Objective The effectiveness of continuous veno-venous hemofiltration (CVVH) in clearing cytokines and reducing mortality in endotoxic shock is still controversial. The purpose of this study was to investigate the effects of CVVH on hemodynamies and plasma proinflammatory cytokines (TNF-?, IL-6, IL-10) during endotoxic shock in sheep. Methods Twelve male sheep weighing 14.5-20.5 kg were randomly divided into two groups of six animals :(A) control group and (B) CVVH group. Endotoxin (L-2880 sigma) 1 mg?kg-1 was infused intravenously(i.v. ) over 30 min and lactated Ringer's solution at 15 mlf44kg-1 f44h-1 for 6h in both groups. In CVVH group (B) CVVH was used for 5 h starting from 1h after the beginning of endotoxin infusion. The animals were anesthetized with midazolam and vecuronium. After tracheal intubation the animals were mechanically ventilated. Femoral artery was cannulated for continuous direct BP monitoring. 5F Swan-Ganz catheter was inserted into pulmonary artery via right internal jugular vein. Cardiac output ( CO), stroke volume ( SV), cardiac index (CI), MPAP, PAWP, SVRI, PVRI and LVSWI were measured, calculated and recorded before endotoxin infusion (T0 , baseline) and at 30, 60, 90, 120, 210 and 360 min (T6) after endotoxin infusion was started. Blood and ultrafiltrate samples were taken at T6 for determination of TNF-a,IL-6 and IL-10 concentrations. Results MAP and SVRI were significantly decreased while HR and SVRI were significantly increased after T, in both groups. MAP and SVRI were significantly higher at T6 in CVVH group than in control group ( P

BACKGROUND:Studies have found that a variety of biological materials can be used for preparing corneal stroma scaffolds that have good biocompatibility, but research on preparation and biocompatibility of the acel ular porcine corneal stroma scaffold is little. OBJECTIVE:To explore the preparation and biocompatibility of the acel ular porcine corneal stroma scaffold. METHODS:Acel ular porcine corneal stroma scaffold and its extract were prepared. Wel-grown human corneal stromal cel s were selected and cultured in the extract of acel ular porcine corneal stroma scaffold (experimental group) or in the complete medium (control group), respectively. After 1, 2 and 3 days of culture, the proliferation ability of human corneal stromal cel s was detected by MTT assay. In the meanwhile, human corneal cel s were directly seeded onto the acel ular porcine corneal stroma scaffold, and then the cel growth on the scaffold was detected using immunochemical method. RESULTS AND CONCLUSION:The number of human corneal stromal cel s was in a rise with time in the two groups, and absorbance values had no significant difference between two groups at different time points of culture. Human corneal stromal cel s grew wel on the scaffold, and were positive for cel integrinβ1, vimentin, aldehyde dehydrogenase 3A1, as wel as CD34, CDK2 and K-Ras. These results show that the acel ular porcine corneal stroma scaffold has no cytotoxicity, and has good biocompatibility.

Objective To study the expression of Ca-A/K channel-related molecules glutamate receptor 2 and 1(GluR2/1) in hippocampus tissues of neonatal rats with hypoxic-ischemic brain damage (HIBD). Methods A total of 60 7-day-old Sprague-Dawley rats were randomly divided into sham operation group and HIBD group. Hippocampal tissues were obtained at 0 h, 1 h, 6 h, 24 h, 48 h and 72 h after HIBD. The expression of GluR2, GluR1 and autophagy marker protein Beclin-1, LC3 were detected by Western blot assay. Results Edema and focal softening and necrosis were observed 6 h after HIBD in the brains of neonatal rats. Compared with Con group, at each time point, the expression levels of GluR2 were lower while the levels of GluR1, Beclin-1 and LC3 were higher significantly in HIBD group (P<0.05). The protein levels of LC3, Beclin-1, GluR1 and GluR2 in hippocampus tissues of HIBD group were significantly different among different time points after the estab-lishment of HIBD model (F=10.65~701.14, P<0.01). The protein level of GluR2 was decreased from 1 h to 24 h after HIBD and reached the lowest level at 24 h. The levels of GluR1, Beclin-1 and LC3 were increased at 6 h, plateaued at 24 h and remained there until 48 h. The levels of these proteins returned back to the initial level at 72 h. Conclusions Ca-A/K channel-related mol-ecules GluR2 and GluR1 play important roles in the autophagic cell death of hippocampus tissues in neonatal rats with hypoxic-ischemic brain damage.

Objective To evaluate effect of dexmedetomidine on mitochondrion-dependent apoptosis during hypoxia-reoxygenation (H/R) injury to hippocampal neurons of rats.Methods The primarily cultured hippocampal neurons of Sprague-Dawley rats were divided into 4 groups (n =40 each) using a random number table method:control group (C group),vehicle group (V group),H/R group and dexmedetomidine group (D group).Hippocampal neurons were subjected to oxygen-glucose deprivation followed by restoration of oxygen supply to establish the model of H/R injury.Dexmedetomidine 1 μmol/L was added at 6 h of reoxygenation in D group.The viability of neurons was measured by methyl thiazolyl tetrazolium assay at 20 h of reoxygenation.The ultrastructure of mitochondria was observed by transmission electron microscopy.The expression of cytochrome c (Cyt c),caspase-3,Fis1 and Drp1 was detected by Western blot.The neuronal apoptosis was detected by flow cytometry,and apoptosis rate was calculated.Results Compared with C group,no significant change was found in the viability of neurons in group V (P＞0.05),and the viability of neurons was significantly decreased,the apoptosis rate was increased,the expression of Cyt c,caspase-3,Fis1 and Drp1 was up-regulated (P＜0.05),and the damage to mitochondrial ultrastructure was accentuated in H/R and D groups.Compared with H/R group,the viability of neurons was significantly increased,the apoptosis rate was decreased,the expression of Cyt c,caspase-3,Fis1 and Drp1 was down-regulated (P＜0.05),and the damage to mitochondrial ultrastructure was significantly attenuated in D group.Conclusion The nechanism by which dexmedetomidine reduces the H/R injury to hippocampal neurons is related to inhibiting mitochondrion-dependent apoptosis in rats.

