tbuckley/cabot-search huggingface dataset:
Effects of Dopamine β-Hydroxylase Inhibition With Nepicastat on the Progression of Left Ventricular Dysfunction and Remodeling in Dogs With Chronic Heart Failure
Authors: Hani N. Sabbah, William C. Stanley, Victor G. Sharov, Takayuki Mishima, Mitsuhiro Tanimura, Claude R. Benedict, Sharath Hegde, Sidney Goldstein
Journal: Circulation (2000)

Background —Inhibition of dopamine β-hydroxylase (DBH) results in a decrease in norepinephrine synthesis. The present study was a randomized, blinded, placebo-controlled investigation of the long-term effects of therapy with the DBH inhibitor nepicastat (NCT) on the progression of left ventricular (LV) dysfunction and remodeling in dogs with chronic heart failure (HF). Methods and Results —Moderate HF (LV ejection fraction [LVEF] 30% to 40%) was produced in 30 dogs by intracoronary microembolization. Dogs were randomized to low-dose NCT (0.5 mg/kg twice daily, n=7) (L-NCT), high-dose NCT (2 mg/kg twice daily, n=7) (H-NCT), L-NCT plus enalapril (10 mg twice daily, n=8) (L-NCT+ENA), or placebo (PL, n=8). Transmyocardial (coronary sinus–arterial) plasma norepinephrine (tNEPI), LVEF, end-systolic volume, and end-diastolic volume were measured before and 3 months after initiating therapy. tNEPI levels were higher in PL compared with NL (86±20 versus 13±14 pg/mL, P &lt;0.01). L-NCT alone and L-NCT+ENA reduced tNEPI toward normal (28±4 and 39±17 pg/mL respectively), whereas HD-NCT reduced tNEPI to below normal levels (3±10 pg/mL). In PL dogs, LVEF decreased but was unchanged with L-NCT and increased with L-NCT+ENA. L-NCT and L-NCT+ENA prevented progressive LV remodeling, as evidenced by lack of ongoing increase in end-diastolic volume and end-systolic volume, whereas H-NCT did not Conclusions —In dogs with HF, therapy with L-NCT prevented progressive LV dysfunction and remodeling. The addition of ENA to L-NCT afforded a greater increase in LV systolic function. NCT at doses that normalize tNEPI may be useful in the treatment of chronic HF.
The Role of Footwear in the Prevention of Foot Lesions in Patients With NIDDM: Conventional wisdom or evidence-based practice?
Authors: Debra K Litzelman, Deanna J Marriott, Frank Vinicor
Journal: Diabetes Care (1997)

OBJECTIVE To conduct a prospective evaluation of footwear characteristics as predictors of diabetic foot wounds. RESEARCH DESIGN AND METHODS A total of 352 patients with NIDDM enrolled in a randomized controlled trial aimed at preventing diabetic foot lesions in an academic general medicine practice were studied. Foot wounds (n = 63) were modeled univariately and multivariably using generalized estimating equations. The dependent variable was a wound classified as a 1.2 or greater according to the Seattle Wound Classification System, indicating at least a superficial or healing minor lesion with no functional interruption of the protective cutaneous barrier. Independent variables included detailed measures of style and material of patients' indoor and outdoor shoes, appropriate length and width, sock fibers, whether the patient had bought new shoes in the past 6 months, and if the patient had been recommended for special shoes. Modeling controlled for intervention status and physiological measures (baseline wound, monofilament abnormalities, and serum HDL level). RESULTS Initial screening (P &amp;lt; 0.20) suggested that a recommendation for special shoes, shoe length, and shoe width were indicative of wounds at follow-up (odds ratios [ORs] 2.19, 1.84, 1.86, respectively), while having bought shoes in the past 6 months was associated with no wound at follow-up (OR 0.60). The final multivariable model included only the recommendation for special shoes (OR 2.19; 95% CI 1.07–4.49). CONCLUSIONS Many variables commonly cited as protective measures in footwear for diabetic patients were not prospectively predictive when controlling for physiological risk factors. Rigorous analyses are needed to examine the many assumptions regarding footwear recommendations for diabetic patients.
The Pendulum Model for Genome Compositional Dynamics: from the Four Nucleotides to the Twenty Amino Acids
Authors: Zhang Zhang, Jun Yu
Journal: Genomics Proteomics & Bioinformatics (2012)

