tbuckley/cabot-search huggingface dataset:
Structural Aspects of Bile Salt-Lecithin Mixed Micelles
Authors: Karl Müller
Journal: Hepatology (1984)

Mixed micells formed by the major constituents of native bile, i.e., bile salts and lecithin, were studied by X-ray scattering differential scanning calorimetry and electron spin resonance spectroscopy. The aim of this study was to find differences in micellar structure and thermodynamic properties which might explain the different abilities of various biles to keep cholesterol in solution at comparable degrees of oversaturation. The data indicate not only that different types of micelles exist but also that different types of complex bile salt/phospholipid arrangements exist within the micelles. It is speculated that the stabilizing and destabilizing factors found by other authors influence the balance between the different micellar structures and thereby the cholesterol solubilization power of bile.
Epithelial surfaces of the trachea and principal bronchi in the rat.
Authors: I Alexander, B C Ritchie, J E Maloney, C R Hunter
Journal: Thorax (1975)

The epithelial surfaces in the trachea and principal bronchi of healthy rats were examined by scanning electron microscopy. A system of four cell types, ciliated, microvillous, brush, and goblet cells, in this order of frequency, were found and intermediate type cells were not seen. An extensive area of the surface examined was covered by densely ciliated epithelium. The presence of other cell types beneath the cilia was confirmed by transmission electron microscopy. Areas up to 1 mm in diameter and randomly distributed were observed where microvillous cells predominated and only occasional ciliated cells were found. Most ciliated cells in these areas were adjacent to glandular openings or goblet cells. The larger microvilli of the brush cells were arranged in a coronal configuration elucidated by the scanning electron microscope. Preparatory techniques recently introduced for the examination of soft tissue in the scanning electron microscope facilitated the confirmation of cell types present and the microarchitecture of the epithelial surface.
“Peptide-based NASH therapy, a first crucial step - soon clinical reality?”
Authors: Daniela Kroy, Christian Trautwein
Journal: Hepatology (2008)

Hepatocytes in fatty livers are hypersensitive to apoptosis and undergo escalated apoptotic activity via death receptor-mediated pathways, particularly that of Fas-FasL, causing hepatic injury that can eventually proceed to cirrhosis and end-stage liver disease. Here we report that the hepatocyte growth factor receptor, Met, plays an important part in preventing Fas-mediated apoptosis of hepatocytes by sequestering Fas. We also show that Fas antagonism by Met is abrogated in human fatty liver disease (FLD). Through structure-function studies, we found that a YLGA amino-acid motif located near the extracellular N terminus of the Met α-subunit is necessary and sufficient to specifically bind the extracellular portion of Fas and to act as a potent FasL antagonist and inhibitor of Fas trimerization. Using mouse models of FLD, we show that synthetic YLGA peptide tempers hepatocyte apoptosis and liver damage and therefore has therapeutical potential.
Efficacy of Antiseptic-Impregnated Central Venous Catheters in Preventing Catheter-Related Bloodstream Infection
Authors: David L. Veenstra, Sanjay Saint, Somnath Saha, Thomas Lumley, Sean D. Sullivan
Journal: JAMA (1999)

ContextCentral venous catheters impregnated with chlorhexidine and silver sulfadiazine have recently been introduced for the prevention of catheter-related infections. However, there remains some uncertainty regarding the efficacy of these catheters because of conflicting reports in the literature.ObjectiveTo evaluate the efficacy of chlorhexidine–silver sulfadiazine–impregnated central venous catheters in the prevention of catheter-related bloodstream infection.Data SourcesStudies identified from a computerized search of the MEDLINE database from January 1966 to January 1998, reference lists of identified articles, and queries of principal investigators and the catheter manufacturer.Study SelectionRandomized trials comparing chlorhexidine–silver sulfadiazine–impregnated central venous catheters with nonimpregnated catheters were included. The outcomes assessed were catheter colonization and catheter-related bloodstream infection confirmed by catheter culture.Data ExtractionTwelve studies met the inclusion criteria for catheter colonization and included a total of 2611 catheters. Eleven studies with a total of 2603 catheters met the inclusion criteria for catheter-related bloodstream infection. Most patients in these studies were from groups considered to be at high risk for catheter-related infections. Summary statistics were calculated using Mantel-Haenszel methods under a fixed-effects model.Data SynthesisThe summary odds ratio for catheter colonization was 0.44 (95% confidence interval [CI], 0.36-0.54; P<.001), indicating a significant decrease in catheter colonization associated with impregnated catheters. The studies examining the outcome of primary interest, catheter-related bloodstream infection, had a summary odds ratio of 0.56 (95% CI, 0.37-0.84; P=.005).ConclusionsCentral venous catheters impregnated with a combination of chlorhexidine and silver sulfadiazine appear to be effective in reducing the incidence of both catheter colonization and catheter-related bloodstream infection in patients at high risk for catheter-related infections.
An Overview of the Environmental Genome Project
Authors: Deborah A. Nickerson, Mark J. Rieder, Dana C. Crawford, Christopher S. Carlson, Robert J. Livingston
Journal: Environmental Health Perspectives (2005)

