Objective: To evaluate the relationship between the change of left ventricular mass and arterial stiffness in the aged patients with diabetes mellitus. Methods: The pulse wave velocity (PWV) and left ventricular mass index(LVMI)were used to estimate the left ventricular mass and arterial stiffness. The relationship between LVMI and PWV and other influencing factors were evaluated with univariate analysis and stepwise regressive analysis in 105 patients with diabetes mellitus. The value of PWV was compared in the subjects of the left ventricular hypertrophy and the non- left ventricular hypertrophy groups. Results: LVMI was positively correlated with PWV, systolic blood pressure, pulse pressure,medical history and body mass index (the values of r were 0.821, 0.792, 0.799, 0.664 and 0.241 respectively,P ＜ 0.01 or P ＜ 0.05). A stepwise regression analysis was used to assess the combined influence of variables on left ventricular hypertrophy. The model included the following variables: PWV, systolic blood pressure and diabetes mellitus medical history. PWV value was significantly higher in patients with left ventricular hypertrophy than that of the patients without left ventricular hypertrophy(t = 9.109,P < 0.01). Conclusion: The increased arterial stiffness is one of the important factors which lead to the increased left ventricular mass index in aged patients with diabetes mellitus.

Objective To identify the mechanisms underlying xCT deficiency by high-resolution proteomic analysis of differential protein expression in Sut and wild melanocytes .Methods The proteins,extracted from Sut and wild melano-cytes,were analyzed by two dimensional electrophoresis and PDQuest software .Subsequent MALDI-TOF mass spectrometry analysis was carried out .The protein identification was based on peptide mass fingerprint combined with the pI and the rela -tive molecular mass ( Mr) .Sequence coverage was performed with the Peptldent software on the NCBnlm website .Also,the autophagy marker protein LC3-Ⅱ, and the autophagic cell death marker protein Beclin 1 were detected by Western blotting . Results and Conclusion Twenty apparently upregulated or downregulated proteins were identified .Strikingly, important modifications in regulators of trafficking and organization of vesicles and autophagy ( Anxa3; Hist 1h2bk, NDRG1, and CaM) and in regulators of invasion and metastasis of carcinoma (S100A-4;S100A-6 and vimentin)are likely to account for dysfunctions in cell viability and cell-extracellular adhesion .These results indicate that the proteins regulating autophagy , vesicles trafficking and MAP kinase related pathways are activated and play a role in xCT-deficiency .

BACKGROUND:Ful-thickness articular cartilage injury is notoriously difficult to be treated in the fields of orthopedics and sports medicine. Al ogeneic bone and cartilage transplantation can offer a transparent cartilage with biological activity and biomechanical properties to repair ful-thickness articular cartilage defects. Al ogeneic osteochondral grafts from osteochondral tissue bank are adequate, and have a good prospect in the treatment of articular cartilage defects.
OBJECTIVE:To summarize the drawn materials, preservation, quality control and clinical monitoring of al ogeneic osteochondral grafts supported by the osteochondral tissue bank.
METHODS:The first author searched PubMed and CNKI for the relevant articles published before 2013 using the key words of“tissue bank, knee, articular cartilage, preservation, transplantation”in English and Chinese, respectively. After retrieval, we summarized the drawn materials, preservation, quality control and clinical monitoring of al ogeneic osteochondral grafts supported by the osteochondral tissue bank.
RESULTS AND CONCLUSION:Nineteen of 194 retrieved articles were enrol ed according to inclusive and exclusive criteria. The results show that al ogeneic bone and cartilage transplantation is an ef ective method for the treatment of articular cartilage defects, and the establishment of the osteochondral tissue bank can provide safe and active tissues for the treatment of articular cartilage defects. Now, the osteochondral tissue bank is stil in the initial stage.

