tbuckley/cabot-search huggingface dataset:
Reply: H3 or H4 histamine receptors: That which contributes to suppressing human cholangiocarcinoma progression still remains to be clarified
Authors: Heather Francis
Journal: Hepatology (2012)

We appreciate that Dr. Xia et al. took an interest in our recent publication. We concur that our study did not address the individual contribution of H3/H4 histamine receptors on human cholangiocarcinoma growth. However, our study demonstrated that clobenpropit inhibits cholangiocarcinoma growth by way of H4HRs.1 We used clobenpropit, an H3HR antagonist / H4HR agonist, and found that stimulation of H4HR decreased cholangiocarcinoma growth both in vitro and in vivo.1 At resubmission, we determined if the effect was due to blocking H3HR or stimulating H4HR. After silencing H3HR, clobenpropit (interacting only with H4HR) decreased cholangiocarcinoma growth. Although specific binding studies using cholangiocarcinoma cells would be better to define the role of H4HR, our study (where H3HR was silenced) provides strong evidence for the involvement of H4HR in cholangiocarcinoma management. Our conclusion that clobenpropit has a higher affinity for H4HR stems from the publications from a well-established group in this field and therefore cannot be dismissed.2, 3 In response to the reference cited by Dr. Xia regarding clobenpropit affinity for H3HR over H4HR, we feel this does not negate our findings. Studies have shown that there is not a biologically significant difference between the affinities of clobenpropit for H4HR and H3HR.4 The structure of clobenpropit, the cell type or tissue being evaluated and conditions impact the affinity of agonist to receptor. Therefore, we would contend that the affinities for clobenpropit and H3HR or H4HR are speculative. Our intent here was to specify that clobenpropit inhibits cholangiocarcinoma growth by way of H4HR. We agree that treating athymic mice (injected with cholangiocarcinoma cells) with clobenpropit does not rule out effects on H3HR since clobenpropit may interact with both H3/H4HRs.5 In vivo clobenpropit reduces tumor growth, decreases mesenchymal characteristics, and blocks the activation of matrix metalloproteinases.1 We agree that our data are more specific to the studies in vitro instead of the data in vivo. Besides some expected limitations of the in vivo studies, we have clearly demonstrated that clobenpropit inhibits cholangiocarcinoma growth by way of H4HRs in vitro. Heather Francis Ph.D.*, * Scott & White Hospital, Temple, TX.
Pavlovian conditioning and multiple chemical sensitivity.
Authors: S Siegel, R Kreutzer
Journal: Environmental Health Perspectives (1997)

Pavlovian conditioning processes may contribute to some symptoms of multiple chemical sensitivity (MCS). This review summarizes the potential relevance of the literature on conditional taste and olfactory aversions, conditional sensitization, and conditional immunomodulation to understanding MCS. A conditioning-based perspective on MCS suggests novel research and treatment strategies.
DUODENAL ULCER SYMPTOM COMPLEX IN PATIENTS NOT HAVING ULCER
Authors: IRVING GRAY
Journal: JAMA (1927)

The pendulum has swung from a state of ignorance concerning duodenal ulcer to a stage at which every symptom complex of pain, food, comfort and pain is diagnosed as due to ulceration of the duodenum. While it is generally acknowledged that the history of the patient is of the greatest importance in arriving at a correct diagnosis, nevertheless, the tendency to make a diagnosis of duodenal ulcer almost on the history alone should be accompanied with a word of caution. The symptoms on which diagnoses are based are, according to MacKenzie,<sup>1</sup>reflex in origin. Whether these reflexes are disturbed by the entrance of the stimulus through the nervous system or through the circulation, the expression of the symptoms in individuals will vary, as pointed out by Libman,<sup>2</sup>according to their sensitiveness. When the difficulties in the diagnosis of duodenal ulcer are considered, the need for more accurate recognition
Alpha-aminoisobutyric acid transport in human leukemic lymphocytes: in vitro characteristics and inhibition by cortisol and cycloheximide
Authors: Daniel T. Baran, Marshall A. Lichtman, William A. Peck
Journal: Journal of Clinical Investigation (1972)

