tbuckley/cabot-search huggingface dataset:
Effects of glucose, insulin and potassium infusion on tissue metabolic changes within first hour of myocardial infarction in the baboon.
Authors: L H Opie, K Bruyneel, P Owen
Journal: Circulation (1975)

The effects of infusions of glucose, insulin and potassium (GIK) on the heart tissue metabolic changes found in adult baboons 60 min after coronary artery ligation were studied. Biopsies taken from 11 baboons without coronary artery ligation gave control values. A second group of 46 baboons had coronary artery ligation. A third group of 17 baboons received an infusion of KCl after coronary artery ligation. A fourth group of 26 baboons received infusion of GIK. Coronary artery ligation resulted in the expected fall of ATP, creatine phosphate, glycogen, tissue (K+/Na+) ratio, and tissue pH, and rise of inorganic phosphate, lactare, lactate/pyruvate ratio and alpha-glycerophosphate in the infarction zones. Compared with ligation, additional infusions of GIK approximately doubled the contents of creatine phosphate and glycogen in the infarct zones, increased the content of ATP in the central infarct zone, and decreased the content of inorganic phosphate in the peripheral infarct zone. Other GIK effects were that the tissue (K+/Na+) ratio rose in the peripheral infarct zone, and the content of both glycogen and lactate rose in the peri-infarct and non-ischemic zones; the pH of tissue homogenates did not decrease. KCl infusions had few effects compared with the ligation group. GIK infusions exerted a beneficial effect when compared with infusions of KCl in that tissue creatine phosphate rose in the peripheral infarct and nonischemic zones; the tissue K+/Na+ ratio rose in the peripheral infarct, peri-infarct, and nonischemic zones; and the lactate/pyruvate ratio fell in the infarct zone. It is proposed that GIK counteracted early tissue metabolic deterioration in the infarcting baboon heart.
ACUTE EDEMA OF THE NASAL SEPTUM.
Authors: J. L. GOODALE
Journal: JAMA (1901)

Acute edematous inflammations of the soft structures of the mouth and throat are comparatively common, especially in the tongue and uvula, but appear to be extremely rare in the nose. Thus, while vascular dilatation of the mucous membrane and the erectile tissue are the usual accompaniments of acute rhinitis, I have not been able to find, in an examination of the literature, any account of acute intranasal inflammations characterized by edema. Two instances, however, of this condition have come under my observation. In one of them it was possible to excise the whole edematous area for microscopic examination.  Case 1.  —The patient, a young married woman, 25 years of age, who had always been in good health, came, Aug. 15, 1898, for a blocking of the left nasal passage, with fulness and impairment of hearing in the left ear, of ten days' duration. There had been a slight sore throat
Abstract 4893: USP7 modulates UV-induced PCNA monoubiquitylation by regulating DNA polymerase eta stability
Authors: Jiang Qian, Qianzhen Zhu, Kyle Pentz, Jinshan He, Qien Wang, Altaf A. Wani
Journal: Cancer Research (2014)

Abstract DNA polymerase eta (Polη), a product of the Xeroderma pigmentosum variant (XPV) gene, plays a unique role in translesion DNA synthesis (TLS). It is a short-lived proteasomally degraded protein and its steady-state level is tightly controlled by multiple pathways. In this study, we have identified the deubiquitylating enzyme ubiquitin-specific protease 7 (USP7) as a novel regulator of Polη stability. Polη and USP7 interact in vitro and in vivo. Overexpression of wild-type USP7, but not its interaction-defective and catalytic mutants, deubiquitylate Polη and increase its steady-state level. The data demonstrate that both physical interaction and catalytic activity of USP7 are necessary for Polη deubiquitylation and stability regulation. Interestingly, knockout of USP7 also increased the steady-state levels and slowed the turnover of both Polη and p53, which is likely caused by destabilizing MDM2, a targeting E3 ligase for ubiquitylation of both Polη and p53. Furthermore, ectopic expression of USP7 upregulated the UV-induced PCNA monoubiquitylation. In contrast, UV-induced PCNA monoubiquitylation was not observed in XPV cells ectopically expressing USP7. Taken together, our results demonstrated that USP7 facilitates UV-induced PCNA monoubiquitylation by directly and indirectly regulating Polη stability. (The work was supported by grants from NIH.) Note: This abstract was not presented at the meeting. Citation Format: Jiang Qian, Qianzhen Zhu, Kyle Pentz, Jinshan He, Qien Wang, Altaf A. Wani. USP7 modulates UV-induced PCNA monoubiquitylation by regulating DNA polymerase eta stability. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4893. doi:10.1158/1538-7445.AM2014-4893
Doctor and Patient: Ethics, Morale, Government
Authors: Richard T. Watson
Journal: JAMA (1964)

