Miracle-dz/UniFAR-FTUs huggingface dataset:
Platelet volume indices in patients with coronary artery disease and acute myocardial infarction: an Indian scenario

Aims: To study platelet volume indices (PVI) in the spectrum of ischaemic heart diseases. Methods: A total of 210 cases were studied; 94 patients had unstable angina (UA) or acute myocardial infarction (AMI) diagnosed on the basis of history, characteristic electrocardiographic changes, and increased cardiac enzyme activities. Seventy patients had stable coronary artery disease (stable CAD) or were admitted for a coronary angiography or coronary artery bypass graft procedure. The third group comprised 30 age and sex matched healthy controls with no history of heart disease and a normal electrocardiogram. Results: All PVI—mean platelet volume (MPV), platelet distribution width (PDW), and platelet large cell ratio (P-LCR)—were significantly raised in patients with AMI and UA (mean MPV, 10.43 (SD, 1.03) fL; mean PDW, 13.19 (SD, 2.34) fL; mean P-LCR, 29.4% (SD, 7.38%)) compared with those with stable CAD (mean MPV, 9.37 (SD, 0.99) fL; mean PDW, 11.35 (SD, 1.95) fL; mean P-LCR, 22.55% (SD, 6.65%)) and the control group (mean MPV, 9.2 (SD, 0.91) fL; mean PDW, 10.75 (SD, l.42) fL; mean P-LCR, 20.65% (SD, 6.14%)). Conclusions: Larger platelets are haemostatically more active and are a risk factor for developing coronary thrombosis, leading to myocardial infarction. Patients with larger platelets can easily be identified during routine haematological analysis and could possibly benefit from preventive treatment. Thus, PVI are an important, simple, effortless, and cost effective tool that should be used and explored extensively, especially in countries such as India, for predicting the possibility of impending acute events.
Discussion of "Capital Regulation and Tail Risk"

During the recent financial crisis, the notion of “tail risk”— exposure to very unlikely yet massive losses—rapidly became the foremost concern of regulators, banks, and other market participants alike. Perotti, Ratnovski, and Vlahu (this issue) analyze how the presence of such risks affects the relationship between bank capital and bank risk taking. With policymakers looking to revamp capital regulations so as to prevent a similar crisis from occurring, there is no question that this is a very timely paper indeed. Perotti, Ratnovski, and Vlahu argue that tail risk differs from the “normal” risks modeled in the banking literature because it can wipe out any amount of bank capital. As a result, the presence of tail risk weakens the effectiveness of capital in reducing risk-shifting incentives. Moreover, when capital is costly to raise, the combination of tail risk and less-catastrophic (“non-tail”) risk can complicate the relationship between capital and risk shifting, making it non-monotonic: although an increase in bank capital from low levels tends to deter risk shifting, at even higher levels the bank may start taking risks again, only to revert to a safer strategy if capital is sufficiently high. This possible reversal arises from the fact that regulatory capital requirements apply not only ex ante but also to the bank’s condition after risks have materialized. The reversal becomes stronger as the probability of tail risks increases. The upshot is that capital regulation is even less effective in the presence of tail risk. This paper makes a number of innovations, including not only the distinction between tail and non-tail risk but also the impact of risk realizations on ex post capital adequacy and how, in the presence of recapitalization costs, this in turn feeds back into initial risk choices. Nevertheless, I think there are several aspects in which it could be
Exercise programs to improve gait performance in people with lower limb amputation: A systematic review

