Objective To investigate the effects of heat injured keratinocytes (KC) supernatant on the expressions of collagen type I, collagen type III, and matrix metalloproteinase 1 (MMP-1) of dermal fibroblasts (Fb). Methods KC and Fb were isolated and cultured. Then the models of heat injured KC and Fb were reproduced in vitro, respectively. The heat injured and normal culture supernatant were collected respectively at 12 hours, and formulated as a 50% concentration of cell-conditioned medium. According to the culture medium, Fb at passage 3-5 was divided into 3 groups. Normal Fb was cultured with the conditioned medium containing 50% heat injured KC culture supernatant (group A), the conditioned medium containing 50% normal KC culture supernatant (group B), and DMEM (group C), respectively. The cells in 3 groups were collected at 24 hours. In addition， the cells in group A were collected at 0, 1, 2, 6, 12, 24, and 48 hours， respectively. Normal Fb was cultured with the conditioned medium containing 50% heat injured Fb culture supernatant. Then, the cells were collected at 0, 1, 2, 6, 12, 24, and 48 hours, respectively. The mRNA levels of the collagen type I, collagen type III, and MMP-1 of Fb were measured by real-time fluorescent quantitative PCR techniques. Results At 24 hours after cultured with supernatant of heat injured KC，mRNA relative expression levels of collagen type I, collagen type III, and MMP-1 in group A were significantly higher than those in groups B and C (P lt; 0.05). The mRNA relative expression levels of collagen type I, collagen type III, and MMP-1 in group A gradually increased with time going, showing significant differences between 0 hour and 2, 6, 12, 24, and 48 hours (P lt; 0.05); significant differences were found between different time points after 2 hours (P lt; 0.05). After Fb was treated with supernatant of heat injured Fb, the mRNA relative expression levels of MMP-1 gradually decreased with time going, showing significant differences between 0 hour and 1, 2, 6, 12, 24, and 24 hours (P lt; 0.05); after 2 hours of culture, significant differences were found among different time points (P lt; 0.05). Conclusion Heat injured KC supernatant may regulate the mRNA expressions of collagen type I, collagen type III, and MMP-1 of Fb.
Objective To explore the effect of epidural analgesia for labor on maternal temperature and the newborns. Methods This randomized trial was performed in West China Second Hospital between December 2015 and July 2016. Fifty puerperants were randomly divided into epidural analgesia (EA) group (natural labor under EA, n=25) or the control group (natural labor using Ramaze breathing method, n=25). Maternal tympanic temperature was recorded once per hour after treating with painless labor or blank control. The serum interleukin-1 beta (IL-1β) and heat shock protein 70 (HSP70) level were measured from the blood of the umbilical cord after the delivery. Apgar scores of the newborns were also recorded. Results There was a significant difference in the temperature between EA and control group one hour after the treatment of painless labor [ (36.9±0.7) and (36.4±0.5)℃]. The level of serum IL-1β and HSP70 were significantly higher in EA group [IL-1β: (0.308±0.036) ng/mL; HSP70: 1.175±0.196] than those in the control group [IL-1β: (0.244±0.031) ng/mL; HSP70: 0.935±0.308] (P<0.05). However, no significant difference was found in the neonatal Apgar score (P>0.05). Conclusions The increase of maternal temperature is greater in the EA labor puerperants compared with that in the controls, which may be related to the increase of IL-1β and HSP70. No adverse effect of labor analgesia on new borns is found
ObjectiveTo investigate the inhibitory effect of heat shock protein 90 (HSP90) inhibitors of 17-propylene amino-17-demethoxy geldanamycin (17-AAG) combining with paclitaxel on human anaplastic thyroid cancer FRO cell line. Method①The proliferation inhibition rates of FRO cells were detected by mmethyl thiazolyl tetrazolium (MTT) assay in different concentration groups (17-AAG: 0.312 5, 0.625 0, 1.2500, 2.5000, and 5.0000 μmol/L; paclitaxel: 0.001 0, 0.0100, 0.1000, and 1.0000 μmol/L; combination group, 17-AAG: 0.625 0 μmol/L, paclitaxel: 0.001 0, 0.0100, 0.1000, and 1.0000 μmol/L) and at different time points (24, 48, and 72 hours). ②The change of cell cycle and apoptosis rates of FRO cells were