Background Paired box gene 6 (Pax6) is a master regulator for eye and brain development.Pax6 mutations or changes in its expression cause a series of ocular diseases including absence of iris,corneal opacity,cataract,glaucoma,abnormal fovea,retinoblastoma,and Wilm's tumor-aniridia-qenital ahormalies-retardation (WAGR).As a transcription factor,it is expressed in the region of anterior surface ectoderm corresponding to the future adenohypophyseal,olfactory and lens placodes,optic vesicle and other parts of the future brain and thus control the development of eye,brain,pituitary grand,nose and pancreas.Pax6 exists in 4 different isoforms,whose functions are subjected to regulation by different post-translation modifications.A complete understanding of the structure and functions of Pax6 and its associations with relevant diseases is helpful for ophthalmologists to investigate the pathogenesis and treatment of implicated ocular diseases caused by Pax6 gene mutation or changing in its expression.

Objective To investigate the effects of Nrf2/ARE pathway activator upregulating the expression of phase Ⅱ detoxifcation enzymes and antioxidant enzymes in islet B cell on its morphological structure in type 2 diabetic rats.Methods Type 2 diabetic rats were divided into diabetes model group (DM group),and tertiary-Butylhydroquinone intervention group(tBHQ group).At the same time,the normal control group (NC group)was set up.All rats were killed after eight-week continuous intervention.Fasting blood glucose (FBG) and fasting insulin (FINS) level were determined.Morphological structure of islet cells and apoptosis were observed.ELISA was used to determine MDA,TNF-α and T-SOD levels in serum and pancreatic tissues and Western blot was used to detect the protein expression levels of total Nrf2 and nulear Nrf2 in pancreatic tissues.Results Compared with NC group,FBG and FINS levels significantly increased and decreased in DM group respectively (all P=0.000).Compared with DM group,FBG and FINS levels significantly decreased and increased in tBHQ group respectively (all P=0.000).Compared with NC group,the number of islet cells significantly decreased and swelling,necrosis and apoptosis occurred in DM group.Islet cells in tBHQ group were significantly better than those in DM group.Compared with NC group,MDA and TNF-α levels in serum and pancreatic tissue significantly increased and TSOD levels significantly decreased in DM group (all P=0.000).Compared with DM group,MDA and TNF-α levels in serum and pancreatic tissue significantly decreased and T-SOD levels significantly increased in DM group(all P=0.000).Total Nrf2 and nulear Nrf2 in protein expression in DM group were significantly lower of than those in NC group (P()=0.000,P nulear Nrf2=0.006).Rats in tBHQ group had significantly higher protein expression of total Nrf2 and nulear Nrf2 than in DM group (all P=0.000).Conclusions Activating Nrf2/ARE pathway can reduce injury of oxidative stress and chronic inflammation on islet B cells further through upregulating the expression of phase Ⅱ detoxifying enzymes and antioxidant enzymes in islet B cells.

BACKGROUND:At present, the common filing materials used to correct secondary unilateral cleft lip nasal deformity include conchae cartilage, costal cartilage, Medpor implants, expanded polytetrafluoroethylene (ePTFE), alogenic acelular dermal matrix. OBJECTIVE:To analyze the therapeutic effects of comprehensive procedures with alogenic acelular dermal matrix or ePTFE for secondary unilateral cleft lip nasal deformity. METHODS: Thirty-six patients with secondary unilateral cleft lip nasal deformity were enroled, including 19 males and 17 females, aged 15-32 years. Alogenic acelular dermal matrix (n=22) or ePTFE (n=14) was used to correct nasal base colapse deformities. Anthropometry method was employed to make measurements. Fixed-point measurement was performed based on patient's pictures before and after correction. Long-term effects of these two kinds of filing materials were analyzed and assessed objectively and quantitatively. RESULTS AND CONCLUSION: After the folow-up of 6 months, al the patients were satisfied with their results, and no infection and no exposure occurred. The treatment effect of the alogenic acelular dermal matrix group was excelent in 16 cases and good in 6 cases; there were 10 cases of excelent and 4 cases of good in the ePTFE group. The objective indicators in the two groups were al improved at 6 months after correction (P < 0.05), but there was no difference between the two groups (P > 0.05). These findings indicate that alogenic acelular dermal matrix or ePTFE is useful to correct secondary unilateral cleft lip nasal deformity.

