Objective:To investigate the effect on proliferation and apoptosis of T-cell leukemia cells by silencing NRP-1 ( Jurkat cells).Methods:The lentivirus plasmid which expresses NRP1 gene specific shRNA was constructed in our preliminary ex-perimental.We transfected the lentivirus plasmid to human T-cell Lymphoma cells.The proliferation of Jurkat cells different groups and effect on cell proliferation after chemotherapy drug EPI-treated were found by CCK-8 kit.The proliferation level and apoptosis rate of the cells were detected by flow cytometry and Annexin-V-FITC/PI method.Results:The proliferation level of NRP-1 /shRNA interference group was decreased significantly in 48 h,72 h,96 h,which was compared with the control groups.The apoptosis rate of the NRP-1/shRNA interference group was increased compared with control groups.The chemotherapy drug sensitivity of epirubicin ( EPI ) test results showed that EPI concentration was 0.025,0.05,0.1,0.2,0.4 μg/ml,the NRP-1/shRNA interference group of cell growth inhibition rate was increased,the corresponding control group difference had statistical significance(P<0.05).We choose the drug con-centration of the EPI IC50 for next experiments.NRP-1/shRNA interference group cell apoptosis rate increased significantly after induction,compared with the control groups difference was statistically significant ( P<0.05 ).Compared with control group, the expression level of Bcl-2 protein was decreased and the expression level of bax protein was increased significantly after EPI induction.The percentage of cells at G0/G1 phase increased significantly,while those at S phase decreased significantly.Conclusion:Plasmid shRNA-NRP1 inhibited the expression of NRP1 in Jurkat cells and decreased the proliferation level of Jurkat cells and promote their apoptosis and enhance their drug sensitivity;the molecular mechanism may relate to down-regulation of Bcl-2 and up-regulation of Bax.and arrested the cell cycle at G0/G1 phase.

Objective:To explore the protective effect and related mechanism of rebamipide on non-steroid anti-inflammatory drug (NSAID) related small intestinal mucosal injury.Methods:A total of 21 C57BL/6 mice were selected and by random number table method, they were divided into negative control group (0.9% NaCl gavage for four days), indomethacin modeling group (20 mg/kg indomethacin gavage for four days) and rebamipide intervention group (20 mg/kg indomethacin gavage for four hours and then 320 mg·kg -1·d -1 rebamipide gavage for four days), seven mice in each group. After modeling, the injury of mice intestinal mucosa of indomethacin modeling group and rebamipide intervention group was evaluated by gross observation as well as pathological analysis. The serum levels of interleukin (IL)-6, IL-10, trefoil factor 3 (TFF3), prostaglandin E2 (PGE2) and epidermal growth factor (EGF) in mice were detected by enzyme-linked immunosorbent assay (ELISA). The expression of IL-6, IL-10, TFF3, cyclooxygenase 2( COX2) and EGF at mRNA level of mice small intestinal tissues were examined by real-time quantitative polymerase chain reaction (qRT-PCR). And the relative expression of TFF3, COX2 and EGF at protein level of mice small intestinal tissues were determined by Western blotting. Levene test and independent sample t test were used for statistical analysis. Results:The scores of gross observation and histopathology of mice small intestinal mucosa injury of rebamipide intervention group were both lower than those of indomethacin modeling group (2.80±0.45 vs. 4.60±1.14, 1.67±0.52 vs. 3.00±0.71), and the differences were statistically significant ( t=2.667 and 3.618, P=0.029 and 0.006). The mouse serum level of IL-6 and the expression of IL-6 at mRNA level in intestinal tissues of indomethacin modeling group were both higher than those of the negative control group, however the serum level of IL-10 was lower than that of the negative control group ((48.83±5.40) ng/L vs. (40.96±5.92) ng/L, 5.23±2.36 vs. 1.12±0.56, (168.50±10.57) ng/L vs. (186.30±7.77) ng/L), and the differences were statistically significant ( t=2.307, 3.372 and 3.366; P=0.047, 0.007 and 0.012). The expression of IL-6 at mRNA level in mice small intestinal tissues of rebamipide intervention group was lower than that of indomethacin modeling