Objective To determine the volume reduction of the primary olfactory cortex (POC) in patients with Alzheimer disease (AD) and investigate the potential relationship of functional olfactory activation and anatomical atrophy changes. Methods Twelve patients with AD, eight patients with mild cognitive impairment (MCI) and twenty normal controls (NC) underwent standardized UPSIT (University of Pennsylvania smell identification test) behavior smell test and neuropsychological tests. Then all of the subjects underwent the high resolution MRI and an olfactory fMRI scan on a 3T system. Volumetric measurement of the POC was conducted and the areas were also saved as a ROI which would be used during the processing of fMRI data to get the activation voxels in local region. The Kruskal-Wallis rank test was used to examine the significance of POC volume and activation in three groups, If P-value was less than 0.05,Bonferroni method was used for multiple comparisons. The correlation between the anatomical volume and functional activation was analyzed with partial correlation adjusted for age. Results The POC volume of NC, MCI and AD groups were 3024--4734, 1409--4553 and 1561--3759 mm~3, and the medians were 3749, 2752 and 2156 mm~3. The activation voxels of each group were 0--2360, 0--2160 and 0--100 mm~3, while the medians were 430, 40 and 0 mm~3. There were significant differences of both POC volume atrophy and activation between the three groups, with a trend of reduction from NC to MCI to AD group (H is 14.942 and 16.587, both P<0.05). The volume of olfactory activation at POC was highly correlated with the volume of POC (r=0.364, P=0.023). Conclusions In this study, we explored the morphological and functional changes in the POC. It is revealed that POC suffers prominent local atrophy and dysfunction as well as hippocampus in AD. These results can provide neuropathological and neurofunctional bases for olfactory deficit in Alzheimer Disease.

Objective To discuss the method and clinical effect of bilobed DIEP flap for repair of degloving injuries of the hand.Methods From June, 2013 to January, 2015, the bilobed DIEP flap were designed to repair 6 cases of degloving injuries of hand, of which the small leaf flap repaired separately defect of thumb, larger leaf flap repair 2nd-5th finger and palm and dorsum.The bilobed DIEP flap design were based upon anatomic study on deep inferior epigastric artery, superior epigastric artery, intercostal artery and its anastomosis.Results The largest area of main flap was 35 cm × 12 cm, and the deputy leaves of flap was 10 cm× 7 cm.All of the 6 flaps survived.One of them experienced distal end necrosis of epidermis.But it was healed by dressing changes.All of the 6 cases were followed up for average of 12 months (range, 6-20 months).All flaps were seen with good appearance, fully recovered protectve sensation and the active motion of the thumb was recovery.Moreover, the donor sites were closed directly and the appearance were satisfactory.Conclusion The bilobed DIEP flap is a satisfying choice in repairing degloving injuries of the hand in that it has reliable blood supply, can obtain the larger area of skin and leaves small injuries in targeted area.

Objective To discuss the clinical application and evaluate the effect of repairing finger injuries using the perforator flap in forearm cubital fossa.Methods From July,2012 to December,2013,8 cases of finger injuries with totaled defect area of 2.5 cm × 4.0 cm-5.5 cm × 7.0 cm were reviewed.Among them,6 cases had phalangeal fracture,7 cases had neurovascular injury and 4 cases combined with tendon injuries.Cubital fossa flaps based on the inferior cubital perforator of radial artery were transplanted to repair the defects.Results All of the 8 flaps survived.One of them experienced distal end necrosis of epidermis and 1 cm long wound dehiscence.But it was healed by dressing change.All of the 8 cases were followed up for an average of 11 months (range,6-20 months).Sensory quality of （S） + was present in all of the flaps with two-point discrimination ranging between 7.5 mm and 9.8 mm with an average of 8.5 mm.All flaps were seen with good appearance,texture and colour.Moreover,function and appearance in donor sites were satisfactory.Conclusion The perforator flap in forearm cubital fossa is a satisfying choice in repairing small skin defects in fingers and other paas in that it is fixed,easy to dissect and leaves small injuries in targeted area.

