Charged rho meson production in neutrino-induced reactions at E_nu = 10 GeV

The neutrinoproduction of charged $\rho$ mesons on nuclei and nucleons is investigated for the first time at moderate energies ($\approx$ 10 GeV), using the date obtained with SKAT bubble chamber. No strong nuclear effects are observed in $\rho^+$ and $\rho^-$ production. The fractions of charged and neutral pions originating from $\rho$ decays are obtained and compared with higher energy data. From analysis of the obtained and available data on $\rho^+$ and $K^{*+}$(892) neutrinoproduction, the strangeness suppression factor in the quark string fragmentation is extracted: $\lambda_s = 0.18\pm0.03$. Estimations are obtained for cross sections of quasiexclusive single $\rho^+$ and coherent $\rho^+$ neutrinoproduction on nuclei. The estimated coherent cross section $\sigma_{\rho^+}^{coh}$ = (0.29$\pm0.16)\cdot 10^{-38}$ cm$^2$ is compatible with theoretical predictions.Comment: 7 pages, 6 figure

A study of the nuclear medium influence on transverse momentum of hadrons produced in deep inelastic neutrino scattering

The influence of nuclear effects on the transverse momentum $(p_T)$ distributions of neutrinoproduced hadrons is investigated using the data obtained with SKAT propane-freon bubble chamber irradiated in the neutrino beam (with $E_{\nu}$ = 3-30 GeV) at Serpukhov accelerator. Dependences of $$on the kinematical variables of inclusive deep-inelastic scattering and of the produced hadrons are measured. It has been observed, that the nuclear effects cause an enhancement of$$ of hadrons (more pronounced for the positively charged ones) produced in the target fragmentation region at low invariant mass of the hadronic system (2 $< W <$ 4 GeV) or at low energies transferred to the current quark (2 $< \nu < 9$ GeV). At higher $W$ or $\nu$, no influence of nuclear effects on $$ is observed. Measurement results are compared with predictions of a simple model, incorporating secondary intranuclear interactions of hadrons (with a formation length extracted from the Lund fragmentation model), which qualitatively reproduces the main features of the data.Comment: 23 pages, 7 figure

Патогенетические факторы, ассоциирующиеся с формированием острого абдоминального болевого синдрома собак при гастроэнтерите

