Miracle-dz/UniFAR-FTUs huggingface dataset:
[Effects of garlic oil on 2, 5-HD induced lipid peroxidation damage in rat nerve tissues].

OBJECTIVE To investigate the effects of garlic oil (GO) against the peroxidation damage of rat nerve tissue and the peripheral motor neuropathy induced by 2, 5-HD. METHODS Male Wistar rats were divided into four groups, with 10 in each group. The model group, and low and high doses of GO groups were administrated with 2, 5-HD (ip, 300 mg/kg), respectively; The control group was treated with sodium chloride, five times per week for six weeks. Pretreatment with GO gavaged (40 mg/kg or 80 mg/kg) started one week be-fore 2, 5-HD treatment, and lasted to the end of the experiment. Neurobehavioral indexes were examined at the zero, second and fourth week. At the end of the experiment, the scores of the gait, and the concentration of MDA and GSH, the level of TAOC and the ability of inhibition of.OH in cerebrum, spinal cord and sciatic nerve were examined. RESULTS Compared with the zero week, except of the control group rats, the hind limb landing foot splay of three groups rats decreased by 44%, 50% and 49% at the fourth week, respectively without significant difference. The threshold value of balance in model, GO low and high doses groups rats decreased by 30%, 45% and 68% at the fourth week, respectively, and lower than the control group rats (P < 0.01). GO low and high doses groups rats showed the serious abnormality at the fourth week, before one week of the model group rats. The scores of gait of model, and GO low and high doses groups rats increased significantly compared with control group rats, and the GO high dose group rats were higher than model group rats (P < 0.05). Increase of the concentration of MDA, and decrease of the level of the ability of inhibition of.OH were induced by 2, 5-HD in cerebrum, spinal cord and sciatic nerve. The concentration of MDA increased, and the level of the ability of inhibition of.OH decreased (P < 0.05 or P < 0.01), respectively. The results showed that the concentration of MDA decreased, and the level of the ability of inhibition of.OH induced by GO in cerebrum, spinal cord and sciatic nerve increased, the concentration of MDA of GO low doses group rats decreased, the level of the ability of inhibition of.OH increased, the concentration of MDA of GO high doses group rats decreased (P < 0.01) respectively, and the level of the ability of inhibition of.OH increased (P < 0.01) in nerve tissue. CONCLUSION GO has antagonist effect on the 2, 5-HD induced peroxidation damage, but can not improve the function of the peripheral motor nerve, indicating that the lipid peroxidation does not play an important role in 2, 5-HD neurotoxicity.
Destruction of the hepatocyte junction by intercellular invasion of Leptospira causes jaundice in a hamster model of Weil's disease

Weil's disease, the most severe form of leptospirosis, is characterized by jaundice, haemorrhage and renal failure. The mechanisms of jaundice caused by pathogenic Leptospira remain unclear. We therefore aimed to elucidate the mechanisms by integrating histopathological changes with serum biochemical abnormalities during the development of jaundice in a hamster model of Weil's disease. In this work, we obtained three‐dimensional images of infected hamster livers using scanning electron microscope together with freeze‐cracking and cross‐cutting methods for sample preparation. The images displayed the corkscrew‐shaped bacteria, which infiltrated the Disse's space, migrated between hepatocytes, detached the intercellular junctions and disrupted the bile canaliculi. Destruction of bile canaliculi coincided with the elevation of conjugated bilirubin, aspartate transaminase and alkaline phosphatase levels in serum, whereas serum alanine transaminase and γ‐glutamyl transpeptidase levels increased slightly, but not significantly. We also found in ex vivo experiments that pathogenic, but not non‐pathogenic leptospires, tend to adhere to the perijunctional region of hepatocyte couplets isolated from hamsters and initiate invasion of the intercellular junction within 1 h after co‐incubation. Our results suggest that pathogenic leptospires invade the intercellular junctions of host hepatocytes, and this invasion contributes in the disruption of the junction. Subsequently, bile leaks from bile canaliculi and jaundice occurs immediately. Our findings revealed not only a novel pathogenicity of leptospires, but also a novel mechanism of jaundice induced by bacterial infection.
Detection of soluble IL‐2 receptor in the serum of patients with myelodysplastic syndromes: induction under therapy with GM‐CSF

