Type 2 diabetes is a polygenic and complex disease.Various approaches, including association analysis, positional cloning, positional candidate gene approach and genome-wide association analysis, were used to identify its susceptible genes.This article summarized the recent findings on susceptible gene mapping of type 2 diabetes.

Objective To evaluate the effectiveness of Nicked-Titanium Shape-Memory alloy net-like stent in the treatment of high risk patients with benign prostatic hyperplasia Methods 35 high risk patients with benign prostatic hyperplasia were treated with Nicked-Titanium Shape-Memory alloy net-like stent from 1995 to 1998. The results were analyzed retrospectirely. Results 34 cases of the disease were treated successfully at the first session, 30 of whom could urinate immediately after treated. 4 patients had a normal urination in 3 days after operation, the total efficacy rate being 97.1% (34/35). Conclusions The present study shows that Nickel-Titanium Shape-Memory alloy net-like stent for patients with benign prostatic hyperplasia is a safe, efficient and ideal method. The long term efficacy of the stent is in progress.

This study was aimed at to investigating the protective effect of a combined treatment with glial cell line derived neurotrophic factor (GDNF) and neurotrophin 3 (NT 3) on noise induced outer hair cell (OHC) damage. Guinea pigs were subjected to receiving infusion of an artificial perilymph containing GDNF (100ng/ml) and NT 3 (2 5?g/ml) into one cochlea via a mini osmotic pump. Three days later, the animals were exposed to a 4kHz narrow band noise at 115 dB SPL for 4h. The control animals received the same treatment except GDNF and NT 3. Thresholds of auditory brainstem responses (ABRs), elicited by clicks, were measured before and 3 days after the surgery of the pump implantation, and 10 days following noise exposure. Then, the subjects were sacrificed and the cochleas were stained with Hoechst 33342. The specimens were examined under a fluorescence microscope for quantitative assessment of the OHC nuclear morphology. The results showed that compared with the control animals, the drug treated ones had significant less swollen OHC nuclei ( P

Objective To study the features and risk factors of ischemic leukoaraiosis (LA) progression in elderly patients aged 80 years and over. Methods The 56 elderly patients with ischemic LA confirmed by MRI were enrolled in this study. The characteristics and risk factors of ischemic LA were comparatively analyzed between baseline and 3 years later by single and multi-variable logistic regression analysis. Results Ischemic LA progressed mostly in the subcortical white matter in elderly patients, especially the frontal lobes (progression of white matter lesion was present in 40% in the frontal lobes at baseline and 52% after 3 years), followed by the parietal lobes (35% at baseline and 36% after 3 years); Furthermore, previous high homocysteine (Hcy) and chronic bronchitis were risk factors of ischemic LA progression. Conclusions Ischemic LA progresses mostly in the subcortical white matter in the elderly, especially the frontal lobes; High Hcy and chronic bronchitis are risk factors of ischemic LA progression in elderly patients.

Repaglinide is one of the most commonly used oral antidiabetic drugs. It can lower postprandial plasma glucose by means of initiating early-phase insulin release through closing the ATP-dependent potassium channels. Phamacogenomics is a branch of genetics which deals with the genetic variability in individual responses to drugs and drug metabolism. The progress of phamacogenomic study on repaglinide is summarized in this article.

ABSTRACT:Many studies show that helminth‐derived molecules can induce immunoregulatory cells to form immune net‐work‐mediated immune ,thereby inhibiting allergic and autoimmune diseases .Helminth parasites can induce immune cell activa‐tion and produce cytokine .And parasites play an inhibitory effect to affect other immune related diseases .However ,the associ‐ation between helminths infections and immune related diseases does not always have an unequivocal outcome .While some hel‐minths infections protect against allergic diseases ,other helminth can exacerbate this immunopathology .

Objective To examine the role of mitochondrial energy-conversion efficiency in regulating the initiation and execution of the apoptotic process in outer hair cells(OHCs)of cochlea following exposure to intense noise.Methods Seventeen adult chinchillas were used in present study.The animals were randomly assigned to one of the two groups,12 animals were exposed to noise and the remaining 5 animals without exposure to noise served as normal control.For all the animals,3-nitropropionic acid solution(3-NP,50mmol/L),an irreversible inhibitor of succinate dehydrogenase(SDH),was dropped onto the round window of the cochlea of the right ear using a micro-syringe to inhibit the mitochondrial energy production,to serve as the test ear.Artificial perilymph solution(AP)was dropped onto the round window of the cochlea of the left ear to serve as the control ear.16h after application of 3-NP and AP,the animals were exposed to 75 pairs of impulse noise at 155 dB pSPL.The cochleae were harvested 2h after the noise exposure.The cochlear basilar membrane was stained with propidium iodide(PI),a DNA intercalating fluorescent probe used to visualize the morphologic viability of hair cell nuclei.All the specimens were examined with a fluorescence microscope.Results In the 3-NP-treated cochlea,medium degree of nuclear condensation of OHCs appeared to be the dominant nuclear pathology,and only a few OHCs showed nuclear fragmentation in the damaged area of the cochlea.In contrast,the AP-treated control ear exhibited a large quantity of nuclear fragments,and a small quantity of medium degree of nuclear condensation.Conclusion The present study indicates that mitochondrial energy-conversion function plays an important role in regulating the apoptotic process.Disruption of the mitochondrial energy can not deter the apoptotic process from initiation,but can slow down the pace of apoptotic progression in outer hair cells of the cochlea following exposure to intense noise.

