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BACKGROUND Weight loss and decline of milk yield in Tibetan sheep was a challenge for the dairy industry in Qinghai-Tibet Plateau, which were considered to be caused by underfeeding of the sheep during the harsh winter. The objective of this study was to assess the role of feed supplementation in the milk performance and rumen microbiome of ewes under forage-based diets. Based on parity, milking period, milk yield, and body weight, ten 1.5-yr-old ewes were allocated randomly into two groups. One group of ewes was fed no supplement Control group (CON) and the other group was fed with concentrate feed supplement (Treatment group, T). Individual milk yield was determined daily; both the milk composition and rumen bacterial characteristics were analyzed after the end of feeding trials. RESULTS Results showed that lactose in the milk of the CON group was significantly lower (P < 0.05) than that of the T group at days 30 and 60. Milk yield in the T group was greater than in the CON group at day 30 (P < 0.05). Additionally, the dominant ruminal bacteria (phyla Bacteroidetes, Firmicutes, and Verrucomicrobia) were shared by both groups through 16S rRNA gene pyrosequencing. Greater relative abundance of Bacteroidales RF16 group in family level, Victivallales in order level, Lentisphaeria in class level, and Lachnospiraceae bacterium in species level were observed in the T group than in the CON group (P < 0.05). CONCLUSIONS These results demonstrated that supplementation of concentrate in the cold season improved milk lactose yield and milk production, and the rumen microbial abundance of Tibetan sheep.

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The role of the cannabinoid receptor 2 (CNR2) is still poorly described in sensory epithelia. We found strong cnr2 expression in hair cells (HCs) of the inner ear and the lateral line (LL), a superficial sensory structure in fish. Next, we demonstrated that sensory synapses in HCs were severely perturbed in larvae lacking cnr2. Appearance and distribution of presynaptic ribbons and calcium channels (Cav1.3) were profoundly altered in mutant animals. Clustering of membrane-associated guanylate kinase (MAGUK) in post-synaptic densities (PSDs) was also heavily affected, suggesting a role for cnr2 for maintaining the sensory synapse. Furthermore, vesicular trafficking in HCs was strongly perturbed suggesting a retrograde action of the endocannabinoid system (ECs) via cnr2 that was modulating HC mechanotransduction. We found similar perturbations in retinal ribbon synapses. Finally, we showed that larval swimming behaviors after sound and light stimulations were significantly different in mutant animals. Thus, we propose that cnr2 is critical for the processing of sensory information in the developing larva.

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Biochar amendment has been extensively used to improve plant performance and suppress disease in monoculture systems; however, few studies have focused on the underlying control mechanisms of replanting disease. In this study, we assessed the effects of biochar application on Radix pseudostellariae plant growth, rhizosphere soil microbial communities, and the physiological properties of microorganisms in a consecutive monoculture system. We found that biochar addition had little impact on the physiological parameters of tissue cultures of R. pseudostellaria but did significantly mediate microbial abundance in the rhizosphere soil of different consecutive monoculture years, leading to decreases in the abundance of pathogenic Fusarium oxysporum, Talaromyces helicus, and Kosakonia sacchari. Furthermore, biochar amendment had negative effects on the growth of beneficial bacteria, such as Burkholderia ambifaria, Pseudomonas chlororaphis, and Bacillus pumilus. Metabolomic analysis indicated that biochar significantly influenced the metabolic processes of F. oxysporum while inhibiting the mycelial growth and abating the virulence on plants. In summary, this study details the potential mechanisms responsible for the biochar-stimulated changes in the abundances and metabolism of rhizosphere bacteria and fungi, decreases in the contents of pathogens, and therefore improvements in the environmental conditions for plants growth. Further research is needed to evaluate the effects of biochar in long-term field trials.

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X-linked intellectual disability (XLID) has been associated with various genes. Diagnosis of XLID, especially for non-syndromic ones (NS-XLID), is often hampered by the heterogeneity of this disease. Here we report the case of a Chinese family in which three males suffer from intellectual disability (ID). The three patients shared the same phenotype: no typical clinical manifestation other than IQ score ≤ 70. For a genetic diagnosis for this family we carried out whole exome sequencing on the proband, and validated 16 variants of interest in the genomic DNA of all the family members. A missense mutation (c.710G > T), which mapped to exon 6 of the Rab GDP-Dissociation Inhibitor 1 (GDI1) gene, was found segregating with the ID phenotype, and this mutation changes the 237th position in the guanosine diphosphate dissociation inhibitor (GDI) protein from glycine to valine (p. Gly237Val). Through molecular dynamics simulations we found that this substitution results in a conformational change of GDI, possibly affecting the Rab-binding capacity of this protein. In conclusion, our study identified a novel GDI1 mutation that is possibly NS-XLID causative, and showed that whole exome sequencing provides advantages for detecting novel ID-associated variants and can greatly facilitate the genetic diagnosis of the disease.

