tbuckley/cabot-search huggingface dataset:
Mechanisms whereby exogenous adenine nucleotides improve rabbit renal proximal function during and after anoxia.
Authors: L J Mandel, T Takano, S P Soltoff, S Murdaugh
Journal: Journal of Clinical Investigation (1988)

When a suspension of rabbit proximal tubules is subjected to anoxia, ATP falls by 80-90% during 40 min of anoxia, and upon reoxygenation (reox) the cells only recover 25-50% of their initial ATP. Addition of Mg-ATP (magnesium chloride-treated ATP), Mg-ADP, or Mg-AMP (five aliquots of 200 nmol/ml added 10 min apart) during anoxia causes complete recovery of ATP levels, and respiratory and transport function after 40 min of reox. Similar additions of adenosine (ADO), or inosine (INO), or Mg-ATP only during reox are less effective. Lactate dehydrogenase (LDH) release after 40 min of anoxia is 30-40% under control conditions, only 10-15% when adenine nucleotides or ADO are added during anoxia, and 20% when INO is added, suggesting that these additions may stabilize the plasma membrane during anoxia and help preserve cellular integrity. During reox, recovery may depend on the entry of ATP precursors and, therefore, we explored the mechanism whereby exogenous ATP increases the intracellular ATP content. Additions of Mg-ATP, Mg-ADP, or Mg-AMP to continuously oxygenated tubules increase cellular ATP content three- to fourfold in 1 h. The added ATP and ADP are rapidly degraded to AMP, and more slowly to ADO, INO, and hypoxanthine. Furthermore, the ATP-induced increase in cellular ATP is abolished by the exogenous addition of adenosine deaminase, which converts extracellular ADO to INO. These results suggest that the increase in cellular ATP requires extracellular ADO. The ADO obtained from the breakdown of AMP may be preferentially transported into the renal cells to be resynthesized into cellular AMP and ATP.
Aortic Annular Sizing for Transcatheter Aortic Valve Replacement Using Cross-Sectional 3-Dimensional Transesophageal Echocardiography
Authors: Hasan Jilaihawi, Niraj Doctor, Mohammad Kashif, Tarun Chakravarty, Asim Rafique, Moody Makar, Azusa Furugen, Mamoo Nakamura, James Mirocha, Mitch Gheorghiu, Jasminka Stegic, Kazuaki Okuyama, Daniel J. Sullivan, Robert Siegel, James K. Min, Swaminatha V. Gurudevan, Gregory P. Fontana, Wen Cheng, Gerald Friede, Takahiro Shiota, Raj R. Makkar
Journal: Journal of the American College of Cardiology (2013)
Intravenous Fluids — Getting the Balance Right
Authors: Elizabeth M. Molyneux, Kath Maitland
Journal: New England Journal of Medicine (2005)

Acute infections are a major cause of illness and death in children worldwide. In Africa, 50 percent of in-hospital deaths of children occur within 24 hours of admission, and shock complicates many cases.1 The provision of emergency advanced life support for critically ill children would have an important effect on survival in the developing world, where acute infections are common.1,2 Ways must be found of ensuring emergency care in resource-poor settings, where sophisticated point-of-care analyses, intensive monitoring, and specialist care are rarely present; basic laboratory studies cannot be done in a timely fashion; the choice of intravenous fluids is . . .
A rare type.
Authors: E Graham
Journal: BMJ (1985)

You just can't do that, Elinor! said my husband. His illness had just been diagnosed at King's College Hospital liver unit. I had suggested to Alfred that we should make arrangements for his tissues to be offered after his death to researchers into his rare metabolic disorder. We know the names of people who have written articles, I had said. Let's write to them and get the post mortem organised with a 'shopping list' of everyone's require? ments. Alfred disagreed: You can't mention post mortems to doctors who are striving to keep me alive. It would be an insult. But if I die away from King's, find out whether they would like a post mortem. And that is what I did . . . and more.
The Mammogram That Cried Wolfe
Authors: Karla Kerlikowske
Journal: New England Journal of Medicine (2007)

