tbuckley/cabot-search huggingface dataset:
PATHOGENESIS OF CHRONIC DISEASE ASSOCIATED WITH PERSISTENT LYMPHOCYTIC CHORIOMENINGITIS VIRAL INFECTION
Authors: Michael B. A. Oldstone, Frank J. Dixon
Journal: The Journal of Experimental Medicine (1969)

Mice infected shortly after birth with lymphocytic choriomeningitis (LCM) virus are not immunologically tolerant, although they carry the virus throughout life. These LCM carrier mice make anti-LCM antibody, which apparently complexes with viral antigen in the circulation and these complexes accumulate in the glomeruli. LCM carrier mice of different strains vary significantly as to concentration of detectable infectious virus in their tissue, amount and time of appearance of anti-LCM antibody, and development of an associated chronic disease. The chronic disease consists primarily of glomerulonephritis, focal hepatic necrosis, and disseminated lymphoid infiltrations. LCM carriers of the SWR/J strain contain high tissue concentrations of virus, considerable anti-LCM antibody detectable in the glomeruli by 3 wk to 2 months of age and develop chronic disease within the first 2-3 months of life. In contrast, C(3)H strain LCM carriers contain 1/1000 as much infectious virus, less detectable anti-LCM antibody, and have not, over a 24 month observation period, developed any detectable disease. B10D2 old and new carrier mice with intermediate amounts of virus develop chronic disease during the latter half of the first year of life. The pathogenesis of the glomerulonephritis of chronic LCM disease is apparently related to the formation of circulating virus-antibody complexes which are trapped in the glomerular filter. There is no evidence for direct glomerular injury by the virus nor for any autoimmune response by the host.
Delayed recovery of intracellular acidosis during reperfusion prevents calpain activation and determines protection in postconditioned myocardium
Authors: J. Inserte, I. Barba, V. Hernando, D. Garcia-Dorado
Journal: Cardiovascular Research (2008)

Indirect data suggest that delayed recovery of intracellular pH (pHi) during reperfusion is involved in postconditioning protection, and calpain activity has been shown to be pH-dependent. We sought to characterize the effect of ischaemic postconditioning on pHi recovery during reperfusion and on calpain-dependent proteolysis, an important mechanism of myocardial reperfusion injury. Isolated Sprague–Dawley rat hearts were submitted to 40 min of ischaemia and different reperfusion protocols of postconditioning and acidosis. pHi was monitored by 31P-NMR spectroscopy. Myocardial cell death was determined by lactate dehydrogenase (LDH) and triphenyltetrazolium staining, and calpain activity by western blot measurement of α-fodrin degradation. In control hearts, pHi recovered within 1.5 ± 0.24 min of reperfusion. Postconditioning with 6 cycles of 10 s ischaemia–reperfusion delayed pHi recovery slightly to 2.5 ± 0.2 min and failed to prevent calpain-mediated α-fodrin degradation or to elicit protection. Lowering perfusion flow to 50% during reperfusion cycles or shortening the cycles (12 cycles of 5 s ischemia–reperfusion) resulted in a further delay in pHi recovery (4.1 ± 0.2 and 3.5 ± 0.3 min, respectively), attenuated α-fodrin proteolysis, improved functional recovery, and reduced LDH release (47 and 38%, respectively, P < 0.001) and infarct size (36 and 32%, respectively, P < 0.001). This cardioprotection was identical to that produced by lowering the pH of the perfusion buffer to 6.4 during the first 2 min of reperfusion or by calpain inhibition with MDL-28170. These results provide direct evidence that postconditioning protection depends on prolongation of intracellular acidosis during reperfusion and indicate that inhibited calpain activity could contribute to this protection.
Enhancing Activity of Various Immunoaugmenting Agents on the Delayed- Type Hypersensitivity Response in Mice
Authors: Anna Bartocci, Elizabeth L. Read, Roy D. Welker, Erich Schlick, Vasilios Papademetriou, Michael A. Chirigos
Journal: Cancer Research (1982)

