tbuckley/cabot-search huggingface dataset:
Spontaneous pneumomediastinum; analysis of 23 cases
Authors: Sebastian Gagatek, Marta García Clemente, Nelson Fuentes Martínez, Herminia Buchelli Ramirez, Miguel Ariza Prota, Pere Casán Clará
Journal: European Respiratory Journal (2013)

Introduction:  Pneumomediastinum(PM) is an unfrequent disease, which characterize by the presence of air in the mediastinum.  Aim:  A review of all cases diagnosed of PM in the last 10 years in our hospital. To determine the clinical course and possible complications.  Methods:  A retrospective study from 2001 until 2012. Data was recollected from medical history using a standart form.  Results: 34 patients, 24 males(70.6%) and 10 women(29,4%), of whom 17 had a smoking history. 23 cases(67,6%) were diagnosed of spontaneous PM and 11(32,4%) as secondary PM. The average age of spontaneous PM was 24,87±15,6 and 55,91±25,42 for secondary PM (p=0.002). We have analyzed 23 cases of spontaneous PM. The most frequent symptoms were: chest pain(74%), shortness of breath(47,8%), sore throat(26,1%), cough(21,7%), neck pain(21,7%) and hoarseness(26,1%). Subcutaneous emphysema have been observed in 18(78,3%) cases. No pneumothorax was observed. 22(96%) patients were admitted to the hospital, with an average length stay of 4.57+3 days. The diagnosis was held by chest X-ray in all cases and chest CT scan was performed in 13 (56,5%)patients. In 3 cases esophageal contrast media was supplied. The most prevalent concomitant disease was asthma, presented in 5(21,7%). Treatment was conservative in all cases: 21(91,3%) oxygen therapy, 20(87%) rest and analgesia 17(74%). No recurrence was observed, having all of them good clinical course.  Conclusions:  Spontaneous PM is a benign condition, which occur principally in young men and have an excellent response to the conservative treatment with no complications or recurrency. Therefore a follow up don9t seem to be necessary and patients could be treated in an outpatient clinic.
Idiopathic portal hypertension
Authors: Jurgen Ludwig, Etsuko Hashimoto, Hiroshi Obata, William P. Baldus
Journal: Hepatology (1993)

old Japanese woman was admitted to the hospital because of hematemesis.The clinical history was negative; she drank no alcohol and did not smoke.She did not recall episodes of jaundice and had not received needle sticks or transfusions.The patient had been well until she became nauseated after a meal and vomited some blood.On physical examination, she weighed 45 kg with a height of 148 cm.Her temperature was 36.7"C, her pulse was 70 beats per minute, her respiratory rate was 16 per minute and her blood pressure was 124/60 mm Hg.She had no rash or lymphadenopathy; stigmata of chronic liver disease such as spider angiomas or palmar erythema were absent.She was not jaundiced.The abdomen was soft, and the liver could not be felt.However, mild splenomegaly was noted.She had no peripheral edema.The remainder of the physical examination was negative.After a blood transfusion the hemoglobin level was 11.4 gm/dl, and the hematocrit was 32%; she had pancytopenia with 3,374,000 erythrocytes, 2,500 WBCs and 30,000 platelets.Levels of serum constituents were as follows: total bilirubin, 0.8 mgidl; alkaline phosphatase, 220 U/L (expected, 108 to 282); AST, 25 U/L (expected, less than 20); ALT, 15 U/L (expected, less than 24); total protein, 6.8 gnddl; total globulin, 2.7 gm/dl; and albumin, 3.6 gm/dl.The prothrombin time was normal (11.4 sec).Serological test results for the presence of antimitochondrial antibodies and for the detection of hepatitis B (core and surface) antibodies and antigens were negative.A test for hepatitis C was not available at the time.The urine was negative for protein and sugar.Endoscopy demonstrated esophageal and cardiac varices with cherry-red-spots.
The tim Mutant of the Drosophila Rhythm Gene timeless Manifests Allele-Specific Interactions with period Gene Mutants
Authors: Joan E Rutila, Hongkui Zeng, Myai Le, Kathryn D Curtin, Jeffrey C Hall, Michael Rosbash
Journal: Neuron (1996)

