tbuckley/cabot-search huggingface dataset:
Efficacy and Safety of Atorvastatin in the Prevention of Cardiovascular End Points in Subjects With Type 2 Diabetes
Authors: Robert H. Knopp, Michael d’Emden, Johan G. Smilde, Stuart J. Pocock
Journal: Diabetes Care (2006)

Cardiovascular disease (CVD) risk is increased in type 2 diabetes. The purpose of this study was to assess the effect of 10 mg of atorvastatin versus placebo on CVD prevention in subjects with type 2 diabetes and LDL cholesterol levels below contemporary guideline targets.Subjects were randomly assigned to receive 10 mg of atorvastatin or placebo in a 4-year, double-blind, parallel-group study. The composite primary end point comprised cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, recanalization, coronary artery bypass surgery, resuscitated cardiac arrest, and worsening or unstable angina requiring hospitalization.A total of 2,410 subjects with type 2 diabetes were randomized. Mean LDL cholesterol reduction in the atorvastatin group over 4 years was 29% versus placebo (P < 0.0001). When we compared atorvastatin versus placebo, composite primary end point rates were 13.7 and 15.0%, respectively (hazard ratio 0.90 [95% CI 0.73-1.12]). In the subset of 1,905 subjects without prior myocardial infarction or interventional procedure, 10.4% of atorvastatin- and 10.8% of placebo-treated subjects experienced a primary end point (0.97 [0.74-1.28]). In the 505 subjects with prior myocardial infarction or interventional procedure, 26.2% of atorvastatin- and 30.8% of placebo-treated subjects experienced a primary end point (0.82 [0.59-1.15]). Relative risk reductions in fatal and nonfatal myocardial infarction were 27% overall (P = 0.10) and 19% (P = 0.41) and 36% (P = 0.11) for subjects without and with prior myocardial infarction or interventional procedure, respectively.Composite end point reductions were not statistically significant. This result may relate to the overall study design, the types of subjects recruited, the nature of the primary end point, and the protocol changes required because of changing treatment guidelines. For these reasons, the results of the Atorvastatin Study for Prevention of Coronary Heart Disease Endpoints in Non-Insulin-Dependent Diabetes Mellitus (ASPEN) did not confirm the benefit of therapy but do not detract from the imperative that the majority of diabetic patients are at risk of coronary heart disease and deserve LDL cholesterol lowering to the currently recommended targets.
Citrate in oral rehydration therapy
Authors: D D K Rolston, M J G Farthing, M L Clark, A M Dawson
Journal: Gut (1985)

Citrate in oral rehydration therapy SIR,-We read with interest the recent paper by Islam et al (Gut 1984; 25: 900-4).We would like to point out that 2-94 g/l of the tribasic salt of sodium citrate (the amount used by these workers) would result in a 10 mmol/l citrate solution and not a 30 mmol/l citrate solution.The latter would require 8&82 g/l of the tribasic salt.One must, therefore, conclude from their study that a 10 mmol/l citrate based oral rehydration solution (and not a 30 mmol/l citrate based solution) is as effective as a WHO oral rehydration solution (which contains 30 mmol/l bicarbonate) in correcting the acidosis and dehydration in their patients.
Reversal of Angiogenesis In Vitro, Induction of Apoptosis, and Inhibition of Akt Phosphorylation in Endothelial Cells by Thromboxane A <sub>2</sub>
Authors: Yunling Gao, Ryoji Yokota, Shaoqing Tang, Anthony W. Ashton, J. Anthony Ware
Journal: Circulation Research (2000)

