Miracle-dz/UniFAR-FTUs huggingface dataset:
Comparative effects of rosuvastatin and atorvastatin on glucose metabolism and adipokine levels in non‐diabetic patients with dyslipidaemia: a prospective randomised open‐label study

Aims: The impact of statins on glucose metabolism and adipokines remains controversial. We compared the effects of rosuvastatin and atorvastatin on glucose homeostasis, insulin sensitivity (IS), adiponectin and leptin levels as well as systemic inflammation in non‐diabetic patients with dyslipidaemia.
Establishment of a Cell Model Based on FKBP12 Dimerization for Screening of FK506-like Neurotrophic Small Molecular Compounds

FK506 is an efficient immunosuppressive agent with an increasing number of clinical applications. It has been approved to prevent rejection in transplant patients and be efficacious in several autoimmune diseases. Its immunosuppressive activity results from binding to receptor proteins designated as immunophilins (i.e., FKBP12, FK506 binding protein). Recent studies have suggested that FK506 can promote neurite outgrowth as a 2nd activity. Furthermore, it has been shown that the neurotrophic property of FK506 is independent of its immunosuppressive action. Although the mechanism of its neurotrophic activity has not yet been well elucidated, FKBP12 is identified as a drug target, and much effort has been directed toward the design of FKBP12-binding molecules, which are neurotrophic but nonimmunosuppressive, for clinical use. In this present study, the authors constructed a stable cell line, which underwent apoptosis upon treatment by AP20187, a wholly synthesized, cell-permeable dimeric FK506 derivative, based on FKBP12-mBax dimerization. This AP20187-mediated apoptosiswas rapidly reversed by the addition of an FKBP12-binding competitormolecule (FK506 or rapamycin), indicating that this cell line might be used to screen FK506 derivatives. Using the screening model, hundreds of synthetic FK506 analogs were analyzed. A promising compound, named N308, was obtained. The results showed that N308 could inhibit AP20187-induced gene-modified target cell apoptosis and elicit augmentation of neurite extension from both cultured PC-12 cells and chicken dorsal root ganglia cultures.
Creating a typology of analytics Master’s degrees in UK universities: Implications for employers and educators

Abstract In recent years there has been a growth in specialised analytics Master’s degrees, in the UK and beyond. However, there has been little research into the contents of such degrees. In particular, the role disciplines such as operational research play within them remains an under-explored area. Using a mixed-methods approach, this article analyses UK Master’s degrees in analytics to determine a typology of provisions. Firstly, a support vector classifier is used to identify the traditional disciplines analytics degrees most closely align with. Secondly, a hybrid approach to analyse the modules included in analytics curricula is employed, as part of which a new metric (module topic weighting) is presented. The analysis identifies two main categories of degrees, the first aligning with machine learning and computing topics; the second operational research and business themes. The paper concludes by evaluating the implications this has for students, employers, educators and the operational research discipline.
Clinical Significance of the Champagne Bottle Neck Sign in the Extracranial Carotid Arteries of Patients with Moyamoya Disease

