China is facing the double burden of high incidence of lung cancer and tuberculosis epidemic. Lung cancer combined with tuberculosis has a high incidence and complexity in clinical practice. High-risk groups include immunocompromised people, long-term smokers and people with a history of tuberculosis. The coexistence of the two diseases not only increases the difficulty of diagnosis and treatment decision-making, but also increases the risk of treatment-related adverse reactions and drug interactions. The guideline was developed by Committee of Integrated Rehabilitation for Lung Cancer, Chinese Anti-Cancer Association; Chinese and Western Integrated Lung Cancer Committee of Chinese Anti-Cancer Association; Society of Tuberculosis, Chinese Medical Association, aiming to standardize the diagnosis and treatment of lung cancer complicated with pulmonary tuberculosis. The guideline emphasizes the core position of combined diagnosis of multimodal imaging, etiology and pathology. It is proposed that anti-tuberculosis and anti-tumor treatment should be coordinated under the framework of multidisciplinary team, and drug interactions and timing optimization should be paid attention to. For surgical treatment, minimally invasive resection combined with systematic lymph node dissection is recommended after infection control. Systemic therapy requires individualized risk stratification and dynamic monitoring of efficacy and adverse reactions. Based on evidence-based medicine and Chinese clinical practice, combined with the accessibility of drugs and technologies, this guideline proposes a whole-process management pathway covering screening, diagnosis, treatment and follow-up, in order to improve the prognosis and quality of life of patients.

Objective:To screen key differentially expressed genes(DEGs)in dead mice with sepsis by spleen high-through-put sequencing combined with bioinformatics.Methods:①A mouse sepsis model was set up by intraperitoneal injection of lipopolysac-charide(LPS),a 7-day survival curve of mice was drawn,and the modeling doses of survival group and death group were screened out.②Expressions of TNF-α,IL-1β,IL-6 and IL-10 in peripheral blood of mice in control group,survival group and death group were verified by ELISA.③High-throughput sequencing was conducted on spleens of survival group and death group,and the key genes were screened by bioinformatics analysis of DEGs.④Expressions of key genes and proteins were detected by RT-PCR and Western blot.Results:①LPS dosage in survival group was 15 mg/kg(with a mortality of 30%),and LPS dosage in death group was 30 mg/kg(with a mortality of 80%).②Expression levels of IL-6,TNF-α and IL-1β in sepsis mice were significantly higher than those of control group,while expression level of IL-10 was decreased(P<0.05).Comparison of sepsis model groups showed that levels of pro-inflammatory factors in death group were higher than those in survival group,while level of IL-10 was lower than that in survival group(P<0.05).③A total of 2999 DEGs in survival group and death group were screened out by bioinformatics,among which 1185 genes were up-regulated and 1814 genes were down-regulated.Top 5 DEGs enrichment pathways were screened out:"hematopoietic cell lineage""primary immunodeficiency""African trypanosomiasis""leishmaniasis"and"B-cell receptor signaling pathway".Ifit1,Ifit3 and Mx1 were three key genes that were screened out.④Compared with survival group,expressions of genes and proteins of Ifit1,Ifit3 and Mx1 were down-regulated in spleen tissues of the death group(P<0.05).Conclusion:By high-throughput sequencing and bioinformatics,Ifit1,Ifit3 and Mx1 are screened out as key genes related to the death outcome of sepsis,which probably influence the outcome of sepsis through the immune mechanism related to virus infection.

Transtibial tunnel reconstruction is one of the classical surgical techniques for posterior cruciate ligament (PCL) reconstruction. However, this surgical technique inevitably produces the "killer turn" effect. Specifically, during the transtibial tunnel reconstruction, there is a sharp tunnel edge at the exit of the tibial tunnel, and the graft has a large stress at this edge, which leads to the failure of transplantation due to the repeated friction between the graft and the tunnel edge. The "killer turn" effect may lead to the "residual laxity", thus resulting in postoperative knee instability, affecting the long-term efficacy of reconstructive surgery and reducing the postoperative satisfaction of patients. In recent years, many scholars have proposed a series of improved techniques for PCL reconstruction in dealing with the "killer turn" effect, including tibial inlay technique and improved transtibial tunnel technique. The authors review the formation mechanism of "killer turn" effect and methods to eliminate or reduce the effect, in order to provide a reference for improving the effect in PCL reconstruction.