Intercorrelative relationships between various clinical and laboratory parameters in dogs with acute gastroenteritis were studied. In dogs with acute alimentary gastroenteritis (n = 31), pain rating scale score significantly (p 0.05) correlated with pulse rate (r = 0.58), respiratory rate (r = 0.50), hematocrit (r = 0.47), ESR (r = 0.72), number of erythrocytes (r = 0.50) and leukocytes (r = 0.77), concentration of albumins (r = -0.52), globulins (r = 0.59), 1-globulins (r = 0.49), 2-globulins (r = 0.42), -globulins (r = -0.36), -globulins (r = 0.59), C-reactive protein (r = 0.82), serum activity of ALT (r = 0.70), AST (r = 0.39), -amylase (r = 0.38), alkaline phosphatase (r = 0.83) and serum concentration of creatinine (r = 0.42), tumor necrosis factor- (r = 0.82), interleukin-4 (r = 0.92), interleukin-6 (r = 0.92), interferon- (r = 0.91), interleukin-1 (r = 0.85), interleukin-8 (r = 0.91). The following changes were noted in the body of dogs with acute gastroenteritis: local and systemic immune-inflammatory response activated, pain, intoxication, dehydration syndrome, disorders of motor, secretory, absorption, excretory function of gastrointestinal tract formed, secondary hepatopathy and pancreatopathy developed. In dogs with acute gastroenteritis, there were also statistically significant (p 0.05) correlations between the number of erythrocytes and hematocrit (r = 0.65), MCHC (r = 0.32), ESR (r = 0.35), hemoglobin concentration (r = 0.73) and leukocyte count (r = 0.35); between MCV and hematocrit (r = 0.62), MCHC (r = -0.64); between MCV and MCHC (r = -0.64); MCH and MCHC (r = 0.40); ESR and leukocyte count (r = 0.53). Changes in intercorrelative relationships between clinical and laboratory parameters in dogs with acute gastroenteritis can be considered as predictors of severity of the pathological process.Исследовались интеркореллятивные связи между разнообразными клиническими и лабораторными показателями у собак, больных острым гастроэнтеритом. Показатель шкалы оценки боли достоверно (р ≤ 0,05) коррелировал с частотой пульса (r = 0,58), частотой дыхания (r  =  0,50), гематокритом (r = 0,47), СОЭ (r = 0,72), количеством эритроцитов (r = 0,50) и лейкоцитов (r = 0,77), концентрацией альбуминов в сыворотке крови (r = –0,52), глобулинов (r = 0,59), α1‑глобулинов (r = 0,49), α2‑глобулинов (r = 0,42), β-глобулинов (r = –0,36), γ-глобулинов (r = 0,59), С-реактивного белка (r = 0,82), сывороточной активностью аланиновой (r = 0,70) и аспарагиновой аминотрасфераз (r = 0,39), α-амилазы (r = 0,38), щелочной фосфатазы (r = 0,83) и сывороточной концентрацией креатинина (r = 0,42), фактора некроза опухоли-α (r = 0,82), интерлейкина‑4 (r = 0,92), интерлейкина‑6 (r = 0,92), интерферона-γ (r = 0,91), интерлейкина‑1α (r = 0,85), интерлейкина‑8 (r = 0,91). В организме собак, больных острым гастроэнтеритом, происходит активизация локальной и системной иммуновоспалительной реакции организма, возникает болевой, интоксикационный, дегидратационный синдром, происходят нарушения моторной, секреторной, всасывательной, экскреторной функции желудочно-­кишечного тракта, формируется вторичная гепатопатия и панкреатопатия. Также констатировано наличие статистически значимых (р ≤ 0,05) коррелятивных связей между количеством эритроцитов и показателем гематокрита (r = 0,65), MCHC (r = 0,32), СОЭ (r = 0,35), концентрацией гемоглобина (r = 0,73) и количеством лейкоцитов (r = 0,35); между MCV и гематокритом (r = 0,62), MCHC (r = –0,64); между MCV и MCHC (r = 0,64); MCH и MCHC (r = 0,40); СОЭ и количеством лейкоцитов (r = 0,53). Изменения интеркоррелятивных связей между клинико-­лабораторными параметрами у больных острым гастроэнтеритом собак можно рассматривать как предикторы тяжести патологического процесса

The total yields of K^+(892), Sigma^+(1385) and Sigma^0 in neutrino-induced reactions at <E_nu> = 10 GeV

Using the data obtained with SKAT bubble chamber, the total yields of $K^+(892)$, $\Sigma^+(1385)$ and $\Sigma^0$ are estimated for the first time in neutrino-induced reactions at moderate energies ($$ = 10.4 GeV). It is shown, that the recently observed \cite{ref1,ref2} enhancement of the $K^0$ and $\Lambda$ yields in $\nu A$ interactions (as compared to $\nu N$ interactions) is contributed only slightly by the $K^+(892)$ and $\Sigma^+(1385)$ production, respectively. The decay contribution to the $K^0$ and $\Lambda$ yields is found to be in qualitative agreement with higher energy ($\geq$ 40 GeV) data. It is shown, that the energy dependence of the $K^+(892)$ mean multiplicity in $\nu N$ interactions is approximately linear in the range of $\approx$ 10-60 GeV, while that for $\Sigma^0$ in $\nu A$ interactions (for $A$ = 20-21) is approximately logarithmic in the range of $\approx$ 10-150 GeV.Comment: 6 pages, 3 figure

