tbuckley/cabot-search huggingface dataset:
A Longitudinal Study of Indoor Nitrogen Dioxide Levels and Respiratory Symptoms in Inner-City Children with Asthma
Authors: Nadia N. Hansel, Patrick N. Breysse, Meredith C. McCormack, Elizabeth C. Matsui, Jean Curtin-Brosnan, D’Ann L. Williams, Jennifer L. Moore, Jennifer L. Cuhran, Gregory B. Diette
Journal: Environmental Health Perspectives (2008)

BackgroundThe effect of indoor nitrogen dioxide concentrations on asthma morbidity among inner-city preschool children is uncertain.ObjectivesOur goal was to estimate the effect of indoor NO2 concentrations on asthma morbidity in an inner-city population while adjusting for other indoor pollutants.MethodsWe recruited 150 children (2–6 years of age) with physician-diagnosed asthma from inner-city Baltimore, Maryland. Indoor air was monitored over a 72-hr period in the children's bedrooms at baseline and 3 and 6 months. At each visit, the child's caregiver completed a questionnaire assessing asthma symptoms over the previous 2 weeks and recent health care utilization.ResultsChildren were 58% male, 91% African American, and 42% from households with annual income < $25,000; 63% had persistent asthma symptoms. The mean (± SD) in-home NO2 concentration was 30.0 ± 33.7 (range, 2.9–394.0) ppb. The presence of a gas stove and the use of a space heater or oven/stove for heat were independently associated with higher NO2 concentrations. Each 20-ppb increase in NO2 exposure was associated significantly with an increase in the number of days with limited speech [incidence rate ratio (IRR) = 1.15; 95% confidence interval (CI), 1.05–1.25], cough (IRR = 1.10; 95% CI, 1.02–1.18), and nocturnal symptoms (IRR = 1.09; 95% CI, 1.02–1.16), after adjustment for potential confounders. NO2 concentrations were not associated with increased health care utilization.ConclusionsHigher indoor NO2 concentrations were associated with increased asthma symptoms in preschool inner-city children. Interventions aimed at lowering NO2 concentrations in inner-city homes may reduce asthma morbidity in this vulnerable population.
An In Vitro and Clinical Comparison of Corneal Storage with Chondroitin Sulfate Corneal Storage Medium with and without Dextran
Authors: Jonathan H. Lass, William J. Reinhart, Debra L. Skelnik, William E. Bruner, Richard P. Shockley, Juliana Y. Park, David L. Hom, Richard L. Lindstrom
Journal: Ophthalmology (1990)
Public health implications of components of plastics manufacture. Flame retardants.
Authors: E M Pearce, R Liepins
Journal: Environmental Health Perspectives (1975)

The four processes involved in the flammability of materials are described and related to the various flame retardance mechanisms that may operate. Following this the four practical approaches used in improving flame retardance of materials are described. Each approach is illustrated with a number of typical examples of flame retardants or synthetic procedures used. This overview of flammability, flame retardance, and flame retardants used is followed by a more detailed examination of most of the plastics manufactured in the United States during 1973, their consumption patterns, and the primary types of flame retardants used in the flame retardance of the most used plastics. The main types of flame retardants are illustrated with a number of typical commercial examples. Statistical data on flame retardant market size, flame retardant growth in plastics, and price ranges of common flame retardants are presented.
Abdominal adipose tissue distribution, obesity, and risk of cardiovascular disease and death: 13 year follow up of participants in the study of men born in 1913.
Authors: B Larsson, K Svardsudd, L Welin, L Wilhelmsen, P Bjorntorp, G Tibblin
Journal: BMJ (1984)

In a prospective study of risk factors for ischaemic heart disease 792 54 year old men selected by year of birth (1913) and residence in Gothenburg agreed to attend for questioning and a battery of anthropometric and other measurements in 1967. Thirteen years later these baseline findings were reviewed in relation to the numbers of men who had subsequently suffered a stroke, ischaemic heart disease, or death from all causes. Neither quintiles nor deciles of initial indices of obesity (body mass index, sum of three skinfold thickness measurements, waist or hip circumference) showed a significant correlation with any of the three end points studied. Statistically significant associations were, however, found between the waist to hip circumference ratio and the occurrence of stroke (p = 0.002) and ischaemic heart disease (p = 0.04). When the confounding effect of body mass index or the sum of three skinfold thicknesses was accounted for the waist to hip circumference ratio was significantly associated with all three end points. This ratio, however, was not an independent long term predictor of these end points when smoking, systolic blood pressure, and serum cholesterol concentration were taken into account. These results indicate that in middle aged men the distribution of fat deposits may be a better predictor of cardiovascular disease and death than the degree of adiposity.
Diagnostic Value of Plasma Amylase, especially after Gastrectomy
Authors: G. K. McGowan, M. R. Wills
Journal: BMJ (1964)