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Abstract X-linked intellectual disability (XLID) has been associated with various genes. Diagnosis of XLID, especially for non-syndromic ones (NS-XLID), is often hampered by the heterogeneity of this disease. Here we report the case of a Chinese family in which three males suffer from intellectual disability (ID). The three patients shared the same phenotype: no typical clinical manifestation other than IQ score ≤ 70. For a genetic diagnosis for this family we carried out whole exome sequencing on the proband, and validated 16 variants of interest in the genomic DNA of all the family members. A missense mutation (c.710G > T), which mapped to exon 6 of the Rab GDP-Dissociation Inhibitor 1 (GDI1) gene, was found segregating with the ID phenotype, and this mutation changes the 237th position in the guanosine diphosphate dissociation inhibitor (GDI) protein from glycine to valine (p. Gly237Val). Through molecular dynamics simulations we found that this substitution results in a conformational change of GDI, possibly affecting the Rab-binding capacity of this protein. In conclusion, our study identified a novel GDI1 mutation that is possibly NS-XLID causative, and showed that whole exome sequencing provides advantages for detecting novel ID-associated variants and can greatly facilitate the genetic diagnosis of the disease.

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PURPOSE:: To investigate the effects of dexmedetomidine (DEX) on amino acid contents and the cerebral ultrastructure of rats with cerebral ischemia-reperfusion injury (I/R). METHODS:: Thirty-six, male, Wistar rats were randomly divided into three groups: the sham operation group (group C), the ischemia-reperfusion group (group I/R), and the DEX group (group D). The middle cerebral artery occlusion model was prepared by the modified Longa method. The time of ischemia was 180 min, and 120 min after reperfusion, the amount of glutamate (Glu), and γ-aminobutyric acid (GABA) in the brain were measured, and the ultrastructure-level changes in the cerebral cortex were examined using electron microscopy. RESULTS:: Compared to group C, Glu contents in group D, and I/R significantly increased. Compared to group I/R, Glu contents in group D significantly decreased. Compared to group C, GABA contents in group D, and I/R significantly increased, and those in group D significantly increased, as compared to group I/R. The cerebral ultrastructure was normal in group C. Vacuolar degeneration in the plastiosome and nervous processes, was more critical than in group D. Vascular endothelial cells (VEC) were damaged. On the contrary, these changes in group D significantly improved. CONCLUSION:: Dexmedetomidine is capable of decreasing glutamergic content, and increasing GABAergic content, in order to decrease the injury of the cerebral ultrastructure, following cerebral ischemia-reperfusion injury.

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Purpose: To investigate the effects of dexmedetomidine (DEX) on amino acid contents and the cerebral ultrastructure of rats with cerebral ischemia-reperfusion injury (I/R). Methods: Thirty-six, male, Wistar rats were randomly divided into three groups: the sham operation group (group C), the ischemia-reperfusion group (group I/R), and the DEX group (group D). The middle cerebral artery occlusion model was prepared by the modified Longa method. The time of ischemia was 180 min, and 120 min after reperfusion, the amount of glutamate (Glu), and -aminobutyric acid (GABA) in the brain were measured, and the ultrastructure-level changes in the cerebral cortex were examined using electron microscopy. Results: Compared to group C, Glu contents in group D, and I/R significantly increased. Compared to group I/R, Glu contents in group D significantly decreased. Compared to group C, GABA contents in group D, and I/R significantly increased, and those in group D significantly increased, as compared to group I/R. The cerebral ultrastructure was normal in group C. Vacuolar degeneration in the plastiosome and nervous processes, was more critical than in group D. Vascular endothelial cells (VEC) were damaged. On the contrary, these changes in group D significantly improved. Conclusion: Dexmedetomidine is capable of decreasing glutamergic content, and increasing GABAergic content, in order to decrease the injury of the cerebral ultrastructure, following cerebral ischemia-reperfusion injury.(AU)

