Chronic wound biofilms: diagnosis and therapeutic strategies / 中华医学杂志(英文版)

OBJECTIVE@#To review the diagnosis of chronic wound biofilms and discuss current treatment approaches.@*DATA SOURCES@#Articles included in this review were obtained from the following databases: Wanfang, China National Knowledge Infrastructure, PubMed, and the Web of Science. We focused on research published before August 2019 with keywords including chronic wound, biofilm, bacterial biofilms, and chronic wound infection.@*STUDY SELECTION@#Relevant articles were selected by carefully reading the titles and abstracts. Further, different diagnosis and clinical treatment methods for chronic wound biofilm were compared and summarized from the selected published articles.@*RESULTS@#Recent guidelines on medical biofilms stated that approaches such as the use of scanning electron microscopy and confocal laser scanning microscopy are the most reliable types of diagnostic techniques. Further, therapeutic strategies include debridement, negative pressure wound therapy, ultrasound, antibiotic, silver-containing dressing, hyperbaric oxygen therapy, and others.@*CONCLUSION@#This review provides the identification and management of biofilms, and it can be used as a tool by clinicians for a better understanding of biofilms and translating research to develop best clinical practices.

Chronic wound biofilms: diagnosis and therapeutic strategies / 中华医学杂志(英文版)

Objective@#To review the diagnosis of chronic wound biofilms and discuss current treatment approaches.@*Data sources@#Articles included in this review were obtained from the following databases: Wanfang, China National Knowledge Infrastructure, PubMed, and the Web of Science. We focused on research published before August 2019 with keywords including chronic wound, biofilm, bacterial biofilms, and chronic wound infection.@*Study selection@#Relevant articles were selected by carefully reading the titles and abstracts. Further, different diagnosis and clinical treatment methods for chronic wound biofilm were compared and summarized from the selected published articles.@*Results@#Recent guidelines on medical biofilms stated that approaches such as the use of scanning electron microscopy and confocal laser scanning microscopy are the most reliable types of diagnostic techniques. Further, therapeutic strategies include debridement, negative pressure wound therapy, ultrasound, antibiotic, silver-containing dressing, hyperbaric oxygen therapy, and others.@*Conclusion@#This review provides the identification and management of biofilms, and it can be used as a tool by clinicians for a better understanding of biofilms and translating research to develop best clinical practices.

Protective effect of Sestrin2 on apoptosis of dendritic cells induced by high mobility group box-1 protein / 解放军医学杂志

Objective To investigate the potential role of Sestrin2 (SESN2) in regulating the apoptosis of dendritic cells (DCs) induced by high mobility group box-1 protein (HMGB1).Methods DCs (the murine DC cell line DC2.4) were cultured with or without HMGB1 stimulation (cultured with 10ng/ml HMGB1 for 8,24 and 48 hours,or cultured with HMGB1 for 48 hours at different concentrations of 1,10 and 100ng/ml,respectively,n=4).The protein level of SESN2,cleaved-caspase-3 and Bcl-2 were analyzed with Western blotting.Localization of SESN2 in cells was observed under confocal laser microscope (LSCM).Cell apoptosis was analyzed with flow cytometry.In addition,DC2.4 cells were transfected with lentivirus containing SESN2 LV-RNA,SESN2 siRNA sequence expressing plasmids or blank vector (NC,NS,n=4).These cells were then stimulated with HMGB1 (100ng/ml)for 48 hours,and the apoptosis was accessed as mentioned above.Results Compared with the control group,the expression of SESN2 was obviously up-regulated after HMGB1 (10ng/ml) stimulation for 24 and 48 hours (P＜0.05).In a dose-dependent response,the expression of SESN2 was markedly enhanced in treatment with 1,10,100ng/ml HMGB1 for 48 hours (P＜0.05).Compared with the control group (7.35％ ± 1.33％),the percentage of apoptosis was significantly increased with 10,100ng/ml HMGB1 for 48 hours [(17.02％ ± 4.85％,17.48％ ± 4.04％,respectively,P＜0.05 or P＜0.01].After transfection,compared with blank vector group,the apoptosis of SESN2 siRNA group obviously elevated [(65.96％ ± 2.50％) vs.(50.01％ ± 2.07％),P＜0.05],and cleaved-caspase-3 expression significantly increased while Bcl-2 expression obviously decreased.In SESN2 LV-RNA group,the apoptosis significantly decreased [(35.57％ ± 1.69％) vs.(49.04％ ± 4.87％),P＜0.05],and cleaved-caspase-3 expression decreased and Bcl-2 expression obviously increased compared with blank vector group (P＜0.05).Conclusion SESN2 has a protective effect against HMGB 1 induced apoptosis of D C2.4 cells.

