Angiotensin I ; Hepatic Stellate Cells ; Insulin-Like Growth Factor Binding Protein 2 ; Peptide Fragments ; Peptidyl-Dipeptidase A

Objective To investigate the clinical feature and prevalence of chronic actinic dermatitis in a four-generation family with both monovular twins affected by chronic actinic dermatitis.Methods The clinical and laboratory findings from monovular twins simultaneously affected by chronic actinic dermatitis and their four-family members were analyzed.Results There were 76 members in the four-generation family,with 22 members (including 14 males and 8 females) diagnosed with chronic actinic dermatitis.No positive results were found from laboratory examinations or environmental survey.Conclusion Chronic actinic dermatitis was inherited in an autosomal mode in this family.

Humans ; Liver ; cytology ; metabolism ; Liver Diseases ; metabolism ; pathology ; therapy ; Receptors, Angiotensin ; metabolism ; Receptors, Cell Surface ; metabolism ; Receptors, Endothelin ; metabolism ; Receptors, Vasopressin ; metabolism

Objective To investigate the expression of unfolded protein response (UPR) gene glucose regulated protein 78(GRP78) and X-box binding protein 1(XBP1) in esophageal squamous cell carcinoma, its effect on activation of the endoplasmic reticulum stress (ERS) and its mechanism in the growth of esophageal squamous cell carcinoma. Methods The expressions of GRP78 and XBP1 were detected by immunohistochemistry in 30 samples of esophageal squamous cell carcinoma and 30 samples of normal esophageal squamous epithelium. The correlation between expressions of both proteins and prognosis was analyzed. Results GRP78 positive rate was 83.3 %(25/30) in esophageal carcinoma, while the proportion was 20.0 %(6/30) in normal esophageal (χ2=25.833, P<0.05). XBP1 positive rate was 70.0 % (21/30) in esophageal carcinoma, while the proportion was 26.7%(8/30) in normal esophageal(χ2=20.872, P<0.05). The positive rates of GRP78 and XBP1 in invasive muscular layer of esophageal squamous cell carcinoma were significantly higher than those in invasive mucous layer. Conclusion GRP78 and XBP1 are highly expressed in esophageal squamous cell carcinoma, which may involve the occurrence and development of the esophageal carcinoma.

Nuclear factor-erythroid 2-related factor-2 (Nrf2) is an important transcription factor for cells to resist oxidative stress. It interacts with antioxidant response elements to induce the expression of downstream protective phase II detoxification enzymes and antioxidant enzymes and thus exerts a protective effect on cells. Oxidative stress is the common pathogenesis of many liver diseases, and the Nrf2-ARE antioxidant pathway is an important anti-oxidative stress pathway in vivo. It can induce the expression of downstream target genes and thus plays an important role in the development, progression, and prevention of liver diseases. This article briefly describes the mechanism of action of the Nrf2 antioxidant pathway in the development and progression of liver diseases and points out that Nrf2 may be a potential target for the prevention or treatment of liver diseases.

Objective: To study the effect of benazepril on the expression of nuclear factor E2 related factor 2 (Nrf2), nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) and reactive oxygen species (ROS) concentration in rats with hepatic fibrosis and to explore the possible antifibrotic mechanism of benazepril. Methods: Twenty-two healthy male Sprague-Dawley rats were randomly divided into 3 groups: control group (6 rats), model group (8 rats) and benazepril treatment group (8 rats). Two rats died during modeling and treatment in the model group and the benazepril treatment group, and a model of hepatic fibrosis induced by carbon tetrachloride (CCL₄) was established. The rats in benazepril group were given benazepril for 8 weeks by gastric gavage. The assessment of liver tissue damage in each group was measured using conventional hematoxylin-eosin and Masson staining. The mRNA level of Nrf2, NOX4 in liver tissue was detected by RT-PCR, and serum ROS concentration was determined by colorimetry. All data were expressed in mean ± standard deviations, and were analyzed using SPSS21.0 statistical software. The data were compared using one-way analysis of variance, and the LSD-t method was used for pairwise comparison between the two groups. The correlation analysis was performed by Spearman’s correlation analysis. Results: In the liver of the model group, with the aggravation of liver fibrosis the expression of Nrf2mRNA, NOX4 mRNA and ROS concentration were higher than control group [(4.01 ± 3.40), (31.78 ± 3.96), (1.82 ± 0.46) μg/ ml vs. (0.12 ± 0.11), (2.03 ± 0.31), (1.56±0.84) μg/ml, P < 0.05]. After benazepril treatment, NOX4 mRNA expression and ROS concentration were decreased than the model group [(15.93 ± 5.01), (0.78 ± 0.44) μg/ml vs. (31.78 ± 3.96), (1.82 ± 0.46) μg /ml, P < 0.05], while Nrf2 mRNA expression was higher than the model group [(6.69 ± 4.86) vs. (4.01 ± 3.40), P < 0.05]. There was a positive correlation between Nrf2 and NOX4, Nrf2 and ROS, and NOX4 and ROS (r = 0.616, 0.411, 0.802, P < 0.05). Conclusion Benazepril may exert an anti-hepatic fibrosis effect by activating Nrf2 expression, or may inhibit the ROS-mediated oxidative stress in response to NOX4.

