tbuckley/cabot-search huggingface dataset:
The Anatomy of a Disparity in Infant Mortality
Authors: Paul H. Wise
Journal: Annual Review of Public Health (2003)

▪ Abstract This article suggests that while disparities in infant mortality have been longstanding, the mechanisms of disparity creation are undergoing intense change. This dynamic character is explored by first developing an analytic model that examines the interaction between social factors and the public health and clinical capacity to intervene. Disparities in infant mortality are then broken down into their component parts and linked to specific arenas of intervention. Disparities in postneonatal mortality are being shaped by differential access to interventions designed to prevent infant death from congenital anomalies and the Sudden Infant Death Syndrome. Disparities in neonatal mortality are primarily determined by factors that influence the birthrate of extremely premature infants and access to specialized obstetrical and pediatric care. This analysis suggests that the epidemiology and social meaning of disparities in infant mortality are intensely dynamic and increasingly reflect the interaction between social forces and technical innovation.
Functional and metabolic effects of ribose in combination with prazosin, verapamil and metoprolol in rats in vivo
Authors: S. LORTET, H.-G. ZIMMER
Journal: Cardiovascular Research (1989)

Journal Article Functional and metabolic effects of ribose in combination with prazosin, verapamil and metoprolol in rats in vivo Get access SYLVIANE LORTET, SYLVIANE LORTET From the Department of Physiology, University of Munich, Munich, Federal Republic of Germany Address for correspondence and reprints: Dr H-G Zimmer, Department of Physiology, University of Munich, Pettenkoferstrasse 12, D-8000 München 2, Federal Republic of Germany. Search for other works by this author on: Oxford Academic PubMed Google Scholar HEINZ-GERD ZIMMER HEINZ-GERD ZIMMER From the Department of Physiology, University of Munich, Munich, Federal Republic of Germany Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 23, Issue 8, August 1989, Pages 702–708, https://doi.org/10.1093/cvr/23.8.702 Published: 01 August 1989 Article history Accepted: 17 March 1989 Published: 01 August 1989
Directly acting drugs prostacyclin or nitroglycerine and endothelin receptor blocker bosentan improve cell engraftment in rodent liver
Authors: Ralf Bahde, Sorabh Kapoor, Sriram Bandi, Kuldeep K. Bhargava, Christopher J. Palestro, Sanjeev Gupta
Journal: Hepatology (2012)

Abstract To optimize strategies for liver-directed cell therapy, prevention of initial transplanted cell losses is particularly important for subsequent liver repopulation. After cell transplantation in hepatic sinusoids, perturbations in hepatic microcirculation along with changes in various liver cell types are among the earliest changes. Therefore, for advancing further concepts in cell engraftment we studied vascular and related events in the liver after transplanting syngeneic hepatocytes into dipeptidyl peptidase IV-deficient rats. We treated rats with vascular drugs to define whether deleterious cell transplantation-induced events could be controlled followed by improvements in transplanted cell engraftment and proliferation. We found cell transplantation altered liver gene expression related to vessel tone, inflammation, cell adhesion, thrombosis, or tissue damage/remodeling. This was due to hepatic ischemia, endothelial injury, and activation of neutrophils, Kupffer cells, and hepatic stellate cells. Treatment of rats before cell transplantation with the angiotensin converting enzyme blocker, lisinopril, or angiotensin II receptor blocker, losartan, did not improve cell engraftment. By contrast, direct-acting nitroglycerine or prostacyclin improved cell engraftment and also kinetics of liver repopulation. These drugs lowered hepatic ischemia and inflammation, whereas pretreatment of rats with the dual endothelin-1 receptor blocker, bosentan, improved cell engraftment independently of hepatic ischemia or inflammation, without improving liver repopulation. However, incubation of hepatocytes with bosentan protected cells from cytokine toxicity in vitro and produced superior cell engraftment and proliferation in vivo . Conclusion : Cell transplantation-induced changes in hepatic microcirculation contributed to transplanted cell clearances from liver. Vascular drugs, such as nitroglycerine, prostacyclin, and bosentan, offer opportunities for improving cell therapy results through superior cell engraftment and liver repopulation. Ongoing clinical use of these drugs will permit rapid translation of the findings in people. (Hepatology 2013)
A Randomized Trial of Colchicine for Acute Pericarditis
Authors: Massimo Imazio, Antonio Brucato, Roberto Cemin, Stefania Ferrua, Stefano Maggiolini, Federico Beqaraj, Daniela Demarie, Davide Forno, Silvia Ferro, Silvia Maestroni, Riccardo Belli, Rita Trinchero, David H. Spodick, Yehuda Adler
Journal: New England Journal of Medicine (2013)