A past-president of the Royal College of Physicians is one of the few people privileged to write exactly what he feels about medicine. Sir Robert Platt has formulated in this short monograph the thoughts, often controversial, from 40 years of medical practice. He writes about doctors and their patients, and the organization of medical care with particular reference to general practice; he gives his views on human experiments and on drugs; starting with the axiom that it is impossible to practice good medicine unless you derive satisfaction from the task, he emphasizes the importance of the family doctor. Good general practice can be very good. Undergraduate training in general practice and suitable post-graduate work could combine the best features of American and British medicine and produce general practitioners equal to American internists in knowledge, who, nevertheless, remain family doctors. Succinctly described are the difficulties of having the government of the
BOWENS DISEASK. A Case Report.
Authors: S. N. Chaudhuri, G. Panja
Journal: British Journal of Dermatology (1959)

Journal Article BOWENS DISEASK. A Case Report. Get access S. N. Chaudhuri, B.Sc, M.B., B.S., S. N. Chaudhuri, B.Sc, M.B., B.S. Calcutta Search for other works by this author on: Oxford Academic Google Scholar G. Panja, M.B., D.B. G. Panja, M.B., D.B. Calcutta Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 71, Issue 3, 1 March 1959, Pages 117–119, https://doi.org/10.1111/j.1365-2133.1959.tb13395.x Published: 01 March 1959
Rupture of a Cold Abscess into the Bronchus
Authors: Z. Fastner
Journal: BMJ (1955)

the form of the diacetate of 10.040, and latterly in the form of the dihydrochloride, laboratory tests having shown no difference between these two salts.Throughout the 18 months that the cream has been in use, no cases of idiosyncrasy to the antiseptic have occurred.During the period of this clinical trial not only have the number of clinical cases been reduced, but there have been no patients with serious staphylococcal infections in the hospital: but possibly of greater significance is the obser- vation that those staphylococcal infections which did occur no longer appeared as groups in particular wards, but were scattered sporadically throughout the hospital.It may well be that other factors played a part in the remarkable results achieved and that the use of the antiseptic hand cream was not alone responsible.Nevertheless, the improvement was very real.X
O69 ALBUMIN INFUSION FOR BACTERIAL INFECTIONS OTHER THAN SPONTANEOUS BACTERIAL PERITONITIS IN CIRRHOTIC PATIENTS: A MULTICENTER RANDOMIZED CONTROLLED STUDY (ALB-CIRINF STUDY)
Authors: T. Thévenot, C. Bureau, F. Oberti, R. Anty, A. Louvet, A. Plessier, M. Rudler, A. Heurgué-Berlot, I. Rosa, N. Talbodec, T. Dao, V. Ozenne, N. Carbonell, X. Causse, O. Goria, A. Minello, V. De Ledinghen, R. Amathieu, H. Barraud, E. Nguyen-Khac, C. Becker, T. Paupard, D. Botta-Fridlung, N. Abdelli, F. Guillemot, E. Monnet, V. Di Martino
Journal: Journal of Hepatology (2014)
Abstract 734: Development of small molecule inhibitors of the phosphatase Shp2 by fragment screening
Authors: Xin Wu, Latanya Scott, Liwei Chen, Harshani R. Lawrence, Yunting Luo, Said M. Sebti, Jerry Wu, Nicholas J. Lawrence
Journal: Cancer Research (2010)