The plasma-amylase level is almost invariably raised at the height of an attack of acute pancreatitis.However, the diag- nostic value of this is limited by the occasional finding of .quallyhigh levels in patients with acute abdominal conditions which are not primarily acute pancreatitis.In our experience such " false-positive " findings have been commonly associated with a history of gastrectomy.In order to study this relation- ship we have reviewed, for the 10-year period January 1952 to December 1961, the 119 patients whose plasma-amylase levels were found to be above 1,000 units (Somogyi)/100 ml.Of these, 113 had acute abdominal symptoms resembling those of acute pancreatitis. Method of Amylase EstimationPlasma amylase was estimated by the method of Somogyi '1938) as described by King (1946).In order to exclude false high results due to bacterial decomposition of the starch sub- strate the latter has been measured in 2-ml.quantities into rubber-capped tubes, sterilized by heating to 60' C. for one hour on three successive days, and stored in the refrigerator.Where the amylase level has been high enough to reduce the digestion time below four minutes the estimation has been repeated after diluting the plasma with saline.Precautions were taken to avoid contamination with saliva.We find that hospital patients without obvious pancreatic disease, including those who have undergone abdominal operations, have levels of amylase in the plasma up to 300 units/100 ml.We accept a level of I,000 units/100 ml. as the minimum necessary to support a diagnosis of acute pancreatitis. Subjects InvestigatedPrimary acute pancreatitis is best treated conservatively.If the diagnosis of acute pancreatitis is made wrongly, the error will not be serious if the appropriate treatment for the condition actually present is conservative also.If, however, the condition As one which demands urgent surgery, the mistake is likely to be fatal for the patient.The main clinical value of the amylase tlst lies in the differentiation of these two groups, and we have therefore classified the patients with high plasma-amylase levels into two major groups: (1) 91 patients with primary acute mncreatitis or some other condition (including secondary pacreatitis) not requiring urgent surgery, and (2) 22 patients with acute abdominal conditions (also including secondary pancrtatitis) which usually require urgent surgery (see Table I).irn fact, several patients in group 1 were operated on, and several in group 2 were not. Group 1A. In the first subgroup of 90 patients with acute pancreatitis the classical syndrome and course of the disease were seen.In 36 the disease was " primary," though 42 had a history suggest- ing disease of the biliary tract ; plasma-amylase levels ranged up to 16,000, and confirmation of the diagnosis was obtained at
Cardiac-Specific Overexpression of Tumor Necrosis Factor-α Causes Oxidative Stress and Contractile Dysfunction in Mouse Diaphragm
Authors: Xia Li, Melanie R. Moody, David Engel, Stacey Walker, Fred J. Clubb, Natarajan Sivasubramanian, Douglas L. Mann, Michael B. Reid
Journal: Circulation (2000)

Background —We have developed a transgenic mouse with cardiac-restricted overexpression of tumor necrosis factor-α (TNF-α). These mice develop a heart failure phenotype characterized by left ventricular dysfunction and remodeling, pulmonary edema, and elevated levels of TNF-α in the peripheral circulation from cardiac spillover. Given that TNF-α causes atrophy and loss of function in respiratory muscle, we asked whether transgenic mice developed diaphragm dysfunction and whether contractile losses were caused by oxidative stress or tissue remodeling. Methods and Results —Muscles excised from transgenic mice and littermate controls were studied in vitro with direct electrical stimulation. Cytosolic oxidant levels were measured with 2′,7′-dichlorofluorescin diacetate; emissions of the oxidized product were detected by fluorescence microscopy. Force generation by the diaphragm of transgenic animals was 47% less than control (13.2±0.8 [±SEM] versus 25.1±0.6 N/cm 2 ; P &lt;0.001); this weakness was associated with greater intracellular oxidant levels ( P &lt;0.025) and was partially reversed by 30-minute incubation with the antioxidant N -acetylcysteine 10 mmol/L ( P &lt;0.01). Exogenous TNF-α 500 μmol/L increased oxidant production in diaphragm of wild-type mice and caused weakness that was inhibited by N -acetylcysteine, suggesting that changes observed in the diaphragm of transgenic animals were mediated by TNF-α. There were no differences in body or diaphragm weights between transgenic and control animals, nor was there evidence of muscle injury or apoptosis. Conclusions —Elevated circulating levels of TNF-α provoke contractile dysfunction in the diaphragm through an endocrine mechanism thought to be mediated by oxidative stress.
Evidence for modulation of genes involved in vascular adaptation by prolonged exposure of endothelial cells to shear stress
Authors: M Bongrazio
Journal: Cardiovascular Research (2000)