To identify new components of the Drosophila circadian clock, we screened chemically mutagenized flies for suppressors or enhancers of the long periods characteristic of the period (per) mutant allele per L. We isolated a novel mutant that maps to the rhythm gene timeless (tim). This novel alleletimSL, alters the temporal pattern of per L protein nuclear localization and restores temperature compensation to perL flies. timSL more generally manifests specific interactions with different per alleles. The identification of this first period-altering tim allele provides further evidence that TIM is a major component of the clock, and the allele-specific interactions with PER provide evidence that the PER/TIM heterodimer is a unit of circadian function. Although timSL fails to restore PER-L/TIM temperature insensitivity in yeast, it alters the TIM phosphorylation pattern during the late night. The effects on phosphorylation suggest that timSL functions as a partial bypass suppressor of per L and provide evidence that the TIM phosphorylation program contributes to the circadian timekeeping mechanism.
Impact of Self-Reported Patient Characteristics Upon Assessment of Glycemic Control in the Veterans Health Administration
Authors: Miriam Maney, Chin-Lin Tseng, Monika M. Safford, Donald R. Miller, Leonard M. Pogach
Journal: Diabetes Care (2007)

OBJECTIVE— The purpose of this article was to evaluate the impact of self-reported patient factors on quality assessment of Veterans Health Administration medical centers in achieving glycemic control. RESEARCH DESIGN AND METHODS— We linked survey data and administrative records for veterans who self-reported diabetes on a 1999 national weighted survey. Linear regression models were used to adjust A1C levels in fiscal year 2000 for socioeconomic status (education level, employment, and concerns of having enough food), social support (marital status and living alone), health behaviors (smoking, alcohol use, and exercise level), physical and mental health status, BMI, and diabetes duration. Medical centers were ranked by deciles, with and without adjustment for patient characteristics, on proportions of patients achieving A1C &amp;lt;7 or &amp;lt;8%. RESULTS— There was substantial medical center level variation in patient characteristics of the 56,740 individuals from 105 centers, e.g., grade school education (mean 15.3% [range 2.3–32.7%]), being retired (38.3% [19.9−59.7%]) or married (65.2% [43.7–77.8%]), food insufficiency (13.9% [7.2–24.6%]), and no reported exercise (43.2% [31.1–53.6%]). The final model had an R2 of 7.8%. The Spearman rank coefficient comparing the thresholds adjusted only for age and sex to the full model was 0.71 for &amp;lt;7% and 0.64 for &amp;lt;8% (P &amp;lt; 0.0001). After risk adjustment, 4 of the 11 best-performing centers changed at least two deciles for the &amp;lt;7% threshold, and 2 of 11 changed two deciles for the &amp;lt;8% threshold. CONCLUSIONS— Adjustment for patient self-reported socioeconomic status and health impacts medical center rankings for glycemic control, suggesting the need for risk adjustment to assure valid inferences about quality.
Dissection of experimental asthma with DNA microarray analysis identifies arginase in asthma pathogenesis
Authors: Nives Zimmermann, Nina E. King, Johanne Laporte, Ming Yang, Anil Mishra, Sam M. Pope, Emily E. Muntel, David P. Witte, Anthony A. Pegg, Paul S. Foster, Qutayba Hamid, Marc E. Rothenberg
Journal: Journal of Clinical Investigation (2003)

Asthma is on the rise despite intense, ongoing research underscoring the need for new scientific inquiry. In an effort to provide unbiased insight into disease pathogenesis, we took an approach involving expression profiling of lung tissue from mice with experimental asthma. Employing asthma models induced by different allergens and protocols, we identified 6.5% of the tested genome whose expression was altered in an asthmatic lung. Notably, two phenotypically similar models of experimental asthma were shown to have distinct transcript profiles. Genes related to metabolism of basic amino acids, specifically the cationic amino acid transporter 2, arginase I, and arginase II, were particularly prominent among the asthma signature genes. In situ hybridization demonstrated marked staining of arginase I, predominantly in submucosal inflammatory lesions. Arginase activity was increased in allergen-challenged lungs, as demonstrated by increased enzyme activity, and increased levels of putrescine, a downstream product. Lung arginase activity and mRNA expression were strongly induced by IL-4 and IL-13, and were differentially dependent on signal transducer and activator of transcription 6. Analysis of patients with asthma supported the importance of this pathway in human disease. Based on the ability of arginase to regulate generation of NO, polyamines, and collagen, these results provide a basis for pharmacologically targeting arginine metabolism in allergic disorders.
Combined Epidermal Growth Factor Receptor Targeting with the Tyrosine Kinase Inhibitor Gefitinib (ZD1839) and the Monoclonal Antibody Cetuximab (IMC-C225)
Authors: Pablo Matar, Federico Rojo, Raúl Cassia, Gema Moreno-Bueno, Serena Di Cosimo, José Tabernero, Marta Guzmán, Sonia Rodriguez, Joaquín Arribas, José Palacios, José Baselga
Journal: Clinical Cancer Research (2004)

