Objective To explore the protective effect and mechanism of miR-202-5p on acute respiratory distress syndrome(ARDS)-induced lung injury in neonatal rats.Methods Sixty newborn SD rats were randomly divided into six groups:the control group(intraperi-toneal injection of normal saline by tail vein),ARDS group(ARDS model established via intraperitoneal injection of 4 mg/kg lipopolysac-charide by tail vein),ARDS+miR-NC group(ARDS rats receiving 2 mg/kg miR-NC via tail vein injection once every 4 h,with intervention for 12 h),ARDS+miR-202-5p group(ARDS rats receiving 2 mg/kg miR-202-5p via tail vein injection once every 4 h,with intervention for 12 h),ARDS+miR-202-5p+ov-NC group,and ARDS+miR-202-5p+ov-ROCK1 group(ARDS rats receiving 2 mg/kg miR-202-5p once every 4 h,with intervention for 12 h;with 6 × 108 plaque-forming units control or overexpression ROCK adenovirus administered via tail vein 3 days before lipopolysaccharide injection).Real-time quantitative PCR was employed to measure miR-202-5p and ROCK1 mRNA expression in rat lung tissue.Hematoxylin and eosin staining was performed to assess pathological lung injury.The lung tissue wet-to-dry weight ratio was determined to evaluate pulmonary edema.Western blotting was utilized to analyze ROCK1,Toll-like receptor 4(TLR4),phosphorylated-nuclear factor κB(p-NF-κB)p65,and phosphorylated-inhibitor of nuclear factor-κBα(p-IκBα)protein expression in lung tissue.The interaction between miR-202-5p and ROCK1 was validated using dual-luciferase reporter gene experiments.Results miR-202-5p expression was significantly down-regulated in ARDS rat lung tissue,while overexpression of miR-202-5p ameliorated pathological injury and pulmonary edema in ARDS rats.ROCK1 mRNA was upregulated in ARDS rat lung tissue;however,overexpression of miR-202-5p decreased the expression of ROCK1 in lung tissue of ARDS rats,while overexpression of ROCK1 reversed the protective effect of overexpression of miR-202-5p on lung injury in ARDS rats.Furthermore,miR-202-5p overexpression suppressed TLR4,p-NF-κB p65,and p-IκBα protein expression in ARDS rat lung tissue,an effect that was reversed by ROCK1 overexpression.Dual-luciferase reporter gene experiments confirmed that miR-202-5p directly targets ROCK1 mRNA 3'UTR.Conclusion miR-202-5p ameliorates ARDS-in-duced lung injury in neonatal rats through targeted suppression of ROCK1 expression,with the underlying mechanism potentially involving inhibition of ROCK1-mediated TLR4/NF-κB signaling pathway activation.

Objective To explore the protective effect and mechanism of miR-202-5p on acute respiratory distress syndrome(ARDS)-induced lung injury in neonatal rats.Methods Sixty newborn SD rats were randomly divided into six groups:the control group(intraperi-toneal injection of normal saline by tail vein),ARDS group(ARDS model established via intraperitoneal injection of 4 mg/kg lipopolysac-charide by tail vein),ARDS+miR-NC group(ARDS rats receiving 2 mg/kg miR-NC via tail vein injection once every 4 h,with intervention for 12 h),ARDS+miR-202-5p group(ARDS rats receiving 2 mg/kg miR-202-5p via tail vein injection once every 4 h,with intervention for 12 h),ARDS+miR-202-5p+ov-NC group,and ARDS+miR-202-5p+ov-ROCK1 group(ARDS rats receiving 2 mg/kg miR-202-5p once every 4 h,with intervention for 12 h;with 6 × 108 plaque-forming units control or overexpression ROCK adenovirus administered via tail vein 3 days before lipopolysaccharide injection).Real-time quantitative PCR was employed to measure miR-202-5p and ROCK1 mRNA expression in rat lung tissue.Hematoxylin and eosin staining was performed to assess pathological lung injury.The lung tissue wet-to-dry weight ratio was determined to evaluate pulmonary edema.Western blotting was utilized to analyze ROCK1,Toll-like receptor 4(TLR4),phosphorylated-nuclear factor κB(p-NF-κB)p65,and phosphorylated-inhibitor of nuclear factor-κBα(p-IκBα)protein expression in lung tissue.The interaction between miR-202-5p and ROCK1 was validated using dual-luciferase reporter gene experiments.Results miR-202-5p expression was significantly down-regulated in ARDS rat lung tissue,while overexpression of miR-202-5p ameliorated pathological injury and pulmonary edema in ARDS rats.ROCK1 mRNA was upregulated in ARDS rat lung tissue;however,overexpression of miR-202-5p decreased the expression of ROCK1 in lung tissue of ARDS rats,while overexpression of ROCK1 reversed the protective effect of overexpression of miR-202-5p on lung injury in ARDS rats.Furthermore,miR-202-5p overexpression suppressed TLR4,p-NF-κB p65,and p-IκBα protein expression in ARDS rat lung tissue,an effect that was reversed by ROCK1 overexpression.Dual-luciferase reporter gene experiments confirmed that miR-202-5p directly targets ROCK1 mRNA 3'UTR.Conclusion miR-202-5p ameliorates ARDS-in-duced lung injury in neonatal rats through targeted suppression of ROCK1 expression,with the underlying mechanism potentially involving inhibition of ROCK1-mediated TLR4/NF-κB signaling pathway activation.