Abstract Protein tyrosine phosphorylation, which is controlled by tyrosine kinase (PTK) and tyrosine phosphatase (PTP), regulates numerous cellular processes, including proliferation, survival, differentiation, migration and apoptosis. Accumulating evidence has shown that defective function of PTPs leads to aberrant protein phosphorylation, which is associated with many humane diseases, including cancer. Src homology 2 phosphatase-2 (Shp2) is a cytoplasmic, nonreceptor protein tyrosine phophatase. It is the first proto-oncogene identified in the PTP superfamily. The structure of Shp2 consists of two SH2 (N-SH2 and C-SH2) domains, a single PTP region and a C-terminal hydrophilic tail. In the basal state, Shp2 displays a low catalytic activity due to close interactions between the N-SH2 and PTP domains that keep the phosphatase in an autoinhibited closed conformation. Upon growth factor or cytokine stimulation, the SH2 domains of Shp2 binds to tyrosine phosphorylated docking proteins such as Gab1 and Gab2, which activates Src, Ras, and the Erk1/2 (Erk) mitogen-activated protein (MAP) kinase pathway. Shp2 gain-of-function mutations are found in leukemias and solid tumors and are linked to Noonan syndrome. Although Shp2 is involved in pathogenesis of human cancers, it is not clear how Shp2 mediates tumorigenesis. To aid chemical biology studies and ultimately experimental therapy, we have been actively engaged in the search potent and selective Shp2 inhibitors. We will describe the results of a fragment-based screen as a method for identifying Shp2 inhibitors. The fragment libraries were both purchased and constructed in-house with a bias towards compounds that would potentially function as phosphotyrosine mimics. This has revealed compounds with moderate to low activity (IC50 200-500 µM) that have served as the starting pints for fragment-to-lead development. The emerging structure-activity relationships will be discussed as well as synthesis, modeling and X-ray studies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 734.
The Latest Report From Finland
Authors: Oglesby Paul
Journal: JAMA (1991)

Not surprisingly, the investigator in the biological sciences relishes the setting in which nature has provided a discrete, well-defined disease in which a single causative factor has been identified and for which a preventive or curative agent has become available. Coronary heart disease is not such an entity, which thereby complicates the design, execution, and interpretation of human clinical studies. The pathological and physiological aspects of coronary disease reflect this complexity. Although the atheroma in the arterial wall has been identified for over 100 years as the chief lesion, it is known that an altered coagulation state plays a variable primary or secondary role, with the interplay of thrombosis on the one hand and thrombolysis on the other. Further, the existence of primary and/or secondary coronary arterial spasm has become recognized as a significant element. Although none of these can be regarded as totally separate and
Inhibition of GSK3β by Postconditioning Is Required to Prevent Opening of the Mitochondrial Permeability Transition Pore During Reperfusion
Authors: Ludovic Gomez, Mélanie Paillard, Hélène Thibault, Geneviève Derumeaux, Michel Ovize
Journal: Circulation (2008)

Background— Opening of the mitochondrial permeability transition pore (mPTP) is a crucial event in lethal reperfusion injury. Phosphorylation (inhibition) of glycogen synthase kinase-3β (GSK3β) has been involved in cardioprotection. We investigated whether phosphorylated GSK3β may protect the heart via the inhibition of mPTP opening during postconditioning. Methods and Results— Wild-type and transgenic GSK3β-S9A mice (the cardiac GSK3β activity of which cannot be inactivated) underwent 60 minutes of ischemia and 24 hours of reperfusion. At reperfusion, wild-type and GSK3β-S9A mice received no intervention (control), postconditioning (3 cycles of 1 minute ischemia and 1 minute of reperfusion), the mPTP inhibitor cyclosporine A (CsA; 10 mg/kg IV), or the GSK3β inhibitor SB216763 (SB21; 70 μg/kg IV). Infarct size was assessed by triphenyltetrazolium chloride staining. The resistance of the mPTP to opening after Ca 2+ loading was assessed by spectrofluorometry on mitochondria isolated from the area at risk. In wild-type mice, infarct size was significantly reduced by postconditioning, CsA, and SB21, averaging 39±2%, 35±5%, and 37±4%, respectively, versus 58±5% of the area at risk in control mice ( P &lt;0.05). In GSK3β-S9A mice, only CsA, but not postconditioning or SB21, reduced infarct size. Postconditioning, CsA, and SB21 all improved the resistance of the mPTP in wild-type mice, but only CsA did so in GSK3β-S9A mice. Conclusion— These results suggest that S9-phosphorylation of GSK3β is required for postconditioning and likely acts by inhibiting the opening of the mitochondrial permeability transition pore.
Conditional disruption of IκB kinase 2 fails to prevent obesity-induced insulin resistance
Authors: Mathias Röhl, Manolis Pasparakis, Stephanie Baudler, Julia Baumgartl, Dinesh Gautam, Marion Huth, Rossana De Lorenzi, Wilhelm Krone, Klaus Rajewsky, Jens C. Brüning
Journal: Journal of Clinical Investigation (2004)

