tbuckley/cabot-search huggingface dataset:
Nosocomial Infections in a Newborn Intensive-Care Unit
Authors: Val G. Hemming, James C. Overall, Michael R. Britt
Journal: New England Journal of Medicine (1976)

We detected a 24.6 per cent nosocomial infection rate (222 infections in 138 infants) among 904 infants hospitalized for over 48 hours in a regional newborn intensive-care during 41 months of surveillance. Surface infections accounted for 40.1 per cent of the total, pneumonia for 29.3 per cent, bacteremia for 14.0 per cent, surgical-wound infection for 8.1 per cent, urinary-tract infection for 4.5 per cent, and meningitis for 4.0 per cent. Staphylococcus aureus (47.3 per cent) and gram-negative enteric bacilli (45.1 per cent) were the most common organisms recovered. Nosocomial infection rates were significantly higher in infants with a birth weight less than 1500 g (P less than 0.001). The mortality rate in infants with any nosocomial infection was 33 per cent in contrast to 14 per cent in non-infected babies (P less than 0.001). Nosocomial infections are a major problem in newborn intensive-care units.
Alteration of some functional and metabolic characteristics of resident mouse peritoneal macrophages by lymphocyte mediators.
Authors: J K Lazdins, A L Kühner, J R David, M L Karnovsky
Journal: The Journal of Experimental Medicine (1978)

Resident mouse peritoneal macrophages were incubated in Sephadex G-100 fractions of supernates from concanavalin A-stimulated lymphocytes. A significant effect of the lymphocyte supernatant fractions containing mediators on macrophage 5'-nucleotidase, glucose-1 14C oxidation, cell maintenance, and migration is reported. The 5'-nucleotidase was depressed to an extent similar to that seen in activated macrophages obtained from Listeria-infected mice. On the other hand, glucose-1-14C oxidation was enhanced, but not to the same degree as seen in the counterparts in vivo. Whereas migration inhibitory factor (MIF) and cell adherence-augmenting activity were found in a number of adjacent fractions, the metabolic effects were found predominantly in a single fraction. Resident peritoneal macrophages or those elicited by the injection of a lymphocyte-derived chemotactic factor were more responsive with respect to the biochemical changes than caseinate-elicited macrophages. On the other hand, caseinate-elicited macrophages appeared to be more sensitive with respect to the effects of mediator(s) on cell retention. A possible dissociation between MIF and cell-adherence augmenting activity, on the one hand, and the entities that stimulate glucose-1-14C oxidation is reported, based on fractionation studies, and loss of the latter activity upon storage of lymphocyte supernates.
The African Exchange: Toward a Biological History of Black People
Authors: Richard Allen Williams
Journal: JAMA (1989)

<i>Ex Africa semper aliquid novi</i>, said the Roman philosopher Pliny the Elder in expressing his amazement that something new was always coming out of Africa. This book, edited by a professor of history at Bowling Green State University in Bowling Green, Ohio, is intended to fill a gap in our knowledge of the biological past of black people by investigating the circumstances under which blacks developed infectious diseases such as smallpox, malaria, yellow fever, tuberculosis, and cholera. Moreover, the book's major thrust is an underlying hypothesis that purports to demonstrate a spread of infectious diseases from Africa to the New World and to other areas such as Brazil via the slave trade and to some extent in the reverse direction; hence the idea of an "African exchange." The volume consists of a survey of literature written recently about the biological past of blacks as well as a number of contributed
How Accurate Are 3 Risk Prediction Models in US Women?
Authors: Erin D. Michos, Roger S. Blumenthal
Journal: Circulation (2012)

C ardiovascular disease (CVD) is the leading cause of death for US women, and nearly two thirds who died suddenly of CVD had no previous symptoms. 1Therefore, it is of great importance to identify "at-risk" women early, so that effective primary prevention strategies can be instituted.A universal recommendation of prevention guidelines is that all asymptomatic women should undergo a global risk assessment.
Refractoriness to Antivascular Endothelial Growth Factor Treatment: Role of Myeloid Cells
Authors: Farbod Shojaei, Napoleone Ferrara
Journal: Cancer Research (2008)

