tbuckley/cabot-search huggingface dataset:
Mortality Experience of a Low-Income Population With Young-Onset Diabetes
Authors: Baqiyyah N. Conway, Michael E. May, Lisa B. Signorello, William J. Blot
Journal: Diabetes Care (2012)

In young-onset diabetes, insulin therapy status is a rough marker of diabetes type. We describe the mortality experience of a low-income, predominantly minority population with diabetes diagnosed before age 30 years, stratified by insulin therapy.A total of 1,098 adults aged 40-79 years (median 49) diagnosed with diabetes before age 30 years and 49,914 without diabetes were recruited from community health centers. Individuals with diabetes were categorized by insulin therapy at baseline: group A, insulin therapy only; group B, insulin therapy and an oral hypoglycemic agent; and group C, no insulin therapy. Cox models were used to compute hazard ratios (HRs) and 95% CI for cause-specific mortality based on both underlying and contributing causes of death from death certificates.During follow-up (mean 3.9 years), 15.0, 12.5, and 7.3% of groups A, B, and C, respectively, and 4.6% without diabetes died. Compared with individuals without diabetes, HRs (CI) for all-cause mortality were 4.3 (3.4-5.6), 4.2 (2.8-6.3), and 2.0 (1.4-2.8) in groups A, B, and C, respectively. The leading cause of death was renal failure (end-stage renal disease [ESRD]) in group A, ESRD and coronary artery disease (CAD) in group B, and CAD in group C and individuals without diabetes. HRs for these conditions were at least twice as high as the HRs for all-cause mortality, reaching 17.3 (10.2-29.3), 17.9 (8.3-38.7), and 5.1 (2.3-11.7) in groups A, B, and C, respectively, for ESRD.Excess mortality persists among people with young-onset diabetes of long duration, with ESRD and CAD as the leading contributors to mortality.
P48 Attendance rates and response to pulmonary rehabilitation
Authors: C. Nolan, K. Ingram, R. Fowler, A. Clark, W. Man
Journal: Thorax (2010)

<h3>Background</h3> Although randomised controlled trials and meta-analyses have demonstrated that pulmonary rehabilitation (PR) improves exercise capacity, there is a variability of response and a proportion of PR participants have not shown clincally significant improvements. We hypothesised that attendance record is an important determinant of exercise response to PR. <h3>Methods</h3> 116 consecutive participants, who attended and completed an outpatient PR programme between September 2009 and June 2010, were included in the study. Subjects attended supervised PR twice per week for 8 weeks, with daily unsupervised home exercise. 107 subjects had pre- and post-PR data. Attendace rate at the supervised sessions was recorded, and good attendance was defined a priori as 75% or more attendance. Changes in incremental shuttle walk (ISW) pre- and post-PR were calculated for good and poor attendance groups and compared using Mann–Whitney test. Spearman rank correlation and univariate regression was used to assess the relationship between attendance rate and change in ISW following PR. <h3>Results</h3> Results were expressed as mean (SD) or median (25th – 27th centiles). Patient baseline characteristics were as follows: 55M, 52F, age: 69 (63, 76), FEV1: 1.28 (0.85, 1.89), MRC dyspnoea score; 3 (3, 4), BMI: 27.4 (23.7, 32.1) and ISW: 180 (80, 320). Mean attendance rate was 83 (17)%. There was no significant difference in age, MRC dyspnoea score and ISW between good and poor attendance groups. Median change in ISW following PR was significantly better in the good attendance group compared with the poor attendance group (60 vs 10 m; &lt;0.02). Although Spearman rank correlation was significant (Spearman r=0.21; p=0.03), there was no significant linear relationship (r2=0.01; p=0.35) between attendance rate and change in ISW following PR. <h3>Discussion</h3> Patients attending more than 75% of PR sessions improve ISW distance in response to PR more than those attending less than 75% although the effects of confounding factors cannot be excluded. There is no linear relationship between attendance rate and improvement in ISW. There are likely to be multiple factors determining response to PR.
The effect of latent adenovirus 5 infection on cigarette smoke-induced lung inflammation
Authors: TZ Vitalis, I Kern, A Croome, H Behzad, S Hayashi, JC Hogg
Journal: European Respiratory Journal (1998)

