tbuckley/cabot-search huggingface dataset:
HYPERCHLOREMIC ACIDOSIS FOLLOWING URETEROSIGMOIDOSTOMY
Journal: JAMA (1953)

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
Normalized Diastolic Properties After Left Ventricular Assist Result From Reverse Remodeling of Chamber Geometry
Authors: Alessandro Barbone, Mehmet C. Oz, Daniel Burkhoff, Jeffrey W. Holmes
Journal: Circulation (2001)

Background Normalization of diastolic properties after left ventricular (LV) assist may result from a change in myocardial material properties, chamber size, or both. This study tested the hypothesis that reported normalization of LV diastolic properties is primarily due to remodeling of chamber geometry. Methods and Results Hearts were obtained at transplantation from 8 patients with dilated cardiomyopathy (DCM), 6 patients with DCM plus 33±5 days of LV assist, and 3 patients with no evidence of heart failure. LV assist normalized passive pressure-volume curves. Chamber dimensions decreased without a change in the ratio of radius to wall thickness. Midwall stress-stretch relations predicted from pressure-volume and dimension data were not different for DCM and LV assist hearts. Passive stress-stretch relations were measured in endocardial trabeculae and were not different for DCM and LV assist hearts. Myocyte size and collagen area fraction were unchanged at this brief duration of support. Conclusions These findings are all consistent with the hypothesis that early normalization of diastolic properties after LV assist device support results from remodeling of chamber geometry, not from changes in tissue stiffness. These data emphasize the importance of geometry to ventricular mechanics and demonstrate that reduction of heart size does not necessarily produce a reduction in wall stress.
Advances in early diagnosis of perinatal HIV infection
Authors: E. Connor
Journal: JAMA (1991)

Early intervention using antiretroviral therapy and prophylaxis for infections has become the standard of care for adults and children infected with human immunodeficiency virus (HIV). Advances in the field of HIV treatment have resulted in improvement in quality and/or duration of life for patients of all ages. Zidovudine therapy is now approved and routinely indicated for treatment of symptomatic HIV-infected children and for those with evidence of immunodeficiency.<sup>1</sup>Prophylaxis for<i>Pneumocystis carinii</i>pneumonia is routinely recommended for children with significant CD4 lymphocyte depletion, and intravenous γ-globulin has been shown to reduce the rate of serious bacterial infections in some HIV-infected chiidren.<sup>2,3</sup>However, for therapeutic interventions to be applied optimally, it is essential for the diagnosis of HIV infection to be made as early in the course as possible,<i>before</i>immunodeficiency and symptomatic illness are manifest. For children with perinatally acquired HIV infection, this is particularly problematic.<sup>4,5</sup>
Regulation of human liver cytochromes P-450 in family 3A in primary and continuous culture of human hepatocytes
Authors: E Schuetz
Journal: Hepatology (1993)