Objective: Shear stress is known to modulate gene expression. However, the molecular link between blood flow and long-time vessel adaptation is still unclear. In this study, the variations of gene expression by prolonged shear stress exposure was investigated in order to identify genes possibly involved in flow dependent vascular adaptation. Methods: Human umbilical vein endothelial cells (HUVECs) were exposed to laminar shear stress (6 dyn/cm2; 24 h) and analyzed by differential display (DDRT-PCR). Flow-modulation of differentially expressed genes by different exposure times (4, 24, 48 h) and in human cardiac microvascular endothelial cells (HCMECs) (24 h exposure) was analyzed by RT-PCR and northern blotting. Results: DDRT-PCR analysis displayed 13 down- and 20 up-regulated products in response to flow. Four known genes were identified: Angiopoietin-2, a protein reported to reduce vessel stability, was progressively (4–48 h) down-regulated by shear stress. The induction of the anti-angiogenic metalloproteinase METH-1 was maximal after 4 h exposure and sustained over the time (24–48 h). Growth arrest-specific mRNA 3 (gas3) and calpactin 1 light chain (p11) were up-regulated only by prolonged exposure (24–48 h). Analysis of the expression of angiopoietin-2, METH-1, gas3, and p11 in shear stress exposed (24 h) HCMECs showed modulation patterns comparable to those observed in HUVECs. Conclusion: Since angiopoietin-2 and METH-1 are known to be involved in vessel regression/stabilization, the reported modulation of these genes by prolonged shear stress exposure strongly suggests their participation in flow-dependent vascular adaptation.
Obstructive Lung Disease after Allogeneic Marrow Transplantation
Authors: Joan G. Clark
Journal: Annals of Internal Medicine (1989)

To describe the clinical presentation and progression of obstructive lung disease after marrow transplantation, we examined a sequential sample of 35 patients who had allogeneic marrow transplantation between January 1980 and January 1987, were 16 years or older, had normal pulmonary function tests before transplantation, and developed airflow obstruction defined as FEV1/FVC less than 70% and FEV1 less than 80% predicted 50 days or more after transplantation. Cases were selected from 1029 adult (older than 16 years) patients who underwent allogeneic marrow transplantation during the same period. Patients with airflow obstruction presented with symptoms of cough, dyspnea, or wheezing, or a combination. In 80% the chest radiograph was normal. Airflow obstruction was diagnosed within 1.5 years after transplantation in 33 of 35 patients. Clinical, extensive, chronic graft-versus-host disease was present in 24 patients. Only 4 patients had a complete response to primary therapy of chronic graft-versus-host disease. Serum IgG and IgA levels were decreased in 15 and 25 patients, respectively. The FEV1 declined rapidly (decrease in FEV1 > 30% between tests) in 21 patients, but 14 patients with slowly progressive or reversible disease were identified. Mortality was 65% at 3 years after transplant, a significantly higher value (P = 0.016) than the 3-year mortality rate of 44% in a comparison group of 412 concurrent patients with chronic graft-versus-host disease who were 16 years or older, survived more than 80 days after transplantation, and had normal pulmonary function. We concluded that obstructive lung disease after marrow transplantation may be variable with respect to time of onset and rate of progression. Obstructive lung disease was frequently associated with serum immunoglobulin deficiency and clinical, extensive, chronic graft-versus-host disease that was not readily responsive to treatment. Mortality was high but long-term survivors were identified.
The first description of tropical sprue
Authors: C. C. Booth
Journal: Gut (1964)

