Objective In order to study the etiology and the hearing status of the deaf students in Hubei province, a survey was carried out from April 1999 to June 2000.Methods A total number of 813 deaf students in Hubei province were examined with audiometer and investigated through questionnaire. The pedigress analysis was conducted in deaf students with family history.Results The pedigrees of 227 familes with deafness were obtained, the inheritance pattern of 167 families could be ascertained. 232(28.5%) deaf students were diagnosed congenital deafness, 581 (71.5%) students were diagnosed acquired deafness. The degrees of deafness could be ascertained with 359(44.1%) students of profound deafness, 323(39.7%) students of severe deafness, 111(13.7%) students with moderate to severe deafness, 11(1.4%) students of moderate deafness, and 9(1.1%) students of mild deafness.Conclusion The hearing loss of deaf students is very serious, and genetic factor and ototoxic antibiotics were a principal causation in the occurrence of deafness.

The in-vivo bioavailability of Qingxintong administrated by intramuscular injection, intravenous injection and gastric infusion was compared. Experimental results showed that Qingxintong was rapidly absorbed and excreted. The half-life time for absorption was 0.05 - 0.07 h and the half-life time for elimination was 0.14 - 0.29 h. The bioavailability of Qingxintong in the dose of 10 mg/kg by intramuscular injection or by intravenous injection was 94.71 %, and was 9.16% in the dose of 60 mg/kg by gastric infusion or in the dose of 10mg/kg by intramuscular injection.

Colorectal cancer (CRC) is one of the leading causes of death worldwide. Thus, the development of new therapeutic targets for CRC treatment is urgently needed. SGK1 is involved in various cellular activities, and its dysregulation can result in multiple cancers. However, little is known about its roles and associated molecular mechanisms in CRC. In present study, we found that SGK1 was highly expressed in tumor tissues compared with peri-tumor samples from CRC patients. In vitro experiments revealed that SGK1 overexpression promoted colonic tumor cell proliferation and migration and inhibited cell apoptosis induced by 5-fluorouracil (5-FU), while SGK1 shRNA and inhibitors showed the inverse effects. Using CRC xenograft mice models, we demonstrated that knockdown or therapeutic inhibition of SGK1 repressed tumor cell proliferation and tumor growth. Moreover, SGK1 inhibitors increased p27 expression and promoted p27 nuclear accumulation in colorectal cancer cells, and p27 siRNAs could attenuate the repression of CRC cell proliferation induced by SGK1 inhibitors. Collectively, SGK1 promotes colorectal cancer development via regulation of CRC cell proliferation, migration and survival. Inhibition of SGK1 represents a novel strategy for the treatment of CRC.
Animals ; Apoptosis ; Cause of Death ; Cell Proliferation ; Colon ; Colorectal Neoplasms* ; Fluorouracil ; Heterografts ; Humans ; In Vitro Techniques ; Mice ; Repression, Psychology ; RNA, Small Interfering