tbuckley/cabot-search huggingface dataset:
Effects of Glucagon on Lipolysis and Ketogenesis in Normal and Diabetic Men
Authors: John E. Liljenquist, James D. Bomboy, Stephen B. Lewis, Bruce C. Sinclair-Smith, Philip W. Felts, William W. Lacy, Oscar B. Crofford, Grant W. Liddle
Journal: Journal of Clinical Investigation (1974)

The effect of glucagon (50 ng/kg/min) on arterial glycerol concentration and net splanchnic production of total ketones and glucose was studied after an overnight fast in four normal and five insulin-dependent diabetic men. Brachial artery and hepatic vein catheters were inserted and splanchnic blood flow determined using indocyanine green. The glucagon infusion resulted in a mean circulating plasma level of 4,420 pg/ml. In the normal subjects, the glucagon infusion resulted in stimulation of insulin secretion indicated by rising levels of immunoreactive insulin and C-peptide immunoreactivity. Arterial glycerol concentration (an index of lipolysis) declined markedly and net splanchnic total ketone production was virtually abolished. In contrast, the diabetic subjects secreted no insulin (no rise in C-peptide immunoreactivity) in response to glucagon. Arterial glycerol and net splanchnic total ketone production in these subjects rose significantly (P=<0.05) when compared with the results in four diabetics who received a saline infusion after undergoing the same catheterization procedure.Net splanchnic glucose production rose markedly during glucagon stimulation in the normals and diabetics despite the marked rise in insulin in the normals. Thus, the same level of circulating insulin which markedly suppressed lipolysis and ketogenesis in the normals failed to inhibit the glucagon-mediated increase in net splanchnic glucose production. It is concluded (a) that glucagon at high concentration is capable of stimulating lipolysis and ketogenesis in insulin-deficient diabetic man; (b) that insulin, mole for mole, has more antilipolytic activity in man than glucagon has lipolytic activity; and (c) that glucagon, on a molar basis, has greater stimulatory activity than insulin has inhibitory activity on hepatic glucose release.
The Role of Endotoxin during Typhoid Fever and Tularemia in Man. II. Altered Cardiovascular Responses to Catecholamines*
Authors: Sheldon E. Greisman, Richard B. Hornick, Frank A. Carozza, Theodore E. Woodward
Journal: Journal of Clinical Investigation (1964)

Since 1959, studies of tularemia and typhoid fever during vaccine trials have led to reproducible clinical forms of the disease in man (1).Such clinical models have permitted observations of a variety of physiologic parameters in the same subject before, during, and after infection and have provided a unique opportunity to evaluate the role of endotoxin in the pathogenesis of these illnesses.Previously (2), the acquisition of significant tolerance to the pyrogenic activity of bacterial endotoxins was described in volunteers convalescent from induced typhoid fever and tularemia.In contrast, no tolerance was acquired after infection with the viral agent of sandfly fever.These findings suggested the release of physiologically active quantities of circulating endotoxin during human typhoid fever and tularemia.The present study is a continuation of such investigations de- signed to evaluate the role of endotoxin in medi- ating the pathophysiologic derangements during gram-negative bacterial infections in man.The introduction of bacterial endotoxins into the blood stream of man and other mammals re- sults in profound alterations in circulatory homeostasis (3).Although the manner of mediation of such disturbances is uncertain, alterations in vascular reactivity to catecholamines may constitute one important mechanism.In the intact rabbit and rat, marked hyperreactivity of the cutaneous
Androgen Receptor Regulation by Physiological Concentrations of the Isoflavonoid Genistein in Androgen-Dependent LNCaP Cells Is Mediated by Estrogen Receptor β
Authors: Jasmin Bektic, Andreas P Berger, Karina Pfeil, Gabriele Dobler, Georg Bartsch, Helmut Klocker
Journal: European Urology (2003)
Selective Killing of Adriamycin-Resistant (G2 Checkpoint-Deficient and MRP1-Expressing) Cancer Cells by Docetaxel
Authors: Zoya N. Demidenko, Dorota Halicka, Jan Kunicki, James A. McCubrey, Zbigniew Darzynkiewicz, Mikhail V. Blagosklonny
Journal: Cancer Research (2005)