Until relatively recently the term 'intestinal malabsorption syndrome' has enshrouded our ignorance of a wide variety of disorders which may interfere with absorption. Some of these, coeliac disease for instance, were first clearly described nearly a century ago (Gee, 1888). Others, such as some of the absorption defects due to pancreatic disease, have only been recognized in the last 30 years (Anderson, 1938). The term 'sprue' has often been used as a synonym for 'intestinal malabsorption' and this has led to considerable confusion in the literature. The credit for the first description of sprue is usually given to Kaetelaer, who gave an account of what might possibly have been an adult form of coeliac disease in Holland in 1669 (Kaetelaer, 1669). The clinical syndrome which is known as tropical sprue is quite different from any of the diseases of temperate climates. Tropical sprue is a particular form of intestinal malabsorption, probably of infective origin, that occurs in tropical parts of the world. It has a very curious geographical distribution. It occurs all over the Far East, but no certain case has hitherto been described from Africa. It also occurs in the West Indian Islands of Barbados and Puerto Rica, but has never been seen in Jamaica (Manson Bahr, 1954). When it occurs it is usually endemic and liable to sporadic epidemics. The primary pathology lies in the intestinal mucosa; this shows histological abnormalities (Butterworth and Perez Santiago, 1957) which are readily recognized when biopsy material is examined under a dissecting microscope (Fig. 1). The first clear description of tropical sprue was given by Dr. William Hillary over 200 years ago, and it was in Barbados that he described it. Since this year is the 200th anniversary of Hillary's death, it seems fitting that gastroenterologists should remind themselves of the clinical description which has earned him an assured place in medical history. Hillary was not in any position to define the geographical distribution of tropical sprue, although this is implied in his statement that he had never seen it in England. But he did note its epidemic nature in Barbados. 'After I came there in 1747' he
Abstract 4512: AT rich interactive domain 3A (ARID3A) overexpression correlates with good prognosis in colorectal cancer
Authors: Meiying Song, Chang Hoon Shin, Misun Park, Hoguen Kim, Hyunki Kim
Journal: Cancer Research (2012)

Abstract AT Rich Interactive Domain 3A (ARID3A) is a member of the ARID family of DNA-binding proteins. Previous studies have shown that ARID3A controls the cell growth through p53-dependent manner, whereas its significance in the prognosis of colorectal cancer (CRC) is not yet fully understood. In this study, formalin-fixed, paraffin-embedded tumors and matched normal mucosae from 690 patients who underwent surgery for CRC were constructed into tissue microarrays. The expression of ARID3A was investigated by immunohistochemistry. We detected a nuclear positive expression of ARID3A in a subset of colorectal cancers, whereas ARID3A was completely negative in all normal mucosae. Of the 690 cases, 195 tumors (28.3%) were strong positive for ARID3A, 187 tumors (27.1%) were weak positive and 308 tumors (44.6%) were negative. We examined p53 expression status by immunohistochemistry simultaneously. Among the 690 tumors, 358 tumors (51.9%) were positive for p53 expression and 332 tumors (48.1%) were negative for p53 expression. Kaplan-Meier method and Cox proportional hazards modeling were used to analyze the overall survival between ARID3A negative or weak expression group and ARID3A strong expression group. The ARID3A expression in CRCs was significantly correlated with age (P=0.003), degree of differentiation (P&amp;lt;0.001), depth of invasion (P=0.001), lymph node metastasis (P=0.008), distant metastasis (P=0.007), TNM stage (P&amp;lt;0.001), status of microsatellite instability (P&amp;lt;0.001), and CEA levels (P=0.003). Moreover, the strong expression of ARID3A and the negativity of p53 were statistically correlated (P=0.045). The survival of CRC patients with ARID3A strong expression was significantly longer than that of patients with ARID3A negative or weak expression (P=0.002), however the effect of ARID3A on the survival rate of CRCs might differ by p53 status. Combined analysis of ARID3A and p53 expression indicated that CRC group with ARID3A-strong positive and p53-negative showed better prognosis compared with the remaining groups (P=0.003). On multivariate analysis, ARID3A overexpression was proven to be an independent predictor for better prognosis in CRC (95% CI: 0.44-0.96; P=0.031). In conclusion, this study strongly suggests the usefulness of ARID3A as a biomarker to predict the prognosis of colorectal cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4512. doi:1538-7445.AM2012-4512
The stepped wedge cluster randomised trial: rationale, design, analysis, and reporting
Authors: K. Hemming, T. P. Haines, P. J. Chilton, A. J. Girling, R. J. Lilford
Journal: BMJ (2015)