The cytochrome P-450 3A gene family comprises the dominant forms of cytochrome P-450 found in human liver. We examined as a possible useful system for studying the regulation of cytochrome P-450 3A under controlled conditions in vitro, primary monolayer cultures of human hepatocytes and compared the results with those obtained from the study of cytochrome P-450 3A in the human hepatoblastoma cell line HepG2 or in the human hepatocellular carcinoma cell line TONG/HCC. Using 3A antibodies, 3A cDNAs and 3A3, 3A4, 3A5 and 3A7 isozyme-specific oligonucleotides as probes, we determined that primary human hepatocyte cultures routinely expressed a 3A3/4* immunoreactive protein and 3A mRNA. These gene products were well maintained for many days and were induced by treatment of the cultures with dexamethasone, phenobarbital, macrolide antibiotics, the HMG CoA reductase inhibitor lovastatin or an antifungal agent, clotrimazole. Of six donor livers examined, only two contained mRNA or protein for 3A5, a form found in only a few adult human subjects. In cultures prepared from one of these two livers, 3A5 mRNA was detectable for several days. In cultures of hepatocytes from the remaining four human livers that did not contain 3A5 mRNA or protein, we detected neither spontaneous nor inducible 3A5 proteins or mRNAs. HepG2 cells contained only 3A7 protein, a form found in human fetal liver, even after treatment with inducers. Treatment of HepG2 cells with dexamethasone, macrolide antibiotics, phenobarbital and phenobarbital-like inducers or lovastatin produced dose-dependent induction of 3A7 mRNA and 3A7 immunoreactive protein. TONG/HCC cells contained 3A3, 3A4 and 3A5 mRNAs, but only 3A5 immunoreactive protein could be detected. Treatment of TONG/HCC cells with dexamethasone, macrolide antibiotics or phenobarbital induced 3A3 and 3A4 mRNAs, as observed in primary cultures, but failed to increase 3A5 mRNA or protein. We conclude that, in addition to primary cultures of human hepatocytes, replicating human hepatic lines HepG2 and TONG/HCC may be useful models for examining regulation of cytochrome P-450 3A genes polymorphically expressed in the living human being. (HEPATOLOGY 1993;18:1254-1262).
Correction
Authors: D Fry, R Johnson, C Cameron, I Lord, J Symons, J Revill, C Rigby, Hilary Saunders, H Weinbren, E Brough, 6pamela Burrill, A Coates, 3m Conolly, G Currie, A Forman, I Hepner, 3m Jeffery, 5r Marsh, A Minns, 3e Shinebourne, 6w Singer, I Talbot, Margaret Watts, Elisabeth Abbott, A Addison, A Albeedh, Pamela Aldis, A Amery, H Amir-Ahmadi, J Anderson, Mildred Anderson, J Andlaw, D Angel, P Arey, Jean Armstrong, K Arnold, Jacqueline Arnold, J Ashby, A Ashton, R Asmal, A Aubrey, N Austin, D Baillie, Eva Bancroft, Valerie Banky, Sarah Bard, Anita Barker, J Barltrop, Maureen Barrett, Katherine Bartlett, J Beale, A Bean, C Beeley, S Bell, A Benady, Enid Benison, E Bennett, R Bennett, Elizabeth Bergel, D Binsted, F Bird, Diana Birkett, R Bishop, N Blake-James, A Blakeney-Edwards, Margaret Boakes, J Bolam, J Bootes, B Booth, Janet Boothroyd Brooks, Ann Boulton, N Bowdler, Annette Boyd, M Bray, Valerie Briggs, Marjorie Broadbent, Margaret Brooks, C Brown, C Bulloch, Barbara Bulpitt, R Burgess, N Caine, P Cameron, Anne Camm, J Campbell, A Candy, Joy Cargill, Maureen Catling, P Chamberlain, J Chan, Jane Child, J Clarke, K Clarke, Anne Cliff, Valerie Cockayne, G Codman, Jennifer Coles, D Connor, J Cook, G Cooke, Patricia Cornel, Ann Coutts Milne, Gillian Coxon, Anne Craig, A Crocker, J Cumberland, D Cumming, P Curran, J Dale, F Darracott, D Davidson, R Davies, T Davies, . Davis, J Day, P Deaner, Brenda De Souza, J Dickinson, F Diabanor, A Doherty, B Doney, B Doran
Journal: BMJ (1963)
Non-human Infection
Journal: Gut (1995)

We have shown that chronic infection by H. heilnannii-like bacteria results in gastric ulceration in Balb/c mice.The purpose of this study was to determine the effect of bedding ingestion and fasting stress on ulcerogenesis in H. heilnannii-infected mice.Mice were inoculated with either gastric homogenate containing H. heibnannii, uninfected gastric homogenate, or sterile Brucella broth, and housed on corn cob bedding.Eight months after inoculation, mice were randomly divided into 3 groups.Group A was fasted on bedding for 24 hours prior to sacrifice.Group B was removed from the corn cob bedding, placed in cages with wire inserts and no bedding, and fasted for 24 hours.Group C was not fasted and not removed from the bedding.At sacrifice, the stomachs were scored for the presence of H. heilmannii and gastritis, and for the number and severity of ulcers.All mice given infected gastric homogenate became infected with H. heilmannii, and all developed gastritis and lymphofollicular and epithelial hyperplasia.The stomachs of group A mice contained corn cob bedding, the stomachs of Group C mice contained lab chow, and the stomachs of group B mice were empty.Of the infected mice, gastric ulcers were grossly apparent in 4/8 Group A mice, 2/8 group B mice, and 1/8 group C mice, but were not present in any uninfected mice.Histologically, ulcers or erosions were detected in 11/24 of the infected mice: 5/8 in Group A (ulcer score, 1.375), 4/8 in Group B (ulcer score, 0.875), and 2/8 in Group C (ulcer score, 0.125).Gastric erosions were present in 6/48 uninfected mice: 2/16 in Group A and 4/16 in Group B (ulcer score, 0.145).Ulcers were more common and severe in infected fasted mice than in unfasted mice or uninfected mice and were more severe in mice fasted on bedding than in mice fasted on wire.Mechanical trauma due to ingestion of bedding, stress due to fasting, or both may exacerbate gastric ulcerogenesis in mice infected with H. heilmannii.
Reminiscences of a Four Months' Stay with Professor A. Von Graefe in Berlin
Authors: A. Samelson
Journal: BMJ (1866)