Thromboxane A(2) (TxA(2)) causes platelet aggregation, vasoconstriction, and inhibition of endothelial cell (EC) migration and prevents vascular tube formation via its specific receptors (TP), of which there are two isoforms (TPalpha and TPbeta), both expressed in human ECs. In this study, we demonstrate that the TxA(2) mimetic IBOP increases apoptosis of human ECs and inhibits the phosphorylation of Akt kinase, an intracellular mediator required for cell survival. Treatment with IBOP destroyed EC networks formed on a basement membrane matrix in vitro. To distinguish the role of the TP isoforms, each isoform was expressed in TP-null ECs to create TPalpha and TPbeta ECs. IBOP induced apoptosis and inhibited phosphorylation of Akt kinase in both TPalpha and TPbeta. IBOP increased cAMP levels in TPalpha but not in TPbeta. Apoptosis induced by IBOP in TPalpha was not affected by either the adenylyl cyclase activator forskolin or the protein kinase A inhibitor 14-22 amide or H-89, whereas that in TPbeta was suppressed by forskolin and enhanced by the protein kinase A inhibitor 14-22 amide or H-89, suggesting that the TP isoforms differ in their signal pathways in mediating apoptosis. In conclusion, apoptosis may be the mechanism by which TxA(2)-mediated destruction of vascular structures in ECs occurs; although both TP isoforms induce apoptosis, possibly via inhibiting Akt phosphorylation, the signaling differs in each isoform, in that activation of the adenylyl cyclase pathway prevents apoptosis caused by TPbeta, but not by TPalpha, stimulation.
(24) Lichen sclerosus et atrophicus treated with cryotherapy
Authors: R.H. Meyrick Thomas, J.D.T. Kirby
Journal: British Journal of Dermatology (1985)

Journal Article (24) Lichen sclerosus et atrophicus treated with cryotherapy Get access R.H. Meyrick Thomas, R.H. Meyrick Thomas St Bartholomew's Hospital, London EC1 Search for other works by this author on: Oxford Academic Google Scholar J.D.T. Kirby J.D.T. Kirby St Bartholomew's Hospital, London EC1 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 113, Issue s29, 1 July 1985, Pages 67–68, https://doi.org/10.1111/j.1365-2133.1985.tb13039.x Published: 01 July 1985
Component-resolved diagnosis of wheat flour allergy in baker's asthma
Authors: Cristina Gómez-Casado, María Garrido-Arandia, Catia Pereira, Manuela Catarino, Víctor Parro, Alicia Armentia, Santiago Quirce, Blanca Armentia, Paloma Barranco, Miguel Blanca, Paloma Campo, Araceli Díaz-Perales
Journal: Journal of Allergy and Clinical Immunology (2014)
A phase II study of sorafenib in patients with chemo-naive castration-resistant prostate cancer
Authors: K.N. Chi, S.L. Ellard, S.J. Hotte, P. Czaykowski, M. Moore, J.D. Ruether, A.J. Schell, S. Taylor, C. Hansen, I. Gauthier, W. Walsh, L. Seymour
Journal: Annals of Oncology (2007)
Peritoneal Transport Characteristics with Glucose Polymer–Based Dialysis Fluid in Children
Authors: Esther Rusthoven, Raymond T. Krediet, Hans L. Willems, Leo A.H. Monnens, Cornelis H. Schro[Combining Diaeresis]der
Journal: Journal of the American Society of Nephrology (2004)

Scarce data are available on the use of glucose polymer-based dialysate in children. The effects of glucose polymer-based dialysate on peritoneal fluid kinetics and solute transport were studied in pediatric patients who were on chronic peritoneal dialysis, and a comparison was made with previously published results in adult patients. In nine children, two peritoneal equilibration tests were performed using 3.86% glucose and 7.5% icodextrin as a test solution. Dextran 70 was added as a volume marker to calculate fluid kinetics. Serum and dialysate samples were taken for determination of urea, creatinine, and sodium. After calculation of the initial transcapillary ultrafiltration (TCUF) rate, it was possible to calculate the contribution of aquaporin-mediated (AQP-mediated) water transport to ultrafiltration for icodextrin and 3.86% glucose and the part of L(p)S (the product of the peritoneal surface area and the hydraulic permeability) caused by AQP. In children, the transport parameters were similar for the two solutions, except for TCUF, which was lower for icodextrin (0.9 ml/min per 1.73 m(2)) as compared with 3.86% glucose (4 ml/min per 1.73 m(2)). Transport parameters were similar in children and adults for glucose, but with icodextrin, TCUF and marker clearance were significantly lower in children. AQP-mediated water flow was 83 versus 50% with glucose (child versus adult; P < 0.01) and 18 versus 7% with icodextrin (P < 0.01). Data indicate that transport parameters in children using icodextrin are similar to glucose except for TCUF. Differences are explained by the absence of crystalloid osmosis and that TCUF was determined after a 4-h dwell. Comparison of transport parameters and peritoneal membrane characteristics between children and adults reveal that there seem to be differences in the amount and functionality of AQP. However, there are no differences in clinical efficacy of this transport pathway because the absolute flow through the AQP is identical in both groups using 3.86% glucose.
Acute hand and wrist injuries in experienced rock climbers
Authors: A J Logan, N Makwana, G Mason, J Dias
Journal: British Journal of Sports Medicine (2004)