Abstract Chemotherapy of cancer is limited by toxicity to normal cells. Drug resistance further limits the therapy. Here, we investigated selective killing of drug-resistant cancer cells by antagonistic drug combinations, which can spare (because of drug antagonism) normal cells. We used paired cell lines that are resistant to Adriamycin due to either expression of MRP1 or lack of G2 checkpoints. The goal was to selectively kill Adriamycin-resistant cancer cells with Docetaxel (Taxotere), while protecting parental (Adriamycin-sensitive) cells, using cytostatic concentrations of Adriamycin. Taxotere kills cells in mitosis. Therefore, by arresting parental cells in G2, 20 to 40 ng/mL of Adriamycin prevented cell death caused by Taxotere. Also, Adriamycin prevented the effects of Taxotere in normal human lymphocytes. In contrast, Taxotere selectively killed MRP1-expressing leukemia cells, which did not undergo G2 arrest in the presence of Adriamycin. Also, in the presence of Adriamycin, HCT116-p21−/− cancer cells with a defective G2 checkpoint entered mitosis and were selectively killed by Taxotere. Finally, 20 ng/mL of Adriamycin protected normal FDC-P1 hematopoietic cells from Taxotere. Whereas parental cells were protected by Adriamycin, the mitogen-activated protein/extracellular signal-regulated kinase inhibitor PD90598 potentiated the cytotoxic effect of Taxotere selectively in Raf-1–transformed FDC-P1 leukemia cells. We propose a therapeutic strategy to prevent normal cells from entering mitosis while increasing apoptosis selectively in mitotic cancer cells.
The Spectrum of Symptoms and QT Intervals in Carriers of the Gene for the Long-QT Syndrome
Authors: G. Michael Vincent, Katherine W. Timothy, Mark Leppert, Mark Keating
Journal: New England Journal of Medicine (1992)

The familial long-QT syndrome is characterized by a prolonged QT interval on the electrocardiogram, ventricular arrhythmias, and sudden death. It is not certain, however, that the length of the QT interval is a sensitive or a specific diagnostic criterion. Recently, we identified genetic markers on chromosome 11 that distinguished between carriers and noncarriers of the gene for the long-QT syndrome in three families. In this study, we compared the clinical features of carriers and noncarriers and assessed the diagnostic accuracy of the QT interval.
Correction of renal tubular acidosis in carbonic anhydrase II-deficient mice with gene therapy.
Authors: L W Lai, D M Chan, R P Erickson, S J Hsu, Y H Lien
Journal: Journal of Clinical Investigation (1998)

Carbonic anhydrase II (CAII) deficiency in humans is associated with a syndrome of renal tubular acidosis, osteopetrosis, and cerebral calcification. A strain of mice of CAII deficiency due to a point mutation also manifests renal tubular acidosis. We report here that retrograde injection of cationic liposome complexed with a CAII chimeric gene, using a cytomegalovirus (CMV) promoter/enhancer as an expression cassette to drive human CAII cDNA, into the renal pelvis of CAII-deficient mice results in expression of CAII in the kidney. The levels of both the CAII gene and its corresponding mRNA were highest by day 3 after treatment, diminishing thereafter, but remaining detectable by 1 mo. After gene therapy, CAII-deficient mice restored the ability to acidify urine after oral administration of ammonium chloride. The ability to acidify urine was maintained at 3 wk after gene therapy, and was eventually lost by 6 wk. Immunohistochemistry studies using anti-CAII antibodies showed that CAII was expressed in tubular cells of the outer medulla and corticomedullary junction. The gene therapy was not associated with nephrotoxicity as assessed by blood urea nitrogen levels and renal histology. To our knowledge, this is the first successful gene therapy of a genetic renal disease. Our results demonstrate the potential of gene therapy as a novel treatment for hereditary renal tubular defects.
P162Sitagliptin reduces fatty-acids uptake in detriment of glucose in experimental type-II diabetic hearts
Authors: B Picatoste, E Ramirez, MA Morcillo, A Caro-Vadillo, J Egido, J Tunon, O Lorenzo Gonzalez
Journal: Cardiovascular Research (2014)

Objective: To study the effect of sitagliptin on glucose and fatty-acids uptake in the myocardium of type-II diabetic rats.
The Effect of Pancreatectomy on Lipemia, Tissue Lipidosis and Atherogenesis in Chicks
Authors: J. STAMLER, L. N. KATZ, C. Bolene
Journal: Circulation (1951)

