After major operation,a series of complicated pathological and physiological changes will occur during the trauma and stress state.The protein synthesis is affected,which results in negative nitrogen balance.In addition,the release of inflammatory factors can damage the capillary endothelial cells and increase the permeability of micrangium,induce vascular colloidal albumin leakage to the extravascular tissue,decrease plasma albumin,make wound edema,eventually lead to postoperative hypoproteinemia.Except for albumin supplement,it should be aimed at the mechanism to control the stress response and reduce the leakage caused by the release of inflammatory factors to solve this problem radically in clinical work.The reports about the causes and treatment of hypoproteinemia after major surgery were reviewed to provide evidence for clinical treatment.

Carbapenem-resistance is an emerging problem in Chinese neonatal intensive care units.Carbapenem-resistant enterobacteriaceae(CRE)can hydrolyze almost all β-lactam antibiotics including carbapenems by producing carbapenemase.There are three groups of carbapenemases, namely Amber A, B and D groups, which have different hydrolytic activities to specific β-lactam antibiotics.Currently, Chinese NICUs have been facing high colonization and infection rates of CRE, with high fatality rate and rapid transmission.The treatment of neonatal CRE infections is extremely difficult.The limited choice of antibiotics, the lack of pharmacokinetic and pharmacodynamic data and the uncertainty of the optimal dose and interval bring great challenges to the effective therapy of neonatal CRE infections.The main antimicrobial agents for CRE in adults and children include carbapenems, ceftazidime/averbactam, fosfomycin, polymyxin, aztreonam, etc., but there are few studies in neonates.Once infants are colonized or infected by CRE, decolonization and treatment are very difficult.Therefore, strict implementation of infection control and neonatal antimicrobial stewardship programs to reduce CRE production, transmission and infection, are the most important measures to cope with the prevalence of CRE.

The morbidity of obesity-related glomerulopathy(ORG) is on the increase in recent years.Studies have demonstrated that the chronic inflammation may play a key role in the pathogenesis of obesity related metabolic dysfunction.LipoxinA4 (LXA4) is an important anti-inflammatory lipid mediator,which is well known as the stop signal of the inflammatory reaction that can promote the resolution of inflammation.This review will provide a survey of recent advances on ORG and LXA4.

Objective: To determine the relationship between serum omentin-1 concentration and bone mineral desity in postmenopausal women, and the adipose influence of tissue on bone mineral density (BMD). Methods: BMD values of 336 participants were measured by dual-energy-x-ray absorptiometry (DEXA) at various skeletal sites: the anteroposterior spine, femeral neck, total hip (T-hip) and total body BMD (TBMD). Body compositions including lean tissue mass (LTM) and body fat mass (FBM) were measured by DEXA. hTe plasma concentrations of adipocytokines (omentin-1, adiponectin,leptin,resistin,visfatin, andapelin) were measured by ELISA. Results: hTe overweight and obese groups had higher T-hip,femerol neck, intertrochanter BMDthan the nomal weight group. Plasma omentin-1 was negatively correlated with anteroposterior spine, femeral neck, trochanter, intertrochanter, T-hip and Ward’s BMD, after adjustment for age, BMI and fat body mass, and the correlation was not significant. Multiple stepwise regression anlysis revealed that lean body mass, menopause duration and estrogen level were the most important variables affecting the BMD and each explained 12.2%–13.7%, 6.9%–13.1%, 0.9%–1.7% of the variance. Serum adiponectin was independently associated with T-hip, lumbar spine and total BMD. Conclusion: Plasma omentin-1 is not significantly correlated with BMD in postmenopausal women. Lean body mass, menopause duration and estrogen level are the most important variables affecting the BMD. Serum adiponectin is an independent predictor of T-hip, lumbar spine and total BMD.