Background: Few studies have explored the effects of exercise on gait performance in people with lower limb amputations. Objectives: To (1) summarize the effects of exercise programs on gait performance and (2) assess the overall quality of the evidence for adults ambulating with leg prostheses. Study design: Systematic review. Methods: Six databases were searched for one- and two-group studies published through June 2013 reporting effects of exercise on gait speed, a universal measure of performance in lower limb prosthetic users. The search adhered to a predetermined protocol following Cochrane Collaboration guidelines. Results: In all, 623 citations were reviewed and eight studies included. The quality level of the combined evidence was low with few randomized control trials and multiple sources of bias evident within the heterogeneous group of studies. The 11 exercise programs, including three control conditions, demonstrated small to large effect size improvements in self-selected gait speed. Use of exercise to improve gait speed was supported by low-quality level evidence, with low–moderate quality evidence to suggest that specific functional exercise programs were more effective than supervised walking. Conclusion: Using exercise to improve gait speed in people with lower limb amputation received a B grade recommendation. Future high-quality research is required. Clinical relevance Supervised walking, muscle strengthening, balance exercises, gait training, and functional training programs demonstrated small to large effect size gait performance improvements in people with lower limb amputation. Self-selected gait speed was the most consistent outcome measure. Exercise programs emphasizing resisted gait and functional training were more effective than supervised walking.
The Molecular Scaffold KSR1 Regulates the Proliferative and Oncogenic Potential of Cells

ABSTRACT The specificity of signaling through mitogen-activated protein kinase pathways has been attributed to both the control of intensity and duration of signaling and the actions of protein scaffolds. Here we demonstrate that the molecular scaffold KSR1 regulates the intensity and duration of ERK activation to modulate a cell's proliferative and oncogenic potential. Deletion of KSR1 eliminates the prolonged phase of ERK activation induced by platelet-derived growth factor and blocks RasV12-induced transformation. The introduction of KSR1 into KSR1−/− mouse embryo fibroblasts causes a concentration-dependent increase in signaling and transformation, to a maximum at 14 times the wild-type KSR1 expression levels, but inhibits these responses at higher expression levels. An increase in KSR1 expression to levels that are optimal for signaling leads to a threefold increase in proliferative capacity and is coincident with the level of KSR1 expression that maximally associates with all members of the Raf/MEK/ERK cascade. These data reveal that cells contain a reserve proliferative capacity that is accessible by the optimal expression of a noncatalytic signaling component and that altering the expression level of a molecular scaffold can modulate the actions of growth factors and oncogenes.
Association between circulating oxidized low-density lipoprotein and incidence of the metabolic syndrome.

CONTEXT Experimental data support the hypothesis that oxidized low-density lipoprotein (LDL) is associated with the metabolic syndrome. However, this hypothesis has not been tested in humans. OBJECTIVE To establish the relation of oxidized LDL with metabolic syndrome in the general community. DESIGN, SETTING, AND PARTICIPANTS The Coronary Artery Risk Development in Young Adults (CARDIA) study is a population-based, prospective, observational study. We studied 1889 participants who were between the ages of 18 and 30 years at the time of recruitment in 1985 and 1986 and living in 1 of 4 US metropolitan areas (41% African American; 56% women) and were seen both at year 15 (2000-2001, ages 33-45 years) and year 20 examinations (2005-2006). MAIN OUTCOME MEASURE The longitudinal association of oxidized LDL and incident metabolic syndrome. Oxidized LDL was measured with a monoclonal antibody-based enzyme-linked immunosorbent assay. The metabolic syndrome was defined according to the Adult Treatment Panel III of the National Cholesterol Education Program. RESULTS Incident metabolic syndrome was diagnosed at the year 20 follow-up in 12.9% (243 of 1889) of participants who did not have metabolic syndrome at the 15-year follow-up. The odds ratios (ORs) for incident metabolic syndrome after 5 years' follow-up and adjusted for age, sex, race, study center, cigarette smoking, body mass index, physical activity, and LDL cholesterol levels by quintiles of oxidized LDL were 2.1 (95% confidence interval [CI], 1.1-3.8) for the second quintile (55.4-69.1 U/L); 2.4 (95% CI, 1.3-4.3) for the third quintile (69.2-81.2 U/L); 2.8 (95% CI, 1.5-5.1) for the fourth quintile (81.3-97.3 U/L); and 3.5 (95% CI, 1.9-6.6) for the fifth quintile (> or =97.4 U/L). The adjusted ORs for incidence of dichotomous components of metabolic syndrome in the highest vs the lowest quintile of oxidized LDL were 2.1 (95% CI, 1.2-3.6) for abdominal obesity, 2.4 (95% CI, 1.5-3.8) for high fasting glucose, and 2.1 (95% CI, 1.1-4.0) for high triglycerides. Low-density lipoprotein cholesterol was not associated with incident metabolic syndrome or with any of its components in the fully adjusted model containing oxidized LDL. CONCLUSION Higher concentration of oxidized LDL was associated with increased incidence of metabolic syndrome overall, as well as its components of abdominal obesity, hyperglycemia, and hypertriglyceridemia.
Improving game-tree search with evolutionary neural networks