BACKGROUND AND PURPOSE: The champagne bottle neck sign represents a rapid reduction in the extracranial ICA diameters and is a characteristic feature of Moyamoya disease. However, the clinical significance of the champagne bottle neck sign is unclear. We investigated the relationship between the champagne bottle neck sign and the clinical and hemodynamic stages of Moyamoya disease. MATERIALS AND METHODS: We analyzed 14 patients with Moyamoya disease before revascularization (5 men, 9 women; age, 43.2 ± 19.3 years). The ratio of the extracranial ICA and common carotid artery diameters was determined using carotid ultrasonography or cerebral angiography; a ratio of < 0.5 was considered champagne bottle neck sign–positive. The clinical disease stage was determined using the Suzuki angiographic grading system. CBF and cerebral vasoreactivity also were measured. RESULTS: The ICA/common carotid artery ratio (expressed as median [interquartile range]) decreased as the clinical stage advanced (stages I–II, 0.71 [0.60–0.77]; stages III–IV, 0.49 [0.45–0.57]; stages V–VI, 0.38 [0.34–0.47]; P < .001). Lower ICA/common carotid artery ratio tended to occur in symptomatic versus asymptomatic arteries (0.47 [0.40–0.53] versus 0.57 [0.40–0.66], respectively; P = .06). Although the ICA/common carotid artery ratio was not related to cerebral perfusion, it decreased as cerebral vasoreactivity decreased (P < .01). All champagne bottle neck sign–positive arteries were classified as Suzuki stage ≥III, 73% were symptomatic, and 89% exhibited reduced cerebral vasoreactivity. In contrast, all champagne bottle neck sign–negative arteries were Suzuki stage ≤III, 67% were asymptomatic, and all showed preserved cerebral vasoreactivity. CONCLUSIONS: The champagne bottle neck sign was related to advanced clinical stage, clinical symptoms, and impaired cerebral vasoreactivity. Thus, detection of the champagne bottle neck sign might be useful in determining the clinical and hemodynamic stages of Moyamoya disease.
Chromosomal loss and breakage in mouse bone marrow and spleen cells exposed to benzene in vivo.

Benzene is a widely recognized human and animal carcinogen. In spite of considerable research, relatively little is known about the genotoxic events that accompany benzene exposure in vivo. To gain insights into the mechanisms underlying the genotoxic effects of benzene, we have characterized the origin of the micronuclei that are formed in bone marrow erythrocytes and splenic lymphocytes of benzene-treated mice using two molecular cytogenetic approaches: (a) fluorescence in situ hybridization with a centromeric DNA probe; and (b) staining with the calcinosis-Raynaud's phenomenon-esophageal dismobility-sclerodactyly-telangiectasia syndrome of scleroderma (CREST) antibody, an antibody recognizing a centromeric protein. Following the p.o. administration of benzene (220 or 440 mg/kg) to male CD-1 mice, a significant increase in micronuclei was observed in the bone marrow erythrocytes. In situ hybridization with a centromeric DNA probe and immunofluorescent staining with the CREST antibody indicated that the micronuclei in bone marrow erythrocytes were formed from both chromosome loss and breakage. The majority of the micronuclei originated from chromosome breakage. A dose-related increase in micronucleated cells was also observed in splenocyte cultures established from these benzene-treated animals. In contrast to the bone marrow erythrocyte results, the majority of benzene-induced micronuclei in the cytokinesis-blocked splenocytes labeled with the CREST antibody indicating that these micronuclei were the result of whole chromosome loss. These data demonstrate that both aneuploidy and chromosomal breakage are early genotoxic events induced by benzene or its metabolites in vivo and also indicate that the nature of the chromosomal alterations may vary depending on the target organ or cell type.
Analysis of bipolar maintenance treatment with lithium versus olanzapine utilizing Multi‐state Outcome Analysis of Treatments (MOAT)

Survival analysis has superseded most other analytic techniques for maintenance treatment studies over recent decades, despite providing results based solely on a single time‐point predefined event. The aim of the present study was to develop the Multi‐state Outcome Analysis of Treatments (MOAT), to provide more pragmatic information for clinicians and investigators in guiding maintenance treatment decisions. The present study was one of two published studies on the development of MOAT procedures, involving a one‐year comparison of olanzapine versus lithium in recently manic patients.
Return Reversal in UK Shares

