Miracle-dz/UniFAR-FTUs huggingface dataset:
The effects of dietary N-3 and antioxidant supplementation on erythrocyte membrane fatty acid composition and fluidity in exercising horses.

REASONS FOR PERFORMING STUDY Fatty acid supplementation could modulate erythrocyte membrane fluidity in horses at rest and during exercise, but information is lacking on the effect of exercise. OBJECTIVES To assess the effect of exercise with, and without, an oral antioxidant supplementation enriched with n-3 fatty acids on erythrocyte membrane fluidity (EMF) and fatty acid composition in eventing horses. METHODS Twelve healthy and regularly trained horses were divided randomly into 2 groups: group S received an oral antioxidant cocktail enriched in n-3 fatty acid (alphatocopherol, eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) whereas group P was placebo-treated. At the end of 4 weeks, all horses performed a standardised exercise test (ET) under field conditions. Venous blood was sampled before starting treatment (TO), immediately before (T1) as well as 15 min (T2) and 24 h (T3) after ET. Spin labelled (16-DOXYL-stearic acid) red blood cell membranes were characterised using the relaxation correlation time (Tc in inverse proportion to EMF). Fatty acid composition (%) of the membrane was determined by gas-liquid chromatography. RESULTS Supplementation did not induce changes in EMF (T1 vs. TO) but significant changes in membrane composition were observed and there were increases in n-3 polyunsaturated fatty acid PUFA, n-3/n-6 ratio, and total n-3 fatty acids. Exercise (T2 vs. T1) induced a significant decrease of EMF in group P (Tc: +19%, P<0.05) and nonsignificant decrease in group S (Tc: +5%), whereas membrane fatty acid composition did not change in either group. During the recovery period (T3 vs. T2), EMF decreased significantly in group S (Tc: +29%, P<0.05) and nonsignificantly in group P (Tc: +18%) without any significant changes in fatty acid composition. CONCLUSION AND POTENTIAL RELEVANCE An enriched oral antioxidant supplementation induced changes in membrane composition, which modulated the decrease in EMF induced by exercise. Long chain n-3 fatty acid supplementation might therefore be beneficial.
Cerebral Microbleeds Are Associated with the Progression of Ischemic Vascular Lesions

Background: Despite their different appearance on imaging, hemorrhagic and ischemic vascular lesions frequently co-occur in the brain and are hypothesized to progress concurrently. Although silent hemorrhagic and ischemic vascular brain lesions are highly prevalent in the general population, the concomitant progression of these lesions has only been studied to a limited extent in this population. We therefore aimed to investigate whether pre-existing and incident cerebral microbleeds (CMBs) are related to the progression of ischemic lesions in the general population. Methods: In the prospective population-based Rotterdam Scan Study, 803 individuals aged ≥60 years underwent magnetic resonance imaging at baseline and after an average interval of 3.4 years. The presence of microbleeds and lacunes was visually rated by trained research physicians, and white matter lesions (WMLs) were automatically segmented at both time points. Logistic regression was used to investigate the association of microbleeds with incident lacunes, and linear regression was used to investigate the relation between microbleeds and progression of WML volume. All analyses were adjusted for age, sex and the time interval between baseline and follow-up scanning. The analyses were repeated after additional adjustments for cardiovascular risk factors: blood pressures; total and high-density lipoprotein cholesterol; smoking; diabetes mellitus; lipid lowering, antihypertensive and antiplatelet medications, and apolipoprotein E ε4. The analyses involving WMLs were also adjusted for intracranial volume. Results: We found that pre-existing microbleeds in any location of the brain were related to a higher incidence of lacunes (odds ratio [OR] adjusted for age, sex and scan interval: 4.67; 95% confidence interval [CI]: 1.84-11.85). Pre-existing microbleeds were not related to progression of WML volume (mean difference in WML volume increase: -0.03; 95% CI: -0.15 to 0.09). Additional adjustments for cardiovascular risk factors did not change the results considerably. Incident microbleeds in any location of the brain were associated with a higher incidence of lacunes (OR: 9.18; 95% CI: 3.61-23.35), whereas only incident microbleeds located in cortico-subcortical regions were related to progression of WML volume (mean difference in WML volume increase: 0.41; 95% CI: 0.21-0.62). Again, adjustments for cardiovascular risk factors did not change the results significantly. Conclusions: Our findings suggest that in the general population, CMBs serve as a predictor of ischemic brain lesions and may represent an imaging marker of active vasculopathy. These results support the hypothesis of a common underlying pathway in the development of ischemic and hemorrhagic brain lesions.
Ovarian inhibin subunit gene expression: regulation by gonadotropins and estradiol.

