Targeted cancer therapy is one of the modalities to increase efficiency and decrease adverse effects of chemotherapy,and the selection of drug vector system is of importance for targeted therapy.An ideal adriamycin targeted vector system should have maximal efficacy and minimal adverse effects in inhibiting cancer cells through different mechanisms.This article reviews the recent progress in adriamycin targeted therapy,including the modes of adriamycin administration,the selection of drug vectors,as well as other chemotherapeutic drugs in targeted therapy of liver carcinoma.

Objective To establish a method for determination of copper, manganese and cadmium in human urine by transversely heated GFAAS.Methods Matrix modifiers were used and background absorption was deducted, copper, manganese and cadmium in human urine were determined by transversely heated GFAAS after digestion.Results 5 g/L Mg(NO3)2 was taken as the matrix modifier when copper and manganese were determined and 0.3 g/L Mg(NO3)2 and 5 g/L NH4H2PO4 was taken as the matrix modifier when cadmium was determined.Under the designed standard conditions, the detection limits of copper, manganese and cadmium were 0.028-0.060 ?g/L;RSDs were 1.1%-5.1%;Recovery rates were 94.2%-107.5%.Conclusion The method is simple, accurate and sensitive, and is applicable to the determination of copper, manganese and cadmium in human urine.

Objective To investigate the changes of PTX3,NT -ProBNP level and the correlation between them and the prognosis of the patients with AMI combined T2DM.Methods 143 patients with primary AMI were enrolled,of which 63 patients with type 2 diabetes (observation group)and 80 patients with no diabetes (control group).Plasma PTX3 values were measured with ELISA method and NT -ProBNP was detected by the electrochemi luminescence method.All patients were observed for the occurrence of MACE during hospitalization and 12 months after discharge.The correlation between PTX3,NT -ProBNP concentration and occurrence of MACE in observation group were analyzed.Results The PTX3,NT -ProBNP concentration[(8.95 ±5.06)ng/mL,(1 609 ±1 049)pg/mL]in the observation group were significantly higher than those in the control group[(7.03 ±3.70)ng/mL,(1 198 ± 809)pg/mL](P =0.010,P =0.009);The number(n =26)of patients with occurrence of MACE in the observation group was significantly higher than 15 cases in the control group(P =0.003).In the observation group,the PTX3, NT -ProBNP concentration[(10.98 ±5.45)ng/mL,(2 007 ±1 097)ng/mL]in patients with MACE were signifi-cantly higher than those in patients without MACE[(7.53 ±4.28)ng/mL,(1330 ±930)ng/mL](P =0.007,P =0.010),and in MACE group,the PTX3,NT -ProBNP concentration[(13.88 ±6.84)ng/mL,(2 596 ±1 333)ng/mL] in patients with death weresignificantly higher than those in patients without death[(9.18 ±3.52)ng/mL,(1 639 ± 751)ng/mL](P =0.029,P =0.023).Conclusion More strong chronic inflammatory reaction and serious myocar-dial injury might occur in the patients with AMI combined and T2DM,and those patients would have poorer prognosis. The combined detection of PTX3,NT -ProBNP has an important significance in evaluating of the degree of myocardial damage and the prognosis of the patients with AMI combined T2DM.

Objective:To construct the pET30a-EgG1Y162-2 prokaryotic expression plasmid and induce the expression of EgG1Y162-2 protein, so as to provide a research basis for development of Echinococcus granulosus vaccine. Methods:Using Echinococcus granulosus cDNA as a template, the target gene of EgG1Y162-2 was synthesized by PCR, and after digestion with restriction enzymes EcoRⅠ and Hind Ⅲ, it was connected to the prokaryotic expression vector pET30a to construct the recombinant plasmid pET30a-EgG1Y162-2. The recombinant plasmid was transformed into competent cell BL21 (DE3) and induced by isopropyl β-D-thiogalactoside (IPTG) to express a large number of proteins. The recombinant protein was purified by affinity chromatography. The purification level was analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), and the expression product was identified by Western blotting. Results:The recombinant plasmid pET30a-EgG1Y162-2 was successfully constructed. After inducting expression, the bacterial supernatant and the eluate were both at a relative molecular weight of about 15 × 10 3, and the protein antigen component eluted with 200 mmol/L imidazole was relatively pure. Western blotting results showed that the purified recombinant protein EgG1Y162-2 with His tag could be recognized by His monoclonal antibody. Conclusion:The pET30a-EgG1Y162-2 prokaryotic expression plasmid of Echinococcus granulosus is successfully constructed, and the recombinant protein of EgG1Y162-2 is induced to express, laying a foundation for further study on anti- Echinococcus granulosus vaccine.