Abstract CD11b+Gr1+ cells, which include neutrophils, macrophages, and myeloid-derived suppressor cells, have been shown to contribute to tumor angiogenesis. Recently, we found that accumulation of CD11b+Gr1+ in tumors renders them refractory to angiogenic blockade by vascular endothelial growth factor (VEGF) antibodies. This effect was traced to a pathway of CD11b+Gr1+–mediated angiogenesis that is, at least in part, driven by the secreted protein Bv8, which is up-regulated by the important myeloid growth factor granulocyte colony-stimulating factor (G-CSF). Thus, G-CSF may promote tumor angiogenesis through a Bv8-dependent pathway that bypasses VEGF and renders tumors refractory to anti-VEGF therapy. [Cancer Res 2008;68(14):5501–4]
Bone and joint changes in haemochromatosis.
Authors: E N Wardle, J T Patton
Journal: Annals of the Rheumatic Diseases (1969)

<h3>Summary</h3> Foraging is a common decision problem in natural environments. When new exploitable sites are always available, a simple optimal strategy is to leave a current site when its return falls below a single average reward rate. Here, we examined foraging in a more structured environment, with a limited number of sites that replenished at different rates and had to be revisited. When participants could choose sites, they visited fast-replenishing sites more often, left sites at higher levels of reward, and achieved a higher net reward rate. Decisions to exploit-or-leave a site were best explained with a computational model estimating separate reward rates for each site. This suggests option-specific information can be used to construct a threshold for patch leaving in some foraging settings, rather than a single average reward rate.
Human HLA-DR beta gene hypervariable region homology in the biobreeding BB rat: selection of the diabetic-resistant subline as a rheumatoid arthritis research tool to characterize the immunopathologic response to human type II collagen.
Authors: W C Watson, J P Thompson, K Terato, M A Cremer, A H Kang
Journal: The Journal of Experimental Medicine (1990)

Collagen arthritis (CA), an autoimmune model of rheumatoid arthritis (RA), has been studied in various animals. However, it has not been studied in an animal with a genetic background relevant to RA. We selected rats from a diabetic-resistant (DR) subline of the diabetic BB rat because they have an autoimmune disease-prone background, but not the immunodeficiencies of the diabetic BB rat, and the third hypervariable region (HVRIII) of the BB RT1.D beta gene appeared to encode a nucleotide sequence of the human HLA DR beta gene, which has been reported to be associated with susceptibility to RA. We synthesized oligonucleotide primers flanking the RT1.D beta HVRIII, cloned polymerase chain reaction-amplified DNA into M13mp18, and confirmed the presence of the susceptibility sequence (SS) (RRRAA) by the dideoxy sequencing method in a colony of DR BB/Wor-UTM rats. When immunized with human type II collagen (CII) in incomplete Freunds adjuvant (IFA), arthritis developed rapidly by day 10 with 100% incidence. Light and electron microscopy revealed an unusually severe and aggressive, bidirectional pattern of cartilage resorption by synovial and subchondral mononuclear and multinucleated inflammatory cells. These findings coincided with a predominant humoral response to the cyanogen bromide (CB) 11 fragment of the human CII molecule by the pathogenic IgG2a isotype. This study provides further support to the role of CA as a relevant RA model, the specific roles of the CB11 fragment as a major site of arthritogenic epitopes, and of antibody mechanisms in the pathogenesis of CA. Furthermore, the identification of an RA SS in an immune response gene of the DR BB rat presents a novel opportunity to determine with an animal model the role of other antigens as well as this SS in RA.
Abstract 970: Obesity promotes melanoma metastasis by modulating Snai1 and KiSS1 expression
Authors: Kyoko Kushiro, Nomeli P. Nunez
Journal: Cancer Research (2011)