Inhibin and FSH maintain a dynamic inverse relationship throughout the rat estrous cycle. In particular, inhibin alpha- and beta A-subunit messenger RNAs (mRNAs) have been shown to be maximally expressed immediately after the midcycle gonadotropin surge, when both circulating estradiol (E2) and inhibin are also elevated. The current study was designed to investigate the regulation of inhibin subunit gene expression and secretion in vivo by recombinant human FSH (rhFSH) and estradiol. Initially, we determined if physiological levels of rhFSH regulated ovarian inhibin subunit gene expression and secretion. Hypophysectomized (HYPOX) adult female rats received hCG (10 IU, sc) and were then treated for 24 h with either rhFSH (0.5-20 IU every 6 h, i.v.) or saline. Hypophysectomy reduced inhibin subunit mRNAs as well as serum inhibin and estradiol. Although 0.5 IU rhFSH was ineffective in increasing inhibin subunit mRNAs, all doses between 2.5-20 IU increased inhibin subunit gene expression and inhibin secretion. Inhibin alpha-, beta A-, and beta B-subunit mRNAs were increased to a similar degree (3- to 5-fold) by all rhFSH doses of 5 IU or more. Similarly, serum E2 and inhibin were increased 2- and 3-fold, respectively, above HYPOX values after all doses of rhFSH of 5 IU or more. To investigate the role of a pure FSH signal in a physiological dose on inhibin subunit gene expression, HYPOX rats were given either rhFSH (5 IU, i.v., every 6 h for 24 or 48 h), hCG (10 IU, sc), or their combination. Neither gonadotropin when given alone altered inhibin subunit gene expression or serum E2 concentrations. Inhibin secretion rose in response to rhFSH alone, but not to hCG. The combination of hCG and rhFSH resulted in increased inhibin subunit mRNAs (3- to 5-fold) as well as circulating E2 and inhibin concentrations. We next studied the effects of E2 replacement in HYPOX rats at both physiological (serum approximately equal to 40 pg/ml) and higher doses (serum approximately equal to 800 pg/ml, to mimic intraovarian concentrations) in the presence or absence of exogenous gonadotropins (for 24 and 48 h). Although not as effective as gonadotropins, both E2 regimens increased inhibin alpha to a similar degree (2-fold), whereas beta-subunit mRNAs were unchanged at 24 h. Serum inhibin concentrations were increased only 48 h after high dose E2 treatments. As the actions of E2 and gonadotropins on alpha-subunit mRNA were not additive, E2 appears to mediate gonadotropin regulation of alpha-subunit gene expression. (ABSTRACT TRUNCATED AT 400 WORDS)
Estrogen and Androgen Protection of Human Neurons against Intracellular Amyloid β1-42 Toxicity through Heat Shock Protein 70

Intracellular amyloidβ peptide (iAβ1-42) accumulates in the Alzheimer's disease brain before plaque and tangle formation (Gouras et al., 2000) and is extremely toxic to human neurons (Zhang et al., 2002). Here, we investigated whether androgen and estrogen could prevent iAβ1-42 toxicity, because both these hormones have a wide range of neuroprotective actions. At physiological concentrations, 17-β-estradiol, testosterone, and methyl testosterone reduce iAβ1-42-induced cell death by 50% in neurons treated after the injection and by 80-90% in neurons treated 1 hr before the injection. The neuroprotective action of the hormones is mediated by receptors, because the estrogen receptor (ER) antagonist tamoxifen and the androgen receptor (AR) antagonist flutamide completely block the estrogen- and androgen-mediated neuroprotection, respectively. Transcriptional activity is required for the neuroprotective action, because dominant negative forms of the receptors that block the transcriptional activity of the ER and AR prevent estrogen- and androgen-mediated neuroprotection. Proteomics followed by Western blot analyses identified increased levels of heat shock protein 70 (Hsp70) in testosterone- and estrogen-treated human neurons. Comicroinjection of Hsp70 with the iAβ1-42 blocks the toxicity of iAβ1-42. We conclude that estrogen and androgens protect human neurons against iAβ1-42 toxicity by increasing the levels of Hsp70 in the neurons.
Anatomic variation of the spinal origins of lateral and medial pectoral nerves

