tbuckley/cabot-search huggingface dataset:
Adiponectin and lipid metabolism in skeletal muscle
Authors: Bonggi Lee, Jianhua Shao
Journal: Acta Pharmaceutica Sinica B (2012)

White adipose tissue (WAT) is a key energy depot in humans and most animals. Traditionally, it is believed that WAT passively accumulates triglycerides or releases fatty acids to accommodate systemic energy metabolism. However, recent studies have demonstrated that WAT also actively participates in energy metabolism mainly through its secretion of cytokines and hormones. Therefore, at this time, WAT is recognized as an endocrine organ. Adiponectin is one of the key adipocyte-derived hormones that regulate systemic or tissue lipid and glucose metabolism. In contrast to most other adipocyte-derived hormones, adiponectin increases insulin sensitivity and improves lipid and glucose metabolism. Although the insulin-sensitizing function of adiponectin has been well established, recent studies have demonstrated that adiponectin also regulates metabolism through pathways independent of insulin signaling. Due to the massive tissue mass of skeletal muscle, lipid uptake and subsequent fatty acid oxidation in skeletal muscle have a big impact on maintaining systemic energy homeostasis. Furthermore, adiponectin gene expression is regulated by energy intake. Therefore, adiponectin serves as a coordinator of energy balance amongst WAT, skeletal muscle and other tissues. We summarize the regulatory effects of adiponectin on lipid and glucose metabolism in skeletal muscle. Future research directions have also been proposed.
Atypical Depression: A Reappraisal
Authors: Gordon Parker, Kay Roy, Philip Mitchell, Kay Wilhelm, Gin Malhi, Dusan Hadzi-Pavlovic
Journal: American Journal of Psychiatry (2002)

OBJECTIVE: The study evaluated the DSM-IV definition of the atypical features specifier for a major depressive episode in major depressive disorder. METHOD: Nonpsychotic patients with major depressive disorder were assessed to determine if the DSM-IV model and decision rules for the atypical features specifier for a major depressive episode could be supported. RESULTS: The five clinical features of the DSM-IV atypical features specifier for a major depressive episode showed weak internal consistency, and the mandatory criterion A feature of mood reactivity did not show specificity in relation to any of the four criterion B accessory symptoms. The more severe the depression, the less likely the patient was to report criterion A and hence to meet criteria for the atypical features specifier. Remodeling the five features favored the personality style descriptor of interpersonal rejection sensitivity as an alternate primary feature. A reformulated model also suggested lifetime panic disorder and social phobia as higher-order determinants of atypical features in major depressive disorder. Additional analyses of criteria suggested that interpersonal rejection sensitivity and leaden paralysis had a phenomenological base in anxiety, that mood reactivity was linked with irritability, and that neither weight gain nor hypersomnia were clearly aligned with anxiety or depression, raising questions about their status as symptoms. CONCLUSIONS: The current definition and modeling of the DSM-IV atypical features specifier for a major depressive episode in major depressive disorder appears problematic. As suggested by earlier descriptions of atypical depression, certain expressions of anxiety may have primacy, and some clinical features associated with the DSM-IV model may be adaptive homeostatic responses rather than pathological symptoms.
TRPC1 Is Essential for In Vivo Angiogenesis in Zebrafish
Authors: Peng-chun Yu, Shan-ye Gu, Ji-wen Bu, Jiu-lin Du
Journal: Circulation Research (2010)

Wiring vascular and neural networks are known to share common molecular signaling pathways. Activation of transient receptor potential type C channels (TRPCs) has recently been shown to underlie chemotropic guidance of neural axons. It is thus of interest to examine whether TRPCs are also involved in vascular development.To determine the role of TRPC1 in angiogenesis in vivo during zebrafish development.Knockdown of zebrafish trpc1 by antisense morpholino oligonucleotides severely disrupted angiogenic sprouting of intersegmental vessels (ISVs) in zebrafish larvae. This angiogenic defect was prevented by overexpression of a morpholino oligonucleotide-resistant form of zebrafish trpc1 mRNA. Cell transplantation analysis showed that this requirement of Trpc1 for ISV growth was endothelial cell-autonomous. In vivo time-lapse imaging further revealed that the angiogenic defect was attributable to impairment of filopodia extension, migration, and proliferation of ISV tip cells. Furthermore, Trpc1 acted synergistically with vascular endothelial growth factor A (Vegf-a) in controlling ISV growth, and appeared to be downstream to Vegf-a in controlling angiogenesis, as evidence by the findings that Trpc1 was required for Vegf-a-induced ectopic angiogenesis of subintestinal veins and phosphorylation of extracellular signal-regulated kinase.These results provide the first in vivo evidence that TRPC1 is essential for angiogenesis, reminiscent of the role of TRPCs in axon guidance. It implicates that TRPC1 may represent a potential target for treating pathological angiogenesis.
Recurrent acute renal failure due to antibiotic-induced interstitial nephritis.
Authors: D Saltissi, C D Pusey, D J Rainford
Journal: BMJ (1979)