Sera of 15 healthy controls and 33 patients suffering from myelodysplastic syndromes (MDS) were investigated for soluble interleukin‐2 receptor (sIL‐2R) expression with a cell‐free enzyme‐linked immunosorbent assay (ELISA) system (T‐Cell Sciences; Cambridge, U. S. A.). The upper limit of the assay is indicated with 477 U/ml. According to the FAB classification eight refractory anaemia (RA). 15 refractory anaemia with excess of blasts (RAEB), five refractory anaemia with excess blasts in transformation (RAEBt) and five chronic myelomonocytic leukaemia (CMML) were examined. None of the patients had reported infectious episodes or been under treatment with cytotoxic agents and/or cytokines within the previous 3 months. Significant differences in sIL‐2R levels between RA (median 368 U/ml), RAEB (median 675 U/ml) and RAEBt (median 971 U/ml) and between RA and CMML (median 723 U/ml) were detected.
The enhancer of human papillomavirus type 16: binding sites for the ubiquitous transcription factors oct-1, NFA, TEF-2, NF1, and AP-1 participate in epithelial cell-specific transcription

The enhancer of human papillomavirus type 16 (HPV-16) is considered to be specific for epithelial cells, in particular for cervical carcinoma-derived cell lines. We reexamined this hypothesis with the complete enhancer as well as nonoverlapping subclones and found all clones to be active in epithelial cell lines derived from the epidermis and from carcinomas of the cervix, mammary gland, and colon, but inactive in fibroblast, lymphoma, and embryonal carcinoma cells. Although the virus infects only human mucosal epithelia, enhancer activity was independent of the exact type or of the species of origin of the transfected epithelial cell. In spite of epithelial cell specificity, we found that the activity of the HPV-16 enhancer varied strongly from a cytomegalovirus enhancer and the simian virus 40 enhancer in a cell line-dependent manner. This suggests varying quantitative contributions of enhancer elements rather than regulation by an all-or-none switch. Cell type specificity was maintained by a 91-bp subclone of the 400-bp enhancer. Most of the enhancer activity of this fragment was eliminated by alternative mutations in binding sites for the ubiquitous factors AP-1, nuclear factor 1 (NF1), or TEF-2. These three types of factors bind this 91-bp enhancer without cooperation, although activation appears to be synergistic. Outside the 91-bp fragment, a motif typical for papillomavirus enhancers, namely an octamerlike sequence flanked by an NF1-binding site, contributes to enhancer function, as the activity was strongly reduced upon its deletion. In HPV-16, this motif is bound by the oct-1 factor as well as by a probably novel factor, NFA, whereas a related motif of HPV-11 is recognized only by NFA. On examination, none of the five types of transcription factors involved in HPV enhancer activation was restricted to epithelial cells, but NF1, AP-1, and oct-1 were present in higher concentration in HeLa cells than in fibroblasts. Only NF1 showed some qualitative cell type-specific differences. We propose that the epithelial specificity of the HPV-16 enhancer is brought about via binding sites for supposed ubiquitous transcription factors. The mechanism of this activation apparently involves synergism between factors that vary in concentration and may include cell-specific functional differences residing outside the DNA-binding domain of these factors.
Morphologic Changes in the Cervical Neural Foramen due to Flexion and Extension: In Vivo Imaging Study

Study Design. Dimensional measurement of cervical neural foramen at various positions, using reformatted computed tomography. Objectives. To examine the morphologic changes in the neural foramen during flexion and extension of the cervical spine in vivo. Summary of Background Data. Previous cadaveric studies have shown the effect of cervical spinal motion on dimensions of the neural foramen. However, little information is available about dynamic morphologic changes in the cervical neural foramen in vivo. Methods. Cervical CT images of seven healthy volunteers were taken at the neutral position, maximum extension, and maximum flexion, and were reconstructed in the oblique plane perpendicular to the long axis of each neural foramen from the C3–C4 to C6–C7 level. Measured parameters included foraminal height, width, cross-sectional area, and segmental sagittal rotation at each spinal level. Differences in neural foraminal dimensions among these positions were analyzed. Correlations of segmental sagittal rotation with differences in dimensions between flexion and extension were analyzed. Results. Flexion significantly increased the foraminal height (by 1.0 mm; 11%), foraminal width (by 1.0 mm; 16%), and foraminal area (by 12 mm2; 28%) (P < 0.01). Extension significantly decreased the foraminal height (by 0.9 mm; 10%), foraminal width (by 1.4 mm; 22%), and foraminal area (by 8.0 mm2; 17%) (P < 0.01). Segmental sagittal rotation significantly positively correlated with % change in foraminal height (r = 0.434, P < 0.01) and area (r = 0.504, P < 0.01). Conclusions. The present results are consistent with those of previous in vitro studies and may explain the clinical observation that cervical extension aggravates symptoms in patients with cervical radiculopathy and that flexion often relieves them.
The Correlation Between Human Capital and Gross Added Value in the Bioeconomy Sectors at the European Union (EU) Country Level