The inhibitor of NF-κB (IκB) kinases (IKK1[α] and IKK2[β]), the catalytic subunits of the IKK complex, phosphorylate IκB proteins on serine residues, targeting them for degradation and thus activating the transcription factor NF-κB. More recently, IKK2 has been implicated in mediation of insulin resistance caused by obesity, lipid infusion, and TNF-α stimulation, since salicylate and aspirin, known inhibitors of IKK activity, can reverse insulin resistance in obese mouse models. To further genetically elucidate the role of IKK2 in obesity-mediated insulin resistance, we have conditionally inactivated the mouse IKK2 gene in adult myocytes by Cre-loxP–mediated recombination in vivo. We have investigated the development of obesity-induced insulin resistance in muscle-specific IKK2 knockout mice and mice exhibiting a 50% reduction of IKK2 expression in every tissue and have found that, after gold thioglucose treatment, wild-type and mutant mice developed obesity to a similar extent. Surprisingly, no difference in obesity-induced insulin resistance was detectable, either at a physiological or at a molecular level. Moreover, impaired glucose tolerance resulting from a high-fat diet occurred to the same degree in control and IKK2 mutant mice. These data argue against a substantial role for muscular IKK2 in mediating obesity-induced insulin resistance in these models in vivo.
Abstract 39: FANCA regulates MUS81-EME1 mediated DNA incision in a damage-dependent manner
Authors: Anaid Benitez, Fenghua Yuan, Satoshi Nakajima, Leizhen Wei, Liangyue Qian, Richard Myers, Jennifer J. Hu, Li Lan, Yanbin Zhang
Journal: Cancer Research (2014)

Abstract MUS81-EME1 is a DNA endonuclease involved in replication-coupled repair of DNA interstrand crosslinks (ICL). A prevalent hypothetical role of MUS81-EME1 in ICL repair is to unhook the damage by incising the leading strand at the 3′ side of an ICL lesion. In this study, we report that purified MUS81-EME1 incises DNA at the 5′ side of a psoralen ICL residing in fork structures. Intriguingly, interstrand crosslink repair protein, FANCA, greatly enhances MUS81-EME1-mediated ICL incision. On the contrary, FANCA exhibits a two-phase incision regulation when DNA is undamaged or the damage affects only one DNA strand. Studies using truncated FANCA proteins indicate that both the N- and C-moieties of the protein are required for the incision regulation. Using laser-induced psoralen ICL formation in cells, we find that FANCA interacts with and recruits MUS81 to ICL lesions. This report clarifies the incision specificity of MUS81-EME1 on ICL damage and establishes that FANCA regulates the incision activity of MUS81-EME1 in a damage-dependent manner. Citation Format: Anaid Benitez, Fenghua Yuan, Satoshi Nakajima, Leizhen Wei, Liangyue Qian, Richard Myers, Jennifer J. Hu, Li Lan, Yanbin Zhang. FANCA regulates MUS81-EME1 mediated DNA incision in a damage-dependent manner. [abstract]. In: Proceedings of the AACR Special Conference: Cancer Susceptibility and Cancer Susceptibility Syndromes; Jan 29-Feb 1, 2014; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(23 Suppl):Abstract nr 39. doi:10.1158/1538-7445.CANSUSC14-39
Variant Angina Pectoris
Authors: Charles A. Marsh
Journal: JAMA (1976)

A 30-year-old man with variant angina pectoris and ventricular arrhythmias had an angiographically demonstrable 60% obstructive lesion of the proximal left anterior descending coronary artery that was observed to progress to 100% during spasm. Control of pain and arrhythmia by pharmacologic means was unsuccessful. Aortocoronary saphenous vein-internal mammary coronary bypass was associated with an anteroseptal wall myocardial infarction and relief from both angina pectoris and arrhythmias. It is suggested that infarction of the ischemic myocardium played a role in the successful management of this case. (<i>JAMA</i>235:833-837, 1976)
Remarks on Death during Chloroform Anaesthesia
Authors: T. L. Brunton
Journal: BMJ (1891)

In givinig a slhort description of the results of the Hyderabad Chloroformii Coimiimissioi I may remind you that the object of the researelc was esseintially a practical one it was to save people's lives, to use the words of his Higlhness the Nizam hiimself, to wlhose generous and enliglitened liberality the Commission owed its existence.The Commission was originally suggested to the Nizam andhis ministers by Surgeon-
Insurers are required to offer coverage for mental problems similar to that for physical ones
Authors: M. McCarthy
Journal: BMJ (2013)

Most US health plans that offer coverage for mental health and substance misuse problems must now provide these benefits on the same terms as they offer medical and surgical benefits, under a new rule announced by the Obama administration on Friday 8 November.

