Objective:To observe the clinical effect of Yiqi Yangjing recipe combined with sticking therapy on lung cancer pleural effusion.Methods:From December 2017 to August 2019, 68 patients with advanced lung cancer and pleural effusion in Pudong New Area Hospital of Traditional Chinese Medicine were selected and randomly divided into two groups by random number table method, with 34 cases in each group.The control group was given furosemide orally on the basis of routine nutritional support treatment, and the treatment group was given Yiqi Yangjing prescription orally and traditional Chinese medicine sticking therapy on the basis of the control group.Both two groups were treated for 6 weeks.The changes of pleural fluid volume and quality of life scores were observed and compared between the two groups.Results:The total effective rate in the treatment group was 70.5%(24/34), which in the control group was 47.1%(16/34), the difference was statistically significant between the two groups(χ 2=3.886, P<0.05). The total effective rate of TCM syndrome integral was 64.7%(22/34) in the treatment group, and 35.3%(12/34) in the control group, the difference was statistically significant between the two groups(χ 2=5.800, P<0.05). After treatment, the overall quality of life score of the treatment group(55.74±5.15)points, which was higher than that of the control group[(51.91±5.20)points]( t=56.130, P<0.05). Conclusion:Yiqi Yangjing recipe combined with traditional Chinese medicine sticking therapy can effectively improve the clinical efficacy of lung cancer hydrothorax, improve the quality of life of patients.

Objective:To investigate the correlation between thromboelastography (TEG) and portal vein thrombosis in patients with cirrhotic esophagogastric varices.Methods:210 hospitalized patients with cirrhotic esophagogastric varices treated in Zhongshan Hospital Affiliated to Fudan University from December 2016 to December 2017 were retrospectively included. They were divided into portal vein thrombosis group (PVT group) and non portal vein thrombosis group (NPVT group) according to whether they were complicated with portal vein thrombosis. The correlation between the results of TEG coagulation reaction time (R value), coagulation time (K value), αAngle, maximum amplitude (MA) and coagulation composite index (CI) and portal vein thrombosis was analyzed. The characteristics of coagulation status in patients with portal vein thrombosis in cirrhosis were compared.Results:A total of 91 patients (43.3%) were complicated with portal vein thrombosis. The R value in the PVT group was significantly lower than that of NPVT group [5.49(5.22-5.77) vs 5.98(5.76-6.20), P=0.006]. Logistic regression analysis showed that Child Pugh grade ( OR=2.883, 95% CI: 1.630-5.098, P<0.001) and R value ( OR=0.739, 95% CI: 0.575-0.950, P=0.018) were independently associated risk factors of PVT. The R value of patients was significantly correlated with Child Pugh grade ( r=0.147, P=0.034), platelet ( r=-0.358, P<0.001), prothrombin time (PT) ( r=0.334, P<0.001) and international standardized ratio (INR) ( r=0.328, P<0.001). Conclusions:The decrease of TEG-R value is closely related to PVT in liver cirrhosis.