Objective::This study aimed at investigating the expression of nuclear factor kappa B (NF-κB) and mammalian target of rapamycin (mTOR) related signal pathways in liver tissues of intrahepatic cholestasis of pregnancy animal models.Methods::Estrogen (EE)-induced cholestasis and a placental ischemia-reperfusion (IR) model were established in pregnant rats. All pregnant rats were divided into four groups by random number table: EE-IR group ( n= 6), EE-sham group ( n = 6), control-IR group ( n= 6) and control-sham group ( n= 6). Liver expression of mTOR, its upstream regulator DNA damage response-1 (REDD1), and downstream factor glucose transporter type-1 (GLUT1), accompanied by NF-κB (p65 is the most important component), its activator toll-like receptor 4 (TLR4), and inhibitor IκBα, were detected by western blot analysis and real-time polymerase chain reaction. The intergroup comparisons were performed with a one-way analysis of variance, the comparisons among groups were analyzed with the nonparametric Kruskal-Wallis test. Results::Giving pregnant rats EE alone reduced the hepatic expression of IκBα (0.72 ± 0.20 vs. 1.01 ± 0.07, P= 0.008). Meanwhile, giving pregnant rats placental IR alone increased liver levels of REDD1 (3.24 ± 0.98 vs. 1.06 ± 0.24, P= 0.025), GLUT1 (2.37 ± 0.82 vs. 1.09 ± 0.10, P= 0.039), TLR4 (2.12 ± 0.29 vs. 1.20 ± 0.28, P= 0.010), and p65 (2.09 ± 0.85 vs. 1.04 ± 0.06, P= 0.023), and decreased hepatic mTOR (0.50 ± 0.07 vs. 1.01 ± 0.03, P= 0.001) and IκBα (0.61 ± 0.08 vs. 1.01 ± 0.07, P= 0.014) expression. Subjecting EE-treated rats to placental IR did not further alter liver levels of GLUT1 (2.02 ± 0.45 vs. 1.79 ± 0.39, P= 0.240), TLR4 (2.10 ± 0.74 vs. 1.60 ± 0.36, P= 0.129), or p65 (2.41 ± 0.83 vs. 1.65 ± 0.46, P= 0.145), whereas it did decrease hepatic mTOR (0.42 ± 0.09 vs. 0.90 ± 0.14, P= 0.008) and IκBα (0.43 ± 0.09 vs. 0.72 ± 0.20, P= 0.004) expression and enhance REDD1 expression (4.46 ± 0.65 vs. 2.05 ± 0.47, P= 0.009). Placental IR stress did impact the hepatic expression of REDD1-mTOR-GLUT1 and TLR4/NF-κB/IκBα in pregnant rats. Conclusion::Placental IR-induced hepatic GLUT1, TLR4, and p65 alternation, which responded efficiently in control rats, were impaired in EE-induced ICP rats.

