tbuckley/cabot-search huggingface dataset:
Inhibition of hypoxic pulmonary vasoconstriction in isolated rat resistance arteries by atrial natriuretic peptide
Authors: TK Rogers, JS Thompson, AH Morice
Journal: European Respiratory Journal (1997)

Atrial natriuretic peptide (ANP) is a vasodilator secreted by the heart in response to right atrial stretch. We have hypothesized that ANP may be released to attenuate pulmonary hypertension due to hypoxia. We have examined whether ANP inhibits hypoxic pulmonary vasoconstriction (HPV) in isolated pulmonary resistance vessels (PRV) from chronically hypoxic (CH) rats, compared to air-breathing, control (C) rats. After at least 17 days of chronic hypoxia, vessels (n = 29) were dissected from CH and C littermates and mounted in an automated myograph. The inhibitory effect of ANP on the rapid first contractile phase of HPV, and the relaxant effect of ANP on vessels tonically contracted in the second phase of HPV, were studied. ANP caused concentration-dependent inhibition of HPV in both C and CH vessels (p &lt; 0.001), whilst vehicle had no effect (mean maximum inhibition was 88 and 101%, respectively, at 17 nM ANP). ANP also caused significant concentration-dependent relaxation of the second contractile phase of HPV, which was similar in C and CH vessels (mean maximum relaxation of 89 and 94%, respectively; median effective concentrations were 2.4 and 2.0 nM, respectively). We conclude that atrial natriuretic peptide is a potent antagonist of both contractile phases of hypoxic pulmonary vasoconstriction in isolated rat pulmonary resistance vessels at concentrations similar to those observed in hypoxic pulmonary hypertension in life. There was no difference between vessels from chronically hypoxic and control animals.
Response to Letter Regarding Article “Effectiveness of Bystander-Initiated Cardiac-Only Resuscitation for Patients With Out-of-Hospital Cardiac Arrest”
Authors: Taku Iwami, Takashi Kawamura, Atsushi Hiraide, Robert A. Berg, Yasuyuki Hayashi, Tatsuya Nishiuchi, Kentaro Kajino, Hisashi Sugimoto, Naohiro Yonemoto, Hidekazu Yukioka, Hiroyuki Kakuchi, Kazuhiro Sase, Hiroyuki Yokoyama, Hiroshi Nonogi
Journal: Circulation (2008)
Parent education and biologic factors influence on cognition in sickle cell anemia
Authors: Allison A. King, John J. Strouse, Mark J. Rodeghier, Bruce E. Compas, James F. Casella, Robert C. McKinstry, Michael J. Noetzel, Charles T. Quinn, Rebecca Ichord, Michael M. Dowling, J. Philip Miller, Michael R. DeBaun
Journal: American Journal of Hematology (2013)

Children with sickle cell anemia have a high prevalence of silent cerebral infarcts (SCIs) that are associated with decreased full-scale intelligence quotient (FSIQ). While the educational attainment of parents is a known strong predictor of the cognitive development of children in general, the role of parental education in sickle cell anemia along with other factors that adversely affect cognitive function (anemia, cerebral infarcts) is not known. We tested the hypothesis that both the presence of SCI and parental education would impact FSIQ in children with sickle cell anemia. A multicenter, cross-sectional study was conducted in 19 US sites of the Silent Infarct Transfusion Trial among children with sickle cell anemia, age 5-15 years. All were screened for SCIs. Participants with and without SCI were administered the Wechsler Abbreviated Scale of Intelligence. A total of 150 participants (107 with and 43 without SCIs) were included in the analysis. In a multivariable linear regression model for FSIQ, the absence of college education for the head of household was associated with a decrease of 6.2 points (P = 0.005); presence of SCI with a 5.2 point decrease (P = 0.017); each $1000 of family income per capita with a 0.33 point increase (P = 0.023); each increase of 1 year in age with a 0.96 point decrease (P = 0.023); and each 1% (absolute) decrease in hemoglobin oxygen saturation with 0.75 point decrease (P = 0.030). In conclusion, FSIQ in children with sickle cell anemia is best accounted for by a multivariate model that includes both biologic and socioenvironmental factors.
Cancer incidence among patients with a hospital diagnosis of pruritus: a nationwide Danish cohort study
Authors: S.A. Johannesdottir, D.K. Farkas, G.R. Vinding, L. Pedersen, A. Lamberg, H.T. Sørensen, A.B. Olesen
Journal: British Journal of Dermatology (2014)

