Clinical characteristics of remote Zeus robot-assisted laparoscopic cholecystectomy:A report of 40 cases

瞄准：总结表现必需品并且分析遥远的宙斯帮助机器人的 laparoscopic 胆囊炎的特征。方法：帮助机器人的 laparoscopic 胆囊炎在在 2004 年 5 月和 2005 年 7 月之间的 40 个病人被执行。操作过程和许多临床的参数被记录并且分析。结果：四十个 laparoscopic 胆囊炎过程成功地与宙斯机器的系统被完成。并且没有手术后的复杂并发症。全部的操作时间，系统安装时间和表现时间是 100.3 +/- 18.5 min， 27.7 +/- 8.8 min 和 65.6 +/- 18.3 min 分别地。失血和手术后的医院停留是 30.6 +/- 10.2 mL 和 2.8 +/- 0.8 d 分别地。为起作用的地调整使用的照相机空地时间和时间是 1.1+/- 1.0 min 和 2.0 +/- 0.8 min 分别地。起作用的错误是 7.5% 。结论：跟随 laparoscopic 操作的原则的帮助机器人的 laparoscopic 胆囊炎有特定的表现必需品。它保存最低限度地侵略的外科的好处并且提供控制操作地的提高的能力，精确、稳定的起作用的操作。

Diagnosis and Treatment of Cholangiocarcinoma: A Consensus from Surgical Specialists of China

Cholangiocarcinoma refers to malignant tumors that develop in epithelial lining of biliary system, and it is divided into two categories according to tumor location, intrahepatic cholangiocarcinoma （ICC） and extrahepatic cholangiocarcinoma （ECC）. ICC occurs from the epithelial cells of the intrahepatic bile duct, its branches and interlobular biliary tree; and ECC is divided into hilar cholangiocarcinoma and distal cholangiocarcinoma by the circumscription at the confluence of cystic duct and the common hepatic duct.

Factors influencing a low rate of hepatitis C viral RNA clearance in heroin users from Southern China

AIM: To study the virological and host factors influencing hepatitis C infection outcomes in heroin users in southern China. METHODS: HCV RNA and associated factors were analyzed among 347 heroin users from Guangxi Zhuang Autonomous Region, southern China who were hepatitis C virus (HCV) EIA positive for two or more consecutive visits. RESULTS: Using the COBAS AMPLICOR HCV TEST, a remarkably low HCV RNA negative rate of 8.6% was detected. After multivariate logistic regression analysis, HCV RNA clearance was significantly associated with the presence of HBsAg (OR = 8.436, P < 0.0001), the lack of HIV-1 infection (OR = 0.256, P = 0.038) and age younger than 25 (OR = 0.400, P = 0.029). CONCLUSION: Our study suggests HCV infection among Chinese heroin users results in high levels of viral persistence even amidst factors previously found to enhance viral clearance. Prospective studies of a possible genetic component within the Chinese population and the pathogenicity of non-genotype 1 HCV infections are needed.

TRAF3 activates STING-mediated suppression of EV-A71 and target of viral evasion

Innate immunity represents one of the main host responses to viral infection.1,2,3 STING(Stimulator of interferon genes),a crucial immune adapter functioning in host cells,mediates cGAS(Cyclic GMP-AMP Synthase)sensing of exogenous and endogenous DNA fragments and generates innate immune responses.4 Whether STING activation was involved in infection and replication of enterovirus remains largely unknown.In the present study,we discovered that human enterovirus A71(EV-A71)infection triggered STING activation in a cGAS dependent manner.EV-A71 infection caused mitochondrial damage and the discharge of mitochondrial DNA into the cytosol of infected cells.However,during EV-A71 infection,cGAS-STING activation was attenuated.EV-A71 ^(pro)teins were screened and the viral ^(pro)tease 2A^(pro) had the greatest capacity to inhibit cGAS-STING activation.We identified TRAF3 as an important factor during STING activation and as a target of 2A^(pro).Supplement of TRAF3 rescued cGAS-STING activation suppression by 2A^(pro).TRAF3 supported STING activation mediated TBK1 phosphorylation.Moreover,we found that 2A^(pro) ^(pro)tease activity was essential for inhibiting STING activation.Furthermore,EV-D68 and CV-A16 infection also triggered STING activation.The viral ^(pro)tease 2A^(pro) from EV-D68 and CV-A16 also had the ability to inhibit STING activation.As STING activation prior to EV-A71 infection generated cellular resistance to EV-A71 replication,blocking EV-A71-mediated STING suppression represents a new anti-viral target.

The SARS-CoV-2 main protease induces neurotoxic TDP-43 cleavage and aggregates

Dear Editor,Neurologic manifestations associated with many COVID-19 patients,including acute infection with severe acute respiratory syndrome coronavirus-2(SARS-CoV-2)and long COVID,have been proven by increasing evidence.1 To date,most studies have focused on how SARS-CoV-2 invades the nervous system and the consequent neuropathological changes.2,3 In contrast,the specific mechanism by which SARS-CoV-2 infection leads to neurological disease remains unclear.

Unique and complementary suppression of cGAS-STING and RNA sensing- triggered innate immune responses by SARS-CoV-2 proteins

The emergence of SARS-CoV-2 has resulted in the COVID-19 pandemic,leading to millions of infections and hundreds of thousands of human deaths.The efficient replication and population spread of SARS-CoV-2 indicates an effective evasion of human innate immune responses,although the viral proteins responsible for this immune evasion are not clear.In this study,we identified SARS-CoV-2 structural proteins,accessory proteins,and the main viral protease as potent inhibitors of host innate immune responses of distinct pathways.In particular,the main viral protease was a potent inhibitor of both the RLR and cGAS-STING pathways.Viral accessory protein 0RF3a had the unique ability to inhibit STING,but not the RLR response.On the other hand,structural protein N was a unique RLR inhibitor.0RF3a bound STING in a unique fashion and blocked the nuclear accumulation of p65 to inhibit nuclear factor-KB signaling.3CL of SARS-CoV-2 inhibited K63-ubiquitin modification of STING to disrupt the assembly of the STING functional complex and downstream signaling.Diverse vertebrate STINGs,including those from humans,mice,and chickens,could be inhibited by 0RF3a and 3CL of SARS-CoV-2.The existence of more effective innate immune suppressors in pathogenic coronaviruses may allow them to replicate more efficiently in vivo.Since evasion of host innate immune responses is essential for the survival of all viruses,our study provides insights into the design of therapeutic agents against SARS-CoV-2.

Anisotropic nanowire growth via a self-confined amorphous template process： A reconsideration on the role of amorphous calcium carbonate

Calcium carbonate crystals with various morphologies have been found in a variety of biospecimens and artificially synthesized structures. Usually, the diversity in morphology can be attributed to different types of interactions between the specific crystal faces and the environment or the templates used for the growth of CaCO3 crystals. On the other hand, isotropic amorphous calcium carbonate （ACC） has been recognized as the precursor of other crystalline calcium carbonate forms for both in vivo and in vitro systems. However, here we propose a self-confined amorphous template process leading to the anisotropic growth of single-crystalline calcite nanowires. Initiated by the assembly of precipitated nanoparticles, the calcite nanowires grew via the continuous precipitation of partly crystallized ACC nanodroplets onto their tips. Then, the crystalline domains in the tip, which were generated from the partly crystallized nanodroplets, coalesced in the interior of the nanowire to form a single-crystalline core. The ACC domains were left outside and spontaneously formed a protective shell to retard the precipitation of CaCO3 onto the side surface of the nanowire and thus guided the highly anisotropic growth of nanowires as a template.