group (1.74±0.82 vs. 5.23±2.36), however, the expression of IL-10 at mRNA level was higher than that of indomethacin modeling group (6.44±3.46 vs. 1.22±0.83), and the differences were statistically significant ( t=3.409 and 3.025, P=0.008 and 0.014). The serum levels of TFF3, PGE2 and EGF, the expression of TFF3 at mRNA level of small intestinal tissues, the relative expression of COX2 and EGF at protein level of small intestinal tissues of indomethacin modeling group were all lower than those of the negative control group ((131.20±16.37) ng/L vs. (150.30±9.66) ng/L, (32.68±6.88) ng/L vs. (41.51±3.20) ng/L, (112.70±17.17) ng/L vs. (138.20±10.10) ng/L, 0.43±0.22 vs. 1.20±0.50, 0.33±0.25 vs. 1.30±0.43, 0.28±0.19 vs. 1.15±0.10), and the differences were statistically significant ( t=2.290, 2.645, 2.867, 3.097, 3.405 and 7.106; P=0.048, 0.021, 0.025, 0.017, 0.027 and 0.002). The mice serum levels of PGE2 and EGF, expression of TFF3, COX2 and EGF at mRNA level of small intestinal tissues, as well as the expression of TFF3 and EGF at protein level of small intestinal tissues of rebamipide intervention group were all higher than those of indomethacin modeling group ((43.55±5.28) ng/L vs. (32.68±6.88) ng/L, (153.30±15.66) ng/L vs. (112.70±17.17) ng/L, 2.48±1.70 vs. 0.43±0.22, 2.95±1.56 vs. 0.88±0.45, 3.97±2.54 vs. 0.98±0.76, 1.47±0.26 vs. 0.72±0.35, 1.08±0.36 vs. 0.28±0.19), and the differences were statistically significant ( t= 2.711, 3.658, 2.656, 2.856, 2.524, 3.013 and 3.435; P=0.024, 0.008, 0.026, 0.019, 0.033, 0.039 and 0.026). Conclusions:Rebamipide alleviates small intestinal mucosal injury induced by indomethacin by inhibiting the expression of inflammatory factors and promoting the expression of intestinal mucosal protective factors suggesting that rebamipide plays a protective role in NSAID related small intestinal injury by maintaining the chemical barrier of the intestinal mucosal.

Objective:To analyze the effects of different anesthesia depths on serum S100β protein level and postoperative cognitive function in patients undergoing minimally invasive McKeown esophagectomy with bispectral index (BIS) monitoring.Methods:A total of 120 patients who received minimally invasive McKeown esophagectomy in the Second Hospital of Shanxi Medical University from April 2018 to April 2019 were selected, and they were divided into light anesthesia group (L group, 40 cases, BIS 46-60), deep anesthesia group (D group, 40 cases, BIS 35-45) and control group (C group, 40 cases, no BIS monitoring) by using the random number table method. Elbow venous blood was taken from each group to detect serum S100β protein levels before induction (T 0), 10 minutes after extubation (T 3), the first day after surgery (T 4), and the third day after surgery (T 5). The mini-mental state examination scale (MMSE) score and the monterey cognitive assessment scale (MoCA) score were performed before surgery and on day 1, 3, and 7 after surgery to count the incidence of postoperative cognitive dysfunction(POCD). Results:There was no statistical difference in serum S100β protein levels between the three groups at T 0 (F = 0.083, P = 0.920). The level of serum S100β protein in D group [(1.08±0.05) μg/L] was significantly higher than that in C group and L group [(0.98±0.10) μg/L and (0.84±0.09) μg/L] at T 3, and the level of serum S100β protein in L group was lower than that in C group, the differences between the three groups were statistically significant (P < 0.05). There was no statistical difference in the incidence of POCD among the three groups on day 7 after surgery (χ 2 = 2.914, P = 0.233). The incidence rates of POCD in D group on day 1 and 3 after surgery (57.1% and 37.1%) were significantly higher than those in C group (41.7% and 38.9%) and L group (20.0% and 14.3%), and the incidence of POCD in L group were lower than those in C group, the differences among the three groups were statistically significant (χ 2 = 10.187, P = 0.006; χ 2 = 6.296, P = 0.043). Conclusions:For patients undergoing minimally invasive McKeown esophagectomy, intraoperative BIS monitoring maintains a light anesthetic state, which can effectively reduce serum S100β protein level and POCD. The mechanism may be related to reducing serum S100β protein level and improving brain damage.