Colchicine is effective for the treatment of recurrent pericarditis. However, conclusive data are lacking regarding the use of colchicine during a first attack of acute pericarditis and in the prevention of recurrent symptoms.In a multicenter, double-blind trial, eligible adults with acute pericarditis were randomly assigned to receive either colchicine (at a dose of 0.5 mg twice daily for 3 months for patients weighing >70 kg or 0.5 mg once daily for patients weighing ≤70 kg) or placebo in addition to conventional antiinflammatory therapy with aspirin or ibuprofen. The primary study outcome was incessant or recurrent pericarditis.A total of 240 patients were enrolled, and 120 were randomly assigned to each of the two study groups. The primary outcome occurred in 20 patients (16.7%) in the colchicine group and 45 patients (37.5%) in the placebo group (relative risk reduction in the colchicine group, 0.56; 95% confidence interval, 0.30 to 0.72; number needed to treat, 4; P<0.001). Colchicine reduced the rate of symptom persistence at 72 hours (19.2% vs. 40.0%, P=0.001), the number of recurrences per patient (0.21 vs. 0.52, P=0.001), and the hospitalization rate (5.0% vs. 14.2%, P=0.02). Colchicine also improved the remission rate at 1 week (85.0% vs. 58.3%, P<0.001). Overall adverse effects and rates of study-drug discontinuation were similar in the two study groups. No serious adverse events were observed.In patients with acute pericarditis, colchicine, when added to conventional antiinflammatory therapy, significantly reduced the rate of incessant or recurrent pericarditis. (Funded by former Azienda Sanitaria Locale 3 of Turin [now Azienda Sanitaria Locale 2] and Acarpia; ICAP ClinicalTrials.gov number, NCT00128453.).
Interplay among BRAF, p16, p53, and MIB1 in pediatric low-grade gliomas
Authors: C. Horbinski, M. N. Nikiforova, J. M. Hagenkord, R. L. Hamilton, I. F. Pollack
Journal: Neuro-Oncology (2012)

BRAF rearrangements and BRAF V600E point mutations are recurring events in pediatric low-grade gliomas. However, their clinical significance, including possible interactions between these markers and other glioma biomarkers, is unclear. In this study a retrospective cohort of 198 pediatric low-grade gliomas (including 40 treated with adjuvant therapy) was analyzed for BRAF rearrangements, BRAF V600E, p16/CDKN2A deletion, p53 expression, and MIB1 proliferation index. In tumors with BRAF rearrangement, homozygous p16 deletion correlated with shorter progression-free survival (P = .04). A high MIB1 proliferation index trended toward worse response to adjuvant radiotherapy compared to BRAF-rearranged, p16-intact tumors (P = .08). On multivariate analysis, the 2 most consistently powerful independent adverse prognostic markers were midline location (P = .0001) and p16 deletion (P = .03). Tumors with BRAF V600E had a strong trend toward an increased risk for progression (hazard ratio = 2.48, P = .07), whereas those with BRAF rearrangement had a milder trend toward reduced risk (hazard ratio = .54, P = .15). These data suggest that p16 deletion adversely impacts the outcomes of BRAF-driven gliomas, that high proliferation index may be a better marker of progression risk than BRAF, that BRAF rearrangement and BRAF V600E might not necessarily produce comparable outcomes, and that none of these markers is stronger than tumor location in determining prognosis in pediatric low-grade gliomas.
Predictive Model for Survival in Patients With Advanced Cancer
Authors: Edward Chow, Mohamed Abdolell, Tony Panzarella, Kristin Harris, Andrea Bezjak, Padraig Warde, Ian Tannock
Journal: Journal of Clinical Oncology (2008)