The rule is the latest of a series issued as part of the implementation of the Mental Health Parity and Addiction Equity Act, a 2008 law that banned large group health plans and health …
Preclinical Dose-Finding Study With a Liver-Tropic, Recombinant AAV-2/8 Vector in the Mouse Model of Galactosialidosis
Authors: Huimin Hu, Elida Gomero, Erik Bonten, John T Gray, Jim Allay, Yanan Wu, Jianrong Wu, Christopher Calabrese, Arthur Nienhuis, Alessandra d'Azzo
Journal: Molecular Therapy (2011)

Galactosialidosis (GS) is a lysosomal storage disease linked to deficiency of the protective protein/cathepsin A (PPCA). Similarly to GS patients, Ppca-null mice develop a systemic disease of the reticuloendothelial system, affecting most visceral organs and the nervous system. Symptoms include severe nephropathy, visceromegaly, infertility, progressive ataxia, and shortened life span. Here, we have conducted a preclinical, dose-finding study on a large cohort of GS mice injected intravenously at 1 month of age with increasing doses of a GMP-grade rAAV2/8 vector, expressing PPCA under the control of a liver-specific promoter. Treated mice, monitored for 16 weeks post-treatment, had normal physical appearance and behavior without discernable side effects. Despite the restricted expression of the transgene in the liver, immunohistochemical and biochemical analyses of other systemic organs, serum, and urine showed a dose-dependent, widespread correction of the disease phenotype, suggestive of a protein-mediated mechanism of cross-correction. A notable finding was that rAAV-treated GS mice showed high expression of PPCA in the reproductive organs, which resulted in reversal of their infertility. Together these results support the use of this rAAV-PPCA vector as a viable and safe method of gene delivery for the treatment of systemic disease in non-neuropathic GS patients. Galactosialidosis (GS) is a lysosomal storage disease linked to deficiency of the protective protein/cathepsin A (PPCA). Similarly to GS patients, Ppca-null mice develop a systemic disease of the reticuloendothelial system, affecting most visceral organs and the nervous system. Symptoms include severe nephropathy, visceromegaly, infertility, progressive ataxia, and shortened life span. Here, we have conducted a preclinical, dose-finding study on a large cohort of GS mice injected intravenously at 1 month of age with increasing doses of a GMP-grade rAAV2/8 vector, expressing PPCA under the control of a liver-specific promoter. Treated mice, monitored for 16 weeks post-treatment, had normal physical appearance and behavior without discernable side effects. Despite the restricted expression of the transgene in the liver, immunohistochemical and biochemical analyses of other systemic organs, serum, and urine showed a dose-dependent, widespread correction of the disease phenotype, suggestive of a protein-mediated mechanism of cross-correction. A notable finding was that rAAV-treated GS mice showed high expression of PPCA in the reproductive organs, which resulted in reversal of their infertility. Together these results support the use of this rAAV-PPCA vector as a viable and safe method of gene delivery for the treatment of systemic disease in non-neuropathic GS patients.
Endoscopic Removal of Inverted Sigmoid Diverticulum - Is it a Dangerous Procedure?
Authors: S. D. Ladas, S. P. Prigouris, C. Pantelidaki, S. A. Raptis
Journal: Endoscopy (1989)

See also: Polyp-simulating Mucosal Prolapse Syndrome in (Pre-) Diverticular DiseaseEndoscopy 1986; 18(03): 84-86DOI: 10.1055/s-2007-1018337 See also: Reply to the Letter to the EditorEndoscopy 1989; 21(05): 244-244DOI: 10.1055/s-2007-1012961
Is tobacco a risk factor for chronic pancreatitis and alcoholic cirrhosis?
Authors: M Bourliere, M Barthet, P Berthezene, J P Durbec, H Sarles
Journal: Gut (1991)

In a case control study alcohol intake and tobacco use were assessed between 1975 and 1987 in 103 male patients suffering from alcoholic cirrhosis of the liver, in 145 patients with chronic pancreatitis, and in 264 control subjects. The patients with chronic pancreatitis were significantly younger than the patients with cirrhosis (mean (SD) age 41.92 (2.4) v 60.9 (11.6) years). Among the patients with chronic pancreatitis, 94% were both smokers and drinkers compared with 83% of patients with cirrhosis of the liver. The relative risks for each disease were calculated by conditional multiple logistic regression. Whereas daily intake of alcohol was a major risk factor for both cirrhosis of the liver and chronic pancreatitis, smoking was significantly related only to the risk of having chronic pancreatitis. Moreover, the mean age at onset of pancreatitis was lower among smokers.