Objective::This study aimed at investigating the expression of nuclear factor kappa B (NF-κB) and mammalian target of rapamycin (mTOR) related signal pathways in liver tissues of intrahepatic cholestasis of pregnancy animal models.Methods::Estrogen (EE)-induced cholestasis and a placental ischemia-reperfusion (IR) model were established in pregnant rats. All pregnant rats were divided into four groups by random number table: EE-IR group ( n= 6), EE-sham group ( n = 6), control-IR group ( n= 6) and control-sham group ( n= 6). Liver expression of mTOR, its upstream regulator DNA damage response-1 (REDD1), and downstream factor glucose transporter type-1 (GLUT1), accompanied by NF-κB (p65 is the most important component), its activator toll-like receptor 4 (TLR4), and inhibitor IκBα, were detected by western blot analysis and real-time polymerase chain reaction. The intergroup comparisons were performed with a one-way analysis of variance, the comparisons among groups were analyzed with the nonparametric Kruskal-Wallis test. Results::Giving pregnant rats EE alone reduced the hepatic expression of IκBα (0.72 ± 0.20 vs. 1.01 ± 0.07, P= 0.008). Meanwhile, giving pregnant rats placental IR alone increased liver levels of REDD1 (3.24 ± 0.98 vs. 1.06 ± 0.24, P= 0.025), GLUT1 (2.37 ± 0.82 vs. 1.09 ± 0.10, P= 0.039), TLR4 (2.12 ± 0.29 vs. 1.20 ± 0.28, P= 0.010), and p65 (2.09 ± 0.85 vs. 1.04 ± 0.06, P= 0.023), and decreased hepatic mTOR (0.50 ± 0.07 vs. 1.01 ± 0.03, P= 0.001) and IκBα (0.61 ± 0.08 vs. 1.01 ± 0.07, P= 0.014) expression. Subjecting EE-treated rats to placental IR did not further alter liver levels of GLUT1 (2.02 ± 0.45 vs. 1.79 ± 0.39, P= 0.240), TLR4 (2.10 ± 0.74 vs. 1.60 ± 0.36, P= 0.129), or p65 (2.41 ± 0.83 vs. 1.65 ± 0.46, P= 0.145), whereas it did decrease hepatic mTOR (0.42 ± 0.09 vs. 0.90 ± 0.14, P= 0.008) and IκBα (0.43 ± 0.09 vs. 0.72 ± 0.20, P= 0.004) expression and enhance REDD1 expression (4.46 ± 0.65 vs. 2.05 ± 0.47, P= 0.009). Placental IR stress did impact the hepatic expression of REDD1-mTOR-GLUT1 and TLR4/NF-κB/IκBα in pregnant rats. Conclusion::Placental IR-induced hepatic GLUT1, TLR4, and p65 alternation, which responded efficiently in control rats, were impaired in EE-induced ICP rats.

Non-small cell lung cancer (NSCLC) is the most common pathological type of lung cancer. The systemic antitumor therapy of advanced NSCLC has undergone renovations of chemotherapy, targeted therapy and immunotherapy, which results in greatly improved survival for patients with advanced NSCLC. Immune checkpoint inhibitors (ICIs), especially targeting programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1), has changed the treatment paradigm of NSCLC. ICIs have become the standard treatment for advanced NSCLC without epidermal growth factor receptor(EGFR) mutation or anaplastic lymphomakinase(ALK) translocation in the first- or second-line setting, and for locally advanced NSCLC following concurrent radiotherapy and chemotherapy. ICIs are also promising in adjuvant/neoadjuvant therapy. More and more ICIs have been approved domestically for the treatment of NSCLC. Led by the NSCLC expert committee of Chinese Society of Clinical Oncology (CSCO), this consensus was developed and updated based on thoroughly reviewing domestic and foreign literatures, clinical trial data, systematic reviews, experts' discussion and the consensus(2019 version). This consensus will aid domestic clinicians in the treatment of NSCLC with ICIs.
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Non-small cell lung cancer (NSCLC) is the most common pathological type of lung cancer, most NSCLC patients are at advanced stage at the time of diagnosis. For patients without sensitive driven-oncogene mutations, chemotherapy is still the main treatment at present, the overall prognosis is poor. Improving outcomes and obtaining long-term survival are the most urgent needs of patients with advanced NSCLC. In recent years, immunotherapy has developed rapidly. Immune checkpoint inhibitors (ICIs), especially targeting programmed death-1 (PD-1)/programmed death-ligand 1 (PD-L1), have made a breakthrough in the treatment of NSCLC, beneficial to patients' survival and changed the treatment pattern for NSCLC. It shows more and more important role in the treatment of NSCLC. Led by NSCLC expert committee of Chinese society of clinical oncology (CSCO), relevant experts in this field were organized. On the basis of referring to domestic and foreign literature, systematically evaluating the results of Chinese and foreign clinical trials, and combining the experiences of the experts, the experts group reached an agreement to develop this consensus. It will guide domestic counterparts for better application of ICIs to treat NSCLC.

