Objective To develop a method of quantitative analysis of multi-components by single marker( QAMS) for determination of quercetin, kaempferide,isohamnetin in Chuipencao granules,providing method to control the quality of Chuipencao granules.Methods The analysis was performed at 30 ℃,on an Shimadzu C18 column(250 mm ×4.6 mm,5μm),and the mobile phase was methanol-0.4% phosphoric acid solution .The flow rate was 1.0 mL/min, and the injection volume was 10 μL.Quercetin as a reference to establish the relative correction factor kaempferol and between isorhmnetin, the method was evaluated for reproducibility, and the difference between calculated and measured values was compared. Results Quercetin, kaempferol and isorhmnetin respectively 32.36-426.43μg, 11.56-136.87μg, 10.45-155.68μg showed a good linear relationship, and the regression equation was: Y=3625.8X-13658 (R2 =0.9998), Y=2682.9X-10253(R2 =0.9999), Y=3012.2X-11223 (R2 =0.9999).The average recoveries were 99.3%, 99.6%, 98.5% (RSD were less than 1.0%).Determination of 10 batches of Chuipencao granules with QAMS and external standard method, kaempferol and isorhamnetin were measured, and measured values were basically the same.Conclusion The QAMS method is reliable and accurate, which might be used for the quality control of Chuipencao granules.

Objective To observe the influence of Kuailvning capsule(KLN)and its drug serum on the concentration of Ca2 + in rat ventricular muscle cells.Methods SD rats were randomly divided into five groups:the control group,serum control group,KLN high -dose group,KLN medium -dose group and KLN low -dose group,six mice in each group.The rat ventricular myocytes were separated by enzymatic hydrolysis.The influence of KLN and its drug serum on the concentration of Ca2 + in rat ventricular muscle cells were observed by Fluo -3 /AMprobe.Results The mean fluorescence intensity of cytosolic Ca2 + in the KLN high -dose group,KLN medium -dose group and KLN low -dose group after 50s,100s,150s,200s,250s were [(18.75 ±1.55),(16.69 ±0.93),(17.76 ±1.26)], [(25.47 ±1.118),(17.86 ±1.49),(17.81 ±1.13)],[(29.05 ±1.31),(20.14 ±1.73),(18.26 ±1.37)], [(35.21 ±1.33),(23.19 ±0.97),(18.18 ±1.46)],[(41.08 ±1.21),(26.34 ±1.69),(17.91 ±1.01)], which were higher than those in the control group(F =5.556,7.007,8.816,10.208,12.232,all P <0.01 ).The mean fluorescence intensity of cytosolic Ca2 + in the KLN high -dose group after 50s,100s,150s,200s,250s were (17.85 ±1.69),(18.95 ±1.73),(21.85 ±1.39),(23.01 ±1.48),(24.07 ±1.42),which were higher than those in the serum control group(t =3.642,4.406,6.074,7.402,8.625,all P <0.01 ).The mean fluorescence intensity of cytosolic Ca2 + in the KLN medium -dose group after 100s,150s,200s,250s were (18.01 ±1.42), (18.76 ±1.22),(19.73 ±1.37),(21.04 ±1.16),which were higher than those in the serum control group(t =3.902,4.033,4.126,4.326,all P <0.01).There were no statistically significant difference between the KLN low -dose group and the serum control group(P >0.05).Conclusion KLN drug serum can promote myocardial cell spon-taneous extracellular calcium influx,the mechanism of KLN antiarrhythmic effect may be related to the Ca2 + channel.

Objective To investigate the relationship of the initiative-aggressive behavior and D2S1338,D19S433 loci.Methods PCR and electrophoresis method were used to conduct genotype analysis on D2S1338 and D19S433 in the peripheral blood of 187 male initiative-aggressive violent offenders and 459 healthy men living in Jiangsu area.Results D2S1338 and D19S433 loci in initiative-aggressive behavior group and healthy group were found to coincide with Hardy-Weinberg equilibrium (P ＞ 0.05).There were significant difference in locus D19S433 (P ＜ 0.05)between initiative-aggressive behavior group and healthy group,but not on locus D2S1338 (P＞0.05).Univariate analysis showed significant differences at allele 14.2 and genotype 14-14 on locus D19S433 between the two groups (P =0.0011,P =0.0008) with the OR values being 0.50 (95 ％ CI:0.33-0.76) and 3.49(95％ CI:1.62-7.52),respectively.Conclusion Locus D19S433 may be related to with initiative-aggressive behavior with allele 14.2 being the resistant factor and genotype 14-14 being the susceptible factor.

