenol or phenylephrine, which was partially suppressed by N(G)-nitro-L-arginine methyl ester (L-NAME). Four weeks after transverse aortic constriction (TAC) in C57BL/6 male mice, the ratio of heart weight to body weight (mg/g) (8.70+/-0.42 in TAC, 6.61+/-0.44 with celiprolol 100 mg x kg(-1) x d(-1) PO, P<0.01) and the ratio of lung weight to body weight (mg/g) (10.27+/-1.08 in TAC, 7.11+/-0.70 with celiprolol 100 mg x kg(-1) x d(-1) PO, P<0.05) were lower and LV fractional shortening was higher in the celiprolol-treated groups than in the TAC group. All of these improvements were blunted by L-NAME. Celiprolol treatment significantly increased myocardial eNOS and activated phosphorylation of eNOS. Myocardial mRNA levels of natriuretic peptide precursor type B and protein inhibitor of NO synthase, which were increased in the TAC mice, were decreased in the celiprolol-treated mice.These findings indicated that celiprolol attenuates cardiac myocyte hypertrophy both in vitro and in vivo and halts the process leading from hypertrophy to heart failure. These effects are mediated by a selective beta1-adrenergic receptor blockade and NO-dependent pathway.
Role of recombinant interferon alfa-2a maintenance in patients with limited-stage small-cell lung cancer responding to concurrent chemoradiation: a Southwest Oncology Group study.
Authors: K Kelly, J J Crowley, P A Bunn, M B Hazuka, K Beasley, C Upchurch, G R Weiss, W J Hicks, D R Gandara, S Rivkin
Journal: Journal of Clinical Oncology (1995)

PURPOSE This study was designed to determine if recombinant interferon alfa-2a (rIFN alpha-2a) could prolong remission duration and/or survival in patients with limited-stage small-cell lung cancer (SCLC) who achieved an objective response to chemoradiotherapy. A secondary end point was to assess the toxicity of chronic IFN administration. PATIENTS AND METHODS One hundred seventy-one of 215 eligible patients achieved an objective response and were eligible to receive rIFN alpha-2a (3 million units [MU]/m2 subcutaneously three times per week escalated to 9 MU/m2 as tolerated) or observation for 2 years. RESULTS One hundred thirty-two of 140 registered patients were eligible. Sixty-four patients were randomized to receive IFN and 68 to observation alone. The median time from randomization to progression was 9 months on the IFN arm and 10 months on the observation arm (P = .72). The overall median survival time was 16 months on the observation arm versus 13 months on the IFN arm (P = .77). Significant toxicities occurred in the rIFN alpha-2a arm. Grade 3 or higher toxicities included malaise, fatigue, and/or lethargy (30%), leukopenia (14%), neutropenia (13%), dyspnea (13%), nausea (11%), and respiratory infection (6%). Forty-three patients discontinued treatment due to intolerable side effects. CONCLUSION rIFN alpha-2a in the dose and schedule used in this study failed to prolong response duration or survival in patients with limited-stage SCLC who had previously responded to an induction chemoradiotherapy program. Failure may have been partly related to poor tolerance and inability to complete therapy.
Increased risk of acute myeloid leukaemia due to polymorphisms in detoxification and DNA repair enzymes
Authors: M.T. Voso, E. Fabiani, F. D'Alo', F. Guidi, A. Di Ruscio, S. Sica, L. Pagano, M. Greco, S. Hohaus, G. Leone
Journal: Annals of Oncology (2007)
Photolocalized eruption associated with acute hepatitis B virus infection
Authors: K. HAYAKAWA, T. SHIOHARA
Journal: British Journal of Dermatology (1996)

We describe a 24-year-old woman with acute hepatitis B virus infection who developed extensive erythematous papules in a photolocalized distribution. The eruption occurred during the prodromal phase, and subsided with the development of jaundice. She had had moderate sunburn 18 days prior to the development of the eruption, which was accentuated on the tanned area. To our knowledge, this is the first case of a photolocalized eruption due to hepatitis B virus infection.
FAS Ligand Triggers Pulmonary Silicosis
Authors: Valéria M. Borges, Haroldo Falcão, José H. Leite-Júnior, Luciana Alvim, Gerlinde P. Teixeira, Momtchilo Russo, Alberto F. Nóbrega, Marcela F. Lopes, Patricia M. Rocco, Wendy F. Davidson, Rafael Linden, Hideo Yagita, Walter A. Zin, George A. DosReis
Journal: The Journal of Experimental Medicine (2001)

