Objective To compare the efficacy and tolerability of the novel bowel-cleansing agent TCIC-001 and the traditional polyethylene glycol (PEG) regimen for bowel preparation prior to colonoscopy. Methods Prospective inclusion of 62 patients who were scheduled to undergo colonoscopy at Zhongshan Hospital, Fudan University from July 2021 to July 2022. They were randomly divided into TCIC-001 group (n=31) and PEG group (n=31) using a random number table method. The TCIC-001 group took TCIC-001 orally, drinking water in stages, with a total liquid intake of 1 500 mL; the PEG group took PEG orally, taking it in 4 doses, with a total liquid intake of 3 000 mL. The primary endpoint indicator is the quality of intestinal hygiene evaluated by the Boston Bowel Preparation Scale (BBPS), the secondary endpoint indicators were medication adherence, medication duration, frequency of bowel movements, duration of bowel movements, and incidence of adverse events between two groups. Results No significant differences were observed in sex, age, or defecation frequency between the two groups. For efficacy, both groups achieved equivalent bowel cleanliness, with a “good preparation” rate of 93.55% and comparable BBPS score of each intestinal segment and total scores. For tolerability, the TCIC-001 group had a shorter medication duration compared to the PEG group ([48.8±25.9] min vs [82.8±28.4] min, P<0.001), a longer defecation duration ([288.6±74.0] min vs [236.5±74.3] min, P<0.001), and a lower incidence of first defecation before medication completion (9.68% vs 41.94%, P=0.004). Regarding safety, no significant differences were observed between the TCIC-001 group and the PEG group in incidences of chloride disturbances (0% vs 9.68%) and calcium disturbances (3.23% vs 6.45%), and no other adverse events. Conclusions TCIC-001 demonstrated comparable bowel-cleansing efficacy to PEG while significantly improving tolerability (reduced medication time and lower risk of premature defecation) and maintaining favorable safety.

Objective:Explore the protective effect and mechanism of methyl badosolone (CDDO-Me) on rats with traumatic brain injury (TBI).Methods:A total of 72 SPF-grade SD rats aged 8 weeks were randomly (random number) divided into 4 groups ( n=18) using the random number table method: Sham, TBI, TBI+Vehicle, and TBI+CDDO-Me. The rat TBI model was established using the hydraulic impact head injury method. The TBI+CDDO-Me group was administered CDDO-Me (dissolved in 1% DMSO, at a dose of 10 mg/kg) via intraperitoneal injection 30 minutes after modeling, twice a day for a total of 3 days. On the third day after modeling, brain tissue was collected for pathological and water content detection after mNSS scoring. Immunofluorescence double staining was used to detect the expression of nuclear factor erythroid2 related factor 2 (Nrf2); immunohistochemical staining was used to detect the expression of ionized calcium binding adapter molecule-1(Iba-1); ELISA was used to detect the levels of tumor necrosis factor-α(TNF-α), interleukin (IL)-1β, and IL-18 in serum; kits were used to detect the levels of malondialdehyde (MDA) and reactive oxygen species (ROS); Western blot was used to detect the expression of the Nrf2 pathway, B-cell lymphoma-2 (BCL-2), and BCL-2 associated X protein (BAX). Results:(1) Compared with the Sham group, the mNSS scores and water content in the injured cortex of the TBI group rats were significantly increased (both P<0.05), and both significantly decreased after CDDO-Me intervention (both P<0.05). (2) Compared with the Sham group, the proportion of Nissl-stained injured neurons and apoptotic positive cells in the TBI group rats were significantly increased (both P<0.05), and both significantly decreased after CDDO-Me intervention (both P<0.05), accompanied by a decrease in BAX protein expression and upregulation of BCL-2 protein expression (both P<0.05). (3) Immunofluorescence and Western blot results showed that compared with the Sham group, the expression of total Nrf2, nuclear Nrf2, HO-1, and NQO1 proteins in the TBI group were all increased (all P<0.05), and the increase was more significant after CDDO-Me intervention (all P<0.05). (4) Immunohistochemistry and ELISA results showed that compared with the Sham group, the levels of MDA, ROS, Iba-1 in brain tissue and the levels of TNF-α, IL-1β, and IL-18 in serum in the TBI group rats were all significantly increased (all P<0.05), and all significantly decreased after CDDO-Me intervention (all P<0.05). Conclusion:CDDO-Me helps to reduce oxidative stress and inflammatory responses in TBI rats, and the mechanism may be related to the activation of the Nrf2/HO-1 antioxidant stress pathway.