Lateral and medial pectoral nerves are distributed to the pectoralis major and minor muscles. The purpose of this study was to identify the spinal origins of lateral and medial pectoral nerves and to evaluate the participating amounts of each spinal nerve composing both pectoral nerves. Two types of spinal origins appeared in lateral pectoral nerves. The first type was composed of nerve fibers from C5, C6, and C7 with a frequency of 50.0% and the second type was composed of nerve fibers from C6 and C7 at a frequency of 50.0%. Regarding the average participating diameter to the lateral pectoral nerve, C7 was the thickest with a value of 1.60 ± 0.35 mm (mean ± SD), next was C6 at 0.83 ± 0.18 mm, and C5 was the third at 0.42 ± 0.24 mm. Three types of spinal origin appeared in the medial pectoral nerve. The first type was comprised of nerve fibers from C8 and T1 in 73.3% of cases. The second type was comprised of C8 only in 23.4% of cases, and the third type was comprised of T1 only in 3.3% of cases. The average participating diameter was 0.71 ± 0.22 mm from C8 and 0.52 ± 0.17 mm from T1. These results show that the spinal origins of the both pectoral nerves were various. Participating amounts of the lateral pectoral nerve appeared sequentially in the order of C7, C6, and C5. In the medial pectoral nerve, C8 participated more amounts than T1. Clin. Anat. 20:915–918, 2007. © 2007 Wiley‐Liss, Inc.
White blood cell count to mean platelet volume ratio: A novel and promising prognostic marker for ST-segment elevation myocardial infarction.

BACKGROUND Increased white blood cell (WBC) count is associated with increased mortality in patients with ST-segment elevation myocardial infarction (STEMI). We aimed to evaluate predictive value of admission WBC to mean platelet volume (MPV) ratio (WMR) on prognosis in patients undergoing primary percutaneous coronary intervention (pPCI) for STEMI. METHODS A total of 2,603 consecutive patients with STEMI who underwent pPCI were recruited for the study. Follow-up data were obtained from digital records, patient files or by telephone interview with patients, family members, or primary care physicians. RESULTS WMR has the highest area under receiver operating characteristic (ROC) curve and pairwise comparisons of the ROC curves revealed that WMR has the higher discriminative ability for long-term mortality than WBC, MPV, red blood cell distribution with (RDW), WBC-MPV combination, and platelet to lymphocyte ratio and neutrophil to lymphocyte ratio (PLR-NLR) combination in patients undergoing pPCI for STEMI (a WMR value of 1,653.47 was also found as threshold value for mortality with 75.4% sensitivity and 87.3% specificity by ROC curve analysis). CONCLUSIONS Higher WMR value on admission was associated with worse outcomes in patients with STEMI and independently better predicted the long-term mortality than other complete blood count components, such as MPV, RDW, PLR-NLR and WBC-MPV combinations.
Poly[[tris(μ3-2-oxidopyridinium-3-carboxylato)manganese(II)sodium(I)] monohydrate]

In the crystal structure of the title compound, {[MnNa(C6H4NO3)3]·H2O}n, the MnII cation is located on a threefold rotation axis and is chelated by three 2-oxidopyridinium-3-carboxylate (opc) anions in an octahedal coordination. The NaI cation is located on a threefold rotation axis and is surrounded by six O atoms from three opc anions. The opc anions link the Mn and Na cations, forming a three-dimensional polymeric structure. The uncoordinated water molecule, located on a threefold rotation axis, is equally disordered over two sites. The three-dimensional network is consolidated by N—H⋯O hydrogen bonds.
Adolescent suicidal behavior: associations with preadolescent physical abuse and selected risk and protective factors.

