tbuckley/cabot-search huggingface dataset:
Systematic review and economic evaluation of Helicobacter pylori eradication treatment for non-ulcer dyspepsia
Authors: P. Moayyedi
Journal: BMJ (2000)

<h3>Abstract</h3> <b>Objectives:</b> To evaluate efficacy and cost effectiveness of <i>Helicobacter pylori</i> eradication treatment in patients with non-ulcer dyspepsia infected with <i>H pylori</i>. <b>Design:</b> Systematic review of randomised controlled trials comparing <i>H pylori</i> eradication with placebo or another drug treatment. Results were incorporated into a Markov model comparing health service costs and benefits of <i>H pylori</i> eradication with antacid treatment over one year. <b>Data sources:</b> Six electronic databases were searched for randomised controlled trials from January 1966 to May 2000. Experts in the field, pharmaceutical companies, and journals were contacted for information on any unpublished trials. Trial reports were reviewed according to predefined eligibility and quality criteria. <b>Main outcome measures:</b> Relative risk reduction for remaining dyspeptic symptoms (the same or worse) at 3-12 months. Cost per dyspepsia-free month estimated from Markov model based on estimated relative risk reduction. <b>Results:</b> Twelve trials were included in the systematic review, nine of which evaluated dyspepsia at 3-12 months in 2541 patients. <i>H pylori</i> eradication treatment was significantly superior to placebo in treating non-ulcer dyspepsia (relative risk reduction 9% (95% confidence interval 4% to 14%)), one case of dyspepsia being cured for every 15 people treated. <i>H pylori</i> eradication cost £56 per dyspepsia-free month during first year after treatment. <b>Conclusion:</b><i>H pylori</i> eradication may be cost effective treatment for non-ulcer dyspepsia in infected patients but further evidence is needed on decision makers9 willingness to pay for relief of dyspepsia.
Abnormalities of Cell-Membrane Fluidity in the Pathogenesis of Disease
Authors: Howard L. Bleich, Emily S. Boro, Richard A. Cooper
Journal: New England Journal of Medicine (1977)

Early in this century, colloid chemists debated about whether cells were bounded by a surface membrane. Today, they debate about the organization of molecules within that membrane. The research involved has led to two images of the cell membrane — as a sea of lipid with islands of protein and as a matrix of protein with lakes of lipid. Both concepts suggest that zones of fluid lipid within the membrane form the environment for membrane proteins. Much of this lipid is in the form of a bilamellar leaflet with hydrophilic portions that face the aqueous environment on either side and . . .
Elevated circulating levels of the serum acute-phase protein YKL-40 (chitinase 3-like protein 1) are a marker of obesity and insulin resistance in prepubertal children
Authors: Ioannis Kyrgios, Assimina Galli-Tsinopoulou, Charilaos Stylianou, Eleni Papakonstantinou, Malamatenia Arvanitidou, Anna-Bettina Haidich
Journal: Metabolism (2011)
Is There a Relationship between Exercise Systolic Blood Pressure Response and Left Ventricular Mass?
Authors: Michael S. Lauer, Daniel Levy, Keaven M. Anderson, Jonathan F. Plehn
Journal: Annals of Internal Medicine (1992)

Objective: To assess the association between an exaggerated exercise systolic blood pressure response and the occurrence of left ventricular hypertrophy in healthy, normotensive individuals. Design: Cross-sectional survey using M-mode echocardiography to measure left ventricular mass and to detect left ventricular hypertrophy. Setting: The Framingham Heart Study. Subjects: Eight-hundred sixty men and 1118 women were studied who were free of cardiovascular or pulmonary disease, who were not taking any antihypertensive or cardiovascular medications, and who successfully achieved at least 90% of their age-predicted maximum heart rate during a monitored exercise treadmill test. All subjects had normal baseline and exercise electrocardiograms. Measurements and Main Results: Men with a peak exercise systolic blood pressure of 210 or more and women with a peak exercise systolic blood pressure of 190 or more were considered to have an "exaggerated" blood pressure response; 122 men and 67 women met these criteria. Subjects with an exaggerated exercise systolic blood pressure response had 10% higher left ventricular mass than those with a normal exercise systolic blood pressure response (in men: 115 ± 25 compared with 105 ± 24 g/m, P < 0.001; in women: 86 ± 22 compared with 73 ± 16 g/m, P < 0.001); they also had a higher prevalence of left ventricular hypertrophy (in men: odds ratio, 1.34, 95% Cl, 1.00 to 1.80; in women: odds ratio, 2.12, Cl, 1.48 to 3.03). After adjusting for age, resting systolic blood pressure, and body mass index, however, subjects with an exaggerated exercise systolic blood pressure response had only 5% higher left ventricular mass (in men: 111 ± 2.1 compared with 106 ± 0.8 g/m, P = 0.02; in women: 80 ± 1.8 compared with 74 ± 0.4 g/m, P = 0.002), and they no longer had a statistically increased prevalence of left ventricular hypertrophy (in men: odds ratio, 1.21, Cl, 0.87 to 1.67; in women: odds ratio, 1.30, Cl, 0.84 to 2.01). Conclusions: The apparent relation between exercise systolic blood pressure response and left ventricular mass is confounded by age, resting systolic blood pressure, and body mass; the degree of confounding is such that the biologic significance of this relationship should be questioned.
PRELIMINARY STEPS IN THE INVESTIGATION OF GASTRIC FUNCTIONS.
Authors: B. ONUF (ONUFROWICZ)
Journal: JAMA (1906)