Abstract Purpose: The epidermal growth factor receptor (EGFR) is abnormally activated in cancer and two classes of anti-EGFR agents, monoclonal antibodies and low-molecular-weight tyrosine kinase inhibitors, have shown antitumor activity in patients. Because these two classes of antireceptor agents target the EGFR at different sites, we decided to explore whether the combined administration of gefitinib, a tyrosine kinase inhibitor, and cetuximab, a monoclonal antibody, had superior antitumor activity than either agent given alone. Experimental Design: We studied the effects of the combination of gefitinib and cetuximab in a panel of human cancer cell lines and in an EGFR-dependent human tumor xenograft model (A431). The effects of these two agents on EGFR signaling, proliferation, apoptosis, and vascularization were evaluated. In addition, we analyzed, with cDNA arrays, changes in gene expression profiles induced by both agents. Results: The combined treatment with gefitinib and cetuximab resulted in a synergistic effect on cell proliferation and in superior inhibition of EGFR-dependent signaling and induction of apoptosis. In a series of in vivo experiments, single-agent gefitinib or cetuximab resulted in transient complete tumor remission only at the highest doses. In contrast, suboptimal doses of gefitinib and cetuximab given together resulted in a complete and permanent regression of large tumors. In the combination-treated tumors, there was a superior inhibition of EGFR, mitogen-activated protein kinase, and Akt phosphorylation, as well as greater inhibition of cell proliferation and vascularization and enhanced apoptosis. Using cDNA arrays, we found 59 genes that were coregulated and 45 genes differentially regulated, including genes related to cell proliferation and differentiation, transcription, DNA synthesis and repair, angiogenesis, signaling molecules, cytoskeleton organization, and tumor invasion and metastasis. Conclusions: Our findings suggest both shared and complementary mechanisms of action with gefitinib and cetuximab and support combined EGFR targeting as a clinically exploitable strategy.
The non-H pylori helicobacters: their expanding role in gastrointestinal and systemic diseases
Authors: J G Fox
Journal: Gut (2002)

The number of species in the genus <i>Helicobacter</i> has rapidly expanded over the past decade. The genus now includes at least 24 formally named species as well as numerous other helicobacters awaiting formal naming. This review highlights the expanding role that other helicobacters, although not as well known as <i>H pylori</i>, play in gastrointestinal and systemic disease in humans.
IgE Mediated Food Allergy in Childhood: Novel Concepts in Allergic Immune Response
Authors: S. Donnanno, M. Rosado, G. Trimarco, F. Capolunghi, S. Cascioli, M.C. Artesani, R. Carsetti, G. Cavagni
Journal: Journal of Allergy and Clinical Immunology (2007)
Metformin Disrupts Crosstalk between G Protein–Coupled Receptor and Insulin Receptor Signaling Systems and Inhibits Pancreatic Cancer Growth
Authors: Krisztina Kisfalvi, Guido Eibl, James Sinnett-Smith, Enrique Rozengurt
Journal: Cancer Research (2009)