BACKGROUND:Previous study has proved that implantation of the tissue-engineering bone with vascular bundles or sensory nerve tracts can promote bone formation, which may be related to the expression of sensory neuropeptide receptors. OBJECTIVE:To investigate the effect of implantation of tissue-engineered bone containing vascular bundles and sensory nerve tracts on the middle-and long-term expression of calcitonin gene-related peptide type Ⅰ receptor (CGRP1R) in the repair of rabbit large femoral defects. METHODS:Thirty-six New Zealand white rabbits were enrol ed and modeled into 1.5 cm femoral defects, and then randomized into three groups. Bone marrow mesenchymal stem cells (BMSCs) were subjected to osteoblastic induction for 7 days, and then seeded onto the β-calcium phosphate scaffold to construct the tissue-engineered scaffold.In sensory nerve group, the tissue-engineered scaffold was implanted into the defect region, and autologous sensory nerve bundles were implanted into the lateral groove of the tissue-engineered bone;in vascular bundle group, the tissue-engineered scaffold was implanted, and autologous femoral blood bundles were implanted into the lateral groove of the tissue-engineered bone;in blank control group, only the tissue-engineered scaffold was implanted. X-ray examination, immunohistochemistry and real-time PCR were performed at 24 and 48 weeks postoperatively. RESULTS AND CONCLUSION:The X-ray scores in the sensory nerve and vascular bundle groups were significantly higher than that in the control group (P<0.05), but no significant difference was found between sensory nerve and vascular bundle groups. Real-time PCR found that the expression level of CGRP1R mRNA in the vascular bundle group was significantly higher than that in the other two groups (P<0.05), but showed no significant difference between sensory nerve and blank control groups.Immunohistochemistry findings showed that CGRP1R positive expression rate in the sensory nerve and vascular bundle groups was higher than that in the blank control group. These results reveal that implantation of the tissue-engineered bone containing vascular bundles can promote the CGRP1R expression.

Microfluidic chip is a novel technology platform, in which microchannels are fabricated in different materials. The ability to precisely control the microflows makes it possible to mimic the microenvironment of cells in physiological or pathological states, which provides many distinct advantages for cell research. In this paper are reviewed the design and fabrication of microfluidic chip, the application of microfluidic chip in cell culture and cell researches; the enormous advantages of microfluidic chips in precise experimental control of the cellular microenvironment are introduced.
Cell Adhesion ; Cell Culture Techniques ; Cell Movement ; Cells, Cultured ; Cellular Microenvironment ; Humans ; Microfluidic Analytical Techniques ; methods

Objective To investigate the respiratory burst function of neutrophils in very low birth weight infants (VLBWI).Methods Twenty two VLBWI was divided into two groups:neonatal respiratory distress syndrome (NRDS) and non NRDS (11 in each).The respiratory burst function of neutrophils in the peripheral blood of VLBWI within 48 hours after birth was determined using the flow cytometrydihydrorhodamine 1,2,3 method before and after the chemical stimulation of phorbol-12-myrismte 14 acetate (PMA),and the gp91Phox was also measured in resting neutrophils by flow cytometry.Twenty healthy term neonates served as controls.Mann-Whitney U test was used for statistical analysis.Results Before the stimulation of PMA,the percentage of activated neutrophils of VLBWI [(49.10±20.19) ％] producing a respiratory burst was higher than that of term neonates [(18.73 ±6.81) ％] (Z--4.911,P=0.000),however,after the stimulation of PMA,the percentage of activated neutrophils of VLBWI [(96.58 ± 3.44) ％] was lower than that of term neonates [(99.20±0.62) ％] (Z--3.186,P=0.001),and the stimulation index (SI) of VLBWI (171.40 ± 103.35) was lower than that of term neonates (306.30 ± 138.47),with significant difference (Z=-3.413,P=0.001).The geometric mean of gp91Phox in VLBWI (21.66± 19.87) was higher compared with term neonates (19.60±8.03),however,the difference was not significant (P=0.350).The percentage of neutrophils that expressed gp91Phox [(56.11 ± 29.40) ％] was lower in VLBWI than that in term neonates [(80.14± 14.87) ％],with significant difference (Z=-2.374,P=0.018).Before the stimulation of PMA,the percentage of activated neutrophils of VLBWI with NRDS (63.40± 16.45) ％] was higher than that of VLBWI without NRDS [(34.80± 11.65) ％],with significant difference (Z=-3.382,P=0.001),the SI of VLBWI with NRDS (129.46 ± 75.36) was significantly lower than that of VLBWI without NRDS (213.35 ± 113.49) (Z=-2.331,P=0.020).Conclusions Neutrophils producing a respiratory burst in both VLBWI and term neonates are active without stimulation of PMA,while the phenomenon is more obvious in VLBWI.Neutrophils in VLBWI and term infants can be activated by the stimulation of PMA,and express gp91Phox.The activation and gp91Phox expression of neutrophils in VLBWI with NRDS tend to be lower than those in VLBWI without NRDS.