We investigated the role of Fas ligand in murine silicosis. Wild-type mice instilled with silica developed severe pulmonary inflammation, with local production of tumor necrosis factor (TNF)-α, and interstitial neutrophil and macrophage infiltration in the lungs. Strikingly, Fas ligand–deficient generalized lymphoproliferative disease mutant (gld) mice did not develop silicosis. The gld mice had markedly reduced neutrophil extravasation into bronchoalveolar space, and did not show increased TNF-α production, nor pulmonary inflammation. Bone marrow chimeras and local adoptive transfer demonstrated that wild-type, but not Fas ligand–deficient lung macrophages recruit neutrophils and initiate silicosis. Silica induced Fas ligand expression in lung macrophages in vitro and in vivo, and promoted Fas ligand–dependent macrophage apoptosis. Administration of neutralizing anti-Fas ligand antibody in vivo blocked induction of silicosis. Thus, Fas ligand plays a central role in induction of pulmonary silicosis.
Type 1 Diabetes Increases the Expression of Proinflammatory Cytokines and Adhesion Molecules in the Artery Wall of Candidate Patients for Kidney Transplantation
Authors: Javier Triñanes, Eduardo Salido, Julián Fernández, Margarita Rufino, José Manuel González-Posada, Armando Torres, Domingo Hernández
Journal: Diabetes Care (2011)

Diabetes may accelerate atheromatosis in uremic patients. Our aim was to assess the influence of type 1 diabetes on the atheromatosis-related inflammation in patients with chronic kidney disease (CKD).We analyzed the expression of proinflammatory cytokines and adhesion molecules in the inferior epigastric artery walls of type 1 diabetic patients with CKD (n = 22) and compared it with nondiabetic uremic patients (n = 92) at the time of kidney transplantation. We evaluated the expression of interleukin (IL)-6, monocyte chemotractant protein (MCP)-1, vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule-1, and the activation of nuclear factor-κβ p65 (NFkB-p65). Common carotid intima-media thickness (c-IMT) was determined by conventional echography.IL-6, MCP-1, and VCAM-1 proteins were elevated in type 1 diabetic patients compared with nondiabetic subjects (P < 0.05). The nuclear localization of NFkB-p65 was higher in type 1 diabetic patients (P < 0.01) and correlated with the levels of MCP-1 in this group (r = 0.726, P < 0.001). Arterial fibrosis correlated with IL-6 and MCP-1 levels (r = 0.411, P < 0.001 and r = 0.378, P = 0.001). A significant correlation was observed between VCAM-1 levels and both the degree of arterial narrowing and c-IMT.Type 1 diabetes produces a proinflammatory state in the arteries of end-stage CKD patients, with increased levels of IL-6, MCP-1, and VCAM-1, as well as a greater degree of p65 activation, which are associated with more severe vascular lesions and higher c-IMT. Although causality is not demonstrated, these findings support the major role of inflammation in type 1 diabetic patients with CKD.
A phase II, multicenter, open-label randomized study of motesanib or bevacizumab in combination with paclitaxel and carboplatin for advanced nonsquamous non-small-cell lung cancer
Authors: G.R. Blumenschein Jr, F. Kabbinavar, H. Menon, T.S.K. Mok, J. Stephenson, J.T. Beck, K. Lakshmaiah, K. Reckamp, Y.-J. Hei, K. Kracht, Y.-N. Sun, R. Sikorski, L. Schwartzberg
Journal: Annals of Oncology (2011)
Myocardial Contractility Is Not Constant During Spontaneous Atrial Fibrillation in Patients
Authors: Carl I. O. Brookes, Paul A. White, Maurice Staples, Paul J. Oldershaw, Andrew N. Redington, Peter D. Collins, Mark I. M. Noble
Journal: Circulation (1998)

Background —The variation in stroke volume and pulse pressure characteristic of atrial fibrillation is usually ascribed to time-dependent ventricular filling, implying a single positive relationship between end-systolic pressure and volume, which defines a single state of myocardial contractility. We tested the hypothesis that contractility also varies. Methods and Results —We measured the left ventricular pressure and volume continuously with a conductance catheter with catheter-tip micromanometer introduced retrogradely into the left ventricle. The end-systolic pressure-volume relationship was determined in 6 patients in atrial fibrillation undergoing cardiac catheterization for diagnostic purposes and 4 control patients in sinus rhythm undergoing coronary artery bypass graft surgery. The normal positive relationship between end-systolic pressure and volume was found in the control patients, but no such positive relationship was found in any patient in atrial fibrillation. In the latter, the slopes of the linear regressions were either not significantly different from zero or significantly negative ( r values &lt;0.08), both results indicating a change in contractility from beat to beat. Significantly negative relationships were found between end-systolic volume and preceding R-R interval (−0.82&lt; r &lt;−0.24), indicating the presence of mechanical restitution. Significantly positive relationships were found between end-systolic volume and the R-R interval before the preceding R-R interval (0.35&lt; r &lt;0.74), indicating the presence of postextrasystolic potentiation. Conclusions —Myocardial contractility is constantly changing from beat to beat in atrial fibrillation because of the influence of the force-interval relationships.
Histochemical Comparison of Naphthol AS-Phosphates for the Demonstration of Phosphatases
Authors: M. S. Burstone
Journal: JNCI Journal of the National Cancer Institute (1958)

Journal Article Histochemical Comparison of Naphthol AS-Phosphates for the Demonstration of Phosphatases Get access M. S. Burstone M. S. Burstone National Institute of Dental Research,3Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 20, Issue 3, March 1958, Pages 601–615, https://doi.org/10.1093/jnci/20.3.601 Published: 01 March 1958 Article history Received: 23 September 1957 Published: 01 March 1958