A study on the status and influencing factors of anxiety and depression among the people affected by leprosy / 预防医学

Objective To learn the status and influencing factors of anxiety and depression among the people affected by leprosy.Methods A total of 60 leprosy patients was enrolled.An investigation including questionnaire and two mental scales namely Self -Rating Anxiety Scale (SAS)and Self -Rating Depression Scale (SDS)were conducted.Results The rate of anxiety and depression was 41.67% (25 /60)and 21.67% (13 /60)respectively.There was no statistical difference on the rate of anxiety and depression between genders.Multiple logistic regression analysis showed that treatment status (OR =23.78,95%CI =2.13 -265.26),disability (OR =7.68,95%CI =2.01 -29.40)and income (OR =4.54,95%CI =1.05 -19.68)were the risk factors of anxiety,and disability (OR =34.77,95%CI =2.84 -425.07) and treatment status (OR =19.28,95%CI =1.86 -199.62)were the risk factors of depression.Conclusion The people affected by leprosy has a high level of anxiety and depression.Disability and treatment status were the major risk factors of anxiety and depression among the people.

Implementation effect analysis of Global Fund for Tuberculosis Control Project on designated hospital in Wenzhou City of Zhejiang Province / 上海预防医学

Objective] To analyze the implementation effect of the Global Fund for tuberculosis ( TB) control project on designated hospital , and provide basis and recommendation for TB control in Wenzhou City of Zhejiang Province . [ Methods] According to the data from the National TB Manage-ment Information System,quarterly reports of project were collected and analyzed . [Results] The X-ray check rate and sputum test rate of newly diagnosed patients both reached more than 97%.The registration rate of active pulmonary TB and smear-positive TB were 71.45 per 100 000 and 26.41 per 100 000.A total of 1 393 new smear-positive pulmonary TB cases were detected .The completion of case finding target for new smear-positive pulmonary TB was 119.67%.The cure rate and treatment success rate for new smear-positive cases were 88.08%and 90.52%.And 1 657 cases have accepted psychological support .The psychological support rates were 36 .05%.A total of 39 361 person times for TB cases received free liver function test , and the test rate was 100%. [ Conclusion ] This project was implemented well in Wenzhou , and obtained good achievement .The discovery of new smear-positive patients , treatment outcome , psychological support and free liver function test for TB patients have reached the project requirements .

Effect of high mobility group box-1 protein on immune cells and its regulatory mechanism / 中国应用生理学杂志

High mobility group box-1 protein (HMGB1), which is a nuclear protein, participates in chromatin architecture and transcriptional regulation. When released from cells, HMGB1 also plays a well-established role as a pro-inflammatory mediator during innate immune responses to injury. In the initial stage of injury, there is a release of large quantities of early pro-inflammatory mediators to initiate or perpetuate immune responses against pathogens, but this pro-inflammatory period is transient, and it is followed by a prolonged period of immune suppression. At present, several lines of evidences have suggested that HMGB1 is a late cytokine provoking delayed endotoxin morbidity, which may enhance the production of early proinflammatory mediators, and it can contribute potently to the activation of different immune cells and play a role in the development of host cell-mediated immunity. The biology of HMGB1 has been extensively studied as a pro-inflammatory cytokine of systemic inflammation, however, this review will attempt to provide a summary of the effects of HMGB1 on different immune cells and its regulatory mechanism in acute insults.