Objective To explore the protective role of lipoxin A4 (LXA4) during early process of atherosclerosis formation in rats with juvenile metabolic syndrome (MS).Methods Rat models of juvenile MS were established with 3-week Sprague-Dawley (SD) rats fed on high-carbonhydrates and high-fat diet for 6 weeks.The other qualified ones were randomly grouped into model group,LXA4 low-dose group,LXA4 middle-dose group,and LXA4high dose group,and a control group fed with normal forage.The low,middle,high-dose groups were injected different doses of LXA4 daily,while the model group and control group were injected with the same dose of isotonic NaCl solution for 2 consecutive weeks.After 2-week medication,the visceral adipose tissue were isolated by laparotomy and heart blood collected by thoracotomy under anesthesia,followed the fixation of thoracic and abdominal aortas in the immobilized rats.The mRNA expression level of inflammation cytokines interleukin-6 (IL-6),tumor necrosis factor-α (TNF-α),C-reactive protein (CRP) in the adipose tissue were determined by semi-quantitative reverse transcription PCR (RT-PCR),respectively.Secretions of IL-6,and TNF-α in serum were determined by enzyme linked immunosorbent assay (ELISA).Immunocytochemistry was used to label endomembrane and middle-membrane of thoracic aorta,and endothelial cell layer in each group and the ratios of thickness of endomembrane and middle-membrane were compared.Results Compared with the control group,weight,body length and abdominal circumference of juvenile MS rats increased significantly (all P ＜ 0.05),and levels of fasting plasma glucose (FPG),triglyceride (TG),high density lipoprotein cholesterol (HDL-C) and insulin in models increased significantly (P ＜ 0.05).RT-PCR showed that the mRNA expressions of inflammatory cytokines IL-6,TNF-α and CRP in adipose tissue in model rats were upexpressed (all P ＜ 0.05).Compared with model rats,mRNA of IL-6,TNF-oα,and CRP in mid,high-dose rats were downexpressed (all P ＜ 0.05),mRNA of TNF-α in low-dose rat downexpressed (all P ＜ 0.05),and there were no significant differences between mRNA expressions of IL-6,CRP in low-dose and model rats according to statistics (all P ＞0.05).Compared with control group,inflammatory cytokines IL-6,TNF-α secreted in serum of model rats were increased significantly (all P ＜ 0.05),and inflammatory cytokines secreted in serum of intervention rats were decreased significantly compared with model rats (P ＜ 0.05).Pathological changes were as follows:HE staining:compared to model group,aortic tunica intima of model rats were remarkably thickened and endothelial cell layer was fragmented and incomplete,which was attenuated in each intervention group.The ratios of endomembrane and middle-membrane in rats:at the end of consecutive medication for 2 weeks,the ratios of endomembrane and middle-membrane in model rats were significantly greater than those of control group (P ＜ O.05),and the ratios of endomembrane and middle-membrane in high-dose intervention rats were significantly smaller than those of the model group (P ＜ 0.05),but still greater than control group,while there were no statistical differences between the ratios in low,middle-dose intervention rats and model rats (P ＞ 0.05).Conclusions The increasing inflammatory cytokines are involved in early process of atherosclerosis formation in rats with juvenile MS.LXA4 by reducing the expression of inflammatory factor level in adipose tissue,thereby reducing the inflammatory cytokines in serum,alleviate the damage of arterial wall.