Objective:Mesenchymal stem cells( MSCs) have self-renewal capacity and potential to differentiate into the cells.It was reported that the expression of miR-30a changed in some immune diseases.But it remains unclear the effect of miR-30a on the im-munoregulatory functions of MSCs.Here we studied the impact of miR-30a on the phenotype,cell viability,apoptosis,cell cycle and im-munoregulatory functions of MSCs.Methods: The mixed enzyme methods were used for the isolation of human umbilical cord MSCs.Flow cytometry(FCM)was used to investigate the effect of overexpressed miR-30a on the phenotype of MSCs.CCK-8 was used to examine the cell viability of miR-30a-overexpressed MSCs.Annexin V/PI was used for the detection of apoptosis of MSCs.Q-PCR and Western blot were used to investigate the effect of miR-30a on the expression of Cyclin E2( CCNE2).CCNE2 was one putative target of miR-30a predicted by Targetscan database.The effects of miR-30a-overexpressed MSCs on the maturation of dendritic cells(DCs)were determined.Results:Overexpression of miR-30a blocked the cell cycle of MSCs in the G0/G1 phase by inhibiting the expression of CCNE2,but did not affect the phenotype, cell viability and apoptosis of MSCs.When co-cultured with DCs, although MSCs down-regulated the expression of CD40 and CD86 on DCs,overexpression of miR-30a more significantly enhanced the suppressive impact of MSCs on the maturation of DCs.Conclusion: miR-30a affects the cell cycle of MSCs and enhances its immunosuppressive effect on DCs.

Objective To explore the clinical efficacy and safety of umbilical cord derived mesenchymal stem cells transplantation(UC-MSCT)for patients with refractory systemic lupus erythematosus (SLE).Methods Twelve patients with refractory SLE were enrolled in this study.UC-MSCs(≥106/kg cell number)were infused intravenously for each patient. The clinical manifestations and laboratory parameters were compared before and after MSCT. Results The twelve patients were followed up for one to twenty-six months after MSCT.The systemic lupus erythematosus disease activity index(SLEDAI)score decreased from 18±4 to 10±4 one month after MSCT(n=12,P＜0.01)and then decreased to 7±4 at three month follow-up.Nine patients showed improvement of 24 h proteinuria[(2103±749)mg vs(3359±1248)mg,P＜0.01]one month after MSCT.Further improvement of 24 h proteinuria was observed in eight patients[(1427±616)mg vs(3342±1333)mg,P＜0.01]at three months post MSCT.Serum creatinine of five patients decreased significantly and ten patients showed an increase of serum albumin. Serum complement C3 increased in three patients and four patients showed obvious amelioration of hematological abnormalities. There was no transplantation related complications for all the patients. Conclusion UC-MSCT is effective and safe for refractory SLE,but further observation is required to evaluate its long term efficacy.

It is the intent of this study to estimate the progression or regression of edema at the bedside continuously. Based on the theoretic model, the Adaptive Genetic Algorithm (AGA) has been applied in the calculation of conductivity reconstruction. Dynamic crossover and mutation operators which are based on Haiming Distance are brought forward in this paper to maintain generation's diversity. Then, both AGA and Standard GA (SGA) have been applied in the conductivity reconstruction of edema in human brain. It is shown that AGA not only has attained a higher degree of efficiency but also has enhanced the capability to converge to the best answer.
Algorithms ; Brain Injuries ; complications ; pathology ; Computer Simulation ; Edema ; pathology ; Electric Impedance ; Humans ; Models, Biological