Objective To explore the effects of thrombelastogram (TEG) on preventing deep venous thrombosis (DVT) and hemorrhage after surgery for varicosity of lower extremities. Methods Totally 200 patients with varicosity of lower extremities who received exfoliation of great saphenous veins combined with transilluminated powered phlebectomy (TIPP) in a ClassⅢ Grade A hospital in Hebei Province from March 2016 to May 2017 by convenient sampling, and divided into the observation group (n=101) and the control group (n=99) according to the random number table. Patients in the observation group were evaluated with Caprini's DVT Assessment Model 24 hours before surgery. Patients who scored 3 or above received TEG monitoring 24 hours before surgery and on days 1, 3 and 7 post surgery, and received hierarchical interventions. Patients in the control group received conventional nursing care during the perioperative period, and empirical anticoagulation measures were taken based on the results of blood and coagulation routine examinations. Color Doppler ultrasonography was used to observe the incidence of DVT in both extremities in the patients one week post surgery, and the incidence of hemorrhage were also observed in patients in the two groups, including hemorrhage running out of dressings, incision bleeding and subcutaneous hematoma. Results DVT was found in 1 patient in the observation group (0.99%) and 8 patients in the control group (8.08%); hemorrhage running out of dressings was found in 3 patients in the observation group, incision bleeding in 2 patients and subcutaneous hematoma in 5 patients, while hemorrhage running out of dressings was found in 10 patients in the control group, incision bleeding in 9 patients and subcutaneous hematoma in 13 patients. There were statistical differences between the two groups (P＜0.05). Conclusions TEG dynamic monitoring combined with Caprini's DVT Assessment Model used in hierarchical interventions for patients with varicosity of lower extremities who receive exfoliation of great saphenous veins combined with TIPP reduces the incidence of DVT and hemorrhage, effectively avoids adverse events postoperatively, and ensures the patients' safety.

Objective:To study the prevalence and clinical characteristics of hepatitis D patients.Methods:A total of 832 144 HBsAg positive persons who were from infectious department of Southwest Hospital Affiliated to Army Military Medical University were screened from January 1, 2010 to December 31, 2020. A total of 13 585 subjects completed relevant Hepatitis Delta virus (HDV) biomarker tests, 157 HDV patients were evaluated. The mean age was 53 ± 13 years, with a range of 22-85 years. The majority of these subjects were male. The prevalence, clinical characteristics, the outcome of 28 days follow-up and the influencing factors of the outcome were analyzed.Results:In recent 10 years, the screening rate related to hepatitis D was only 1.6% (13 585/832 144), and the screening rate was the highest in 2011, up to 4.13% (962/23 289); The positive rate of screening was only 1.17% (157/13 346). In 2012, the positive rate of screening was the highest, up to 3.56% (58/1627). In Southwest Hospital, the source of disease was 66.24% (104/157) in Chongqing, 22.93% (36/157) in Sichuan, 8.28% (13/157) in Guizhou, 1.27% (2/157) in Yunnan, and 0.64% (1/157) in each of Jiangxi and Tibet. Of 157 patients, 29 (18.47%) had non-cirrhotic with chronic low bilirubin hepatitis, 23.57% (37/157) was non-cirrhotic with chronic high bilirubin hepatitis, 28.66% (45/157) had acute-on-chronic liver failure (ACLF), 27.39% (42/157) had compensated cirrhosis or decompensated cirrhosis, and 1.91% (3/157) had primary hepatocellular carcinoma. The incidence of disease progression was 48.89% (22/48) of chronic-on-acute liver failure>33.33%(1/3) of primary hepatocellular carcinoma>25.58%(11/43) of compensated or decompensated cirrhosis>18.92%(7/37) of non-cirrhotic with chronic high bilirubin hepatitis>6.90%(2/29) of non-cirrhotic with chronic low bilirubin hepatitis ( P<0.05). Among them, 7.64%(12/157) had hepatic encephalopathy, and the rate of disease progression was 83.33%(10/12) ( P<0.05); 3.82% (6/157) of them had combined with other hepatophilic viruses including hepatitis C virus (HCV), Epstein-barr virus, (EBV), Cytomegalovirus (CMV) infections. Logistic regression analysis showed that old age, complication with hepatic encephalopathy, hyperbilirubinemia and prolonged coagulation time were independent risk factors affecting the outcome of hepatitis D. Conclusions:In recent 10 years, the screening rate of hepatitis D is low and the positive rate is not high. It should be noted that HDV infection can accelerate the progress of hepatitis and increase the risk of adverse liver outcomes.