<h3>Objective</h3> Appendicitis is considered the most frequent surgical emergency in children. While the management of paediatric appendicitis is evolving, the precise amount of unpublished completed trials, potentially introducing bias into meta-analyses, is unknown. Controversial issues include the appropriate choice of surgical procedures, criteria for diagnosis of appendicitis, the role of antibiotic treatment and pain management. Selective reporting may introduce bias into evidence-based clinical decision-making, and the current, precise extent of unpublished results in paediatric appendicitis is unknown. We therefore assessed the publication status of completed clinical studies involving children registered on ClinicalTrials.gov. <h3>Design</h3> Cross sectional analysis. STrengthening the Reporting of OBservational studies in Epidemiology criteria were applied for design and analysis. <h3>Setting and participants</h3> ClinicalTrials.gov was queried for completed studies which were matched to publications on ClinicalTrials.gov, PubMed or Google Scholar. If no publication could be identified, principal investigators were contacted. <h3>Interventions/exposure</h3> Observational analysis. <h3>Primary and secondary outcome measures</h3> The proportion of published and unpublished studies was calculated. Subgroup analysis included studies on surgical procedures, diagnosis, antibiotic treatment and pain management. <h3>Results</h3> Out of n=52 completed clinical studies involving children with appendicitis, n=33 (63%) were published and n=19 (37%) were unpublished. Eighty-three per cent (n=43/52) of clinical trials assessed the above-listed controversial issues. Diagnostic studies were most rigorously published (91% of trials reported), data on surgical procedures, antibiotic and pain management were less transparent. Sixty-six per cent of interventional studies and 60% of randomised studies were published. Median time-to-publication, for example, the delay between completion of the trial until public availability of the results was 24 (IQR 12–36), range 2–92 months. <h3>Conclusion</h3> Despite the importance of appendicitis in clinical practice for the paediatric surgeon, there remains scientific uncertainty due to unpublished clinical trial results with room for improvement in the future. These data are helpful in framing the shifting paradigms in paediatric appendicitis because it adds transparency to the debate.
Increased mortality of preterm infants transferred between tertiary perinatal centres.
Authors: E. Bowman, L. W. Doyle, L. J. Murton, R. N. Roy, W. H. Kitchen
Journal: BMJ (1988)

Over 18 months almost one quarter of infants born before 30 weeks9 gestation in a tertiary perinatal centre who required intensive care had to be transferred to other tertiary centres because intensive care facilities were fully occupied. When infants with lethal congenital malformations were excluded half of the 34 infants who were transferred died; this was twice the mortality (24%) in the 111 infants remaining. The difference between the groups was significant (relative odds = 3.1) and remained so after adjustment for any discrepancies in gestational age (relative odds = 4.0). After adjustment for potential confounding variables by logistic function regression the risk of dying for those transferred remained significantly higher than that for infants who remained (relative odds = 4.6, 95% confidence interval 1.8 to 12.1). As the requirement for neonatal intensive care is episodic and unpredictable more flexibility has to be built into the perinatal health care system to enable preterm infants delivered in tertiary perinatal centres to be cared for where they are born.
Simultaneous Uptake of I-131 and F-18 FDG by a Renal Metastasis of Thyroid Papillary Cancer
Authors: Jong-Ryool Oh, Jae-Hoon Lim, Shin-Young Jeong, Suk-Hee Heo, Ari Chong, Jung-Joon Min
Journal: Clinical Nuclear Medicine (2011)