Abstract The paper aims to prove the link between human capital and gross added value in bioeconomy sectors in the EU countries. Data from EUROSTAT data base regarding employment and gross added value in 6 bioeconomy sectors were used in a cross-country regression analysis. The econometric analysis of cross-country data shows a positive correlation between human capital in bioeconomy sectors and their gross output in 2015 in 26 European countries. It is found also that the correlation is stronger in the highly developed economies as in the central-eastern countries, as well as in the European economy.
[Effect of electroacupuncture intervention on expression of testicular P 450 scc/17 β-HSD3 in rats with partial androgen deficiency].

OBJECTIVE To observe the effect of electroacupuncture (EA) intervention on expression of cytochrome P 450 side chain cleavage (P 450 scc) and 17 β-hydroxysteroid dehydrogenase 3 (17 β-HSD3) in the testis in partial androgen deficiency of aging male (PADAM) rats so as to reveal its mechanism underlying improving PADAM. METHODS Thirty male SD rats were randomly and equally divided into control, model, and EA groups. The PADAM model was established by intraperitoneal injection of cyclophosphamide (20 mg · kg(-1) · d(-1)), once daily for 5 days. EA (20-30 Hz, 1-3 mA) was applied to bilateral "Shenshu" (BL 23) and "Guanyuan" (CV 4) for 15 min, once daily for 8 weeks. Serum total testosterone (TT) and free testosterone (FT) levels were measured using enzyme-linked immunosorbent assay (ELISA). The expression levels of P 450 scc/17 β-HSD3 proteins and mRNA in the testis tissue were assayed by immunohistochemistry, Western bolt (WB) and RT-polymerase chain reaction (RT-PCR), separately. RESULTS Compared with the control group, both serum TT, FT levels and expression levels of P450 scc/17 β-HSD3 proteins and mRNA in the testis tissue in the model group were significantly down-regulated (P<0.01). After EA intervention, compared with the model group, the cyclophosphamide-induced decrease of serum TT, FT levels and the expression levels of P 450 scc/17 β-HSD3 proteins and mRNA in the testis was reversed in the EA group (P<0.01). CONCLUSION EA intervention is effective in up-regulating serum TT and FT, testicular P 450 scc and 17 β-HSD3 proteins and mRNA levels in PADAM rats, which may be one of its mechanisms underlying improvement of PADAM.
Host location by visual and olfactory floral cues in an oligolectic bee: innate and learned behavior

Oligolectic bees collect pollen from only a few related plant taxa, and our understanding of both the bees' innate and learned behavior in host-plant recognition is incomplete. For the oligolectic bee Chelostoma rapunculi, whose host plants are within Campanula, we conducted choice tests on foraging-naive individuals to investigate the bee's innate preference for visual and olfactory floral cues of its host plants over those of nonhost plants. In addition, we tested both foraging-naive and foraging-experienced individuals to determine the relative importance of these 2 sensory modalities in the bee's innate and learned host-flower location. Visual and olfactory cues of Campanula trachelium flowers, both separately and combined, attracted significantly more foraging-naive bees than equivalent cues of nonhost plants. Furthermore, for both foraging-naive and -experienced bees, the visual cues of host plants were more attractive than the olfactory ones, and the 2 cues combined attracted more bees than either alone. In foraging-naive bees, visual and olfactory cues alone elicited almost exclusively approaches, whereas after the bees gained foraging experience, landings became more frequent in response to visual cues but not to olfactory cues; in both bee groups, the combination of visual and olfactory cues was most effective in promoting landings. We conclude that Ch. rapunculi has an innate preference for the floral cues of its host plants over those of nonhost species and that both foraging-naive and foraging-experienced bees integrate visual and olfactory cues to find their host flowers, with a slightly greater reliance on visual cues in bees with foraging experience.
Analysis of Size Portfolios and Risk Factor Loadings of Asset Pricing Models – Threshold Regression Approach