Objective:To investigate the molecular mechanism of autophagy and apoptosis induced by ultrafine carbon black in human bronchial epithelial cells (BEAS-2B cells), and to study the intervention effect and mechanism of N-acetylcysteine (NAC) on ultrafine carbon black-induced oxidative damage in BEAS-2B cells.Methods:In March 2023, BEAS-2B cells were used as research object, an in vitro airway model exposed to ultrafine carbon black was constructed. A control group and three carbon black exposure groups (50, 100, 200 μg/ml) were set up, and the cells were treated with corresponding concentrations of ultrafine carbon black for 24 hours. In addition, the experiment was divided into control group, NAC+ control group, 100 μg/ml carbon black exposure group and NAC+ exposure group. The corresponding groups were treated with 2 mmol/L NAC for 1 h and 100 μg/ml ultrafine carbon black for 24 h, respectively. Cell viability was measured by CCK-8 assay. Intracellular reactive oxygen species (ROS) level was detected by chemical fluorescence method. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), as well as the content of malondialdehyde (MDA) were detected by colorimetry. The mRNA and protein expressions of autophagy-related genes[Atg5, Atg7, Beclin1, microtubule-associated protein light chain 3B (LC3B), p62 and lysosome-associated membrane protein 2 (LAMP2) ] and apoptosis-related genes [B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase3, Caspase9 and poly (ADP-ribose) polymerase 1 (PARP1) ] were determined by fluorescence quantitative PCR and Western blot. Cell apoptosis was determined by flow cytometry.Results:Compared with the control group, the relative survival rates of BEAS-2B cells in 50, 100, 200 μg/ml carbon black exposure groups were significantly decreased, the levels of ROS and MDA were significantly increased, and the activities of SOD, GSH-Px and CAT were significantly decreased ( P<0.05). The relative survival rate, ROS and MDA levels, SOD, GSH-Px and CAT activities were significantly correlated with the exposure dose of ultrafine carbon black ( rs=-0.755, 0.826, 0.934, -0.810, -0.880, -0.840, P<0.05). Compared with the control group, the relative expression levels of Atg5, Atg7, Beclin1, LC3B, p62, LAMP2, Bax, Caspase3, Caspase9, PARP1 mRNA and Atg5, Atg7, Beclin1, LC3BⅡ, p62, LAMP2, Bax, cleaved Caspase3 (C-Caspase3), cleaved Caspase9 (C-Caspase9), cleaved PARP1 (C-PARP1) protein and the ratio of LC3BⅡ/LC3BⅠ in 50, 100 and 200 μg/ml carbon black exposure groups were significantly increased, while the relative expression levels of Bcl-2 mRNA and protein were significantly decreased ( P<0.05). The changes of the above indexes were significantly correlated with the exposure dose of carbon black ( rs=0.892, 0.879, 0.944, 0.892, 0.828, 0.880, 0.814, 0.794, 0.931, 0.918, 0.813, 0.866, 0.774, 0.695, 0.918, 0.761, 0.794, 0.944, 0.833, 0.866, 0.905, -0.886, -0.748, P<0.05). Compared with 100 μg/ml carbon black exposure group, the relative survival rate, the activities of SOD, GSH-Px and CAT in NAC+exposure group were significantly increased, while the levels of ROS and MDA were significantly decreased, and the relative expression levels of LC3B, p62 and Caspase3 mRNA and protein as well as the ratio of LC3BⅡ/LC3BⅠ were significantly decreased, and the differences were statistically significant ( P<0.05). Compared with the control group, the apoptosis rates of BEAS-2B cells in 50, 100, 200 μg/ml carbon black exposure groups were significantly increased ( P<0.05), and there was a significant positive correlation between ultrafine carbon black exposure dose and cell apoptosis rate ( rs=0.944, P<0.05). While compared with 100 μg/ml carbon black exposure group, the apoptosis rate of NAC+exposure group was significantly decreased, and the difference was statistically significant ( P<0.05) . Conclusion:Cell autophagy and apoptosis may be important pathophysiological mechanisms of ultrafine carbon black-induced oxidative damage in BEAS-2B cells. NAC can alleviate the occurrence of BEAS-2B cell damage caused by ultrafine carbon black by regulating oxidative stress and the cascading autophagy and apoptosis pathways.