In making preparations for the investigation of the gastric functions of epileptics, particularly in idiopathic epilepsy, for which the Craig Colony for Epileptics seemed to offer a favorable field, worthy of careful and intelligent investigation, the fact appeared that the methods in vogue were not commensurate to scientific needs, as they do not offer that degree of exactness which would recognize beyond all doubt deviations from the normal, if such were not present in a very marked degree.  So many points have to be considered before conclusions regarding one special pointcan be made that if accuracy of method and analytic discrimination are not introduced in this field of research, results must necessarily be of such a vague character as not to allow any definite conclusions. This fact impressed the writer particularly in taking up the chemopathology of gastric secretion. It seemed absolutely necessary first to establish standards by means of
Effect of Deoxyribozymes Targeting c-Jun on Solid Tumor Growth and Angiogenesis in Rodents
Authors: G. Zhang, C. R. Dass, E. Sumithran, N. Di Girolamo, L.-Q. Sun, L. M. Khachigian
Journal: JNCI Journal of the National Cancer Institute (2004)

Background: The basic region-leucine zipper protein c-Jun has been linked to cell proliferation, transformation, and apoptosis. However, a direct role for c-Jun in angiogenesis has not been shown. Methods: We used human microvascular endothelial cells (HMEC-1) transfected with a DNAzyme targeting the c-Jun mRNA (Dz13), related oligonucleotides, or vehicle in in vitro models of microvascular endothelial cell proliferation, migration, chemoinvasion, and tubule formation, a rat model of corneal neovascularization, and a mouse model of solid tumor growth and vascular endothelial growth factor (VEGF)–induced angiogenesis. All statistical tests were two-sided. Results: Compared with mock-transfected cells, HMEC-1 cells transfected with Dz13 expressed less c-Jun protein and possessed lower DNA-binding activity. Dz13 blocked endothelial cell proliferation, migration, chemoinvasion, and tubule formation. Dz13 inhibited the endothelial cell expression and proteolytic activity of MMP-2, a c-Jun–dependent gene. Dz13 inhibited VEGF-induced neovascularization in the rat cornea compared with vehicle control (Dz13 versus vehicle: 4.0 neovessels versus 30.7 neovessels, difference = 26.7 neovessels; P = .004; area occupied by new blood vessels for Dz13 versus vehicle: 0.35 mm2 versus 1.52 mm2, difference = 1.17 mm2; P = .005) as well as solid melanoma growth in mice (Dz13 versus vehicle at 14 days: 108 mm3 versus 283 mm3, difference = 175 mm3; P = .006) with greatly reduced vascular density (Dz13 versus vehicle: 30% versus 100%, difference = 70%; P<.001). Conclusion: DNAzymes targeting c-Jun may have therapeutic potential as inhibitors of tumor angiogenesis and growth.
Androgen Abuse by Athletes
Authors: JEAN D. WILSON
Journal: Endocrine Reviews (1988)