Abstract Malignant melanoma accounts for 75% of deaths associated with skin cancer. Its lethality comes from its aggressive metastasis to secondary sites such as the lungs. Epidemiological and animal studies suggest that obesity may increase the ability of melanomas to metastasize. The objective of these studies was to determine the mechanism by which obesity increases the aggressiveness of melanomas to metastasize. To this end, we used ob/ob mice as a model of obesity, as well as different cell culture conditions which mimic obesity, to investigate the molecular mechanism by which obesity affects the metastatic phenotype of B16BL6 mouse metastatic melanoma cells in vitro. In cell culture, we showed that serum from obese mice increased the ability of melanoma cells to invade. We showed that both obese mouse serum and conditioned medium collected from mature 3T3L1 adipocytes promoted a mesenchymal phenotype, as seen by an increased expression of genes associated with this phenotype, such as Snai1, and a corresponding decreased expression of the metastasis suppressor gene KiSS1. Our preliminary results suggest that obesity may increase the metastatic ability of melanomas via the pro-inflammatory cytokine Interleukin 6 (IL-6). Therefore, our hypothesis is that obesity promotes melanoma metastasis by promoting the epithelial-to-mesenchymal transition (EMT) and its associated phenotypic changes by up-regulating Snai1 and down-regulating KiSS1 through IL-6. These findings will help us understand how obesity affects melanoma metastasis and allow us to identify key cellular signaling pathways that can be used to prevent or possibly inhibit melanoma metastasis. 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 970. doi:10.1158/1538-7445.AM2011-970
Case of Rupture of the Heart from External Violence without Penetrating Wound
Authors: H. Handford
Journal: BMJ (1880)

years.The surgeon who brought the lady to nie had a very good case of instruments, and as he undertook, with I)r.Grabham, the charge of the patient after operation, I was able (although I had not extracted a cataract for about twenty years) to remove both lenses, and thus save this old lady the voyage to Lisbon; and I have lately heard from Dr.
HETEROGENEOUS UPREGULATION OF APAMIN-SENSITIVE CURRENTS (IKAS) IN FAILING HUMAN VENTRICLES
Authors: Po-Cheng Chang, John C. Lopshire, Isik Turker, Christopher L. Corr, Susan P. Straka, Jason B. Garlie, Zhenhui Chen, Su-Kiat Chua, Mitsunori Maruyama, Thomas C. Wozniak, John W. Brown, Mark W. Turrentine, Jacqueline A. O'Donnel, Irmina Gradus-Pizlo, Shien-Fong Lin, Peng-Sheng Chen, Tomohiko Ai
Journal: Journal of the American College of Cardiology (2011)
Traveler's amnesia. Transient global amnesia secondary to triazolam
Authors: H. H. Morris
Journal: JAMA (1987)

Three neuroscientists traveled on different occasions from New York to Europe to attend scientific meetings. In an attempt to minimize "jet lag," they all took triazolam, 0.5 mg, during the flight. In addition to the medication, they also consumed ethyl alcohol to a variable degree, none to clinical intoxication. All three experienced an episode of anterograde amnesia that lasted several hours. In two of the individuals, neurologists associated with them did not detect any memory disturbance at the time. These episodes of transient global amnesia were evidently secondary to the triazolam or the combination of triazolam and ethyl alcohol. These episodes suggest caution if using this medication to avoid jet lag, especially if ethyl alcohol will be consumed. (<i>JAMA</i>1987;258:945-946)
A PILOT STUDY OF L-GLUTAVITE IN HOSPITALIZED "AUTISTIC" AND "HYPERACTIVE" CHILDREN
Authors: SEYMOUR LEYEN, ARTHUR S. IMPASTATO
Journal: American Journal of Psychiatry (1961)

Of 18 children receiving L-Glutavite in the blind study only 2 showed appreciable improvement in their behavior. Of the 17 children receiving the placebo 3 displayed the same degree of improvement. L-Glutavite in the dose administered during this 6-week study did not cause any marked improvement in "hyperactive" or "autistic" children.
Predominance of Dense Low-Density Lipoprotein Particles Predicts Angiographic Benefit of Therapy in the Stanford Coronary Risk Intervention Project
Authors: Bonnie D. Miller, Edwin L. Alderman, William L. Haskell, Joan M. Fair, Ronald M. Krauss
Journal: Circulation (1996)

LDL particles differ in size and density. Individuals with LDL profiles that peak in relatively small, dense particles have been reported to be at increased risk of coronary artery disease. We hypothesized that response to coronary disease therapy in such individuals might differ from response in individuals whose profiles peak in larger, more buoyant LDL. We examined this hypothesis in the Stanford Coronary Risk Intervention Project, an angiographic trial that compared multifactorial risk-reduction intervention with the usual care of physicians.For 213 men, a bimodal frequency distribution of peak LDL density (g/mL) determined by analytical ultracentrifugation was used to classify baseline LDL profiles as "buoyant mode" (density < or = 1.0378) or "dense mode" (density > 1.0378). Coronary disease progression after 4 years was assessed by rates of change (mm/y, negative when arteries narrow) of minimum artery diameter. Rates for buoyant-mode subjects were -0.038 +/- 0.007 (mean +/- SEM) in usual care (n = 65) and -0.039 +/- 0.010 in intervention (n = 56; P = .6). Rates for dense-mode subjects were -0.054 +/- 0.012 in usual care (n = 51) and -0.008 +/- 0.009 in intervention (n = 41, P = .007). Lipid changes did not account for this difference in angiographic response.Different types of LDL profile may predict different-responses to specific therapies, perhaps because metabolic processes determine both LDL profiles and responses to therapies.
Aortic Replacement
Authors: ALBERT STARR, M. LOWELL EDWARDS, COLIN W. MCCORD, HERBERT E. GRISWOLD
Journal: Circulation (1963)