Objective To establish a scientific training program that takes into account both anaerobic and aerobic training for pilots,and to explore the appropriate ratio of aerobic and anaerobic training.Methods According to the physical examination standards for pilots,a total of 16 healthy subjects aged 18-24 were selected from two batches.The two batches of subjects were trained with different aerobic and anaerobic ratios.Training period was 3 months.The changes in cardiopulmonary function of the subjects before and after training were evaluated using the cardiopulmonary function exercise testing system(CPET),and the changes in anaerobic capacity were evaluated using changes in strength as an indicator.Results After training,the weight load of the subjects in the two training programs,including barbell squats,leg flexion and hard pull,and barbell under 10RM and 3RM,was significantly increased(P<0.001),and there was no statistically significant difference in anaerobic strength growth between the two groups.The results of CPET showed that the maximum load,maximum heart rate,and respiratory quotient in the two groups were significantly increased after than before the training(P<0.01).The maximum load(Experiment group 1:29.12±19.69,Experiment group 2:72.00±46.24)and respiratory quotient(Experiment grouop 1:0.11±0.09,Experiment group 2:0.28±0.16)of the subjects in experiment group 2 before and after training were greater than those in experiment group 1.The difference was statistically significant(P<0.05).Conclusion The anaerobic and aerobic capacities of the subjects in the experiment group 2 are effectively improved,indicating that ratio of aerobic and anaerobic of the training scheme is better.

Background It has been found that fluoride may cause cardiomyocyte damage. c-Jun N-terminal kinases (JNK) signaling pathway plays an important role in apoptosis, but its role in fluorosis-induced cardiomyocyte damage is still unknown yet. Objective To explore the toxic effect of sodium fluoride (NaF) on H9c2 cardiomyocytes of rats and whether NaF affects cardiomyocyte apoptosis through the JNK signaling pathway. Methods According to the concentrations of sodium fluoride and whether sp600125 (JNK inhibitor) was added, cardiomyocytes of rats were divided into six groups, including control group, SP600125 group (SP group), 0.24, 0.48, and 0.96 mmol·L⁻¹ NaF groups, and 0.96 mmol·L⁻¹ NaF+SP600125 group (NaF+SP group). Cardiomyocytes exposed to NaF for 24 h were observed using a fluorescence inverted microscope. The changes of cell viability at 24, 48, and 72 h after the treatment were detected by CCK-8 method. The levels of reactive oxygen species (ROS) at 24 h after the treatment in H9c2 cardiomyocytes were determined by fluorescent probe method. The expression levels of Bcl-2, Bax, Caspase-3, and JNK mRNA at 24 h after the treatment were detected by real-time PCR. The protein expression levels of Bcl-2, Bax, Caspase-3, and p-JNK at 24 h after the treatment were detected by Western blotting. Results Compared with the control group, after being exposed to 0.48 and 0.96 mmol·L⁻¹ NaF for 24 h, the cell growth density decreased. With the increase of NaF concentration, rounded cells and some suspended dead cells appeared. At 24h after exposure to NaF, the cell viability of the 0.48 and 0.96 mmol·L⁻¹ NaF groups decreased compared with the control group (P<0.05). At 48h and 72h after exposure to NaF, the cell viability levels of the NaF treated groups were significantly lower than that of the control group (P<0.05). After NaF exposure for 24 h, compared with the control group, the intracellular ROS levels were increased (P<0.05); the mRNA expression levels of Bcl-2 were decreased to varying degrees, especially in the 0.48 and 0.96 mmol·L⁻¹ NaF groups (P<0.05); the mRNA expression levels of Bax, Caspase-3, and JNK were increased (P<0.05); the protein expression levels of Bcl-2 were reduced (P<0.05); the protein expression levels of Bax, Caspase-3, and p-JNK were elevated (P<0.05). Compared with the 0.96 mmol·L⁻¹ NaF group, the cell viability of the NaF+SP group was increased, the intracellular ROS level was decreased, the mRNA expression levels of Bax, Caspase-3, and JNK were decreased, the protein expression level of Bcl-2 was increased, and the protein expression levels of Bax, Caspase-3, and p-JNK were decreased (P<0.05); the expression level of Bcl-2 mRNA had a rising trend but showed no statistical significance (P>0.05). Conclusion Cardiomyocyte damage after excessive fluoride exposure may result from fluoride inducing excessive ROS production in cardiomyocytes, which may activate the JNK signaling pathway and induce cardiomyocyte apoptosis.