detected in 17-AAG group (0.625 0 μmol/L), paclitaxel group (0.1000 μmol/L), and combination group (17-AAG: 0.625 0 μmol/L, paclitaxel: 0.1000 μmol/L) by flow cytometry at 24 hours after treatment. ③activity of Caspase-3 and Caspase-9 in FRO cells of 17-AAG group (0.625 0 μmol/L), paclitaxel group (0.1000 μmol/L), and combination group (17-AAG: 0.625 0 μmol/L, paclitaxel: 0.1000 μmol/L) was detected by Caspase-3 detection reagent box and Caspase-9 detection reagent box respectively. FRO cells of normal control group were treated without any drug, but culture solution. Results①The proliferation inhibition rates of FRO cells increased with the increase of concentra-tion (17-AAG, paclitaxel, combination of 17-AAG and paclitaxel), there was significant difference between any 2 groups (normal control group included), P<0.05. In addition, the proliferation inhibition rates of FRO cells in any concentration group (normal control group excluded) increased over time (24, 48, and 72 hours), there was significant difference between any 2 time points (P<0.05). The proliferation inhibition rates of FRO cells in combination group were all higher than those of 17-AAG group and paclitaxel group in condition of same time point and same concentration (P<0.05). The q value of combination group was higher than 1.15 at 3 time points in all concentration, that meant 17-AAG could increase the efficiency of paclitaxel. ②The apoptosis rate of FRO cells in normal control group was lower than those of 17-AAG group, paclitaxel group, and combination group (P<0.05), and apoptosis rate of FRO cells in combination group was higher than those of 17-AAG group and paclitaxel group (P<0.05). ③Activity of Caspase-3 and Caspase-9 of FRO cells in normal control group were lower than those of 17-AAG group, paclitaxel group, and combination group (P<0.05), and activity of Caspase-3 and Caspase-9 of FRO cells in combination group were higher than those of 17-AAG group and paclitaxel group (P<0.05). Conclusions17-AAG and paclitaxel can significantly inhibit the proliferation and induce the apoptosis of FRO cells. The combination of the two kinds of drugs may generate synergy, with dose-dependence effect.
Objective To review the advancement of heat shock protein 70 (HSP70) vaccine in alimentary canal cancer. Methods Related articles were reviewed. Results HSP70 can integrate with tumor special antigen to form HSP70 polypeptide compound. To activate the special and nonspecial immune response of body, HSP70 can participate in the process of tumor immunity as a “molecular partner”. Conclusion HSP70 has shown alluring perspective in the precaution and treatment of alimentary canal cancer.
Objective To retrospectively analyze the clinical characteristics of heat stroke (HS) and HS-acute kidney injury (AKI), analyze the risk factors leading to death in patients, and provide new ideas for the prevention and treatment of HS. Methods Patients with HS who visited 13 hospitals in Sichuan subtropical monsoon climate and HS high-incidence areas between July 2019 and September 2023 were retrospectively selected. According to whether in-hospital death or AKI occurred, the patients were divided into survival group and death group, AKI group and non-AKI group. According to serum creatinine level, patients in the AKI group were divided into AKI stage 1 group, AKI stage 2 group and AKI stage 3 group. The main clinical manifestations and important clinical data of the patients were analyzed, and the risk factors affecting the death of patients were analyzed by multivariate logistic regression. Results A total of 195 patients with HS and 115 patients with HS-AKI were included. The results of multivariate logistic regression analysis showed that AKI, abnormal coagulation function, nervous system injury, neutrophil/lymphocyte ratio, and D-dimer were independent risk factors for death (P＜0.05). The results of clinical characteristics analysis of HS-AKI showed that the mortality rate of patients with AKI stage 2 and AKI stage 3 was higher (P＜0.05). Conclusions AKI, abnormal coagulation function, nervous system injury, neutrophil/lymphocyte ratio, and D-dimer are independent risk factors for death in HS. Therefore, active treatment of patients with HS combined with AKI, abnormal coagulation function, and nervous system injury in the future will help reduce the risk of death in patients.