Six immunoaugmenting agents were tested in the delayed-type hypersensitivity reaction (DTH) in normal BALB/c X DBA/2 mice. The agents tested, levan, lentinan, mannozym, maleic anhydride divinyl ether, polyriboinosinic-polycytidylic acid-poly-L-lysine, and highly purified L-cell interferon, gave significant increases in the DTH response above the sheep red blood cell control. The schedule of doses for each agent corresponded with previous experiments from this laboratory of the maximum natural killer cell activity, macrophage activation, and interferon induction. Highly purified L-cell interferon was capable of eliciting a significant DTH response when given 4 hr after the initial challenge with sheep erythrocytes. In addition, lambda-carrageenan, a macrophage-cytotoxic agent which can render the macrophage inactive, was found to suppress the DTH response to levels slightly above phosphate-buffered saline controls. The carrageenan-induced suppression of the DTH response could be abrogated by coadministration with immunoaugmenting agents to levels attained with the immunoaugmenting agents alone.
Disease of the airways in chronic obstructive pulmonary disease
Authors: M.G. Cosio Piqueras, M.G. Cosio
Journal: European Respiratory Journal (2001)

The pathological hallmarks of chronic obstructive pulmonary disease (COPD) are inflammation of the small airways (bronchiolitis) and destruction of lung parenchyma (emphysema). The functional consequence of these abnormalities is airflow limitation. Airway abnormalities and emphysema interact in a complex fashion in the development of airflow limitation in COPD. In an attempt to improve understanding of the role of the airways in COPD, the morphological counterparts of airflow limitation, the cellular inflammatory infiltrate in the airways and the relationship between emphysema type and airway abnormalities are reviewed. Significant correlation between airway remodelling and functional measurements are found in earlier stages of COPD. In advanced COPD, airflow limitation is reflected by airway narrowing, airway deformity and extent of emphysema. The cellular inflammatory infiltrate is mainly composed of neutrophils in early stages of COPD. However, the presence of CD8+ T-cells seems to differentiate smokers with COPD from smokers that would not develop the disease. The inflammatory changes and remodelling found in the airways and their contribution to airflow obstruction might be modulated by the type of emphysema smokers develop, with centrilobular emphysema showing more severe inflammatory changes and narrower airways than panlobular emphysema. In conclusion, the degree of airway involvement in chronic obstructive pulmonary disease can vary greatly for the same degree of airflow obstruction, depending on the type of emphysema smokers develop. If the underlying lung abnormalities in chronic obstructive pulmonary disease vary, as the evidence suggests, the study of cigarette-induced lung disease as a single entity will further delay understanding of chronic obstructive pulmonary disease.
Pulmonary Tumors in Germfree Mice: Induction With Urethan
Authors: Nelson A. Burstein, K. Robert McIntire, Anthony C. Allison
Journal: JNCI Journal of the National Cancer Institute (1970)

Germfree (GF) mice develop fewer urethan-induced pulmonary adenomas than do conventional (CONV) mice. Twenty-four weeks after one intraperitoneal injection of urethan (~1 mg/g body weight), 9 of 17 GF BALB/c mice and 17 of 20 CONV BALB/c mice developed tumors. Untreated GF and CONV BALB/c mice did not develop tumors. In contrast to GF mice, all CONV mice became naturally infected with pneumonia virus of mice or Sendai virus. None of the 12 common murine viruses tested was necessary for urethan oncogenesis.
Micro <scp>RNA</scp> profiling reveals differentially expressed micro <scp>RNA</scp> signatures from the skin of patients with nonsegmental vitiligo
Authors: M.S. Mansuri, M. Singh, M. Dwivedi, N.C. Laddha, Y.S. Marfatia, R. Begum
Journal: British Journal of Dermatology (2014)

Funding sources: This work was supported by grants to R.B. from the Gujarat State Biotechnology Mission, Gandhinagar, Gujarat, India (GSBTM/MD/PROJECTS/SSA/453/2010‐2011). M.S.M. thanks the University Grants Commission, New Delhi, India, for the awarding of a Junior Research Fellowship. N.C.L. thanks the Council of Scientific and Industrial Research, New Delhi, India, for the awarding of a Senior Research Fellowship. Conflicts of interest: none declared. Dear Editor, Vitiligo is an acquired depigmentation disorder characterized by milky white patches on skin that occur as a result of the destruction of melanocytes. The precise modus operandi of the pathogenesis of vitiligo has remained elusive. The onset and progression of vitiligo are thought to be driven by multiple inherited genes and environmental triggers.1 MicroRNAs (miRNAs) have been shown to be promising biomarkers for different diseases.2 Shi et al.3 elucidated the serum miRNA expression profile in patients with nonsegmental vitiligo (NSV). Nevertheless, the role of miRNAs in the skin microenvironment of vitiligo lesions remains to be explored. In this study, we aimed to detect differentially expressed miRNAs and to explore the potential role of miRNAs in the pathogenesis of vitiligo by miRNA expression profiling of lesional and nonlesional skin from patients with NSV compared with healthy skin from controls.
Placement of an Arterial Line
Authors: Ken Tegtmeyer, Glenn Brady, Susanna Lai, Richard Hodo, Dana Braner
Journal: New England Journal of Medicine (2006)

