Diabetic retinopathy is the leading cause of blindness in those of working age.It is well known that the retinal vasculature is altered during diabetes.More recently,it has emerged that neuronal,glial dysfunction and electroretinogram changes occur in those with diabetes.Current research is directed at understanding these neuronal and glial changes because they may be an early manifestation of disease processes that ultimately lead to vascular abnormality.This review will highlight the recent advances in our understanding of the neuronal,glial dysfunction,electroretiongram changes that occur during diabetes.

Objective To investigate the expression and resistant gene of integron in multidrug-resistant Acinetobacter baumannii (MDR-Ab).Methods 51 strains of MDR-Ab isolated from a hospital in August-October 2012 were collected, antimicrobial susceptibility testing was performed.Class I(Int I),II (Int II)and III (Int III)of integrase genes and inte-gron variable region gene cassettes were detected by polymerase chain reaction (PCR),and the homology of integron varia-ble region was analyzed by detection results of restriction fragment length polymorphism (RFLP)and DNA sequencing. Results Positive rate of integrase gene in MDR-Ab was 78.43%(40/51).All genes belonged to Int I,while IntⅡand IntⅢ were not found.Variable region cassettes were detected in 97.50% (n=39)of Int I,there were 5 types of integron gene cassettes:aacA4 in 14 strains,aacA4+catB8 in 22 strains,arr-3 +aacA4 in 1 strain,dfrA15 in 1 strain and arr-3 in 1 strain.Conclusion MDR-Ab isolated from this hospital may be related with Int I expression.Int I carried gene cassettes as follows:aacA4,aacA4+catB8,arr-3+aacA4,dfrA15 and arr-3.

Objective To investigate whether delayed treatment with exogenous kallikrein on neurogenesis after focal cortical infarction in stroke-prone renovascular hypertensive rats (RHRSP). Methods Seventy-two RHRSP were divided into 3 groups. Twenty-four rats were given human tissue kallikrein ( 1.6 × 10-2 PNAU/kg) and 24 rats were given vehicle through tail venous daily for 2 or 6 days consecutively starting at the 24th hour after distal middle cerebral artery occlusion (MCAO). 24 rats underwent sham-operation. Cell proliferation was examined by using 5'-bromo-2'-deoxyuridine (BrdU, 50 mg/kg). Rats were respectively sacrificed 3, 7, 14 or 28 days after MCAO. Results Treatment with kallikrein significantly increased the number of BrdU+ cells in the ipsilateral subventricular zone (SVZ) (304.0±73. 9 vs 167.0±32.2 vs 56.0±12.2 at 7 d after operation, q =7.165, 12.916 and 5.751 respectively,all P<0.05) and in the peri-infarction region (490.0±82.0 vs 308.0±51.5 vs 49.0± 9.5 at 7 d after operation, q = 7.920, 19.184 and 11.264 respectively, all P < 0.01 ), and increased the number of BrdU+/DCX+ cells (225.0±13.6 vs 98.0±9.6 vs 23.0±5.6 at 7 d after operation, q = 30.731,48.735 and 18.004 respectively,all P < 0.01) in the ipsilateral SVZ compared with the vehicle group or the sham-operated group, which began on the 3 day, peaked in 7--14 days after MCAO, and then gradually decreased. Compared with the vehicle group, exogenous kallikrein markedly increased the number of BrdU+/NeuN+ cells (21.0±3.4 vs 13.0±2.6 at 14 d, P =0.001 ) in the peri-infarction region after MCAO. The kallikrein group showed a better functional improvement than the vehicle group after stroke ( all P < 0.05). Conclusion Our study suggests that administration of exogenous kallikrein at 24 h after cortical infarction enhances the SVZ neuroblasts proliferation, migration, and selective differentiation and improves functional recovery after stroke.

Objective To investigate the secondary degeneration of corticospinal tracts in cervical spinal cord following a recently cerebral infarct with diffusion tensor imaging(DTI) and its potential impact on neurological recovery.Methods Twenty-six patients with a focal cerebral infract underwent DTI at the first week, the fourth and twelfth week after stroke onset, respectively.The NIH Stroke Scale (NIHSS), the Fugl-Meyer motor scale (FM) and the barthel index (BI) were used to evaluate the neurological function before every DTI.Twenty-six gender and age match healthy volunteers underwent DTI three times at same time points.The DTI parameters of mean diffusivity (MD) and fractional anisotropy (FA value) were measured at the cervical spinal cord and initial lesion.Results Compared to the controls, the FA values of the contralateral side corticospinal tracts in the cervical spinal cord in patients significantly decreased at every observed time point (P<0.01).In patients group, the FA values of the contralateral side corticospinal tracts in the cervical spinal cord decreased progressively from 1~(st) week to 12~(th) week (P<0.01), but MD remained unchange.The absolute value of the percent reduction of FA value of the contralateral side corticospinal tracts in the cervical spinal cord in patients associated negatively with the absolute value of the percent change of NIHSS and FM (P<0.05), but not with the absolute value of the percent change of BI(P>0.05).Conclusions Conclusions: The secondary degeneration of the corticospinal tracts resulted from cerebral infarction may extend to the cervical spinal cord.Which may last at lest three months and thus hamper the process of neurological recovery.