The aim of this study was to test the hypothesis that latent adenovirus (Ad) 5 infection increases the lung inflammation that follows a single acute exposure to cigarette smoke. A recently developed model of latent adenoviral infection in guinea-pigs was used. Twelve animals were infected with Ad5 (10(8) plaque-forming units) and 12 animals were sham-infected. Thirty five days later six Ad5-infected and six sham-infected animals were exposed to the smoke from five cigarettes. The remaining animals were used as controls for both infection and smoking. As markers of inflammation, the volume fraction of macrophages, T-lymphocytes, neutrophils and eosinophils were measured by quantitative histology. We found that latent Ad5-infection alone, doubled the number of macrophages in the lung parenchyma and that smoking alone, doubled the volume fraction of neutrophils in the airway wall and the volume fraction of macrophages in the lung parenchyma. Neither viral infection nor smoking, alone, had an effect on T-lymphocytes or eosinophils. However, the combination of viral infection and smoking doubled the T-lymphocyte helper cells and quadrupled the volume fraction of macrophages in the lung parenchyma. We conclude that in guinea-pigs, latent adenovirus 5 infection increases the inflammation that follows a single acute exposure to cigarette smoke, by increasing the volume fraction of macrophages and T-lymphocyte helper cells.
Note on the Treatment of Relapsing Acne
Authors: L. Phillips
Journal: BMJ (1897)

TREATMENT OF RELAPSING ACNE.[I 10M 797 months in some of the largest hospitals in this country, re- presenting 8o,ooo in-patients and several hundred thousand out-patients, Mayo Robson) that I have ventured to relate these two cases to you.Both of them are interesting, the first in being complicated with cystitis and a general debili- tated condition which rendered diagnosis almost impossible; the second in the absence of symptoms until obstruction occurred, and in the rapid and favourable termination of the case.In neither case was there a history of jaundice or colic, and no attack of a similar nature had prA'viously occurred.
W(h)ither the exercise ECG?
Authors: S. R. Underwood
Journal: BMJ (2010)

Bourdillon questions guidance from the National Institute for Health and Clinical Excellence (NICE) that exercise electrocardiography (ECG) has no role in diagnosing obstructive coronary disease causing angina (or in diagnosing angina, as NICE says incorrectly).1 2 Perhaps a more cogent reason for questioning this conclusion is that NICE considered only diagnosis and took no account of downstream testing or …
The Plexin-A1 Receptor Activates Vascular Endothelial Growth Factor-Receptor 2 and Nuclear Factor-κB to Mediate Survival and Anchorage-Independent Growth of Malignant Mesothelioma Cells
Authors: Alfonso Catalano, Raffaella Lazzarini, Silvia Di Nuzzo, Silvia Orciari, Antonio Procopio
Journal: Cancer Research (2009)

Abstract The semaphorins and their receptors, the neuropilins and the plexins, are constituents of a complex regulatory system that controls axonal guidance. Moreover, many types of tumor cells express various members of semaphorins and receptors, but the biological activities within tumor mass and the signal transduction mechanism(s) they use are largely unknown. Here, we show that in asbestos-related malignant pleural mesothelioma (MPM), Semaphorin-6D (Sema6D) and its receptor plexin-A1 are frequently expressed and trigger a prosurvival program that promotes anchorage-independent growth of MPM cells. Interestingly, the same response is also controlled by the tyrosine kinase receptors of vascular endothelial growth factor (VEGF) through a nuclear factor-κB (NF-κB)–dependent pathway. We found that in MPM cells, plexin-A1 and VEGF-receptor 2 (VEGF-R2) are associated in a complex. Moreover, the presence of Sema6D promotes the tyrosine phosphorylation of VEGF-R2 in a plexin-A1–dependent manner. This is necessary for basal and Sema6D-induced NF-κB transcriptional activity, and NF-κB mediates tumor cell survival. Expression of Sema6D and plexin-A1 is induced by asbestos fibers and overexpression of plexin-A1 in nonmalignant mesothelial cells inhibits cell death after asbestos exposure. This work identifies a new biological function of semaphorins in cancer cells and suggests the involvement of an undescribed survival pathway during MPM tumorigenesis. [Cancer Res 2009;69(4):1485–93]
Number and Proliferation of Clara Cells in Normal Human Airway Epithelium
Authors: JAMES E. BOERS, ANTON W. AMBERGEN, FREDERIK B. J. M. THUNNISSEN
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