That mammographic density is an important risk factor for breast cancer was first recognized by Wolfe in the 1970s. His pioneering observation has since been confirmed in more than 42 studies, the vast majority of which have shown an association between increased mammographic density and the risk of breast cancer.1 Women in the highest quartile of mammographic density have a risk of breast cancer that is approximately four to six times as high as that among women of similar age who are in the lowest quartile. Only two other factors increase the risk of breast cancer more than mammographic density: . . .
Full-Time Practice in the Community Hospital
Authors: Robert R. Henderson
Journal: JAMA (1970)

During the last 30 years, we have noted a change in the faculty of most medical schools, from predominately part-time teachers of clinical medicine to predominately full-time physicians, many interested in basic research. During the past 15 years, we have noted a somewhat similar but slower change in the staffing pattern of many community hospitals, particularly those larger institutions in urban areas. Often the change is initiated by the addition of a full-time salaried director of medical education and followed by full-time directors of key services who are responsible for the quality of care. I would like to describe and briefly discuss the advantages of medical teaching programs in the milieu of the community hospital with a full-time staff. The Hunterdon Medical Center, located in Flemington, NJ, serves a county of 440 square miles with a population of approximately 75,000 persons. It is the only general medical facility in the
Cerebyx Labels Changed
Authors: Stuart L. Nightingale
Journal: JAMA (1999)

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
Risk of Amniocentesis for Prenatal Diagnosis
Authors: Aubrey Milunsky
Journal: New England Journal of Medicine (1975)

Amniocentesis for prenatal genetic studies is now a well established diagnostic tool in the obstetrician's armamentarium. This technic, in general use for about six years, however, is grossly under-utilized. In Massachusetts, for example, where 3979 women 35 years of age and older had babies in 1974, only 4.1 per cent availed themselves of the opportunities afforded by prenatal diagnosis. There may be many reasons for the low utilization of early diagnostic amniocentesis. Lack of knowledge by physician and patient alike of the indications for amniocentesis,1 and objections on the basis of religious belief, are perhaps less important than the obstetrician's . . .
Abstract 1309: ERβ1 induces apoptosis in lung cancer cells by regulating growth factor signaling.
Authors: Christoforos Thomas, Fotis Nikolos, Gayani Rajapaksa, Igor Bado, Jan-Ake Gustafsson
Journal: Cancer Research (2013)

Abstract Estrogens have recently been associated with the clinical outcome of patients with non-small cell lung cancer (NSCLC). The wild-type estrogen receptor β (ERβ1) one of the mediators of the estrogen signaling in cells is expressed in lung cancer. However, the role of ERβ1 in NSCLC cell growth has not been fully elucidated. Here we show that induction of ERβ1 expression inhibited cell growth in H1299 and A549 NSCLC cells. Treatment of these cells with the ERβ agonists 17β-estradiol or 3β-Adiol further decreased cell proliferation and induced apoptosis. ERβ1 was found to induce apoptosis through stimulation of the intrinsic apoptotic pathway that involves upregulation of the proapoptotic protein Bim. Inactivation of the extracellular-signal-regulated kinases ERK1/2 was found to be involved in the ERβ1-mediated induction of apoptosis since treatment with EGF that activates ERK1/2 abolished the ability of ERβ1 to sustain the apoptotic phenotype. These results suggest that, by regulating NSCLC cell growth, ERβ1 could be an important factor in biology of lung cancer and a potentially useful component in the clinical management of the disease. Citation Format: Christoforos Thomas, Fotis Nikolos, Gayani Rajapaksa, Igor Bado, Jan-Ake Gustafsson. ERβ1 induces apoptosis in lung cancer cells by regulating growth factor signaling. [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 1309. doi:10.1158/1538-7445.AM2013-1309
Promising New Procedure Offers Hope for Patients With Intracerebral Hemorrhage
Authors: Mike Mitka
Journal: JAMA (2011)