Objective:To investigate the effects of propofol combined with sevoflurane intravenous-inhalational anesthesia and propofol intravenous anesthesia on implicit memory, explicit memory and stress response in patients undergoing gynecological cancer surgery.Methods:A total of 48 patients undergoing gynecologic cancer surgery in the Second Hospital of Shanxi Medical University from August 2018 to May 2019 were selected. Random number table was used to divide patients into propofol intravenous anesthesia group (group A) and propofol combined with sevoflurane intravenous-inhalational anesthesia group (group B), 24 cases in each group. During the operation, the patients in group A were given continuous intravenous anesthesia with propofol and the patients in group B were given continuous intravenous anesthesia with propofol combined with sevoflurane. Minimal alveolar concentration (MAC) of sevoflurane was 0.5, and midazolam was not utilized throughout the whole anesthesia for both groups. The bispectral index (BIS) value of the two groups ranged from 45 to 55 during the operation. The concentration of cortisol, adrenocorticotropic hormone (ACTH) and prolactin(PRL) in elbow venous blood was measured before anesthesia induction (T 1) and 10 minutes after intraoperative auditory recording (T 2). Implicit and explicit memory scores were measured 12-24 h after operation. Results:Neither group produced explicit memory compared with 0 (group A: 0.012±0.007, t = 1.554, P > 0.05; group B: 0.016±0.002, t = 1.942, P > 0.05), and there was no significant difference in explicit memory score between the two groups ( t = -0.417, P > 0.05). Both groups produced implicit memory (group A: 0.089±0.050, t = 8.726, P < 0.05; group B: 0.189±0.060, t = 15.415, P < 0.05), and implicit memory score was higher in group B ( t = -6.215, P < 0.05). The level of cortisol, ACTH and PRL at time T 1 was not significantly different between the two groups (all P > 0.05), and the level of cortisol, ACTH and PRL in group B was higher than that in group A at time T 2 [(276±35) μg/L vs. (96±33) μg/L; (228±42.3) pg/ml vs. (14.1±1.7) pg/ml; (4 208±213) mU/ml vs. (3 805±196) mU/ml; t value was 18.634, 34.879, 12.605, all P < 0.05]. Conclusion:Propofol intravenous anesthesia can better inhibit the production of implicit memory and intraoperative stress response compared with propofol combined with sevoflurane intravenous-inhalational anesthesia.

Objective: To determine the contribution of follow-up formula (FUF) to the nutrient intake of 7-24-month-old infants and young children. Methods: The cluster random sampling method and the convenience sampling method were used in combination, and geographic and economic factors were taken into consideration. Four areas of China (Beijing, Hebei, Guangxi, Guangdong) were selected, with 120 infants chosen from each of these areas (half of which were 7-12 months old, and half were 13-24 months old). A dietary survey was completed by a continuous 24-hour weighing method over two days. Questionnaires were completed by their caregivers which included weighing the FUF and supplementary food given to the infant, and recording the frequency of breast feeding and any supplementary nutrients. A total of 518 questionnaires were distributed, and 472 questionnaires qualified for inclusion. Nutrient intake was calculated using the China food composition, infant formula food nutrient content and infant nutrition supplement brand-label information databases, and then the nutrient intake proportion (the percentage of estimated energy requirement (EER%), recommended nutrient intake (RNI%) or adequate intake (AI%)), and the contribution rate of FUF were analyzed. Results: A total of 472 infants were investigated (227 infants aged 7-12 months old, 245 infants aged 13-24 months old). The findings revealed that the median energy intake of 7- 12-month-old and 13- 24-month-old infants were 2 530.08 kJ and 3 445.48 kJ, respectively, which accounted for 85.18% and 94.14% of EER, respectively; and the median intake of protein reached 91.50% and 105.88% of their RNI/AI, respectively. For micronutrients, the median intake of vitamin B₁, vitamin B₂, niacin, vitamin E, potassium, zinc and manganese in 7- 12-month-old infants and vitamin B₂, vitamin E, potassium, magnesium, iron and manganese in 13-24-month-old children accounted for 82.00% and 114.29% of RNI/AI (RNI%/AI%), respectively. The intake of vitamin B₆, iron and selenium in 7-12-month-old infants and vitamin B₁, vitamin B₆, vitamin C, calcium and selenium in 13-24-month-old children was less than 80% RNI/AI. Furthermore, some nutrients showed higher intake levels, such as vitamin A, calcium, phosphorus and magnesium in 7-12-month-old infants and vitamin A and phosphorus in 13-24-month-old children, which were higher than 130% RNI/AI. In total, 40.53% (92) of infants aged 7-12 months and 52.65% (129) of children aged 13- 24 months were fed FUF as part of their diet, and its contribution rate to macronutrients was 29.69% for carbohydrates and 51.77% for fats, and to micronutrients was 2.04% for manganese and 74.24% for vitamin C. Conclusion FUF contributes to the nutrient intake of infants and young children aged from 7-24 months old at different rates depending on the macronutrient or micronutrient analyzed.