Abstract Recently, we identified a novel crosstalk between insulin and G protein–coupled receptor (GPCR) signaling pathways in human pancreatic cancer cells. Insulin enhanced GPCR signaling through a rapamycin-sensitive mTOR-dependent pathway. Metformin, the most widely used drug in the treatment of type 2 diabetes, activates AMP kinase (AMPK), which negatively regulates mTOR. Here, we determined whether metformin disrupts the crosstalk between insulin receptor and GPCR signaling in pancreatic cancer cells. Treatment of human pancreatic cancer cells (PANC-1, MIAPaCa-2, and BxPC-3) with insulin (10 ng/mL) for 5 minutes markedly enhanced the increase in intracellular [Ca2+] induced by GPCR agonists (e.g., neurotensin, bradykinin, and angiotensin II). Metformin pretreatment completely abrogated insulin-induced potentiation of Ca2+ signaling but did not interfere with the effect of GPCR agonists alone. Insulin also enhanced GPCR agonist–induced growth, measured by DNA synthesis, and the number of cells cultured in adherent or nonadherent conditions. Low doses of metformin (0.1–0.5 mmol/L) blocked the stimulation of DNA synthesis, and the anchorage-dependent and anchorage-independent growth induced by insulin and GPCR agonists. Treatment with metformin induced striking and sustained increase in the phosphorylation of AMPK at Thr172 and a selective AMPK inhibitor (compound C, at 5 μmol/L) reversed the effects of metformin on [Ca2+]i and DNA synthesis, indicating that metformin acts through AMPK activation. In view of these results, we tested whether metformin inhibits pancreatic cancer growth. Administration of metformin significantly decreased the growth of MIAPaCa-2 and PANC-1 cells xenografted on the flank of nude mice. These results raise the possibility that metformin could be a potential candidate in novel treatment strategies for human pancreatic cancer. [Cancer Res 2009;69(16):6539–45]
<i>Chlamydia pneumoniae</i> Serology, Lung Function Decline, and Treatment for Respiratory Disease
Authors: DAVID PETER STRACHAN, DAVID CARRINGTON, MICHAEL MENDALL, BARBARA KAREN BUTLAND, JOHN WILLIAM GORDON YARNELL, PETER ELWOOD
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

Associations have been reported between Chlamydia pneumoniae seropositivity and both acute and chronic obstructive airway diseases. Plasma specimens collected between 1979 and 1983 from 1,773 men 45 to 59 yr of age in Caerphilly, South Wales, were tested for IgG and IgA antibodies to C. pneumoniae (TW183) by microimmunofluorescence. Subsequent mortality and medication for obstructive airway disease were ascertained at 5-yr follow-up examinations. Spirometry was performed at the first and second examinations and analyzed both cross-sectionally and longitudinally; 642 men (36%) had IgG antibodies at a titer of 1:16 or above, of whom 362 also had detectable IgA antibodies. No statistically significant associations were found between either IgG titer or IgA titer and any of the outcome measures: inhaler therapy at entry; commencement of inhalers during follow-up; death from respiratory causes; baseline FEV1, FVC, and FEV1/FVC ratio; and decline in FEV1 (p > 0.1 throughout). Men with high IgG titers ( ⩾ 1:64) had a slower rate of decline of FEV1 than did seronegative subjects (adjusted mean difference in 5-yr change in FEV1: + 22 ml, 95% confidence interval: − 31 ml to + 76 ml). Men with high IgA titers ( ⩾ 1:16) had a slightly faster rate of decline ( − 12 ml, − 96 ml to + 71 ml). This first prospective assessment suggests that chronic C. pneumoniae infection is not a major risk factor for progressive airflow obstruction. Strachan DP, Carrington D, Mendall M, Butland BK, Yarnell JWG, Elwood P. Chlamydia pneumoniae serology, lung function decline and treatment for respiratory disease.
Tuberculous pericarditis in Birmingham.
Authors: H C Gooi, J M Smith
Journal: Thorax (1978)

Forty-one patients with acute tuberculous pericarditis were studied retrospectively. Anti-tuberculosis chemotherapy alone was effective in thirty. Five patients died, two from unrelated causes, two due to delayed diagnosis, and one after pericardiectomy. Constrictive pericarditis developed in seven patients, six of whom had successful pericardiectomy. Corticosteroids could not be shown to have reduced the risk of developing constriction. When constriction occurred it did so within the first six months of illness in all cases in contrast to a separate series of 15 patients who presented with constrictive pericarditis. These had had no previous history of tuberculosis, and in 10 cases where pericardiectomy was done, no histological evidence of tuberculosis was found. They were European with an average age of 49 years whereas in the group with acute tuberculous pericarditis 33 were Asian and the average age was 36 years.
Lipomatous hypertrophy of the interatrial septum: in vivo diagnosis.
Authors: J M Isner, C S Swan, J P Mikus, B L Carter
Journal: Circulation (1982)