Objective Apoptosis and necrosis are two forms of hair cell death in cochlea following exposure to intense impulse noise.The present study was designed to examine the activity of caspase-3,caspase-8 and caspase-9 in the basilar membrane of cochlea,and investigate the cellular signal pathway associated with noise-induced hair cell death in cochlea.Methods Twenty-seven adult chinchillas were used in present study.The animals were randomly assigned into test group(no.15) and control group(no.12).The animals in test group were exposed to noise for the detection of the activity of caspase-3,caspase-8 and caspase-9,respectively,each with 5 animals.Animals in control group were not exposed to noise.Chinchillas were exposed to impulse noise at 155 dB peak sound pressure level(pSPL) for 75 times.Two hours after noise exposure,both cochleae were perfused with approximately 30?l of freshly prepared solution containing one of the three caspases(caspase-3,-8 and-9) respectively using a micro-syringe.One hour after perfusion,the animals were sacrificed and the cochleae were harvested.The Corti organs were double stained with propidium iodide(PI),and a DNA intercalating fluorescent probe was used to visualize the morphologic viability of hair cell nuclei.All the specimens were observed with a fluorescence microscope.Results The normal cochlea did not exhibit green fluorescence for any of the three caspases in Corti organ.Strong caspase-3,-8 and-9 green fluorescence appeared in the outer hair cells with condensed or fragmented nuclei,a sign of apoptosis,whereas no fluorescence was observed for any of the three caspases in the swollen outer hair cell nuclei,a sign of necrosis,in the cochleae exposed to intense impulse noise.Conclusion It is indicated that caspase-9 is involved in the intrinsic and caspase-8 involved in the extrinsic apoptotic pathway which occur simultaneously in apoptotic outer hair cells.No caspase activation occurs in necrotic outer hair cell in the cochlea following exposure to intense impulse noise.

Objective To compare the prevalence of apoptosis and necrosis, and investigate the primary death pathway of outer hair cells of rat cochlea following styrene exposure. Methods Fourteen adult Long Evans rats were used in the present study. The animals were randomly assigned into test group (n=8) and control group (n=6). Animals in test group were exposed to styrene by gavage at 400 mg/kg (2g styrene was mixed with 1ml olive oil). Treatment was performed once a day, 5 days per week for 3 weeks. Animals in control group were fed by gavage the same volume of olive oil on an identical time schedule used for the test group. The auditory brainstem response (ABR) thresholds of both ears elicited with clicks were measured before and at the end of the 3-week styrene or olive oil treatment. After hearing was re-assessed, animals were sacrificed and cochleae were quickly removed from the skull. Following fixation, whole specimens comprising the basilar membrane with Corti's organ were separated from the modiolus. Apoptotic, necrotic and missing outer hair cells (OHCs) were distinguished by combined assays of nuclear staining with propidium iodide (PI), TUNEL assay and filamentous actin(F-actin)staining with FITC-phalloidin. Each Corti's organ was thoroughly examined by fluorescence microscopy. The numbers of damaged OHCs (apoptotic, necrotic and missing OHCs) were documented. Results Neither threshold shift of ABR nor sign of hair cell (HC) damage was found in the cochlea of control animals. The animals of test group showed both physiological and pathological changes in the cochleae following the 3-week styrene treatment. ABR testing revealed an average of 15 dB of threshold shifts. F-actin staining exhibited the maximal level of OHCs damage in the middle portion of Corti's organ. The major damage occurred in the third row of OHCs, followed by the second and first rows of OHCs. Three types of morphological changes in damaged OHC nuclei were revealed by PI labeling: nuclear condensation, nuclear swelling and nuclear missing. Strong TUNEL green fluorescence appeared in the OHCs with condensed nuclei. Quantitative analysis showed that the average number of apoptotic OHCs was approximately three times greater than the number of necrotic OHCs (P=0.01). Conclusion It is indicated that apoptosis is the primary death pathway of OHCs leading to generation of the cochlear lesion following styrene exposure.

Objective To quantitatively analyze the occurrence of apoptotic and necrotic outer hair cells (OHCs) and to evaluate the changes of these parameters with time after noise exposure. Methods Chinchillas were exposed to a narrow band noise at either 104 or 108 dB SPL for 1 hour. The animals were executed and dissected at either 1, 4 and 30 days after the noise exposure and the cochleas were collected for detection of OHC death mode. The apoptotic and necrotic OHCs were distinguished by examining the OHC nuclear morphology and confirmed by staining for caspase 3 activity or TUNEL assay. ABR thresholds for click stimuli were used to monitor changes in auditory function. Results The number of apoptotic cells were significantly greater than those of necrotic cells shortly after the noise exposure at day 1 for the 104 dB group, day1 and day4 for 108 dB group ( P =0 01, P =0 03, P =0 01) and the difference between the number of apoptotic cells and necrotic cells became statistically insignificant at day 4 and day 30 for the 104 dB group and day 30 for 108 dB group ( P =0 67, P =0 29, P =0 52). By day 30, apoptotic and necrotic pathologies continued, although in small quantity in both 104 dB group and 108 dB group. Conclusions The results of the study indicated that the early expansion of cochlear lesion is contributed primarily by apoptosis, whereas the later stage of lesion expansion is likely contributed equally by apoptosis and necrosis. The death of OHCs not only takes place during a noise exposure, but also continues for at least 30 days after noise exposure