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.
ObjectiveTo investigate the expression of heat shock proteins 90α(HSP90α) in human hepatocellular carcinoma and the relationship between its expression and biologic behavior of tumor and prognosis. MethodsUsing the immunohistochemical SP method, HSP90α expression was detected in liver tissue from 10 normal individuals, 40 patients with hepatocellular carcinoma(HCC) and adjacent noncancerous liver tissues. ResultsThe positive expression rate of HSP90α was 10.0%,52.5%,72.5% in normal liver tissues,adjacent noncancerous liver tissues,hepatocellular carcinous tissues respectively. A significantly higher distribution of HSP90α positive expression in HCC tissues compared with adjacent noncancerous liver tissues and normal liver tissues was obtained （P＜0.05）. The positive expression of HSP90α in HCC was correlated with clinical stage, tumor differentiation, serosal condition and lymph node metastasis （P＜0.05）, but not to tumor number （P＞0.05）. It was also correlated with prognosis of HCC. The mean tumorfree survival of patients with HSP90α negative expression was 38.6 months while that of HSP90α positive expression was 25.5 months （P＜0.05）. ConclusionHSP90α is overexpressed in human hepatocellular carcinoma. HSP90α could be used as an indicator to judge the clinical stage, tumor differentiation, serosal condition, lymph node metastasis and prognosis of HCC.
Objective To study the advantages of heat and moisture exchangers compared with heated humidifiers in reducing the incidence of ventilator-associated pneumonia ( VAP) . Methods We searched PubMed as well as reference lists from publications to collect randomized controlled trials which comparing heat and moisture exchangers with heated humidifiers in preventing VAP for mechanically ventilated patients. Meta-analysis was performed using software Review Manager 5. 0. Results Fifteen randomized controlled trials were included. There was no difference in incidence of VAP among the patients managed with moisture exchangers or heated humidifiers ( OR1. 18, 95% CI [ 0. 96, 1. 44] ) . The subgroup of patients using moisture exchangers had lower VAP incidence compared with those using heated humidifiers without heated wire circuits ( OR 1. 39, 95% CI [ 1. 08, 1. 79] ) . There were no differences between the compared groups in mortality, length of intensive care unit stay, or duration of mechanical ventilation. Conclusion The available evidence indicates that moisture exchangers are superior to heated humidifiers without heated wire circuits, and not to heated humidifiers with heated wire circuits to prevent VAP.
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.
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 investigate the role and mechanism of heat shock protein 60 (HSP60) in induction of murine skin allograft tolerance. Methods At the age of 8-12 weeks, inbred female BALB/C (H-2d) mice (n=45) and CBA/N (H-2k)mice (n=15) were used as transplantation donors and C57BL/6 (H-2b) mice (n=60) as recipients. Recipients C57BL/6 (H-2b) mice were randomized into 4 groups (n=15). In group A, 1 cm × 1 cm Wolfe-Krause skin graft was excised from the back of BALB/C (H-2d) mice and hypoderma was scraped off aseptically, and then transplanted to the back of C57BL/6 (H-2b)mice. The method of skin transplantation in the other 3 groups was the same as to group A. In group B, C57BL/6 (H-2b) mice were treated with imcompleted Freund’s adjuvant (IFA) administration into the back 2 weeks before transplantation of BALB/C (H-2d) mice skin. In group C, C57BL/6 (H-2b) mice were administered HSP60 emulsified in IFA into the back 2 weeks before transplantation of BALB/C (H-2d) mice skin. In group D, C57BL/6 (H-2b) mice were treated with HSP60 emulsified in IFA into the back and followed by skin transplantation of CBA/N (H-2k) mice 2 weeks later. The delayed type hypersensitivity was determined 7 days after transplantation. One-way mixed lymphocyte reaction, the concentration of cytokines in the mixed lymphocyte reaction culture supernatant was determined 7 days and 25 days after transplantation. The survival time of skin allograft was observed. Results The survival time of skin allograft in groups A, B, C and D was 12.4 ± 0.5, 11.6 ± 0.8, 29.3 ± 2.6 and 27.6 ± 2.1 