Following complete pancreatectomy, chicks exhibit an excessive hypercholesterolemia when fed a diet containing cholesterol plus cottonseed oil. This inordinate hypercholesterolemia is accompanied by intensified atherogenesis, compared with unoperated controls on the same diet. Dietary neutral fat is essential for these excessive cholesterolemic and atherogenic responses. The possible significance of these findings for the pathogenesis of atherosclerosis in diabetic man is discussed.
Influence of Cholesterol Feeding on Phospholipid Metabolism of Connective Tissue
Authors: ESTHER L. McCANDLESS, ROBERT E. BAILEY, D. B. ZILVERSMIT
Journal: Circulation Research (1960)

Subcutaneous injection of carrageenan, a sulfated polygalactose extracted from the red algae Chondrus crispus , stimulated the production of fibrous connective tissue in the rabbit. Animals fed cholesterol for 3 and 5 weeks had significantly higher phospholipid concentrations in this connective tissue than did control rabbits, but no alteration in phospholipid specific activity. These results are similar to those obtained in preliminary studies of connective tissue cultured by the sponge implantation technic. Significant increases occurred in cephalin, lecithin, and sphingomyelin concentrations in tissue proliferated after cearrageenan injection. The cholesterol content of connective tissue was increased 7- to 8-fold. Histologically, the tissue taken after 3 weeks of cholesterol feeding could not be distinguished from that of control animals. At 5 weeks, connective tissue from cholesterol-fed rabbits contained mature fat cells and macrophages resembling foam cells, in addition to the fibroblasts and collagen present in control tissue. Development of collagenous fibers and alterations in lipids were not found to be directly related. It is suggested that the elaboration of collagen and the accumulation of phospholipid, both of which occur in experimental atheromatosis, represent independent processes of connective tissue cells.
Course and Prognosis in Rheumatoid Arthritis
Authors: J. J. R. Duthie, P. E. Brown, J. D. E. Knox, M. Thompson
Journal: Annals of the Rheumatic Diseases (1957)

In a previous communication (Duthie, Thompson, Weir, and Fletcher, 1955), the results of treatment in hospital and the subsequent progress of a group of patients with rheumatoid arthritis were described.At the time of the first report the mean duration of follow-up was 24-4 months.Certain factors which might influence prognosis were considered.It was concluded that improvement following treatment in hospital was reasonably well maintained in the majority of patients if subsequent medical and social supervision were adequate.The most important factors in prognosis proved to be the duration of disease on admission, sex, and type of course run up to the time of admission.Patients admitted within one year of the onset of symptoms fared substantially better than those admitted at a later stage of the disease; the prognosis in males was better than in females; an acute onset followed by a rapidly progressive course in the early stages seemed to indicate a more benign form of the disease.Age at onset, the erythrocyte sedimentation rate (E.S.R.), haemoglobin level, and activity of the disease on admission gave no useful indication regarding the subsequent course of the disease.The present report is concerned with the further study of this group of patients.* Paper presented at a Plenary Session of the IX International Congress of The Rheumatic Diseases at Toronto, in June, 1957.patients because of active disease, the presence of deformities, or a combination of both. 30per cent. of males and 18 per cent. of females were admitted within Mean Age at Third Assessment (yrs) 54-1 55*3Mean Duration of Disease on Admission (yrs).
THE TYPE OF TUBERCLE BACILLUS COMMONLY PRESENT IN TUBERCULOUS LESIONS IN BONES AND JOINTS: TWO CASES WITH UNUSUAL NUMBERS OF TUBERCLE BACILLI IN THE DISCHARGES
Authors: L. Cobbett
Journal: BMJ (1928)

t HTHICAITISM u" 626APRIL 'r4, ~UERULUSBOESAN~JINSMEDICAL JOUR'NAY.- of gastr ic ulcer.In the present state of kniowledge it is the only method which brings relief to a number of victims of the disease.While sticli is the case there is sure to be controversy as to miiethods.I lhave striveni to present these problemiis to you, an-d have suggested wha-t I regar-d as the best solutions to themii.
Why Change? A Look at the Current System of Disability Determination and Workers' Compensation for Occupational Lung Disease
Authors: STEPHEN I. RICHMAN
Journal: Annals of Internal Medicine (1982)