The high incidence of bleeding after peripherally inserted central catheter (PICC) catheterization increases the risk of puncture site infection and unplanned extubation. Hemostatic dressings should be used in the early stages of catheterization to reduce blood infiltration. However, new hemostatic dressings have various types and advantages, which makes them difficult to choose dressings for medical staff. This paper introduces the types and hemostatic characteristics of novel functional hemostatic dressings, reviews the hemostatic mechanism and hemostatic effect of chitosan, cyanoacrylate gum, alginate, gelatin sponge and oxycellulose dressings in PICC puncture respectively, and prospects the development of new functional hemostatic dressings. It is expected that future hemostatic dressings will move towards multifunctionality and compositeness.
Humans ; Bandages ; Catheterization, Peripheral/instrumentation* ; Hemorrhage/prevention & control* ; Hemostatics/therapeutic use*

Sacroiliac complex injuries are commonly seen in high-energy pelvic fractures. The injuries make a big difference in treatment patterns due to the diverse injury types, posing considerable challenges in formulating optimal treatment strategies, and hence are persistent clinical difficulties in orthopedic trauma. The clinical management of sacroiliac complex injuries presents several key challenges such as a non-negligible rate of missed diagnoses in associated vascular and visceral injuries, absence of standardized protocols for surgical approaches and reduction-fixation strategies across different injury patterns, and ongoing controversies regarding surgical indications and optimal timing for patients combined with concomitant lumbosacral plexus injuries. Currently, no systematic clinical guidelines are available for the diagnosis and treatment of sacroiliac complex injuries both domestically and internationally. To this end, the Pelvic and Acetabular Surgery Group, Orthopedic Branch, China International Exchange and Promotive Association for Medical and Health Care and Orthopedic Physician Branch, Chinese Medical Doctor Association organized a panel of domestic experts in the field to develop the Clinical guideline for the diagnosis and treatment of sacroiliac complex injuries ( version 2025), based on evidence-based medicine and adhering to the principles of scientific rigor, clinical applicability, and innovation. These guidelines provided 11 recommendations covering diagnosis, therapeutic principles and techniques, management protocols for lumbosacral plexus injuries, outcome evaluation, and postoperative rehabilitation pathways, etc., aiming to standardize the clinical management of sacroiliac complex injuries.

Sacroiliac complex injuries are commonly seen in high-energy pelvic fractures. The injuries make a big difference in treatment patterns due to the diverse injury types, posing considerable challenges in formulating optimal treatment strategies, and hence are persistent clinical difficulties in orthopedic trauma. The clinical management of sacroiliac complex injuries presents several key challenges such as a non-negligible rate of missed diagnoses in associated vascular and visceral injuries, absence of standardized protocols for surgical approaches and reduction-fixation strategies across different injury patterns, and ongoing controversies regarding surgical indications and optimal timing for patients combined with concomitant lumbosacral plexus injuries. Currently, no systematic clinical guidelines are available for the diagnosis and treatment of sacroiliac complex injuries both domestically and internationally. To this end, the Pelvic and Acetabular Surgery Group, Orthopedic Branch, China International Exchange and Promotive Association for Medical and Health Care and Orthopedic Physician Branch, Chinese Medical Doctor Association organized a panel of domestic experts in the field to develop the Clinical guideline for the diagnosis and treatment of sacroiliac complex injuries ( version 2025), based on evidence-based medicine and adhering to the principles of scientific rigor, clinical applicability, and innovation. These guidelines provided 11 recommendations covering diagnosis, therapeutic principles and techniques, management protocols for lumbosacral plexus injuries, outcome evaluation, and postoperative rehabilitation pathways, etc., aiming to standardize the clinical management of sacroiliac complex injuries.