To derive and validate a simple predictive model for survival of patients with metastatic cancer attending a palliative radiotherapy clinic.We described previously a model predicting survival of patients referred for palliative radiotherapy using six prognostic factors: primary cancer site, site of metastases, Karnofsky performance score (KPS), and the fatigue, appetite, and shortness of breath subscales from the Edmonton Symptom Assessment Scale. Here we simplified the model to include only three factors: primary cancer site, site of metastases, and KPS. Each factor was assigned a value proportional to its prognostic weight, and the weighted scores for each patient were summed to obtain a survival prediction score (SPS). Patients were also grouped according to their number of risk factors (NRF): nonbreast cancer, metastases other than bone, and KPS < or = 60. The three- and six- variable models were evaluated for their ability to predict survival in patients referred during a different time period and of those referred to a different cancer center.A training set of 395 patients, a temporal validation set of 445 patients, and an external validation set of 467 patients were used. The ability of the three- and six-variable models to separate patients into three prognostic groups and to predict their survival was similar using both SPS and NRF methods in the training, temporal, and external validation data sets. There was no statistically significant difference in the performance of the models.The three-variable NRF model is preferred because of its relative simplicity.
Cytokine-stimulated human vascular smooth muscle cells synthesize a complement of enzymes required for extracellular matrix digestion.
Authors: Z S Galis, M Muszynski, G K Sukhova, E Simon-Morrissey, E N Unemori, M W Lark, E Amento, P Libby
Journal: Circulation Research (1994)

Vascular matrix remodeling occurs during development, growth, and several pathological conditions that affect blood vessels. We investigated the capacity of human smooth muscle cells (SMCs) to express matrix metalloproteinases (MMPs), enzymes that selectively digest components of the extracellular matrix (ECM), in the basal state or after stimulation with certain cytokines implicated in vascular homeostasis and pathology. Enzymatic activity associated with various proteins secreted in the culture media was detected by gelatin or casein sodium dodecyl sulfate-polyacrylamide gel electrophoresis zymography. Proteins were identified by immunoprecipitation and mRNA by Northern blotting. SMCs constitutively secreted a 72-kD gelatinase and the tissue inhibitors of MMPs (TIMPs) types 1 and 2. SMCs stimulated with interleukin-1 or tumor necrosis factor-alpha synthesized de novo 92-kD gelatinase, interstitial collagenase, and stromelysin. Several lines of evidence suggest that when stimulated by cytokines, SMCs produce activated forms of MMPs. Together, the constitutive and the cytokine-induced enzymes can digest all the major components of the vascular ECM. Moreover, since these mediators augment the production of MMPs without appreciably affecting the synthesis of TIMPs, locally secreted cytokines may tip the regional balance of MMP activity in favor of vascular matrix degradation.
Unhealthy behaviours and disability in older adults: Three-City Dijon cohort study
Authors: F. Artaud, A. Dugravot, S. Sabia, A. Singh-Manoux, C. Tzourio, A. Elbaz
Journal: BMJ (2013)

<b>Objectives</b> To examine the individual and combined associations of unhealthy behaviours (low/intermediate physical activity, consuming fruit and vegetables less than once a day, current smoking/short term ex-smoking, never/former/heavy alcohol drinking), assessed at start of follow-up, with hazard of disability among older French adults and to assess the role of potential mediators, assessed repeatedly, of these associations. <b>Design</b> Population based cohort study. <b>Setting</b> Dijon centre of Three-City study. <b>Participants</b> 3982 (2410 (60.5%) women) French community dwellers aged 65 or over included during 1999-2001; participants were disability-free at baseline when health behaviours were assessed. <b>Main outcome measure</b> Hierarchical indicator of disability (no, light, moderate, severe) combining data from three disability scales (mobility, instrumental activities of daily living, basic activities of daily living) assessed five times between 2001 and 2012. <b>Results</b> During the 12 year follow-up, 1236 participants (861 (69.7%) women) developed moderate or severe disability. Interval censored survival analyses (adjusted for age, sex, marital status, and education) showed low/intermediate physical activity (hazard ratio 1.72, 95% confidence interval 1.48 to 2.00), consuming fruit and vegetables less than once a day (1.24, 1.10 to 1.41), and current smoking/short term ex-smoking (1.26, 1.05 to 1.50) to be independently associated with an increased hazard of disability, whereas no robust association with alcohol consumption was found. The hazard of disability increased progressively with the number of unhealthy behaviours independently associated with disability (P&lt;0.001); participants with three unhealthy behaviours had a 2.53 (1.86 to 3.43)-fold increased hazard of disability compared with those with none. Reverse causation bias was verified by excluding participants who developed disability in the first four years of follow-up; these analyses on 890 disability events yielded results similar to those in the main analysis. 30.5% of the association between the unhealthy behaviours score and disability was explained by body mass index, cognitive function, depressive symptoms, trauma, chronic conditions, and cardiovascular disease and its risk factors; the main contributors were chronic conditions and, to a lesser extent, depressive symptoms, trauma, and body mass index. <b>Conclusions</b> An unhealthy lifestyle is associated with greater hazard of incident disability, and the hazard increases progressively with the number of unhealthy behaviours. Chronic conditions, depressive symptoms, trauma, and body mass index partially explained this association.
Controlled Study of Biofeedback-Assisted Relaxation in Type I Diabetes
Authors: Angele McGrady, Barbara K Bailey, Marion P Good
Journal: Diabetes Care (1991)