AIM: To investigate the effect of gastrodin on the expression of brain-derived neurotrophic factor (BDNF) and interleukin-6 (IL-6) in the striatum of cerebral ischemia rats, and to explore the potential mechanism of gastrodin in treating cerebral ischemia. METHODS: The rats were randomly divided into four groups: normal, sham, model, and gastrodin groups, each consisting of 10 rats. After successful modeling using middle cerebral artery occlusion (MCAO), the gastrodin group received intraperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days. Pathological changes in striatal neurons were observed using Nissl staining. Immunohistochemistry was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum. Additionally, immunoblot analysis was performed to determine the expression levels of BDNF and IL-6 proteins in the striatum. RESULTS: Nissl staining revealed clear and intact structures of striatal neurons in the normal and sham groups, with tightly arranged cells. In the model group, the number of cells was significantly reduced compared to the sham group (P<0.01), and there was a noticeable cytosolic atrophy and loose cell arrangement. The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group (P<0.01), and there was also a significant improvement in cell morphology. The results of immunohistochemistry and immunoblot were consistent, and there was no statistically significant difference in BDNF and IL-6 protein expression between the normal group and the sham group (P>0.05). Compared to the sham group, the model group showed a decrease in the protein expression level of BDNF in the striatum on the ischemic side (P<0.01) and an increase in the protein expression level of IL-6 (P<0.05, P<0.01). In contrast, the gastrodin group showed an increase in the protein expression level of BDNF in the striatum on the ischemic side (P<0.05, P<0.01) and a decrease in the protein expression level of IL-6 (P< 0.05, P<0.01) compared to the model group. CONCLUSION: Gastrodin has a significant protective effect on striatal injury caused by cerebral ischemia, and its mechanism may be related to the up-regulation of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

Gastric cancer is a common malignant tumor with complex pathological mechanisms， a low early diagnosis rate， and a high mortality rate. However， surgical treatment， targeted therapy， and chemotherapy have their treatment limitations and toxic side effects. Therefore， exploring the pathogenesis and mechanism of gastric cancer and finding effective treatment methods are important. At present， researches has found that tumor epithelial cells exhibit individual differences in molecular characteristics and exhibit metabolic heterogeneity that affects cell phenotype and function. The interaction between metabolites and cytokines can inhibit the formation of the tumor immune microenvironment and promote malignant progression. Therefore， metabolic reprogramming is regarded as a key feature of tumors and plays an important role in the process of tumor occurrence and development. However， the continuous deterioration of gastric cancer may be closely related to changes in the energy metabolism of cancer cells. Gastric cancer cells may regulate the dysregulation of synthesis or decomposition pathways such as glucose metabolism， amino acid metabolism， lipid metabolism， and nucleotide metabolism and activate associated signaling pathways， key proteins， and genes， leading to proliferation， invasion， and metastasis of cancer cells. In recent years， there has been a close relationship between the effective intervention by traditional Chinese medicine in gastric cancer and the regulation of metabolic reprogramming. There has been some progress in the intervention research on effective ingredients and formulas of traditional Chinese medicine for cancer. This article summarized existing Chinese and foreign literature on how gastric cancer cells affect disease progression by regulating their related metabolic networks， such as glucose metabolism， amino acid metabolism， lipid metabolism， and nucleotide metabolism， as well as how effective ingredients and formulas of traditional Chinese medicine enhance anti-tumor effects through targeted metabolism. It reviewed metabolic reprogramming intervention in gastric cancer， providing a reference for research on metabolic reprogramming regulation by traditional Chinese medicine and new targets and strategies for the treatment and prognosis of gastric cancer.

Werner syndrome (WS) is a premature aging disorder that mainly affects tissues derived from mesoderm. We have recently developed a novel human WS model using WRN-deficient human mesenchymal stem cells (MSCs). This model recapitulates many phenotypic features of WS. Based on a screen of a number of chemicals, here we found that Vitamin C exerts most efficient rescue for many features in premature aging as shown in WRN-deficient MSCs, including cell growth arrest, increased reactive oxygen species levels, telomere attrition, excessive secretion of inflammatory factors, as well as disorganization of nuclear lamina and heterochromatin. Moreover, Vitamin C restores in vivo viability of MSCs in a mouse model. RNA sequencing analysis indicates that Vitamin C alters the expression of a series of genes involved in chromatin condensation, cell cycle regulation, DNA replication, and DNA damage repair pathways in WRN-deficient MSCs. Our results identify Vitamin C as a rejuvenating factor for WS MSCs, which holds the potential of being applied as a novel type of treatment of WS.
Animals ; Ascorbic Acid ; pharmacology ; Cell Cycle Checkpoints ; drug effects ; Cell Line ; Cellular Senescence ; drug effects ; DNA Damage ; DNA Repair ; drug effects ; DNA Replication ; drug effects ; Disease Models, Animal ; Heterochromatin ; metabolism ; pathology ; Humans ; Mesenchymal Stem Cells ; metabolism ; pathology ; Mice ; Nuclear Lamina ; metabolism ; pathology ; Reactive Oxygen Species ; metabolism ; Telomere Homeostasis ; drug effects ; Werner Syndrome ; drug therapy ; genetics ; metabolism