Objective To investgate the effect of Tiao qi xing shui decoction combined with peritoneal injection DDP and IL-2 on Bax,Caspase-3, TGF-β1 gene expression in mouse with ascetes hepatoma,and explore its mechanism from molecular biology.Methods 72 pure lines of Kunming mice were randomly divided into control group,Chinese medicine group,combination of traditional Chinese and Western medicine,in high,middle,low dose group and Western medicine group,each had 12.All mices were killed after treatment,and the expression of Bax,Caspase-3,GF-β1 protein in mouse liver tumor tissues were detected by Immunohistochemical. Results Immunohistochemical results showed that,the positive expression of apoptosis gene Bax protein in high dose group of TCMand Western Medicine was higher than that of control group(P<0.01),and the positive expression of apoptosis gene Caspase-3,TGF-β1 protein in high and middle dose group of TCMand Western Medicine were higher than that of control group(P<0.01).Conclusion The high dose group of TCM and Western Medicine can significantly increase the expression of Bax protein,the high and middle dose guoup of TCMand Western Mdicine can significantly increase the expression of Caspase-3,TGF-β1 protein,induction apoptosis.

Objective Platelet aggregation, activation induced by bubbles is the main cause of decompression sick-ness.Clopidogrel(Clo) can decrease platelet aggregation through inhibiting the bind of fibrinogen and ADP .This study is designed to find if Clopidogrel can paly a protective role in decompression sickness and explore the intervention mechanism . Methods Totally 111 male SD rats divided into 3 groups:normal control group (n=20), decompression sickness(DCS) group(n=46), and DCS+Clo(Clopidogrel)treated decompression sickness (DCS+Clo)group(n=45).The rats in DCS and DCS+Clo group were placed in chamber and compressed to 1.5 MPa at speed of 2t/4 , the time of compression and res-idence was 4.5 min totally, then decompressed to surface at a speed of 3 m/s.The mortality and behavioral of rats were ob-served within 30 min post decompression .The pathology and the wet/dry ratio of lung , WBC and platelet counts in periph-eral blood, the expression of activated platelets , and immunohistochemical detection of lung tissue CD 41 expression were also been tested .Results We found Clo reduces the DCS mortality risk ( mortality rate:11/45 in DCS+Clo group vs 28/46 in DCS group, P<0.01).Clo reduced the lung injury, the wet/dry ratio of lung, the accumulation of platelet and leu-kocyte in lung , the WBC counts and activated platelets in peripheral blood .Conclusion Clo can play a protective role in decompression sickness through reducing post-decompression platelet consumption and activation , decreasing the activation of leukocytes .

MicroRNAs(miRNAs)are a class of small RNA molecules which play a pivotal role in the regulation of genes involved in diverse processes.Recently,many viral-encoded miRNAs have been discovered,which suggests that viruses also use this fundamental mode of gene regulation.Although the functions of most viral- encoded miRNAs are unknown,some of them are involved in evading CTL,mediating latent infection,apoptosis suppression,etc.Uncovering the role of viral miRNAs in the pathopoiesis offers an immense opportunity not only to develope effective antiviral therapies,but also to identifying novel molecular targets for developing antiviral reagents.Therefore,recent progress on vmiRNAs was reviewed.

MicroRNAs (miRNAs) are a newly identified class of non-protein-coding small RNAs that play important roles in multiple biological processes. Recent evidence indicates that the expression of many miRNAs is both temporally and spatially regulated by RNA editing, differential processing and tissue-specific enhancers, and the potential for ultimately designing molecular medicines based on the modulation of miRNAs seems good. A better understanding of the mechanism which regulates miRNAs is very helpful to reveal the pathogenesis of some diseases, discover novel molecular targets for treatment by interference, and develop an effective gene therapy. Therefore, the latest progress in the mechanism regulating miRNAs is summarized.