OBJECTIVES To determine whether preadolescent physical abuse raises the risk of adolescent suicidal behavior, to examine potential mediators and moderators of the relationship between preadolescent abuse and adolescent suicidality, and to examine whether distal (preadolescent) risk factors add to proximal (adolescent) factors in predicting suicidality. METHOD Seventy-five physically abused preadolescents on the New York City Maltreatment Register and 78 controls were studied at ages 10.5 and 16.5 years. Adolescent suicidal ideation and attempts and hypothesized risk and protective factors were assessed by self-report, parent interview, and teacher ratings. Data were analyzed by logistic regression. RESULTS Preadolescent physical abuse was a robust, largely unmediated, independent predictor of adolescent suicidality. Only adolescent internalizing problems mediated the relationship. No risk factors moderated the relationship. Adolescent attachment to parents and internalizing problems contributed independently to the prediction of suicidality risk in abused and control subjects. No preadolescent risk or protective factors added to the predictions beyond risk deriving from preadolescent abuse. CONCLUSIONS The association between preadolescent physical abuse and adolescent suicidality is largely unmediated and unmoderated by well-documented risk factors for suicidality. Therefore, comprehensive interventions to reduce abusive parenting must begin when families enter the child protection system, along with therapeutic interventions with the children and adolescents themselves.
Monitoring of brain interstitial total tau and beta amyloid proteins by microdialysis in patients with traumatic brain injury.

OBJECT Damage to axons contributes to postinjury disabilities and is commonly observed following traumatic brain injury (TBI). Traumatic brain injury is an important environmental risk factor for the development of Alzheimer disease (AD). In the present feasibility study, the aim was to use intracerebral microdialysis catheters with a high molecular cutoff membrane (100 kD) to harvest interstitial total tau (T-tau) and amyloid beta 1-42 (Abeta42) proteins, which are important biomarkers for axonal injury and for AD, following moderate-to-severe TBI. METHODS Eight patients (5 men and 3 women) were included in the study; 5 of the patients had a focal/mixed TBI and 3 had a diffuse axonal injury (DAI). Following the bedside analysis of the routinely measured energy metabolic markers (that is, glucose, lactate/pyruvate ratio, glycerol, and glutamate), the remaining dialysate was pooled and two 12-hour samples per day were used to analyze T-tau and Abeta42 by enzyme-linked immunosorbent assay from Day 1 up to 8 days postinjury. RESULTS The results show high levels of interstitial T-tau and Abeta42 postinjury. Patients with a predominantly focal lesion had higher interstitial T-tau levels than in the DAI group from Days 1 to 3 postinjury (p < 0.05). In contrast, patients with DAI had consistently higher Abeta42 levels when compared with patients with focal injury. CONCLUSIONS These results suggest that monitoring of interstitial T-tau and Abeta42 by using microdialysis may be an important tool when evaluating the presence and role of axonal injury following TBI.
The N-Terminal Regulatory Domain of Stp1p Is Modular and, Fused to an Artificial Transcription Factor, Confers Full Ssy1p-Ptr3p-Ssy5p Sensor Control

ABSTRACT Stp1p and Stp2p are homologous and redundant transcription factors that are synthesized as latent cytoplasmic proteins with N-terminal regulatory domains. In response to extracellular amino acids, the plasma membrane-localized Ssy1p-Ptr3p-Ssy5p (SPS) sensor induces an endoproteolytic processing event that cleaves away the N-terminal regulatory domains. The shorter forms of Stp1p and Stp2p are targeted to the nucleus, where they bind and activate the transcription of amino acid permease genes. A novel genetic screen, specifically designed to search for rare mutations that affect the SPS-sensing pathway, identified the F-box protein Grr1p as an obligatory factor required for Stp1p/Stp2p processing. Additionally, we have found that a null mutation in the ASI1 (amino acid sensor-independent) gene enables full-length unprocessed Stp1p/Stp2p to enter the nucleus and derepress SPS sensor-dependent genes. The N-terminal domains of Stp1p/Stp2p contain two conserved motifs that are required for proper nuclear exclusion and proteolytic processing. These motifs function in parallel; mutations that abolish processing inhibit signaling, whereas mutations that interfere with cytoplasmic retention result in constitutive derepression of SPS sensor-regulated genes independently of processing. The N-terminal domain of Stp1p is functionally autonomous and transferable to other transcription factors, where its presence confers ASI1-dependent nuclear exclusion and SPS sensor-induced proteolytic processing.
Adaptive radiation with regard to nutrient sequestration strategies in the carnivorous plants of the genus Nepenthes