Objective: To study the outcome of perforator flap combined with mesh in repairing cicatricial abdominal hernia after deep burn. Methods: From June 2000 to June 2016, 11 cases of cicatricial abdominal wall hernia after deep burn were treated. 8 cases were caused by electrical burn, 2 cases by stove burn and 1 case by molten iron burn. All of them were Ⅳ degree burn of abdominal wall. The overall treatment time was 1-11 years, with the average of 4.1 years. The hernias were 6 cm × 6 cm to 12 cm × 11 cm in size. The abdominal wall hernia was repaired following the process of scar excision, mesh and perforator flap transfer and defect repairment. 3 kinds of mesh materials were used, polypropylene mesh (n=7), composite mesh (n=2), and acellular allogenic dermis (n=2). The size of meshes ranged from 8 cm ×8 cm to 16 cm ×13 cm. Meanwhile, paraumbilical perforator flaps were used in 5 patients, and anterolateral thigh perforator flaps were 6. The flaps were 18 cm ×10 cm to 22 cm ×13 cm in size. Results: All 11 cases of abdominal wall hernia were repaired. Follow-up period was 6 months to 2 years. There was no recurrence was found. The shape of the flap was satisfying. Conclusions The perforator flap combined with mesh is a good method to repair cicatricial abdominal wall hernia after deep burn.

Objective: To explore the methods and effects of wound repair and functional reconstruction of high-voltage electrical burns in wrists. Methods: From January 2009 to June 2016, 71 patients with high-voltage electrical burns in wrists were hospitalized, with 118 wrist wounds including 21 of type Ⅰ, 69 of type Ⅱ, 9 of type Ⅲ, and 19 of type Ⅳ. According to the wrist injuries, different surgical operations were performed. Forearm amputation was conducted in 20 wrists with necrosis in the distal end. On the basis of fasciotomy for decompression, early debridement was performed on the other 98 wrist wounds. After debridement, wounds with area ranging from 10 cm×7 cm to 30 cm×18 cm were repaired with tissue flaps with abundant blood supply. Thirty-two wounds were repaired with pedicled groin flaps, 11 wounds with pedicled paraumbilical flaps, 3 wounds with pedicled anterolateral thigh island flaps, 9 wounds with combined abdominal axial pattern flaps, 37 wounds with free skin flaps or myocutaneous flaps, and 6 wounds with flow-through descending branch of lateral femoral circumflex artery flaps, with tissue flap area ranging from 12 cm×8 cm to 34 cm×20 cm. Ulnar artery or radial artery vascular reconstruction was performed in 20 wrist wounds. Forty-one donor sites were sutured directly, while 14 were closed by thin split-thickness skin grafts from same-side thighs, and 43 were closed by thin split-thickness skin grafts from opposite-side thighs. Fifty-three wrist wounds were performed with tendon and nerve repair surgery, of which 20 were performed with simple tendon and nerve release surgery. Flexor digitorum profundus tendons and (or) flexor pollicis longus tendons were reconstructed with autologous or allogeneic tendon transplantation in 33 wrist wounds, and the median nerve was repaired with sural nerve graft in 21 wrist wounds. In 6 to 24 months after the last operation, tendon function of 53 wrist wounds which had tendon repair was evaluated with finger total active motion (TAM) method, while median nerve function of 21 wrist wounds which had median nerve repair was evaluated with integrate estimation method. Results: (1) After forearm amputation, the incisions of 20 wrists with necrosis in the distal end were healed. (2) Among the 98 tissue flaps, 90 had good blood flow, while 8 had distal necrosis, of which 6 were healed after necrotic tissue removal and skin grafting, and two were sutured directly after debridement. Infection occurred under 7 flaps, of which 3 were healed by dressing change, and 4 were healed after second debridement. Twenty wrist wounds which had radial artery or ulnar artery repair had good blood supply of hand and amputation was avoided. During follow-up of 1 to 3 years, the incisions and flaps of patients who had tissue flap repair surgery healed well. (3) The excellent and good rate of TAM in each finger of the corresponding affected limbs of 53 wrist wounds which had tendon and nerve repair surgery was 51%. (4) Twenty wrists which had simple tendon and nerve release surgery were followed up for 1 to 2 years. The strength of muscle dominated by the median nerve was restored to grade Ⅴ in 1 wrist, grade Ⅳ in 3 wrists, and grade Ⅲ in 2 wrists. The strength of muscle dominated by the ulnar nerve was restored to grade Ⅳ in 3 wrists, with no recovery in other wrists. Sensory function examination showed grade S0 in 4 wrists, grade S1 in 2 wrists, grade S2 in 3 wrists, grade S3 in 8 wrists, and grade S4 in 3 wrists. Twenty-one wrists which had median nerve repair were followed up for 1 to 2 years. There was no recovery in muscle strength dominated by the median nerve. Sensory function examination showed grade S0 in 3 wrists, grade S1 in 5 wrists, grade S2 in 8 wrists, and grade S3 in 5 wrists. Conclusions It is a good method to sequentially conduct early fasciotomy for decompression, early debridement, vascular reconstruction, transplant of tissue flap with abundant blood supply, tendon and nerve repair in repairing electrical burn wounds of wrists, avoiding amputation, and reconstructing hand function according to the condition of electrical burns of wrists.