ANDROGEN abuse by athletes constitutes only a portion of the problem of androgen misuse by the general population (1) and only a minor aspect of the doping of athletes with drugs presumed to enhance athletic ability (2, 3). Indeed, of the drugs banned by the International Olympic Committee, steroids account only for about 15% (4). This particular form of drug abuse stems from the convergence of several separate misconceptions. The first was the recognition that the administration of androgens to hypogonadal males causes an increase in nitrogen retention and an increase in muscle mass and lean body weight (5). It followed that the differences in muscle mass between men and women are largely due to differences in testosterone levels, and it was assumed that the administration of androgens in supraphysiological amounts to normal men would do even more than the normal amount. The second misconception was that the anabolic (muscle promoting) and androgenic (virilizing) actions of the hormone are exerted by different mechanisms and that pure anabolic agents could be devised that would be devoid of or have minimal androgenic effects (6, 7). In fact, androgenic and anabolic effects are not due to different actions of the hormone but result from interaction of the hormone with the same receptor molecule in different tissues (1). In men with normal levels of plasma androgens the androgen receptor in most tissues appears either to be saturated or downregulated. Thus, it has not been possible to separate the two types of actions at the pharmacological or physiological levels, and in normal men any anabolic actions obtained from exogenous androgens are inevitably limited in scope. The third misconception, at least in the United States, stemmed from international competitiveness in sports. According to a widely accepted account, John B. Ziegler, a physician for the US weight lifting team, was told by a Russian team physician at the 1954 world weight lifting championship in Vienna that some members of the Russian team used androgens (8–10). Ziegler assumed that androgens would enhance athletic performance, and he began to experiment in American weight lifters with the various agents that had been developed as candidates for pure anabolic steroids (8). He subsequently concluded that the effects of androgens are purely psychological (9, 10).
MENTAL SYMPTOMS OF CEREBRAL SYPHILIS.
Authors: JAMES H. McBRIDE
Journal: JAMA (1901)

Syphilis may be the cause, either immediate or remote, of every form of disease of the nervous system, from neurasthenic conditions to coarse brain disease, or insanity. The reference to cases that follow will relate chiefly to conditions of mental disorder. Insanity due to syphilis has, in many cases, characteristics which though not easy to describe, are indicative of a specific origin. There is however a small proportion of syphilitic insanity that is represented by the usual forms of mental disorder. It is quite correct to say, therefore, that syphilitic insanity may mimic every known form of mental derangement, simulating acute mania, ordinary melancholia, terminal dementia or resembling so closely paretic dementia that experts may differ in their diagnosis. There is nothing characteristic in the mania of syphilis while the maniacal stage lasts, and the same statement applies to forms of depression due to syphilis. The history of the entire
Side-effects of guanoxan.
Authors: S. G. Cotton, E. Montuschi
Journal: BMJ (1966)

BRNALscreening test.Negative plates and those with light or mixed growth can be confidently discarded.A heavy pure growth in all four lines is designated positive, and the result confirmed by our routine method.Identification and sensitivity testing can be performed on the primary growth, and where necessary treatment instituted without awaiting confirmatory results.While proper mid-stream specimens are desirable we suspect that they are not always obtained, and immediate direct plating reduces the growth of contaminants to a minimum.If patients bathe before attending clinic vulval cleansing appears unnecessary.This method has been compared with our semi-quantitative method, which is essentially the same as that of Guttmann and Stokes,2 on 350 antenatal cases and 100 others.No significant discrepancies were found, and the incidence of bacteriuria of pregnancy demonstrated was 6%, correlating well with other series.It is also currently in use in investi- gating asymptomatic bacteriuria of non- pregnant women, and in an investigation in general practice.Inoculated plates can be sent direct to the laboratory for incubation, but urinary pathogens will grow, though more slowly, at room temperature.Plates can therefore be inoculated and kept by the prac- titioner, and only " positives " sent for identification and sensitivity testing.Mac-Conkey plates inhibit the swarming of Proteus species, and at room temperature keep without deterioration for considerable periods, especially in plastic bags.They are readily available from routine stock in all laboratories, and dare one suggest that pre-poured plates might eventually become available through the Ministry for domiciliary use.This is, we believe, a really simple test which should be easily available to all doctors and their patients.-Weare, etc.,
INTESTINAL OBSTRUCTION
Authors: J. V. Cooke, F. H. Rodenbaugh, G. H. Whipple
Journal: The Journal of Experimental Medicine (1916)