The objective of the study is to analysis portfolio returns and the performance of asset pricing models in the context of macroeconomic variables. Portfolios have been constructed on the basis of firms’ size; two equally weighted decile portfolios and two value weighed decile portfolios representing the cluster of the largest and smallest firms are included in the analysis along with market portfolio. Portfolio returns are regressed with the factor loadings of CAPM, three factor and five factor Fama and French asset pricing models. The relationship of portfolio returns and asset pricing models is evaluated in the presence of four macroeconomic variables namely interest rate, industrial production, producer price index and exchange rate; each macroeconomic variable is introduced separately in threshold regression to the identify regime shift effect. Analyses are performed on monthly returns of securities listed on PSX during the period from 2000 to 2010. Results of the study have revealed that only interest rate and exchange rate are found to have threshold effect on the portfolio returns. According to the results, threshold effect is frequently captured through three factors Fama French model. Finally, the results also suggest that the threshold effect is only evident with large firms portfolios.
Layer-Specific fMRI Responses to Excitatory and Inhibitory Neuronal Activities in the Olfactory Bulb

High-resolution functional magnetic resonance imaging (fMRI) detects localized neuronal activity via the hemodynamic response, but it is unclear whether it accurately identifies neuronal activity specific to individual layers. To address this issue, we preferentially evoked neuronal activity in superficial, middle, and deep layers of the rat olfactory bulb: the glomerular layer by odor (5% amyl acetate), the external plexiform layer by electrical stimulation of the lateral olfactory tract (LOT), and the granule cell layer by electrical stimulation of the anterior commissure (AC), respectively. Electrophysiology, laser-Doppler flowmetry of cerebral blood flow (CBF), and blood oxygenation level-dependent (BOLD) and cerebral blood volume-weighted (CBV) fMRI at 9.4 T were performed independently. We found that excitation of inhibitory granule cells by stimulating LOT and AC decreased the spontaneous multi-unit activities of excitatory mitral cells and subsequently increased CBF, CBV, and BOLD signals. Odor stimulation also increased the hemodynamic responses. Furthermore, the greatest CBV fMRI responses were discretely separated into the same layers as the evoked neuronal activities for all three stimuli, whereas BOLD was poorly localized with some exception to the poststimulus undershoot. In addition, the temporal dynamics of the fMRI responses varied depending on the stimulation pathway, even within the same layer. These results indicate that the vasculature is regulated within individual layers and CBV fMRI has a higher fidelity to the evoked neuronal activity compared with BOLD. Our findings are significant for understanding the neuronal origin and spatial specificity of hemodynamic responses, especially for the interpretation of laminar-resolution fMRI. SIGNIFICANCE STATEMENT Functional magnetic resonance imaging (fMRI) is a noninvasive, in vivo technique widely used to map function of the entire brain, including deep structures, in animals and humans. However, it measures neuronal activity indirectly by way of the vascular response. It is currently unclear how finely the hemodynamic response is regulated within single cortical layers and whether increased inhibitory neuronal activities affect fMRI signal changes. Both laminar specificity and the neural origins of fMRI are important to interpret functional maps properly, which we investigated by activating discrete rat olfactory bulb circuits.
Acute vasoconstriction after subarachnoid hemorrhage.