process at several points on the edges of the sore, and pain in it was reduced to a minimum.As for the case of the breast, the woman herself had so much improved in health, that it would have been difficult to recognise in her, the same thin, cachectic- looking creature of three months back, for her on 9 July
Book Reviews
Journal: Allergy (1983)

Books reviewed in this article: Nawotny, A. (ed.): Pathological membranes. Vol. 11. Ball, G. N. (ed.): Allergy and clinical immunology. Clark, T.J. H. (ed.): Steroids in asthma. A reappraisal in the light of inhalation therapy. Hillary, I. B. &amp; Hennessen, W. (eds.): Enteric infections in man and animals: standardization of immunological procedures. Developments in biological standardization. Vol. 53. Axelsen, N. H. (ed.): Handbook of immunoprecipitation‐in‐gel techniques. Inman, F. P. &amp; Kindt, T. J. (ed.): Contemporary topics in molecular immunology. Maurer, Th. : Contact and photo‐contact allergens. A manual of predictive test methods. In: Dermatology Series, Vol. 3.
Toxicity of PBBs with Special Reference to Porphyrinogenic Action and Spectral Interaction with Hepatic Cytochrome P-450
Authors: J. J. T. W. A. Strik
Journal: Environmental Health Perspectives (1978)

Some of the polyhalogenated aromatic compounds (PHAs) which are able to produce porphyria are presently known as environmental contaminants. Chronic exposure to PHAs causes hepatic porphyria in different species. Qualitatively PBBs act comparable to PHAs. An increase in accumulation of porphyrins caused by PHAs is not simply related to an increase of delta-ALAS activity in liver. Heme cannot exert a feedback when porphyria develops. Induction of P-450 mediated drug enzymes is needed. The PHAs interact with P-450 in vitro. The PHAs are converted into a reactive intermediate, not a known metabolite, which depletes liver GSH and then becomes reactive to tissue structures. Mitochondria are damaged; fluorescence of porphyrins is detected in the region of central veins where degenerative change in hepatocytes is most marked. A possible pathological change in the cell membrane permeability is assumed too. In this porphyric stage uropophyrinogen decarboxylase (urogen decarboxylase) is inhibited. The proportion of steroid hormones product by ovaries and testes compared to each other are possibly involved in sensitivity to porphyrinogenic compounds.
Die Behandlung des Hallux valgus.
Journal: JAMA (1930)

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
Committee for Research on Tobacco and Health Holds First Meeting
Journal: JAMA (1964)

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
Expression of X protein and hepatitis B virus replication in chronic hepatitis
Authors: Y Haruna
Journal: Hepatology (1991)