Pruritus is a frequent complaint in patients with cancer. However, no large study has examined pruritus as a marker of undiagnosed cancer. To examine the association between inpatient, outpatient and emergency hospital diagnoses of pruritus and subsequent cancer diagnoses. In this nationwide Danish cohort study, we used medical databases to identify all patients (n =12 813) with a diagnosis of pruritus during the period 1978–2011 and followed them until a first‐time cancer diagnosis, emigration, death or 31 December 2011. We computed standardized incidence ratios (SIRs) for cancer as the observed to expected number of cancers based on national cancer incidence rates. We calculated the 1‐year absolute risk of cancer, treating death as a competing risk. The overall SIR of cancer was 1·13 [95% confidence interval (CI) 1·07–1·20]: 1·22 (95% CI 1·13–1·33) among men and 1·05 (95% CI 0·97–1·14) among women. The SIR was 1·20 (95% CI 1·08–1·33) among patients with a previous diagnosis of dermatological disease and 1·10 (95% CI 1·02–1·18) among patients without such a diagnosis. Both haematological and various solid cancers were observed at increased rates. Overall, the highest SIRs were observed during the first 3 months of follow‐up, declining rapidly thereafter. The 1‐year absolute risk of a cancer diagnosis was 1·63% and 155 patients with pruritus would have needed to be examined to detect one excess cancer. Pruritus may be a marker of occult cancer. Further studies are needed to assess the prognostic benefit of screening for cancer in patients with pruritus.
Impact of Obesity on Biochemical Control After Radical Prostatectomy for Clinically Localized Prostate Cancer: A Report by the Shared Equal Access Regional Cancer Hospital Database Study Group
Authors: Stephen J. Freedland, William J. Aronson, Christopher J. Kane, Joseph C. Presti, Christopher L. Amling, David Elashoff, Martha K. Terris
Journal: Journal of Clinical Oncology (2003)

Given the limited information regarding the impact of obesity on treatment outcomes for prostate cancer, we sought to examine the relationship between body mass index (BMI) and cancer control after radical prostatectomy (RP).
Elucidation of Prinzmetal's variant form of preexcitation.
Authors: A Munsif, B J Scherlag, R Lazzara
Journal: Circulation (1994)

In 1952, Prinzmetal induced preexcitation in the normal dog heart using subthreshold stimulation (SS) delivered to the right ventricle.In 12 dogs we recorded ECG leads II, aVR, His (Hb) and proximal right bundle potentials with electrode catheters at the aortic root and a special electrode that was inserted through the right ventricular (RV) free wall. In 12 others, SS was delivered to the Hb area by a catheter placed under the septal leaflet of the tricuspid valve. During SS, the HV interval shortened from 35 +/- 4 milliseconds (mean +/- SD) to 19 +/- 7 milliseconds (P = .0001), but AH intervals were unchanged. The ECG showed delta waves with aberrant QRS complexes. Endocardial electrograms showed that the origin of activation in the preexcitation beats was localized to the muscle adjacent to the Hb or proximal right bundle. When vagal stimulation induced sudden AV block, no ventricular excitation was seen, confirming the subthreshold nature of the applied stimulation. By adjusting the levels of SS, latent forms of preexcitation could be induced, eg, early local septal muscle activation but no change in the ECG leads. Premature ventricular stimuli delivered to the RV apex or outflow tract could cause manifest preexcitation in the ECG leads or inhibit expression of latent preexcitation in endocardial recordings.SS delivered to the RV apex or Hb area causes ventricular preexcitation, as shown previously by Prinzmetal et al. SS delivered at the insertion sites of an accessory pathway may facilitate localization of such abnormal connections, particularly when preexcitation is concealed.
C-Reactive Protein, Diabetes, and Attendance at Religious Services
Authors: Dana E. King, Arch G. Mainous, William S. Pearson
Journal: Diabetes Care (2002)