Lipomatous hypertrophy of the interatrial septum (LHIS), a finding associated with obesity and advancing age, consists of the accumulation of adipose tissue, including fetal adipose tissue, in the interatrial septum cephalad and caudad to the fossa ovalis. Previous descriptions of this entity have been limited to autopsy examination. We report a patient in whom the diagnosis of LHIS was established during life by the use of computed tomographic cardiac imaging. As is often the case in patients discovered at autopsy to have LHIS, this patient had atrial fibrillation and, while in normal sinus rhythm, an abnormal P-wave morphology. This patient represents the first patient in whom the diagnosis of LHIS has been established during life. LHIS should be considered in the differential diagnosis of atrial fibrillation and other supraventricular rhythm/conduction disturbances, particularly in obese, elderly patients.
Spontaneous release of interleukin 2 by lung T lymphocytes in active pulmonary sarcoidosis is primarily from the Leu3+DR+ T cell subset.
Authors: C Saltini, J R Spurzem, J J Lee, P Pinkston, R G Crystal
Journal: Journal of Clinical Investigation (1986)

The inflammation within the lower respiratory tract of individuals with pulmonary sarcoidosis is dominated by large numbers of helper T lymphocytes that proliferate and spontaneously release interleukin 2 (IL-2). To identify the lymphocyte subpopulation that releases IL-2 in this disorder, lung lymphocytes recovered by bronchoalveolar lavage were characterized using the monoclonal antibodies Leu4 (T lymphocyte), Leu3 (helper/inducer), Leu2 (suppressor/cytotoxic), and anti-HLA-DR, and separated by panning and flow cytometry. The majority of the IL-2 spontaneously released by T cells in the sarcoid lung was contributed by the Leu3+ cell population (Leu3+65 +/- 23 IL-2 units released/10(6) cells per 24 h; Leu2+ 9 +/- 8, P less than 0.04). Further characterization of the lung Leu3+ T cells in sarcoid demonstrated that 30 +/- 3% were expressing HLA-DR molecules on their surface compared with 6 +/- 1% in normals (P less than 0.01). Importantly, the subpopulation of Leu3+ lung T lymphocytes expressing a high intensity of HLA-DR molecules on their surface was responsible for the majority of the release of IL-2 in the sarcoid lung (Leu3+ high-intensity DR 42 +/- 17 U/10(6) cells per 24 h, Leu3+ low-intensity DR 8 +/- 1 U/10(6) cells per 24 h; P less than 0.01). Thus, the spontaneous release of IL-2 in the lung of sarcoid patients appears to be localized to a subset of Leu3+ high-intensity DR ("activated" lung helper/inducer) T lymphocytes. Because the sarcoid lung is characterized by markedly increased numbers of these cells, it is likely that this compartmentalized T cell population plays a major role in sustaining the exaggerated localized immune processes of this disorder.
Replacement of Connexin40 by Connexin45 in the Mouse
Authors: Sébastien Alcoléa, Thérèse Jarry-Guichard, Jacques de Bakker, Daniel Gonzàlez, Wouter Lamers, Steven Coppen, Luis Barrio, Habo Jongsma, Daniel Gros, Harold van Rijen
Journal: Circulation Research (2003)

Gap junction channels, required for the propagation of cardiac impulse, are intercellular structures composed of connexins (Cx). Cx43, Cx40, and Cx45 are synthesized in the cardiomyocytes, and each of them has a unique cardiac expression pattern. Cx40 knock-in Cx45 mice were generated to explore the ability of Cx45 to replace Cx40, and to assess the functional equivalence of these two Cxs that are both expressed in the conduction system. ECGs revealed that the consequences resulting from the biallelic replacement of Cx40 by Cx45 were an increased duration of the P wave, and a prolonged and fractionated QRS complex. Epicardial mapping indicated that the conduction velocities (CV) in the right atrium and the ventricular myocardium, as well as conduction through the AV node, were unaffected. The significant reduction of the CV in the left atrium would be the most likely cause of the P-wave lengthening. In the right ventricle, a changed and prolonged activation in sinus rhythm was found in homozygous mutant mice, which may explain the prolongation and splitting of the QRS complex. Electrical mapping of the His bundle branches revealed that this was due to slow conduction measured in the right branch. The CV in the left branch was unchanged. Therefore, in the absence of Cx40, the upregulation of Cx45 in the heart results in a normal impulse propagation in the right atrium, the AV node, and the left His bundle branch only.