The X protein can act on the enhancer of hepatitis B virus in an in vitro system and elevate the transcriptional level of hepatitis B virus. However, because no relationship had been reported between X protein expression and hepatitis B virus replication in patients with chronic hepatitis B, we focused on its expression in the liver in comparison with markers of hepatitis B virus replication. Liver biopsy samples and sera from 59 carriers with HBsAg were examined immunohistochemically for X protein using rabbit IgG against recombinant X protein. There was a significant difference in the serum hepatitis B virus DNA level between X protein–positive and –negative patients (p < 0.001). Serum pre-S1 and pre-S2 antigens were also measured quantitatively by enzyme immunoassay using monoclonal antibodies specific against each antigen. The titers of pre-S1 antigen in patients positive for X protein were significantly higher (p < 0.001) than those of the X protein–negative patients (3.02 ± 0.99 vs. 2.00 ± 0.59, respectively). Similarly, the titers of pre-S2 antigen were 2.98 ± 0.91 vs. 1.94 ± 0.54, respectively (p < 0.001). The rate of positivity of the X protein was higher (38 of 49; 77.6%) in the replicative group (serum HBeAg, serum hepatitis B virus DNA or HBcAg in liver positive) compared with that observed in the nonreplicative group (3 of 10; 30% – serum HBeAg, serum hepatitis B virus DNA and HBcAg in liver negative) (p < 0.01). Our findings indicate that the X protein is closely correlated with hepatitis B virus replication and may have an important role in viral replication in chronic hepatitis B virus infection. (HEPATOLOGY 1991;13:417–421.)
<i>QuickStats:</i> Changes* in Late Preterm Birth Rates,<sup>†</sup> by State — National Vital Statistics System, United States, 2014 and 2016
Authors: Michelle Osterman
Journal: MMWR Morbidity and Mortality Weekly Report (2018)

Signi cant increase Nonsigni cant increase Nonsigni cant decline DC * Increases and declines; significant at p<0.05.† Late preterm birth rate is the number of births delivered at 34 to 36 completed weeks of gestation per 100 total births.The late preterm birth (34 to 36 weeks of gestation) rate rose 4.0% in the United States, from 6.82% in 2014 to 7.09% in 2016.Increases in late preterm birth rates occurred in 24 states and the District of Columbia during 2014-2016.Increases in an additional 23 states were not statistically significant.Nonsignificant declines in late preterm births were observed in three states.
Addition to Author Contributions
Journal: JAMA Psychiatry (2014)

Martin Grosshans, MD; Emanuel Schwarz, PhD; Jan Malte Bumb, MD; Carola Schaefer, MPharm; Cathrin Rohleder, PhD; Christian Vollmert, MD; Sabine Vollstädt-Klein, PhD; Heike Tost, MD, PhD; Andreas Meyer-Lindenberg, MD, PhD; Falk Kiefer, MD; F. Markus Leweke, MD
DO WE CODDLE THE HEART?
Journal: JAMA (2005)

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
Essentials of Surgery. A Textbook of Surgery for Students and Graduate Nurses and for Those Interested in the Care of the Sick.
Journal: JAMA (1923)

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
Treatment of patients with hepatitis C and cirrhosis
Authors: Teresa L. Wright
Journal: Hepatology (2002)

Recommendations for treatment of hepatitis C in patients with cirrhosis are difficult. Few prospective studies have focused on treatment of patients with advanced disease, and response rates appear to be lower and serious side effects more frequent in patients with cirrhosis. In patients with compensated cirrhosis, combination therapy with interferon alfa (3 million units [MU] 3 times a week) and ribavirin (1,000 or 1,200 mg/d) results in a sustained virological response (SVR) in 33% to 41% of patients. Responses to combination therapy are not significantly higher using peginterferon alfa 2a (180 μg/wk; 43%) or peginterferon alfa 2b (1.5 μg/kg/wk; 44%) compared with standard interferon. In using peginterferon in combination therapy, the benefits of once weekly dosing need to be weighed against the higher risks of cytopenias and greater costs with the pegylated formulations. Combination therapy results in some degree of histological improvement even in patients who are virological non-responders. These findings provide the scientific basis for ongoing studies of maintenance therapy with peginterferon to prevent complications of cirrhosis in non-responder patients with hepatitis C. Recommendations for management of decompensated cirrhosis and of recurrent hepatitis C after liver transplantation are difficult because of limitations of data, most of which are derived from uncontrolled case series. Combination therapy is poorly tolerated in both groups and rates of response are low. Thus, while the medical need is great, treatment of patients with decompensated cirrhosis or with recurrent hepatitis C after transplantation should be undertaken cautiously and only within the confines of prospective clinical trials. (Hepatology 2002;36:S185-S194).
Prevention of Cervical Cancer in Low-Resource Settings
Authors: Eric J. Suba, Kim R. Geisinger, Matthew A. Zarka, Stephen S. Raab
Journal: JAMA (2006)

To the Editor: Dr Denny and colleagues1 studied screen-and-treat approaches to cervical cancer screening in low-resource settings. We question whether these approaches should be characterized as safe, effective, or resource-appropriate in a real-world setting.