Connexin26 Gap Junction Mediates miRNA Intercellular Genetic Communication in the Cochlea and Is Required for Inner Ear Development

Organ development requires well-established intercellular communication to coordinate cell proliferations and differentiations. MicroRNAs (miRNAs) are small, non-coding RNAs that can broadly regulate gene expression and play a critical role in the organ development. In this study, we found that miRNAs could pass through gap junctions between native cochlear supporting cells to play a role in the cochlear development. Connexin26 (Cx26) and Cx30 are predominant isoforms and co-express in the cochlea. Cx26 deficiency but not Cx30 deficiency can cause cochlear developmental disorders. We found that associated with Cx26 deletion induced the cochlear developmental disorders, deletion of Cx26 but not Cx30 disrupted miRNA intercellular transfer in the cochlea, although inner ear gap junctions still retained permeability after deletion of Cx26. Moreover, we found that deletion of Cx26 but not Cx30 reduced miR-96 expression in the cochlea during postnatal development. The reduction is associated with the cochlear tunnel developmental disorder in Cx26 knockout (KO) mice. These data reveal that Cx26-mediated intercellular communication is required for cochlear development and that deficiency of Cx26 can impair miRNA-mediated intercellular genetic communication in the cochlea, which may lead to cochlear developmental disorders and eventually congenital deafness as previously reported

Structural design of a silicon six-wafer micro-combustor under the effect of heat transfer boundary condition at the outer walls

The aim of this investigation was to establish a methodology for designing highly stressed micro fabricated structures by studying the structural design issues associated with a silicon six–wafer micro combustor under the effect of heat transfer boundary condition at the outer walls. Some experimental and numerical simulation results have indicated that the flame can not be sustained in the micro combustor if the poor heat transfer coefficients at the outer wall are present. This could cause the combustor wall temperature higher than the auto ignition temperature of reactants and results in the upstream burning. Since silicon has relatively poor high temperature strength and creep resistance when the temperature is above the brittle to ductile transition temperature (BDTT), e.g. 900K, the combustion in the recirculation jacket could possibly damage the micro combustor due to the high wall temperature

MiRNA-145 increases therapeutic sensibility to gemcitabine treatment of pancreatic adenocarcinoma cells.

Pancreatic adenocarcinoma is one of the most leading causes of cancer-related deaths worldwide. Although recent advances provide various treatment options, pancreatic adenocarcinoma has poor prognosis due to its late diagnosis and ineffective therapeutic multimodality. Gemcitabine is the effective first-line drug in pancreatic adenocarcinoma treatment. However, gemcitabine chemoresistance of pancreatic adenocarcinoma cells has been a major obstacle for limiting its treatment effect. Our study found that p70S6K1 plays an important role in gemcitabine chemoresistence. MiR-145 is a tumor suppressor which directly targets p70S6K1 for inhibiting its expression in pancreatic adenocarcinoma, providing new therapeutic scheme. Our findings revealed a new mechanism underlying gemcitabine chemoresistance in pancreatic adenocarcinoma cells

Prevalence survey on pterygium among people aged 40 and above in Hengli Town of Dongguan

AIM:To investigate the prevalence of pterygium of the household population aged 40 and above in Hengli Town of Dongguan.<p>METHODS: Using the method of cluster random sampling, select 3 628 people aged 40 and above in four villages and one community for visual examination, intraocular pressure check, slit lamp examination and questionnaire.<p>RESULTS: The actual number of subjects was 3 393 people, and examination rate was 93.52%. We detected 843 patients with pterygium. The prevalence of pterygium was 24.85%.<p>CONCLUSION: There is high prevalence of pterygium in Dongguan area. The prevalence of pterygium is related with age and working environment, but has no relation with gender

A Deafness Mechanism of Digenic Cx26 (\u3cem\u3eGJB2\u3c/em\u3e) and Cx30 (\u3cem\u3eGJB6\u3c/em\u3e) Mutations: Reduction of Endocochlear Potential by Impairment of Heterogeneous Gap Junctional Function in the Cochlear Lateral Wall

Digenic Connexin26 (Cx26, GJB2) and Cx30 (GJB6) heterozygous mutations are the second most frequent cause of recessive deafness in humans. However, the underlying deafness mechanism remains unclear. In this study, we created different double Cx26 and Cx30 heterozygous (Cx26+/−/Cx30+/−) mouse models to investigate the underlying pathological changes and deafness mechanism. We found that double Cx26+/−/Cx30+/− heterozygous mice had hearing loss. Endocochlear potential (EP), which is a driving force for hair cells producing auditory receptor current, was reduced. However, unlike Cx26 homozygous knockout (Cx26−/−) mice, the cochlea in Cx26+/−/Cx30+/− mice displayed normal development and had no apparent hair cell degeneration. Gap junctions (GJs) in the cochlea form two independent networks: the epithelial cell GJ network in the organ of Corti and the connective tissue GJ network in the cochlear lateral wall. We further found that double heterozygous deletion of Cx26 and Cx30 in the epithelial cells did not reduce EP and had normal hearing, suggesting that Cx26+/−/Cx30+/− may mainly impair gap junctional functions in the cochlear lateral wall and lead to EP reduction and hearing loss. Most of Cx26 and Cx30 in the cochlear lateral wall co-expressed in the same gap junctional plaques. Moreover, sole Cx26+/− or Cx30+/− heterozygous mice had no hearing loss. These data further suggest that digenic Cx26 and Cx30 mutations may impair heterozygous coupling of Cx26 and Cx30 in the cochlear lateral wall to reduce EP, thereby leading to hearing loss