Thermostable L-arabinose isomerase (L-AI) is the most potential enzyme for the biological production of D-tagatose from D-galactose, a novel functional factor. Gene araA encoding the L-arabinose isomerase from Bacillus stearothermophilis IAM 11001 was cloned and expressed in Escherichia coli. The araA gene of 1491 bp has 95% identity with L-AI from Thermus sp. IM6501. The GenBank accession number for the nucleotide sequence of this araA gene determined in this work is EU394214.The bacterium was induced by IPTG and analyzed by SDS-PAGE, approximately 59 kDa exogenous protein was observed on the SDS-PAGE. The recombinant L-AI was purified to electrophoretical homogeneity with affinity chromatography, and the activity of recombinant L-AI was also studied. The bioconversion rate of D-galactose to D-tagatose reached 39.4% after 24h whole cell reaction.

L-arabinose isomerase (L-AI) can isomerize L-arabinose and D-galactose into L-ribulose and D-tagatose, respectively, which is currently the most effective biological catalyst for D-tagatose production. The crystal structure of L-AI has been solved recently and its gene has been cloned, sequenced and overex- pressed. L-AI improved by protein engineering will be the dominant enzyme for industrial production of D-tagatose. This paper reviewed researches on protein structure and function, properties and application in D-tagatose production of L-AI, and the long-term potential development of L-AI was prospected.

Objective To investigate the expression of CD14/CD16 by monocytes and the anti-inflammatory effects of hypertonic saline plus dextran (HSD) in adult blunt trauma patients in hemonhagic shock. Method A total of 30 adult patients were eligible for inclusion in the study if they sustained blunt trauma from March to October 2007 and had at least one recorded episode of hypotension (systolic blood pressure ≤ 90 mm Hg) with clear evidence of blood loss (external or internal including the thorax, abdomen or retroperitoneum). Patients were excluded if they refused to participate, were admitted ≥ 6 hours after injury, were pregnant, or had chronic disease. The enrolled patients were randomly divided in a double-blinded manner into an HSD group which was administered 7.5% Nad plus 6% dextran - 70, and a control group which was administered 0.9% NaCl. A single 250 ml dose of either HSD or NaO was immediately administered to the patients in each of the two groups while they were in the emergency room. The primary outcomes were to measure the changes in CD4/CD16 expression by monocytes and the levels of anti-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-lra and IL-10. Patient demographics, fluid requirements, organ dysfunction, infection and death were recorded. Results A total of 28 patients were enrolled with no significant differences in their clinical measurements. Hyperosmolarity was modest and transient. HSD altered the shock-induced monocyte redistribution pattern by reducing the drop in the "classic" CD14 ++ subset and remarkably affecting the expansion of the "pro-inflammatory" CD14+CD16+ subsets. In parallel, HSD significamly reduced pro-inflammatory TNF-α production while increasing anti-inflammatory IL-lra and IL-10 production. Conclusions This human trial demonstrates that HSD has anti-inflammatory and immunologic properties for trauma patients in hemorrhagic shock. HSD exerts profound immunomodulatory effects, promoting more balanced pro-/anti-inflammatory responses and reducing post-traumatic complications. Therefore, it could be useful in attenuating post-trauma multiorgan dysfunction (MOD).

Objectives To evaluate the effects of hypertonic-hyperoncotic solution (HHS) on cardiac function and extravascular lung water in children after open-heart surgery for congenital cardiac disease. Methods 50 children with congenital cardiac disease were randomly assigned to 2 groups. The HHS group received HHS (7.5% sodium chloride with 6% hydroxyethyl-stareh 200 kDa). The ISS group received isotonic saline solution (ISS 0.9% sodium chloride). Cardiac index (CI), extravascular lung water index (ELWI), stroke volume index (SVI), mean arterial pressure (MAP), and systemic vascular resistance index (SVRI) were measured. Immediately after sur-gery, patients were loaded either with HHS or with ISS (4 ml/kg). Sodium concentration, osmolality, thrombocyte count(TC), fibrinogen, and arterial blood gases were detected before operation, immediately after loading, 15 minutes, 1,4, 12, and 24 hours after the end of vol-ume loading. Hemodynamic parameters were recorded at the same time. The total amount of dobutamine required was documented. Results In HHS group, MAP, SVI and CI increased, and SVRI decreased significantly after the administration of HHS, compared with ISS group and before administration(P<0.01 or 0.05). Both CVP and HR were unchanged in both groups. In HHS group, ELWI decreased signifi-cantly, compared with before volume administration. But ELWI increased directly and remained elevated for 60 minutes after the administra-tion of ISS. Sodium concentration increased immediately after infusion of HHS. The postoperative need for infused dobutamine in the patients in HHS group was decreased, compared with ISS group (P<0.05). All patients left the hospital in a clinically sufficient state. Condu-sions A single infusion of HHS after cardiac surgery is safe. After cardiopuimonary bypass surgery, the administration of HHS increased CI by elevating SVI in combination with a decreased SVRI. ELWI significantly decreased, which suggest that HHS effectively counteracts, the capillary leakage.

