Cross-modality modulation of auditory midbrain processing of intensity information.

In nature, animals constantly receive a multitude of sensory stimuli, such as visual, auditory, and somatosensory. The integration across sensory modalities is advantageous for the precise processing of sensory inputs which is essential for animals to survival. Although some principles of cross-modality integration have been revealed by many studies, little insight has been gained into its functional potentials. In this study, the functional influence of cross-modality modulation on auditory processing of intensity information was investigated via recording neuronal activity in the auditory midbrain (i.e., inferior colliculus, IC) under the conditions of visual, auditory, and audiovisual stimuli, respectively. Results demonstrated that combined audiovisual stimuli either enhanced or suppressed the responses of IC neurons compared to auditory stimuli alone, even though the same visual stimuli alone induced no response. Audiovisual modulation appeared to be strongest when the combined audiovisual stimuli were located at the best auditory azimuth of neurons as well as when presented with intensity at near-threshold levels. Additionally, the rate-intensity function of IC neurons to auditory stimuli was expanded or compressed by audiovisual modulation, which was highly dependent on the minimal threshold (MT) of neurons. Lowering of the MT and greater audiovisual modulation for the neuron indicated an intensity-specific enhancement of auditory intensity sensitivity by cross-modality modulation. Overall, evidence suggests a potential functional role of cross-modality modulation in IC that serves to instruct adaptive plasticity to enhance the auditory perception of intensity information.

IL-17A G197A gene polymorphism contributes to susceptibility for liver cirrhosis development from patients with chronic hepatitis B infection in Chinese population.

BACKGROUND: IL-17A G197A and IL-17F A7488G gene polymorphisms are found to be associated with the risk of several diseases, however few studies have focused on their correlation with risk of liver cirrhosis (LC). AIMS: The aim of this study was to assess the impact of IL-17A G197A and IL-17F A7488G gene polymorphisms on development of LC from chronic hepatitis B (CHB) in Chinese patients. METHODS: A total of 163 HBV-related LC patients and 168 CHB patients were enrolled in the present study. IL-17A and IL-17F gene polymorphisms were analyzed using a polymerase chain reaction (PCR) restriction fragment length polymorphism assay (PCR-RFLP). RESULTS: Frequencies of IL-17A G197A genotype AA and allele A were significantly higher in LC patients compared with that in CHB patients (AA 42.33% vs 27.98%, P = 0.032; A 56.34% vs 46.15%, P=0.011, respectively); While no significant difference in frequencies of genotypes and alleles of IL-17F A7488G was found between the two groups. The AA genotype of IL-17A G197A significantly increased LC risk (OR 4.186, 95% CI: 1.479-11.844), while A allele carriers were also associated with an increased LC risk (OR 1.856, 95% CI: 1.161-2.967). CONCLUSION: IL-17A G197A is a candidate gene that confers the genetic susceptibility for LC development from CHB in Chinese population.

[Genetic transformation of Pinellia ternata with Agrobacterium tumefaciens-mediated sHSP genes].

OBJECTIVE: To establish an efficient genetic transformation system of Pinellia ternata. METHOD: With petioles from test-tube seedlings of P. ternata as explants, Agrobacterium tumefaciens mediation method was adopted to explore the effect of phenolic substances, A. tumefaciens's concentration, infection time, pre-incubation time and co-cultivation time on genetic transformation efficiency of P. ternata. RESULT AND CONCLUSION: The genetic transformation efficiency could be effectively enhanced by infecting in A. tumefaciens culture containing AS 40 mg x L(-1) for 15 min for three days. The petioles were put into the differentiation medium containing 150 mg x L(-1) Kan and 350 mg x L(-1) Carb to screening and cultivation. After around 30 days, microtubers could be observed at both sides of the petioles. Gus staining and PCR verification on the regenerated plants showed that the exogenous gene sHSP had been integrated into genome of P. ternata.

[The analysis of IL-10 and its methylation in the patients with acute on chronic liver failure].

OBJECTIVE: To investigate the effect of IL-10 and the methylation of its promoter in acute on chronic liver failure (ACLF). METHODS: Patients were divided into three groups: 25 with ACLF, 25 with CHB, 10 healthy controls. Respectively detect the serum level of IL-10 via ELISA, and the methylation of IL-10 promoter via MSP, to analyze the difference among the three groups. RESULTS: Both the ACLF group and the CHB group have significant increase in serum level of IL-10 compared with the control group (P < 0.05); the ACLF group's level is higher than the CHB group, however without statistical significance (P > 0.05). The serum level of IL-10 in ACLF group has no significant relativity with ALT and HBV-DNA( r = -0.022, r = 0.033, respectively; P > 0.05); has positive relativity with TBIL and MELD ( r = 0.566, r = 0.443, respectively; P < 0.05); and negative relativity with PTA (r = -0.581, P < 0.05). The distribution of the methylation of IL-10 promoter in ACLF group is significantly different from the other two. CONCLUSION: The serum level of IL-10 in hepatitis patients is significantly higher and increases with the degree of liver failure. The promoter methylation may be important in the gene inactivation.

[Hypomethylation of TNF-alpha gene promoter in the patients with acute-on-chronic hepatitis B liver failure].

OBJECTIVE: The present study was designed to investigate the possible epigenetic alteration in the promoter of TNF-alpha in the patients with acute-on-chronic hepatitis B liver failure (ACHBLF). METHODS: The methylation of TNF-alpha promoter in peripheral blood mononuclear cells (PBMCs) was measured by methylation specific PCR (MSP). The level of serum TNF-alpha was determined by enzyme-linked immunosorbent assay (ELISA). Model for End-stage Liver Disease (MELD) was performed for the evaluation of liver failure. RESULTS: The serum level of TNF-alpha in patients with ACHBLF(44.9260 +/- 26.48523) was higher than that in CHB (18.92505 +/- 9.04461) and healthy controls (11.9172 +/- 5.04612) (P < 0.05). Moreover, the serum TNF-alpha level was significantly decreased in methylation group as compared to unmethylaiton group in patients with ACHBLF (P < 0.05). MELD was not significantly different between methylated and unmethylated group of ACHBLF patients (P > 0.05). In addition, the serum level of TNF-alpha was found to be positively correlated with serum total bilirubin (r = 0.891, P < 0.01) and MELD score (r = 0.792, P < 0.01), but to be negatively correlated with prothrombin activity (r = - 0.511, P < 0.05) in patients with ACHBLF. CONCLUSION: The TNF-alpha methylation patten is stable for the liver failure, suggesting the effect of environment on methylation.