Arterial Line Placement (Introduction) This video will demonstrate arterial line placement in the radial artery using two of the many techniques available for arterial line placement, an over-the-wire technique and an over-the-needle technique. Placement of an arterial line is indicated for continuous monitoring of arterial pressure and direct arterial blood sampling. The radial pulse is palpated between the distal radius and the flexor carpi radialis tendon. Prior to line placement, perfusion of the extremity should be checked. For radial arterial catheters, an Allen test or a modified Allen test may be performed. While the value of the Allen test has . . . .
Non-HDL Cholesterol and Apolipoprotein B in the Dyslipidemic Classification of Type 2 Diabetic Patients
Authors: Ana Maria Wägner, Antonio Pérez, Edgar Zapico, Jordi Ordóñez-Llanos
Journal: Diabetes Care (2003)

OBJECTIVE—To compare non-HDL cholesterol (HDLc) and apolipoprotein B (apoB) in the identification of nonconventional high-risk dyslipidemic phenotypes in type 2 diabetic patients. RESEARCH DESIGN AND METHODS—Total cholesterol and triglycerides, HDLc, LDL cholesterol, non-HDLc, apolipoprotein B (apoB), and LDL size were determined in 122 type 2 diabetic patients (68% male, aged 59.6 ± 9.7 years, and HbA1c 7.5% [range 5.2–16.0]). They were then classified as normo- and hypertriglyceridemic if their triglyceride concentrations were below/above 2.25 mmol/l, as normo/hyper-non-HDLc if non-HDLc concentrations were below/above 4.13 mmol/l, and as normo- and hyperapoB if apoB concentrations were below/above 0.97 g/l. Both classifications were compared (concordance assessed with the κ index), and low HDLc and LDL phenotype B were identified in each category. RESULTS—A total of 26 patients were hypertriglyceridemic and 96 were normotriglyceridemic. All hypertriglyceridemic subjects had increased non-HDLc, whereas 24 had increased apoB (κ= 0.95). In the normotriglyceridemic group, 44 had increased non-HDLc, 68 had increased apoB, and 25 of the 52 patients with normal non-HDLc had increased apoB (κ= 0.587). Low HDLc and LDL phenotype B were similarly distributed into the equivalent categories. CONCLUSIONS—Non-HDLc and apoB are equivalent risk markers in hypertriglyceridemic patients, but apoB identifies additional patients with high-risk dyslipidemic phenotypes in normotriglyceridemic type 2 diabetic patients.
Use of Prescription Weight Loss Pills among U.S. Adults in 1996–1998
Authors: Laura Kettel Khan, Mary K. Serdula, Barbara A. Bowman, David F. Williamson
Journal: Annals of Internal Medicine (2001)

Pharmacotherapy is recommended for the treatment of obese persons with a body mass index of 30 kg/m(2) or higher or a body mass index of at least 27 kg/m(2) plus an obesity-related comorbid condition.To estimate the prevalence of use of prescription weight loss pills in the United States in 1996-1998.1998 Behavioral Risk Factor Surveillance System, a nationally representative telephone survey.United States.139 779 adults 18 years of age and older.Self-reported pill use for 1996-1998, body mass index (current and before pill use), age, sex, and race or ethnicity.The 2-year prevalence of pill use was 2.5% (95% CI, 2.1% to 2.9%), or 4.6 million U.S. adults. Use was higher in women than in men (4.0% vs. 0.9%, respectively) and highest among Hispanic respondents (3.2%). Of pill users, 25% were not overweight (body mass index < 27 kg/m(2) before using pills.Nearly 5 million U.S. adults used prescription weight loss pills in 1996-1998. However, one quarter of users were not overweight, suggesting that weight loss pills may be inappropriately used, especially among women, white persons, and Hispanic persons.
GNPAT variant is not associated with severe iron overload in Irish C282Y homozygotes
Authors: Eleanor Ryan, Jennifer Russell, John D Ryan, John Crowe, Stephen Stewart
Journal: Hepatology (2015)