OBJECTIVE—Previous studies have shown an association between attendance at religious services and health, particularly cardiovascular morbidity and mortality. People with diabetes have higher risk of cardiovascular mortality and higher C-reactive protein (CRP) levels than people without diabetes. The purpose of this study was to explore the relationship between religious attendance and CRP in people with diabetes. RESEARCH DESIGN AND METHODS—This study used cross-sectional survey and examination of a nationally representative sample of noninstitutionalized U.S. adults aged ≥40 years, derived from the National Health and Nutrition Examination Survey III 1988–1994 (n = 10,059). There were 556 people with diabetes. The primary outcome measure was the presence of elevated CRP. RESULTS—There were no differences between people with diabetes compared with people without diabetes in the percentage of those who attended religious services (62.29 vs. 62.0%, P = 0.36). Religious service nonattenders with diabetes were more likely than attenders to have an elevated CRP (odds ratio [OR] 2.17 [95% CI 1.15–4.09]). In people without diabetes, the association between attendance and CRP was not significant (P &amp;gt; 0.05). Among people with diabetes, after adjusting for demographic variables, health status, smoking, social support, mobility, and BMI, the association between religious attendance and CRP remained significant for respondents with diabetes (1.90 [1.03–3.51]). CONCLUSIONS—These findings revealed that people with diabetes who have not attended religious services in the previous year are more likely to have elevated levels of CRP. Further research should be conducted to evaluate this association to improve our understanding of the psychological and religious factors that influence diabetes.
Interleukin-2 treatment potentiates induction of oral tolerance in a murine model of autoimmunity.
Authors: L V Rizzo, N E Miller-Rivero, C C Chan, B Wiggert, R B Nussenblatt, R R Caspi
Journal: Journal of Clinical Investigation (1994)

The present study addresses the feasibility of potentiating oral tolerance by immunomanipulation, using the murine model of experimental autoimmune uveoretinitis (EAU) induced by immunization with the retinal antigen interphotoreceptor retinoid binding protein (IRBP). Three feedings of 0.2 mg IRBP every other day before immunization did not protect against EAU, whereas a similar regimen of five doses was protective. However, supplementing the nonprotective 3x regimen with as little as one injection of 1,000 U of human recombinant interleukin-2 (IL-2) resulted in disease suppression that was equal to that of the protective 5x regimen. The protective effect was maintained across a range of IL-2 doses and times of administration; none of the IL-2 regimens tested resulted in disease enhancement. Peyer's Patch cells of 3x-fed and IL-2-treated mice showed greatly increased production of TGF-beta, IL-4, and IL-10 compared with animals given the nonprotective 3x regimen and to animals given the protective 5x regimen. We propose that IL-2 treatment enhances protection from EAU at least in part by stimulating production of antiinflammatory cytokines by regulatory cells in Payer's Patches. Moreover, the observed lymphokine production patterns suggest that whereas protection induced by the 3x + IL-2 regimen is likely to involve antiinflammatory cytokines, protection induced by the 5x regimen might involve anergy or deletion of the uveitogenic T cells. These results could have practical implications for use of IL-2 as a safe and effective way of potentiating oral tolerance.
Oxidative metabolism of halothane in the production of altered hepatocyte membrane antigens in acute halothane-induced hepatic necrosis
Authors: J Neuberger, G. Mieli-Vergani, J M Tredger, M Davis, R. Williams
Journal: Gut (1981)

Previous investigations have shown that patients with fulminant hepatic failure after halothane anaesthesia have a circulating antibody which reacts with an antigen present on the surface of halothane-altered hepatocytes. In the present study, it has been shown that the expression of the antigen is associated with the oxidative metabolism of halothane, in contrast with results of other groups which have shown that the reductive route is involved in the direct hepatotoxic reaction attributed to halothane.
Correlation between response to neoadjuvant chemotherapy and survival in locally advanced breast cancer patients
Authors: A. Romero, J.A. García-Sáenz, M. Fuentes-Ferrer, J.A. López Garcia-Asenjo, V. Furió, J.M. Román, A. Moreno, M. de la Hoya, E. Díaz-Rubio, M. Martín, T. Caldés
Journal: Annals of Oncology (2012)
Changes in PESI scores predict mortality in intermediate-risk patients with acute pulmonary embolism
Authors: Lisa Moores, Celia Zamarro, Vicente Gómez, Drahomir Aujesky, Leticia García, Rosa Nieto, Roger Yusen, David Jiménez
Journal: European Respiratory Journal (2012)