The genetic code serves as one of the natural links for life's two conceptual frameworks-the informational and operational tracks-bridging the nucleotide sequence of DNA and RNA to the amino acid sequence of protein and thus its structure and function. On the informational track, DNA and its four building blocks have four basic variables: order, length, GC and purine contents; the latter two exhibit unique characteristics in prokaryotic genomes where protein-coding sequences dominate. Bridging the two tracks, tRNAs and their aminoacyl tRNA synthases that interpret each codon-nucleotide triplet, together with ribosomes, form a complex machinery that translates genetic information encoded on the messenger RNAs into proteins. On the operational track, proteins are selected in a context of cellular and organismal functions constantly. The principle of such a functional selection is to minimize the damage caused by sequence alteration in a seemingly random fashion at the nucleotide level and its function-altering consequence at the protein level; the principle also suggests that there must be complex yet sophisticated mechanisms to protect molecular interactions and cellular processes for cells and organisms from the damage in addition to both immediate or short-term eliminations and long-term selections. The two-century study of selection at species and population levels has been leading a way to understand rules of inheritance and evolution at molecular levels along the informational track, while ribogenomics, epigenomics and other operationally-defined omics (such as the metabolite-centric metabolomics) have been ushering biologists into the new millennium along the operational track.
The Effects of Type 1 Diabetes on Cognitive Performance
Authors: Augustina M.A. Brands, Geert Jan Biessels, Edward H.F. de Haan, L. Jaap Kappelle, Roy P.C. Kessels
Journal: Diabetes Care (2005)

OBJECTIVE—To investigate the exact nature and magnitude of cognitive impairments in patients with type 1 diabetes and the possible association with other disease variables, such as recurrent episodes of hypoglycemia and metabolic control. RESEARCH DESIGN AND METHODS—MedLine and PsycLit search engines were used to identify studies on cognitive performance in patients with type 1 diabetes. Effect sizes (Cohen’s d), which are the standardized differences between the experimental and the control group, were calculated. In the meta-analysis, a combined d value was calculated, expressing the magnitude of associations across studies. RESULTS—A total of 33 studies were identified that met the inclusion criteria. Compared with nondiabetic control subjects, the type 1 diabetic group demonstrated a significantly lowered performance on the following cognitive domains: intelligence (d = −0.7), speed of information processing (d = −0.3), psychomotor efficiency (d = −0.6), visual (d = −0.4) and sustained attention (d = −0.3), cognitive flexibility (d = −0.5), and visual perception (d = −0.4). Lowered cognitive performance in diabetic patients appeared to be associated with the presence of microvascular complications but not with the occurrence of severe hypoglycemic episodes or with poor metabolic control. CONCLUSIONS—In patients with type 1 diabetes, cognitive dysfunction is characterized by a slowing of mental speed and a diminished mental flexibility, whereas learning and memory are spared.The magnitude of the cognitive deficits is mild to moderate, but even mild forms of cognitive dysfunction might hamper everyday activities since they can be expected to present problems in more demanding situations.
EPITHELIOID HAEMANGIOMA-LIKE VASCULAR PROLIFERATION IN AIDS: MANIFESTATION OF CAT SCRATCH DISEASE BACILLUS INFECTION?
Authors: PhilipE. Leboit, BarbaraM. Egbert, MarkH. Stoler, JamesA. Strauchen, TimothyG. Berger, T.S.Benedict Yen, ThomasA. Bonfiglio, CharlesK. English, DouglasJ. Wear
Journal: The Lancet (1988)

Papular and nodular skin lesions that clinically resembled Kaposi sarcoma, but histologically showed a distinct epithelioid haemangioma-like appearance, were noted in seven patients with the acquired immunodeficiency syndrome. Clusters of bacteria that had the structure of gram-negative rods were identified within each of the vascular proliferations by electron microscopy. The bacteria did not stain with the Brown-Brenn, acid-fast, or other histochemical stains for infectious organisms, but did stain with Warthin-Starry—ie, the staining profile was that described for the cat scratch disease (CSD) bacillus. Immunoperoxidase staining, using antisera raised in rabbits against cultured CSD bacillus, showed a positive reaction with the bacterium in all five cases tested. The two surviving patients have both given histories of having been scratched by a cat. In several patients, the vascular lesions regressed after therapy with antibiotics appropriate for CSD bacillus infection.
A cytoplasmic serine protein kinase binds and may regulate the Fanconi anemia protein FANCA
Authors: Hiroshi Yagasaki, Daiki Adachi, Tsukasa Oda, Irene Garcia-Higuera, Nii Tetteh, Alan D. D'Andrea, Makoto Futaki, Shigetaka Asano, Takayuki Yamashita
Journal: Blood (2001)
TECHNIC FOR QUANTITATIVE ESTIMATION OF SUGAR IN VERY SMALL AMOUNTS OF BLOOD
Authors: BENJAMIN KRAMER
Journal: JAMA (1923)