Objective The effect of biofeedback-assisted relaxation was tested in a randomized trial in 18 adults with insulin-dependent (type I) diabetes. Research Design And Methods Pretreatment and posttreatment blood glucose values and insulin dosages in the group trained for 10 wk in biofeedback-assisted relaxation were compared with those in the untrained group. Results Significantly lower average blood glucose levels, percentage of fasting blood glucose levels at target, and percentage of glucose values &amp;lt; 11.2 mM were observed in the trained group at posttest compared with the untrained group. Conclusions These differences could not be explained by increases in insulin. It is suggested that stress management be considered as an adjunct to the medical management of people with type I diabetes.
Collagen-induced arthritis in mice. Localization of an arthritogenic determinant to a fragment of the type II collagen molecule.
Authors: K Terato, K A Hasty, M A Cremer, J M Stuart, A S Townes, A H Kang
Journal: The Journal of Experimental Medicine (1985)

Purified chick type II collagen was cleaved with cyanogen bromide (CB), and the resulting peptides isolated and renatured. Sera from arthritic DBA/1 mice, immunized with chick type II collagen, were tested for reactivity with each peptide. The sera preferentially recognized peptides 11, 10, and 8, in that order. Some reactivity was also detected to peptides 9, 7, and 12. Because arthritis depends upon binding of antibody to autologous type II collagen in the joint, sera were also tested for reactivity with mouse type II collagen. There was a strong positive correlation between reactivity with peptide 11 and reactivity with mouse collagen, but no correlation was found with any of the other peptides. Peptides 11, 10, and 8 were also used for immunization. Antibodies were detected in response to each of these peptides, but arthritis developed only in mice immunized with peptide 11. We conclude that a major immunogenic and arthritogenic epitope on type II collagen resides in the region of the molecule represented by CB peptide 11.
Interleukin‐13 and ‐4 expression in the central airways of smokers with chronic bronchitis
Authors: D. Miotto, M.P. Ruggieri, P. Boschetto, G. Cavallesco, A. Papi, I. Bononi, C. Piola, B. Murer, L.M. Fabbri, C.E. Mapp
Journal: European Respiratory Journal (2003)

The aim of this study was to determine whether the T‐helper 2‐type cytokines interleukin (IL)‐13 and ‐4 are involved in mucus hypersecretion, the hallmark of chronic bronchitis (CB). Surgical specimens were examined from 33 subjects undergoing lung resection for localised peripheral malignant pulmonary lesions: 21 smokers with symptoms of CB, 10 asymptomatic smokers (AS) and two nonsmokers with normal lung function. The number of IL‐4 and ‐13 positive (+) cells in the central airways was quantified. To better assess the cytokine profile, a count was also made of IL‐5+ and interferon (IFN)‐γ+ cells. Compared to AS, the CB group had an increased number of IL‐13+ and ‐4+ cells in the bronchial submucosa, while the number of IL‐5+ and IFN‐γ+ cells were similar in all the groups. No significant associations were found between the number of cells expressing IL‐13 or ‐4 and the number of inflammatory cells. Double labelling showed that 13.2 and 12.9% of IL‐13+ cells were also CD8+ and CD4+, whereas 7.5 and 5% of IL‐4+ cells were CD8+ and CD4+, respectively. In conclusion, T‐helper‐2 and ‐1 protein expression is present in the central airways of smokers and interleukin‐4 and ‐13 could contribute to mucus hypersecretion in chronic bronchitis.
Smooth Muscle Cell Plasticity
Authors: Anh T. Nguyen, Delphine Gomez, Robert D. Bell, Julie H. Campbell, Alexander W. Clowes, Giulio Gabbiani, Cecilia M. Giachelli, Michael S. Parmacek, Elaine W. Raines, Nancy J. Rusch, Mei Y. Speer, Michael Sturek, Johan Thyberg, Dwight A. Towler, Mary C. Weiser-Evans, Chen Yan, Joseph M. Miano, Gary K. Owens
Journal: Circulation Research (2012)
Nitric Oxide–Induced Motility in Aortic Smooth Muscle Cells
Authors: Yingzi Chang, Bogdan Ceacareanu, Madhulika Dixit, Nair Sreejayan, Aviv Hassid
Journal: Circulation Research (2002)