Although the Pulmonary Embolism Severity Index (PESI) accurately identifies 35% of patients with acute pulmonary embolism (PE) as being low risk, some patients deemed high risk by the PESI on admission might be treated safely in the outpatient environment. This retrospective cohort study included a total of 304 consecutive patients with acute PE, classified at the time of hospital admission into PESI class III. The PESI was recalculated 48 h after admission (PESI 48 ) and each patient reclassified into the corresponding risk category. The primary outcome of the study was all-cause mortality between day 2 and day 30 after PE diagnosis. 26 (8.5%) patients (95% CI 5.4–11.7%) died between day 2 and day 30 after PE diagnosis. Investigators reclassified 83 (27.3%) patients (95% CI 22.3–32.3%) as low risk (classes I and II) at 48 h. 30-day mortality in these patients was 1.2% (95% CI 0–3.5%) as opposed to 11.3% (95% CI 7.1–15.5%) in those who remained high risk. The net improvement in reclassification was estimated at 54% (p&lt;0.001). In a cohort of intermediate-risk patients with acute PE, calculation of the PESI 48 allows identification of those patients at very low risk of dying during the first month of follow-up.
Efficient and robust RNA-seq process for cultured bacteria and complex community transcriptomes
Authors: Georgia Giannoukos, Dawn M Ciulla, Katherine Huang, Brian J Haas, Jacques Izard, Joshua Z Levin, Jonathan Livny, Ashlee M Earl, Dirk Gevers, Doyle V Ward, Chad Nusbaum, Bruce W Birren, Andreas Gnirke
Journal: Genome biology (2012)

Abstract We have developed a process for transcriptome analysis of bacterial communities that accommodates both intact and fragmented starting RNA and combines efficient rRNA removal with strand-specific RNA-seq. We applied this approach to an RNA mixture derived from three diverse cultured bacterial species and to RNA isolated from clinical stool samples. The resulting expression profiles were highly reproducible, enriched up to 40-fold for non-rRNA transcripts, and correlated well with profiles representing undepleted total RNA.
Acute inflammatory response secondary to intrapleural administration of two types of talc
Authors: V. F. Rossi, F. S. Vargas, E. Marchi, M. M. P. Acencio, E. H. Genofre, V. L. Capelozzi, L. Antonangelo
Journal: European Respiratory Journal (2009)

Intrapleural instillation of talc has been used in the treatment of recurrent pleural effusions but can, in rare instances, result in respiratory failure. Side-effects seem to be related to composition, size and inflammatory power of talc particles. The aim of this study was to evaluate the inflammatory response to intrapleural injection of talc containing small particles (ST) or talc containing particles of mixed size (MT). 100 rabbits received intrapleural talc, 50 with ST (median 6.41 μm) and 50 with MT (median 21.15 μm); the control group was composed of 35 rabbits. Cells, lactate dehydrogenase, C-reactive protein (CRP), interleukin (IL)-8 and vascular endothelial growth factor were evaluated in serum and bronchoalveolar lavage at 6, 24, 48, 72 and 96 h. Lung histology and the presence of talc were also analysed. Statistics were performed using ANOVA and an unpaired t-test. Most of the parameters showed greater levels in the animals injected with talc than in the controls, suggesting a systemic and pulmonary response. Higher serum levels of CRP and IL-8 were observed in the animals injected with ST. Talc particles were observed in both lungs with no differences between groups. Lung cell infiltrate was more evident in the ST group. In conclusion, talc with larger particles should be the preferred choice in clinical practice in order to induce safer pleurodesis.
Regulation of Mitochondrial Dynamics by Dynamin-Related Protein-1 in Acute Cardiorenal Syndrome
Authors: Maki Sumida, Kent Doi, Emi Ogasawara, Tetsushi Yamashita, Yoshifumi Hamasaki, Taro Kariya, Eiki Takimoto, Naoki Yahagi, Masaomi Nangaku, Eisei Noiri
Journal: Journal of the American Society of Nephrology (2015)