Adult ; Heart Aneurysm ; congenital ; Heart Atria ; pathology ; Humans ; Male

OBJECTIVE:To investigate effectiveness and safety of rh-endostatin in the treatment of keloid.METHODS:Sixty-four keloid patients in Nanchong Central Hospital during Jan.2015-Jan:2016 were divided into observation group and control group by random number table,with 32 cases in each group.Both group received fractional CO2 laser treatment.After surgery,control group was given antioxidant drug and antibiotics routinely.Observation group was additionally given Rh-endostatin injection 0.1-0.2 mg/cm2 via keloid body,once a month,for twice,on the basis of control group.Clinical efficacy,symptom score after laser treatment and 2 months after laser treatment,wound healing time,wound pigmentation area and keloid area before and after treatment,the occurrence of ADR were compared between 2 groups.RESULTS:There was no statistical significance in total re sponse rate (93.75％ vs.87.50％) and the incidence of ADR (15.63％ vs.12.50％) between observation group and control group (P＞0.05).There was no statistical significance in symptom score of control group between after laser treatment and after 2 months of treatment (P＞0.05).The erythema,edema and pigmentation scores of observation group were significantly lower than before treatment and control group,with statistical significance (P＜0.05);there was no statistical significance in skin itching and burning sensation score between 2 groups (P＞0.05).The wound incrustation time,decrustation time and wound healing time of observation group were significantly shorter than those of control group,with statistical significance (P＜0.05).Pigmentation area and keloid area of 2 groups were significantly smaller than before,and the observation group was significantly smaller than the control group,with statistical significance (P＜0.05).CONCLUSIONS:Rh-endostatin can alleviate erythema,edema,pigmenta tion and other symptoms effectively,shorten healing time,and inhibit pigmentation and keloid regeneration effectively with good safety.

OBJECTIVETo investigate the effect of different pressure oxygen pre-breathing in preventing decompression sickness of rats.

METHODSForty male SD rats were randomly divided into 4 groups: decompression sickness (DCS) group and three oxygen pre-breathing groups with 1 ATA, 2 ATA and 3 ATA pressure respectively. The rats of DCS group were placed in the hyperbaric chamber and the chamber was compressed evenly within 3 minutes to depths of 7 absolute atmosphere(ATA) and held at the designated depth for 60 min, then decompressed (3 min) at constant speed to the surface pressure. After that, the rats were taken out for further detection. While the rats of oxygen pretreatment groups pre-breathed different pressure oxygen for 20 min before entering into chamber. The mortality and behavioral of rats were observed with 30 min post decompression. The dry/wet ratio of the lung, protein levels in the bronchoalveolar lavage fluid (BALF), and the inflammatory cytokine tumor necrosis factor (TNF-alpha) expression were also tested.

RESULTSCompared with that of the DCS group, the mortality and morbidity of oxygen pre-breathe groups didn't change obviously. But the total BALF protein level and the inflammatory cytokine TNF-alpha expression of 1 ATA oxygen pre-breathe group were obviously decreased, while the dry/wet ratio of lung as obviously increased instead (P < 0.05).

CONCLUSIONAlthough preoxygenation can' t obviously change the mortality and mobidity of rats, normal pressure oxygen pre-breathing can mitigate the protein infiltration in BALF and the expression of inflammatory cytokine in lung tissue.

Animals ; Bronchoalveolar Lavage Fluid ; chemistry ; Decompression Sickness ; Diving ; Lung ; pathology ; Oxygen ; physiology ; Pressure ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; metabolism

Objective To study the expression levels of microRNA (miR)-16 and miR-146a in rat lungs of decompres-sion sickness (DCS) caused by fast buoyancy ascent escape or diving .Methods At 0.5 h after fast buoyancy ascent es-cape or diving, the pathological changes in rat lungs and expression levels of miR-16,and miR-146a were detected by re-verse transcription-quantitive polymerase chain reaction and compared with normal control group .Results The pathological characteristics of lungs in two DCS groups were tissue damage .At 0.5 h after DCS caused by fast buoyancy ascent escape , the lung tissue expression levels of miR-16 and miR-146a did not significantly change compared with normal control and diving DCS groups ,but the rat lung tissue expression level of miR-146 a in diving DCS group was obviously increased , com-pared with normal control group .Conclusion miR-146a may play a role in post-transcriptional regulation in the process of diving DCS .