Objective:To analyze the clinical data of 203 discharged patients with corona virus disease 2019(COVID-19), and to investigate the predictors for the severe cases.Methods:Confirmed COVID-19 cases hospitalized at Zhongnan Hospital of Wuhan University from January 1 to February 1, 2020 were consecutively enrolled, who were divided into severe group and non-severe group.The clinical data of enrolled patients were collected and the clinical manifestations, laboratory results, imaging, treatments and prognosis of patients in the two groups were analyzed. Mann-Whitney U rank sum test and chi-square test were used for statistical analysis. Results:A total of 203 discharged patients with COVID-19 were enrolled. The common clinical manifestations included fever (89.2%, 181/203), dry cough (60.1%, 122/203), chest distress (35.5%, 72/203), shortness of breath(29.1%, 59/203)and myalgia or arthralgia (26.6%, 54/203). The time from disease onset to hospital admission was 5.8 days (1.0 to 20.0 days). Among 203 enrolled patients, 107(52.7%) were divided into severe group and 96(47.3%) were non-severe group. The age in severe group was 60 years (23 to 91 years), which was significantly older than non-severe group (47 years (20 to 86 years)), the difference was statistically significant ( Z=-6.12, P<0.01). There were 63.6%(68/107) patients in severe group with at least one underlying disease, which was significantly more than non-severe group (20.8% (20/96)), the difference was statistically significant ( χ2=37.60, P<0.01). The proportions of patients with increased white blood cells, decreased lymphocytes and albumin, elevated alanine aminotransferase, aspartate aminotransferase, creatinine, lactic acid dehydrogenase, creatine kinase, fasting blood glucose, D-dimer, erythrocyte sedimentation rate, C-reactive protein, interleukin-6, and procalcitonin in severe group were all higher. On admission, 172 patients (84.7%) had bilateral patchy shadows or ground glass opacity in the lungs on chest imaging study, 20(9.9%) presented pleural effusion. Fifty-five cases (27.1%) showed progressions of lung lesions on computed tomography (CT) rescan at an average interval of five days. Among 203 patients, 123(60.6%) were given oxygen therapy upon admission, 107(52.7%) were given short-term glucocorticoid therapy, and 131(64.5%) received antiviral therapy; and 26(12.8%) died. The hospital stay was 11.0 days (1.0 to 45.0 days). Conclusions:Fever is the most common symptoms in COVID-19 patients.Elderly and patients with underlying diseases are risk factors for progression to severe cases. The elderly patients should be strengthened early monitoring, paid attention to the control of underlying diseases, and reduce the occurrence of critical diseases.

The widespread application of next generation sequencing (NGS) in clinical settings has enabled testing, diagnosis, treatment and prevention of genetic diseases. However, many issues have arisen in the meanwhile. One of the most pressing issues is the lack of standards for reporting genetic test results across different service providers. The First Forum on Standards and Specifications for Clinical Genetic Testing was held to address the issue in Shenzhen, China, on October 28, 2017. Participants, including geneticists, clinicians, and representatives of genetic testing service providers, discussed problems of clinical genetic testing services across in China and shared opinions on principles, challenges, and standards for reporting clinical genetic test results. Here we summarize expert opinions presented at the seminar and report the consensus, which will serve as a basis for the development of standards and guidelines for reporting of clinical genetic testing results, in order to promote the standardization and regulation of genetic testing services in China.

The effects of tanshinone IIA on the proliferation of the human non-small cell lung cancer cell line A549 and its possible mechanism on the VEGF/VEGFR signal pathway were investigated. The exploration of the interaction between tanshinone IIA and its target proteins provides a feasible platform for studying the anticancer mechanism of active components of herbs. The CCK-8 assay was used to evaluate the proliferative activity of A549 cells treated with tanshinone IIA (2.5-80 μmol/L) for 24, 48 and 72 h, respectively. Flow cytometry was used for the detection of cell apoptosis and cell cycle perturbation. VEGF and VEGFR2 expression were studied by Western blotting. The binding mode of tanshinone IIA within the crystal structure of the VEGFR2 protein was evaluated with molecular docking analysis by use of the CDOCKER algorithm in Discovery Studio 2.1. The CCK-8 results showed that tanshinone IIA can significantly inhibit A549 cell proliferation in a dose- and time-dependent manner. Flow cytometry results showed that the apoptosis rate of tested group was higher than the vehicle control, and tanshinone IIA-treated cells accumulated at the S phase, which was higher than the vehicle control. Furthermore, the expression of VEGF and VEGFR2 was decreased in Western blot. Finally, molecular docking analysis revealed that tanshinone IIA could be stably docked into the kinase domain of VEGFR2 protein with its unique modes to form H-bonds with Cys917 and π-π stacking interactions with Val848. In conclusion, tanshinone IIA may suppress A549 proliferation, induce apoptosis and cell cycle arrest at the S phase. This drug may suppress angiogenesis by targeting the protein kinase domains of VEGF/VEGFR2.