Objective To explore the MRI T 1WI features of the hyperacute intracerebral hematoma by super-low-field MR.Methods 160 patients with hyperacute intracerebral hematoma were examined by using MR unit of 0.04T magnetic(WDLMW-400) and PS3D T 1WI(TR=125 ms,TE=25 ms).Results Hematomas located in basal ganglia(140 cases),cerebral lobe(13 cases),cerebellum(5 cases) and brain stem ( 2 cases) respectively.All of the hyperacute hematomas showed short T 1 signal intensity in PS3D T 1WI;the mass effects and perihematoma edema also can be found in all of the 160 cases.Conclusion This study shows that the super-low-field MRI is superior to medium and high field MRI in diagnosis of hyperacute intracerebral hematoma.

AIM:To investigate the effects of MG132,one of the proteasomal peptide aldehydes inhibitors,on lipopolysaccharide(LPS)-induced nuclear transcription factor-kappa B(NF-?B) activation,the production of nitric oxide(NO) and tumor necrosis factor-alpha(TNF-?),as well as the expression of inducible nitric oxide synthase(iNOS) in murine macrophage line RAW264.7.METHODS:Reporter gene assay was used to examine the activity of NF-?B by pNiFty-SEAP/HEK293 cells,which were transfected with the pNiFty reporter plasmid into human embryo kidney cells(HEK293).Fluorescence substrate DAF-2DA was used to testify NO level in Raw264.7 cell line induced by LPS.Furthermore,the secretion of TNF-? was examined by ELISA.Western blotting was used to reveal the expression of iNOS and I?B-?.RESULTS:MG132 significantly decreased the secretion of TNF-? induced by LPS,with the inhibitory rates of 36.7% and 60.4% to 5 ?mol/L and 10 ?mol/L MG132,respectively.The pro-inflammatory mediator NO production was decreased in a dose-dependent manner with the inhibitory rates increasing from 29.5%(2 ?mol/L) to 55.9%(10 ?mol/L).Pretreatment with MG132 reduced the expression of iNOS,but restored the I?B restrain caused by LPS treatment.Observed by a reporter gene assay,TNF-?-induced NF-?B activity was decreased gradually by addition of increasing concentration of MG132(2.5-10 ?mol/L).CONCLUSION:Our results suggest an anti-inflammation effect of MG132 by the suppression of LPS-induced the production of pro-inflammatory mediators including NO and TNF-?,and the expression of iNOS,which probably mediates the blockage of I?B degradation and NF-?B activation.

Objective To study the damage of rat articular cartilage induced by different doses of T-2 toxin, and to explore the relationship between mini-dose T-2 toxin and articular cartilage damage. Methods A total of 120 Wistar rats, weighing 50 - 70 g, were randomly divided into four groups according to their body weights: T-2 toxin group 0(control), 100, 200, 300 μg/kg, 30 rats in each group. Animals in the control group were fed standard rat chow, and animals in the three T-2 toxin groups were fed T-2-toxin-contaminated chow (the dose was 100, 200, 300 μg/kg, respectively). After 6 months, rats were euthanized by ether asphyxiation. The bilateral knee joints were collected and section prepared. The articular cartilage was examined by light and electronic microscope. Results Light microscope showed, the rat articular chondrocytes were clear and arranged orderliness in the control group. The rat articular chondrocytes were disarranged in 100 μg/kg T-2 toxin group.Degeneration and necrosis were found in 200 μg/kg group. Chondrocytes were shrunken with hypereosinophilia cytoplasm and fragmented pyknotic nuclei, extensive areas of chondrocyte loss and chondrocyte clones were visible in 300 μg/kg group. Scanning electronic micrograph(SEM) showed, the rat articular chondrocytes were clear, well formed and arranged tidy in the control group. The surface of articular cartilage was rough in 100 μg/kg group.Collagen fasciculi ruptured and stacked up in 200 μg/kg group. Presented a typical articular dryness phenomenon,the cartilage surface collapsed and many pits appeared in 300 μg/kg group. Transmission electronic microscope (TEM) showed that chondrocytes were abundant with cytoplasm, well-developed rough endoplasmic reticulum in the control group; agglomerate chromatin scattered along the karyotheca, nuclear membrane was thickening, with vacuolar degeneration of the endoplasmic reticulum in the 100 μg/kg group; endoplasmic reticulum expended, with protein retention and organelles breaks in the 200 μg/kg group. A large number of chondrocytes lost organdles, the membrane structures disrupted and the cartilage matrix stromatolyzed in the 300 μg/kg group. Conclusions Within the range of 100 - 300 μg/kg, T-2 toxin induces dose-related articular cartilage injury, the greater the dose, the more serious damage.