tbuckley/cabot-search huggingface dataset:
Elder Self-neglect and Abuse and Mortality Risk in a Community-Dwelling Population
Authors: Xin Qi Dong, Melissa Simon, Carlos Mendes De Leon, Terry Fulmer, Todd Beck, Liesi Hebert, Carmel B Dyer, Gregory Paveza, Denis Evans
Journal: JAMA (2009)

Both elder self-neglect and abuse have become increasingly prominent public health issues. The association of either elder self-neglect or abuse with mortality remains unclear.To examine the relationship of elder self-neglect or abuse reported to social services agencies with all-cause mortality among a community-dwelling elderly population.Prospective, population-based cohort study (conducted from 1993 to 2005) of residents living in a geographically defined community of 3 adjacent neighborhoods in Chicago, Illinois, who were participating in the Chicago Health and Aging Project (CHAP; a longitudinal, population-based, epidemiological study of residents aged > or = 65 years). A subset of these participants had suspected elder self-neglect or abuse reported to social services agencies.Mortality ascertained during follow-up and by use of the National Death Index. Cox proportional hazard models were used to assess independent associations of self-neglect or elder abuse reporting with the risk of all-cause mortality using time-varying covariate analyses.Of 9318 CHAP participants, 1544 participants were reported for elder self-neglect and 113 participants were reported for elder abuse from 1993 to 2005. All CHAP participants were followed up for a median of 6.9 years (interquartile range, 7.4 years), during which 4306 deaths occurred. In multivariable analyses, reported elder self-neglect was associated with a significantly increased risk of 1-year mortality (hazard ratio [HR], 5.82; 95% confidence interval [CI], 5.20-6.51). Mortality risk was lower but still elevated after 1 year (HR, 1.88; 95% CI, 1.67-2.14). Reported elder abuse also was associated with significantly increased risk of overall mortality (HR, 1.39; 95% CI, 1.07-1.84). Confirmed elder self-neglect or abuse also was associated with mortality. Increased mortality risks associated with either elder self-neglect or abuse were not restricted to those with the lowest levels of cognitive or physical function.Both elder self-neglect and abuse reported to social services agencies were associated with increased risk of mortality.
Pulmonary arteriovenous fistula in a patient with renal cell carcinoma
Authors: S. Kopetz, C. Jimenez, S-M. Tu, P. Sharma
Journal: European Respiratory Journal (2007)

Arteriovenous (AV) fistulas are common in renal cell carcinoma. These are usually small and asymptomatic. Case reports have previously described symptomatic fistulas in primary renal cell tumour or, less commonly, bone metastases. The current study describes a patient with lung metastases from renal cell carcinoma who developed a symptomatic pulmonary AV fistula. The patient presented with debilitating progressive shortness of breath, which resolved after coiling of the pulmonary AV fistula. Supporting radiographs include a unique ventilation–perfusion finding of perfusion tracer in the kidney that is diagnostic of a pulmonary shunt. This is the first report of a pulmonary fistula from renal cell carcinoma. This rare complication of renal cell carcinoma reflects its diverse clinical presentations and unique tumour biology.
DERMATOLOGICAL MANIFESTATIONS OF CROHN'S DISEASE*
Authors: D. I. McCallum, P. D. C. Kinmont
Journal: British Journal of Dermatology (1968)

SUMMARY— A part from occasional case reports Crohn's disease has received little attention in the dermatological literature. Of 138 cases studied 44% were found to suffer from skin complications including abscess formation and ulceration in the peri-anal regions, groins or anterior abdominal wall. Less frequent were erythema nodosum, pyoderma gangrenosum and the skin manifestations of a malabsorption syndrome. The literature on the pathology and clinical features of Crohn's disease is briefly reviewed. The skin complications encountered are described, and their diagnostic importance is emphasized since their onset may precede any clinical manifestations of intestinal disturbance.
Therapeutic implications of tumor interstitial fluid pressure in subcutaneous RG-2 tumors
Authors: Y. Navalitloha
Journal: Neuro-Oncology (2006)