Understanding the causes of common diseases such as cancer, asthma, diabetes, hypertension, and atherosclerosis, which have high population prevalence, is a significant priority for public health research and a major goal in biomedical studies. The influences on susceptibility to common disease are thought to arise from multiple factors, each conferring a low level of relative risk for disease. These low levels of disease risk probably reflect interactions between genotypes at multiple loci (epistasis), interactions between genotypes and environment, and more stochastic epigenetic events such as methylation (Belinsky 2004; Berwick 2000; Hayward 2003; Hegele 1997). Because the risk of any given effect is small (Lander and Schork 1994; Moffatt and Cookson 1999; Pritchard and Cox 2002; Reich and Lander 2001; Risch and Merikangas 1996), detecting these influences will require larger sample sizes, making populationbased association studies more practical for tracing the underlying genetic risks (Risch and Merikangas 1996). Association studies will also be key for exploring genetic links to environmental exposures (Bell and Taylor 1997). In 1997 Dr. Kenneth Olden, director of the National Institute of Environmental Health Sciences (NIEHS), convened a historic conference titled “The Environmental Genome Project” held 17–18 October 1997 in Bethesda, Maryland. This symposium explored the feasibility of the Environmental Genome Project (EGP) and generated significant discussion. The EGP is designed to explore the relationship between common genetic polymorphisms and environmentally induced disease in human populations E s s a y o n The Environmental Genome Project
Acquired Brown's syndrome in a patient with SLE.
Authors: J McGalliard, A L Bell
Journal: Annals of the Rheumatic Diseases (1993)

Letters to the editor samples were tested by both solid phase assays.None of the 25 serum samples tested was positive for the anti-29 kilodalton ELISA.Four out of 27 serum samples were positive for the anti-myeloperoxidase ELISA and negative for antinuclear antibody testing.Anti-myeloperoxidase positive serum samples were P-ANCA positive (n=3) or immunofluorescence negative (n= 1).No marked hypergammaglobulinaemia could explain 'false' positive results by non-specific Fc receptor binding.No association was found between the presence of ANCA and either vasculitis or glomerulonephritis.The serum of one patient with relapsing polychondritis-Wegener's granulomatosis overlap contained P-ANCA at a titre of 1/20.Among the eight patients positive for ANCA, relapsing polychondritis was active in seven, whereas it was active in only 12 out of 25 ANCA negative patients (p=0 1, two tailed Fisher's test).These results suggest that low titres of C-ANCA are not specific for Wegener's granulomatosis and that ANCA (either diffuse or perinuclear) may be present in 24% of serum samples from patients with re- lapsing polychondritis, especially during the active phase of the disease.
Use of Blood in Elective Surgery
Authors: Deba P. Sarma
Journal: JAMA (1980)

A retrospective study of blood-ordering practices and blood use for elective surgical procedures at the Veterans Administration Medical Center of New Orleans shows a cross match-to-transfusion ratio of 4.29. To reduce this ratio, a guideline for ABO-Rh type and antibody screen (type and screen) is implemented. This avoids routine cross matching for those surgical procedures where blood is seldon transfused.
Human Herpesvirus 6 in Lung Tissue from Patients with Pneumonitis after Bone Marrow Transplantation
Authors: Richard W. Cone, Robert C. Hackman, Meei-Li W. Huang, Raleigh A. Bowden, Joel D. Meyers, Mark Metcalf, Judith Zeh, Rhoda Ashley, Lawrence Corey
Journal: New England Journal of Medicine (1993)