Renal metastasis of thyroid papillary cancer is rare and only a few cases have been reported. Most metastases of well-differentiated thyroid cancer alternatively accumulate either I-131 or F-18 fluorodeoxyglucose (FDG), according to tumor differentiation, and only a few metastases exhibit simultaneous I-131 and F-18 FDG uptake. This study shows the simultaneous I-131 and F-18 FDG uptake of metastatic renal mass in a patient with a 10-year history of thyroid papillary cancer. In our knowledge, this is the first report of thyroid cancer with renal metastasis as imaged by both I-131 SPECT/CT and F-18 FDG PET/CT.
Varicella in the Immunocompromised Host
Authors: Stephen R. Preblud, Phillip I. Nieburg, Neal A. Halsey
Journal: JAMA (1978)

<h3>To the Editor.—</h3> We would like to comment on a recent article by Keene and colleagues (239:45-46, 1978) discussing a 17-year-old girl with disseminated varicella complicating ulcerative colitis. The approach taken to varicella in the immunocompromised host is a function of the point at which the diagnosis is entertained. In a patient receiving steroid therapy in whom varicella develops after an unsuspected exposure, therapy should consist of immediate tapering of steroid dosage to physiological levels insofar as is possible.<sup>1,2</sup>In addition, two other modes of therapy may be useful in such patients. Adenosine arabinoside, an investigational antiviral agent, is available to immunocompromised patients with either disseminated varicella or disseminated herpes zoster through Richard Whitely, MD, or the University of Alabama Medical Center, Birmingham (205-934-5316 or 205-822-6459). Ann Arvin, MD, and Thomas Merigan, MD, of Stanford University, Stanford, Calif (415-497-5715, 415-321-6015, or 415-854-3788) are making interferon, another investigational agent, available
Pancreatic Cholera Syndrome: Effect of a Synthetic Somatostatin Analog on Intestinal Water and Ion Transport
Authors: William C. Santangelo, Thomas M. O'dorisio, Jong G. Kim, Gene Severino, Guenter J. Krejs
Journal: Annals of Internal Medicine (1985)

The effect of a synthetic somatostatin analog was studied in a patient with severe secretory diarrhea due to pancreatic cholera syndrome. Basal intestinal perfusion studies indicated an absence of water and sodium absorption, and active chloride secretion in the small bowel. Intravenous administration of the somatostatin analog (1 µg/kg · h) changed zero net water movement to absorption (122 mL/30 cm of the jejunum per hour). Chloride secretion changed to absorption (5.0 to 7.9 meq/30 cm · h), and plasma vasoactive intestinal polypeptide concentration was reduced from 330 to 45 pmol/L (normal, less than 51). When the analog was given subcutaneously, 100 µg twice daily, stool weight decreased, and plasma vasoactive intestinal polypeptide concentration fell toward the normal range (67 pmol/L). Plasma concentration of pancreatic polypeptide was initially elevated and dropped during intravenous infusion of somatostatin analog but returned to baseline on maintenance therapy with the analog delivered subcutaneously. The patient has not had further diarrhea during 9 months of therapy.
Polymorphisms in the Drug Transporter Gene ABCB1 Predict Antidepressant Treatment Response in Depression
Authors: Manfred Uhr, Alina Tontsch, Christian Namendorf, Stephan Ripke, Susanne Lucae, Marcus Ising, Tatjana Dose, Martin Ebinger, Marcus Rosenhagen, Martin Kohli, Stefan Kloiber, Daria Salyakina, Thomas Bettecken, Michael Specht, Benno Pütz, Elisabeth B. Binder, Bertram Müller-Myhsok, Florian Holsboer
Journal: Neuron (2008)
Nosocomial Bloodstream Infections in the Critically III-Reply
Authors: Richard P. Wenzel
Journal: JAMA (1994)

<h3>In Reply.</h3> —Dr Heiselman correctly notes that nosocomial bloodstream infections from IV lines can be associated with significant morbidity and economic burden; he also stresses the fact that appropriate time of replacement or removal of IV lines is essential for preventing secondary bloodstream infection. In our study population, IV lines were responsible for at least 20 (23%) of the 86 episodes of bloodstream infection. The attributable mortality from the infection in this subpopulation was 25% (nine cases vs four controls died). When only matched case-control pairs who survived bloodstream infection (n=11) were considered among patients with infections of IV line origin, cases stayed an additional 6.5 days in the surgical intensive care unit (SICU) (median stay, 15.5 days for cases vs 9 days for controls); extra costs attributable to the infection averaged $28 690 per survivor. Nosocomial bloodstream infection from IV lines occurred on average 8.4 days (median, 6 days)
Keeping the Pace
Authors: Elizabeth B. Fortescue
Journal: JAMA (2014)