Objective:To evaluate the role of Homer1a/metabotropic glutamate receptor 5 (mGluR5) signaling pathway in sleep deprivation-induced cognitive dysfunction in aged rats.Methods:One hundred and four SPF healthy male Sprague-Dawley rats, aged 22-24 months, weighing 320-360 g, were divided into 4 groups ( n=26 each) using a random number table method: normal control group (group Control), sleep deprivation+ vehicle group (group SD+ Vehicle), sleep deprivation+ mGluR5 forward allosteric agent CDPPB group (group SD+ CDPPB), and sleep deprivation+ mGluR5 antagonist MPEP group (group SD+ MPEP). A 48-h sleep deprivation model was developed by sleep-deprived rod method. At the beginning of developing the model and 24 h after developing the model, CDPPB 10 mg/kg, MPEP 10 mg/kg and the equal volume of 1% Tween 80 were intraperitoneally injected in group SD+ CDPPB, group SD+ MPEP and group SD+ Vehicle, respectively.Morris water maze and novel object recognition tests were conducted to evaluate cognitive function after development of the model. The expression of Homer1a and mGluR5 in the hippocampus was detected by Western blot, the dendritic spine density in the hippocampal CA1 region was detected by Golgi staining, and the field excitatory postsynaptic potential (fEPSP) slope in the hippocampal CA1 region was detected by isolated electrophysiology. Results:Compared with Control group, the number of crossing the original platform, time of staying at the target quadrant, and novel object recognition index at 1 and 24 h after training were significantly decreased, the expression of Homer1a in the hippocampus was up-regulated, the expression of mGluR5 in the hippocampus was down-regulated, and the density of dendritic spine and fEPSP slope in the hippocampal CA1 region were decreased in group SD+ Vehicle ( P<0.05). Compared with group SD+ Vehicle, the number of crossing the original platform, time of staying at target quadrant, and novel object recognition index at 1 and 24 h after training were significantly increased, the expression of mGluR5 in hippocampus was up-regulated, and the density of dendritic spines and fEPSP slope in the hippocampal CA1 region were increased in group SD+ MPEP( P<0.05), and no statistically significant change was found in the parameters mentioned above in group SD+ CDPPB ( P>0.05). Conclusions:Sleep deprivation impairs the synaptic plasticity of hippocampal neurons by regulating Homer1a/mGluR5 signaling pathway, and thus mediating the process of cognitive dysfunction in aged rats.

Objective:To evaluate the role of sonic hedgehog (Shh)/glioma-associated oncogene homolog 1 (Gli1) signaling pathway in sleep deprivation-induced cognitive impairment in young mice.Methods:Forty-eight SPF healthy male C57BL/6 mice, aged 4 weeks, weighing 14-16 g, were divided into 3 groups ( n=16 each) by the random number table method: control group (C group), sleep deprivation group (SD group) and Shh agonist SAG group (SD+ SAG group). Multi-platform water environment method was used to prepare the sleep deprivation model in mice, and the sleep deprivation was 20 h a day for 10 consecutive days.In SD+ SAG group, SAG 10 mg/kg was intraperitoneally injected at 5 min before each sleep deprivation, while the equal volume of normal saline was intraperitoneally injected in group C and group SD.The mice underwent novel object recognition and Y-maze tests at 24 h after development of the model.Mice were sacrificed after the behavioral testing, and the hippocampi were isolated for determination of the density of dendritic spines in hippocampal CA1 region (by Golgi staining), expression of Gli1 and brain-derived neurotrophic factor (BDNF) in hippocampal tissues (by Western blot), and expression of Gli1 and BDNF mRNA in hippocampal tissues (by quantitative real-time polymerase chain reaction). Results:Compared with group C, the preference index in novel object recognition and Y-maze tests and density of dendritic spines in CA1 region were significantly decreased, and the expression of Gli1 and BDNF protein and mRNA in hippocampus was down-regulated in group SD ( P<0.05). Compared with group SD, the preference index in novel object recognition and Y-maze tests and density of dendritic spines in CA1 region were significantly increased, and the expression of Gli1 and BDNF protein and mRNA in hippocampus was up-regulated in group SD+ SAG ( P<0.05). Conclusions:Inhibition of Shh/Gli1 signaling pathway and reduction of plasticity of dendritic spines of hippocampal neurons are involved in sleep deprivation-induced cognitive impairment in young mice.

Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease caused by abnormal accumulation of fat in the hepatocytes. Its prevalence is rising globally and has become the most common cause of chronic liver disease worldwide. The pathogenesis of NAFLD is multifaceted, involving insulin resistance, genetic and epigenetic factors, chronic systemic inflammation, mitochondrial dysfunction, endoplasmic reticulum stress, diet, gut microbiota, and other significant contributors. This article primarily delves into the mechanisms of mitochondrial dysfunction and endoplasmic reticulum stress in the development of NAFLD, aiming to provide new insights and therapeutic strategies for NAFLD.