Experimental pathologic studies suggest that Clara cells are one of the types of airway stem cells but the proliferation of Clara cells in human lungs has not yet been examined. The purpose of this study was to assess in conducting airways of normal human lungs: (1) the number of Clara cells; and (2) the contribution of Clara cells to the proliferation compartment. Samples of histologic normal tissue were taken from seven lungs obtained by autopsy. A triple sequential (immuno)histochemical staining was performed, using MIB-1 as a proliferation marker and anti-CC10 for the identification of Clara cells; subsequently, a PAS stain was carried out as a marker for goblet cells, as these cells were reported to be CC10-immunoreactive in an unknown proportion. Clara cells were virtually absent in the proximal airway epithelium. The number of Clara cells in the terminal bronchioles was 11 +/- 3% (mean +/- SD) and in respiratory bronchioles 22 +/- 5%. The overall proliferation compartment of the conducting airway epithelium was 0.83 +/- 0.47%; the contribution of Clara cells was 9%. In the terminal bronchioles 15% of proliferating airway epithelial cells were Clara cells, and in the respiratory bronchioles this number increased to 44%. The contribution of Clara cells to the proliferation compartment of normal human tracheobronchial epithelium is substantial, demonstrating a role of the Clara cell in the maintenance of the normal epithelium of the distal conducting airways in humans.
Global nucleosome occupancy in yeast.
Authors: Bradley E Bernstein, Chih Long Liu, Emily L Humphrey, Ethan O Perlstein, Stuart L Schreiber
Journal: Genome biology (2004)

Abstract Background Although eukaryotic genomes are generally thought to be entirely chromatin-associated, the activated PHO5 promoter in yeast is largely devoid of nucleosomes. We systematically evaluated nucleosome occupancy in yeast promoters by immunoprecipitating nucleosomal DNA and quantifying enrichment by microarrays. Results Nucleosome depletion is observed in promoters that regulate active genes and/or contain multiple evolutionarily conserved motifs that recruit transcription factors. The Rap1 consensus was the only binding motif identified in a completely unbiased search of nucleosome-depleted promoters. Nucleosome depletion in the vicinity of Rap1 consensus sites in ribosomal protein gene promoters was also observed by real-time PCR and micrococcal nuclease digestion. Nucleosome occupancy in these regions was increased by the small molecule rapamycin or, in the case of the RPS11B promoter, by removing the Rap1 consensus sites. Conclusions The presence of transcription factor-binding motifs is an important determinant of nucleosome depletion. Most motifs are associated with marked depletion only when they appear in combination, consistent with a model in which transcription factors act collaboratively to exclude nucleosomes and gain access to target sites in the DNA. In contrast, Rap1-binding sites cause marked depletion under steady-state conditions. We speculate that nucleosome depletion enables Rap1 to define chromatin domains and alter them in response to environmental cues.
Relationship between Epicardial S-T Segment Changes and Myocardial Metabolism during Acute Coronary Insufficiency
Authors: JAN KARLSSON, GORDON H. TEMPLETON, JAMES T. WILLERSON
Journal: Circulation Research (1973)

Canine left ventricular wall metabolites (ATP, creatine phosphate, glycogen, glucose, glucose-6-phosphate, and lactate) were assessed in the ischemic region of the wall after 17 minutes of ligation of the left anterior descending coronary artery at its midlevel. Variations in the degree of lactate accumulation were found between different sites in the same ischemic region and between the outer and the inner left ventricular wall at the same site. High levels of lactate were associated with S-T segment elevation in the epicardial electrocardiogram, but no lactate accumulation or only mild lactate accumulation was found at isoelectric sites. Lactate accumulation at isoelectric sites was higher in the outer wall than it was in the inner wall; the opposite tendency was observed at sites of S-T segment elevation. In addition to high lactate levels, sites of S-T segment elevation demonstrated a more pronounced depletion of ATP and creatine phosphate, indicating not only a marked anaerobic glycolysis but also a more pronounced overall anaerobic stress. No relationship was found, however, between the absolute magnitude of S-T segment elevation and the degree of lactate accumulation or ATP depletion at sites of S-T segment elevation within the ischemic region. The data obtained in this study demonstrate that during myocardial ischemia epicardial sites of S-T segment elevation are sites of pronounced subendocardial and epicardial ischemia and of anaerobic metabolism.
The mechanisms responsible for the flash-lag effect cannot provide the motor prediction that we need in daily life
Authors: Jeroen B. J. Smeets, Eli Brenner
Journal: Behavioral and Brain Sciences (2008)

Abstract The visual prediction that Nijhawan proposes cannot explain why the flash-lag effect depends on what happens after the flash. Moreover, using a visual prediction based on retinal image motion to compensate for neuronal time delays will seldom be of any use for motor control, because one normally pursues objects with which one intends to interact with ones eyes.
Both interleukin 2 and a second T cell-derived factor in EL-4 supernatant have activity as differentiation factors in IgM synthesis.
Authors: K Nakanishi, T R Malek, K A Smith, T Hamaoka, E M Shevach, W E Paul
Journal: The Journal of Experimental Medicine (1984)