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
Regulation of VLA-4 in lupus monocytes objectives
Authors: H. Rahami
Journal: Annals of the Rheumatic Diseases (2011)

<h3>Objectives</h3> The development of atherosclerosis and subsequent increased risk of cardiovascular disease (CVD) is known to be associated with inflammation. Studies have shown an increased risk of CVD in systemic lupus erythematosus (SLE). Inflammation seen in atherosclerosis involves various immune mediators, including interactions between adhesion molecules on endothelial cells and on monocytes. Very late antigen-4 (VLA-4) is an adhesion molecule in the integrin family found on monocytes and has been implicated in monocyte recruitment during development of atherosclerosis. A recent study noted an increased expression of VLA-4 in SLE monocytes, but the regulation is poorly understood. We aimed to further define variables governing the expression of VLA-4 on monocytes in patients with SLE compared to healthy controls. <h3>Methods</h3> CD14+ human monocytes were obtained from whole blood of healthy adult patients and SLE patients. Flow cytometry was used to measure expression of VLA-4 at rest and upon exposure to various agents, including interferon γ, interferon α, interleukin-4 and vitamin D. VLA-4 mRNA expression in SLE and healthy monocytes was measured using qRT-PCR. Healthy monocytes were incubated in control and SLE sera, and VLA-4 was expression evaluated using flow cytometry and immunofluorescence (IF). <h3>Results</h3> VLA-4 (CD49d) expression was significantly higher on control monocytes compared to SLE monocytes as measured by mean fluorescence intensity (p &lt; 0.05). However, levels of VLA-4 mRNA were significantly lower in control monocytes compared to SLE monocytes (p &lt; 0.05). Exposure of healthy monocytes to healthy human sera compared to SLE sera did not result in differences in cell surface expression of VLA-4; however, VLA-4 was redistributed to the interior of the cell. IF staining of VLA-4 of healthy monocytes incubated in SLE sera demonstrated VLA-4 in a vesicular compartment whereas healthy monocytes incubated in healthy sera or RPMI media alone exhibited VLA-4 staining on the surface or diffusely in the cytoplasm. <h3>Conclusion</h3> There was a significant downregulation of cell surface expression of VLA-4 in SLE monocytes as compared to the healthy population although mRNA levels were increased. We demonstrated that exposure to SLE sera causes increased internal IF staining of VLA-4, suggesting that decreased surface expression, in spite of increased RNA levels, in SLE is due to altered distribution. VLA-4 has increased expression in atherosclerosis, and understanding its upregulation in SLE patients could have implications for the prevention and treatment of advanced atherosclerosis in SLE. In addition, VLA-4 is capable of intracellular signalling. If there is an altered distribution of VLA-4 in SLE monocytes, this might affect the inflammatory pathway in SLE. These data provide a context for considering novel therapeutics to treat atherosclerosis in SLE.
Role of Kanamycin in the Management of Infections
Authors: Gordon M. Koota, Fritz B. Schweinburg, Alexander M. Rutenburg
Journal: New England Journal of Medicine (1960)

THE efficacy of kanamycin for the treatment of infections due to gram-positive and gram-negative bacteria has been established,1 2 3 4 5 6 7 8 9 10 11 and the hazards of injudicious administration of the drug delineated.1 2 3 4 5 6 7 8 9 10 11 12 13 This is a report of experience with the use of this compound in the management of surgical infections in 163 patients.Route of Administration and DosageIntramuscular AdministrationKanamycin was administered intramuscularly to 163 patients. Of these, 25 also received the drug intravenously, and 12 intraperitoneally.The average daily intramuscular dose was 1 to 2 gm., 1 gm. as the initial dose and 0.5 gm. every six hours thereafter for forty-eight hours, . . .
Pocket programmable computers in clinical practice.
Authors: M F Ryan, N Corbett, I Clark, M Peters
Journal: BMJ (1990)

high scores and little room for improvement (that is, there was a ceiling effect).The section on evaluation also mentions the use of several other tests, including a letter cancellation task, a 10 word recognition task, and paired associate memory tests.The results of tests are omitted from the results section.Thus the methodology of this trial makes it impossible to draw any conclusions about the effect of tacrine, and the negative results reported are as open to doubt as the positive results in the original paper by Summers et al,< which Dr Chatellier and colleagues have attempted to replicate.
Iron-Loading Anemia
Authors: Lewis R. Weintraub, Marcel E. Conrad, William H. Crosby
Journal: New England Journal of Medicine (1966)