We investigate whether shares that have experienced extreme stock market performance over a five year period become mis-priced leading to opportunities for exploiting that mis-pricing. The results cast serious doubt on the efficiency of the UK stock market to price these shares. This means that managers of these companies may be receiving distorted signals from the market, which will have a knock-on effect on a range of managerial decisions, from the estimation of the equity cost of capital to the timing of share issues. More specifically we find that the 10 per cent of shares with the worst total share return record over five years go on to produce the highest returns in the subsequent five years with an average out-performance of 8.9% per year - defying those who would write these companies off as the 'dogs' of the market. Those that are currently flying high on the market (the 10% best performers over five years) go on to under-perform by 47% over the next five years - suggesting that the 'darlings' of the market tend to become over-priced leading to the possibility of excessive resource allocation in their favour. This systematic long-term reversal of share returns is observed over the entire period 1960-2002. Loser shares (the worst performing shares in the prior five years) out-perform winner shares (the best performing shares over the prior five years) by about 14% per year. By separating the firm size (market capitalization) effect from the return reversal effect we show the presence of both. This evidence is in direct contradiction to Clare and Thomas (1995), who found no return reversal in UK shares following an adjustment for size. Return reversal is a feature of large as well as small companies and a seven-part consideration of risk does not substantiate the argument that loser out-performance is compensation for risk. We also consider some the arguments concerning the behavioural and institutional constraints that may permit the continuance of the return reversal effect over a long period with insufficient arbitrage pressure to eliminate it.
Regulation of the glutamine transporter SN1 by extracellular pH and intracellular sodium ions

The glutamine transporter SN1 has recently been identified as one of the major glutamine transporters in hepatocytes and brain astrocytes. It appears to be the molecular correlate of system N amino acid transport. Two different transport mechanisms have been proposed for this transporter. These are an electroneutral mechanism, in which glutamine uptake is coupled to an exchange of 1Na+ and 1H+, or an electrogenic mechanism coupled to the exchange of 2Na+ against 1H+. This study was performed to solve these discrepancies and to investigate the reversibility of the transporter. When SN1 was expressed in Xenopus laevis oocytes, glutamine uptake was accompanied by a cotransport of 2–3 Na+ ions as determined by 22Na+ fluxes. However, at the same time a rapid release of intracellular Na+ was observed indicating an active exchange of Na+ ions. The driving force of the proton electrochemical gradient was equivalent to that of the sodium electrochemical gradient. Acidification of the extracellular medium caused the transporter to run in reverse and to release glutamine. Determination of accumulation ratios at different driving forces were in agreement with an electroneutral 1Na+‐glutamine cotransport‐1H+ antiport. Inward currents that were observed during glutamine uptake were much smaller than expected for a stoichiometric cotransport of charges. A slippage mode in the transporter mechanism and pH‐regulated endogenous oocyte cation channels are likely to contribute to the observed currents.
A COLORIMETRIC MICRO-METHOD FOR THE DETERMINATION OF GLUTATHIONE.

1. A rapid colorimetric and apparently specific micromethod for the determination of total glutathione in small amounts of tissue is described. Generally, less than 30mg. of tissue is sufficient and this is homogenized in ice-cold 3% metaphosphoric acid. The product is filtered through sintered glass and neutralized or diluted before being added to a cuvette containing phosphate buffer, pH7.1, 5,5'-dithiobis-(2-nitrobenzoic acid), EDTA and glutathione reductase. Addition of NADPH(2) to the system initiates a progressive reduction of 5,5'-dithiobis-(2-nitrobenzoic acid) by catalytic amounts of GSH, and this causes a colour increase at 412mmu. The rate of this change, calculated over 5min. , is proportional to the total amount of glutathione present, and consequently unknown concentrations may be determined by reference to standards. 2. A preparation (based on that of Racker, 1955) of a suitable sample of glutathione reductase from yeast is described. 3. A less specific and less sensitive determination of extracted thiol groups with 5,5'-dithiobis-(2-nitrobenzoic acid) at pH8.0, based on observations of Ellman (1959) and Jocelyn (1962), is also described. 4. Although the precise nature of the reaction is not known, evidence is put forward to support a process of cyclo-reduction. GSSG is reduced enzymically to GSH, which reacts with 5,5'-dithiobis-(2-nitrobenzoic acid) to produce a coloured ion: [Formula: see text] (E(max.) 412mmu) and a mixed disulphide. This disulphide reacts with further quantities of GSH to liberate another ion and GSSG, which then re-enters the cycle.
Comparison of the effectiveness of duloxetine in depressed patients with and without a family history of affective disorders in first-degree relatives