Objective To estimate any influence of strong pulsed magnetic fields on the expression of growth-related genes in human bladder cancer BIU-87 cells. Methods Human BIU-87 cells were cultured in vitro and randomly divided into a magnetic field group and a control group. Each group was further divided into 24 h, 48 h and 72 h sub-groups. The magnetic field group cells were exposed to an 8 T magnetic field pulsed at 15 Hz for 2 h every day. The control group cells also placed on the same environment, but not exposed to any strong, pulsed magnetic field. The expression of B cell lymphoma/leukemia gene-2 (Bcl-2) mRNA, Bax mRNA and caspase-3 mRNA was measured with RT-PCR, and flow cytometry was used to evaluate the expression of the Bcl-2, Bax and caspase-3 genes of the tumor cells in vitro. Results The expression of Bax mRNA and protein was significantly higher in the cells exposed to the magnetic field than in the control groups. The expression of Bcl-2 mRNA and protein was significantly less. The expression of caspase-3 mRNA and protein in the two groups showed no significant differences.Conclusions A strong, pulsed magnetic field can inhibit the growth of bladder tumor BIU-87 cells and promote their apoptosis. The mechanism is probably related with the magnetic field promoting Bax mRNA and protein expression and inhibiting Bcl-2 mRNA and protein expression.

Objective: To analyze the molecular epidemiology, genetic variations and evolution of enterovirus 71 (EV71) strains isolated in Jiangsu Province from 2009 to 2018. Methods: Statistical methods were used to analyze the data about epidemiological characteristics and results of pathogen detection in cases with EV71 infection in Jiangsu Province from 2009 to 2018. The complete VP1 sequences of 80 EV71 strains were amplified and sequenced for analysis of diversity and phylogenesis. Results: A total of 41 858 enterovirus-positive hand, foot and mouth disease cases were reported in Jiangsu Province from 2009 to 2018. EV71 was the predominant pathogen, accounting for 36.52%, and responsible for most of the severe cases. However, the percentage of EV71 among all pathogens gradually decreased over time. EV71 infection reached the peak in April to June and mainly occurred in children aged six months to five years old with higher incidence in males than in females. In terms of regional distribution, EV71 infections were characterized by area clustering in Jiangsu Province, mainly detected in Nanjing, Suzhou, Wuxi and Lianyungang. The 80 EV71 isolates belonged to C4a genotype. Nucleotide differences between them and three vaccine strains (H07, FY23 and FY7VP5)were 0.6%-5.5%, 0.8%-5.7% and 1.9%-6.9% and amino acid difference were 0-1.4%, 0.3%-2.0% and 0.3%-2.0%, respectively. Amino acid mutations in the epitopes of the 80 EV71 strains did not marked by years or regions. Conclusions EV71 strains showed obvious epidemiological characteristics in time, population and regional distribution in Jiangsu Province from 2009 to 2018.All of the 80 EV71 isolates belonged to C4a subgenotype. The nucleotide sequences between them and the vaccine strains varied greatly, but the homology of amino acids was relatively high, indicating the existence of some synonymous mutations and no risk of antigenic drift. This study would provide reference for EV71 vaccination in Jiangsu Province.