With continuous improvement of people's living standards, great efforts have been paid to environmental protection. Among those environmental issues, soil contamination by petroleum hydrocarbons has received widespread concerns due to the persistence and the degradation difficulty of the pollutants. Among the various remediation technologies, in-situ microbial remediation enhancement technologies have become the current hotspot because of its low cost, environmental friendliness, and in-situ availability. This review summarizes several in-situ microbial remediation technologies such as bioaugmentation, biostimulation, and integrated remediation, as well as their engineering applications, providing references for the selection of in-situ bioremediation technologies in engineering applications. Moreover, this review discusses future research directions in this area.
Biodegradation, Environmental ; Humans ; Hydrocarbons ; Petroleum ; Soil ; Soil Microbiology ; Soil Pollutants

Objective To analyze the survival rate of HIV /AIDS patients receiving highly active antiretroviral therapy(HAART)since the implementation of the national Four Free and One Carepolicy against HIV in Hangzhou.Methods Clinical data of 2370 AIDS patients were collected from National AIDS Comprehensive Treatment Information System Treatment Library from 2004 to 2014.The data, including basic information,viral load,CD4 +T lymphocyte counts,starting time of treatment,WHO clinical stage,infection pathways and follow-up were respectively analyzed.Kaplan-Meier and Cox proportional hazards models were used to analyze the survival rate and the factors affecting survival.Results The total follow-up time was 3968.14 person years and 57 patients died in 2370 patients with a mortality rate of 1 .44 /100 person years (57 /3968.14).Kaplan-Meier method showed that the cumulative survival rates of the first,third and fifth year were 98.08%,96.20% and 95.24%,respectively.The overall mortality rate fell from 6.06 /100 person years in 2006 to 1 .44 /100 person years in 2014.The mortality rate of AIDS-related disease declined from 1 .10 /100 person years in 2009 to 0.90 /100 person years in 2014.Multivariate Cox regression analysis showed that the risk of death for patients with CD4 +T 200-349 cells/μL was 0.466 times(95%CI 0.246-0.882)as that for patients with CD4 +T cells <200 /μL.The risk of death was 3.408 times(95%CI 1 .365-8.506)in patients aged≥ 50 years,3.788 times(95%CI 1 .645-8.718)in patients aged 40 to <50 years,and 2.593 times(95%CI 1 .139-5.905)in patients aged 30 to 40 years as that in patients aged <30 years.The mortality risk for patients with baseline WHO stage Ⅲ and Ⅳ was 1 .960 times as patients with WHO stage Ⅰ and Ⅱ (95% CI 1 .117-3.439 ).Conclusions Patients with increased age,low CD4 +T counts and baseline WHO stage Ⅲ or Ⅳ are main risk factors affecting survival rate of HIV /AIDS patients,early antiviral therapy is the key for improving the survival rate of patients.