Potential conflict of interest: Nothing to report. Author names in bold denote shared co‐first authorship. To the Editor: Following the recent publication by McLaren et al. whereby the rs11558492 polymorphism in the GNPAT gene (p.D519G) was demonstrated to be a modifier of the hereditary hemochromatosis (HH) phenotype in a cohort of male C282Y homozygotes, we sought to examine this polymorphism in the Irish HH population.1 We looked at the polymorphism in our C282Y homozygous HH population as a whole (n = 263), in males only (n = 177), and in males categorized according to a serum ferritin value at diagnosis of (1) ≥1000 μg/L (n = 57, median serum ferritin 1650 μg/L, interquartile range 1196‐1947 μg/L) and (2) <1000 μg/L (n = 100, median serum ferritin 558 μg/L, interquartile range 420‐810 μg/L). Allele frequencies of GNPAT p.D519G were similar across all groups (chi‐squared test, P = 0.632). The allele frequency of GNPAT p.519G was 24.5% for the whole population and 23.7% for males only, in agreement with frequencies reported in 35 male C282Y homozygotes resident in the United States, Canada, and Australia (24.3%) and in 274 French male C282Y homozygotes (26.3%).1 Independent t tests did not demonstrate a significant difference in the allele frequency of p.D519G or mean age in males with a diagnostic serum ferritin of ≥1000 μg compared to those with a diagnostic serum ferritin of <1000 μg/L, 19.3% versus 25.5% (P = 0.593), and mean age 50 ± 10 years versus 47 ± 13 years (P = 0.094), respectively. The allele frequency of 19.3% in those with a diagnostic serum ferritin of ≥1000 μg/L contrasts with that reported by McLaren et al. of 38.6% in a cohort comprising 22 males with a diagnostic serum ferritin of >1000 μg/L.1 Excess alcohol intake was noted in nine individuals (two of whom had serum ferritin ≥1000 μg/L), and when these were removed from the analysis on the whole population, the p.D519G allele frequency was 24.2% The relationship between diagnostic serum ferritin and the GNPAT p.D519G variant was examined using Pearson product‐moment correlation coefficient analysis. Correlation analysis failed to demonstrate any association between the presence of GNPAT p.D519G and diagnostic serum ferritin across all cohorts. In summary, our data show that GNPAT p.D519G is not associated with a high iron phenotype (diagnostic serum ferritin ≥1000 μg/L) in Irish C282Y homozygotes. Thus, our data disagree with the findings of McLaren et al.1 but agree with the findings of Bardou‐Jacquet et al.2 and indeed De Tayrac et al.,3 who did not find the rs11558492 polymorphism to be a significant genetic modifier of the C282Y HH phenotype in a genome‐wide association study. Further studies are warranted in order to clarify the role of the GNPAT p.D519G variant as a modifier of the HH phenotype.
Proteomic Patterns and Prediction of Glomerulosclerosis and Its Mechanisms
Authors: Baogang J. Xu, Yu Shyr, Xiubin Liang, Li-jun Ma, Ellen M. Donnert, Jeremy D. Roberts, Xueqiong Zhang, Valentina Kon, Nancy J. Brown, Richard M. Caprioli, Agnes B. Fogo
Journal: Journal of the American Society of Nephrology (2005)

Protein expression profiles linked to sclerosis in the 5/6 nephrectomy (Nx) rat model of focal segmental glomerulosclerosis were investigated. Sections of control glomeruli from normal baseline Nx tissue and nonsclerotic and sclerotic glomeruli from 12 wk after 5/6 Nx were isolated by laser capture microdissection. Protein profiles were acquired directly by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Classification accuracy was 99.2% for distinguishing normal versus sclerotic glomeruli and 96.7 and 97.8% for nonsclerotic versus normal and sclerotic glomeruli, respectively. The proteomic pattern of the nonsclerotic glomeruli was more similar to sclerotic than normal glomeruli (P < 0.0001). Thymosin beta4, a protein with relevant interactions with plasminogen activator inhibitor-1, angiogenesis, and wound healing, was identified as a key differentially expressed protein. Thymosin beta4 immunostaining was increased in sclerotic glomeruli, predominantly in endothelial cells. Downregulation of thymosin beta4 by RNAi in cultured glomerular endothelial cells decreased angiotensin II-induced plasminogen activator inhibitor-1 expression. In conclusion, proteomic patterns can accurately distinguish normal versus nonsclerotic versus sclerotic glomeruli. The closely related proteomic patterns of nonsclerotic and sclerotic glomeruli suggest early activation of prosclerotic mechanisms even in seemingly intact glomeruli. Thymosin beta4 is a marker of such early events and may even contribute to sclerosis.
AGGRESSIVE BEHAVIOR DISORDERS OF CHILDHOOD: A FOLLOW-UP STUDY
Authors: H. H. MORRIS, P. J. ESCOLL, R. WEXLER
Journal: American Journal of Psychiatry (1956)