Objective To evaluate the efficacy of reduced glutathione (GSH) for preventing thalidomide-induced peripheral neuropathy (TiPN) in multiple myeloma (MM). Methods A total of 40 cases of MM in Jiading District Central Hospital Affiliated to Shanghai University of Medicine & Health Sciences from October 2014 to September 2016 were chosen as research objects. According to the randomized double blind principle, the patients were divided into two groups, the patients in the treatment group were treated with GSH and thalidomide in combination with chemotherapy, and the patients in the control group were treated without thalidomide and chemotherapy. The occurrence of TiPN between the two groups were observed and analyzed. Results The total incidence of TiPN in the treatment group was 25 % (5/20), while that in the control group was 45 % (9/20), there was no significant difference between the two groups (χ2= 1.758, P>0.05). There were no statistically significant differences in neuromotor conduction velocity (MCV), compound muscle action potential (CMAP) and sensory conduction velocity (SCV) between the two groups (all P> 0.05). There were no statistically significant difference in SNAP of median nerve and ulnar nerve between the two groups (both P>0.05). But the sensory nerve action potential (SNAP) of superficial peroneal nerve in the treatment group was higher than that in the control group [(7.5 ±4.6) vs. (4.9 ±2.6)], and the difference was statistically significant (t= 2.221, P< 0.05). Conclusion GSH has a certain effect on the prevention of TiPN.

Objective: To study the effects of different anesthesia depths on stress response during single-lung ventilation in patients with thoracoscopic lobectomy. Methods: Sixty patients selected for elective thoracoscopic lobectomy in the Second Hospital of Shanxi Medical University from September 2018 to May 2019 were randomly divided into three groups according to the digital random table method, with 20 patients in each group. Group A maintained deep anesthesia with the bispectral index (BIS) 36-45, group B maintained moderate anesthesia with BIS 46-55, and group C did not undergo BIS monitoring. The changes of heart rate, mean arterial pressure (MAP), stress indexes cortisol and blood glucose before anesthesia induction (T₀), immediately after one-lung ventilation (T₁), 60 min after one-lung ventilation (T₂) and immediately after skin suture (T₃) in the three groups were compared. Results: The concentration of blood glucose in group A at T₁, T₂ and T₃ was (5.28±0.49) mmol/L, (5.34±0.49) mmol/L and (5.40±0.47) mmol/L, and the cortisol was (142.75±31.45) ng/ml, (181.36±19.62) ng/ml and (153.81±33.92) ng/ml; the blood glucose in group B was (5.63±0.35) mmol/L, (6.06±0.19) mmol/L and (5.79±0.44) mmol/L, and the cortisol was (168.45±31.16) ng/ml, (171.09±25.28) ng/ml and (159.39±18.77) ng/ml; the blood glucose in group C was (6.35±0.56) mmol/L, (7.04±0.26) mmol/L and (6.17±0.54) mmol/L, and the cortisol was (191.13±46.00) ng/ml, (283.25±30.07) ng/ml and (183.01±19.71) ng/ml, respectively. The blood glucose and cortisol levels in group C at T₁, T₂ and T₃ were higher than those in group A and group B (all P < 0.05). The MAP in group A at T₁, T₂ and T₃ were (69±5) mmHg (1 mmHg= 0.133 kPa), (67±6) mmHg and (75±7) mmHg, respectively, and group B was (80±8) mmHg, (79±4) mmHg and (84±9) mmHg, the differences between the two groups were statistically significant (all P < 0.05). There was significant difference in cortisol between group A and group B at T₁ (P < 0.05). The heart rate and MAP at T₁, T₂ and T₃ in group A and group C were significantly different from those at T₀ (all P < 0.05). The heart rate and MAP at T₁ and T₂ in groups B were significantly different from those at T₀ (all P < 0.05). Conclusion BIS anesthesia depth monitoring should be performed during single-lung ventilation in thoracic surgery, and BIS should be maintained at 46-55, which can not only inhibit the stress response but also have a slight effect on hemodynamics.