Intestinal obstruction, as a rule, is associated with an increasing amount of non-coagulable nitrogen in the blood. With acute intoxication the rise in non-coagulable nitrogen may be rapid and reach as high as three or even ten times normal. With more chronic intoxication there may be little or no rise in the blood non-coagulable nitrogen. Closed intestinal loops show exactly the same picture, and, when combined with obstruction, may give very high nitrogen readings. Acute proteose intoxication due to injection of a pure proteose will show a prompt rise in blood non-coagulable nitrogen, even an increase of 100 per cent within 3 or 4 hours. These intoxications also show a high blood content of creatinine and urea. The residual or undetermined nitrogen may be very high. A human case of intestinal obstruction with autopsy presents blood findings exactly similar to those observed in many animal experiments. Clinically the non-coagulable nitrogen of the blood may give information of value in intestinal obstruction. A high reading means a grave intoxication, but a low reading may be observed in some fatal cases and gives no assurance that a fatal intoxication may not supervene. The kidneys in practically all these experiments are normal in all respects. It is possible that protein or tissue destruction rather than impaired eliminative function is responsible for the rise in non-coagulable nitrogen of the blood in these acute intoxications. Transfusions of dextrose solutions often benefit intestinal obstruction, and may depress the level of the non-coagulable nitrogen in the blood. Some cases show no change in non-coagulable nitrogen following transfusions and diuresis, and, as a rule, such cases present the most severe intoxication.
Abstract 910: Synergistic combinations of targeted therapy and chemotherapy for neuroendocrine cancer.
Authors: Richard D. Dinnen, Yuehua Mao, Daniel P. Petrylak, Robert L. Fine
Journal: Cancer Research (2013)

Abstract We previously developed and reported a novel laboratory-derived chemotherapeutic regimen of capecitabine and temozolomide (TMZ) (CapTem). The CapTem regimen is highly active, well-tolerated with minor toxicities and may prolong survival and palliate symptoms in patients with well differentiated neuroendocrine tumors (NET). Further studies with CapTem in our laboratory indicated that sunitinib, a tyrosine kinase inhibitor (TKI), was highly synergistic with 5-Fluorouracil (5-FU) in killing BON (NET) cells. (Capecitabine is enzymatically converted to 5-FU in the tumor). Synergy was observed at a low concentration of 1.0 μM 5-FU and 1 nM sunitinib. Addition of 100 nM sunitinib resulted in a 4.5 fold increase in cell death (14.2 vs 64.5%). In addition, if sunitinib was combined with the CapTem regimen, (5-FU followed by TMZ), a synergistic response was observed with both 5-FU and TMZ over a range of concentrations, giving a maximal cell death of 74.4%. This contrasts with the cell death obtained with 5-FU, TMZ and sunitinib alone, resulting in 9.0, 6.8 and 10.2% annexin V+ cells, respectively. Sorafinib, a TKI closely related to sunitinib, not only did not synergize with 5-FU or TMZ, it inhibited cell death observed with sunitinib and 5-FU/ TMZ. In addition, K-252a, a potent inhibitor of tyrosine kinases, reduced the cell death induced by 5-FU/sunitinib suggesting a tyrosine kinase was involved. Considering the IC-50 of sunitinib for PDGF β is 75 nM, whereas for sorafinib it is 1129 nM, a difference of 15 fold, we hypothsized that the PDGF-β pathway might be involved. Addition of the PDGF-ββ form resulted in an enhancement of 5-FU/TMZ (CapTem) cell death. However, there was no effect on sunitinib-induced cell death, suggesting that the PDGF-β pathway may be involved but to an unknown extent in the cell death pathway induced by CapTem. Exposure of BON cells to TMZ and 5-FU may mimic the in vivo exposure to these drugs in patients and the resulting cell line resistance may be similar to resistance in tumors. Preliminary studies with four resistant BON cell lines: TMZ-Resistant, 5-FU-Resistant, TMZ+5FU-Resistant, (concurrent exposure to TMZ and 5-FU) and TMZ -&amp;gt; 5FU-Resistant, (sequential exposure to 5FU and TMZ) found that cells resistant to CapTem still retain sensitivity to sunitinib. This suggests that addition of sunitinib can overcome CapTem resistance in BON cells. Citation Format: Richard D. Dinnen, Yuehua Mao, Daniel P. Petrylak, Robert L. Fine. Synergistic combinations of targeted therapy and chemotherapy for neuroendocrine cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 910. doi:10.1158/1538-7445.AM2013-910
Joint Effects of Common Genetic Variants on the Risk for Type 2 Diabetes in U.S. Men and Women of European Ancestry
Authors: Marilyn C. Cornelis, Lu Qi, Cuilin Zhang, Peter Kraft, Jo Ann Manson, Tianxi Cai, David J. Hunter, Frank B. Hu
Journal: Annals of Internal Medicine (2009)