We have studied the transport of alpha-aminoisobutyric acid (AIB)-3-(14)C and its response to cortisol and cycloheximide in vitro in blood lymphocytes from untreated patients with chronic lymphocytic leukemia. The accumulation of AIB-3-(14)C increased in a linear fashion for 60 min, and reached an apparent steady state in 120 min. The initial rate of AIB accumulation (V(o)) varied from 1.1 to 10.2 mumoles/kg cell H(2)O per min in cells from 16 different patients; however, V(o) was reproducible in cells from five of six patients which were studied repeatedly over 1-9 months, and correlated positively with the lymphocyte count (r = 0.51, P = < 0.01). Virtually total inhibition of protein synthesis with cycloheximide was found to decrease the accumulation of AIB in cells from four patients which had high rates of AIB transport, but had no effect on transport in cells from four patients which accumulated AIB more slowly. These results indicate that active transport depends, in part, upon the presence of labile protein with a turnover rate which varies among different cell populations. Treatment with 10 muM cortisol for 240 min in vitro reduced the initial rate of AIB-3-(14)C accumulation (V(o)) by 43.4+/-4.1% (SE) (range, 9-66%) in cells from 16 patients. The degree of inhibition did not vary appreciably over a 9 month period in four of five patients. The effect of cortisol was proportional to its starting concentration, and developed at low concentrations (0.1-1.0 muM). Cortisol appears to decrease AIB accumulation by inhibiting active uptake, since it neither enhanced the exodus of AIB, nor inhibited apparently nonsaturable transport. Inhibition was noncompetitive in type, suggesting that cortisol decreases the total capacity of the active transport mechanism.Cortisol inhibited AIB transport indirectly by a process which involved de novo protein synthesis, since inhibition (a) appeared only after 60 min of treatment, (b) was present in treated cells which were subsequently incubated for 60 min in cortisol-free medium, and (c) failed to develop during simultaneous blockade of protein synthesis with cycloheximide, even when cycloheximide itself did not decrease AIB transport.
Active downregulation of myocardial energy requirements during prolonged moderate ischemia in swine.
Authors: A E Arai, G A Pantely, C G Anselone, J Bristow, J D Bristow
Journal: Circulation Research (1991)

We studied the effects of rapid atrial pacing during the final 10 minutes of a 70-minute, 31% reduction in coronary blood flow in anesthetized swine to understand the significance of apparent metabolic improvements during the initial 60 minutes of segmental ischemia. Within 5-10 minutes of ischemia, subendocardial phosphocreatine (PCr) and ATP were depleted to 47% and 63% of control, respectively; lactate accumulated within the subendocardium to 300% of control; and net arteriovenous lactate production occurred. Despite continued ischemia and no significant changes in the external determinants of myocardial oxygen consumption, by 60 minutes subendocardial PCr and lactate contents returned to near control levels and there was net arteriovenous lactate consumption. Ischemic left ventricular wall thickening and ATP levels remained depressed throughout the experiment. Atrial pacing during the final 10 minutes of ischemia again resulted in depletion of PCr and lactate production. Since the myocardium was capable of hydrolyzing PCr in response to atrial pacing at 60 minutes of ischemia, we conclude it was capable of hydrolyzing PCr during the period of constant ischemia when instead it was accumulating PCr. We propose the ischemic myocardium downregulates regional energy requirements below blood flow-limited rates of energy production during ischemia. This appears to be an active adaptation to ischemia and not a result of passive damage or cellular injury.
The Prevention of Malaria in the Federated Malay States. A Record of Twenty Years' Progress.
Authors: Malcolm Watson, P. S. Hunter, A. R. Wellington, Ronald Ross
Journal: JAMA (1922)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Hospital Credentialing and Privileging of Surgeons
Authors: Jason C. Pradarelli, Darrell A. Campbell, Justin B. Dimick
Journal: JAMA (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Using the NO TEARS tool for medication review
Authors: Tessa Lewis
Journal: BMJ (2004)

