tbuckley/cabot-search huggingface dataset:
Swedish national study reports improved survival for extremely preterm infants
Authors: J. Hopkins Tanne
Journal: BMJ (2009)

More than two thirds (70%) of babies born alive before 27 weeks’ gestation survive to one year, according to a prospective, three year national study in Sweden ( JAMA 2009;301:2225-33, doi:10.1001/jama.2009.771).

“The most important finding in this study is the high survival of extremely preterm infants born alive,” the authors say. The one year survival was 9.8% for babies born at 22 weeks, 53% at 23 weeks, 67% at 24 weeks, 82% at 25 weeks, and 85% at 26 weeks. Of babies surviving to one year, 45% had no serious morbidity.

Preterm births are increasing worldwide, and neonatal intensive care can save even extremely immature babies, said the lead investigator, Karel Marsal, of Lund University Hospital. He was speaking at a media briefing on child health organised by JAMA in New York last week.

The Extremely Preterm …
Association between antiviral treatment and extrahepatic outcomes in patients with hepatitis C virus infection
Authors: Adriaan J van der Meer
Journal: Gut (2015)

Chronic infection with the hepatitis C virus (HCV) is a slow progressive disease. While fibrosis development may not be linear over time, it has been estimated that 15–20% of patients will establish cirrhosis within 20 years of HCV acquisition.1 Once cirrhosis is present, it is clear that the patient's prognosis is heavily affected, with a 3–5% annual risk of liver failure as well as hepatocellular carcinoma (HCC). Although liver transplantation may be lifesaving in selected cases, organ shortage remains an important limitation. As a result, cirrhosis-related complications are considered to be one of the main reasons why chronic HCV infection is associated with an impaired overall survival.2 Fortunately, many HCV-infected patients are not expected to develop advanced hepatic fibrosis. Are these patients unaffected by the virus? Probably not. Chronic HCV infection remains a multifaceted disease, which is not restricted to the liver. Patients may experience a variety of liver-unrelated discomforts such as fatigue, nausea, abdominal or musculoskeletal pain, loss of weight, and neuropsychiatric symptoms including depression, irritability and malaise. These symptoms are non-specific and can often be attributed to extrahepatic manifestations of HCV infection. Extrahepatic manifestations are reported in up to 74% of patients, can be present long before the stage of advanced liver disease, and may be largely responsible for the frequent impaired health-related quality of life among patients with chronic HCV infection.3 Among the best known manifestations are mixed …
Recurrent Oral Ulcers
Authors: Eric T. Stoopler, Thomas P. Sollecito
Journal: JAMA (2015)

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
Signatures of tumour immunity distinguish Asian and non-Asian gastric adenocarcinomas
Authors: Suling J Lin, Johann A Gagnon-Bartsch, Iain Beehuat Tan, Sophie Earle, Louise Ruff, Katherine Pettinger, Bauke Ylstra, Nicole van Grieken, Sun Young Rha, Hyun Cheol Chung, Ju-Seog Lee, Jae Ho Cheong, Sung Hoon Noh, Toru Aoyama, Yohei Miyagi, Akira Tsuburaya, Takaki Yoshikawa, Jaffer A Ajani, Alex Boussioutas, Khay Guan Yeoh, Wei Peng Yong, Jimmy So, Jeeyun Lee, Won Ki Kang, Sung Kim, Yoichi Kameda, Tomio Arai, Axel zur Hausen, Terence P Speed, Heike I Grabsch, Patrick Tan
Journal: Gut (2014)