Research on the Determination of Cadmium in Grain by Rapid Digestion-Standard Addition

Rapid digestion-standard addition based on graphite furnace atomic absorption spectrometry(GFAAS) for determining cadmium in grain of four kinds of matrix (brown rice, corn, wheat and rice) is established, by studying on digestion conditions, optimizing the proportion of sample and nitric acid, and using digested sample to prepare standard solution. The results show that the correlation coefficients are 0.995 to 0.999. The detection limit of method is 0.003 mg/kg. The relative error between the test result and the standard value is –3.8% to –1.1%. The standard recoveries of cadmium in low, medium and high gradient are 99.1% to 103.4%, and the RSD values of the standard substances and real samples are 1.2% to 2.7%.Compared with the results of microwave digestion method, the detection values of cadmium have no significant difference (P>0.05). The method have shown advantages in terms of accuracy and precision, and it is a rapid and accurate method to calculate cadmium in large quantities of grain samples

The investigation of status of human parasites in children from Yushu

目的  调查青海省玉树县震后转移安置学生的肠道寄生虫感染情况。方法  粪便直接涂片法检查虫卵。结果  512份粪便样品中，寄生虫阳性粪便31份，感染率为6.05%。其中，结肠内阿米巴20例，感染率为3.91%；蓝氏贾第鞭毛虫8例，感染率为1.56%；蛔虫3例，感染率0.59%。结论  玉树的学生肠道寄生虫的感染率均不高于全国平均水平。Objective: To investigate the status of human parasites in children who have been evacuated here from Yushu after earthquake. Methods: Detect the eggs from smear feces samples. Results: 512 stool samples were collected and examined by microscope. The total infection rate was 6.05%, where the infection rate for entamoeba coli Grassi was 3.91%, Giardia lamblia stile was 1.56%, Ascaris Lumbricoides was 0.59%. Conclusion: Our results suggest that the infection rate of human parasites is not higher than normal rate in China

Deficiency of Mkrn2 causes abnormal spermiogenesis and spermiation, and impairs male fertility.

Although recent studies have shed insights on some of the potential causes of male infertility, new underlining molecular mechanisms still remain to be elucidated. Makorin-2 (Mkrn2) is an evolutionarily conserved gene whose biological functions are not fully known. We developed an Mrkn2 knockout mouse model to study the role of this gene, and found that deletion of Mkrn2 in mice led to male infertility. Mkrn2 knockout mice produced abnormal sperms characterized by low number, poor motility, and aberrant morphology. Disruption of Mkrn2 also caused failure of sperm release (spermiation failure) and misarrangement of ectoplasmic specialization (ES) in testes, thus impairing spermiogenesis and spermiation. To understand the molecular mechanism, we found that expression of Odf2, a vital protein in spermatogenesis, was significantly decreased. In addition, we found that expression levels of Odf2 were decreased in Mkrn2 knockout mice. We also found that MKRN2 was prominently expressed in the sperm of normal men, but was significantly reduced in infertile men. This result indicates that our finding is clinically relevant. The results of our study provided insights into a new mechanism of male infertility caused by the MKRN2 downregulation

Genome-wide gene responses in a transgenic rice line carrying the maize resistance gene Rxo1 to the rice bacterial streak pathogen, Xanthomonas oryzae pv. oryzicola

Abstract Background Non-host resistance in rice to its bacterial pathogen, Xanthomonas oryzae pv. oryzicola (Xoc), mediated by a maize NBS-LRR type R gene, Rxo1 shows a typical hypersensitive reaction (HR) phenotype, but the molecular mechanism(s) underlying this type of non-host resistance remain largely unknown. Results A microarray experiment was performed to reveal the molecular mechanisms underlying HR of rice to Xoc mediated by Rxo1 using a pair of transgenic and non-transgenic rice lines. Our results indicated that Rxo1 appeared to function in the very early step of the interaction between rice and Xoc, and could specifically activate large numbers of genes involved in signaling pathways leading to HR and some basal defensive pathways such as SA and ET pathways. In the former case, Rxo1 appeared to differ from the typical host R genes in that it could lead to HR without activating NDR1. In the latter cases, Rxo1 was able to induce a unique group of WRKY TF genes and a large set of genes encoding PPR and RRM proteins that share the same G-box in their promoter regions with possible functions in post-transcriptional regulation. Conclusions In conclusion, Rxo1, like most host R genes, was able to trigger HR against Xoc in the heterologous rice plants by activating multiple defensive pathways related to HR, providing useful information on the evolution of plant resistance genes. Maize non-host resistance gene Rxo1 could trigger the pathogen-specific HR in heterologous rice, and ultimately leading to a localized programmed cell death which exhibits the characteristics consistent with those mediated by host resistance genes, but a number of genes encoding pentatricopeptide repeat and RNA recognition motif protein were found specifically up-regulated in the Rxo1 mediated disease resistance. These results add to our understanding the evolution of plant resistance genes.</p