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Abstract Purpose: To investigate the effects of dexmedetomidine (DEX) on amino acid contents and the cerebral ultrastructure of rats with cerebral ischemia-reperfusion injury (I/R). Methods: Thirty-six, male, Wistar rats were randomly divided into three groups: the sham operation group (group C), the ischemia-reperfusion group (group I/R), and the DEX group (group D). The middle cerebral artery occlusion model was prepared by the modified Longa method. The time of ischemia was 180 min, and 120 min after reperfusion, the amount of glutamate (Glu), and γ-aminobutyric acid (GABA) in the brain were measured, and the ultrastructure-level changes in the cerebral cortex were examined using electron microscopy. Results: Compared to group C, Glu contents in group D, and I/R significantly increased. Compared to group I/R, Glu contents in group D significantly decreased. Compared to group C, GABA contents in group D, and I/R significantly increased, and those in group D significantly increased, as compared to group I/R. The cerebral ultrastructure was normal in group C. Vacuolar degeneration in the plastiosome and nervous processes, was more critical than in group D. Vascular endothelial cells (VEC) were damaged. On the contrary, these changes in group D significantly improved. Conclusion: Dexmedetomidine is capable of decreasing glutamergic content, and increasing GABAergic content, in order to decrease the injury of the cerebral ultrastructure, following cerebral ischemia-reperfusion injury.

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OBJECTIVE: To delineate the relationship between traumatic brain injury (TBI) and mood disorders from population-based data in Taiwan. STUDY DESIGN: This prospectively followed cohort study involved a subset of the National Health Insurance Research Database containing complete inpatient and outpatient data of 1 million randomly drawn beneficiaries. We included 10- to 24-year-old patients (n = 15,203) receiving the diagnosis of TBI in ambulatory visits or hospitalization from 2000-2004 and their age- and sex-matched comparison insureds using health service in the same year (n = 76,015). Diagnosis of mood disorders was recorded within 5 years after the traumatic event or index use of health service. Baseline demographics, clinical characteristics, and premorbid psychiatric conditions were compared using χ(2) analysis. Increased risk during the 5-year follow-up period was represented by crude and adjusted hazard ratios with 95% CI using a Cox proportional hazard regression. RESULTS: A total of 451/15,203 patients with TBI (2.97%) received a diagnosis of mood disorders in the 5-year follow-up period compared with 1153/97,445 individuals (1.52%) without antecedent TBI. After adjusting for select premorbid comorbidities, TBI remained a significant predisposing factor with a 1.96-fold (95% CI 1.74-2.22) increase in risk of mood disorders. CONCLUSIONS: Our findings show a higher likelihood of manifesting mood disorders in adolescents and young adults who sustained a prior TBI. Health professionals should carefully monitor both the physical and psychological impacts of head trauma.

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OBJECTIVES: The aim of this study was to assess the in vitro activities of nemonoxacin (a novel non-fluorinated quinolone), doripenem, tigecycline and 16 other antimicrobial agents against the Nocardia species. METHODS: MICs of 19 antimicrobial agents for 125 clinical isolates of the Nocardia species were determined by the broth microdilution method. RESULTS: Nocardia brasiliensis (n = 61), Nocardia asteroides (n = 45), Nocardia flavorosea (n = 5), Nocardia otitidiscaviarum (n = 4), Nocardia farcinica (n = 3), Nocardia beijingensis (n = 2), Nocardia puris (n = 2) and one each of Nocardia nova, Nocardia jinanensis and Nocardia takedensis were identified based on a 16S rRNA gene sequencing analysis. For N. brasiliensis isolates, the MIC(90)s of the tested quinolones were in the order nemonoxacin < gemifloxacin = moxifloxacin < levofloxacin = ciprofloxacin, and the MIC(90)s of the tested carbapenems were in the order doripenem = meropenem < ertapenem < imipenem. Tigecycline had a lower MIC(90) (1 mg/L) than linezolid (8 mg/L). For N. asteroides isolates, the MIC(90)s of the tested quinolones were in the order nemonoxacin < gemifloxacin = moxifloxacin < levofloxacin < ciprofloxacin, and the MIC(90)s of the tested carbapenems were in the order doripenem = meropenem = imipenem < ertapenem. For the other 19 Nocardia species isolates, nemonoxacin showed good activity with the lowest MIC(90) of the tested quinolones. Among the four tested carbapenems, doripenem and meropenem had comparatively lower MIC(90)s. CONCLUSIONS: The results of this in vitro study suggest that nemonoxacin, linezolid and tigecycline show promise as treatment options for nocardiosis. Further investigation of their clinical role is warranted.

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