Under the current system of disability determination and workers' compensation for occupational lung disease, disabled workers or their survivors can reasonably count on being compensated. However, by rejecting established scientific truth in order to pay workers' compensation in circumstances where disability or death had not been due to occupation, the system has operated unfairly and has undermined public confidence and respect. To gain more scientific integrity and fairness, the system should be changed to provide for adjudication by scientifically informed disability boards. The adversary system sould be retained, however, as needed protection against bias, quackery, and mendacity.
Metabolic Syndrome and Risk of Development of Atrial Fibrillation
Authors: Hiroshi Watanabe, Naohito Tanabe, Toru Watanabe, Dawood Darbar, Dan M. Roden, Shigeru Sasaki, Yoshifusa Aizawa
Journal: Circulation (2008)

Background— The metabolic syndrome consists of a cluster of atherosclerotic risk factors, many of which also have been implicated in the genesis of atrial fibrillation (AF). However, the precise role of the metabolic syndrome in the development of AF is unknown. Methods and Results— This prospective, community-based, observational cohort study was based on an annual health check-up program in Japan. We studied 28 449 participants without baseline AF. We used 2 different criteria for the metabolic syndrome—the guidelines of the National Cholesterol Education Program Third Adult Treatment Panel (NCEP-ATP III) and those of the American Heart Association/National Heart, Lung, and Blood Institute (AHA/NHLBI)—to study the risk of development of new-onset AF. The metabolic syndrome was present in 3716 subjects (13%) and 4544 subjects (16%) using the NCEP-ATP III and AHA/NHLBI definitions, respectively. During a mean follow-up of 4.5 years, AF developed in 265 subjects (105 women). Among the metabolic syndrome components, obesity (age- and sex-adjusted hazard ratio [HR], 1.64), elevated blood pressure (HR, 1.69), low high-density lipoprotein cholesterol (HR, 1.52), and impaired insulin tolerance (HR, 1.44 [NCEP-ATP III] and 1.35 [AHA/NHLBI]) showed an increased risk for AF. The association between the metabolic syndrome and AF remained significant in subjects without treated hypertension or diabetes by the NCEP-ATP III definition (HR, 1.78) but not by the AHA/NHLBI definition (HR, 1.28). Conclusions— The metabolic syndrome was associated with increased risk of AF. The metabolic derangements of the syndrome may be important in the pathogenesis of AF.
Evaluation of the Association between Persistent Organic Pollutants (POPs) and Diabetes in Epidemiological Studies: A National Toxicology Program Workshop Review
Authors: Kyla W. Taylor, Raymond F. Novak, Henry A. Anderson, Linda S. Birnbaum, Chad Blystone, Michael DeVito, David Jacobs, Josef Köhrle, Duk-Hee Lee, Lars Rylander, Anna Rignell-Hydbom, Rogelio Tornero-Velez, Mary E. Turyk, Abee L. Boyles, Kristina A. Thayer, Lars Lind
Journal: Environmental Health Perspectives (2013)

Diabetes is a major threat to public health in the United States and worldwide. Understanding the role of environmental chemicals in the development or progression of diabetes is an emerging issue in environmental health.We assessed the epidemiologic literature for evidence of associations between persistent organic pollutants (POPs) and type 2 diabetes.Using a PubMed search and reference lists from relevant studies or review articles, we identified 72 epidemiological studies that investigated associations of persistent organic pollutants (POPs) with diabetes. We evaluated these studies for consistency, strengths and weaknesses of study design (including power and statistical methods), clinical diagnosis, exposure assessment, study population characteristics, and identification of data gaps and areas for future research.Heterogeneity of the studies precluded conducting a meta-analysis, but the overall evidence is sufficient for a positive association of some organochlorine POPs with type 2 diabetes. Collectively, these data are not sufficient to establish causality. Initial data mining revealed that the strongest positive correlation of diabetes with POPs occurred with organochlorine compounds, such as trans-nonachlor, dichlorodiphenyldichloroethylene (DDE), polychlorinated biphenyls (PCBs), and dioxins and dioxin-like chemicals. There is less indication of an association between other nonorganochlorine POPs, such as perfluoroalkyl acids and brominated compounds, and type 2 diabetes. Experimental data are needed to confirm the causality of these POPs, which will shed new light on the pathogenesis of diabetes. This new information should be considered by governmental bodies involved in the regulation of environmental contaminants.
A tungsten supplemented diet attenuates bacterial translocation in chronic portal hypertensive and cholestatic rats: role of xanthine dehydrogenase and xanthine oxidase
Authors: G Schimpl, M A Pabst, G Feierl, A Kuesz, H Ozbey, S Takahashi, M E Hollwarth
Journal: Gut (1999)

