ABSTRACT
On March 24, 2017, a patient with Von Hippel-Lindau syndrome (VHL) characterized by bilateral adrenal pheochromocytoma and pancreatic tumors was admitted to our hospital, who underwent simultaneous pancreatic body and tail tumor resection, bilateral adrenal tumor resection and Omentum transplantation of the right adrenal gland.Intraoperative hormone therapy was used. Part of the normal adrenal tissue was preserved and embedded in the omentum, but an adrenal crisis occurred on the first day after the operation.The hormone replacement was used. Postoperative hormone replacement therapy was performed for 6 months. After 4 years of follow-up, blood pressure was normal, no cortical dysfunction, no tumor recurrence or other related lesions appeared. The preserved part of adrenal tissue during simultaneous multi-organ tumor resection for such patients can reduce long-term hormone replacement after surgery and prevent late adrenal cortex dysfunction.
ABSTRACT
Objective@#To observe the effects of oxymatrine(OM) on the expression and release of high mobility group box 1(HMGB1) in rat pancreatic acinar cell line AR42J stimulated by hydrogen peroxide.@*Methods@#MTT method was used to detect the effects of H2O2 in different concentrations on the survival of AR42J cells. AR42J cells cultured in vitro were divided into control group, H2O2 group and H2O2+ OM group. An equal volume of H2O2(final concentration 0.16 mmol/L) was added in H2O2 group and H2O2+ OM group, respectively, while an equal volume of triple distilled water was added in control group. In H2O2+ OM group, OM(final concentration 0.5 g/L)was added 0.5 h before the addition of H2O2, and cell samples and supernatant were collected after 24 h culture. The expression of HMGB1 protein was detected by Western blotting, the level of HMGB1 protein in cell supernatant was detected by enzyme-linked immunosorbent assay, and the intracellular distribution of HMGB1 protein was detected by immunofluorescence.@*Results@#In the H2O2 group, the expression of HMGB1, the secretion of HMGB1 in the supernatant and the proportion of cytoplasmic HMGB1 in the total HMGB1 were significantly higher than those in the control group[1.04±0.04 vs 0.69±0.02, (4.84±0.13)μg/L vs (2.68±0.07)μg/L, (35.7±2.5)% vs (10.7±1.9)%], and all the differences were statistically significant (all P<0.05). After OM intervention, HMGB1 protein expression, secretion and cytoplasmic proportion were [0.82±0.02, (3.97±0.10)μg/L and (27.3±1.7)%], respectively, which were obviously lower than those in the H2O2 group, and all the differences were statistically significant (all P<0.05).@*Conclusions@#H2O2 can induce the expression and release of HMGB1 in rat pancreatic acinar cells; OM treatment could alleviate the severity of oxidative stress injuries induced by H2O2 in AR42J cells.
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ObjectiveTo systematically evaluate the clinical effect of epidermal growth factor receptor (EGFR)-targeted agents in the treatment of advanced pancreatic cancer. MethodsEMbase, PubMed, Cochrane Library, Clinical Trials, CNKI, Wanfang Data, and VIP were searched for randomized controlled trials (RCTs) of EGFR-targeted therapies for advanced pancreatic cancer. Eligible RCTs were screened out based on quality and related criteria, and RevMan 5.3 and STATA 12.0 were used to perform the meta-analysis. ResultsA total of 8 RCTs were included, with 2382 patients in total. The results of the meta-analysis showed that compared with the control group, the experimental group had no increases in overall survival time (hazard ratio ［HR］=0.86, 95% confidence interval ［CI］: 0.74-1.02, P＞0.05) and objective response rate (risk ratio ［RR］=1.00, 95%CI: 0.76-1.32, P＞0.05), but had significant increases in progression-free survival time (HR=0.78, 95%CI: 0.62-0.98, P＜0.05) and disease control rate (RR=1.22, 95%CI: 1.04-1.43, P＜0.05). The subgroup analysis showed that after the source of heterogeneity was identified and the studies with high heterogeneity were excluded, the experimental group had a significant increase in overall survival time (HR=0.85, 95%CI: 0.77-0.94, P＜0.05), and the patients with rash appeared to be more sensitive to the therapies (HR=0.70, 95%CI: 0.54-0.92, P＜0.05). ConclusionFor patients with advanced pancreatic cancer, EGFR-targeted therapies can effectively prolong overall survival time and improve quality of life.
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Objective:To observe the effects of oxymatrine(OM) on the expression and release of high mobility group box 1(HMGB1) in rat pancreatic acinar cell line AR42J stimulated by hydrogen peroxide.Methods:MTT method was used to detect the effects of H 2O 2 in different concentrations on the survival of AR42J cells. AR42J cells cultured in vitro were divided into control group, H 2O 2 group and H 2O 2+ OM group. An equal volume of H 2O 2(final concentration 0.16 mmol/L) was added in H 2O 2 group and H 2O 2+ OM group, respectively, while an equal volume of triple distilled water was added in control group. In H 2O 2+ OM group, OM(final concentration 0.5 g/L)was added 0.5 h before the addition of H 2O 2, and cell samples and supernatant were collected after 24 h culture. The expression of HMGB1 protein was detected by Western blotting, the level of HMGB1 protein in cell supernatant was detected by enzyme-linked immunosorbent assay, and the intracellular distribution of HMGB1 protein was detected by immunofluorescence. Results:In the H 2O 2 group, the expression of HMGB1, the secretion of HMGB1 in the supernatant and the proportion of cytoplasmic HMGB1 in the total HMGB1 were significantly higher than those in the control group[1.04±0.04 vs 0.69±0.02, (4.84±0.13)μg/L vs (2.68±0.07)μg/L, (35.7±2.5)% vs (10.7±1.9)%], and all the differences were statistically significant (all P<0.05). After OM intervention, HMGB1 protein expression, secretion and cytoplasmic proportion were [0.82±0.02, (3.97±0.10)μg/L and (27.3±1.7)%], respectively, which were obviously lower than those in the H 2O 2 group, and all the differences were statistically significant (all P<0.05). Conclusions:H 2O 2 can induce the expression and release of HMGB1 in rat pancreatic acinar cells; OM treatment could alleviate the severity of oxidative stress injuries induced by H 2O 2 in AR42J cells.