Objective To study the pathological changes of lung tissues during fast floating escape-induced decompres-sion sickness.Methods Eighty male SD rats were randomly divided into 2 groups, 60 in fast floating escape group (escape group) , and 20 in control group .Rats in the control group were only put in a cabin under the same atmospheric pressure (ATM).Rats in escape group were pressurized to 1.5 MPa by pressure air at the 2t/7 exponential rate and stayed for 4 min till decompression.Then the rats′survival rate was observed after 0.5 h, lung tissue specimens were collected from each rat, the pathological score was taken , according to the degree of lung injury and the R language was used for statistical analysis.Results The mortality rate was 50%.Lung tissues of these rats were pathologically characterized by stromal lung thickening, edema, and hyperemia.Kruskal non-parametric test analysis found a significant difference (P=0.0016) between the two groups .Nemenyi test was used in pairwise comparison .The death and survival animals in escape group compared with the control group, the scores were significantly different (P<0.05).The scores had no significant difference between the deach and survival animal in escape group .Conclusion Decompression sickness caused by fast floating es-cape can significantly damage the blood-lung barrier to cause pulmonary edema .

Objective To observe the protection of carbachol on intestinal barrier function in patients with trauma. Methods A prospective randomized controlled trial was conducted. Seventy patients after trauma with a definite diagnosis of multiple organ dysfunction syndrome(MODS)from Department of Critical Care Medicine in Hebei United University Affiliated Hospital were included. According to random number table,the patients were divided into a carbachol treatment group(37 cases)and a mosapride citrate treatment group(33 cases),and all the patients in the two groups were treated by antibacterial drugs,supportive agents for organ function,surgery, etc symptomatic treatment. Based on the conventional treatment,in the carbachol treatment group,carbachol was administered through a stomach tube at the dose of 0.2 mg/kg,twice a day,and the dose was doubled if no exhaust or defecation persisted for 3 days after treatment,while in the mosapride group,mosapride citrate was given at the dose of 5 mg once and thrice a day,the therapeutic course of both groups being 7 days. On the 1st,3rd,5th, 7th day after admission,peripheral venous fasting blood in early morning was collected,the activity of diamine oxidase(DAO),expression rates of CD11b+and CD18+in polymorphonuclear neutrophil(PMN),contents of tumour necrosis factor-α(TNF-α)and interleukin-10(IL-10) were detected,and the clinical curative effects were observed. Results Compared to the mosapride citrate treatment group,the total effective rate was significantly higher in the carbachol treatment group on the 7th day after treatment〔70.3%(26/37)vs. 45.5%(15/33),P<0.05〕. The activity of DAO,expression rates of CD11b+and CD18+in PMN,contents of TNF-αand IL-10 in the carbachol treatment group were decreased with the extension of time,and reached valley values on the 7th day,the differences were statistically significant in the comparisons with those in mosapride citrate treatment group at the same time point〔DAO(mg/L):3.21±0.52 vs. 3.93±0.51,CD11b+:(14.89±2.16)% vs.(28.92±1.59)%,CD18+:(53.67±2.44)% vs. (72.46±4.08)%, TNF-α(ng/L):111.44±16.42 vs. 129.73±18.74, IL-10(ng/L):67.71±38.83 vs. 121.45±40.23,all P<0.05〕. At the various time points,the above indexes had no obvious changes in mosapride citrate treatment group. Conclusion Carbachol can ameliorate the ischemic/reperfusion(I/R)injury in patients with intestinal barrier dysfunction after trauma,decrease the release of inflammatory cytokines in vivo,and promote peristalsis of intestinal tract,therefore carbachol has clinical value of protecting intestinal barrier function.