ABNORMALITIES in iron metabolism associated with anemia have been demonstrated in nutritional pyridoxine deficiency in several animal species.1 2 3 4 However, a similar condition in human beings has been produced only once, in an eight-month-old mentally retarded boy.5 Removal of this essential vitamin and the addition of the antagonist 4-desoxypyridoxine to the diet of human adults has not resulted in any hematologic disturbance despite the appearance of other clinical and laboratory manifestations of pyridoxine deficiency.6 In 1956 Harris et al.7 described a patient with a hypochromic microcytic anemia and iron overload who had a partial hematologic response to pyridoxine therapy. In this . . .
1169 THE −1195 G&gt;A CYCLOOXYGENASE-2 PROMOTER POLYMORPHISM IS ASSOCIATED WITH HEPATIC INFLAMMATION AND FIBROSIS IN PATIENTS WITH CHRONIC HEPATITIS C
Authors: M. Miyashita, T. Ito, M. Sakaki, A. Kajiwara, H. Nozawa, K. Hiroishi, M. Kobayashi, H. Kumada, M. Imawari
Journal: Journal of Hepatology (2011)
The influence of nanoscale grooved substrates on osteoblast behavior and extracellular matrix deposition
Authors: Edwin Lamers, X. Frank Walboomers, Maciej Domanski, Joost te Riet, Falco C.M.J.M. van Delft, Regina Luttge, Louis A.J.A. Winnubst, Han J.G.E. Gardeniers, John A. Jansen
Journal: Biomaterials (2010)
Concentration of thyroxine-binding globulin: value of direct assay.
Authors: W A Burr, D B Ramsden, S E Evans, T Hogan, R Hoffenberg
Journal: BMJ (1977)

The concentration of thyroxine-binding globulin (TBG) in the serum can now be measured by direct assays that are simple and inexpensive. Comparison of a direct measurement of TBG concentration with a widely used indirect method (Thyopac-3) showed that the indirect method was inaccurate when TBG concentrations were high. This will result in an increase in the derived free thyroxine index (FTI), so that euthyroid patients with a raised TBG concentration may be at risk of being labelled thyrotoxic. Correction of serum total thyroxine (T4) concentration according to the actual TBG concentration (T4:TBG ratio) provided a better correlation with thyroid state than FTI.
Can the States Nullify Health Care Reform?
Authors: Timothy S. Jost
Journal: New England Journal of Medicine (2010)

On February 1, the Virginia Senate passed a bill stating that "No resident of this Commonwealth . . . shall be required to obtain or maintain a policy of individual insurance coverage." In considering this legislation, Virginia joins numerous other states with pending legislation aimed at limiting, changing, or opposing national health care reforms (see map).1 What is going on here?Whereas states generally adopt laws to achieve a legal effect, nullification laws are pure political theater. On its face, the Virginia bill exempts residents of the Commonwealth from having to comply with a law requiring the purchase of health insurance. Although . . .
Treatment of homozygous familial hypercholesterolaemia: an informative sibship.
Authors: R West, P Gibson, J Lloyd
Journal: BMJ (1985)

In a family in which both parents had the heterozygous form of familial hypercholesterolaemia four of the children had the homozygous form. The three oldest homozygous children, two of whom did not receive any treatment and in one of whom treatment did not lower the plasma cholesterol concentration, developed xanthomas in early childhood and died aged 3, 9, and 10 years. The fourth homozygous child was treated with diet and drugs from the age of 1 and at the age of 15 had no xanthomas, no clinical evidence of heart disease, and a virtually normal coronary angiogram. His plasma cholesterol concentration was reduced by about 30% but remained considerably raised. It is concluded that treatment, if started before atherosclerosis develops, can delay the onset of atheroma and coronary heart disease even though normal plasma cholesterol concentrations are not achieved.