A ball-valve prosthesis for aortic replacement has been described which, while it is similar to the mitral ball valve in terms of materials and construction, is quite different in sewing margin and internal geometry. Implantation is greatly facilitated by the flexibility of the prosthesis in terms of external diameter, and by the availability of a full set of varying sizes for obtaining a proper fit. Widening of the aortic root by patch grafting has not been necessary. Long-term survival has been achieved in the dog, and early clinical results are most promising. While the selection of the ideal aortic valvular replacement must await further experience with all types of prostheses, continued evaluation of the ball valve in the aortic position, in carefully chosen patients, is indicated.
Vitamin B12c in Pernicious Anaemia and Subacute Combined Degeneration of Cord
Authors: C. C. Ungley, H. Campbell
Journal: BMJ (1951)

BRiusH 1 2 M IA ORA homocystine as an alternative to methionine only when vitamin B12 is given (Jukes, Stokstad, and Broquist, 1950; see also Schaefer et al., 1950).Dubnoff (1950) has shown that vitamin B12 augments the reduction of S-S compounds in liver slices.Jukes, Broquist, and Stokstad (1950) have put forward an ingenious scheme relating the activities in bacterial metabolism of vitamin B12, certain deoxyribosides, folic acid, and "citrovorum factor" ("folinic acid"; see Bardos et al., 1949).Traina (1950aTraina ( , 1950b) ) found that vitamin B12 has an antihistamine and anti-anaphylactic effect, but we have failed to confirm the former (Sharpe, Woollett, and Cuthbertson, 1950).Swendseid et al. (1947) showed that liver extract diminishes the excessive urinary excretion of phenols which occurs in pernicious anaemia.Abbott and James (1950) have confirmed this phenomenon with crystalline vitamin B12' This may be connected with the suggested toxic factor of pernicious anaemia, production of which ceases on administration of vitamin B12' In due time these observations will doubtless be welded together into a coherent theory of the mode of action of vitamin B12, but as yet they provide little clue to the mechanism of its haemopoietic activity, beyond its suggested function in the building of nucleic acids.
Hypoxia-inducible factor induces local thyroid hormone inactivation during hypoxic-ischemic disease in rats
Authors: Warner S. Simonides, Michelle A. Mulcahey, Everaldo M. Redout, Alice Muller, Marian J. Zuidwijk, Theo J. Visser, Frank W.J.S. Wassen, Alessandra Crescenzi, Wagner S. da-Silva, John Harney, Felix B. Engel, Maria-Jesús Obregon, P. Reed Larsen, Antonio C. Bianco, Stephen A. Huang
Journal: Journal of Clinical Investigation (2008)

Thyroid hormone is a critical determinant of cellular metabolism and differentiation. Precise tissue-specific regulation of the active ligand 3,5,3′-triiodothyronine (T3) is achieved by the sequential removal of iodine groups from the thyroid hormone molecule, with type 3 deiodinase (D3) comprising the major inactivating pathway that terminates the action of T3 and prevents activation of the prohormone thyroxine. Using cells endogenously expressing D3, we found that hypoxia induced expression of the D3 gene DIO3 by a hypoxia-inducible factor–dependent (HIF-dependent) pathway. D3 activity and mRNA were increased both by hypoxia and by hypoxia mimetics that increase HIF-1. Using ChIP, we found that HIF-1α interacted specifically with the DIO3 promoter, indicating that DIO3 may be a direct transcriptional target of HIF-1. Endogenous D3 activity decreased T3-dependent oxygen consumption in both neuronal and hepatocyte cell lines, suggesting that hypoxia-induced D3 may reduce metabolic rate in hypoxic tissues. Using a rat model of cardiac failure due to RV hypertrophy, we found that HIF-1α and D3 proteins were induced specifically in the hypertrophic myocardium of the RV, creating an anatomically specific reduction in local T3 content and action. These results suggest a mechanism of metabolic regulation during hypoxic-ischemic injury in which HIF-1 reduces local thyroid hormone signaling through induction of D3.
Can there be fair funding for fundholding practices?
Authors: J Dixon
Journal: BMJ (1994)