<h3>Abstract</h3> Unlike other European countries, the human population genetics and demographic history of Metropolitan France is surprisingly understudied. In this work, we combined newly genotyped samples from various zones in France with publicly available data and applied both allele frequency and haplotype-based methods in order to describe the internal structure of this country, by using genome-wide single nucleotide polymorphism (SNP) array genotypes. We found out that French Basques are genetically distinct from all other populations in the <i>Hexagone</i> and that the populations from southwest France (namely the Gascony region) share a large proportion of their ancestry with Basques. Otherwise, the genetic makeup of the French population is relatively homogeneous and mostly related to Southern and Central European groups. However, a fine-grained, haplotype-based analysis revealed that Bretons slightly separated from the rest of the groups, due mostly to gene flow from the British Isles in a time frame that coincides both historically attested Celtic population movements to this area between the 3th and the 9th centuries CE, but also with a more ancient genetic continuity between Brittany and the British Isles related to the shared drift with hunter-gatherer populations. Haplotype-based methods also unveiled subtle internal structures and connections with the surrounding modern populations, particularly in the periphery of the <i>Hexagone</i>.
Nonbinding inhibitory antiinsulin receptor antibodies. A new type of autoantibodies in human diabetes.
Authors: G Boden, Y Fujita-Yamaguchi, R Shimoyama, J J Shelmet, L Tappy, I Rezvani, O E Owen
Journal: Journal of Clinical Investigation (1988)

Sera and their IgG from 10/104 diabetic patients (five with insulin-dependent and five with noninsulin-dependent diabetes, NIDDM), contained antibodies that bound 125I-labeled purified human insulin receptors. 9 of these 10 sera failed to inhibit insulin binding (to rat hepatocytes and human placental membranes), did not stimulate glucose oxidation (by isolated rat adipocytes), and did not bind human placental IGF-1 receptors. Only one serum (and its IgG) modestly inhibited insulin binding and stimulated glucose oxidation. We conclude (a) that sera from 9/104 diabetics (five insulin-dependent and four noninsulin-dependent) contained a newly identified species of IgG antiinsulin receptor autoantibodies (AIRA), which bound to the insulin receptor at a locus different from the insulin binding site and did not inhibit insulin binding; and (b) that only 1/104 diabetic sera contained low-titer "conventional" antiinsulin receptor autoantibodies that bound to the insulin receptor at or near the insulin binding site, inhibited insulin binding and caused a clinical condition, which was difficult to distinguish from typical NIDDM.
Thymosin β4 Is Not Required for Embryonic Viability or Vascular Development
Authors: Indroneal Banerjee, Thomas Moore Morris, Sylvia M. Evans, Ju Chen
Journal: Circulation Research (2013)

Rossdeutsch et al describe a requirement for thymosin β4 (Tβ4) in vascular development. Impaired mural cell migration, differentiation, partial embryonic lethality, and hemorrhaging were observed after analysis of 2 lines of mice, one of which was germline null for Tβ4 and another in which Tβ4 was knocked down by endothelial-specific expression of Tβ4 short hairpin RNA. These data are in direct contrast to our published global and cardiac-specific Tβ4-knockout lines. Thus, the role of Tβ4 needs to be clarified to understand its importance in cardiovascular development.To investigate and clarify the role of Tβ4 in vascular smooth muscle cell development and vessel stability.Examination of Tβ4 global knockouts did not demonstrate embryonic hemorrhaging, altered mural cell development, or lethality. Endothelial-specific knockouts also did not exhibit any embryonic lethality and were viable to adulthood.Analysis of our Tβ4 global and cardiac- and endothelial-specific knockout models demonstrated that Tβ4 is dispensable for embryonic viability and vascular development.
Alopecia areata arising in patients receiving cyclosporin immunosuppression
Authors: M.G. Davies, P.W. Bowers
Journal: British Journal of Dermatology (2006)