days, respectively. There was significant difference between groups A, B and groups C, D (P﹤0.05), while there was no significant difference between group A and group B as well as between group C and group D (P gt; 0.05). The counts of per minute impulse (cpm) of mixed lymphocyte reaction 7 days after transplantation in groups A, B, C and D was 12 836 ± 1 357, 11 876 ±1 265, 6 581 ± 573 and 6 843 ± 612, respectively. There was significant difference between groups A, B and group C and group D (P lt; 0.05), while there was no significant difference between group A and group B as well as between group C and group D (P gt; 0.05). The cpm of mixed lymphocyte reaction at 25 days after transplantation in group A, B, C and D was 13 286 ±1 498, 12 960 ± 1 376, 11 936 ± 1 265 and 12 374 ± 1269, respectively. There was no significant difference among 4 groups (P gt;0.05).The concentration of IL-10 in the mixed lymphocyte reaction culture supernatant in groups C, D were higher than that in groups A, B, and IL-2 and IFN-γ were lower than that in groups A, B 7 days after transplantation (P lt; 0.05), while there was no significant difference between group A and group B as well as between group C and group D (P gt; 0.05). There was no significant difference in cytokines among the 4 groups 25 days after transplantation (P gt; 0.05). The delayed type hypersensitivity in groups A, B, C and D 7 days after transplantation was 0.84 ± 0.09, 0.81 ± 0.07, 0.43 ± 0.05 and 0.46 ± 0.03 mm, respectively. There was significant differences between groups A, B and groups C, D (P lt; 0.05). While there was no significant difference between group A and group B as well as between group C and group D (P gt; 0.05). Conclusion HSP60 may play a role in induction and maintenance of murine skin allograft tolerance.
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.
By using biochemical assessment technique and histological examination,a comparative study of the cutaneous tissues in 16 patients with lymphedema of the lower extremity before and after the heating and bandage therapy, and it was noted thatthe heating and bandage therapy might:(1) the content of hydroxyproline in the affected skin would be decreased; (2) the thickness of skin was decreased and the water content was reduced; (3) the microcirculation of local tissues was enhanced, and (4) the activity of the macrophages was increased. In conjunction with the criteria of clinical observation, the action mechanism of heating and bandage therapy might be as follows: (1) improve the local microcirculation and enhance the resorption of tissue fluid and the protein, and (2) increase the activity of the macrophages, and minimize the extent of fibrosis of the affected tissues.
Objective To investigate the relationship of the expression between heat shock protein (HSP) 70 and 90, and Survivin and its effects on the proliferative activity in retinoblastoma (RB) cells. Methods Expression of Survivin, HSP70 and 90, and Ki-67 in conventional paraffin samples from 43 patients with RB and 6 healthy people was detected by streptavidin-biotin peroxidase (SP) immunohistochemical method. Ki67 labeling index was used to evaluate the proliferative activity in RB. Results In 43 cases of RB, positive expression of HSP70 and 90 and Survivin was found in 28 (65.12%), 37 (86.05%) and 27 (62.79%) cases, respectively. None of the 6 normal retinal tissue expressed HSP70, HSP90 or Survivin. Positive expression of Survivin was more frequent in positive expressions of HSP90 than that in negative expressions of HSP90 (P＜0.05). Ki67 labeling index was higher in positive expressions of HSP90 and positive expressions of Survivin than that in their negative expressions respectively (P＜0.05). Meanwhile, higher Ki67 labeling index was found in positive HSP90Survivin expressions than that in negative HSP90Survivin expressions and those cases where only HSP90 or Survivin was found (P＜0.05). Expression of HSP70 did not correlate with that of Survivin, nor had any significant effect on Ki67 labeling index (P＞0.05). Expression of HSPs and Survivin and Ki67 labeling index did not correlate with histological types (P＞0.05). Conclusion Expression of HSP90 correlates with that of Survivin in RB. Co-existence of Survivin and HSP90 probably plays an important role in the genesis of RB.