Long-Cheng Tang, Li Zhao and Li-Zhi Guan
Jin-qian Zhang, Li-cheng Zhang, Na Ren, Ming Zhang, Li-min Guo, Xing-wang Li and Jun Cheng
Objective Patients with H1N1 virus infection were hospitalized and quarantined, and some of them developed into acute respiratory failure, and were transfered to the medical intensive care unit of Beijing Ditan Hospital, Capital Medical University in Beijing, China.
Methods The clinical features and preliminary epidemiologic findings among 30 patients with confirmed H1N1 virus infection who developed into acute respiratory failure for ventilatory support were investigated.
Results A total of 30 patients (37.43 ± 18.80 years old) with 2009 influenza A (H1N1) related acute respiratory distress syndrome (ARDS) received treatment with mechanical ventilation, 15 cases of whom were male and 17 cases died of ARDS. Fatal cases were significantly associated with an APACHE Ⅱ score (P = 0.016), but not with PaO2/FIO2 (P = 0.912) and chest radiograph (P = 0.333). The most common complication was acute renal failure (n = 9). Five patients received extracorporeal membrane oxygenation (ECMO), 3 of whom died and the others survived. The major causes of death were multiple organ dysfunction syndrome (MODS) (39%), intractable respiratory failure (27%) and sepsis (20%).
Conclusions Most patients with respiratory failure due to influenza A (H1N1) virus infection were young, with a high mortality, particularly associated with APACHE ∥ score, secondary infection of lung or type 2 diabetes mellitus.
Jun Cheng, Min Quan, Min Li, Shun-ai Liu and Qi Wang
Hepatitis B virus (HBV) circulates in blood and replicates in the presence of quasispecies. During HBV replication, HBV DNA polymerase lacks fidelity and proofreading function partly because its exonuclease activity is either absent or deficient. Therefore, HBV genome is mutated with unusually high frequency. And these mutations can affect more than one open reading frame due to overlapping genes. Otherwise, natural substitutions, deletions or insertions involving the Cp/EN∥ locus in the X gene can significantly alter the extent of viral replication activity. Particular selection pressures such as host immune system and antiviral therapy readily select out escape mutants from this pre-existing quasispecies pool. Antiviral drug resistance in chronic hepatitis B (CHB) can be caused by the viral mutation frequency, the intrinsic mutability of the antiviral target site, the selective pressure exerted by the drug, the magnitude and rate of virus replication, the overall replication fitness of the mutant, the genetic barrier of the compound and the availability of replication space. Potent inhibition of HBV replication could be able to prevent the development of drug resistance because mutagenesis is replication dependent. Viral load may decline to a point where the continued production of quasispecies with the potential to resist new drug treatments no longer occurs, if viral replication can be suppressed for a sufficient length of time.
Jun Cheng, Min Li, Ping Gao, Jin-ling Dong and Qi Wang
Liver steatosis is a pathological hallmark in patients with chronic hepatitis C (CHC). Increased lipid uptake, decreased lipid secretion, increased lipid synthesis and decreased lipid degradation are all involved in pathogenesis of steatosis induced by hepatitic C virus (HCV) infection. Level of low density lipoprotein receptor (LDL-R) and activity of peroxisome proliferator-activated receptor (PPAR) α is related to liver uptake of lipid from circulation, and affected by HCV. Secretion via microsomal triglyceride transfer protein (MTTP), and formation of very low density lipoprotein (VLDL) have been hampered by HCV infection. Up-regulation of lipid synthesis related genes, such as sterol regulatory element-binding protein (SREBP)-1, SREBP-2, SREBP-1c, fatty acid synthase (FASN), HMG CoA reductase (HMGCR), liver X receptor (LXR), acetyl-CoA carboxylase 1 (ACC1), hepatic CB (1) receptors, retinoid X receptor (RXR) α, were the main stay of liver steatosis pathogenesis. Degradation of lipid in liver is decreased in patients with CHC. There is strong evidence that heterogeneity of HCV core genes of different genotypes affect their effects of liver steatosis induction. A mechanism in which steatosis is involved in HCV life cycle is emerging.
Jun Cheng, Min Quan, Min Li, Shun-ai Liu and Qi Wang
Covalently closed circular (ccc) DNA of hepatitis B virus (HBV) existed in the nuclei of HBV infected hepatocytes with a half-life time of 14.3 years in a mathematic model. Viral protein feedback regulation in HBV life cycle to maintain vital viral replication is an important mechanism. Interleukin-6, epithelial growth factor, heme oxygenase-1, histones, and hepatocyte nuclear factors are demonstrated as the key regulators for HBV life cycle. CpG island structure and methylation status are involved in the regulation of HBV DNA replication. Nucleos(t)ide analogues are widely used in the clinical practice for the treatment of chronic hepatitis B patients, although no evidence indicating a direct inhibiton of HBV cccDNA. In the future, along with the study of HBV life cycle, new drugs including RNA interference technique, will pave the way to eliminate the HBV cccDNA from infected hepatocytes resulting final cure of chronic hepatitis B.