Human herpesvirus 6 (HHV-6) is a recently described herpesvirus that is epidemiologically and biologically similar to cytomegalovirus. It is the cause of exanthem subitum (roseola) in children.
Two mutations within a feline mucopolysaccharidosis type VI colony cause three different clinical phenotypes.
Authors: A C Crawley, G Yogalingam, V J Muller, J J Hopwood
Journal: Journal of Clinical Investigation (1998)

Mucopolysaccharidosis type VI (MPS VI) is a lysosomal storage disease caused by a deficiency of N-acetylgalactosamine-4-sulfatase (4S). A feline MPS VI model used to demonstrate efficacy of enzyme replacement therapy is due to the homozygous presence of an L476P mutation in 4-sulfatase. An additional mutation, D520N, inherited independently from L476P and recently identified in the same family of cats, has resulted in three clinical phenotypes. L476P homozygotes exhibit dwarfism and facial dysmorphia due to epiphyseal dysplasia, abnormally low leukocyte 4S/betahexosaminidase ratios, dermatan sulfaturia, lysosomal inclusions in most tissues including chondrocytes, corneal clouding, degenerative joint disease, and abnormal leukocyte inclusions. Similarly, D520N/D520N and L476P/D520N cats have abnormally low leukocyte 4S/betahexosaminidase ratios, mild dermatan sulfaturia, lysosomal inclusions in some chondrocytes, and abnormal leukocyte inclusions. However, both have normal growth and appearance. In addition, L476P/D520N cats have a high incidence of degenerative joint disease. We conclude that L476P/D520N cats have a very mild MPS VI phenotype not previously described in MPS VI humans. The study of L476P/D520N and D520N/ D520N genotypes will improve understanding of genotype to phenotype correlations and the pathogenesis of skeletal dysplasia and joint disease in MPS VI, and will assist in development of therapies to prevent lysosomal storage in chondrocytes.
Is HbA1c Affected by Glycemic Instability?
Authors: Rachel Derr, Elizabeth Garrett, Gerald A. Stacy, Christopher D. Saudek
Journal: Diabetes Care (2003)

OBJECTIVE—HbA1c is a standard clinical assessment of glycemia and the basis of most data relating glycemic control to complications. It remains unclear, however, whether HbA1c is affected by glycemic variation and mean glycemia. RESEARCH DESIGN AND METHODS—To test this question, we analyzed the statistical relationship between HbA1c levels and glycemic variability as measured by self-monitoring of blood glucose (SMBG). The records of 256 subjects were studied. SMBG data for the preceding 3 months were downloaded, and HbA1c was measured by ion-exchange high-performance liquid chromatography. Simple- and random-effects linear regression models were used to assess the independent contributions of mean blood glucose (BG) and SD of BG to HbA1c, after adjusting for the mean BG. RESULTS—Mean ± SD for HbA1c was 7.66 ± 1.11% and for BG was 8.5 ± 1.9 mmol/l (153.3 ± 34.9 mg/dl); SD of BG for individual subjects was 3.5 mmol/l (63.3 mg/dl), varying from 0.4 mmol/l (8.1 mg/dl; very stable glycemia) to 8.4 mmol/l (152.5 mg/dl; very unstable glycemia). A close correlation between mean BG and HbA1c was demonstrated (r = 0.62). Also, within-subject SD of BG correlated with HbA1c (r = 0.375), indicating that people with poorer glycemic control had higher BG variance. After adjusting for mean BG in a linear regression model, however, the effect of the within-subject SD of BG on the HbA1c was insignificant. Several further analyses confirmed the strength of the observation. CONCLUSIONS—HbA1c reflects mean glycemia and is not meaningfully affected by glycemic instability after adjusting for mean BG.
Abstract 470: Role of Fli1 in hematopoietic stem cell-derived fibroblast promotion of tumor cell migration and invasion
Authors: Lindsay T. McDonald, Daniel J. Neitzke, Victoria J. Findlay, David P. Turner, Patricia M. Watson, Dennis K. Watson, Amanda C. LaRue
Journal: Cancer Research (2011)