<h3>Objective</h3> Differences in gastric cancer (GC) clinical outcomes between patients in Asian and non-Asian countries has been historically attributed to variability in clinical management. However, recent international Phase III trials suggest that even with standardised treatments, GC outcomes differ by geography. Here, we investigated gene expression differences between Asian and non-Asian GCs, and if these molecular differences might influence clinical outcome. <h3>Design</h3> We compared gene expression profiles of 1016 GCs from six Asian and three non-Asian GC cohorts, using a two-stage meta-analysis design and a novel biostatistical method (<i>RUV-4</i>) to adjust for technical variation between cohorts. We further validated our findings by computerised immunohistochemical analysis on two independent tissue microarray (TMA) cohorts from Asian and non-Asian localities (n=665). <h3>Results</h3> Gene signatures differentially expressed between Asians and non-Asian GCs were related to immune function and inflammation. Non-Asian GCs were significantly enriched in signatures related to T-cell biology, including CTLA-4 signalling. Similarly, in the TMA cohorts, non-Asian GCs showed significantly higher expression of T-cell markers (CD3, CD45R0, CD8) and lower expression of the immunosuppressive T-regulatory cell marker FOXP3 compared to Asian GCs (p&lt;0.05). Inflammatory cell markers CD66b and CD68 also exhibited significant cohort differences (p&lt;0.05). Exploratory analyses revealed a significant relationship between tumour immunity factors, geographic locality-specific prognosis, and postchemotherapy outcomes. <h3>Conclusions</h3> Analyses of &gt;1600 GCs suggest that Asian and non-Asian GCs exhibit distinct tumour immunity signatures related to T-cell function. These differences may influence geographical differences in clinical outcome, and the design of future trials particularly in immuno-oncology.
Relationship of oxidative stress and endothelial dysfunction in sleep apnoea
Authors: B Jurado-Gámez, M C Fernandez-Marin, J L Gómez-Chaparro, L Muñoz-Cabrera, J Lopez-Barea, F Perez-Jimenez, J Lopez-Miranda
Journal: European Respiratory Journal (2010)

The aim of the present study was to evaluate ischaemic reactive hyperaemia (IRH) in obstructive sleep apnoea (OSA) and its relationship with oxidative stress. We studied 69 consecutive patients referred to our Sleep Unit (Reina Sofia University Hospital, Cordoba, Spain). Patients with chronic diseases or those taking medication were excluded. IRH was assessed before and after polysomnography. Morning IRH and oxidative stress markers were compared between patients with (apnoea–hypopnoea index (AHI) ≥5) and without (AHI &lt;5) OSA. Measurements were repeated in 25 severe OSA patients after continuous positive airway pressure (CPAP) therapy. We included 46 OSA patients (mean± sd AHI 49±32.1) and 23 non-OSA subjects (AHI 3±0.9). The OSA patients showed a significant worsening of morning IRH, and a significant increase in malondialdehyde and 8-hydroxydeoxyguanosine levels. Only the oxygen desaturation index independently explained morning IRH, while malondialdehyde levels showed a weak effect on IRH. In severe OSA patients, IRH improved significantly after CPAP treatment, as did malondialdehyde, 8-hydroxydeoxyguanosine and protein carbonyl levels. In OSA patients, endothelial dysfunction and oxidative stress were observed, and IRH worsened after sleep. The increase in oxidative stress was not associated with IRH, while intermittent hypoxia was strongly associated with IRH. In severe OSA patients, CPAP treatment improved oxidative stress and endothelial function.
Renal tubular NEDD4-2 deficiency causes NCC-mediated salt-dependent hypertension
Authors: Caroline Ronzaud, Dominique Loffing-Cueni, Pierrette Hausel, Anne Debonneville, Sumedha Ram Malsure, Nicole Fowler-Jaeger, Natasha A. Boase, Romain Perrier, Marc Maillard, Baoli Yang, John B. Stokes, Robert Koesters, Sharad Kumar, Edith Hummler, Johannes Loffing, Olivier Staub
Journal: Journal of Clinical Investigation (2013)