Objective To investigate the effete of chitosan on rabbit carotid artery internal jugular vein fistula intimal hyperplasia and its regulation on TLR4/NF-κB signaling.Methods A total of 28 New Zealand white rabbits were randomly divided into the control group(n=4),the model group(n=12) and the chitosan group(n=12).Model group and chitosan group rabbits were established respectively carotid artery internal jugular vein fistula models.After AVF surgery,chitosan was smeared on venous blood vessels and anastomosis.After 4,6 and 8 weeks,the rabbits were separately sacrificed and the AVF venous vascular tissues were taken.The pathological changes of AVF venous vascular tissue in each group were observed.The changes of α-SMA were detected by immunohistochemistry method.The mRNA expressions of PCNA and TLR4 in the tissues were measured by Real-time PCR.At the same time,the protein expressions of PCNA,TLR4,MyD88 and NF-κB were detected by Western blotting.The experimental data were processed by two-factor analysis of variance in statistics.Results (1) After 4 weeks,vascular intimal was thicked in mdel group.In intimal hyperplasia,α-SMA was staining,and then proliferation of vascular smooth muscle cell was significant.As time increasing,more intimal hyperplasia shown obviously,the expression of α-SMA significantly increased.Compared with model group,chitosan group significantly reduced the degree of intimal hyperplasia,the level of α-SMA was significantly decreased,vascular smooth muscle cell proliferation was also extraordinarily decreased.(2) Compared with control group,the expression levels of PCNA,TLR4,MyD88 and NF-κB increased with time.The indices of Chitosan group were markedly higher than control group,but significantly lower than model groups.Conclusion Chitosan can inhibit the proliferation of rabbit VSMCs.The mechanism may be concerned in down regulating TLR4-mediated signaling pathway,reducing the possibility of intimal hyperplasia of rabbit AVF venous blood vessels.

Objective To explore the effect of chitosan on vascular smooth muscle cells inhibited proliferation from rabbit arteriovenous fistula and its mechanisms.Methods Established rabbit fistula model on carotid arteryinternal jugular vein.After 1 month cultured VSMCs with primary culture by tissue-pieces inoculation.Cultured VSMCs were divided into three groups:①normal control group.②FBS-treated group:cell were treated with 5％,10％,20％ for 48 h,respectively; established the model of rabbit VSMCs proliferation.③chitosan-treated group:VSMCs cultured with 20％ FBS were exposed to different doses of chitosan(10,100,500,1000,2000μg/ml) for 48 h.And VSMCs were treated for different time (0,12,24,48 h) with Chitosan 1000 μg/ml.Expression levels of PCNA and TLR4/ NF-κB were detected by Western blotting.RT-PCR were applied to measure the mRNA expression of PCNA and TLR4.The protein levels of TLR4 and NF-κB were detected by immunofluorescence.Results Compared with low concentration serum group,FBS-treated VSMCs exhibited a increase in mRNA and protein expression of PCNA and TLR4.FBS-induced protein expression of PCNA and TLR4/NF-κB were reduced by chitosan.Also mRNA expression of PCNA and TLR4 were reduced.They were dependent on concentration and time.In rabbit VSMCs TLR4 was mainly expressed in the cytoplasm and NF-κB expressed mainly in the nucleus.Compared with normal control group,TLR4 and NF-κB protein expression were significantly decreased by chitosan.Conclusion High concentration serum induced VSMCs proliferation.Chitosan can inhibit the proliferation of rabbit VSMCs.It is speculated that the mechanism may be related to the expression of TLR4 receptor activation,reducing expression of downstream factor MyD88 and NF-κB.It is suggest that chitosan can become potential new drugs of arteriovenous fistula prevention of intimal hyperplasia.

To produce recombinant phospholipase A(1) (PLA(1)) by Escherichian coli, the pla gene encoding PLA(1) was amplified from Serratia liquefaciens by PCR and cloned into two vectors pET20-b(+) and pET28-a(+). The two recombinant plasmids were then transformed into E. coli BL21 (DE3) individually to express PLA(1). E. coli BL21(DE3)/pET28a-pla yielded extracellular PLA(1) with an activity of 40.8 U/mL in batch cultivations of shaken flasks by auto-induction, which was accounted for 91% of total enzyme activity. On the basis of primal auto-induction medium, the optimized fermentation medium of PLA(1) contained tryptone 10 g/L, yeast extract 5 g/L, glucose 0.8 g/L, lactose 5 g/L, Na2HPO4 25 mmol/L, KH2PO4 25 mmol/L and 1 mmol/L MgSO4 (final concentration). Glycine (7.5 g/L) was added 6 h after inoculated. After incubated at 37 degrees C for 24 h, extracellular enzyme activity reached 128.7 U/mL.
Cloning, Molecular ; Culture Media ; Escherichia coli ; genetics ; growth & development ; metabolism ; Fermentation ; Lactose ; pharmacology ; Phospholipases A1 ; biosynthesis ; genetics ; Recombinant Proteins ; biosynthesis ; genetics ; Serratia liquefaciens ; enzymology