Increased interstitial fluid pressure (IFP) in brain tumors results in rapid removal of drugs from tumor extracellular space. We studied the effects of dexamethasone and hypothermia on IFP in s.c. RG-2 rat gliomas, because they could potentially be useful as means of maintaining drug concentrations in human brain tumors. We used dexamethasone, external hypothermia, combined dexamethasone and hypothermia, and infusions of room temperature saline versus chilled saline. We measured tumor IFP and efflux half-time of 14C-sucrose from tumors. In untreated s.c. tumors, IFP was 9.1 +/- 2.1 mmHg, tumor temperature was 33.7 degrees C +/- 0.7 degrees C, and efflux half-time was 7.3 +/- 0.7 min. Externally induced hypothermia decreased tumor temperature to 8.9 degrees C +/- 2.9 degrees C, tumor IFP decreased to 3.2 +/- 1.1 mmHg, and efflux half-time increased to 13.5 min. Dexamethasone decreased IFP to 2.4 +/- 1.0 mmHg and increased efflux half-time to 15.4 min. Combined hypothermia and dexamethasone further increased the efflux half-time to 17.6 min. We tried to lower the tumor temperature by chilling the infusion solution, but at an infusion rate of 48 mul/min, the efflux rate was the same for room temperature saline and 15 degrees C saline. The efflux rate was increased in both infusion groups, which suggests that efflux due to tumor IFP and that of the infusate were additive. Since lowering tumor IFP decreases efflux from brain tumors, it provides a means to increase drug residence time, which in turn increases the time-concentration exposure product of therapeutic drug available to tumor.
Cardiomyocyte-Specific Overexpression of Nitric Oxide Synthase 3 Improves Left Ventricular Performance and Reduces Compensatory Hypertrophy After Myocardial Infarction
Authors: Stefan Janssens, Peter Pokreisz, Luc Schoonjans, Marijke Pellens, Pieter Vermeersch, Marc Tjwa, Peter Jans, Marielle Scherrer-Crosbie, Michael H. Picard, Zsolt Szelid, Hilde Gillijns, Frans Van de Werf, Desire Collen, Kenneth D. Bloch
Journal: Circulation Research (2004)

Nitric oxide (NO) is an important modulator of cardiac performance and left ventricular (LV) remodeling after myocardial infarction (MI). We tested the effect of cardiomyocyte-restricted overexpression of one NO synthase isoform, NOS3, on LV remodeling after MI in mice. LV structure and function before and after permanent LAD coronary artery ligation were compared in transgenic mice with cardiomyocyte-restricted NOS3 overexpression (NOS3-TG) and their wild-type littermates (WT). Before MI, systemic hemodynamic measurements, echocardiographic assessment of LV fractional shortening (FS), heart weight, and myocyte width (as assessed histologically) did not differ in NOS3-TG and WT mice. The inotropic response to graded doses of isoproterenol was significantly reduced in NOS3-TG mice. One week after LAD ligation, the infarcted fraction of the LV did not differ in WT and NOS3-TG mice (34±4% versus 36±12%, respectively). Four weeks after MI, however, end-systolic LVID was greater, and fractional shortening and maximum and minimum rates of LV pressure development were less in WT than in NOS3-TG mice. LV weight/body weight ratio was greater in WT than in NOS3-TG mice (5.3±0.2 versus 4.6±0.5 mg/g; P &lt;0.01). Myocyte width in noninfarcted myocardium was greater in WT than in NOS3-TG mice (18.8±2.0 versus 16.6±1.6 μm; P &lt;0.05), whereas fibrosis in noninfarcted myocardium was similar in both genotypes. Cardiomyocyte-restricted overexpression of NOS3 limits LV dysfunction and remodeling after MI, in part by decreasing myocyte hypertrophy in noninfarcted myocardium.
Cockroach allergen (Bla g 1) in school dust
Authors: Sampson B. Sarpong, Robert A. Wood, Theodore Karrison, Peyton A. Eggleston
Journal: Journal of Allergy and Clinical Immunology (1997)