The A - dependence of K0K^{0} and Λ\Lambda neutrinoproduction on nuclei

For the first time, the A- dependence of the production of $K^0$, $\Lambda$ and, for comparison, $\pi^-$ mesons is investigated in neutrinonuclear reactions, using the data obtained with SKAT bubble chamber. An exponential parametrization ($\sim A^{\beta}$) of the particle yields results in ${\beta}_{V^0} = 0.20 \pm 0.05$ for $V^0$ particles (combined $K^0$ and $\Lambda$), while for $\pi^-$ mesons the A- dependence is much weaker, ${\beta}_{\pi^-} = 0.068 \pm 0.007$. A nuclear enhancement of the ratio $K^0/\pi^-$ is found; this ratio increases from $0.055 \pm 0.013$ for $\nu N$- interactions up to $0.070 \pm 0.011$ at $A \approx 21$ and $0.099 \pm 0.011$ at $A \approx 45$. It is observed, that the multiplicity rise of $V^0$'s occures predominantely in the backward hemisphere of the hadronic c.m.s. It is shown, that the A- dependence of the nuclear enhancement of the ${\Lambda}^0$ and $\pi^-$ yields can be reproduced in the framework of a model, incorporating the secondary intranuclear interactions of pions originating from the primary $\nu N$- interactions, while only (29$\pm$9)% of that for $K^0$ at $A \approx 45$ can be attributed to intranuclear interactions.Comment: 18 pages, 8 figure

Vitamin D serum level predicts stroke clinical severity, functional independence, and disability—A retrospective cohort study

BackgroundStroke is a leading cause of mortality and disability and one of the most common neurological conditions globally. Many studies focused on vitamin D as a stroke risk factor, but only a few focused on its serum level as a predictor of stroke initial clinical severity and recovery with inconsistent results. The purpose of this study was to assess the relationship between serum vitamin D levels and stroke clinical severity at admission and functional independence and disability at discharge in Saudi Arabia.MethodologyA retrospective cohort study of adult ischemic stroke patients who had their vitamin D tested and admitted within 7 days of exhibiting stroke symptoms at King Abdulaziz Medical City (KAMC) Jeddah, Saudi Arabia. Based on vitamin D level, the patients were categorized into normal [25(OH)D serum level ≥ 75 nmol/L], insufficient [25(OH)D serum level is 50–75 nmol/L], and deficient [25(OH)D serum level ≤ 50 nmol/L]. The primary outcome was to assess the vitamin D serum level of ischemic stroke patients’ clinical severity at admission and functional independence at discharge. The National Institute of Health Stroke Scale (NIHSS) was used to assess the clinical severity, whereas the modified Rankin scale (mRS) was used to assess functional independence and disability.ResultsThe study included 294 stroke patients, out of 774, who were selected based on the inclusion and exclusion criteria. The mean age of the participants was 68.2 ± 13.4 years, and 49.3% were male. The patients’ distribution among the three groups based on their vitamin D levels is: normal (n = 35, 11.9%), insufficient (n = 66, 22.5%), and deficient (n = 196, 65.6%). After adjusting for potential covariates, regression analysis found a significant inverse relationship of NIHSS based on 25(OH)D serum level (beta coefficient: −0.04, SE: 0.01, p = 0.003). Patients with deficient serum vitamin D level also had significantly higher odds of worse functional independence in mRS score [OR: 2.41, 95%CI: (1.13–5.16), p = 0.023] when compared to participants with normal vitamin D level.ConclusionLow vitamin D levels were associated with higher severity of stroke at admission and poor functional independence and disability at discharge in patients with acute ischemic stroke. Further randomized clinical and interventional studies are required to confirm our findings

Does α-Amino-β-methylaminopropionic Acid (BMAA) Play a Role in Neurodegeneration?

The association of α-amino-β-methylaminopropionic acid (BMAA) with elevated incidence of amyotrophic lateral sclerosis/Parkinson’s disease complex (ALS/PDC) was first identified on the island of Guam. BMAA has been shown to be produced across the cyanobacterial order and its detection has been reported in a variety of aquatic and terrestrial environments worldwide, suggesting that it is ubiquitous. Various in vivo studies on rats, mice, chicks and monkeys have shown that it can cause neurodegenerative symptoms such as ataxia and convulsions. Zebrafish research has also shown disruption to neural development after BMAA exposure. In vitro studies on mice, rats and leeches have shown that BMAA acts predominantly on motor neurons. Observed increases in the generation of reactive oxygen species (ROS) and Ca2+ influx, coupled with disruption to mitochondrial activity and general neuronal death, indicate that the main mode of activity is via excitotoxic mechanisms. The current review pertaining to the neurotoxicity of BMAA clearly demonstrates its ability to adversely affect neural tissues, and implicates it as a potentially significant compound in the aetiology of neurodegenerative disease. When considering the potential adverse health effects upon exposure to this compound, further research to better understand the modes of toxicity of BMAA and the environmental exposure limits is essential