Calreticulin upregulation induced by hypoxic preconditioning relieves oxidative stress injury in rat cardiomyocytes / 生理学报

The present study was aimed to investigate whether calreticulin (CRT) was involved in the protective effect of hypoxic preconditioning (HPC) against oxidative stress injury in rat cardiomyocytes. Neonatal cardiomyocytes were prepared from Sprague-Dawley rats aged 24 h, and cultured in DMEM medium containing 10% fetal bovine serum. The cultured cardiomyocytes were randomly divided into 8 groups as follows: (1) hydrogen peroxide stress (H(2)O(2) group); (2) brief hypoxic exposure for 20 min to simulate HPC (HPC group); (3) hypoxic exposure for 20 min followed by normoxic reoxygenation for 24 h before hydrogen peroxide stress (HPC + H(2)O(2) group); (4) SB203580 (a specific inhibitor of p38 MAPK) + HPC + H(2)O(2) group; (5) CRT antisense oligonucleotide transfection (AS group); (6) AS + H(2)O(2) group; (7) AS + HPC + H(2)O(2) group; (8) control group. Morphological observation, lactate dehydrogenase (LDH) leakage and flow cytometry were employed to assess cell apoptosis and necrosis. RT-PCR and Western blot were used to detect CRT expression and activity of p38 MAPK. All experiments were repeated at least four separate times. The results obtained were as follows: (1) HPC relieved cell injury caused by H(2)O(2). Compared with that in H(2)O(2) group, the cell survival rate increased by 18.0% (P<0.05), apoptotic rate and LDH leakage in culture medium decreased by 19.4% and 53.0%, respectively (P<0.05) in HPC + H(2)O(2) group. (2) H(2)O(2) induced CRT over-expression (7.1-fold increase compared with control, P<0.05), while HPC resulted in mild CRT up-regulation (2.4-fold increase compared with control, P<0.05), suggesting that HPC can relieve the over-expression of CRT induced by H(2)O(2). (3) CRT AS transfection weakened the protection of HPC. Compared with that in HPC + H(2)O(2) group, the cell survival rate decreased by 4% (P<0.05), and apoptotic rate and LDH leakage in culture medium increased by 2.6% and 39.0%, respectively (P< 0.05) in AS + HPC + H(2)O(2) group. (4) The protection of HPC and HPC-induced upregulation of CRT were almost eliminated when SB203580 was administered before HPC. These results suggest that HPC up-regulates CRT expression through the p38 MAPK signaling pathway and protects cardiomyocytes from oxidative stress injury.

Hypoxic preconditioning induces endoplasmic reticulum stress-related cardioprotection mediated by p38 mitogen-activated protein kinase / 生理学报