A group of 90 children, under the age of 15, with aggressive behavior was studied at the Pennsylvania Hospital (Franklin School) between 1925 and 1935. These children came largely from the Middle Atlantic States, and represented a wide [SEE TABLE 2 IN SOURCE PDF.] spread in their social and economic backgrounds. In an attempt to follow these children to maturity in order to assess their subsequent life adjustment, 66 were followed to the age of 18 or over ( excluding one death at age 6½). Of these 66, 13 subsequently became psychotic; 14 eventually made adequate social adjustment; 39 never made adequate adjustment. Twelve of the last group committed at least one crime of record, but only one of these crimes involved violence or destruction. In the original group, the ratio of males to females was 2½ to 1; in the psychotic group, 6 to 7; in the group adjusting well, 6 to 1. The backgrounds of these children show significant deviations from those of 60 post-encephalitic children.
Lung ultrasound for the screening of interstitial lung disease in very early systemic sclerosis
Authors: Tatiana Barskova, Luna Gargani, Serena Guiducci, Silvia Bellando Randone, Cosimo Bruni, Giulia Carnesecchi, Maria Letizia Conforti, Francesco Porta, Alberto Pignone, Davide Caramella, Eugenio Picano, Marco Matucci Cerinic
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Background</h3> A high percentage of patients with systemic sclerosis (SSc) develop interstitial lung disease (ILD) during the course of the disease. Promising data have recently shown that lung ultrasound (LUS) is able to detect ILD by the evaluation of B-lines (previously called ultrasound lung comets), the sonographic marker of pulmonary interstitial syndrome. <h3>Objective</h3> To evaluate whether LUS is reliable in the screening of ILD in patients with SSc. <h3>Methods</h3> Fifty-eight consecutive patients with SSc (54 women, mean age 51±14 years) who underwent a high resolution CT (HRCT) scan of the chest were also evaluated by LUS for detection of B-lines. Of these, 32 patients (29 women, mean age 51±15 years) fulfilled the criteria for a diagnosis of very early SSc. <h3>Results</h3> At HRCT, ILD was detected in 88% of the SSc population and in 41% of the very early SSc population. A significant difference in the number of B-lines was found in patients with and without ILD on HRCT (57±53 vs 9±9; p&lt;0.0001), with a concordance rate of 83%. All discordant cases were false positive at LUS, providing a sensitivity and negative predictive value of 100% in both SSc and very early SSc. <h3>Conclusions</h3> ILD may be detected in patients with very early SSc. The presence of B-lines at LUS examination correlates with ILD at HRCT. LUS is very sensitive for detecting ILD even in patients with a diagnosis of very early SSc. The use of LUS as a screening tool for ILD may be feasible to guide further investigation with HRCT.
Economic Burden of Bladder Cancer Across the European Union
Authors: Jose Leal, Ramon Luengo-Fernandez, Richard Sullivan, J. Alfred Witjes
Journal: European Urology (2015)

More than 120 000 people are diagnosed annually with bladder cancer in the 28 countries of the European Union (EU). With >40 000 people dying of it each year, it is the sixth leading cause of cancer. However, to date, no systematic cost-of-illness study has assessed the economic impact of bladder cancer in the EU. To estimate the annual economic costs of bladder cancer in the EU for 2012. Country-specific cancer cost data were estimated using aggregate data on morbidity, mortality, and health care resource use, obtained from numerous international and national sources. Health care costs were estimated from expenditures on primary, outpatient, emergency, and inpatient care, as well as medications. Costs of unpaid care and lost earnings due to morbidity and early death were estimated. Bladder cancer cost the EU €4.9 billion in 2012, with health care accounting for €2.9 billion (59%) and representing 5% of total health care cancer costs. Bladder cancer accounted for 3% of all cancer costs in the EU (€143 billion) in 2012 and represented an annual health care cost of €57 per 10 EU citizens, with costs varying >10 times between the country with the lowest cost, Bulgaria (€8 for every 10 citizens), and highest cost, Luxembourg (€93). Productivity losses and informal care represented 23% and 18% of bladder cancer costs, respectively. The quality and availability of comparable cancer-related data across the EU need further improvement. Our results add to essential public health and policy intelligence for delivering affordable bladder cancer care systems and prioritising the allocation of public research funds. We looked at the economic costs of bladder cancer across the European Union (EU). We found bladder cancer to cost €4.9 billion in 2012, with health care accounting for €2.9 billion. Our study provides data that can be used to inform affordable cancer care in the EU.