Background It remains unclear whether or not a positive family history of affective disorders predicts the effectiveness of antidepressant treatment of depression. Aims Assess the relationship of a family history of affective disorders to the efficacy of duloxetine in the treatment of depressive disorder. Methods Seventy-seven patients with depressive disorder (as defined by the 10th edition of the International Classification of Diseases, ICD-10) were enrolled in the study and treated with standard doses of duloxetine for 12 weeks. Among these patients 37 had a family history of affective disorder in first-degree relatives and 40 did not. The Hamilton Depression rating scale (HAMD-17), Hamilton Anxiety rating scale (HAMA), Side Effects Rating Scale (SERS), Snaith-Hamilton Pleasure Scale (SHAPS), and Beck Depression Inventory (BDI) were assessed at baseline and at the end of the 2nd, 4th, 6th, 8th, and 12th week after enrollment. Repeated measures analysis of variance and logistic regression were used to analyze the association between a family history of affective disorders and the efficacy of duloxetine. Results Patients with a positive family history of affective disorders had an earlier age of onset, a longer duration of illness, a higher level of psychic anxiety, and more prominent anhedonia. Repeated measures analysis of variance showed a significant improvement in the severity of depression over the 12 weeks but no differences in the magnitude or speed of improvement between the two groups. Treatment was considered effective (i.e., drop in baseline HAMD-17 total score of ≥50%) in 75.7% of those with a family history of affective disorders and in 77.5% of those without a family history (X2=0.04, p=0.850). Conclusions Family history of affective disorders is not associated with the effectiveness of duloxetine in the acute treatment of depressive disorder.
Thermotolerance of heat-shocked Listeria monocytogenes in milk exposed to high-temperature, short-time pasteurization

The effect of prior heat shock (48 degrees C for 15 min) on the thermotolerance of Listeria monocytogenes at the minimal high-temperature, short-time (71.7 degrees C for 15 s) parameters required by the Pasteurized Milk Ordinance was examined. The mean D71.7 degrees C value for heat-shocked L. monocytogenes was 4.6 +/- 0.5 s (control D = 3.0 +/- 1.0 s); the ratio of D to control D was 1.5. The increased thermotolerance of heat-shocked Listeria cells was not significant and appeared unlikely to have practical implications, in terms of risk assessment, for the safety of pasteurized milk.
Catecholamine‐associated refractory hypertension following acute intracranial hemorrhage: Control with propranolol

Seven patients (4 with subarachnoid hemorrhage, 2 with intracerebral hemorrhage, and 1 with massive cerebral infarction) had acute arterial hypertension refractory to control by several antihypertensive drugs (hydralazine, sodium nitroprusside, α‐methyldopa, and trimethaphan camsylate) used singly or in combination. In each case, catecholamine excretion–measured by urinary norepinephrine plus epinephrine–was markedly elevated, averaging 218 m̈g/day. Patients without the acute refractory hypertension had normal or only slightly elevated urinary catecholamine levels (mean, 72 m̈g/day). The β‐adrenergic blocking agent propranolol, in doses between 20 and 40 mg every 6 hours, successfully controlled blood pressure, while other agents failed. The intense sympathetic nervous system discharge resulting in acute refractory hypertension may be due to injury to the diencephalon or brainstem (or both) or to diffuse brain dysfunction from increased intracranial pressure or intracranial blood.
Mass mortality of common dolphins (Delphinus delphis) in south west England due to incidental capture in fishing gear

In the first quarter of 1992, 118 dolphin carcases, of which 54 were positively identified as common dolphins (Delphinus delphis), were found stranded on the coast of Cornwall and Devon. To determine the cause, detailed post mortem examinations were carried out on 38 of the carcases, and the results were compared with those from 20 common dolphins that stranded on the coast of Cornwall and Devon in the previous 15 months. There was no evidence that the deaths were due to an infectious or parasitic disease, or acute intoxication by any of the algal toxins, trace metals or chlorinated hydrocarbons measured. However, 30 of the 38 dolphins showed signs associated with incidental capture in fishing gear. Skin lesions characteristic of capture in a small-meshed net and the predominance of recently ingested Atlantic mackerel (Scomber scombrus) and pilchard (Sardina pilchardus) in the stomachs of the dolphins suggested that they had been caught in the trawl or purse seine nets used for these fish. There is insufficient information to explain why this high mortality occurred in 1992 and not in other years.
Cefalotin as antimicrobial prophylaxis in patients with known intraoperative anaphylaxis to cefazolin.