Journal Article Alopecia areata arising in patients receiving cyclosporin immunosuppression Get access M.G. Davies, M.G. Davies Department of Dermatology, Plymouth and Truro Hospitals, U.K. Search for other works by this author on: Oxford Academic Google Scholar P.W. Bowers P.W. Bowers Department of Dermatology, Plymouth and Truro Hospitals, U.K. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 132, Issue 5, 1 May 1995, Pages 835–836, https://doi.org/10.1111/j.1365-2133.1995.tb00742.x Published: 01 May 1995
EFFECTS OF DEEP X RAYS ON THE CELLS OF THE BLOOD
Authors: W. L. Watt
Journal: BMJ (1929)

PORREPO DBCX I'M -M 8a}tlẽ xperiednce in its application.This implies traininig and practice, whlichl unfortunately is niot available ill every schlool.It is cul-ious how tuberculin is apt to be turned down by meln wiho have seldom used it themselves ior seeni it uised.Celtain physiological principles formii the basis of treat- monit in tuberculosis anid are serviceable miiore or less in all fornms of tuberculosis.Tlleir adjustment in detail requires consider'ation based oni experienlce.This is likewise true
Prevention of Mantle Lymphoma Tumor Establishment by Routing Transferrin Receptor toward Lysosomal Compartments
Authors: Yves Lepelletier, Valérie Camara-Clayette, Hulin Jin, Aurélie Hermant, Séverine Coulon, Michaël Dussiot, Michelle Arcos-Fajardo, Cédric Baude, Danielle Canionni, Richard Delarue, Nicole Brousse, Philippe Benaroch, Marc Benhamou, Vincent Ribrag, Renato C. Monteiro, Ivan C. Moura, Olivier Hermine
Journal: Cancer Research (2007)

Mantle cell lymphoma (MCL) is one of the most frequent of the newly recognized non-Hodgkin's lymphomas. The major problem of MCL therapy is the occurrence of relapse and subsequent resistance to chemotherapy and immunotherapy in virtually all cases. Here, we show that one injection of anti-human transferrin receptor (TfR) monoclonal antibody A24 totally prevented xenografted MCL tumor establishment in nude mice. It also delayed and inhibited tumor progression of established tumors, prolonging mice survival. In vitro, A24 induced up to 85% reduction of MCL cell proliferation (IC(50) = 3.75 nmol/L) independently of antibody aggregation, complement-dependent or antibody-dependent cell-mediated cytotoxicity. A24 induced MCL cell apoptosis through caspase-3 and caspase-9 activation, either alone or synergistically with chemotherapeutic agents. A24 induced TfR endocytosis via the clathrin adaptor protein-2 complex pathway followed by transport to lysosomal compartments. Therefore, A24-based therapies alone or in association with classic chemotherapies could provide a new alternative strategy against MCL, particularly in relapsing cases.
The Effects of Trazodone with <scp>l</scp>-Tryptophan on Sleep-disordered Breathing in the English Bulldog
Authors: SIGRID C. VEASEY, POLINA FENIK, KAREN PANCKERI, ALLAN I. PACK, JOAN C. HENDRICKS
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