A number of methods for the quantitative determination of sugar in small amounts of blood have been described.<sup>1</sup>Of these the method of Folin and Wu<sup>2</sup>is probably the best, because of its simplicity and accuracy. The amount of blood used, though small, is such that it cannot readily be obtained except by venipuncture. This is often a matter of considerable difficulty with infants. When consecutive determinations are to be made within a short time, it is often impossible. For this reason, blood sugar determinations have heretofore been made in this laboratory by the Bang<sup>3</sup>method. This method has the single advantage of requiring only about 100 mg. of blood for a single determination. The technical difficulties of the sugar determination itself are, however, so great that we have recently been compelled to devise a more simple pro cedure. We have therefore so modified the technic of
Ulcerative colitis complicated by Wenckebach atrioventricular block.
Authors: A Ballinger, M J Farthing
Journal: Gut (1992)

Extracolonic manifestations of inflammatory bowel disease are common and diverse. Cardiac complications, however, are rare and of these pericarditis is the most frequently described association. A 57 year old man with a 20 year history of ulcerative colitis presented with a four day history of retrosternal chest pain and exertional dyspnoea. Electrocardiogram showed Wenckebach atrioventricular block. Three days later he developed bloody diarrhoea and sigmoidoscopy showed active proctocolitis. He was treated with oral prednisolone after which the chest pain and diarrhoea settled within 48 hours. At outpatient review two weeks later he was completely well and the electrocardiogram had returned to normal.
Deficiency of the Long Pentraxin PTX3 Promotes Vascular Inflammation and Atherosclerosis
Authors: Giuseppe Danilo Norata, Patrizia Marchesi, Vivek Krishna Pulakazhi Venu, Fabio Pasqualini, Achille Anselmo, Federica Moalli, Irene Pizzitola, Cecilia Garlanda, Alberto Mantovani, Alberico Luigi Catapano
Journal: Circulation (2009)

Background— Immune responses participate in several phases of atherosclerosis; there is, in fact, increasing evidence that both adaptive immunity and innate immunity tightly regulate atherogenesis. Pentraxins are a superfamily of acute-phase proteins that includes short pentraxins such as C-reactive protein or long pentraxins such as PTX3, a molecule acting as the humoral arm of innate immunity. To address the potential role of PTX3 in atherogenesis, we first investigated the expression of PTX3 during atherogenesis, generated double-knockout mice lacking PTX3 and apolipoprotein E, and then studied the effect of murine PTX3 deficiency on plasma lipids, atherosclerosis development, and gene expression pattern in the vascular wall. Methods and Results— PTX3 expression increases in the vascular wall of apolipoprotein E–knockout mice from 3 up to 18 months of age. Double-knockout mice lacking PTX3 and apolipoprotein E were fed an atherogenic diet for 16 weeks. Aortic lesions were significantly increased in double-knockout mice and mice heterozygous for PTX3 compared with apolipoprotein E–knockout mice. Mice lacking PTX3 showed a more pronounced inflammatory profile in the vascular wall as detected by cDNA microarray and quantitative polymerase chain reaction analysis and an increased macrophage accumulation within the plaque. Finally, lesion size correlated with the number of bone marrow monocytes. Conclusion— PTX3 has atheroprotective effects in mice, which, in light of the cardioprotective effects recently reported, suggests a cardiovascular protective function of the long pentraxin 3 through the modulation of the immunoinflammatory balance in the cardiovascular system.
A NOTE ON THE HISTOLOGY OF DERMATITIS EXFOLIATIVA NEONATORUM
Authors: E. F. SKINNER
Journal: British Journal of Dermatology (1910)

Journal Article A NOTE ON THE HISTOLOGY OF DERMATITIS EXFOLIATIVA NEONATORUM Get access E. F. SKINNER, M.A., M.B.Cantab. M.R.C.P. E. F. SKINNER, M.A., M.B.Cantab. M.R.C.P. Clinical Assistant to the Department for Diseases of the Skin, Sheffield Royal Hospital; Medical Officer in Charge of X‐Ray Department, Children's Hospital, Sheffield Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 22, Issue 3, 1 March 1910, Pages 75–88, https://doi.org/10.1111/j.1365-2133.1910.tb16609.x Published: 01 March 1910
Cost-shifting in Oregon
Authors: Celia Margot Witten
Journal: JAMA (1992)