Objective:To investigate the neuroprotective effect of histone deacetylase 3 (HDAC3) specific inhibitor RGFP966 on traumatic brain injury (TBI) and its mechanism in rats.Methods:Forty-eight SD rats were randomly divided into sham-operated group, TBI group, TBI+vehicle group and TBI+RGFP966 group ( n=12). Rats in the later 3 groups accepted hydraulic impact brain injury to establish TBI models; and then, RGFP966 (dissolved in 1% DMSO at a dose of 10 mg/kg) was injected intraperitoneally 30 min after modeling, twice a day for 3 d, in TBI+RGFP966 group; same amount of DMSO was injected into TBI+vehicle group at the same time. Three d after modeling, neurological function was tested by modified neurological severity score (mNSS), water content of brain tissues was detected by dry-wet weight method, proportion of injured neurons at the frontal cortical tissues on the affected side was detected by Nissl staining, expressions of HDAC3 and pyroptosis related proteins were detected by immunohistochemical staining and Western blotting, and serum content of inflammatory factors was detected by ELISA. Results:Three d after modeling, compared with the TBI+vehicle group, the TBI+RGFP966 group had significantly decreased mNSS scores (9.83±0.75 vs. 6.67±0.82), water content of the injured cerebral cortex (82.73%±0.36% vs. 80.92%±0.66%), proportion of damaged neurons (75.60%±7.44% vs. 55.87%±4.10%), and HDAC3 protein expression (0.67±0.09 vs. 0.51±0.07), and significantly increased acetylated H3 (Ace-H3) and acetylated H4 (Ace-H4) protein expressions (0.81±0.02 vs. 1.22±0.02; 0.74±0.01 vs. 1.07±0.02), and statistically decreased protein expressions of nuclear factor-κB (NF-κB, 1.20±0.05 vs. 0.94±0.04), NOD-like receptor thermal protein domain associated protein 3 (NLRP3, 0.72±0.02 vs. 0.40±0.03), Caspase-1 containing cysteine (Caspase-1), dermatin D N-terminal fragment (GSDMD-N, 0.71±0.03 vs. 0.52±0.01), significantly decreased NF-κB and NLRP3 immunohistochemical staining scores, and significantly decreased serum contents of tumor necrosis factor-α, interleukin(IL)-1β and IL-18 ( P<0.05). Conclusion:Early intervention with RGFP966 after TBI can reduce the pyroptosis and inflammatory reaction of nerve cells and play neuroprotective role, whose mechanism may be related to inhibited activation of NF-κB/NLRP3/GSDMD pathway.

Objective:To investigate the effects of positive end-expiratory pressure (PEEP) setting of mechanical ventilation guided by esophageal pressure in the treatment of patients with traumatic craniocerebral injury combined with acute respiratory distress syndrome (ARDS).Methods:The retrospective cohort study was conducted. From June 2016 to June 2018, 55 patients with traumatic craniocerebral injury combined with ARDS who met the inclusion criteria were admitted to Zhengzhou Central Hospital Affiliated to Zhengzhou University. According to PEEP setting method, 28 patients were allocated to esophageal pressure group (17 males and 11 females, aged (40±13) years) and 27 patients were allocated to PEEP-fractional concentration of inspired oxygen (FiO 2) table group (18 males and 9 females, aged (38±10) years). Patients in the 2 groups were treated with mechanical ventilation guided by lung protective ventilation strategy, and the optimal PEEP at 0 (immediately), 24, 48, and 72 h after treatment was determined according to esophageal pressure and PEEP-FiO 2 table, respectively. The mechanical ventilation parameters in the 2 groups were adjusted according to the optimal PEEP. The transpulmonary end-expiratory pressure, pulmonary compliance, oxygen index, central venous pressure, mean arterial pressure, and intracranial pressure at 24, 48, and 72 h after treatment were recorded. Data were statistically analyzed with analysis of variance for repeated measurement, chi-square test, independent sample t test, and Bonferroni correction. Results:The optimal PEEP of patients in esophageal pressure group at 0, 24, 48, and 72 h after treatment was (12.4±3.9), (11.2±3.5), (13.4±2.6), and (13.2±3.6) cmH 2O (1 cmH 2O=0.098 kPa), respectively, which was significantly higher than (8.2±2.5), (7.4±2.2), (8.3±2.3), and (8.5±2.5) cmH 2O in PEEP-FiO 2 table group, respectively ( t=4.702, 4.743, 7.849, 5.623 , P<0.01). The transpulmonary end-expiratory pressure and pulmonary compliance at 24, 48, and 72 h after treatment and oxygen index at 48 and 72 h after treatment of patients in esophageal pressure group were significantly higher than those in PEEP-FiO 2 table group ( t=17.852, 20.586, 19.532, 4.752, 5.256, 7.446, 2.342, 4.178, P<0.05 or P<0.01). The central venous pressure of patients in esophageal pressure group at 24, 48, and 72 h after treatment was significantly higher than that in PEEP-FiO 2 table group ( t=12.632, 5.247, 8.994, P<0.01), and there was no statistically significant difference in mean arterial pressure of patients between the 2 groups at 24, 48, and 72 h after treatment ( P>0.05). The intracranial pressure of patients in esophageal pressure group was higher than that in PEEP-FiO 2 table group at 24, 48, and 72 h after treatment, but there was no statistically significant difference between the 2 groups ( P>0.05). Conclusions:For patients with traumatic craniocerebral injury combined with ARDS, the optimal PEEP can be set under the guidance of esophageal pressure method, and the mechanical ventilation parameters adjusted according to the optimal PEEP can improve lung compliance and accelerate recovery of lung function more effectively, with no adverse effect in mean arterial pressure and intracranial pressure.