Neural networks were evolved to constrain minimax search in the game of Othello. At each level of the search tree, such focus networks decide which moves are to be explored. Based on the evolved knowledge of the minimax algorithm's advantages and limitations the networks hide problem nodes from minimax. Focus networks were encoded in marker-based chromosomes and evolved against a full-width minimax opponent using the same heuristic board evaluation function. The focus network was able to guide the minimax search away from poor information, resulting in stronger play while examining far fewer nodes. <<ETX>>
Modelling a population with Barrett's oesophagus from oesophageal adenocarcinoma incidence data

Objective. A recent study of adenocarcinoma of the oesophagus (ACO) incidence rates in Denmark showed a steep fall in the over-80 population, interpreted as the result of a decline in the prevalence of Barrett's oesophagus (BO) in this age group, for which three hypotheses were advanced: the specific mortality from ACO and, superimposed, either excess mortality from causes of death unrelated to ACO or a birth cohort effect. The aim of this study was to create models estimating the BO population fitting each of these three hypotheses, in order to select the most plausible hypothesis and to gain insight into the Danish BO population. Material and methods. Models were designed for these three hypotheses, conforming to the generally accepted 0.4–0.5% annual ACO incidence in BO patients. These models employed expectation-maximization (EM) algorithms, Danish life tables and the observed ACO incidence rates. The models enabled the estimation of a BO population for each hypothesis. Results. After testing against set criteria, the most plausible model was found to be that describing a birth cohort effect which predicted a ±5% annual rise in the prevalence of BO and, consequently, in the incidence rate of ACO in Denmark. This prediction was borne out over the subsequent decade. Conclusions. This rising ACO incidence rate is likely to continue into the foreseeable future. The use of EM algorithms enabled a first estimate of the BO population at risk of ACO, although, owing to the limitations imposed by the models, the age- and gender-specific ACO risk for the entire Danish BO population could not as yet be ascertained.
Regulation of expression of genes coding for small, acid-soluble proteins of Bacillus subtilis spores: studies using lacZ gene fusions

We constructed in-frame translational fusions of the Escherichia coli lacZ gene with four genes (sspA, sspB, sspD, and sspE) which code for small, acid-soluble spore proteins of Bacillus subtilis, and integrated these fusions into the chromosomes of various B. subtilis strains. With single copies of the fusions in wild-type B. subtilis, beta-galactosidase was synthesized only during sporulation, with the amounts accumulated being sspB much greater than sspE greater than or equal to sspA greater than or equal to sspD. Greater than 97% of the beta-galactosidase was found in the developing forespore, and the great majority was incorporated into mature spores. Less than 2% of the maximum amount of beta-galactosidase was made when these fusions were introduced into B. subtilis strains blocked in stages 0 and II of sporulation, as well as in some stage III mutants. Other stage III mutants, as well as stage IV and V mutants, had no effect on beta-galactosidase synthesis. Increasing the copy number of the sspA-, sspD-, or sspE-lacZ fusions (up to 17-fold for sspE-lacZ) in wild-type B. subtilis resulted in a parallel increase in the amount of beta-galactosidase accumulated (again only in sporulation and with greater than 95% in the developing forespore), with no significant effect on wild-type small, acid-soluble spore protein production. Similarly, the absence of one or more wild-type ssp genes or the presence of multiple copies of wild-type ssp genes had no effect on the expression of the lacZ fusions tested. These data indicate that these ssp-lacZ fusions escape the autoregulation seen for the intact sspA and sspB genes. Strikingly, the kinetics of beta-galactosidase synthesis were identical for all four ssp-lacZ fusions and paralleled those of glucose dehydrogenase synthesis. Similarly, all asporogenous mutants tested had identical effects on both glucose dehydrogenase and ssp-lacZ fusion expression.
WHEN TO CUT A STAND OF TREES?

