Objective To compare the postoperative cognition function after propofol intravenous versus isoflurane inhalation anesthesia in off-pump coronary artery bypass grafting (CABG) patients. Methods 30 ASA Ⅱ - Ⅲ patients undergoing off-pump CABG were randomly assigned to two groups. Following induction of anesthesia,isoflurane inhalation( group A ) or propofol intravenous (group B ) were adjusted to maintain comparable depth of anesthesia state. The mini-mental state examination (MMSE) was used to assess the cognitive function 1 day before and 4 days after the operation. Results There were 5 patients suffered postoperative cognitive dysfunction in group A, and 3 cases in group B . But compared with the preoperative( group A (29.13 ± 0. 83 ), group B (29.13 ±1. 13 ) ) ,the MMSE score at 4 days in group A ( 28.73 ± 1.03 ) were lower( t = 2.45, P ＜ 0.05 ), there was no difference in group B( 28.93 ± 1.16)at 4 days( t = 1.87, P ＞ 0. 05 ). Conclusion Both propofol intravenous anesthesia and isoflurane inhalation anesthesia in off-pump CABG may contribute to postoperative cognitive dysfunction, propofol intravenous anesthesia is advantageous over isoflurane inhalation anesthesia.

OBJECTIVE To investigate the antidepressant effect of triptolide in chronically unpredictable stressed mice and its possible protective effect on brain derived neurotrophic factor(BDNF). METHODS One method was selected from 8 different stress methods each day,and the mice were treated with triptolide(20,40,80 and 160μg·kg-1)10 min before the stress method. A chroni?cally unpredictable stressed model was established and after 14 d stress experiment, the total distance in the locomotor activity and the immobility time in the force swimming test and tail test were observed respectively. Triptolide(20,40,80 and 160μg·kg-1)was given 10 min before the test. In addition, Western blot was used to analyze the expression of phosphorylated cAMP response element binding protein(p-CREB) and BDNF in the hippocampus and frontal cortex. RESULTS There was no effect on the locomotor activity in any group. Compared with the normal control group,the chronically unpre?dictable stressed group showed obvious depressive-like behavior,while the immobility time in the force swimming test decreased from(161 ± 18)s in chronically stressed group to(102 ± 14)s(P<0.05) and(83±14)s(P<0.01)when mice were ip given triptolide 80 and 160μg·kg-1, respectively,and(77± 11)s(P<0.01)in imipramine(IMI)hydrochloride group(10 mg?kg-1),and(96±9)s(P<0.01)in fluox?etine(FLU)group(10 mg?kg-1). The immobility time in the tail suspension test decreased from(128± 8)s in chronically stressed group to(93±9)s(P<0.05),(85±8)s(P<0.01)and(77±11)s(P<0.01)when mice were ip given triptolide 40,80 and 160μg · kg-1 respectively,and(64 ± 9)s(P<0.01)in IMI hydro?chloride 10 mg?kg-1 group,and(72±6)s(P<0.01)in FLU group(10 mg?kg-1). Moreover,the expression of p-CREB in the hippocampus and frontal cortex significantly increased in triptolide 80 and 160μg·kg-1 groups(P<0.05),so did the expression of BDNF in the hippocampus and frontal cortex in triptolide 80 and 160μg·kg-1 groups(P<0.05). CONCLUSION Triptolide can ameliorate the depressive-like behavior in chronically unpredictable stressed mice,which may be related to the cAMP-CREB-BDNF signal transduction cascades.

In this article, methods of measuring and evaluating treatment adherence, based on whether they are objective and subjective, are reviewed upon literature examination, and the advantages and disadvantages of each method for different population segments are also discussed.It is intended to provide medical professionals and researchers with a general framework about adherence assessment methods.During treatment and research, medical professionals and researchers should select the most appropriate methods for their purposes and provide effective and personalized evaluation methods to ultimately evaluate and improve patients' medication adherence.

Tumor-associated macrophages(TAMs)are the predominant cell group in the tumor microenvironment(TME)and are the most important regulatory cells of immune system suppression and tumor cell proliferation in TIME.Src homology-2 domain-containing protein tyrosine phosphatase 2(SHP-2)is a non-receptor protein tyrosine phosphatase that plays an important role in the transmission of signals from the cell surface to the nucleus.SHP-2 is a key intracellular regulatory factor mediating cell proliferation and differentiation and is involved in a variety of growth factor and cytokine signaling pathways linking the cell surface to the nucleus.Recent studies have shown that SHP-2 is a key enzyme in determining the function of TAMs,but because of its variable function,it plays different or even opposite roles in different solid TMEs.This paper reviews the function of SHP-2 in TAMs and related solid tumors to provide a comprehensive reference for tumor immunity and targeted therapy research.

With the improved understanding of driver mutations in non-small cell lung cancer (NSCLC), expanding the targeted therapeutic options improved the survival and safety. However, responses to these agents are commonly temporary and incomplete. Moreover, even patients with the same oncogenic driver gene can respond diversely to the same agent. Furthermore, the therapeutic role of immune-checkpoint inhibitors (ICIs) in oncogene-driven NSCLC remains unclear. Therefore, this review aimed to classify the management of NSCLC with driver mutations based on the gene subtype, concomitant mutation, and dynamic alternation. Then, we provide an overview of the resistant mechanism of target therapy occurring in targeted alternations ("target-dependent resistance") and in the parallel and downstream pathways ("target-independent resistance"). Thirdly, we discuss the effectiveness of ICIs for NSCLC with driver mutations and the combined therapeutic approaches that might reverse the immunosuppressive tumor immune microenvironment. Finally, we listed the emerging treatment strategies for the new oncogenic alternations, and proposed the perspective of NSCLC with driver mutations. This review will guide clinicians to design tailored treatments for NSCLC with driver mutations.
Humans ; Carcinoma, Non-Small-Cell Lung/genetics* ; Lung Neoplasms/genetics* ; Mutation ; Tumor Microenvironment/genetics*