Background: Genome-wide association studies have identified novel type 2 diabetes loci, each of which has a modest impact on risk. Objective: To examine the joint effects of several type 2 diabetes risk variants and their combination with conventional risk factors on type 2 diabetes risk in 2 prospective cohorts. Design: Nested case–control study. Setting: United States. Participants: 2809 patients with type 2 diabetes and 3501 healthy control participants of European ancestry from the Health Professionals Follow-up Study and Nurses' Health Study. Measurements: A genetic risk score (GRS) was calculated on the basis of 10 polymorphisms in 9 loci. Results: After adjustment for age and body mass index (BMI), the odds ratio for type 2 diabetes with each point of GRS, corresponding to 1 risk allele, was 1.19 (95% CI, 1.14 to 1.24) and 1.16 (CI, 1.12 to 1.20) for men and women, respectively. Persons with a BMI of 30 kg/m2 or greater and a GRS in the highest quintile had an odds ratio of 14.06 (CI, 8.90 to 22.18) compared with persons with a BMI less than 25 kg/m2 and a GRS in the lowest quintile after adjustment for age and sex. Persons with a positive family history of diabetes and a GRS in the highest quintile had an odds ratio of 9.20 (CI, 5.50 to 15.40) compared with persons without a family history of diabetes and with a GRS in the lowest quintile. The addition of the GRS to a model of conventional risk factors improved discrimination by 1% (P < 0.001). Limitation: The study focused only on persons of European ancestry; whether GRS is associated with type 2 diabetes in other ethnic groups remains unknown. Conclusion: Although its discriminatory value is currently limited, a GRS that combines information from multiple genetic variants might be useful for identifying subgroups with a particularly high risk for type 2 diabetes. Primary Funding Source: National Institutes of Health.
Visceral leishmaniasis resembling systemic lupus erythematosus
Authors: P V Voulgari, G A Pappas, E N Liberopoulos, M Elisaf, F N Skopouli, A A Drosos
Journal: Annals of the Rheumatic Diseases (2004)

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unknown aetiology. B cell hyperactivity with production of multiple autoantibodies is the hallmark of the disease.1 On the other hand, such polyclonal B cell activation may occur in chronic infectious diseases. In this report we present a patient with visceral leishmaniasis who was diagnosed as having SLE and we discuss the clinical and laboratory findings which may discriminate between these two entities.

A 50 year old man presented in October 2001 with arthralgias, fatigue, weight loss, and low grade fever. Laboratory evaluation revealed haemoglobin 110 g/l, white blood cells 3.9×109/l with normal differential count, platelets 90×109/l, and erythrocyte sedimentation rate (ESR) 50 mm/1st h.

He was admitted to the hospital where physical examination disclosed mild splenomegaly. A laboratory investigation confirmed anaemia, leucopenia, and thrombocytopenia, increased ESR and C reactive protein (CRP) (table 1). Renal, liver and thyroid …
Selective enhancement of lipid peroxidation in plasma membrane in two experimental models of liver regeneration: Partial hepatectomy and acute CCl<sub>4</sub>administration
Authors: I Aguilar-Delfin, F López-Barrera, R Hernández-Munoz
Journal: Hepatology (1996)

It has been proposed that lipid peroxidation (LP) might be a modulator of cell division, influencing initiation and cessation of mitosis in regenerating liver. However, the understanding of the participating role of this event in the onset of liver proliferation has been hampered by the fact that both higher or lower LP have been reported after two–thirds partial hepatectomy (PH). Therefore, the present study deals with the extent of LP in the main subcellular fractions from rat liver at early stages of regeneration, induced by either PH of 70% or acute CCl4 administration. Our results, using several methods to monitor LP, indicate a differential effect in the peroxidative pattern of specific subcellular fractions from regenerating liver after 24 hours of PH: a decrease in microsomes and an increase confined to plasma membrane and cytosolic fractions, peaking after 24 hours of PH. In CCl4–treated rats, higher LP was also noted in plasma membrane and cytosol, being maximal at the replicative stage in this experimental model (48 hours). In addition, increased LP was found in microsomal and nuclear fractions, declining before the 48 hours. In hepatectomized rats, changes in LP seem to be an organ–specific event and related to only PHs capable of triggering a synchronized proliferative response, namely above 40%. These results show that LP, promoted by PH and CCl4 administration, is qualitatively distinct among subcellular fractions and may indeed be a normal cell event of physiological importance in the regenerating liver.