OBJECTIVE Decreased cerebral blood flow (CBF) and cerebral ischemia occurring immediately after subarachnoid hemorrhage (SAH) may be caused by acute microvascular constriction. However, CBF can also be influenced by changes in intracranial pressure (ICP) and cerebral perfusion pressure (CPP). The goal of these experiments was to assess the significance of acute vasoconstriction after SAH and its relationship to changes in CBF, ICP, CPP, and extracellular glutamate concentrations. METHODS Three experiments were performed using the endovascular filament technique to produce SAH. In the first experiment, CBF, ICP, and CPP were measured for 60 minutes after SAH (n = 21) and were correlated with the 24-hour mortality rate. In the second experiment, rats undergoing SAH (n = 23) or a sham procedure (n = 7) were perfused 60 minutes after SAH for measurement of the circumference and wall thickness of the internal carotid and anterior cerebral arteries and correlation with CBF, ICP, and CPP. In the third experiment (n = 11), extracellular glutamate concentrations determined by hippocampal and cortical microdialysis and high performance liquid chromatography were correlated with physiological changes. RESULTS CBF reductions to less than 40% of baseline for 60 minutes after SAH predicted 24-hour mortality with 100% accuracy and were used to define "lethal" SAH. In contrast, ICP and CPP 60 minutes after SAH were not correlated with the mortality rate. The vascular circumference was significantly smaller in lethal than in sublethal SAH or sham-operated rats (P < 0.001). Vessel measurements were correlated with both CBF and hemorrhage size (P < 0.01). Extracellular glutamate concentration increased to 600% of baseline after lethal SAH in both hippocampus and cortex and was inversely correlated with CBF (r = 0.9, P < 0.001) but did not increase after sublethal SAH. CONCLUSION Acute vasoconstriction after SAH occurs independently of changes in ICP and CPP and is associated with decreased CBF, larger hemorrhage size, persistent elevations of extracellular glutamate, and poor outcome. Acute vasoconstriction seems to contribute directly to ischemic brain injury after SAH. Further evaluations of pharmacological agents with the potential to reverse acute vasoconstriction may increase CBF and improve outcome.
A critical comparison of platelet preparation methods

Purpose of reviewPlatelet concentrates may be prepared from whole blood or by plateletpheresis. Currently, the non-evidence-based preponderance of apheresis units in the United States and the 50: 50 ratio in Europe may not optimize the gifts of whole-blood donors or minimize healthcare costs. Post-storage pooled, whole-blood-derived platelets, on the other hand, do not provide the convenience of or an equivalent level of safety as apheresis platelets. Recent findingsSome data suggest that different methods of manufacture of whole-blood-derived platelets (platelet-rich plasma or buffy coat intermediate steps) result in differing degrees of platelet activation, which may impact on the quality of stored concentrates. Recent studies have observed superior radiolabel recovery and post-transfusion increments for platelets derived from apheresis compared with platelet-rich plasma whole-blood-derived platelets. A pre-storage pooling system for whole-blood-derived platelets has just been licensed in the USA, and may eventually combine the benefits of apheresis-derived and whole-blood-derived platelets. The advantages of the European method of manufacture of buffy coat whole-blood-derived platelet concentrate have convinced the Canadian Blood Services to abandon platelet-rich-plasma-derived concentrates. SummaryWe present a literature-based review of the relative merits of apheresis-derived and whole-blood-derived platelets. Additional studies are needed in order to define the optimal proportion of the platelet supply from apheresis collections and the choice of whole-blood-derived production method for US blood providers.
Insulin‐like genes in ascidians: Findings in Ciona and hypotheses on the evolutionary origins of the pancreas

Insulin plays an extensively characterized role in the control of sugar metabolism, growth and homeostasis in a wide range of organisms. In vertebrate chordates, insulin is mainly produced by the beta cells of the endocrine pancreas, while in non‐chordate animals insulin‐producing cells are mainly found in the nervous system and/or scattered along the digestive tract. However, recent studies have indicated the notochord, the defining feature of the chordate phylum, as an additional site of expression of insulin‐like peptides. Here we show that two of the three insulin‐like genes identified in Ciona intestinalis, an invertebrate chordate with a dual life cycle, are first expressed in the developing notochord during embryogenesis and transition to distinct areas of the adult digestive tract after metamorphosis. In addition, we present data suggesting that the transcription factor Ciona Brachyury is involved in the control of notochord expression of at least one of these genes, Ciona insulin‐like 2. Finally, we review the information currently available on insulin‐producing cells in ascidians and on pancreas‐related transcription factors that might control their expression. genesis 53:82–104, 2015. © 2014 Wiley Periodicals, Inc.