This paper revisits the debate over the economic optimality of different timber harvest rules. The traditional Faustmann and Maximum Sustained Yield rotation determinations are confined to a deterministic world. Once stochasticity is introduced into the model formulation and the additional rental and management costs due to postponement of harvest are taken into account, we find that the optimal stopping time becomes random and varies in response to changes in the underlying price and growth processes. As a result, this stochastic optimal stopping time is bounded by the Faustmann cutting age from below if variabilities of the stochastic processes diminish to zero, but not necessarily by the MSY rotation from above.
Genomic and proteomic comparisons between bacterial and archaeal genomes and related comparisons with the yeast and fly genomes.

Bacterial, archaeal, yeast, and fly genomes are compared with respect to predicted highly expressed (PHX) genes and several genomic properties. There is a striking difference in the status of PHX ribosomal protein (RP) genes where the archaeal genome generally encodes more RP genes and fewer PHX RPs compared with bacterial genomes. The increase in RPs in archaea and eukaryotes compared with that in bacteria may reflect a more complex set of interactions in archaea and eukaryotes in regulating translation, e.g., differences in structure requiring scaffolding of longer rRNA molecules, expanded interactions with the chaperone machinery, and, in eukaryotic interactions with endoplasmic reticulum components. The yeast genome is similar to fast-growing bacteria in PHX genes but also features several cytoskeletal genes, including actin and tropomyosin, and several signal transduction regulatory proteins from the 14.3. 3 family. The most PHX genes of Drosophila encode cytoskeletal and exoskeletal proteins. We found that the preference of a microorganism for an anaerobic metabolism correlates with the number of PHX enzymes of the glycolysis pathway that well exceeds the number of PHX enzymes acting in the tricarboxylic acid cycle. Conversely, if the number of PHX enzymes of the tricarboxylic acid cycle well exceeds the PHX enzymes of glycolysis, an aerobic metabolism is preferred. Where the numbers are approximately commensurate, a facultative growth behavior prevails.
Primary Hyperparathyroidism and the Risk of Fracture: A Population‐Based Study

While severe primary hyperparathyroidism (HPT) is clearly associated with osteitis fibrosa cystica, it remains uncertain whether mild, asymptomatic primary HPT adversely affects the skeleton. Thus, we assessed the incidence of age‐related fractures in a large, population‐based inception cohort of 407 cases of primary HPT (93 men and 314 women) recognized during the 28‐year period, 1965–1992. Fracture risk was assessed by comparing new fractures at each site to the number expected from gender‐ and age‐specific fracture incidence rates for the general population (standardized incidence ratios, SIRs). These community patients with primary HPT mostly had mild disease (mean ± SD serum calcium, 10.9 ± 0.6 mg/dl). Altogether, 471 fractures occurred during 5766 person‐years of follow‐up. Overall fracture risk was significantly increased in these patients (SIR 1.3, 95% confidence interval [CI] 1.1–1.5). Primary HPT was associated with an increased risk of vertebral (SIR 3.2, 95% CI 2.5–4.0), distal forearm (SIR 2.2, 95% CI 1.6–2.9), rib (SIR 2.7, 95% CI 2.1–3.5), and pelvic fractures (SIR 2.1, 95% CI 1.1–3.5). The risk of proximal femur fractures was only marginally increased (SIR 1.4, 95% CI 1.0–2.0). By univariate analysis, increasing age and female gender were significant predictors of fracture risk, although higher serum calcium levels were also associated with increased fracture risk, and parathyroid surgery may have had a protective effect. By multivariate analysis, however, only age (relative hazard [RH] per 10‐year increase, 1.6, 95% CI 1.4–1.9) and female gender (RH 2.3, 95% CI 1.2–4.1) remained significant independent predictors of fracture risk. Thus, primary HPT among unselected patients in the community is associated with a significant increase in the risk of vertebral, Colles', rib, and pelvic fractures. These data have important implications for the current trend to recommend nonsurgical management for patients with mild primary HPT.
Abuse of the elderly.