Obstructive sleep apnea hypopnea syndrome (OSAHS) is a prevalent disorder, for which there are no universally effective pharmacotherapeutics. We hypothesized that in OSAHS, excitatory serotoninergic influences are important for maintaining patency of the upper airway in waking, and that in sleep, reduced serotoninergic drive plays a significant role in upper airway collapse and OSAHS. The previously reported small responses in humans with OSAHS to serotoninergics may relate, in part, to study design and the drugs/doses selected. We therefore performed multitrials/dose, multidose, randomized sleep studies testing the effectiveness of a combination of serotoninergics, trazodone, and l-tryptophan, in our animal model of OSAHS, the English bulldog. Trazodone/l-tryptophan caused dose-dependent reductions in respiratory events in non-rapid-eye-movement sleep (NREMS) and rapid-eye-movement sleep (REMS). During NREMS, the respiratory disturbance index (RDI) ± standard error was 6.3 ± 1.4 events/h (placebo) and 0.9 ± 0.3 (highest dose), p < 0.01. During REMS, the RDI was 31.4 ± 6.1 events/h (placebo) and 11.5 ± 4.3 (highest dose), p = 0.002. Trazodone/l-tryptophan dose-dependently reduced sleep fragmentation, p = 0.03, increased sleep efficiency, p = 0.005, enhanced slow-wave sleep, p = 0.0004, and minimized sleep-related suppression of upper airway dilator activity, p < 0.02. Trazodone with l-tryptophan can treat sleep-disordered breathing (SDB) in an animal model of OSAHS; the effectiveness of this therapy may be related to increased upper airway dilator activity in sleep and/or enhanced slow-wave sleep. Veasey SC, Fenik P, Panckeri K, Pack AI, Hendricks JC. The effects of trazodone with l-tryptophan on sleep-disordered breathing in the English bulldog.
Secretin, Cholecystokinin and Newer Gastrointestinal Hormones
Authors: Phillip L. Rayford, Thomas A. Miller, James C. Thompson
Journal: New England Journal of Medicine (1976)

IN 1902, Bayliss and Starling1 demonstrated that the introduction of hydrochloric acid into a denervated loop of small intestine elicited the brisk secretion of pancreatic juice. The implications of this observation were appreciated immediately, and they suggested that some unidentified, blood-borne "chemical messenger" was released from the acidified intestine to mediate this response. According to Babkin,2 the word "hormone" was introduced by Starling on the suggestion of Mr. W.B. Hardy.3 The word is from the Greek, ο͑ρμαω, meaning "I arouse to activity" or "I excite."Although the study of endocrinology may have begun, in one sense, in 1902 with the . . .
Zidovudine-induced mitochondrial disorder with massive liver steatosis, myopathy, lactic acidosis, and mitochondrial DNA depletion
Authors: Patrick Chariot, Irène Drogou, Isabelle de Lacroix-Szmania, Marie-Christine Eliezer-Vanerot, Bénédicte Chazaud, Anne Lombès, Annette Schaeffer, Elie Serge Zafrani
Journal: Journal of Hepatology (1999)
Counterpoint: A Diabetes Outcome Progression Trial (ADOPT): Good for Sulfonylureas?
Authors: Ebaa Al-Ozairi, Latika Sibal, Philip Home
Journal: Diabetes Care (2007)

A Diabetes Outcome Progression Trial (ADOPT) was conceived in the hope that the seemingly inexorable decline in islet B-cell function described with metformin, sulfonylureas, and insulin in the UK Prospective Diabetes Study (UKPDS) might be stopped or inhibited to a major degree by peroxisome proliferator–activated receptor-γ agonists, in particular rosiglitazone (1,2). It was already well recognized that the rapid early efficacy of sulfonylureas in lowering glucose was not retained to 12 months, and that metformin and thiazolidinediones had slow onset of action over months, so the design of the study necessarily had to enable decline of measures of blood glucose control to be assessed for a considerable period from 1 year onwards. However, the extent (degree and time) to which this early efficacy of the sulfonylureas in protecting against hyperglycemia would persist was not accurately known. The study also provided a good opportunity to compare durability of effect of the three classes of drugs directly in the context of some shorter-term studies since published (3).

Metformin is currently well established as first-line therapy in people with type 2 diabetes, usually after lifestyle measures fail to achieve A1C levels <6.5%, although some consensus (as opposed to evidence-based) guidelines have suggested initiation immediately from diagnosis (4,5). This review will not challenge those ideas, although the evidence is not as strong as sometimes assumed. The exceptions to first-line metformin use are where metformin is contraindicated, perhaps where someone is not overweight, and where presentation glucose levels are high and the rapid effect of a sulfonylurea is needed. In situations where metformin is contraindicated, or as second-line add-on therapy to metformin when target levels are no longer met, the alternative choice to a sulfonylurea would be a thiazolidinedione or possibly a gliptin (it is assumed insulin would not usually …