vent onward transmission of HIV, I believe that considerable changes are possible in resources and policy that would lend themselves to further prevention of HIV infection. When benefits outweigh costs by orders of magnitude, we will see changes in the United States. Policy changes will result from logical thinking.” While Cohen noted that he will participate in discussions of policies about who to treat and when, his role as principal investigator of HPTN 052 is “to report the results and let them speak for themselves.” Meanwhile, advocates for HIVinfected patients continue to stress the importance of making drugs available to patients who need them, and the shortsightedness of not doing so. An individual unable to access an ADAP and whose HIV infection progresses to full-blown AIDS may be categorized as disabled and become eligible for Medicaid, Macsata pointed out. Those Medicaid costs, he said, are 2.5 times greater than accessing drugs through ADAPs. “From a public health standpoint, it just doesn’t make sense.” What needs to be done to put ADAPs on a more solid footing throughout the country? “An additional $360 million is necessary for FY 2012 to meet projected needs,” said Penner, “although given the current federal fiscal environment, the request is for an additional $106 million.”
Pyelonephritis in the Diabetic
Authors: Donald B. Halverstadt
Journal: JAMA (1966)

In a study of 80 juvenile diabetic patients, chronic pyelonephritis was found histologically in seven (9%) of open renal biopsies. Twelve patients (15%) had positive urine cultures. No patient had a positive renal-biopsysite culture. Three patients (4%) had positive renal-tissue cultures. There was essentially no correlation found between the presence of positive urine cultures, positive tissue cultures, and the histological diagnosis of chronic pyelonephritis. It is suggested that factors other than the continued presence of bacteria in the kidney may play a role in the pathogenesis of chronic pyelonephritis.
Brain's Clinical Neurology
Authors: Donald J. Dalessio
Journal: JAMA (1985)

Books that last through decades generally have an aura of immortality about them; one comes to look upon them as old friends. Thus it is for<i>Brain's Clinical Neurology</i>, revised by Bannister, which first appeared in 1960 and is now in its third decade of life, extending through six editions. Furthermore, it is an Oxford University Press book, implying a precision in production and printing that is invariably fulfilled. This text is written primarily for nonneurologists and students, if you will, and falls midway between those useful outlines that one peeks at for thirty seconds in a moment of crisis and more comprehensive texts and tomes on neurology that endeavor to be exhaustive, and usually are. The current edition is up-to-date in its inclusion of those new diagnostic techniques that have revolutionized the clinical practice of neurology. It also includes a discussion of neurotransmitters, neuropeptides, and endorphins, which is at
Female Sex and Higher Drug Dose as Risk Factors for Late Cardiotoxic Effects of Doxorubicin Therapy for Childhood Cancer
Authors: Steven E. Lipshultz, Stuart R. Lipsitz, Suzanne M. Mone, Allen M. Goorin, Stephen E. Sallan, Stephen P. Sanders, E. John Orav, Richard D. Gelber, Steven D. Colan
Journal: New England Journal of Medicine (1995)

Late cardiotoxic effects of doxorubicin are increasingly a problem for patients who survive childhood cancer. Cardiotoxicity is often progressive, and some patients have disabling symptoms. Our objective was to identify risk factors for late cardiotoxicity.
Abstract 799: Comprehensive proteomic analysis of cisplatin resistance in ovarian cancer
Authors: Pang-ning Teng, Brian L. Hood, Tracy Litzi, Nicole P. Chappell, Chad A. Hamilton, G. Larry Maxwell, Thomas P. Conrads
Journal: Cancer Research (2012)