B cells cultured with anti-IgM, BSF-p1, and B15-TRF will differentiate into high rate IgM-synthesizing cells in the presence of supernatants from EL-4 cells that have been induced with phorbol myristate acetate. These supernatants contain two molecular species (EL-TRFs) that have differentiative activity. One co-migrates with interleukin 2 (IL-2) and its activity is blocked by antibody to the IL-2 receptor. Furthermore, molecularly cloned IL-2, at concentrations of 100 U/ml or more, expresses such EL-TRF activity. The EL-TRF activity of cloned IL-2 can also be inhibited by antibody to the IL-2 receptor. The other material with EL-TRF activity has a molecular weight of approximately 32,000. This material lacks IL-2 activity. Antibody to the IL-2 receptor does not impair its function. B cells stimulated with anti-IgM and BSF-p1, with or without B15-TRF, express determinants that react with two monoclonal antibodies which recognize distinct epitopes on the T cell IL-2 receptor. These determinants are present at much lower density (approximately 100-fold) on stimulated B cells that on HT-2 cells, an IL-2-dependent T cell line. Very small amounts of [3H]IL-2 (less than 1,000 molecules per cell) bind to activated B cells. These results indicate that IL-2 binds to a receptor on appropriately prepared B cells and causes them to differentiate into high rate IgM-synthesizing cells. The physiologic significance of the B cell differentiative activity of IL-2 remains to be investigated.
Precarious Employment: Understanding an Emerging Social Determinant of Health
Authors: J. Benach, A. Vives, M. Amable, C. Vanroelen, G. Tarafa, C. Muntaner
Journal: Annual Review of Public Health (2014)

Employment precariousness is a social determinant that affects the health of workers, families, and communities. Its recent popularity has been spearheaded by three main developments: the surge in “flexible employment” and its associated erosion of workers' employment and working conditions since the mid-1970s; the growing interest in social determinants of health, including employment conditions; and the availability of new data and information systems. This article identifies the historical, economic, and political factors that link precarious employment to health and health equity; reviews concepts, models, instruments, and findings on precarious employment and health inequalities; summarizes the strengths and weaknesses of this literature; and highlights substantive and methodological challenges that need to be addressed. We identify two crucial future aims: to provide a compelling research program that expands our understanding of employment precariousness and to develop and evaluate policy programs that effectively put an end to its health-related impacts.
Factors associated with coronary artery calcification in young female patients with SLE
Authors: K Manger
Journal: Annals of the Rheumatic Diseases (2003)

<b>Background:</b> With improved survival rates of patients with systemic lupus erythematosus (SLE), damage such as accelerated atherosclerosis gains increasing importance. <b>Objective:</b> To identify the prevalence of coronary artery calcifications (CAC) in asymptomatic patients. <b>Methods:</b> Electron beam tomography (EBT) was performed in 75 female patients with SLE aged &lt;50. The results were correlated with traditional and SLE related factors associated with CAC. 49 women with symptomatic coronary heart disease (CHD) and 279 women without CHD were also analysed. <b>Results:</b> Overall, 21/75 (28%) patients had CAC. Low HDL cholesterol levels &lt;1.40 mmol/l (p=0.03, OR=1.8, 67% <i>v</i> 39%) and cigarette smoking (p=0.01, OR=5.7, 76% <i>v</i> 44%) were identified as factors associated with CAC. Hypertension and high cholesterol were more common in women with CHD (p&lt;0.01) than in those without CHD. SLE related factors were proteinuria (1331 <i>v</i> 465 mg/day, p=0.02), impaired renal function (p=0.02, OR=2.6, 26% <i>v</i> 6%), and high C3 levels (p=0.04, OR=1.8, 65% <i>v</i> 38%). High C3 levels were also more common in symptomatic CHD (p=0.02). The prevalence of Sm antibodies was lower in patients with CAC (15% <i>v</i> 42%, p=0.03). In a multivariate analysis, cigarette smoking, reduced renal function, high C3, and a cumulative steroid dose above 30 g were the most important CAC associated factors in the lupus cohort. <b>Conclusion:</b> A subgroup of patients with SLE with CAC without any clinical symptoms of CHD was identified by EBT. Therefore, EBT is useful for assessing asymptomatic atherosclerosis in this group.
STUDIES ON ENTRY AND EGRESS OF POLIOMYELITIC INFECTION
Authors: Harold K. Faber, Rosalie J. Silverberg, Luther Dong
Journal: The Journal of Experimental Medicine (1953)