Carnivorous pitcher plants of the genus Nepenthes have evolved a great diversity of pitcher morphologies. Selective pressures for maximizing nutrient uptake have driven speciation and diversification of the genus in a process known as adaptive radiation. This leads to the evolution of pitchers adapted to specific and often bizarre source of nutrients, which are not strictly animal-derived. One example is Nepenthes ampullaria with unusual growth pattern and pitcher morphology what enables the plant to capture a leaf litter from the canopy above. We showed that the plant benefits from nitrogen uptake by increased rate of photosynthesis and growth what may provide competitive advantage over others co-habiting plants. A possible impact of such specialization toward hybridization, an important mechanism in speciation, is discussed.
Comparison of hospital length of stay between hospitalized non-valvular atrial fibrillation patients treated with either apixaban or warfarin

Abstract Background. Hospital length of stay (LOS) is an important cost driver for hospitals and payers alike. Hospitalized non-valvular atrial fibrillation (NVAF) patients treated with apixaban may have shorter LOS than those treated with warfarin because of the absence of need for INR monitoring in apixaban. Thus, this study compared hospital LOS between hospitalized NVAF patients treated with either apixaban or warfarin. Methods. This was a retrospective, observational cohort study based on a large US database including diagnosis, procedure, and drug administration information from >600 acute-care hospitals. Patients selected for study were aged ≥18 years and had a hospitalization record with an ICD-9-CM diagnosis code for atrial fibrillation (AF) in any position from 1 January 2013 to 28 February 2014 (index hospitalization). Patients with diagnoses indicative of rheumatic mitral valvular heart disease or a valve replacement procedure during index hospitalization were excluded. Patients were required to have been treated with either apixaban or warfarin, and not treated with rivaroxaban or dabigatran, during index hospitalization. Apixaban patients were propensity score (PS) matched to warfarin patients at a 1:1 ratio, using patient demographic/clinical and hospital characteristics. The study outcome was hospital LOS, calculated as discharge date minus admission date; a sensitivity analysis calculated hospital LOS as discharge date minus first anticoagulant administration date. Sub-analyses were conducted among patients with a primary diagnosis of AF. Results. The study included 832 apixaban patients matched to 832 warfarin patients. Mean [standard deviation (SD)] and median hospital LOS were significantly (p < 0.001) shorter in apixaban patients (4.5 [4.2] and 3 days) than in warfarin patients (5.4 [5.0] and 4). Results were consistent in the sensitivity and sub-analyses. Conclusions. Among NVAF patients, apixaban treatment was associated with shorter hospital LOS when compared with warfarin treatment. These findings may have important clinical and economic implications for hospitals, payers, and patients.
Association of tumour necrosis factor‐alpha G/A ‐238 and G/A ‐308 single nucleotide polymorphisms with juvenile idiopathic arthritis

Juvenile idiopathic arthritis (JIA) is a heterogeneous autoimmune disorder of unknown origin. As proinflammatory cytokines are known to contribute towards the pathogenesis of JIA, this case–control study was performed to examine the associations of certain single nucleotide polymorphisms (SNPs) of tumour necrosis factor‐α (TNF‐α) gene. Fifty‐three patients with JIA participated in this study as patients group and compared with 137 healthy unrelated controls. Genotyping was performed for TNF‐α gene at positions ‐308 and ‐238, using polymerase chain reaction with sequence‐specific primers method. Results of the analysed data revealed a significant positive association for TNF‐α gene at positions ‐308 and ‐238 for A allele in patients group compared with controls (P < 0.01). At the genotypic level, the frequency of TNF‐α gene at positions ‐308 and ‐238 for GG genotype was discovered to be higher in the patients with JIA compared to the healthy controls (P < 0.01), while GA genotype at the same positions was observed to be less frequent in the case group than the controls (P < 0.01). At the haplotypic level, a significant positive association for TNF‐α GG haplotype (positions ‐308, ‐238) together with a notable negative association for TNF‐α AG and GA haplotypes at the same positions were detected in the patients group in comparison with the healthy individuals (P < 0.01). Cytokine gene polymorphisms might affect the development of JIA. Particular TNF‐α gene variants could render individuals more susceptible to JIA.