To establish single- and double-transfected transgenic cells stably expressing hMATE1, hMATE1 cDNA was cloned by RT-PCR from human cryopreserved kidney tissue, and subcloned into pcDNA3.1(+) plasmid by virtue of both HindIII and Kpn I restriction enzyme sites. Subsequently, the recombined pcDNA3.1(+)- hMATE1 plasmid was transfected into MDCK, MDCK-hOCT1 or MDCK-hOCT2 cells using Lipofectamine 2000 Reagent. After a 14-day-cultivation with hygromycin B at the concentration of 400 µg · mL(-1), all clones were screened with DAPI and MPP+ as substrates to identify the best candidate. The mRNA content of hMATE1, the cellular accumulation of metformin with or without cimetidine as inhibitor, or transportation of cimetidine was further valuated. The results showed that all of the three cell models over expressed hMATE1 mRNA. The cellular accumulation of metformin in MDCK-hMATE1 was 17.6 folds of the control cell, which was significantly inhibited by 100 µmol · L(-1) cimetidine. The transcellular transport parameter net efflux ratios of cimetidine across MDCK-hOCT1/hMATE1 and MDCK-hOCT2/hMATE1 monolayer were 17.5 and 3.65, respectively. In conclusion, cell models with good hMATE1 function have been established successfully, which can be applied to study the drug transport or drug-drug interaction involving hMATE1 alone or together with hOCT1/2 in vitro.

Objective To investigate whether tissue engineered bone with implanted vascular bun-dles can up-regulate release of vascular endothelial growth factor (VEGF) in models of femoral defect in rabbits.Methods Thirty-two rabbits were randomized into 2 even groups.In both groups, a segmental bone defect of 15 mm in length was made at the left femur before a tissue engineered bone was inserted into the defect.In the experimental group, a femoral vascular bundle was implanted into the tissue engineered bone.In the control group, there was no vascular implantation.At 2, 4, 8, and 12 weeks after implantation, samples were taken to determine new bone formation by histology and expression level of VEGF by immuno-histochemistry.Results The new bone formation was significantly higher in the experimental group at the end of 4, 8, and 12 weeks(P < 0.05) .The expression level of VEGF in the experimental group was also significantly higher than in the control group at all time points after operation, and the expression of VEGF peaked at 4 weeks.Conclusion Tissue engineered bone with vascular bundle implanted can up-regulate VEGF release in models of femoral defect in rabbits.

Objective To investigate the inhibitory effects of L. monocytogenes expressing melanomainhibiting activity(MIA)gene on malignant melanoma.Methods The plasmid pERL3-hly-MIA was constructed and used to transform live L.monocytogenes by electroporation.Atier culture.the transformed L.monocytogenes,namely LM-hly-MIA,was harvested for the detection of MIA protein by Westem Blot.A total of 24 mice were divided into three groups,namely control group,LM group and LM-hly-MIA group,to be immunized with physiological saline,L.monocytogenes and LM-hly-MIA,respectively.One day after the immunization.mice were subcutaneously inoculated with 0.1 mL of B16 cells at a concentration of 1×107/mL.One week later.reimmunization was performed.The size and weight of tumors were observed and measured in these mice.Results Enzyme digestion and Western blot confirmed the Successful construction of plasmid pERL3-hly-MIA.The average weight of tumors in mice was 4.33±0.91 gram.3.36 ±0.41 gram and 1.89±0.52 gram,respectively in the control group,LM group and LM-hly-MIA group,respectively(P＜0.05).with the inhibition rates of tumor growth being 22.4%and 61.5%in LM group and LM-hly-MIA group.respectively.Conclusion The attenuated strain of L.monocytogenes expressing MIA gene could evidently inhibit melanoma growth.