Experimental evidence has clarified distant organ dysfunctions induced by AKI. Crosstalk between the kidney and heart, which has been recognized recently as cardiorenal syndrome, appears to have an important role in clinical settings, but the mechanisms by which AKI causes cardiac injury remain poorly understood. Both the kidney and heart are highly energy-demanding organs that are rich in mitochondria. Therefore, we investigated the role of mitochondrial dynamics in kidney–heart organ crosstalk. Renal ischemia reperfusion (IR) injury was induced by bilateral renal artery clamping for 30 min in 8-week-old male C57BL/6 mice. Electron microscopy showed a significant increase of mitochondrial fragmentation in the heart at 24 h. Cardiomyocyte apoptosis and cardiac dysfunction, evaluated by echocardiography, were observed at 72 h. Among the mitochondrial dynamics regulating molecules, dynamin-related protein 1 (Drp1), which regulates fission, and mitofusin 1, mitofusin 2, and optic atrophy 1, which regulate fusion, only Drp1 was increased in the mitochondrial fraction of the heart. A Drp1 inhibitor, mdivi-1, administered before IR decreased mitochondrial fragmentation and cardiomyocyte apoptosis significantly and improved cardiac dysfunction induced by renal IR. This study showed that renal IR injury induced fragmentation of mitochondria in a fission-dominant manner with Drp1 activation and subsequent cardiomyocyte apoptosis in the heart. Furthermore, cardiac dysfunction induced by renal IR was improved by Drp1 inhibition. These data suggest that mitochondrial fragmentation by fission machinery may be a new therapeutic target in cardiac dysfunction induced by AKI.
Gastric Cancer Surgery: Morbidity and Mortality Results From a Prospective Randomized Controlled Trial Comparing D2 and Extended Para-Aortic Lymphadenectomy—Japan Clinical Oncology Group Study 9501
Authors: Takeshi Sano, Mitsuru Sasako, Seiichiro Yamamoto, Atsushi Nashimoto, Akira Kurita, Masahiro Hiratsuka, Toshimasa Tsujinaka, Taira Kinoshita, Kuniyoshi Arai, Yoshitaka Yamamura, Kunio Okajima
Journal: Journal of Clinical Oncology (2004)

Radical gastrectomy with regional lymphadenectomy is the only curative treatment option for gastric cancer. The extent of lymphadenectomy, however, is controversial. The two European randomized trials only reported an increase in operative morbidity and mortality, but failed to show survival benefit, in the D2 lymphadenectomy group. We conducted a randomized controlled trial to compare the Japanese standard D2 and D2 + para-aortic nodal dissection.Only experienced surgeons in both procedures from 24 Japanese institutions participated in the study. Patients with potentially curable gastric adenocarcinoma (T2-subserosa, T3, or T4) who were surgically fit were intraoperatively randomized. Postoperative morbidity and hospital mortality were recorded prospectively in a fixed format and were compared between the two groups in this study.A total of 523 patients were randomized between July 1995 and April 2001. Postoperative complications were reported in 24.5% of all patients. Although the morbidity for the extended surgery group (28.1%) was slightly higher than the standard group (20.9%), there was no difference in the incidence of four major complications (anastomotic leak, pancreatic fistula, abdominal abscess, pneumonia) between the two groups. Hospital mortality was reported at 0.80%: one patient in each group died of operative complications, while one from each group died of rapid progressive cancer while inpatient.Specialized surgeons could safely perform gastrectomy with D2 lymphadenectomy in patients with low operative risks. Para-aortic lymphadenectomy could be added without increasing major surgical complications in this setting.
Agonistic Anti-β <sub>1</sub> -Adrenergic Receptor Autoantibodies From Cardiomyopathy Patients Reduce the β <sub>1</sub> -Adrenergic Receptor Expression in Neonatal Rat Cardiomyocytes
Authors: Svenia Podlowski, Hans Peter Luther, Rosemarie Morwinski, Johannes Müller, Gerd Wallukat
Journal: Circulation (1998)

Background —Autoantibodies directed against the β 1 -adrenergic receptor have been described in patients with dilated cardiomyopathy. These autoantibodies exert an agonistic, chronotropic effect on spontaneously beating cultured neonatal rat cardiomyocytes. We studied the effect of such antibodies on β 1 -adrenergic receptor expression. Methods and Results —Cardiomyocytes were incubated with either the β-adrenergic agonist isoproterenol or autoantibodies for 72 hours. β-Adrenergic receptor expression was studied on the mRNA level with semiquantitative reverse transcription–polymerase chain reaction and on the protein level with immunoblotting. Isoproterenol downregulated both mRNA and β 1 - and β 2 -adrenergic receptor protein subtypes, whereas the anti–β 1 -adrenergic receptor autoantibodies decreased only the β 1 -adrenergic receptor mRNA and protein. Long-term incubation of cultured cardiomyocytes with isoproterenol or the anti–β 1 -adrenergic receptor autoantibodies reduced the acute stimulatory effect of isoproterenol on the myocytes. These effects were prevented by incubating the cells with isoproterenol in the presence of propranolol or with anti–β 1 -adrenergic receptor autoantibodies in the presence of bisoprolol. Bisoprolol also abolished the reduction of the β 1 -adrenergic receptor expression caused by longer-term incubation with isoproterenol and the autoantibodies. Conclusions —We conclude that after longer-term treatment with the anti–β 1 -adrenergic receptor autoantibodies, the rat cardiomyocytes showed a β-adrenergic receptor expression similar to that observed in failing hearts from patients with dilated cardiomyopathy.