The sport of rock climbing has its own spectrum of injuries, almost half of which involve the wrist and hand.To examine the incidence of acute wrist and hand injuries in 545 members of The Climbers' Club of Great Britain.A total of 1100 questionnaires were sent to current members of The Climbers' Club of Great Britain for them to detail any hand and wrist injuries sustained to date. In decade years, the climbing grades and time spent climbing at each grade were determined. From these results a total and historic climbing intensity score for each climber could be calculated.Half of the questionnaires were returned complete. The respondents were almost entirely male. There were 235 wrist and hand injuries in 155 climbers (28%). The climbing intensity scores were significantly higher in the injury group than in those who had not suffered a wrist or hand injury (p<0.05). Finger tendon injuries were the most common injury, followed by abrasions/lacerations and fractures.The most common injuries found in rock climbing involve the wrist and hand. The predominant injury to the hand involves the finger tendons or pulleys. The greater the climbing intensity calculated over a climber's career, the greater the likelihood of sustaining these injuries.
Notch1 Expression Predicts an Unfavorable Prognosis and Serves as a Therapeutic Target of Patients with Neuroblastoma
Authors: Hsiu-Hao Chang, Hsinyu Lee, Ming-Kuan Hu, Po-Nien Tsao, Hsueh-Fen Juan, Min-Chuan Huang, Yu-Yin Shih, Bo-Jeng Wang, Yung-Ming Jeng, Christina Ling Chang, Shiu-Feng Huang, Yeou-Guang Tsay, Fon-Jou Hsieh, Kai-Hsin Lin, Wen-Ming Hsu, Yung-Feng Liao
Journal: Clinical Cancer Research (2010)

Notch signaling has been implicated to play a critical role in the tumorigenesis of neuroblastoma (NB) and can modulate calreticulin (CRT) expression that strongly correlates with tumor differentiation and favorable prognosis of NB. We thus sought to determine how Notch regulates CRT expression and affects NB tumor behavior.The Notch-dependent regulation of CRT expression in cultured NB cells was analyzed by confocal microscopy and Western blotting. Notch1 protein expression in 85 NB tumors was examined by immunohistochemistry and correlated with the clinicopathologic/biological characters of NB patients. The progression of NB tumors in response to attenuated Notch signaling was examined by using a xenograft mouse model.We showed that CRT is essential for the neuronal differentiation of NB cells elicited by inhibition of Notch signaling. This effect was mediated by a c-Jun-NH(2)-kinase-dependent pathway. Furthermore, NB tumors with elevated Notch1 protein expression were strongly correlated with advanced tumor stages, MYCN amplification, an undifferentiated histology, as well as a low CRT expression level. Most importantly, the opposing effect between Notch1 and CRT could reciprocally affect the survival of NB patients. The administration of a gamma-secretase inhibitor into a xenograft mouse model of NB significantly suppressed the tumor progression.Our findings provide the first evidence that a c-Jun-NH(2)-kinase-CRT-dependent pathway is essential for the neuronal differentiation elicited by Notch signaling blockade and that Notch1 and CRT can synergistically predict the clinical outcomes of NB patients. The present data suggest that Notch signaling could be a therapeutic target for NB.
Changes in the Incidence and Duration of Periods without Insurance
Authors: David M Cutler, Alexander M Gelber
Journal: New England Journal of Medicine (2009)

Policymakers have recently proposed ways of providing health care coverage for an increased number of uninsured persons. However, there are few data that show how the incidence and duration of periods in which persons do not have insurance have changed over time.We used two data sets from the Survey of Income and Program Participation of the U.S. Census Bureau: one that covered the period from 1983 through 1986 (25,946 persons), and another that covered the period from 2001 through 2004 (40,282 persons). For each set of years, we estimated the probability that a person would be uninsured for some period of time and the probability that a person would subsequently obtain private or public insurance. We also estimated the probabilities that persons in various demographic groups would become uninsured over the course of a year and would remain uninsured for various amounts of time.The percentage of the population that lost insurance in a 12-month period increased from 19.8% in 1983-1986 to 21.8% in 2001-2004 (P=0.04). The percentage that was uninsured for a period of time increased markedly among persons with the lowest educational level and predominantly represented loss of private coverage. The percentage of new uninsured periods that ended within 24 months increased from 73.8% to 79.7% between the two study periods (P<0.001); increases were seen in all age groups and among persons of all educational levels. Transition from no insurance to private insurance decreased from 65.2% to 59.2% (P<0.001). Transition from no insurance to public insurance increased from 8.7% to 20.4% (P<0.001).As compared with the years from 1983 through 1986, from 2001 through 2004, more people, particularly those with the lowest educational level, had periods in which they were not insured. The periods without insurance were shorter in 2001-2004 than they were in 1983-1986, since an increase in transitions to public coverage offset a reduction in transitions to private coverage. Our results portend difficulties if private coverage continues to decline and is not offset by further expansions of public insurance.
Crush injuries of the chest: A follow-up study of patients treated in an artificial ventilation unit
Authors: I. A. Davidson, W. Bargh, A. N. Cruickshank, W. H. Duthie
Journal: Thorax (1969)