OBJECTIVE：To establish the rapid field identification method of Cryptotympana pustulata ecdysis. METHODS ： 3D depth of field synthesis technology was used to identify 50 batches of C. pustulata ecdysis and its adulterants from the length of beak ，size and protrusion degree of upper labial base ，the protrusion degree of the lower labial base ecdysis and the color of its upper transverse groove ，the number and shape of main and lateral spines on the foot ，significance of abdominal valves ，the number of webs ，the number and shape of side plates ，the number of tergum rings ，terminaliae，etc. RESULTS ：Among 50 batches of samples ，S1-S5，S26-S30，S36-S50 were C. pustulata ecdysis；S21-S25 was adulterants of C. pustulata ecdysis after weight gain ；S31-S35 was adulterants of C. pustulata ecdysis after extraction ；S6-S20 were ecdysis from Tibicen flammatus ，C. flammatta，Lyristes pekinensis ，all of which were adulterants. The main distinguishing feature of C. pustulata ecdysis and its adulterants was that abdomen and ventral surface of C. pustulata ecdysis were triangular ，and the abdomen and ventral surface of other species was nearly parallel ；the valve of C. flammatta ecdysis was obvious ，but those of other varieties were not obvious ；the lateral appearance of terminaliae of C. flammatta ecdysis was sharper than those of other species ；there was an acute angle between the front foot accessory thorns and the end thorns of the T. flammatus ecdysis，and an obtuse angle between the front foot accessory thorns and the end thorns of the L. pekinensis ecdysis. CONCLUSIONS ：The method is simple ，reliable and suitable for rapid field identification of C. pustulata ecdysis and its adulterants.

Objective:To study the predictive value of hour-specific total serum bilirubin(TSB) nomogram combined with clinical risk factors in the risk of hyperbilirubinemia.Method:Perinatal clinical data of newborns born in Shanghai Pudong New Area Health Care Hospital for Women and Children, Shanghai Pudong New Area People's Hospital and Shanghai Pudong Hospital from August 2017 to July 2018 were collected in this prospective study. Transcutaneous bilirubin (TcB) was monitored before discharge from hospital. Enrolled neonates were followed up for 28 days. The patients were assigned to neonatal hyperbilirubinemia group (NHB) and non-hyperbilirubinemia group (Non-HB) according to the occurrence of hyperbilirubinemia. The predictive value of models for the risk of hyperbilirubinemia was evaluated by receiver operating characteristic (ROC) curves and Logistic regression analysis.Result:A total of 8 664 newborns were included in this study, with 1 196 cases of hyperbilirubinemia, with an incidence of 13.8%. Logistic regression analysis showed that maternal blood type O, premature rupture of membranes, male gender, gestational age 35~37 weeks, subcutaneous ecchymosis/cranial edema, and breastfeeding were independent risk factors for NHB ( P<0.05). The area under receiver operative characteristic curve (ROC) of predischarge bilirubin risk zone only was 0.874(95% CI 0.861~0.885, P<0.05)and for all independent risk factors was 0.664 (95% CI 0.647~0.680, P<0.05). The area under ROC curve was 0.891 (95% CI 0.880~0.902, P<0.05) by combining predischarge bilirubin risk zone with clinical risk factors. Conclusion:Predischarge bilirubin risk zone combined with clinical risk factors can reasonably predict neonatal hyperbilirubinemia well.

Age-dependent loss of skeletal muscle mass and function is a feature of sarcopenia, and increases the risk of many aging-related metabolic diseases. Here, we report phenotypic and single-nucleus transcriptomic analyses of non-human primate skeletal muscle aging. A higher transcriptional fluctuation was observed in myonuclei relative to other interstitial cell types, indicating a higher susceptibility of skeletal muscle fiber to aging. We found a downregulation of FOXO3 in aged primate skeletal muscle, and identified FOXO3 as a hub transcription factor maintaining skeletal muscle homeostasis. Through the establishment of a complementary experimental pipeline based on a human pluripotent stem cell-derived myotube model, we revealed that silence of FOXO3 accelerates human myotube senescence, whereas genetic activation of endogenous FOXO3 alleviates human myotube aging. Altogether, based on a combination of monkey skeletal muscle and human myotube aging research models, we unraveled the pivotal role of the FOXO3 in safeguarding primate skeletal muscle from aging, providing a comprehensive resource for the development of clinical diagnosis and targeted therapeutic interventions against human skeletal muscle aging and the onset of sarcopenia along with aging-related disorders.
Animals ; Humans ; Sarcopenia/metabolism* ; Forkhead Box Protein O3/metabolism* ; Muscle, Skeletal/metabolism* ; Aging/metabolism* ; Primates/metabolism*