Abstract Cells and paracrine factors of the tumor microenvironment play a central role in tumor angiogenesis, invasion, migration and proliferation, making the tumor microenvironment an exciting therapeutic target. Among the most prominent cell types in the tumor stroma are fibroblasts, termed carcinoma-associated fibroblasts (CAFs). We have identified a novel population of CAFs and CAF precursors (circulating fibroblast precursors, CFPs) that are of hematopoietic stem cell (HSC) origin. These cells preferentially migrate and differentiate in response to tumor and their inhibition results in decreased tumor size. While these studies have identified a novel HSC-derived CAF population, the mechanisms by which these cells promote tumorigenesis are unknown. Previous studies have indicated a critical role for Fli1, an Ets family transcription factor, in regulation of HSCs and differentiation/maturation of hematopoietic lineages. Additionally, loss of Fli1 has been associated with cancer progression. Based on these findings, we hypothesize that HSC-derived CFPs/CAFs directly affect tumor cell migration and invasion and that loss of Fli1 in CFPs/CAFs enhances these effects. To address this hypothesis, we examined the ability of HSC-derived fibroblast populations to affect tumor cell migration and invasion in vitro. Fibroblasts were established from peripheral blood and bone marrow of normal mice and mutant Fli1 mice expressing a truncated Fli1 protein (Fli1ΔCTA) lacking the carboxy-terminal regulatory (CTA) domain. The effects of conditioned media from these fibroblast populations on tumor cell migration and invasion were examined in chemotactic transwell migration assays and matrigel-based invasion assays, respectively. Data show that conditioned media from all HSC-derived fibroblast populations promoted migration and invasion of tumor cells versus control, and that this effect was significantly enhanced using conditioned media from fibroblasts derived from Fli1ΔCTA/Fli1ΔCTA mice. Ongoing studies are directed at identifying the mechanisms by which Fli1 target genes affect HSC-derived fibroblast modulation of tumor cell migration and invasion. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 470. doi:10.1158/1538-7445.AM2011-470
TNF-α Gene Silencing Using Polymerized siRNA/Thiolated Glycol Chitosan Nanoparticles for Rheumatoid Arthritis
Authors: So Jin Lee, Aeju Lee, Seung Rim Hwang, Jong-Sung Park, Jiyeon Jang, Myung Sook Huh, Dong-Gyu Jo, Soo-Young Yoon, Youngro Byun, Sun Hwa Kim, Ick Chan Kwon, Inchan Youn, Kwangmeyung Kim
Journal: Molecular Therapy (2013)

Among various proinflammatory cytokines involved in the pathogenesis of rheumatoid arthritis (RA), tumor necrosis factor (TNF)-α plays a pivotal role in the release of other cytokines and induction of chronic inflammation. Even though siRNA has the therapeutic potential, they have a challenge to be delivered into the target cells because of their poor stability in physiological fluids. Herein, we design a nanocomplex of polymerized siRNA (poly-siRNA) targeting TNF-α with thiolated glycol chitosan (tGC) polymers for the treatment of RA. Poly-siRNA is prepared through self-polymerization of thiol groups at the 5' end of sense and antisense strand of siRNA and encapsulated into tGC polymers, resulting in poly-siRNA-tGC nanoparticles (psi-tGC-NPs) with an average diameter of 370 nm. In the macrophage culture system, psi-tGC-NPs exhibit rapid cellular uptake and excellent in vitro TNF-α gene silencing efficacy. Importantly, psi-tGC-NPs show the high accumulation at the arthritic joint sites in collagen-induced arthritis (CIA) mice. Treatment monitoring data obtained by the matrix metalloproteinase 3-specific nanoprobe and microcomputed tomography show that intravenous injection of psi-tGC-NPs significantly inhibits inflammation and bone erosion in CIA mice, comparable to methotrexate (5 mg/kg). Therefore, the availability of psi-tGC-NP therapy that target specific cytokines may herald new era in the treatment of RA.
Cancer and Eosinophilia
Authors: Paul B. Beeson
Journal: New England Journal of Medicine (1983)

The investigations by Slungaard and colleagues, described in this issue,1 deal with the mechanism of a spectacular elevation of blood eosinophils in a patient with lung cancer and provide us with a satisfying, although not too surprising, explanation for this well-known phenomenon.2 The manifestation always evokes puzzled discussion and usually prompts a search for some other cause of the eosinophilia, such as co-existing parasitic infestation or drug allergy. When these are not found, the question asked is whether the hematologic reaction indicates some peculiar immunologic response to the tumor or points to a special character of the neoplasm.Actually, a . . .
Reply to M.M.J. Zanders et al
Authors: Kathryn L. Penney, Meir J. Stampfer
Journal: Journal of Clinical Oncology (2014)