Background: Cockroach allergen, Bla g 1, is an important indoor allergen. Although household exposure has been documented, little is known about the potential for exposure outside the home. Objective: We investigated the settled dust concentration of Bla g 1 in 147 samples collected from classrooms, kitchens, cafeterias, and other sites in four primary schools in the city of Baltimore. Methods: School authorities were questioned about characteristics of schools, teachers, and students, as well as cockroach control and cleaning procedures. Settled dust samples were collected with a hand-held vacuum cleaner from the floors of all classrooms, food-related areas, and other sites of the schools over a 3-week period. A sample collection in each school took 1 to 2 days. Dust samples from each room were pooled and analyzed as a single sample for Bla g 1 by using a two-site monoclonal ELISA. Results: One hundred two (69%) of the 147 samples had detectable Bla g 1 and were within the range reported by other investigators in inner city homes. There was no difference between the median levels of Bla g 1 in three schools: school 1 (5.2 U/gm), school 2 (3.0 U/gm), and school 4 (2.7 U/gm); but school 3 had a significantly lower level (<0.8 U/gm, p < 0.001). The median level from the food-related areas was significantly higher than the median classroom level (p = 0.048). School 3 had fewer students on subsidized lunch, fewer African-American students, and fewer students per teacher. Bla g 1 levels were compared in the different schools while controlling for potential confounding variables by a stepwise multiple regression analysis with a logit model for ordinal responses. On the basis of this analysis, Bla g 1 levels in schools 1, 2, and 4 differed significantly from levels in school 3 (p < 0.001 in each case). Food-related areas had significantly higher levels than classrooms (p = 0.048). Floor level, the presence of a sink, and the presence of carpeting did not have significant effects. Conclusions: We conclude that Bla g 1 is detectable at potentially significant concentrations in some inner city schools. Furthermore, the level of exposure is different between different schools and between sites within individual schools. (J Allergy Clin Immunol 1997;99:486-90.)
Persistence of the fetal pattern of tropoelastin gene expression in severe neonatal bovine pulmonary hypertension.
Authors: K R Stenmark, A G Durmowicz, J D Roby, R P Mecham, W C Parks
Journal: Journal of Clinical Investigation (1994)

Neonatal hypoxic pulmonary hypertension causes increases and spatial changes in tropoelastin expression in pulmonary arteries. However, it is not clear if this is due to recruitment of quiescent smooth muscle cells (SMC) into an elastin-producing phenotype or persistence of the fetal pattern of tropoelastin gene expression. We evaluated the distribution and relative concentration of tropoelastin mRNA in intralobar pulmonary arteries from late gestation fetuses and in animals exposed to hypobaric hypoxia (430 mmHg) from birth for 1, 3, 7, or 14 d, as well as in age-matched and adult room air-breathing controls. In situ hybridization demonstrated that tropoelastin mRNA was distributed throughout the entire radius of the pulmonary vessel wall in the fetus and newborn calf. By 15 d of age, only cells in the inner third of the media expressed tropoelastin mRNA, and by adulthood no tropoelastin mRNA was detected in the vessel wall. These findings demonstrated that tropoelastin expression shuts off in a spatially specific pattern, moving from the abluminal to the luminal side of the medial in the neonatal pulmonary artery when pressures and resistance are falling. In the aorta of 15-d-old calves, tropoelastin mRNA expression was seen equally throughout the media, indicating tissue-specific regulation of elastin in the neonatal period. In contrast, intralobar pulmonary arteries from calves exposed to hypoxia, which prevented the normal postnatal decline in pulmonary artery pressure, maintained the fetal pattern and levels of tropoelastin mRNA expression at all time points. Thus, rather than causing a recruitment of SMC into an elastin-producing phenotype, neonatal pulmonary hypertension caused a persistence of the fetal pattern of tropoelastin expression in medial SMC. Cell-free translation showed that the same tropoelastin isoforms were made by mRNA from control and hypertensive calves and, unlike the ligamentum nuchae, did not change during the transition from fetal to neonatal life. We conclude that pulmonary hypertension in the neonate perturbs the normal postpartum repression of tropoelastin expression resulting in a persistence of the fetal spacial and isoform patterns of tropoelastin gene expression.
Determinants of Maternal Triglycerides in Women With Gestational Diabetes Mellitus in the Metformin in Gestational Diabetes (MiG) Study
Authors: Helen L. Barrett, Marloes Dekker Nitert, Lee Jones, Peter O’Rourke, Karin Lust, Kathryn L. Gatford, Miles J. De Blasio, Suzette Coat, Julie A. Owens, William M. Hague, H. David McIntyre, Leonie Callaway, Janet Rowan
Journal: Diabetes Care (2013)