The E3 ubiquitin ligase NEDD4-2 (encoded by the Nedd4L gene) regulates the amiloride-sensitive epithelial Na+ channel (ENaC/SCNN1) to mediate Na+ homeostasis. Mutations in the human β/γENaC subunits that block NEDD4-2 binding or constitutive ablation of exons 6–8 of Nedd4L in mice both result in salt-sensitive hypertension and elevated ENaC activity (Liddle syndrome). To determine the role of renal tubular NEDD4-2 in adult mice, we generated tetracycline-inducible, nephron-specific Nedd4L KO mice. Under standard and high-Na+ diets, conditional KO mice displayed decreased plasma aldosterone but normal Na+/K+ balance. Under a high-Na+ diet, KO mice exhibited hypercalciuria and increased blood pressure, which were reversed by thiazide treatment. Protein expression of βENaC, γENaC, the renal outer medullary K+ channel (ROMK), and total and phosphorylated thiazide-sensitive Na+Cl– cotransporter (NCC) levels were increased in KO kidneys. Unexpectedly, Scnn1a mRNA, which encodes the αENaC subunit, was reduced and proteolytic cleavage of αENaC decreased. Taken together, these results demonstrate that loss of NEDD4-2 in adult renal tubules causes a new form of mild, salt-sensitive hypertension without hyperkalemia that is characterized by upregulation of NCC, elevation of β/γENaC, but not αENaC, and a normal Na+/K+ balance maintained by downregulation of ENaC activity and upregulation of ROMK.
Do Measures of Body Fat Distribution Provide Information on the Risk of Type 2 Diabetes in Addition to Measures of General Obesity?
Authors: Marshall K. Tulloch-Reid, Desmond E. Williams, Helen C. Looker, Robert L. Hanson, William C. Knowler
Journal: Diabetes Care (2003)

To investigate which anthropometric measurements of obesity best predict type 2 diabetes in a population of Pima Indians and whether additional information on diabetes risk could be obtained by combining measures of general obesity with measures of body fat distribution.We conducted a prospective study of 624 men and 990 nonpregnant women >18 years of age without diabetes. Subjects were followed a mean of 5.25 years for the development of type 2 diabetes (using 1997 American Diabetes Association criteria).A total of 322 new cases of type 2 diabetes (107 men and 215 women) were diagnosed during follow-up. Baseline obesity measurements were highly correlated and predicted diabetes in proportional hazards models adjusted for age. BMI had the highest hazard ratio in men and women, with age-adjusted hazard ratios per SD of 1.73 (95% CI 1.44-2.07) and 1.67 (1.45-1.91), respectively. According to receiver-operating characteristic analysis, BMI and waist-to-height ratio were the best predictors of diabetes in men, while in women BMI, waist-to-height ratio, waist circumference, and waist-to-thigh ratio were the best predictors. The predictive abilities of models containing BMI were not significantly improved by including other measures of general obesity or measures of the body fat distribution.Throughout its range, BMI was an excellent predictor of type 2 diabetes risk in Pima Indians and was not significantly improved by combining it with other measures of general adiposity or body fat distribution.
CyberKnife for hilar lung tumors: report of clinical response and toxicity
Authors: Keith Unger, Andrew Ju, Eric Oermann, Simeng Suy, Xia Yu, Saloomeh Vahdat, Deepa Subramaniam, K William Harter, Sean P Collins, Anatoly Dritschilo, Eric Anderson, Brian T Collins
Journal: Journal of Hematology & Oncology (2010)

To report clinical efficacy and toxicity of fractionated CyberKnife radiosurgery for the treatment of hilar lung tumors.Patients presenting with primary and metastatic hilar lung tumors, treated using the CyberKnife system with Synchrony fiducial tracking technology, were retrospectively reviewed. Hilar location was defined as abutting or invading a mainstem bronchus. Fiducial markers were implanted by conventional bronchoscopy within or adjacent to tumors to serve as targeting references. A prescribed dose of 30 to 40 Gy to the gross tumor volume (GTV) was delivered in 5 fractions. Clinical examination and PET/CT imaging were performed at 3 to 6-month follow-up intervals.Twenty patients were accrued over a 4 year period. Three had primary hilar lung tumors and 17 had hilar lung metastases. The median GTV was 73 cc (range 23-324 cc). The median dose to the GTV was 35 Gy (range, 30 - 40 Gy), delivered in 5 fractions over 5 to 8 days (median, 6 days). The resulting mean maximum point doses delivered to the esophagus and mainstem bronchus were 25 Gy (range, 11 - 39 Gy) and 42 Gy (range, 30 - 49 Gy), respectively. Of the 17 evaluable patients with 3 - 6 month follow-up, 4 patients had a partial response and 13 patients had stable disease. AAT t a median follow-up of 10 months, the 1-year Kaplan-Meier local control and overall survival estimates were 63% and 54%, respectively. Toxicities included one patient experiencing grade II radiation esophagitis and one patient experiencing grade III radiation pneumonitis. One patient with gross endobronchial tumor within the mainstem bronchus developed a bronchial fistula and died after receiving a maximum bronchus dose of 49 Gy.CyberKnife radiosurgery is an effective palliative treatment option for hilar lung tumors, but local control is poor at one year. Maximum point doses to critical structures may be used as a guide for limiting toxicities. Preliminary results suggest that dose escalation alone is unlikely to enhance the therapeutic ratio of hilar lung tumors and novel approaches, such as further defining the patient population or employing the use of radiation sensitizers, should be investigated.
Acute psoriatric arthropathy precipitated by oxprenolol.
Authors: D G Macfarlane, L Settas
Journal: Annals of the Rheumatic Diseases (1984)

