Objective To compare the efficacy of the radical resection by laparoscopy versus open approach in perioperative period on the patients with rectal carcinoma,and investigate the feasibility,safety and oncological clearance of the laparoscopy.Methods The clinical data of 44 patients who underwent radical resection of rectal carcinoma by laparoscopy in our hospital were reviewed and compared with another 53patients who underwent an open approach in the same period.The surgery-related data,postoperative recovery status,tumor radical resection index,and postoperative complications by laparoscopy were analyzed by statistics,and compared with those by open approach,and evaluated the deference of too kinds of operation.Results This study showed a longer surgical time (260.45 ± 67.46) min vs ( 179.25 ± 40.92) min,P ＜0.05,a less intra-operative blood loss( 125.20 ±61.80) mL vs ( 198.02 ± 131.24) mL,P ＜0.05,in laparoscopic group compared with open approach.Meanwhile,it also showed an earlier recovery of bowel functions for discharge gas from anus,taking in food,and out-of-bed activity (4.34 ± 1.55) d vs(5.45 ± 1.55) d,P ＜0.05,in the laparoscopic group compared with open approach.There was no statistical difference of incidence of post-operative complications (5 cases vs 11 cases,P ＞0.05) between the two groups and the laparoscopic approach was also equal to the open approach as regard to post-operative stay (15.34 ±6.62) d vs (16.82±5.73) d,P ＞0.05,and demand of intra-operative blood transfusion (4 case vs 8 cases,P＞0.05 ).Conclusions Compared with open surgery,the radical resection of rectal carcinoma by laparoscopy has shown obvious advantages in smaller incision,less blood loss,less pain,earlier recovery of bowel and bladder functions,and earlier out-of-bed activity.And it is also possible by laparoscopy approach to decrease the post-operative complications and post-operative stay.Meanwhile,there is no significant deference on oncological clearance for laparoscopy compared with open approach during perioperative period,while the long term follow-up data is still needed to support the results.

Objective To explore the effect ofthymosin alpha-1 (Ta1) on postnatal systemic inflammation-induced learning and memory impairment in mice and their relevant mechanism.Methods (1) Twenty-four neonatal C57BL/6 mice were randomly assigned into normal saline group,lipopolysaccharide (LPS,0.3 mg/kg) group,LPS (0.6 mg/kg) group,and LPS (0.9 mg/kg) group.And the animals were intraperitoneally injected with different doses of LPS or equal volume of saline for 5 days.The variations of body weight,liver weight relative to the body and tumor necrosis factor-α (TNF-α) level in serum and brain tissues were observed to determine the appropriate dose of LPS for simulating neonatal clinical infection.(2) A total of 60 newborn mice were randomly divided into three groups:control group,LPS group and Ta1 treatment group;mice in each group were continuously injected with equal volume saline,LPS (0.6 mg/kg) and Tal (0.4 mg/kg)+LPS (0.6 mg/kg) for 5 days.On day 28 and on day 56,Morris water maze was used to measure the spatial learning and memory abilities of mice;the concentrations of TNF-α,interleukin-1β (IL-1β),brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the hippocampus were examined by ELISA,and the expressions of toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) were measured by Western blotting.Results (1) As compared with the normal saline group,the mice in the LPS group (0.6 mg/kg) had significantly slower growth ([2.23±0.22] g vs.[1.18±0.21] g),increased relative liver weight to the body (0.052±0.004 vs.0.072±0.007) and increased TNF-α levels in serum and brain tissues ([62.01±3.32] pg/mL vs.[151.06± 14.51] pg/mL;[186.03±13.24] pg/mL vs.[298.71±41.61] pg/mL,P＜0.05).(2) As compared with the LPS group,Tal treatment group had significantly shortened average escape latency in place navigation test,prolonged active time in spatial probe test,statistically decreased hippocampal TNF-α,IL-1β,TLR4 and NF-κB levels ([73.32±5.18] pg/mL vs.[58.61 ±4.03] pg/mL;[99.15±8.30] pg/mL vs.[75.56±6.13] pg/mL;2.32±0.29 vs.1.71±0.26;1.77±0.24 vs.1.26±0.14) and significantly increased BDNF and NGF levels ([1.33±0.12] pg/mL vs.[1.69±0.25] pg/mL;[41.45±3.47] pg/mL vs.[50.38±5.02] pg/mL,P＜0.05).Conclusion Tal improves learning and memory functions and alleviates neuro-inflammation in postnatal infection of mice,and the underlying mechanism probably involves in inhibiting TLR4/NF-κB signaling pathway activation and increasing neurotrophic factors.

OBJECTIVETo investigate the role of Tal1 gene, which is aberrantly expressed in 40%-60% of patients with T lymphocytic leukemia (T-ALL), in the proliferation of T-ALL cells.

METHODSWe established stable Jurkat-siTal1 and Jurkat-T1 cell lines by trasnfecting T-ALL Jurkat cells with lentiviral vectors to knock-down or overexpress Tal1. Jurkat cells transfected with negative control siRNAs for Tal1 knock-down (Jurkat-mock1) and over-expression(Jurkat-mock2) served as the control cells. The proliferation of the cells lines was assessed using CCK-8 assay, and the cell cycle distribution was determined by flow cytometry. The mRNA and protein expressions of cyclin-dependent kinase inhibitor 2 (CDKN2A) and cyclin-dependent kinase inhibitor 1 (CDKN2B) were measured by real-time RT-PCR and Western blotting, respectively.

RESULTSJurkat-T1 cells showed more active proliferation in vitro than Jurkat-mock2 cells, while Jurkat-siTal1 cells showed slower growth than Jurkat-mock1 cells. In Jurkat-T1 cells, G0/G1 phase cells were decreased and S phase cells increased compared with Jurkat-mock2 cells, and Jurkat-siTal1 cells showed increased G0/G1 phase cells and decreased S phase cells compared with Jurkat-mock1 cells. Real-time RT-PCR and Western blotting showed that Tal1 inhibited the cellular expression of CDKN2A and CDKN2B at both mRNA and protein levels.

CONCLUSIONTal1 promotes the growth and the transition from G0/G1 phase to S phase in T-ALL cells Jurkat by inhibiting the expressions of G0/G1 and S phase negative regulatory proteins CDKN2A and CDKN2B.

Apoptosis ; Basic Helix-Loop-Helix Transcription Factors ; metabolism ; Cell Cycle ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p15 ; metabolism ; Cyclin-Dependent Kinase Inhibitor p16 ; metabolism ; Humans ; Jurkat Cells ; Lentivirus ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; metabolism ; pathology ; Proto-Oncogene Proteins ; metabolism ; RNA, Small Interfering ; T-Cell Acute Lymphocytic Leukemia Protein 1