Factors associated with increasing maternal triglyceride concentrations in late pregnancy include gestational age, obesity, preeclampsia, and altered glucose metabolism. In a subgroup of women in the Metformin in Gestational Diabetes (MiG) trial, maternal plasma triglycerides increased more between enrollment (30 weeks) and 36 weeks in those treated with metformin compared with insulin. The aim of this study was to explain this finding by examining factors potentially related to triglycerides in these women.Of the 733 women randomized to metformin or insulin in the MiG trial, 432 (219 metformin and 213 insulin) had fasting plasma triglycerides measured at enrollment and at 36 weeks. Factors associated with maternal triglycerides were assessed using general linear modeling.Mean plasma triglyceride concentrations were 2.43 (95% CI 2.35-2.51) mmol/L at enrollment. Triglycerides were higher at 36 weeks in women randomized to metformin (2.94 [2.80-3.08] mmol/L; +23.13% [18.72-27.53%]) than insulin (2.65 [2.54-2.77] mmol/L, P = 0.002; +14.36% [10.91-17.82%], P = 0.002). At 36 weeks, triglycerides were associated with HbA1c (P = 0.03), ethnicity (P = 0.001), and treatment allocation (P = 0.005). In insulin-treated women, 36-week triglycerides were associated with 36-week HbA1c (P = 0.02), and in metformin-treated women, they were related to ethnicity.At 36 weeks, maternal triglycerides were related to glucose control in women treated with insulin and ethnicity in women treated with metformin. Whether there are ethnicity-related dietary changes or differences in metformin response that alter the relationship between glucose control and triglycerides requires further study.
The case of visceral fat: argument for the defense
Authors: Samuel Klein
Journal: Journal of Clinical Investigation (2004)

Increased plasma fatty acid concentrations may be responsible for many of the metabolic abnormalities associated with abdominal obesity. Excessive visceral fat is associated with insulin resistance and other metabolic risk factors for coronary heart disease. A study reported in this issue of the JCI evaluates the relative contribution of fatty acids released during lipolysis of visceral adipose tissue triglycerides to portal and systemic fatty acid flux in human subjects.
First-cycle rash and survival in patients with advanced non-small-cell lung cancer receiving cetuximab in combination with first-line chemotherapy: a subgroup analysis of data from the FLEX phase 3 study
Authors: Ulrich Gatzemeier, Joachim von Pawel, Ihor Vynnychenko, Petr Zatloukal, Filippo de Marinis, Wilfried EE Eberhardt, Luis Paz-Ares, Karl-Maria Schumacher, Thomas Goddemeier, Kenneth J O'Byrne, Robert Pirker
Journal: The Lancet Oncology (2010)
PERIOD OF INFECTIVITY OF PATIENTS WITH HOMOLOGOUS SERUM JAUNDICE AND ROUTES OF INFECTION IN THIS DISEASE
Authors: W. Paul Havens
Journal: The Journal of Experimental Medicine (1946)

1. Pooled specimens of serum obtained from 3 human volunteers three-fourths through their respective 56, 66, and 70 day incubation periods of homologous serum jaundice produced the disease in 1 out of 4 human volunteers following parenteral inoculation. 2. Serum specimens obtained from these same 3 patients during the acute, pre-icteric phase of their homologous serum jaundice produced the disease in 3 out of 4 human volunteers following parenteral inoculation. 3. These same sera, proven to be infectious by parenteral inoculation, failed to produce disease when ingested by 10 other human volunteers. 4. Pooled specimens of serum obtained in the convalescent phase (28 to 32 days after onset) of these 3 patients failed to produce apparent infection when inoculated parenterally into 5 human volunteers. 5. Pooled specimens of feces of 3 patients obtained in the acute phase of homologous serum jaundice, when virus was proven to be in the serum, were not demonstrably infectious when fed to 6 volunteers. 6. These findings are slightly different from those encountered in a similar study with infectious material from cases of infectious hepatitis.
The Role of BRCA1 in the Cellular Response to Chemotherapy
Authors: R. D. Kennedy, J. E. Quinn, P. B. Mullan, P. G. Johnston, D. P. Harkin
Journal: JNCI Journal of the National Cancer Institute (2004)

Germline mutations of the BRCA1 gene account for approximately 5% of breast and ovarian cancer cases, and lower than normal BRCA1 expression or function may be an important contributing factor in sporadic cancers. The major role of BRCA1 is to respond to DNA damage by participating in cellular pathways for DNA repair, mRNA transcription, cell cycle regulation, and protein ubiquitination. Because most chemotherapeutic agents function by directly or indirectly damaging DNA, the role of BRCA1 as a regulator of chemotherapy-induced DNA damage has been the subject of an increasing number of investigations. We review published preclinical and clinical evidence that the level of BRCA1 function in an individual patient's tumor can guide the choice of chemotherapeutic agents for breast and ovarian cancer. We conclude that a loss of BRCA1 function is associated with sensitivity to DNA-damaging chemotherapy and may also be associated with resistance to spindle poisons. We recommend that prospective clinical studies investigating the role of BRCA1 in the response to chemotherapy be conducted.
Therapeutic Targeting of Autophagy
Authors: Amabel M. Orogo, Åsa B. Gustafsson
Journal: Circulation Research (2015)