Abstract We have conducted a comprehensive proteomic analysis of an ovarian cancer cell line (A2780) and its cisplatin resistant daughter line (A2780-CP20) to identify key regulators and signaling pathways that confer cisplatin resistance. Quantitative proteomic profiling was conducted of defined biological compartments including that from global lysates, the nuclear fraction, the phosphoproteome and the secretome. Total cell lysates and nuclear fractions were harvested from A2780 and A2780-CP20 cultured in the presence or absence of cisplatin (3 µM) for 72 h. The secretome fractions were collected from A2780 and A2780-CP20 cultured in serum-free, phenol red-free media in the presence or absence of cisplatin (3 µM) for 24 h. Phosphopeptides were enriched from peptide digests of total lysates of A2780 and A2780-CP20 cultured in the presence or absence of cisplatin (3 µM) for 15 min using TiO2. Sample digests were analyzed by high-resolution LC-MS/MS that resulted in the identification of 2703, 2286, 1815, and 1362 proteins from the global, nuclear, secretome, and phosphoproteome fractions, respectively. Spectral counting was utilized to quantify the relative abundance of proteins identified. Nuclear proteins identified at elevated abundance in the cisplatin resistant A2780-CP20 including an array of chromatin remodeling proteins, such as SATB1, SATB2, coilin, AT-rich interactive domain-containing protein 3A (ARID3A), ARID3B, and ARID3Cwere validated by Western blot and qPCR in A2780/A2780-CP20 as well as other gynecologic cancer cell lines. Modulation of the abundance level of these candidates and the phenotypic impact on cisplatin resistance utilizing shRNA knockdown will be described. Differential proteins selected from the secretome analysis for western blot validation include Fras1-related extracellular matrix protein 2 (FREM2), stanniocalcin-1 (STC1), angio-associated migratory cell protein (AAMP), plasminogen activator inhibitor 1 (SERPINE1), high mobility group protein B1 (HMGB1), and chloride intracellular channel protein 2 (CLIC4), stromelysin-2 (MMP10), interstitial collagenase (MMP2), and CD166 antigen. Validated candidate protein targets from the secretome analysis will be tested by IHC on formalin fixed tissue sections as well as ELISA and multiple reaction monitoring (MRM) by mass spectrometry in serum from recurrent and non-recurrent ovarian cancer patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 799. doi:1538-7445.AM2012-799
A defect in sodium-dependent amino acid uptake in diabetic rabbit peripheral nerve. Correction by an aldose reductase inhibitor or myo-inositol administration.
Authors: D A Greene, S A Lattimer, P B Carroll, J D Fernstrom, D N Finegold
Journal: Journal of Clinical Investigation (1990)

A myo-inositol-related defect in nerve sodium-potassium ATPase activity in experimental diabetes has been suggested as a possible pathogenetic factor in diabetic neuropathy. Because the sodium-potassium ATPase is essential for other sodium-cotransport systems, and because myo-inositol-derived phosphoinositide metabolites regulate multiple membrane transport processes, sodium gradient-dependent amino acid uptake was examined in vitro in endoneurial preparations derived from nondiabetic and 14-d alloxan diabetic rabbits. Untreated alloxan diabetes reduced endoneurial sodium-gradient dependent uptake of the nonmetabolized amino acid 2-aminoisobutyric acid by greater than 50%. Administration of an aldose reductase inhibitor prevented reductions in both nerve myo-inositol content and endoneurial sodium-dependent 2-aminoisobutyric acid uptake. Myo-inositol supplementation that produced a transient pharmacological elevation in plasma myo-inositol concentration, but did not raise nerve myo-inositol content, reproduced the effect of the aldose reductase inhibitor on endoneurial sodium-dependent 2-aminoisobutyric acid uptake. Phorbol myristate acetate, which acutely normalizes sodium-potassium ATPase activity in diabetic nerve, did not acutely correct 2-aminoisobutyric uptake when added in vitro. These data suggest that depletion of a small myo-inositol pool may be implicated in the pathogenesis of defects in amino acid uptake in diabetic nerve and that rapid correction of sodium-potassium ATPase activity with protein kinase C agonists in vitro does not acutely normalize sodium-dependent 2-aminoisobutyric acid uptake.
Impaired Renal Tubular Potassium Secretion in Sickle Cell Disease
Authors: RALPH A. DeFRONZO
Journal: Annals of Internal Medicine (1979)

We examined renal tubular function in six patients with sickle cell hemoglobin. All had normal inulin and para-aminohippurate clearances and impaired urinary concentrating and acidifying abilities. After intravenous potassium chloride administration, maximum excretion of potassium (UKV) was significantly lower in sickle cell patients than in control subjects, and the percentage of potassium load excreted in 5 h was markedly reduced. Urinary potassium excretion after sodium sulfate infusion was also markedly reduced in sickle cell patients compared to control subjects. After 40 mg of oral furosemide, UKV was also diminished in sickle cell patients. Plasma aldosterone response to ACTH and intravenous potassium was similar to that of control subjects. Plasma renin activity increased normally after volume contraction. We conclude that sickle cell patients have a defect in their ability to excrete an acute potassium load that cannot be attributed to abnormal renin or aldosterone secretion. Overall potassium homeostasis is maintained by extrarenal mechanisms during acute potassium loading.
Reduced ferrochelatase activity in fibroblasts from patients with porphyria variegata
Authors: D. J. Viljoen, E. Cayanis, D. M. Becker, S. Kramer, B. Dawson, R. Bernstein
Journal: American Journal of Hematology (1979)

