Child ; Cleidocranial Dysplasia ; diagnosis ; diagnostic imaging ; Humans ; Male ; Radiography

Clinical studies have shown that trastuzumab combined with chemotherapy can significantly improve survival in treatment of HER2-positive metastatic breast cancer as well as in the neoadjuvant and adjuvant therapy for HER2-positive early breast cancer. In patients with HER2-positive and hormone receptor-positive metastatic breast cancer, adding trastuzumab to endocrine therapy improves treatment efficacy. Resistance to trastuzumab may be reversed by incorporating other targeted therapeutic drugs. Patients can still benefit from continuing trastuzumab after their disease progresses.

Aim To establish an animal model of uterine leiomyoma for pathogenesis research and drug screen analysis.Methods Guinea pigs were treated with estradiol benzoate 100 ?g?d~(-1),twice a week,by intramuscular injection for 12 weeks.After the animal were killed,the uteri were dissected out and ultrathin sections were obtained.Compare to that of human being,pathohistologic characteristics were observed under the microscope.Results The uteri treated with estrogen were proliferated and deformated.Uterine nodules were observed in many of the tested animals.According to the results of pathohistology,these cells demonstrate the features of smooth muscle-like cells.Conclusion The uterine leiomyoma induced by estrodiol in guinea pig is similar to that of human being.It has been suggested that the animal model is valuable for pathogenesis research and drug screen analysis,although it still needs more evidence to be demonstrated.

Adult ; Ear Canal ; pathology ; Ear Neoplasms ; Female ; Humans ; Neurofibromatoses

Newborn due to low birth weight caused by preterm or fetal growth restriction will have an adverse effect on kidney development. In adulthood,the long-term adverse effects of low birth weight are associ-ated with a variety of kidney disease. Current studies suggest that low birth weight may participate in a variety of kidney disease development and progression by affecting the nephron number,the function of the vascular struc-ture and the endocrine level. This paper mainly reviews the relationship between low birth weight and kidney dis-ease.

Gallstone disease is highly prevalent in clinic,particularly in women and some specific ethnic groups.The formation of water-insoluble cholesterol crystals is due to a misbalance between the three major lipids present in the bile:cholesterol,bile salts,and phospholipids.Many proteins implicated in biliary lipid secretion in the liver are regulated by several transcription factors,including nuclear receptors LXR and FXR.Human and murine genetic,pathophysiological evidence is consistent with the relevance of these nuclear receptors in gallstone formation.In addition,there is emerging data that also suggests a role for estrogen receptor ESR1 in abnormal cholesterol metabolism leading to gallstone disease.A better comprehension of the role of nuclear receptor function in gallstone formation may help doctors to design new and more effective therapeutic strategies for this highly prevalent disease condition.

Sepsis is a major cause of secondra y pancreatic injury in critically ill children.A lagr e number of inflammatoyr m ediators werer elesa ed after acute ijn ury of the pancreas,which may aggravate the inflammatory reaction and the stress reaction.Nuclear factor E2-related factor 2(Nrf2),an important protec-tive transcription factor,could activate the expression of more than 500 genes.Most of the genes have the function of cytoprotection.Studise have dem onts rated that Nrf2 plays a certain role in cytoprotection,such as regulating the inflammatory response,anti-oxidative stress,improving mitochondrial functoi n and decreasing toxic protein aggregation.This review explored the protective mechanism of Nrf2 in pancreatic injury caused by sepis s.

OBJECTIVE:To study the effects of celastrol on the proliferation and apoptosis of human hepatoma HepG2 cells, and investigate its mechanism. METHODS:CCK-8 method was used to determine the cell activity 24,48,72 h after treated by 2, 5,10 μmol/L celastrol,and the proliferation inhibition rate and half inhibitory concentration(IC50)were calculated;flow cytome-try was conducted to detect the cell apoptosis rate and cycle change 24 h after treated by 2,5,10μmol/L celastrol,and the DMSO was used as negative control;rhodamine 123 staining method was used to determine the mitochondrial membrane potential 48 h af-ter treated by 2,5,10 μmol/L celastrol,and the DMSO was used as negative control;Western blot was adopted to detect the pro-apoptotic related genes Bax and B lymphoma 2(Bcl-2)protein expressions 0,12,24,36 h after treated by 5 μmol/L celastrol. RESULTS:2,5,10 μmol/L celastrol can inhibit cell proliferation,IC50 was 5.834 μmol/L. 2,5,10 μmol/L celastrol can induce apoptosis;5,10 μmol/L celastrol can block cell in G0/G1,S phases,compared with negative control group,with significant differ-ences(P<0.05 or P<0.01),and the above effects all showing certain concentration-dependent manner. 5 μmol/L celastrol can in-crease Bax protein expression and decrease Bcl-2 protein expression after cultured for 12,24,36 h,showing certain time-depen-dent manner;compared with 0 h,there was significant difference(P<0.05 or P<0.01). CONCLUSIONS:Celastrol can obvious-ly inhibit the proliferation of human hepatoma HepG2 cells and induce their apoptosis,and the mechanism may be related with strengthening mitochondrial permeability and promoting the release of apoptosis-inducing factor.

Cancer cells frequently share biological characteristics and energy metabolic processes distinct from normal cells. The specific metabolic phenotype was originally known as the Warburg effect. Researchers later discovered that cancer cells prefer to synthesize fatty acid de novo . Moreover, key enzymes involved in fatty acid synthesis and β-oxidation are overexpressed in tumor tissues, with low or without expression in normal tissues. Abnormal fatty acid metabolism is related to the survival and invasiveness of cancer cells, indicating that abnormal fatty acid metabolism provides the crucial components and energy sources of cancer cells. In recent years, the specific phenotype of abnormal fatty acid metabolism and the exploration of the role of this metabolic alteration in cancer biology and therapeutic strategies targeting the fatty acid metabolic pathways have become attractive focuses in cancer research. The role of active fatty acid metabolism in tumorigenesis and development, as well as the research progress in the development of the specific inhibitors, is reviewed in this paper.

Glutathione (GSH) is the most important small-molecule, active oligopeptide in the maintenance of redox balance. GSH contributes to antioxidant and thiol equilibrium, as well as modulates the activities of many signaling molecules and redox-sensi-tive transcription factors by S-glutathionylation. Several studies have shown that the GSH level increased in various tumors. Additional-ly, increased GSH significantly contributes to drug resistance by eliminating ROS, detoxifying drugs, or participating in DNA repair. GSH-related metabolic enzymes are overexpressed in resistant cells, thereby regulating cellular response to chemotherapy drugs. Deple-tion of GSH or downregulation of GSH-related metabolic enzymes may effectively reverse drug resistance and promote resistant cells to restore sensitivity. This potential indicates that the GSH antioxidant system plays an important role in drug resistance. The GSH anti-oxidant system, as a potential target for antitumor therapy and reversal of drug resistance, has recently become an attractive focus in cancer research. This paper presents a review of the role of the GSH antioxidant system in drug resistance and discusses the therapeutic strategies targeting the GSH antioxidant system.