We used CRISPR/Cas9 to delete plin1 of 3T3-L1 preadipocyte, to observe its effect on lipolysis in adipocytes and to explore regulatory pathways. We cultured 3T3-L1 preadipocytes, and the plin1 knockout vectors were transfected by electroporation. Puromycin culture was used to screen successfully transfected adipocytes, and survival rates were observed after transfection. The optimized "cocktail" method was used to differentiate 3T3-L1 preadipocytes. The glycerol and triglyceride contents were determined by enzymatic methods. The changes in lipid droplet form and size were observed by Oil red O staining. The protein expression of PLIN1, PPARγ, Fsp27, and lipases was measured by Western blotting. RT-PCR was used to measure the expression of PLIN1 and lipases mRNA. After the adipocytes in the control group were induced to differentiate, the quantity of tiny lipid droplets was decreased, and the quantity of unilocular lipid droplets was increased and arranged in a circle around the nucleus. Compared with the control group, the volume of unilocular lipid droplets decreased, and the quantity of tiny lipid droplets increased after induction of adipocytes in the knockout group. The expression of PLIN1 mRNA and protein in the adipocytes was significantly inhibited (P<0.05); glycerol levels increased significantly (0.098 4±0.007 6), TG levels decreased significantly (0.031 0±0.005 3); mRNA and protein expression of HSL and ATGL increased (P<0.05); PPARγ and Fsp27 expression unchanged in adipocytes. The above results indicate that the knockout of plin1 enhances the lipolysis of 3T3-L1 adipocytes by exposing lipids in lipid droplets and up-regulating lipases effects.
3T3-L1 Cells ; Adipocytes ; metabolism ; Animals ; CRISPR-Cas Systems ; Gene Knockout Techniques ; Lipase ; metabolism ; Lipolysis ; genetics ; Mice ; Perilipin-1 ; genetics ; metabolism

Objective:To evaluate the effects of sevoflurane combined with propofol anesthesia on the synaptic plasticity in the hippocampus after operation in rats with mild cognitive impairment (MCI) and the relationship with potassium-chloride cotransporter-2 (KCC2)/sodium-potassium-chloride cotransporter 1 (NKCC1).Methods:Clean-grade healthy male Sprague-Dawley rats, aged 16-18 months, weighing 440-540 g, in which MCI was induced by severe bilateral common carotid artery stenosis (BCAS). Forty-eight rats with MCI were divided into 4 groups ( n=12 each) using a random number table method: sham operation group (group Sham), sevoflurane anesthesia group (group S), propofol anesthesia group (group P), and sevoflurane and propofol anesthesia group (group SP). After disappearance of eyelash reflex, open reduction and internal fixation was performed after tibial fracture was induced in S, P and SP groups.Anesthesia method was as follows: 1.7% sevoflurane was inhaled and propofol 20 mg·kg -1·h -1 was intravenously infused for 3 h in group SP, 3% sevoflurane was inhaled for 3 h in group S, and propofol was intravenously infused at rate of 40 mg·kg -1·h -1 for 3 h in group P. The novel object recognition (NOR) test was performed at 14 days after operation, and the discrimination index in NOR test was calculated.The in vivo electrophysiological experiment was performed on 19 days after operation to measure long-term potentiation and amplitude of the field excitatory postsynaptic potential (fEPSP). The expression of KCC2 and NKCC1 was determined by Western blot, and the ratio of KCC2/NKCC1 was calculated.The density of dendritic spines in the hippocampal CA1 region was determined by Golgi-COX staining performed at 30 days after operation. Results:Compared with Sham group, the discrimination index in NOR test, hippocampal KCC2/NKCC1 ratio, density of dendritic spines in hippocampal CA1 region, and amplitude of fEPSP were significantly decreased in S and P groups ( P<0.05), and no significant change was found in the parameters mentioned above in group SP ( P>0.05). Compared with group S or group P, the discrimination index in NOR test, hippocampal KCC2/NKCC1 ratio, density of dendritic spines in hippocampal CA1 region, and amplitude of fEPSP were significantly increased in group SP ( P<0.05). Conclusion:Sevoflurane combined with propofol anesthesia does not aggravate postoperative cognitive dysfunction in the rats with MCI, which may be related to maintaining the balance of hippocampal KCC2/NKCC1 and protecting the synaptic plasticity in hippocampi.