We have demonstrated a progressive centrifugal migration of poliomyelitis virus from the CNS into various peripheral ganglia and into peripheral nerves, including their distal portions. This phenomenon appears to be a regular occurrence in experimental animals, and is similar to that found in two other neurotropic infections, rabies and Borna disease. Viremia appears to be secondary to primary neural infection. The presence of virus in the lumen of the alimentary tract appears to be secondary to primary neural infection and not to viremia, and to be associated with the centrifugal spread of virus in peripheral nerves. The presence of virus in "extraneural" tissues is not per se referable to infection of their constituent cells but rather to infection of their supplying nerves or, in some instances, to their content of virus-bearing blood. The finding of virus in the vagus nerve may throw light on some of the electrocardiographic changes noted in certain cases of human poliomyelitis. The presence of virus in peripheral nerves may throw light on the etiology of the most frequent clinical manifestations of human poliomyelitis, localized pain and tenderness.
The Hypoxia-Inducible MicroRNA Cluster miR-199a∼214 Targets Myocardial PPARδ and Impairs Mitochondrial Fatty Acid Oxidation
Authors: Hamid el Azzouzi, Stefanos Leptidis, Ellen Dirkx, Joris Hoeks, Bianca van Bree, Karl Brand, Elizabeth A. McClellan, Ella Poels, Judith C. Sluimer, Maarten M.G. van den Hoogenhof, Anne-Sophie Armand, Xiaoke Yin, Sarah Langley, Meriem Bourajjaj, Serve Olieslagers, Jaya Krishnan, Marc Vooijs, Hiroki Kurihara, Andrew Stubbs, Yigal M. Pinto, Wilhelm Krek, Manuel Mayr, Paula A. da Costa Martins, Patrick Schrauwen, Leon J. De Windt
Journal: Cell Metabolism (2013)
Nasal proportional assist ventilation unloads the inspiratory muscles of stable patients with hypercapnia due to COPD
Authors: G. Polese, M Vitacca, L. Bianchi, A. Rossi, N Ambrosino
Journal: European Respiratory Journal (2000)

This study was undertaken to assess the physiological effects of proportional assist ventilation (PAV), administered noninvasively through a nose mask, on ventilatory pattern, arterial blood gases, lung mechanics, and inspiratory muscle effort in stable, hypercapnic patients with chronic obstructive pulmonary disease. In 15 patients, PAV was set by adjusting volume assist (VA) and flow assist (FA) according to the "run-away" technique and the patient's comfort respectively. The level of support was fixed at 80% of the total possible assistance and averaged 13.9+/-4.1 cmH2O x L(-1) and 4.1+/-1.3 cmH2O x L(-1) x s for VA and FA, respectively. Continuous positive airway pressure (CPAP) was established at 2 cmH2O and then increased to 5 cmH2O. Physiological measurements were made during spontaneous breathing (SB), after more than 40 min of PAV, and 20 min after the rise in CPAP. On average, PAV improved ventilation (10.3+/-2.1 to 12.5+/-2.0 L x m(-1)), tidal volume (0.60+/-0.11 to 0.76+/-0.24 L), arterial oxygen tension and arterial carbon dioxide pressure (from 6.7+/-0.7 to 7.1+/-0.9 and from 7.6+/-1.0 to 7.2+/-1.2 kPa, respectively). During SB, pulmonary resistance and dynamic lung elastance averaged 15.0+/-7.6 cmH2O x L(-1) s and 15.8+/-8.0 cmH2O x L(-1), respectively. Assuming a normal chest wall elastance (5 cmH2O x L(-1)), VA and FA relieved respectively approximately 70% of the elastic and 30% of the resistive burden, with PAV set with the procedure of this study. The overall magnitude of the patients' inspiratory effort, measured by means of the oesophageal and diaphragmatic pressure time product in 10 patients was significantly reduced by PAV, on average, 328+/-122 to 226+/-118 (-31%) and 361+/-119 to 254+/-126 (-30%) cmH2O x min(-1), respectively. In 10 patients the electrical activity of the diaphragm (Edi) was also reduced by PAV to approximately 70%, on average, of the SB activity. The rise of CPAP 25 cmH2O did not cause any further significant change in the physiological variables. In all instances there was a good patient-ventilator interaction, the ventilatory breath never entering into the patient's neural expiratory time. These data show that nasal proportional assist ventilation can provide physiological benefits to the stable hypercapnic chronic obstructive pulmonary disease patients. In fact, proportional assist ventilation, which was well tolerated by all patients, unloaded the inspiratory muscles and improved arterial blood gases. Further studies can clarify whether these beneficial physiological effects of nasal proportional assist ventilation can bear profitable consequences in the overall clinical management of chronic obstructive pulmonary disease patients with chronic carbon dioxide retention.