BACKGROUND The most common trigger for intraoperative anaphylaxis in Western Australia for the period 2014-5 was an antibiotic used for surgical prophylaxis, cefazolin. In these patients who subsequently present for surgery, alternative cephalosporins are forbidden by current guidelines because of concerns regarding an increased risk of anaphylaxis. However, consideration of the structure-activity relationships relevant to anaphylaxis suggests that cefalotin is a safe alternative because of structural dissimilarities, although there are no pubished clinical data relevant to the perioperative setting. METHODS Patients diagnosed with intraoperative anaphylaxis to cefazolin at the Western Australian Anaesthetic Allergy Clinic were tested with intradermal cefalotin and, if negative, subsequently challenged i.v. If tolerated, cefalotin was recommended for subsequent surgery, and subjects were followed up to determine the safety of subsequent intraoperative doses. RESULTS Twenty-one subjects diagnosed with immediate hypersensitivity to cephazolin, including 19 subjects with confirmed anaphylaxis, participated. None tested positive to intradermal cefalotin, and all received a graded i.v. challenge to cefalotin without developing signs or symptoms of anaphylaxis. Three subjects subsequently received intraoperative cefalotin 12-139 days later without adverse events. CONCLUSIONS A negative intradermal cefalotin skin test has a good negative predictive value in patients who have previously suffered anaphylaxis to cefazolin, allowing the rational and desirable use of this alternative cephalosporin for future surgery and the avoidance of less desirable antimicrobial agents.
Moderating Effects of Coping on Associations between Autonomic Arousal and Adolescent Internalizing and Externalizing Problems

Few published studies have looked at the moderating role of coping styles on the association between stress reactivity and internalizing/externalizing problems despite theory suggesting that particular constellations of stress reactivity and coping may be uniquely problematic. The present study aimed to test the interactive effects of coping and psychophysiology on self- and parent-report broad-spectrum problems in a normative adolescent sample. Sixty-six late adolescents (ages 16–17; 60% female, 13% ethnic minority) completed questionnaires on coping, stressful life events, and behavioral/emotional problems, with parents also providing data on problems. In addition, skin conductance and heart rate data were obtained during a brief interview designed to elicit the feeling of reexperiencing a recent stressful experience. Path analytic results suggested evidence for several interaction effects between coping and skin conductance. Most commonly, the pattern of effects was consistent with a buffering effect for productive (or problem-focused) coping strategies against elevated internalizing and externalizing problems for individuals who demonstrated high physiological stress reactivity. Evidence for interaction effects related to respiratory sinus arrhythmia was less frequent and less consistent with a priori hypotheses. Although our cross-sectional results should be interpreted cautiously, the interactions reported here suggest that improving coping skills may be particularly beneficial for youth with high psychophysiological arousal.
The Effect of Dalteparin, a Kind of Low Molecular Weight Heparin, on Lung Adenocarcinoma A549 Cell Line In Vitro

The beneficial effects of unfractionated heparin and low molecular weight heparin on cancer progression have been reported. In the study, the effect of dalteparin on pulmonary adenocarcinoma A549 cell line was observed in vitro. Our experiments revealed that: (1) dalteparin can inhibit the cell viability dose-dependently and time-dependently; (2) dalteparin can arrest the A549 cells in G1 phase and induce them to early apoptosis; (3) dalteparin exerts its effects through p21WAF1 and p27KIP1 proteins; and (4) the changes of p21WAF1 and p27KIP1 proteins caused by dalteparin occurred at posttranscriptional levels.