Objective:To explore the effects and underlying mechanisms of azintamide on gastric emptying and gastrointestinal hormone secretion in proton pump inhibitor related low gastric acid environment.Methods:A total of 60 rats were selected and randomly divided into low gastric acid control group, low gastric acid model group, low gastric acid and azintamide intervention group, high gastric acid control group, high gastric acid model group and high gastric acid and azintamide intervention group by random number table, with 10 rats in each group. The rats of low gastric acid control group and high gastric acid control group were all treated with 0.9% sodium chloride solution. The rats of low gastric acid model group and high gastric acid model group were established by intraperitoneal injection of 20 mg/kg omeprazole once per day for seven days, and subcutaneous injection of 2 mg/kg penta gastrin once per day for three days, respectively. The rats of low gastric acid and azintamide intervention group and high gastric acid and azintamide intervention group were gavaged with azintamide 50 mg/kg once per day for three days on the basis of low gastric acid model group and high gastric acid model group, respectively. Only the rats in three low gastric acid groups were analyzed. At Day 0, 2nd, 4th, 6th and 8th after modeling, the body weight of rats were compared. After modeling, the weight of gastric contents and pH of gastric fluid was measured and compared, and the peripheral blood levels of pepsinogen A (PGA), gastrin and cholecystokinin (CCK) were detected by enzyme linked immunosorbent assay. One-way analysis of variance and Tukey′s honestly significant difference post-hoc test were used for statistical analysis.Results:The pH value of gastric fluid in low gastric acid model group and low gastric acid and azintamide intervention group were both higher than that in the low gastric acid control group (2.17±0.53, 2.03±0.69 vs. 1.32±0.17), and the differences were statistically significant ( P=0.026 and 0.041, respectively). While there was no significant difference in pH value between the low gastric acid model group and low gastric acid and azintamide intervention group ( P>0.05). On the Day 0, 2nd, 4th, 6th and 8th after modeling, the body weight of rats of low gastric acid control group, low gastric acid model group and low gastric acid and azintamide intervention group was (285.40±10.86), (283.40±6.38), (282.00±5.04) g; (287.10±10.73), (283.20±5.83), (284.00±5.72) g; (292.20±11.18), (281.90±6.23), (289.00±5.82) g; (296.40±11.12), (277.70±6.96), (292.00±6.82) g; (300.80±11.29), (274.30±8.84), (297.00±4.17) g, respectively. On the Day 6th and 8th after modeling, the body weight of rats of low gastric acid model group was lower than that of the low gastric acid control group; and the body weight of rats of low gastric acid and azintamide intervention group was higher than that of low gastric acid model group, and the differences were statistically significant (both P<0.01). On the Day 0, 2nd, 4th, 6th and 8th, there was no statistically significant difference in body weight of rats between low gastric acid and azintamide intervention group and low gastric acid control group ( P>0.05). On the Day 0, 2nd, 4th, there were no statistically significant differences in body weight of rats between low gastric acid and azintamide intervention group and low gastric acid model group, and between low gastric acid model group and low gastric acid control group (both P>0.05). The weight of gastric contents of low gastric acid model group was heavier than that of low gastric acid control group ((2.36±0.11) g vs. (1.85±0.20) g), the weight of gastric contents of low gastric acid and azintamide intervention group was lighter than that of low gastric acid model group ((1.87±0.42) g vs. (2.36±0.11) g), and the differences were statistically significant ( P=0.019 and 0.016, respectively), and there was no statistically significant difference in weight of gastric contents between the low gastric acid and azintamide intervention group and the low gastric acid control group ( P>0.05). The peripheral blood level of PGA of rats of low gastric acid model group was lower than that of low gastric acid control group ((551.80±190.00) ng/L vs. (857.00±164.80) ng/L), while the peripheral blood level of PGA of the low gastric acid and azintamide intervention group was higher than that of the low gastric acid model group ((799.90±97.80) ng/L vs. (551.80±190.00) ng/L), and the differences were statistically significant ( P=0.011 and 0.037, respectively). There was no significant difference in peripheral blood level of PGA between the low gastric acid control group and the low gastric acid and azintamide intervention group ( P>0.05). The peripheral blood level of gastrin of the low gastric acid model group was higher than that of the low gastric acid control group ((49.31±11.93) ng/L vs. (35.59±5.29) ng/L), and the CCK level of the low gastric acid model group was lower than that of low gastric acid control group ((10.26±5.32) ng/L vs. (25.55±11.62) ng/L), and the differences were statistically significant ( P=0.037 and 0.035, respectively). The peripheral blood level of gastrin of the low gastric acid and azintamide intervention group was lower than that of low gastric acid model group ((35.65±6.49) ng/L vs. (49.31±11.93) ng/L), the level of CCK of the low gastric acid and azintamide intervention group was higher than that of low gastric acid model group ((27.59±11.22) ng/L vs. (10.26±5.32) ng/L), and the differences were statistically significant ( P=0.048 and 0.021, respectively). There were no significant differences in CCK and gastrin between low gastric acid and azintamide intervention group and low gastric acid control group (both P>0.05). Conclusion:Azintamide regulates the levels of gastrointestinal hormones CCK and gastrin under the condition of low gastric acid and affects the expression of pepsinogen A, thereby promoting gastric emptying in a low gastric acid environment.

The original version of this article unfortunately contained some mistakes.