To the Editor.  —I wish to comment on Dr Eddy's thoughtful analysis of Oregon's proposed Medicaid plan that appeared in a recent issue of JAMA . 1 The plan proposed by the Oregon Department of Human Resources categorized medical services into 709 services, and proposes payment for the first 588. The number of people covered is expanded under this plan.  Eddy discussed several potential criticisms of the Oregon proposal. These criticisms included the question of whether the proposal is, in effect, rationing, and the question of whether the proposal puts an unfair burden on women and children. It seems to me that the proposal will actually not have the effect of dropping coverage for some of the previously covered services, but will merely shift the burden to the physician or health care provider caring for the patients involved.  For example, Eddy mentions that treatments for diaper rash, pharyngitis, and superficial
Moving forward on rationing: an economic view
Authors: C. Donaldson, A. Bate, P. Brambleby, H. Waldner
Journal: BMJ (2008)

Twelve years ago (<i>BMJ</i> 1996;312:1553-4) the <i>BMJ</i> argued that health systems needed to be explicit about rationing and published articles describing different ways of rationing fairly. Here a clinician (doi:10.1136/bmj.a1846), two ethicists (doi:10.1136/bmj.a1850), and four health economists discuss how their ideas have developed—and been put into practice—since then
Gene expression in rod shaped cardiac myocytes, sorted by flow cytometry
Authors: C Diez
Journal: Cardiovascular Research (1998)

Objective: Primary cardiac myocyte cultures are usually contaminated with variable parts of different cell types, such as fibroblasts, endothelial cells and smooth muscle cells. Thus, the objective of our study was to analyse the gene expression in a pure population. Methods: To obtain an homogeneous population, cardiac myocytes from adult rats were fixed with ethanol and sorted by flow cytometry. This approach is suitable for isolating either single cells or up to several thousand cells. To measure the messenger ribonucleic acid (mRNA) expression of different genes at the level of a few rod-shaped myocytes, a cDNA library was created by polymerase chain reaction (PCR). Results: Sorting by a fluorescence-activated cell sorter (FACS) resulted in pure rod-shaped cardiac myocytes and isolated RNA from these cells is undegraded, as shown by Northern blotting. We demonstrated both the expression of housekeeping genes, such as β-actin and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as well as the myocyte-specific transcripts, α-cardiac myosin heavy chain (α-MHC) and β-MHC. Furthermore, we showed the induction of the immediately early gene c-fos at the level of ten sorted cells. Conclusions: This method allows one to study gene expression in different cell types within the heart, in tissue samples or to tackle the problem of heterogeneity within a cell population.
Reaction of systemic lupus erythematosus antinative DNA antibodies with native DNA fragments from 20 to 1,200 base pairs.
Authors: M Papalian, E Lafer, R Wong, B D Stollar
Journal: Journal of Clinical Investigation (1980)

Double-stranded DNA fragments of varying sizes were isolated and tested for binding to systemic lupus erythematosus (SLE) antinative DNA antibodies. Fragments of 20-25, 40-50, 90-110, and 160-180 base pairs (bp), along with intermediate-size pieces were isolated by preparative gel electrophoresis of a limited micrococcal nuclease digest of calf thymus DNA. Larger helical polynucleotides of 160-200, 380, 600-1,000, and 1,200 bp were isolated by preparative gel electrophoresis of DNA from chicken erythrocyte nucleosomes and oligonucleosomes. The fragments behaved as base-paired structures as tested by thermal denaturation, resistance to S1 nuclease, and serological assays with antibodies to native or denatured DNA. At a concentration of 0.27 muM, fragments of 20-25 bp were able to react with two SLE sera in competition with native DNA. With these and two other sera, DNA of 40-50 bp was a much more effective competitor. One serum required DNA greater than 180 bp for competition in the concentration range tested. Denatured fragments were much less effective than native fragments. The results emphasize the heterogeneity of SLE antinative DNA antibodies, confirm that secondary structure of the antigen is important for specific binding to these antibodies, and support the suggestion that bivalent binding to one molecule may be important for high functional affinity.
Mice deficient in the urea-cycle enzyme, carbamoyl phosphate synthetase i, die during the early neonatal period from hyperammonemia
Authors: Paul J. Schofield, Paul J. Schofield, Timothy M. Cox, Thomas C. Caskey, Maki Wakamiya
Journal: Hepatology (1999)