Objective: To investigate the effects of angiotensin II type 1 receptor antagonist valsartan on leptin, leptin receptor and collagen in rats with hepatic fibrosis. Methods: Thirty-six male wistar rats were randomly divided into control group, model group and drug-treated group, with 12 rats in each group. Liver fibrosis models were made by subcutaneous injection of carbon tetrachloride on the dorsal of the rats, simultaneously gastric gavage with Valsartan and were killed at the end of 8th week. The degree of liver fibrosis was observed by HE and Masson staining. The serum leptin (LP) and TGFβ1 were determined by ELISA. Liver LP mRNA and leptin receptor mRNA (OB-R mRNA) were detected by RT-PCR. Liver LP, OB-R and collagen I were detected by Western blot. The data of multiple groups were analyzed by one-way analysis variance (ANOVA), and linear correlation was performed between serum LP and TGF β1. Results: After the intervention of valsartan, HE and Masson staining showed that the degree of liver fibrosis was significantly reduced. The levels of serum LP and TGFβ1 in the control group were (18.92 ± 7.10) ng/ml and (9.13 ± 1.58) pg/ml respectively, which were significantly lower than those in the model group (46.92 ± 28.54) ng/ml and (16.39 ± 3.56) pg/ml, And (29.27 ± 7.27) ng/ml and (12.24 ± 2.94) pg/ml in the drug-treated group, respectively. The F values were 7.864 and 20.057 respectively. The P values were < 0.05. The differences were statistically significant. The relative expression levels of LP and OB-R mRNA in the control group were 0.35 ± 0.18 and 0.62 ± 0.18, respectively, which were significantly lower than those in the model group (1.79 ± 1.79 and 1.52 ± 1.44, and drug-treated group 0.48 ± 0.34 and 0.75 ± 0.26, respectively), F values = 6.914,3.894, P values were < 0.05, the differences were statistically significant. The relative expression levels of LP, OB-R and collaten I in liver were 0.71 ± 0.13, 0.81 ± 0.11 and 0.76 ± 0.13 in the model group, 0.97 ± 0.06, 1.04 ± 0.06, and 1.05 ± 0.04 respectively in the drug-treated group and 0.74 ± 0.05, 0.93 ± 0.05 and 0.91 ± 0.05. The F values were 15.425, 13.757 and 19.130 respectively in three groups (P < 0.001), the difference was statistically significant. Conclusion Valsartan, an angiotensin II type 1 receptor antagonist, can reduce the expression of leptin and leptin receptor, reduce the production of TGFβ1 and collaten I, and play an anti-hepatic fibrosis effect.