Fifty-four patients previously treated for a severe chest injury in an artificial ventilation unit have been followed up. An attempt has been made to determine their state of health and activity. Particular attention has been paid to their respiratory function. The significance of the findings has been discussed.
Risk of Coronary Artery Disease Associated With Polymorphism of the Cytochrome P450 Epoxygenase CYP2J2
Authors: Martin Spiecker, Harald Darius, Thomas Hankeln, Muhidien Soufi, Alexander M. Sattler, Jürgen R. Schaefer, Koichi Node, Jan Börgel, Andreas Mügge, Klaus Lindpaintner, Anika Huesing, Bernhard Maisch, Darryl C. Zeldin, James K. Liao
Journal: Circulation (2004)

Cytochrome P450 (CYP) 2J2 is expressed in the vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs). The EETs are potent endogenous vasodilators and inhibitors of vascular inflammation. However, it is not known whether genetic polymorphisms of CYP2J2 are associated with increased cardiovascular risks.All 9 exons of the CYP2J2 gene and its proximal promoter were sequenced in 132 patients to identify potential variants. Functional consequence of a single nucleotide polymorphism (SNP) in the promoter of CYP2J2 was further evaluated by use of transcription factor-binding and reporter assays. A total of 17 polymorphisms were identified. One of the most relevant polymorphisms in terms of frequency and functional importance is located at -50 (G-50T) in the proximal promoter of CYP2J2. Screening of 289 patients with coronary artery disease and 255 control subjects revealed 77 individuals with the G-50T SNP (17.3% of coronary artery disease patients, 10.6% of control subjects; P=0.026). The association of the G-50T polymorphism remained significant after adjustment for age, gender, and conventional cardiovascular risk factors (OR, 2.23; 95% CI, 1.04 to 4.79). The G-50T mutation resulted in the loss of binding of the Sp1 transcription factor to the CYP2J2 promoter and resulted in a 48.1+/-2.4% decrease in CYP2J2 promoter activity (P<0.01). Plasma concentrations of stable EET metabolites were significantly lower in individuals with the G-50T SNP.A functionally relevant polymorphism of the CYP2J2 gene is independently associated with an increased risk of coronary artery disease.
Jejunal microvilli atrophy and reduced sugar transport in rats with advanced liver cirrhosis: improvement by insulin-like growth factor (IGF-I)
Authors: I. Castilla-Cortázar, M. Pascual, E. Urdaneta, M. García, J. Trigueros, J. Quiroga, J. Prieto, S. Santidrián
Journal: Journal of Hepatology (1998)
MOLECULAR ASPECTS OF ALCOHOL METABOLISM: Transcription Factors Involved in Early Ethanol-Induced Liver Injury
Authors: Laura E. Nagy
Journal: Annual Review of Nutrition (2004)

Alcohol metabolism takes place primarily in the liver. Initial exposures to ethanol have a major impact on the hepatic redox state and intermediary metabolism as a consequence of ethanol metabolism via alcohol dehydrogenase. However, upon continued exposure to ethanol, the progression of liver injury involves ethanol metabolism via CYP2E1 and consequent oxidant stress, as well as potential direct effects of ethanol on membrane proteins that are independent of ethanol metabolism. Multiple organ systems contribute to liver injury, including the innate immune system and adipose tissue. In response to ethanol exposure, specific signal transduction pathways, including NFkappaB and the mitogen-activated protein kinase family members ERK1/2, JNK, and p38, are activated. These complex responses to ethanol exposure translate into activation of nuclear transcription factors and altered gene expression within the liver, leading to the development of steatosis and inflammation in the early stages of alcohol-induced liver injury.
Combination of Peritubular C4d and Transplant Glomerulopathy Predicts Late Renal Allograft Failure
Authors: Niamh Kieran, Xiaotong Wang, James Perkins, Connie Davis, Elizabeth Kendrick, Ramaswamy Bakthavatsalam, Nancy Dunbar, Paul Warner, Karen Nelson, Kelly D. Smith, Roberto F. Nicosia, Charles E. Alpers, Nicolae Leca, Jolanta Kowalewska
Journal: Journal of the American Society of Nephrology (2009)