Objective:To investigate the molecular mechanism of autophagy and apoptosis induced by ultrafine carbon black in human bronchial epithelial cells (BEAS-2B cells), and to study the intervention effect and mechanism of N-acetylcysteine (NAC) on ultrafine carbon black-induced oxidative damage in BEAS-2B cells.Methods:In March 2023, BEAS-2B cells were used as research object, an in vitro airway model exposed to ultrafine carbon black was constructed. A control group and three carbon black exposure groups (50, 100, 200 μg/ml) were set up, and the cells were treated with corresponding concentrations of ultrafine carbon black for 24 hours. In addition, the experiment was divided into control group, NAC+ control group, 100 μg/ml carbon black exposure group and NAC+ exposure group. The corresponding groups were treated with 2 mmol/L NAC for 1 h and 100 μg/ml ultrafine carbon black for 24 h, respectively. Cell viability was measured by CCK-8 assay. Intracellular reactive oxygen species (ROS) level was detected by chemical fluorescence method. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), as well as the content of malondialdehyde (MDA) were detected by colorimetry. The mRNA and protein expressions of autophagy-related genes[Atg5, Atg7, Beclin1, microtubule-associated protein light chain 3B (LC3B), p62 and lysosome-associated membrane protein 2 (LAMP2) ] and apoptosis-related genes [B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase3, Caspase9 and poly (ADP-ribose) polymerase 1 (PARP1) ] were determined by fluorescence quantitative PCR and Western blot. Cell apoptosis was determined by flow cytometry.Results:Compared with the control group, the relative survival rates of BEAS-2B cells in 50, 100, 200 μg/ml carbon black exposure groups were significantly decreased, the levels of ROS and MDA were significantly increased, and the activities of SOD, GSH-Px and CAT were significantly decreased ( P<0.05). The relative survival rate, ROS and MDA levels, SOD, GSH-Px and CAT activities were significantly correlated with the exposure dose of ultrafine carbon black ( rs=-0.755, 0.826, 0.934, -0.810, -0.880, -0.840, P<0.05). Compared with the control group, the relative expression levels of Atg5, Atg7, Beclin1, LC3B, p62, LAMP2, Bax, Caspase3, Caspase9, PARP1 mRNA and Atg5, Atg7, Beclin1, LC3BⅡ, p62, LAMP2, Bax, cleaved Caspase3 (C-Caspase3), cleaved Caspase9 (C-Caspase9), cleaved PARP1 (C-PARP1) protein and the ratio of LC3BⅡ/LC3BⅠ in 50, 100 and 200 μg/ml carbon black exposure groups were significantly increased, while the relative expression levels of Bcl-2 mRNA and protein were significantly decreased ( P<0.05). The changes of the above indexes were significantly correlated with the exposure dose of carbon black ( rs=0.892, 0.879, 0.944, 0.892, 0.828, 0.880, 0.814, 0.794, 0.931, 0.918, 0.813, 0.866, 0.774, 0.695, 0.918, 0.761, 0.794, 0.944, 0.833, 0.866, 0.905, -0.886, -0.748, P<0.05). Compared with 100 μg/ml carbon black exposure group, the relative survival rate, the activities of SOD, GSH-Px and CAT in NAC+exposure group were significantly increased, while the levels of ROS and MDA were significantly decreased, and the relative expression levels of LC3B, p62 and Caspase3 mRNA and protein as well as the ratio of LC3BⅡ/LC3BⅠ were significantly decreased, and the differences were statistically significant ( P<0.05). Compared with the control group, the apoptosis rates of BEAS-2B cells in 50, 100, 200 μg/ml carbon black exposure groups were significantly increased ( P<0.05), and there was a significant positive correlation between ultrafine carbon black exposure dose and cell apoptosis rate ( rs=0.944, P<0.05). While compared with 100 μg/ml carbon black exposure group, the apoptosis rate of NAC+exposure group was significantly decreased, and the difference was statistically significant ( P<0.05) . Conclusion:Cell autophagy and apoptosis may be important pathophysiological mechanisms of ultrafine carbon black-induced oxidative damage in BEAS-2B cells. NAC can alleviate the occurrence of BEAS-2B cell damage caused by ultrafine carbon black by regulating oxidative stress and the cascading autophagy and apoptosis pathways.

Nano-engineering-based tissue regeneration and local therapeutic delivery strategies show significant potential to reduce the health and economic burden associated with craniofacial defects, including traumas and tumours. Critical to the success of such nano-engineered non-resorbable craniofacial implants include load-bearing functioning and survival in complex local trauma conditions. Further, race to invade between multiple cells and pathogens is an important criterion that dictates the fate of the implant. In this pioneering review, we compare the therapeutic efficacy of nano-engineered titanium-based craniofacial implants towards maximised local therapy addressing bone formation/resorption, soft-tissue integration, bacterial infection and cancers/tumours. We present the various strategies to engineer titanium-based craniofacial implants in the macro-, micro- and nano-scales, using topographical, chemical, electrochemical, biological and therapeutic modifications. A particular focus is electrochemically anodised titanium implants with controlled nanotopographies that enable tailored and enhanced bioactivity and local therapeutic release. Next, we review the clinical translation challenges associated with such implants. This review will inform the readers of the latest developments and challenges related to therapeutic nano-engineered craniofacial implants.
Humans ; Titanium ; Dental Implants ; Wound Healing ; Surface Properties