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Objective: Through experiment on animals and clinical trials to explore the safety and efficacy of hypoglycemic anti-deafness capsules on diabetic patients with deafness., Methods: Total 296 patients with non-insulin dependent diabetes mellitus (NIDDM) were randomly divided into two groups. A treatment group of 164 patients (208 ears) was treated with hypoglycemic anti-deafness capsules based on TCM syndrome differentiation. A control group of 132 patients (184 ears) was treated with glibenclamide and conventional drug treatment for deafness. The following were observed: hearing, fasting plasma glucose (FPG), 2 h postprandial plasma glucose (2hPG), 24 h urine glucose (24hUG), improvement of main symptoms, platelet function, and changes in superoxide dismutase (SOD) and lipid peroxide (LPO) levels. In animal studies, Kunming mice, weighing 18-22 g were used. Half of the mice were males and half were females. Wistar rats, weighing 80-120 g were used. Half of the rats were males and half were females. Male Wistar rats, weighing 200-220 g, were also used. Their acute and chronic toxicity was studied., Results: The hearing improvement was 56.7% in the treatment group and 26.6% in the control group. FPG, 2hPG, and 24hUG were improved significantly (P < 0.05, P < 0.01, P < 0.01, respectively) in the treatment group and 2hPG and 24hUG improved significantly in the control group (P < 0.05, P < 0.05). The improvement in 2hPG and 24hUG in the treatment group was significantly greater than that in the control group P < 0.01).There was no significant difference in FPG between the two groups (P < 0.05). Main symptoms in the treatment group were significantly more improved than those in the control group (P < 0.05, P < 0.01). In the treatment group, platelet adhesion and aggregation, SOD, and LPO were all significantly improved from before treatment (P < 0.05, P < 0.01). However, in the control group, except LOP (P < 0.05), there were no significant differences from before treatment to after (P < 0.05). In animal studies, no obvious acute or long-term toxicity was observed from capsule administration., Conclusion: Through experiment on animals and clinical trials, we can found that hypoglycemic anti-deafness capsules could decrease blood glucose and serum triglycerides of alloxan-induced diabetic rats. This herbal capsule is effective for safely treating diabetic patients with deafness.

Mutations in the mitochondrial 12S ribosomal RNA gene have been identified to be associated with deafness. Among these, the A to G transition at position 1555 is one of the most common pathogenic mutations associated with hearing loss. In order to evaluate the allele frequency of this mutation in infants with hearing loss, the A1555G mutation was screened in 300 deaf children and 100 age- and sex-matched healthy subjects. Consequently, 5 patients with this mutation were identified, whereas the mutation was absent in healthy controls. Among the patients with the mutation, only one had an obvious family history of hearing impairment. Notably, this pedigree manifested a high penetrance of deafness. In particular, the penetrance of deafness was 80 and 40%, when the aminoglycoside antibiotics (AmAn) was included or excluded, respectively. Clinical evaluation of this family exhibited a wide degree of hearing loss. Furthermore, screening for the complete mitochondrial genes revealed the occurrence of A1555G and transfer (t)RNAThr T15943C mutations, together with other genetic variations belonging to East Asian haplogroup C. Notably, the T15943C mutation, located at the T arm of tRNAThr, could disrupt the 63T-55A base-pairing and impair tRNA metabolism. Therefore, it was hypothesized that the combination of A1555G and T15943C mutations may result in mitochondrial dysfunction that is responsible for deafness. Screening for A1555G, as well as other potential pathogenic mutations in the mitochondrial genome, is critical for clinical diagnosis and prevention of hearing impairment. [ABSTRACT FROM AUTHOR]

In China, approximately 30,000 babies are born with hearing impairment each year. However, the molecular factors causing congenital hearing impairment in the Xiamen area of Fujian province have not been evaluated. To provide accurate genetic testing and counseling in the Xiamen area, we investigated the molecular etiology of non-syndromic deafness in a deaf population from Xiamen. Unrelated students with hearing impairment (n = 155) who attended Xiamen Special Education School in Fujian Province were recruited for this study. Three common deafness-related genes, GJB2, SLC26A4, and mtDNA12SrRNA, were analyzed using all-exon sequencing. GJB2 mutations were detected in 27.1% (42/155) of the entire cohort. The non-syndromic hearing loss (NSHL) hotspot mutations c.109G>A (p.V37I) and c.235delC were found in this population, whereas the Caucasian hotspot mutation c.35delG was not. The allelic frequency of the c.109G>A mutation was 9.03% (28/310), slightly higher than that of c.235delC (8.39%, 26/310), which is the most common GJB2 mutation in most areas of China. The allelic frequency of the c.109G>A mutation was significantly higher in this Xiamen’s deaf population than that in previously reported cohorts (P = 0.00). The SLC26A4 mutations were found in 16.77% (26/155) of this cohort. The most common pathogenic allele was c.IVS7-2A>G (6.13%, 19/310), and the second most common was the c.1079C>T (p.A360V) mutation (1.94%, 6/310) which has rarely been reported as a hotspot mutation in other studies. The mutation rate of mtDNA12SrRNA in this group was 3.87% (6/155), all being the m.A1555G mutation. These findings show the specificity of the common deaf gene-mutation spectrum in this area. According to this study, there were specific hotspot mutations in Xiamen deaf patients. Comprehensive sequencing analysis of the three common deaf genes can help portray the mutation spectrum and develop optimal testing strategies for deaf patients in this area. [ABSTRACT FROM AUTHOR]