Most regional health authorities set budgets for fundholding practices according to the amount of care used by the practice population. This article explains why this funding method can only lead to an inequitable allocation of resources between fundholding and non-fundholding practices. Using the experience of North West Thames region, the efforts made to make funding fairer are discussed. The steps that health authorities could take to investigate and reduce the problem are also outlined. In the absence of a capitation formula for funding fundholding practices, the paper suggests that health authorities should do much more to investigate the amount of money they spend on non-fundholding practices. Regions could develop and use other methods to set budgets rather than rely on activity recorded by practices. Regions and the Department of Health should resolve urgently if and how far the budgets for fundholders should be compensated for increases in provider prices.
Structural features of Salmonella typhimurium lipopolysaccharide required for activation of tissue factor in human mononuclear cells.
Authors: F R Rickles, P D Rick
Journal: Journal of Clinical Investigation (1977)

Activation of mononuclear cell tissue factor was examined utilizing lipopolysaccharides obtained from wild-type and both Rc and Re mutants of Salmonella typhimurium. Wild-type (smooth) lipopolysaccharide, galactose-deficient (Rc) lipopolysaccharide, heptose-deficient (Re) lipopolysaccharide, and lipid A preparations were all active in their ability to generate tissue factor activity in human mononuclear cells grown in tissue culture. Polymyxin B has been reported to prevent some of the lethal effects of endotoxin in vivo, and the drug reportedly binds to the 2-keto-3-deoxyoctulosonate-lipid A region of the lipopolysaccharide molecule. Polymyxin B was effective in inhibiting the tissue factor generating activity of wild-type lipopolysaccharide, Re lipopolysaccharide, and lipid A in a dose-dependent fashion. Treatment of lipid A preparations with mild alkali abolished the ability of these preparations to activate tissue factor in cells. Analogous to many of the other biologic properties of lipopolysaccharide, tissue factor activation in human mononuclear cells appears to depend upon the integrity of the lipid A portion of the molecule.
Obesity: Mediators and Treatment Approaches
Authors: Zachary T. Bloomgarden
Journal: Diabetes Care (2009)

This is the fifth of a series of six articles based on presentations at the American Diabetes Association Scientific Sessions held 6–10 June 2008 in San Francisco, California.

Zofia Zukowska (Washington, DC) discussed the peripheral actions of neuropeptide Y (NPY), an important mediator by which diet and lack of physical activity lead to weight gain. NPY is synthesized as a 97 amino acid precursor, which is processed and amidated to NPY 1–36. NPY 1–36 is cleaved by dipeptidyl peptidase (DPP)-4 to NPY 3–36, which has other biologic activities, leading to the possibility that inhibitors of DPP-4 may potentiate NPY action with potentially adverse (or beneficial) effects. NPY is contained in all sympathetic nerves together with norepinephrine, although their modes of release are somewhat dissimilar. This is, then, a major sympathetic nervous system effector, elevated in stress, hypertension, cardiac and renal failure, and malignancies, which, Zukowska stated, is the most abundant peptide in the brain and heart. There are multiple G protein–coupled receptors for NPY including y1, which is vasoconstrictive, has atherogenic effects, and acts in the brain to reduce anxiety and increase appetite (1), and y2 and y5, which are also involved in the peptide's vascular effects (2). She cited evidence that although stress with increased sympathetic tone causes lipolysis by increasing catecholamine levels, sympathetic activation may also increase NPY, leading to angiogenesis and adipogenesis causing fat cell growth. Cold stress with a fat- and sugar-enriched diet increases body weight. An experimental model of daily 10-min encounters with an aggressive mouse was also associated with increased NPY as well as increased Y2 receptor expression, seen particularly with a high-fat diet and environmental stress. Interestingly, ob/ob mice have a sevenfold increase in NPY expression. NPY has insulin-like effects on release of adipokines and resistin. In vivo, NPY administration by a slow-release …