E Cheng-Guo, Quan-Lin Li and Shiyong Li
Service systems and their cooperation are one of the most important and hot topics in management and information sciences. To design a reasonable allocation mechanism of service systems is the key issue in the cooperation of service systems. In this paper, we systematically introduce the interval Shapley value as cost allocation of cooperative interval games 〈N, V〉 arising from cooperation in a multi-server service system, and provide an explicit expression for the interval Shapley value of cooperative interval games 〈N, V〉. We construct an interval game 〈N, W〉 of a service system which shares the same value for the grand coalition with the original interval game, by using the characteristic function which is dominated by the function of the original interval game. Finally, we prove that the interval game 〈N, W〉 is concave, which means that the interval Shapley value of the interval game 〈N, W〉 is in the interval core of this interval game, and illustrate this conclusion by using numerical examples.
Xiao-ming Li, Jia-yue Yin, He-zuo Qu, Cheng-qiong Bi, Hao-jun Xu and Li Zhu
Hongli Li, Xiaohuai Chen, Yinbao Cheng, Houde Liu, Hanbin Wang, Zhenying Cheng and Hongtao Wang
Due to the variety of measurement tasks and the complexity of the errors of coordinate measuring machine (CMM), it is very difficult to reasonably evaluate the uncertainty of the measurement results of CMM. It has limited the application of CMM. Task oriented uncertainty evaluation has become a difficult problem to be solved. Taking dimension measurement as an example, this paper puts forward a practical method of uncertainty modeling and evaluation of CMM task oriented measurement (called SVCMM method). This method makes full use of the CMM acceptance or reinspection report and the Monte Carlo computer simulation method (MCM). The evaluation example is presented, and the results are evaluated by the traditional method given in GUM and the proposed method, respectively. The SVCMM method is verified to be feasible and practical. It can help CMM users to conveniently complete the measurement uncertainty evaluation through a single measurement cycle.
Tie-long Zheng, Ping-an Wang, Dian-li Wang, Cheng-fu Sun, Yuan Hong, Qi Wang and Jun Cheng
Objective To observe the biological function of human 3-hydroxyisobutyrate dehydrogenase (HIBADH).
Methods Human 3-hydroxyisobutyrate dehydrogenase (HIBADH, 3-hydroxy-2-methyl propanoate: NAD+ oxidoreductase) recombinant protein was expressed in E. coli BL21, and purified by Ni+ column. The special antisera was obtained from rabbits immunized by this purified antigen. On the distribution of HIBADH, it was found that HIBADH over-expressed in the injured liver cells when serious hepatitis occurred. The phenomenon was confirmed in the animal models of SD rats with acute liver cell injury induced by CCl4, but this phenomenon did not exist in the models induced by endotoxin combined with galactosamine. Further more, HIBADH’s overexpression in liver cells will induce cell necrosis through the pathway of oxidative stress.
Results When the liver cells injured by drug or other chemical materials, HIBADH will be compensationally over-expressed for the deficiency of energy, so liver cells can make enough ATP through brand-chain amino acid catabolism. However, the overexpression of HIBADH will be harmful for liver cells through the product of much more active oxygens which will induce the cell necrosis.
Conclusions HIBADH over-expression is a signal of the liver cell metabolism injury, and it can aggravate the liver cell injury through oxidative stress.
Wang Hong, Qi-Sheng Liang, Lan-Ren Cheng, Xiao-Hong Li, Fu Wei, Wen-Tao Dai and Shi-Tong Li
Background: Rocuronium is an alternative to succinylcholine for rapid tracheal intubation after major thermal injury and other forms of critical illness that cause denervation changes in skeletal muscle. Rocuronium may decrease the potencies of non-depolarizing muscle relaxants.
Objectives: Examine whether potency of rocuronium changed during the first month after denervation, and investigate the effects of skeletal muscle denervation on potency of rocuronium.
Methods: The denervation mouse model was developed to create denervated individual cells from the flexor digitorum brevis of the hindfoot. The skeletal muscle cells were examined at day 0 in the innervated control and days 1, 4, 7, 14, 21, and 28 in the denervation group. Nicotinic acetylcholine receptors in the cells were activated with 30 M acetylcholine, alone or in combination with various concentrations of rocuronium. Currents were recorded with a whole-cell patch-clamp technique.
Results: Rocuronium reversibly inhibited acetylcholine-activated currents in a dose-dependent fashion at different times after denervation. The inhibition concentration for the half-maximal responses of rocuronium increased 1.2- (p >0.05), 1.8-, 2.8-, 2.3-, 2.1-, and 1.9-fold (p <0.01) at day 1, 4, 7, 14, 21, and 28 after denervation, respectively, compared to that at day 0 after denervation.
Conclusion: Rocuronium dose required to achieve satisfactory clinical effects changed at different durations after skeletal muscle denervation.