We have previously reported that SHP-2 upregulation is necessary for NO-stimulated motility in differentiated rat aortic smooth muscle cells. We now test the hypothesis that upregulation of SHP-2 is necessary and sufficient to stimulate cell motility. Overexpression of SHP-2 via recombinant adenoviral vector stimulated motility to the same extent as NO, whereas the expression of C463S-SHP-2, the dominant-negative SHP-2 allele, blocked the motogenic effect of NO. On the basis of previous studies, we next tested the hypothesis that NO decreases RhoA activity and that this event is necessary and sufficient to explain NO-induced motogenesis. We found that NO decreased RhoA activity in a concentration-dependent manner. Moreover, a dominant-negative SHP-2 allele, DSH2, blocked the NO-induced inhibition of RhoA activity, indicating that upregulation of SHP-2 is necessary for this event. Expression of G14V-RhoA, the constitutively active RhoA allele, decreased cell motility and blocked the motogenic effect of NO, whereas the expression of T19N-RhoA, the dominant-negative RhoA allele, increased cell motility to an extent similar to that induced by NO. Dominant-negative RhoA reversed the effect of dominant-negative SHP-2, indicating that RhoA functions downstream from SHP-2. To investigate events downstream from RhoA, we treated cells with fasudil, a selective Rho kinase inhibitor, and found that it increased cell motility. These results indicate that upregulation of SHP-2, leading to downregulation of RhoA, which is followed by decreased Rho kinase activity, is a sequence of events necessary and sufficient to explain NO-induced cell motility in differentiated aortic smooth muscle cells. The results may be of relevance to in vivo events such as neointimal formation, angiogenesis, and vasculogenesis.
Acute appendicitis in Japanese soldiers in Burma: support for the "fibre" theory
Authors: J Black
Journal: Gut (2002)

In the last three months of 1946 and the first quarter of 1947, the late Anand Pardhy and I were the graded surgeon and graded physician in a CCS (Casualty Clearing Station) which was acting as a static hospital in the small town of Prome, on the Irrawaddy, in South Burma. In the same area was a camp of 1077 Japanese soldiers awaiting repatriation. They had their own medical officers and sick bay but cases requiring surgery and the more severely ill medical cases were admitted to the CCS. During this period, we admitted from the Japanese camp 10 cases of acute appendicitis, or one case every 2–3 weeks. At the beginning I assisted Pardhy but became so familiar with the technique that I was allowed to do the operation, with Anand Pardhy assisting.

We were intrigued by the high incidence of appendicitis in the Japanese soldiers and thought …
George E. Brown memorial lecture. Local modulation of adrenergic neurotransmission.
Authors: J T Shepherd, P M Vanhoutte
Journal: Circulation (1981)

The cardiovascular reflexes, by regulating the traffic in the sympathetic nerves, govern the amount of norepinephrine released from the nerve endings. However, the final adjustments in the amount of neurotransmitter available to activate the beta 1 receptors in the heart and the alpha receptors in the blood vessels take place at the sympathetic neuroeffector junction. Thus, a decrease in pH, hyperosmolarity, moderate increases in the concentration of K+ ion, adenosine and adenine nucleotides depress the release of norepinephrine at any given level of sympathetic nerve activity. These metabolic changes, which occur in active tissues, and in particular in adenosine, have been proposed as mediators of the accompanying local hyperemia. In addition, they apparently facilitate this local dilatation by disconnecting the blood vessels in the active tissues from sympathetic control. Acetylcholine, histamine and 5-hydroxytryptamine are present in and around certain blood vessels and can activate specific receptors on the prejunctional fibers and cause vasodilatation by reducing the output of neutrotransmitter. Some of the norepinephrine released into the synaptic cleft may depress its continued release by activating prejunctional alpha receptors. In contrast, angiotensin II, by a local action on the nerve endings, can augment the release of transmitter. Decreases in local temperature reduce transmitter release but augment the affinity of the postjunctional alpha receptors for norepinephrine. The role of these local events at the neuroeffector junction, their physiologic significance and potential clinical importance are discussed in this review.