The abuse of older people by family members dates back to ancient times. Until the advent of initiatives to address child abuse and domestic violence in the last quarter of the 20th century it remained a private matter hidden from public view. Initially seen as a social welfare issue and subsequently a problem of ageing abuse of the elderly like other forms of family violence has developed into a public health and criminal justice concern. These two fields – public health and criminal justice – have therefore dictated to a large extent how abuse of the elderly is viewed how it is analysed and how it is dealt with. This chapter focuses on abuse of older people by family members or others known to them either in their homes or in residential or other institutional settings. It does not cover other types of violence that may be directed at older people such as violence by strangers street crime gang warfare or military conflict. (excerpt)
Solid phase testing in the HLA laboratory: implications for organ allocation

This piece was originally requested as a white paper from the Scientific and Clinical Affairs Committee of the American Society for Histocompatibility and Immunogenetics (ASHI), of which the author was then Chairman. Upon review by the ASHI Board of Directors and the Editors of their journal, it was considered too controversial for publication. It is intended to be provocative and controversial; it is not intended as a review of the literature. Though written with a decided ‘American point of view’, it is of importance that the issues facing US transplantation and laboratory testing efforts are shared to varying degrees by the international community, and who, unlike some of their American cousins, may be able to tolerate a spirited discussion. Sadly, we sometimes forget that dissent from dogma can be fun!
Pulmonary tuberculosis, impaired lung function, disability and quality of life in a high-burden setting.

SETTING Tuberculosis treatment clinic in Papua, Indonesia. OBJECTIVE To document the impact of pulmonary tuberculosis (PTB) on lung function, exercise tolerance and quality of life (QOL). DESIGN A prospective cohort study of 115 patients with smear-positive PTB followed for 6 months. Demographics, disease history, sputum microbiology, spirometry, 6-minute weight.walk distance (6MWWD) and QOL (modified St George's Respiratory Questionnaire) were measured at diagnosis and at 2 and 6 months. Analysis was restricted to the 69/115 (60%) subjects who attended all follow-up visits. RESULTS Subjects who attended all visits were less likely than the full cohort to be of Papuan ethnicity (P < 0.05), were more likely to be cured (P < 0.001) and had better lung function at diagnosis (P < 0.05). Significant lung function impairment (forced expiratory volume in 1 second [FEV(1)] <60% predicted) was found in 27/69 (39%) at diagnosis. Although this fell during treatment (P < 0.01), 17/69 (24.6%) had persisting significant lung function impairment at treatment completion. As lung function recovered, exercise tolerance (6MWWD) rose by 12.3% (P < 0.001) and QOL improved (P < 0.001). CONCLUSION In a high-burden setting, PTB causes prolonged, significant impairment of lung function, exercise tolerance and QOL. Current measures of disease burden are likely to underestimate the true impact of disease. Earlier diagnosis and disease-modifying treatments may reduce the long-term impact of PTB.
Na+/H+ exchangers: physiology and link to hypertension and organ ischemia

Purpose of reviewNa+/H+ exchangers (NHEs) are ubiquitous proteins with a very wide array of physiological functions, which are summarized here with an emphasis on the most recent advances. Hypertension and organ ischemia are two disease states of paramount importance in which NHEs have been implicated. The involvement of NHEs in the pathophysiology of these disorders is incompletely understood. This paper reviews the principal findings and current hypotheses linking NHE dysfunction to hypertension and ischemia. Recent findingsWith the advent of large-scale sequencing projects and powerful in-silico analyses, we have come to know what is most likely the entire mammalian NHE gene family. Recent advances have detailed the roles of NHE proteins, exploring new functions such as anchoring, scaffolding and pH regulation of intracellular compartments. Studies of NHEs in disease models, though not conclusive to date, have contributed new evidence on the interplay of ion transporters and the delicate ion balances that may become disrupted. SummaryThis review provides the interested reader with a concise overview of NHE physiology, and addresses the implication of NHEs in the pathophysiology of hypertension and organ ischemia in light of the most recent literature.