A previously normal 58-year-old woman developed a widespread psoriatic rash and asymmetrical peripheral polyarthritis a week after beginning treatment with oxprenolol for hypertension. Skin and joint disease resolved simultaneously after drug withdrawal and have not recurred.
Graft fibrosis after pediatric liver transplantation: Ten years of follow-up
Authors: Rene Scheenstra, Paul M.G.J. Peeters, Henkjan J. Verkade, Annette S. H. Gouw
Journal: Hepatology (2008)

Previously we reported the presence of portal fibrosis in 31% (n = 84) of the grafts in protocol biopsies 1 year after pediatric liver transplantation (LTx). To assess the natural history of graft fibrosis after pediatric liver transplantation, we extended the analysis of graft histology in follow-up protocol biopsy specimens obtained 5 and 10 years after transplantation. We correlated histological results with clinical parameters at the time of LTx and during follow-up, to allow identification of risk factors for the development of fibrosis. From 1 year to 5 years after LTx, the prevalence of fibrosis increased from 31% to 65% (n = 66) but remained stable thereafter (at 10 years, 69%, n = 55). At 10 years after LTx, however, the percentage of patients with severe fibrosis had increased from 10% (at 5 years) to 29%. Of the 69% of children without fibrosis at 1 year post-transplantation, 64% (n = 39) had developed some degree of fibrosis at 10 years. Fibrosis was strongly related to transplant-related factors such as prolonged cold ischemia time, young age at the time of transplantation, high donor/recipient age ratio, and the use of partial grafts (P < 0.05). Fibrosis was not significantly related to rejection, chronic hepatitis, or the nature of the immunosuppressive therapy.Biopsies after pediatric LTx show that most grafts developed fibrosis within 5 years. At 10 years after LTx, the graft fibrosis had progressed to severe fibrosis in at least 25% of the patients. Development of fibrosis, starting either before or after the first year post-LTx, was strongly related to transplant-related factors, indicating the importance of these factors to long-term graft prognosis.
CD4+CD25+ TR Cells Suppress Innate Immune Pathology Through Cytokine-dependent Mechanisms
Authors: Kevin J. Maloy, Laurence Salaun, Rachel Cahill, Gordon Dougan, Nigel J. Saunders, Fiona Powrie
Journal: The Journal of Experimental Medicine (2003)

CD4(+)CD25(+) regulatory T (T(R)) cells can inhibit a variety of autoimmune and inflammatory diseases, but the precise mechanisms by which they suppress immune responses in vivo remain unresolved. Here, we have used Helicobacter hepaticus infection of T cell-reconstituted recombination-activating gene (RAG)(-/-) mice as a model to study the ability of CD4(+)CD25(+) T(R) cells to inhibit bacterially triggered intestinal inflammation. H. hepaticus infection elicited both T cell-mediated and T cell-independent intestinal inflammation, both of which were inhibited by adoptively transferred CD4(+)CD25(+) T(R) cells. T cell-independent pathology was accompanied by activation of the innate immune system that was also inhibited by CD4(+)CD25(+) T(R) cells. Suppression of innate immune pathology was dependent on T cell-derived interleukin 10 and also on the production of transforming growth factor beta. Thus, CD4(+)CD25(+) T(R) cells do not only suppress adaptive T cell responses, but are also able to control pathology mediated by innate immune mechanisms.
Intracoronary Streptokinase after Primary Percutaneous Coronary Intervention
Authors: Murat Sezer, Hüseyin Oflaz, Taner Gören, İrem Okçular, Berrin Umman, Yilmaz Nişanci, Ahmet Kaya Bilge, Yasemin Şanli, Mehmet Meriç, Sabahattin Umman
Journal: New England Journal of Medicine (2007)