Objective:To evaluate the role of Toll-like receptor 4 (TLR4)/nuclear transcription factor κB (NF-κB) signaling pathway in long-term cognitive impairment induced by multiple exposures to sevoflurane anesthesia in neonatal rats.Methods:Seventy-five SPF healthy newborn Sprague-Dawley rats of either sex, aged 6 days, weighing 12-20 g, were divided into 3 groups ( n=25 each) using a random number table method: control group (group C), multiple exposures to sevoflurane anesthesia group (group S) and TLR4 inhibitor plus multiple exposures to sevoflurane anesthesia group (group I+ S). The rats in group S and group I inhaled 3% sevoflurane for 2 h at 6, 7 and 8 days after birth. TLR4 inhibitor TAK-242 10 mg/kg was intraperitoneally injected before each exposure to sevoflurane in group I, and the equal volume of normal saline was given instead in the other two groups. The spontaneous activity was evaluated by open field test on day 29 after birth, and the cognitive function was assessed by Morris water maze test on days 30-34 after birth. After the behavioral test, the blood samples from the abdominal aorta were collected, and then the rats were sacrificed under deep anesthesia to isolate the hippocampal tissues for measurement of the levels of S100β and neuron-specific enolase (NSE) in serum and hippocampal interleukin-1β (IL-1β), IL-6 and tumor necrosis factor α (TNF-α) (by enzyme-linked immunosorbent assay), expression of TLR4, NF-κB p65 and phosphorylated NF-κB p65 (p-NF-κB p65) (by Western blot) and for microscopic examination of the pathological changes of hippocampal CA1 region after HE staining. Results:Compared with group C, the escape latency was significantly prolonged, the number of crossing the original platform was reduced, the TLR4 expression was up-regulated, the ratio of p-NF-κB p65/NF-κB p65 was increased, the levels of serum S100β protein and NSE and hippocampal IL-1β, IL-6 and TNF-α were increased ( P<0.05), and the pathological changes in the hippocampal CA1 region were aggravated in group S. Compared with group S, the escape latency was significantly shortened, the number of crossing the original platform was increased, TLR4 expression was down-regulated, the ratio of p-NF-κB p65/NF-κB p65 was decreased, the levels of S100β and NSE in serum and hippocampal IL-1β, IL-6 and TNF-α were decreased ( P<0.05), and the pathological changes in hippocampal CA1 area were significantly attenuated in group P. Conclusions:The mechanism by which multiple exposures to sevoflurane anesthesia induces long-term cognitive impairment is related to activation of TLR4/NF-κB signaling pathway and increase in hippocampal inflammatory responses in neonatal rats.

Objective:To evaluate the role of nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in edaravone-induced attenuation of long-term cognitive impairment caused by long-time sedation with propofol in the neonatal rats.Methods:Eighty SPF healthy newborn Sprague-Dawley rats of both sexes, aged 7 days, weighing 15-20 g, were divided into 4 groups ( n=20 each) using a random number table method: control group (group C), propofol group (group P), edaravone+ propofol group (group EP) and Nrf2 inhibitor ML385+ edaravone+ propofol group (group MEP). Propofol 75 mg/kg was intraperitoneally injected once a day for 7 consecutive days in P group, EP group and MEP group, respectively, while the equal volume of medium/long chain fat emulsion injection was intraperitoneally injected in C group. Edaravone 3 mg/kg was intraperitoneally injected at 30 min before each propofol injection in EP and MEP groups, and ML385 15 mg/kg was intraperitoneally injected simultaneously in group MEP. The spontaneous activity was evaluated by the open field test on day 29 after birth, and the cognitive function was assessed by Morris water maze test on days 30-34 after birth. The rats were sacrificed after the end of water maze test, and brains were removed and hippocampal tissues were obtained for determination of reactive oxygen species (ROS) levels (by flow cytometry), superoxide dismutase (SOD) and malondialdehyde (MDA) levels (by enzyme-linked immunosorbent assay) and expression of Nrf2 and HO-1 (by Western blot) and for microscopic examination of the pathological changes in the hippocampal CA1 area (using HE staining). Results:There was no significant difference in the speed, distance and time of stay at the center of the open field among the four groups ( P>0.05). Compared with C group, the escape latency was significantly prolonged, the number of crossing the original platform quadrant was reduced, the levels of MDA and ROS were increased, the activity of SOD was decreased, the expression of Nrf2 and HO-1 was down-regulated ( P<0.05), and the pathological injury was observed in the hippocampal CA1 region in group P. Compared with P group, the escape latency was significantly shortened, the number of crossing the original platform quadrant was increased, the levels of MDA and ROS in the hippocampus were decreased, the activity of SOD was increased, the expression of Nrf2 and HO-1 was up-regulated ( P<0.05), and the pathological injury in the hippocampal CA1 region was significantly alleviated in EP group. Compared with EP group, the escape latency was significantly prolonged, the number of crossing the original platform quadrant was reduced, the levels of MDA and ROS were increased, the activity of SOD was decreased, the expression of Nrf2 and HO-1 was down-regulated ( P<0.05), and the pathological injury was aggravated in the hippocampal CA1 region in MEP group. Conclusions:The mechanism by which edaravone attenuates long-term cognitive impairment caused by long-time sedation with propofol is related to activation of Nrf2/HO-1 signaling pathway and inhibition of oxidative stress in the neonatal rats.