ObjectiveTo evaluate the efficacy and safety of heated humidified high-flow nasal cannula (HHHFNC) vs. nasal continuous positive airway pressure (NCPAP) in the treatment of neonatal respiratory distress syndrome (NRDS). MethodsThe PubMed, EMbase, The Cochrane Library (Issue 3, 2017), CBM, VIP, WanFang Data and CNKI were searched up to March 27th, 2017 to collect randomized controlled trials (RCTs) of HHHFNC vs. NCPAP for NRDS. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies. Then, meta-analysis was performed by RevMan 5.3 software.ResultsA total of 11 RCTs involving 1 104 patients were included. The results of meta-analysis showed that: 1) The HHHFNC group reduced the rate of reintubation (OR=0.56, 95%CI 0.32 to 0.98, P=0.04), shortened the time of assisted ventilation (MD=–11.12, 95%CI –13.31 to –8.93, P<0.000 01), hospitalization time (MD=–2.99, 95%CI –3.54 to –2.44, P<0.000 01) and neonatal aspiration of milk (MD=–17.82, 95%CI –21.19 to –14.45, P<0.000 01), shortened partial pressure of carbon dioxide at 48 hours (MD=–4.86, 95%CI –5.94 to –3.78, P<0.000 01), reduced the rate of frequent hemorrhoid (OR=0.32, 95%CI 0.12 to 0.90, P=0.03), the rate of abdominal distension (OR=0.17, 95%CI 0.09 to 0.30, P<0.000 01), the rate of injury of nose (OR=0.08, 95%CI 0.03 to 0.20, P<0.000 01), and the rate of head shape change (OR=0.03, 95%CI 0.00 to 0.23, P=0.000 7). 2) There were no significant differences between two groups in mortality rate, nosocomial infection rate, oxygen exposure time, arterial oxygen pressure and oxygen saturation at 48 hours, intraventricular hemorrhage, patent ductus arteriosus, retinopathy of prematurity, bronchopulmonary dysplasia and neonatal necrotizing enterocolitis, respectively. ConclusionCurrent evidence indicates that HHHFNC can reduce the rate of reintubation, shorten the time of assisted ventilation, length of hospital day and neonatal aspiration of milk, reduce the rate of frequent hemorrhoid, abdominal distension, injury of nose, head shape change. Due to the limitation of quantity and quality of included studies, the long-term follow-up results of HHHFNC for NRDS are needed to analyze with large-scale and multicenter RCTs.
Objectives To detect expressions of heat shock protein 70 (HSP70) and glial fibrillary acidic protein (GFAP) , and to estimate the post-injury interval after concussion of brain via the ratios of percentage of HSP70/GFAP-positive cells. Methods We established a brain concussion model of rat. Tissue levels of HSP70 and GFAP were determined by immunohistochemical staining at different time points after injury. Finally, the relationship between the ratio of percentage of HSP70/GFAP-positive cells and the post-injury interval was measured. Results The ratio of percentage of positive cells (increased from 7.15 to 11.73) and the percentage of HSP70-positive cells (P<0.05, compared with control group) increased, and the percentage of GFAP-positive cells did not change remarkably (P<0.05, compared with control group); the post-injury interval was between 0.5 hour and 3 hours. High ratio (>6.66) and high percentage of HSP70 and GFAP-positive cells (P<0.05, compared with control group) indicated the post-injury interval was between 3 and 12 hours. A low ratio (<6.66) and high percentage of HSP70 and GFAP-positive cells (P<0.05, compared with control group) suggested that the post-injury interval was later than 12 hours. Conclusion By analyzing the variation rule of the ratio of percentage positive cells after brain concussion, the post-injury interval after concussion of brain could be estimated.