OBJECTIVE：To screen the components with better anti-inflammatory effect from Codonopsis Radix polysaccharide and explore the anti-inflammatory mechanism. METHODS ：Using Codonopsis Radix as sample ，the crude polysaccharide （CP） was obtained by water extraction and alcohol precipitation. After CP was separated and purified by Fast Flow DEAE Sepharose ， SephadexG-150 gel column and so on ，the components CP 1-2-1 and CP 3-1-1 were obtained and then characterized. The survival rate of RAW 264.7 cell was determined by MTT method after cultured with CP ，CP1-2-1 and CP 3-1-1（0.01，0.1，1，10，100 μg/mL）for 24 and 48 h respectively. The cells were divided into blank group （blank culture medium ），model group （1 μg/mL LPS）and low-，medium- and high-concentration groups of 3 kinds of Codonopsis Radix polysaccharide （1 μg/mL LPS+25，50， 100 μg/mL CP，CP1-2-1，CP3-1-1 solution）. After cultured for 24 h，NO content in cell culture solution ，mRNA expressions of TLR4，IL-6，NF-κB and TNF-α in cells were determined. RESULTS：The sugar content of CP reached （92.20±0.73）％. CP 1-2-1 was a single neutral polysaccharide composed of fructose with a relative molecular weight of 25.8 kDa. CP 3-1-1 was an acidic heteropolysaccharide composed of arabinose ，rhamnose，galactose and galacturonic acid and so on ，with a relative molecular weight of 49.5 kDa. Cell survival rates were higher than 99％，after cultured with 3 kinds of polysaccharide for 24 and 48 h. Compared with blank group ，NO content in cell culture solution and mRNA expressions of TLR 4，IL-6，NF-κB and TNF-α in cells were increased significantly in model group （P＜0.05 or P＜ . Compared with model group ， NO content in cell 2016CFB412） culture solution of each administration group was significantly reduced，mRNA expressions of TLR 4，NF-κB，TNF-α，IL-6 in cells in 50，100 μg/mL CP group were significantly decreased ong1991@163.com （P＜0.05 or P＜0.01）；mRNA expressi ons of TLR 4，NF-κB in cells in 25 µg/mL CP 1-2-1 group and mRNA expressions of TLR 4，NF-κB，TNF-α，IL-6 in cells in 50，100 µg/mL CP 1-2-1 group were significantly decreased （P＜0.05 or P＜0.01）；mRNA expressionsof IL- 6 in cells in 25 µg/mL CP 3-1-1 group，mRNA expressions of NF-κB，TNF-α，IL-6 in cells in 50 µg/mL CP 3-1-1 group and mRNA expressions of TLR 4，NF-κB，TNF-α，IL-6 in cells in 100 µg/mL CP 3-1-1 group were significantly decreased （P＜0.05 or P＜0.01）. CONCLUSIONS ：CP，CP 1-2-1 and CP 3-1-1 all have certain anti-inflammatory activities. The mechanism may be related to inhibiting the generation and releasing of inflammatory cytokines such as TNF-α，IL-6 by inhibiting the activation of TLR 4/NF-κB pathway.