The stepped wedge cluster randomised controlled trial is a relatively new study design that is increasing in popularity.It is an alternative to parallel cluster trial designs, which are commonly used for the evaluation of service delivery or policy interventions delivered at the level of the cluster.The design includes an initial period in which no clusters are exposed to the intervention.Subsequently, at regular intervals (the "steps") one cluster (or a group of clusters) is randomised to cross from the control to the intervention under evaluation.This process continues until all clusters have crossed over to be exposed to the intervention.At the end of the study there will be a period when all clusters are exposed.Data collection continues throughout the study, so that each cluster contributes observations under both control and intervention observation periods.It is a pragmatic study design, giving great potential for robust scientific evaluations that might otherwise not be possible.
Epithelial-mesenchymal transition in cultured neonatal hepatocytes
Authors: Roser Pagan, Miquel Llobera, Senén Vilaró
Journal: Hepatology (1995)

When hepatocyte-enriched fractions from neonatal rat livers were cultured for different times in the absence of added growth factors, a population of highly proliferating and migrating fibroblastlike cells appeared. Double immunofluorescence with antibodies to cytokeratin and to vimentin showed a progressive reduction in the number of cytokeratin-positive cells parallel to an increase in the vimentin-positive cells. Some cells with transitional epithelial or migrating morphology coexpressed both intermediate filament proteins. Immunofluorescence with antibodies against hepatocyte differentiation markers showed that shortly after seeding most of the cells were positive to anti-albumin antibodies, but after 1 week in culture, only 10% were positive. Cells presenting albumin and cytokeratin appeared morphologically epithelial. Fibroblastlike cells were not positive for albumin, but some cells with transitional epithelial morphology presented some labels for albumin and for vimentin. Immunofluorescence with antibodies to glutathione-S-transferase subunit Pi and vimentin showed that many fibroblastlike cells were positive for both markers, some of them binucleate. Cultures performed in the presence of dexamethasone, absence of arginine, or on collagen type I matrix had no effect on the behavior of neonatal hepatocytes. The appearance of fibroblastlike cells was ontogenically regulated because the highest increase in the percentage of vimentin-positive cells was observed in cell cultures from livers of 7- and 15-day-old animals. These data provide evidence that neonatal hepatocytes in culture have the potential to dedifferentiate by epithelial-mesenchymal transition and contribute to an understanding of hepatic growth development.
Antifertility effects and dominant lethal assays for mutagenic effects of DEHP.
Authors: J Autian
Journal: Environmental Health Perspectives (1982)

Results of past animal studies have indicated the antifertility effects of phthalate esters and additional studies have suggested the potential mutagenic effects at very high doses. A toxicity study in mice has also been conducted in which chronic LD50 values were calculated for a group of phthalate esters. For DEHP, for example, the acute LD50 was 38.35 ml/kg, but after 10 weeks the value fell to 1.37 ml/kg, suggesting that the ester was producing a cumulative toxicity agent even at lower doses in regard to antifertility and mutagenic effects in mice. Preliminary results indicated that antifertility effects occurred with as little as three subcutaneous doses of 1 ml/kg each. Calculations of mutagenic index revealed a dose-dependent effect but no stoichiometric relationship was established.
A Political Economy of Medicine: Great Britain and the United States
Authors: Ronald Andersen
Journal: JAMA (1987)

Should physicians read this book? If you like history and are prepared to give serious consideration to the thesis that it has played a major role in what our health care system is like today or how physicians currently practice medicine —<i>AA Political Economy of Medicine</i>is worth a try. Hollingsworth assumes, with considerable justification, that a comparison of the United States and Great Britain will improve our understanding of the evolution and performance of each system. His readable medical histories of the two systems from 1890 to 1970 suggest that the medical profession in<i>both</i>countries has been more powerful in shaping medical policies and performances of the medical system than have the majority of consumers, or patients. However, consumers have been<i>relatively</i>more powerful in England and Wales, and the medical profession has been<i>relatively</i>more powerful in the United States. He argues these differences contributed to