The histologic associations and clinical implications of peritubular capillary C4d staining from long-term renal allografts are unknown. We identified 99 renal transplant patients who underwent an allograft biopsy for renal dysfunction at least 10 yr after transplantation, 25 of whom were C4d-positive and 74 of whom were C4d-negative. The average time of the index biopsy from transplantation was 14 yr in both groups. Compared with C4d-negative patients, C4d-positive patients were younger at transplantation (29 +/- 13 versus 38 +/- 12 yr; P < 0.05) and were more likely to have received an allograft from a living donor (65 versus 35%; P < 0.001). C4d-positive patients had more inflammation, were more likely to have transplant glomerulopathy, and had worse graft outcome. The combined presence of C4d positivity, transplant glomerulopathy, and serum creatinine of >2.3 mg/dl at biopsy were very strong predictors of rapid graft loss. C4d alone did not independently predict graft loss. Retrospective staining of historical samples from C4d-positive patients demonstrated C4d deposition in the majority of cases. In summary, these data show that in long-term renal allografts, peritubular capillary staining for C4d occurs in approximately 25% of biopsies, can persist for many years after transplantation, and strongly predicts graft loss when combined with transplant glomerulopathy.
The Mammary Progenitor Marker CD61/β3 Integrin Identifies Cancer Stem Cells in Mouse Models of Mammary Tumorigenesis
Authors: François Vaillant, Marie-Liesse Asselin-Labat, Mark Shackleton, Natasha C. Forrest, Geoffrey J. Lindeman, Jane E. Visvader
Journal: Cancer Research (2008)

The cells of origin and mechanisms that underpin tumor heterogeneity in breast cancer are poorly understood. Here, we have examined three mouse models of mammary tumorigenesis (MMTV-wnt-1, MMTV-neu, and p53(+/-)) for changes in their epithelial cell hierarchy during the preneoplastic and neoplastic stages of tumor progression. In preneoplastic tissue, only MMTV-wnt-1 mice showed a perturbation in their epithelial subpopulations. In addition to an expanded mammary stem cell pool, repopulating cells capable of yielding extensive mammary outgrowths in vivo were revealed in the committed luminal progenitor population. These findings indicate that wnt-1 activation induces the appearance of aberrant progenitor cells, and suggest that both mammary stem and progenitor cells can serve as the cellular targets of wnt-1-induced tumorigenesis. In tumors arising in MMTV-wnt-1 tumors, the luminal epithelial progenitor marker CD61/beta3 integrin identified a cancer stem cell (CSC) population that was highly enriched for tumorigenic capability relative to the CD61(-) subset. CD61 expression also defined a CSC subset in 50% of p53(+/-)-derived tumors. No CSCs, however, could be identified in the more homogeneous MMTV-neu/erbB2 model, suggesting an alternative model of tumorigenesis. Overall, our findings show the utility of the progenitor marker CD61 in the identification of CSCs that sustain specific mammary tumors.
High HIV prevalence in male patients with acute hepatitis A in the Rome metropolitan area, Italy 2002–2008
Authors: Enrico Girardi, Paola Scognamiglio, Maria Rosaria Sciarrone, Mariarosaria Loffredo, Claudio Gnesivo, Pasquale Noto, Giorgio Antonucci, Maria Rosaria Capobianchi, Giuseppe Ippolito
Journal: Journal of Hepatology (2010)
Mechanical ventilation aggravates transfusion-related acute lung injury induced by MHC-I class antibodies
Authors: A. P. J. Vlaar, E. K. Wolthuis, J. J. Hofstra, J. J. T. H. Roelofs, L. Boon, M. J. Schultz, R. Lutter, N. P. Juffermans
Journal: Intensive Care Medicine (2010)