The term "confounding by indication" is typically used to denote a particular form of confounding in studies of medications whereby the apparent effect of a medication is actually a result of the condition for which it is prescribed.In this instance (ie, in the study by Margel et al 1 ), all of the comparisons were within patients with diabetes, so the underlying indication for the medication was the same.One might argue that metformin users differ from users of other antidiabetic
Induction of Drug Tolerance to Trimethoprim/Sulfamethoxazole in Non-HIV Patients with a History of Sulfonamide Allergy
Authors: Regan Pyle, Miguel A. Park, Gerald W. Volcheck, Kimberly Poe, Jenna Podjasek, Matthew A. Rank, Joseph H. Butterfield
Journal: Journal of Allergy and Clinical Immunology (2013)
The Language of Pain: Finding Words, Compassion, and Relief
Authors: Preeti N. Malani
Journal: JAMA (2010)

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High-Density Substrate Mapping in Brugada Syndrome
Authors: P.D. Lambiase, A.K. Ahmed, E.J. Ciaccio, R. Brugada, E. Lizotte, S. Chaubey, Ron Ben-Simon, A.W. Chow, M.D. Lowe, W.J. McKenna
Journal: Circulation (2009)

Two principal mechanisms are thought to be responsible for Brugada syndrome (BS): (1) right ventricular (RV) conduction delay and (2) RV subepicardial action potential shortening. This in vivo high-density mapping study evaluated the conduction and repolarization properties of the RV in BS subjects.A noncontact mapping array was positioned in the RV of 18 BS patients and 20 controls. Using a standard S(1)-S(2) protocol, restitution curves of local activation time and activation recovery interval were constructed to determine local maximal restitution slopes. Significant regional conduction delays in the anterolateral free wall of the RV outflow tract of BS patients were identified. The mean increase in delay was 3-fold greater in this region than in control (P=0<0.001). Local activation gradient was also maximally reduced in this area: 0.33+/-0.1 (mean+/-SD) mm/ms in BS patients versus 0.51+/-0.15 mm/ms in controls (P<0.0005). The uniformity of wavefront propagation as measured by the square of the correlation coefficient, r(2), was greater in BS patients versus controls (0.94+/-0.04 versus 0.89+/-0.09 [mean+/-SD]; P<0.05). The odds ratio of BS hearts having any RV segment with maximal restitution slope >1 was 3.86 versus controls. Five episodes of provoked ventricular tachycardia arose from wave breaks originating from RV outflow tract slow-conduction zones in 5 BS patients.Marked regional endocardial conduction delay and heterogeneities in repolarization exist in BS. Wave break in areas of maximal conduction delay appears to be critical in the initiation and maintenance of ventricular tachycardia. These data indicate that further studies of mapping BS to identify slow-conduction zones should be considered to determine their role in spontaneous ventricular arrhythmias.
Hubert Anthony Buck
Authors: D Davies
Journal: BMJ (2004)

An icon in the treatment of Lassa feverIn early 2000 Dr Bill Aldis, then the World Health Organization's representative in Sierra Leone, remembers getting a worried call from Geneva: "I've got an ICRC [International Committee of the Red Cross] staff member with suspected Lassa fever just evacuated from Kenema [in Sierra Leone].What do I do?" Dr Aldis replied, "The best thing you could do is put him on an airplane and get him back to Kenema-there's a hospital there with the world's greatest expert in Lassa fever, a guy named Conteh . .."Such was the reputation of Aniru Conteh, who ran the world's only Lassa fever isolation ward.Born in 1942 in Jawi Folu, Eastern Province, Sierra Leone, Aniru Conteh was the son of the local chief.At the age of 16 he left home to go to school in the country's capital, Freetown, where he went on to study chemistry and biology at Fourah Bay College.Initially he worked as a teacher, but in 1974 he enrolled as a medical student at the University of Ibadan in Nigeria, where he continued to work after qualifying, until he returned to Sierra Leone in 1979 and started working on the Lassa fever programme.Lassa fever takes its name from a small village in Nigeria, where a mysterious outbreak in a mission hospital in 1969 led to the three mission nurses becoming infected.Two of the nurses died, but the third survived and was evacuated to the Colombia Presbyterian Hospital in New York.Wilbur