<h3>BACKGROUND</h3> Bacterial translocation (BT) plays a major role in the pathophysiological process of spontaneous infections in portal hypertension (PH) and cholestatic jaundice. The major mechanisms promoting BT in experimental animal models are the disruption of the intestinal ecological equilibrium and disruption of the intestinal mucosal barrier. The enzymes xanthine dehydrogenase (XD) and xanthine oxidase (XO) are often implicated as a significant source of oxidants which have a major impact on the impairment of intestinal barrier function. <h3>AIM</h3> To investigate the incidence of BT in rats with PH and obstructive jaundice, and to evaluate the impact of XD and XO. <h3>METHODS</h3> Animals were subjected to sham laparotomy (SL), PH by calibrated stenosis of the portal vein, and common bile duct ligation (CBDL). They were fed either a standard pellet diet or a tungsten supplemented molybdenum-free diet. Four weeks after the operative procedure, intestinal colonisation and BT to portal vein, vena cava, mesenteric lymph nodes, liver, and spleen were determined. Intestinal XD and XO activity were measured enzymatically and histochemically. <h3>RESULTS</h3> Significant (p&lt;0.01) intestinal bacterial overgrowth was present in all PH and CBDL groups compared with the SL group. In normally fed animals after SL, BT occurred in 12%. In PH and after CBDL, the rate of BT increased significantly (p&lt;0.05) to 28% and 54% respectively. In the jejunum of normally fed animals subjected to PH or CBDL, a significant increase in XO was observed (p&lt;0.01). Animals fed a tungsten supplemented diet showed a significant attenuation of BT to 14% in PH and 22% after CBDL (p&lt;0.05). Tungsten treatment completely suppressed jejunal XD and XO activities. <h3>CONCLUSIONS</h3> Significant intestinal bacterial overgrowth, BT, and XD to XO conversion occurred in PH and after CBDL. XD and XO inactivation by a tungsten supplemented molybdenum-free diet significantly reduced the incidence of BT without affecting intestinal bacterial overgrowth. These data strongly support the hypothesis that increased XD to XO conversion may contribute to intestinal barrier failure in PH and after CBDL.
An Address on SOME PROBLEMS CONNECTED WITH BENIGN ENLARGEMENT OF THE PROSTATE
Authors: C. A. R. Nitch
Journal: BMJ (1929)

THERE are manv problems connected with benign enlarge- micnt of the prostate which provide miaterial for serious thought and discussion.Some of these problems have not yet been solved satisfactorily, and others are treated in different ways by many of the workers in this field of surgery.Some writers still employ the term " hypertrophy," but this is incorrect, for hypertrophy of an organ implies an ircrease in size of all its component parts, whereas in the pathological prostate the enlargement is essentially glandular.It is now generally agreed that the condition, which for want of a better name is usually called ".enlargement of the prostate," is due to an adenomatous formation, but the actual origin of the adenomata is as yet unsettled.Before discussing the theories which have been advanced to account for these pathological changes, a brief reference to the anatomy and histology of the normal prostate is essential.
Intensive Glucose Control in Elderly Adults
Authors: Thomas E. Finucane
Journal: JAMA (2007)

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A Phase II Tolerability Study of Cisplatin Plus Docetaxel as Adjuvant Chemotherapy for Resected Non-small Cell Lung Cancer
Authors: Christopher G. Azzoli, Lee M. Krug, Vincent A. Miller, Naiyer A. Rizvi, Mark G. Kris, Megan Dunne, Amy Farmer, Barbara Pizzo, Leslie Tyson, Teresa Seeger, Barbara Coleman, Erin Moore, Lauren Lastinger, Ennapadam Venkatraman, Charles M. Rudin
Journal: Journal of Thoracic Oncology (2007)