Objective To study the expression of heat shock protein 47 (HSP47) and its correlation to collagen deposition in pathological scar tissues. Methods The tissues of normal skin(10 cases), hypertrophic scar(19 cases), and keloid(16 cases) were obtained. The expression ofHSP47 was detected by immunohistochemistry method. The collagen fiber content was detected by Sirius red staining and polarization microscopy method. Results Compared with normal skin tissues(Mean IOD 13 050.17±4 789.41), the expression of HSP47 in hypertrophic scar(Mean IOD -521 159.50±272994.13) and keloid tissues(Mean IOD 407 440.30±295 780.63) was significantly high(Plt;0.01). And there was a direct correlation between the expression of HSP47 and the total collagen fiber content（r＝0.386，Plt;0.05）. Conclusion The HSP47 is highly expressed in pathological scartissues and it may play an important role in the collagen deposition of pathological scar tissues.
Objective To detect the expression of heat shock protein 47 mRNA in pathological scar tissue by using real-time fluorescent quantitative reversetranscription-polymerase chain reaction (RT-PCR). Methods The tissues of normal skin(n=6), hypertrophic scar(n=6) and keloid(n=6) were adopted, which were diagnosised by Pathology Department. Based on fluorescent TaqMan methodology, the real-time fluorescent quantitative RT-PCR were adopted to detect the expression ofheat shock protein 47 mRNA. Results Compared with normal skin tissue（0.019±0.021）×105, the expressions of heat shock protein47 cDNA of hypertrophic scar tissue（1.233±1.039）×105 and keloid tissue（1.222±0.707）×105 were higher， being significant differences（Plt;0.05）. Conclusion A fluorescent quantitative method was successfully applied to detecting the expression of heat shock protein 47 mRNA. Heat shock protein 47 may play an important role in promoting the formation of pathological scar tissue.
Objective To investigate the expressions of heat shock protein 27 (HSP27), Bcl-2, and Bax proteins of the nerve cells after spinal cord ischemia/reperfusion injury (SCII) in rats and their relationship. Methods Seventy adult male Sprague Dawley rats (weighing, 200-220 g) were randomly divided into the sham operated group (sham group, n=35) and the SCII group (n=35). Only the left renal artery was exposed with no occlusion of the abdominal aorta in the rats of sham group. The left renal artery was exposed with occlusion of the abdominal aorta for 20 minutes in the rats of SCII group. At 4, 8, and 12 hours and at 1, 2, 3, and 5 days, reperfusion treatment was performed in 5 rats respectively, and then the spinal cord tissue was harvested to detect the expressions of HSP27, Bcl-2, and Bax protein of the nerve cells by using immunohistochemistry staining. Results The HSP27 began to express at 4 hours, reached the peak at 3 days, and decreased at 5 days in SCII group; significant differences were found between at 3 and 5 days and at the other time points (P lt; 0.05). The Bcl-2 expression increased at 4 hours, reached the peak at 1 day and maintained a high level at 2 days, and then gradually decreased; significant differences were found between at 1 and 2 days and at the other time points (P lt; 0.05). The Bax expression reached the peak at 12 hours and 3 days, and decreased at 5 days; significant differences were found between at 12 hours and 3 days and at the other time points (P lt; 0.05). A little expression of each protein was observed in sham group at different time points; the expressions of HSP27, Bcl-2, and Bax proteins in SCII group were significantly higher than those in sham group at different time points (P lt; 0.05). Conclusion There may be the time window of self repair after SCII. High expression of HSP27 has an obvious protective effect on the SCII in rat, by promoting the expression of the anti-apoptotic protein Bcl-2 and reducing the expression of the pro-apoptotic protein Bax so as to inhibit spinal cord cell apoptosis.