Calreticulin (CRT), an important Ca(2+)-binding molecular chaperone in the endoplasmic reticulum (ER), and caspase-12, a pivotal molecule mediating ER-initiated apoptosis, are involved in the ER stress (ERS). Using primary cultured neonatal cardiomyocytes, CRT and caspase-12 expression and activation during hypoxic preconditioning (HPC) and hypoxia/reoxygenation (H/R) were studied to explore the role of ERS in cardioprotection by HPC. And by using SB203580 and SP600125 [the specific inhibitors of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK)] separately, the role of p38 MAPK in HPC-induced ERS was also detected. Neonatal cardiomyocytes were prepared from Sprague-Dawley rats aged 24 h, and cultured in DMEM medium containing 10% fetal bovine serum, and then randomly divided into six groups as follows: H/R, HPC+H/R, SB203580+HPC+H/R, SP600125+HPC+H/R, HPC and control groups. H/R was produced by 2-hour hypoxia/14-hour reoxygenation, and HPC by 20-minute hypoxia/24-hour reoxygenation. Morphological studies, estimation of lactate dehydrogenase (LDH) leakage and flow cytometry were employed to assess cell apoptosis and necrosis. CRT and caspase-12 expression and activation, levels of phospho-p38 MAPK and phospho-JNK were detected by Western blot. All experiments were repeated at least four separate times. The results obtained are as follows: (1) HPC relieved the cell injury caused by H/R. Compared with that in H/R group, cellso survival rate in HPC+H/R group increased by 6.4%, and the apoptosis rate and LDH leakage in the cell culture medium decreased by 6.6% and 70.0%, respectively. (2) H/R induced caspase-12 activation (33.2-fold increase in comparison with control) and CRT expression (8.1-fold increase in comparison with control). HPC itself resulted in mild CRT up-regulation (2.6-fold increase in comparison with control), but the extent of up-regulation was lower than that induced by H/R. HPC before H/R was found to relieve the over-expression of CRT induced by H/R (72.4% decrease), and to inhibit the activation of caspase-12 (59.6% decrease). (3) The protection of HPC and HPC-induced up-expression of CRT and inhibition of caspase-12 activation were almost eliminated when the inhibitor of p38 MAPK, not of JNK, was present before HPC. These results suggest that HPC protects the neonatal cardiomyocytes from severe ERS-induced apoptosis during sustained H/R through pre-invoking proper ERS response. Mild up-expression of CRT and inhibition of caspase-12 activation induced by HPC, which are important protection factors, are mediated by p38 MAPK, not by JNK.

Calreticulin expression increases during delayed cardioprotection induced by hypoxic preconditioning / 生理学报

Both in vivo and cultured cardiomyocyte experiments were performed to investigate the alteration of expression of calreticulin (CRT) during the delayed cardioprotection induced by hypoxic preconditioning (HPC) and the intracellular signal transduction mechanisms of the alteration. (1) Wistar rats were randomly divided into three groups: sham operation group (Sham), myocardial infarction (MI) group induced by left coronary artery ligation and HPC+MI group (4-hour HPC 24 h before MI). Twenty-four hours, 14 d and 28 d after left coronary artery ligation, myocardial function, infarction size and the area at risk were measured. Western blot was used to detect the expression of CRT, the activity of p38 mitogen-activated protein kinase (MAPK) and stress-activated protein kinase (SAPK). (2) Cultured cardiomyocytes from neonatal Sprague-Dawley (SD) rat were divided into six groups: hypoxia/reoxygenation (H/R), HPC, HPC+H/R, p38 MAPK inhibitor SB203580+HPC+H/R (SB+HPC+H/R), SAPK inhibitor SP600125+HPC+H/R (SP+HPC+H/R) and control. Survival rate and apoptosis rate of cardiomyocytes 6 h after H/R and activities of lactate dehydrogenase (LDH) in culture medium in each group were measured. Western blot was used to detect the expression of CRT and activities of p38 MAPK and SAPK. The results are as follows: (1) During in vivo experiment, compared with MI group, HPC significantly improved +dp/dt(max) and -dp/dt(max), reduced infarction size and the area at risk. HPC dramatically changed the expression of CRT. CRT expression in HPC+MI group was 206% of that in MI group (P<0.05) 24 h after infarction, especially in the area at risk. However, 28 d after operation, the expression of CRT decreased by 57%. Correlation analysis indicated a positive correlation between CRT expression and myocardial function (r=0.9867, P<0.05), and negative correlation between CRT expression and infarction size (r=-0.9709, P<0.05). (2) In cultured cardiomyocytes, HPC attenuated cell injury induced by H/R. CRT expression increased moderately to 222% of control (P<0.05) during HPC, but increased dramatically to 503% of control (P<0.05) after H/R. HPC reduced H/R-induced CRT up-regulation to 56% of that in H/R group (P<0.05). Correlation analysis indicated that CRT expression induced by HPC had a positive correlation with p38 MAPK activity (r=0.9021, P<0.05), but a negative correlation with SAPK activity (r=-0.8211, P<0.05). Both in vivo and in vitro results indicate that HPC protects myocardium from ischemia or H/R injury. p38 MAPK is possibly involved in the up-regulation of CRT induced by HPC, while SAPK has a negative influence.