Abstract Ferrochelatase deficiency has been shown in both porphyria variegata (PV) and erythropoietic protoporphyria (EPP). It has been suggested that in PV there is a decrease in the enzyme, whereas in EPP the enzyme is unstable. In the present study ferrochelatase activity was measured in skin fibroblasts from three patients with PV and three normal subjects. The enzymatic activity in the patients with PV (17.5 ± 4.5 pmoles heme formed per 10 7 fibroblasts per hour) was 50% of that of the control group (31.0 ± 3.2 pmoles heme formed per 10 7 fibroblasts per hour). This supports the contention that the enzyme is deficient in PV and that an inactive ferrochelatase is the primary deficiency in this type of porphyria.
A METHOD FOR MAINTAINING PRESSURE OVER ELBOW IN OLECRANON BURSITIS (MINER'S ELBOW), WITHOUT IMMOBILIZING THE JOINT
Authors: Guy S. Van Alstine
Journal: JAMA (1922)

I find, will maintain sufficient pressure to bring about obliteration of the bursal sac without greatly inhibiting the joint action. With this device my patients have been able to continue their usual occupations while under treatment. This treatment is not suitable in old chronic cases with thickened, fibrous sacs, or in acute suppurative bursitis. 2678 East Seventy-Fifth Street.
Abstract 2961: Reactivation of EWS-FLI1 suppressed FOXO1 expression as a novel therapeutic strategy for Ewing's sarcoma
Authors: Stephan Niedan, Max Kauer, Gunhild Jug, Robert L. Walker, Paul S. Meltzer, Udo Kontny, Heinrich Kovar
Journal: Cancer Research (2012)

Abstract The EWS-FLI1 chimeric protein, characterizing Ewing's sarcoma (ESFT), is prototypic for an aberrant oncogenic ETS transcription factor. The mechanisms of transcriptional regulation leading to ETS-driven tumorigenesis are poorly understood. In-silico analysis of time-resolved expression data revealed enrichment of recognition motifs for forkhead box (FOX) proteins in EWS-FLI1 repressed promoters. Several FOX genes were found to be bound by EWS-FLI1 in ChIP-seq and transcriptionally affected by EWS-FLI1 knockdown. We therefore hypothesized that EWS-FLI1 exerts an important part of its repressive activity via inhibiting FOX proteins. Upon silencing of EWS-FLI1, both FOXO1 and FOXO3 proteins were strongly induced in ESFT cells consistent with this hypothesis, but only FOXO1 translocated to the nucleus. However, in the presence of EWS-FLI1, FOXO1 is excluded from the nucleus as a consequence of phosphorylation. Nuclear translocation was restored by either inhibition of CDK2, augmented by chemical inhibition of PI3K, or by mutation of CDK2 or AKT phosphorylation sites. Furthermore, ChIP experiments revealed that EWS-FLI1 directly binds the promoter of FOXO1 in vitro suggesting a multi-layered regulation of FOXO1 expression by transcriptional repression and post-translational modification. Functional restoration of nuclear FOXO1 expression in ESFT cells resulted in impaired proliferation and significantly reduced soft agar colony formation ability. A significant overlap between EWS-FLI1 repressed and FOXO1 activated genes was observed. Treatment of ESFT cell lines with Methyl-Seleninic-Acid (MSA) led to re-activation of endogenous FOXO1 in the presence of EWS-FLI1 in a dose- and time-dependent manner, and induced massive cell death, which we found to be at least partially FOXO1-dependent. Taken together, these data confirm our hypothesis that a repressive sub-signature of EWS-FLI1 regulated genes is due to suppression of FOXO1. FOXO1 re-activation by small molecules may constitute a novel therapeutic strategy in the treatment of ESFT. This study was supported by grant 22328-B09 from the Austrian Science Fund FWF. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2961. doi:1538-7445.AM2012-2961