Autophagy is an evolutionarily conserved process by which long-lived proteins and organelles are sequestered by autophagosomes and subsequently degraded by lysosomes for recycling. Autophagy is important for maintaining cardiac homeostasis and is a survival mechanism that is upregulated during stress or starvation. Accumulating evidence suggests that dysregulated or reduced autophagy is associated with heart failure and aging. Thus, modulating autophagy represents an attractive future therapeutic target for treating cardiovascular disease. Activation of autophagy is generally considered to be cardioprotective, whereas excessive autophagy can lead to cell death and cardiac atrophy. It is important to understand how autophagy is regulated to identify ideal therapeutic targets for treating disease. Here, we discuss the key proteins in the core autophagy machinery and describe upstream regulators that respond to extracellular and intracellular signals to tightly coordinate autophagic activity. We review various genetic and pharmacological studies that demonstrate the important role of autophagy in the heart and consider the advantages and limitations of approaches that modulate autophagy.
An angiogenic role for the human peptide antibiotic LL-37/hCAP-18
Authors: Rembert Koczulla, Georges von Degenfeld, Christian Kupatt, Florian Krötz, Stefan Zahler, Torsten Gloe, Katja Issbrücker, Pia Unterberger, Mohamed Zaiou, Corinna Lebherz, Alexander Karl, Philip Raake, Achim Pfosser, Peter Boekstegers, Ulrich Welsch, Pieter S. Hiemstra, Claus Vogelmeier, Richard L. Gallo, Matthias Clauss, Robert Bals
Journal: Journal of Clinical Investigation (2003)

Antimicrobial peptides are effector molecules of the innate immune system and contribute to host defense and regulation of inflammation. The human cathelicidin antimicrobial peptide LL-37/hCAP-18 is expressed in leukocytes and epithelial cells and secreted into wound and airway surface fluid. Here we show that LL-37 induces angiogenesis mediated by formyl peptide receptor–like 1 expressed on endothelial cells. Application of LL-37 resulted in neovascularization in the chorioallantoic membrane assay and in a rabbit model of hind-limb ischemia. The peptide directly activates endothelial cells, resulting in increased proliferation and formation of vessel-like structures in cultivated endothelial cells. Decreased vascularization during wound repair in mice deficient for CRAMP, the murine homologue of LL-37/hCAP-18, shows that cathelicidin-mediated angiogenesis is important for cutaneous wound neovascularization in vivo. Taken together, these findings demonstrate that LL-37/hCAP-18 is a multifunctional antimicrobial peptide with a central role in innate immunity by linking host defense and inflammation with angiogenesis and arteriogenesis.
Dominant Expression of Multiple Drug Resistance After In Vitro X-irradiation Exposure in Intraspecific Chinese Hamster Ovary Hybrid Cells
Authors: S. McClean, L. K. Hosking, B. T. Hill
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Dominant Expression of Multiple Drug Resistance After In Vitro X-irradiation Exposure in Intraspecific Chinese Hamster Ovary Hybrid Cells Get access Siobhán McClean, Siobhán McClean Laboratory of Cellular Chemotherapy, Imperial Cancer Research FundLondon, England Search for other works by this author on: Oxford Academic PubMed Google Scholar Louise K. Hosking, Louise K. Hosking Laboratory of Cellular Chemotherapy, Imperial Cancer Research FundLondon, England Search for other works by this author on: Oxford Academic PubMed Google Scholar Bridget T. Hill Bridget T. Hill Laboratory of Cellular Chemotherapy, Imperial Cancer Research FundLondon, England Correspondence to : Bridget T. Hill, Ph.D., Laboratory of Cellular Chemotherapy, Imperial Cancer Research Fund, 44, Lincoln's Inn Fields, London WC2A 3PX, England. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 1, 6 January 1993, Pages 48–53, https://doi.org/10.1093/jnci/85.1.48 Published: 06 January 1993 Article history Received: 29 April 1992 Revision received: 17 September 1992 Accepted: 02 October 1992 Published: 06 January 1993