Microvascular perfusion is often impaired after primary percutaneous coronary intervention (PCI). We proposed that in situ thrombosis might contribute to poor myocardial perfusion in this setting. To test this hypothesis, we evaluated the effect of low-dose intracoronary streptokinase administered immediately after primary PCI.Forty-one patients undergoing primary PCI were randomly assigned to receive intracoronary streptokinase (250 kU) or no additional therapy. Two days later, cardiac catheterization was repeated, and coronary hemodynamic end points were measured with the use of a guidewire tipped with pressure and temperature sensors. In patients with anterior myocardial infarction, the deceleration time of coronary diastolic flow was measured with transthoracic echocardiography. At 6 months, angiography, echocardiography, and technetium-99m single-photon-emission computed tomography were performed.Two days after PCI, all measures of microvascular function (means +/-SD) were significantly better in the streptokinase group than in the control group, including coronary flow reserve (2.01+/-0.57 vs. 1.39+/-0.31), the index of microvascular resistance (16.29+/-5.06 U vs. 32.49+/-11.04 U), the collateral-flow index (0.08+/-0.05 vs. 0.17+/-0.07), mean coronary wedge pressure (10.81+/-5.46 mm Hg vs. 17.20+/-7.93 mm Hg), systolic coronary wedge pressure (18.24+/-6.07 mm Hg vs. 33.80+/-11.00 mm Hg), and diastolic deceleration time (828+/-258 msec vs. 360+/-292 msec). The administration of intracoronary streptokinase was also associated with a significantly lower corrected Thrombolysis in Myocardial Infarction frame count (the number of cine frames required for dye to travel from the ostium of a coronary artery to a standardized distal coronary landmark) at 2 days. At 6 months, however, there was no evidence of a difference between the two study groups in left ventricular size or function.In our pilot trial, the administration of low-dose intracoronary streptokinase immediately after primary PCI improved myocardial reperfusion but not long-term left ventricular size or function. These findings require clarification in a larger trial. (ClinicalTrials.gov number, NCT00302419.)
Effect of Paternal Diabetes on Pre-Diabetic Phenotypes in Adult Offspring
Authors: Adela Penesova, Joy C. Bunt, Clifton Bogardus, Jonathan Krakoff
Journal: Diabetes Care (2010)

OBJECTIVE Paternal and maternal type 2 diabetes, exclusive of gestational diabetes, may influence risk factors in the offspring differently (through possible epigenetic effects of parental diabetes) and are difficult to identify without accurate dates of diagnosis. We aimed to examine a metabolic phenotype in three different groups of offspring to see distinct paternal versus maternal effects. RESEARCH DESIGN AND METHODS We examined body composition and insulin action (M) in nondiabetic subjects and insulin secretion tested via acute insulin response (AIR) in normal glucose-tolerant full-heritage Pima Indian adults categorized by disparate parental diabetes status: 1) offspring of fathers with early-onset diabetes (age &amp;lt;35 years) and nondiabetic mothers (ODF; n = 10), 2) offspring of mothers with early-onset diabetes (age &amp;lt;35 years), not exposed to diabetes in utero with nondiabetic fathers (OMED; n = 11), and 3) a control group of offspring of parents without diabetes until &amp;gt;50 years of age (CON; n = 15). RESULTS ODFs were leaner than CONs and OMEDs (percent of body fat [%BF]: least-squares means adjusted for age and sex [95% CI]: 27.3 [23.3–31.3] in ODFs vs. 35.4 [32.2–38.5] in CONs and 32.4 [28.8–36.1] in OMEDs, P = 0.04). ODFs were more insulin sensitive (had a higher M) than OMEDs or CONs, but not after adjustment for age, sex, and %BF. AIR adjusted for M, age, sex, and %BF was lower in ODFs versus CONs and OMEDs (P &amp;lt; 0.05). CONCLUSIONS Adult ODFs were leaner and had lower early insulin secretion, despite being equally insulin sensitive after adjustment for body fat compared to the other groups, indicating a paternal imprinted effect.