ObjectiveTo investigate the influence of heat shock protein A2 (HSPA2) on the biological behavior of pancreatic adenocarcinoma cells and its mechanism. MethodsThe expressions of HSPA2 were determined in the human pancreatic adenocarcinoma cell lines (PANC-1, BxPC-3, and AsPC-1) using the Western blot. Subsequently, the cells with the lowest and highest HSPA2 expressions among these three lines were selected for conducting overexpression and knockdown experiments targeting HSPA2, respectively. The cellular proliferation, cell clonogenesis, migration, and invasion capabilities were assessed using MTT, clonogenic assay, and Transwell assay, respectively. Additionally, the impact of HSPA2 on the expression of key markers of epithelial-mesenchymal transition (EMT) was examined using the Western blot. The potential target molecules of HSPA2 were identified through immunoprecipitation assay and mass spectrometry. The rescue experiments further explored the regulatory relation between the HSPA2 and its target molecules. The influence of HSPA2 on pancreatic adenocarcinoma growth was investigated through establishment of xenograft tumor model in nude mice. ResultsThe HSPA2 exhibited the lowest expression in the PANC-1 cells and the highest expression in the AsPC-1 cells among the three cell lines. Subsequent functional studies demonstrated that the overexpression of HSPA2 in the PANC-1 cells markedly promoted proliferation, cell clonogenesis, migration, and invasion, while the knockdown of HSPA2 expression in the AsPC-1 cells markedly inhibited these processes. The Western blot analysis further showed that the HSPA2 overexpression downregulated E-cadherin expression and upregulated N-cadherin and Vimentin expressiones, whereas the HSPA2 knockdown produced opposite effects. The rescue experiments indicated that the HSPA2 promoted the EMT in pancreatic adenocarcinoma cells by upregulating Yes associated protein (YAP). The subcutaneous xenograft tumor experiments in the nude mice showed that the HSPA2 knockdown inhibited tumor growth. ConclusionThe results of this study suggest that HSPA2 promotes EMT via upregulating YAP, which facilitates proliferation, migration, and invasion of pancreatic adenocarcinoma cells.
ObjectiveTo evaluate the predictive value of mini-fluid challenge for volume responsiveness in patients under shock.MethodsSixty patients diagnosed as shock were included in the study. A 50 mL infusion of physiological saline over 10 seconds and a further 450 mL over 15 minutes were conducted through the central venous catheter. Cardiac output (CO), global end-diastolic volume index (GEDVI), central venous pressure (CVP) and extravascular pulmonary water index (EVLWI) were monitored by the pulse indicator continuous cardiac output monitoring. If the increase of CO after 500 mL volume expansion (ΔCO500) ≥10%, the patient was considered to be with volume responsiveness. The relevance between ΔCO50 and ΔCO500 was analyzed, and the sensitivity and specificity of the ΔCO50 were analyzed by receiver operating characteristic (ROC) curve.ResultsAfter 50 mL volume injection, the heart rate and systolic blood pressure of the two groups did not change obviously. The CVP of non-responders changed slightly higher than that of responders, but neither of them had obviously difference (P>0.05). The CO of responders had increased significantly (P<0.05) which was in accord with that after a further 450 mL volume injection. GEDVI and EVLWI did not change significantly (P>0.05). ΔCO50 and ΔCO500 were strongly correlated (r=0.706, 95%CI 0.677 - 0.891, P>0.05). The area under ROC curve for ΔCO50 was 0.814 (95%CI 0.707 - 0.922).ConclusionThe volume responsiveness of patients under shock can be predicted by mini-fluid challenge study which is related to normal volume expansion and it does not increase the risk of pulmonary edema.
Objective To observe the expression of heat shock protein 70 (HSP70) in human liver after hepatic transplantation, and to study its correlation with the occurrence and progression of acute allograft rejection.Methods Fifteen biopsy specimen of allograft liver after transplantation were collected and divided into three groups according to their pathological changes: control group (no rejection), mild acute rejection group, and moderate/serious acute rejection group. The expressions of HSP70 in grafts were detected by using immunohistochemical method and imaging analysis. Results HSP70 was expressed in all 3 groups, and appeared mainly in hepatocellular cytoplasm. The immunohistochemical imaging analysis of HSP70 showed: integral optical density (IOD) which was 30.99±11.14 in the control group was lower than that in the mild acute rejection group (68.84±21.37) and that in the moderate/serious acute rejection group (71.82±19.99), P＜0.01； and the IOD in the moderate/serious acute rejection group was higher than that in the mild acute rejection group (P＜0.05). Conclusion HSP70 plays a role in cellular protection for allograft liver, and the continuously increasing expression of HSP70 in graft maybe closely relates to the occurrence and progression of acute allograft rejection.
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.
Cardiogenic shock (CS) describes a physiological state of end-organ hypoperfusion characterized by reduced cardiac output in the presence of adequate intravascular volume. Mortality still remains exceptionally high. Veno-arterial extracorporeal membrane oxygenation (VA ECMO) has become the preferred device for short-term hemodynamic support in patients with CS. ECMO provides the highest cardiac output, complete cardiopulmonary support. In addition, the device has portable characteristics, more familiar to medical personnel. VA ECMO provides cardiopulmonary support for patients in profound CS as a bridge to myocardial recovery. This review provides an overview of VA ECMO in salvage of CS, emphasizing the indications, management and further direction.
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 observe the influence of heat shock protein 27 (HSP27) sensibilization to retinal ganglion cells (RGC) apoptosis of rats.
MethodsThirty-five female Wistar rats were randomly divided into HSP27 sensibilization group (15 rats), borate buffer solution (BBS) control group (15 rats) and normal group (5 rats). The rats in HSP27 sensibilization group were received hypodermic injection in rear limb with 100 μg HSP27 and complete freund adjuvant, intraperitoneal injection with 1 μg pertussis toxin. The BBS control group received the same volume of BBS at the same site. The normal group received no intervention. The intraocular pressure was measured 3 days before injection and 1, 2, 4, 6, 8 weeks after injection. Four, 6 and 8 weeks after injection, the retinal frozen sections was made to observe RGC apoptosis by terminal-deoxynucleoitidyl transferase mediated nick end labeling. The anti-HSP27 level in serum and cerebrospinal fluid were detected by enzyme linked immunosorbent assay.
ResultsThere was no obvious change of intraocular pressure in rats in 3 groups before injection (P>0.05). RGC apoptosis was observed in HSP27 sensibilization group 4 weeks after injection, and increased significantly at 6 weeks after injection. There was no RGC apoptosis in BBS control group and normal group. The level of anti-HSP27 in serum and cerebrospinal fluid of HSP27 sensibilization group occurred at 4 and 6 weeks after injection respectively, decreased with prolongation of injection time. Compared with BBS control group and normal group, the RGC apoptosis rate, anti-HSP27 level in serum and cerebrospinal fluid of HSP27 sensibilization group were significantly increased (P<0.05). There was no significant difference of the RGC apoptosis rate, anti-HSP27 level in serum and cerebrospinal fluid between BBS control group and normal group (P>0.05).
ConclusionsHSP27 sensibilization could promote the RGC apoptosis. The variation trend of anti-HSP27 level in cerebrospinal fluid is consistent with the RGC apoptosis.