By-products released from pretreatment process of lignocellulose seriously hinder the development of cellulosic fuel ethanol. Therefore, the great way to increase the efficiency of cellulosic ethanol production is improvement of Saccharomyces cerevisiae tolerance to these inhibitors. In this work, the effects of LCB4 gene overexpression on cell growth and ethanol fermentation in S. cerevisiae S288C under acetic acid, furfural and vanillin stresses were studied. Compared to the control strain S288C-HO, the recombinant strain S288C-LCB4 grew better on YPD solid medium containing 10 g/L acetic acid, 1.5 g/L furfural and 1 g/L vanillin. Ethanol yields of recombinant strain S288C-LCB4 were 0.85 g/(L·h), 0.76 g/(L·h) and 1.12 g/(L·h) when 10 g/L acetic acid, 3 g/L furfural and 2 g/L vanillin were supplemented into the fermentation medium respectively, which increased by 34.9%, 85.4% and 330.8% than the control strain S288C-HO. Meanwhile, ethanol fermentation time was reduced by 30 h and 44 h under furfural and vanillin stresses respectively. Further metabolites analysis in fermentation broth showed that the recombinant strain produced more protective compounds, such as glycerol, trehalose and succinic acid, than the control strain, which could be the reason for enhancing strain tolerance to these inhibitors from pretreatment process of lignocellulose. The results indicated that overexpression of LCB4 gene could significantly improve ethanol fermentation in S. cerevisiae S288C under acetic acid, furfural and vanillin stresses.

Objective To study the association of body mass index (BMI) and waist circumference (WC) with dyslipidemia and the risk of dyslipidemia at different BMI and WC level among adults in Suzhou Industrial Park District. Methods A total of 6219 participants were chosen by stratified random cluster sampling method. Four streets were selected form the district first, then one community as a cluster was selected randomly from each street. Questionnaire survey, physical examination and laboratory tests were done by all subjects. Results The prevalence of dyslipidemia was 35.9％;the rates of overweight, obesity and central obesity were 36.6％, 9.6％ and 49.5％ respectively. The prevalence of dyslipidemia in underweight group, normal weight group, overweight group and obesity group were 13.6％, 30.2％, 47.7％and 59.0％ for male, and 17.2％, 27.3％, 38.6％和 48.8％ for female respectively. The prevalence of dyslipidemia for male and female both rose with BMI (χ2=139.848, P<0.001; χ2=92.387, P<0.001). The prevalence of dyslipidemia in the high waist circumference group and normal group were 50.2％and 30.9％for male, and 40.8％and 23.8％for female respectively. Prevalence of groups with high waist circumference for male and female were significantly higher than normal groups (χ2=108.669, P<0.001; χ2=110.642, P<0.001). Pearson correlation analysis showed that total cholesterol (TC), triglyceride(TG), and low density lipoprotein cholesterol (LDL-C) were positively correlated with BMI ( r=0.153, P<0.001;r=0.227, P<0.001;r=0.192, P<0.001), and were also positively correlated with WC(r=0.138, P<0.001; r=0.234, P<0.001; r=0.159, P<0.001). High density lipoprotein cholesterol(HDL-C) was negatively correlated with BMI (r=-0.189, P<0.001) and WC (r=-0.185, P<0.001). Logistic regression analysis after age adjustment showed that, compared to the group with BMI<24 kg/m2 and WC<85 cm(male)/WC<85 cm (female), odds ratios (OR) for male in group with BMI<24 kg/m2 and WC≥85 cm, group with BMI≥24 kg/m2 and WC<85 cm and group with BMI≥24.0 kg/m2and WC≥85 cm were 1.602, 1.834 and 3.064 respectively, and ORs for female in group with BMI<24.0 kg/m2 and WC≥80 cm and group with BMI≥24.0 kg/m2 and WC≥80 cm were 1.703 and 2.381 respectively, however, the OR for female in group with BMI≥24.0 kg/m2 and WC<85 cm was not statistically significant (P>0.05). Conclusions BMI, waist circumference and dyslipidemia were closely correlated. Waist circumference is more important than BMI for female.

AIM:To discover the effect of MCPH1 on the DNA damage induced by ionizing radiation in esoph-ageal cancer cells.METHODS:ECA109 cancer cells were radiated at dose of 8 Gy.The nuclear foci of relevant factors were detected 1 h after irradiation in the ECA109 cells after silence of MDC1 gene.A cell line was established that was sta-ble low expression of MCPH1.The nuclear foci induced by ionizing radiation after silence of MCPH1 were determined.RE-SULTS:The MCPH1 gene silenced ECA109 cell line was successfully constructed.A strong relationship between MDC1, MCPH1 andγ-H2AX was observed 1 h after 8 Gy irradiation.Silence of MDC1 did not affect the nuclear foci formation ofγ-H2AX and MCPH1.The nuclear foci of MDC1 but notγ-H2AX significantly reduced after silencing of MCPH1.CON-CLUSION:MCPH1 is located in the downstream of H2AX and upstream formation of MDC1, and regulates the nuclear fo-ci formation of MDC1 during DNA damage response.