Ammonia liberated during amino acid catabolism in mammals is highly neurotoxic and is detoxified by the five enzymes of the urea cycle that are expressed within the liver. Inborn errors of each of the urea cycle enzymes occur in humans. Carbamoyl phosphate synthetase I (CPSase I; EC 6.3.4.16) is located within the inner mitochondrial matrix and catalyzes the initial rate–limiting step of the urea cycle. Unless treated, complete deficiency of CPSase I, a rare autosomal recessive disease, causes death in newborn infants. Survivors are often mentally retarded and suffer frequent hyperammonemic crises during intercurrent illness or other catabolic stresses. Biochemically, CPSase I deficiency is characterized by high levels of blood ammonia, glutamine, and alanine, with low or absent citrulline and arginine levels. As a first step toward the development of gene therapy directed to the hepatocyte, we have generated a CPSase I-deficient mouse by gene targeting. Mice with homozygous disruption of CPSase I (CPSase [-/-] mice) die within 36 hours of birth with overwhelming hyperammonemia, and without significant liver pathology. This animal is a good model of human CPSase I deficiency.
Visualization of the Left Branch of the Human Atrioventricular Bundle
Authors: HERMAN N. UHLEY, LAURENCE M. RIVKIN
Journal: Circulation (1959)

Visualization of the atrioventricular node and bundles of His in the human heart has been very difficult in the past, so much so that the very existence of specialized conducting tissue in man has been questioned. The authors present a simplified technic permitting visualization of the left bundle of His that facilitates studies in this area.
Finding Neural Tube 'Zippers' May Let Geneticists Tailor Prevention of Defects
Authors: Paul Cotton
Journal: JAMA (1993)

THE MYSTERY of neural tube defects is unraveling at an increasingly rapid pace. On the heels of the finding that folic acid supplements could prevent 60% to 72% of these common birth defects in North American and Northern European populations (<i>JAMA</i>. 1993;269:1257-1261) comes new evidence published this month that there is not one but five separate closures, or "zippers," involved in normal neural tube fusion (<i>Am J Med Genet.</i>1993;47:5). Until now, a specific cause could be identified in only 10% of cases, and the rest "were all just lumped together in a giant, unknown soup you couldn't do anything about because you didn't know" what environmental or genetic factors might be at fault, says Margot Van Allen, MD, clinical associate professor of medical genetics at the University of British Columbia Faculty of Medicine, Vancouver, and first author on the neural tube closure article. Rigid scientific confirmation of Van Allen's
Inequalities in premature mortality in Britain: observational study from 1921 to 2007
Authors: B. Thomas, D. Dorling, G. D. Smith
Journal: BMJ (2010)

<b>Objective</b> To report on the extent of inequality in premature mortality as measured between geographical areas in Britain. <b>Design</b> Observational study of routinely collected mortality data and public records. Population subdivided by age, sex, and geographical area (parliamentary constituencies from 1991 to2007, pre-1974 local authorities over a longer time span). <b>Setting</b> Great Britain. <b>Participants</b> Entire population aged under 75 from 1990 to 2007, and entire population aged under 65 in the periods 1921-39, 1950-3, 1959-63, 1969-73, and 1981-2007. <b>Main outcome measure</b> Relative index of inequality (RII) and ratios of inequality in age-sex standardised mortality ratios under ages 75 and 65. The relative index of inequality is the relative rate of mortality for the hypothetically worst-off compared with the hypothetically best-off person in the population, assuming a linear association between socioeconomic position and risk of mortality. The ratio of inequality is the ratio of the standardised mortality ratio of the most deprived 10% to the least deprived 10%. <b>Results</b> When measured by the relative index of inequality, geographical inequalities in age-sex standardised rates of mortality below age 75 have increased every two years from 1990-1 to 2006-7 without exception. Over this period the relative index of inequality increased from 1.61 (95% confidence interval 1.52 to 1.69) in 1990-1 to 2.14 (2.02 to 2.27) in 2006-7. Simple ratios indicated a brief period around 2001 when a small reduction in inequality was recorded, but this was quickly reversed and inequalities up to the age of 75 have now reached the highest levels reported since at least 1990. Similarly, inequalities in mortality ratios under the age of 65 improved slightly in the early years of this century but the latest figures surpass the most extreme previously reported. Comparison of crudely age-sex standardised rates for those below age 65 from historical records showed that geographical inequalities in mortality are higher in the most recent decade than in any similar time period for which records are available since at least 1921. <b>Conclusions</b> Inequalities in premature mortality between areas of Britain continued to rise steadily during the first decade of the 21st century. The last time in the long economic record that inequalities were almost as high was in the lead up to the economic crash of 1929 and the economic depression of the 1930s. The economic crash of 2008 might precede even greater inequalities in mortality between areas in Britain.