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.

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

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

Cutaneous wound healing is a complicated multiatep process with numerous mediators that act in a network of activation and inhibition processes. Nonhealing chronic wounds decrease the quality of Life. Recombinant growth factors, currently used in clinic, fail to provide a sustained repair function at the wound due to their inadequate biological availability and transient half-time. Recent attention has focused on gene therapy, which might become a significant treatment modality for those wound healing pathologies refractory to other wound management approaches. This review discusses the potentials and limitations of current genetherapy for the treatment of wounds, current ongoing clinical trials, and possible future directions in this exciting field.

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.

Objective To report a pedigree of generalized atrophic benign epidermolysis bullosa (GABEB),a special type of junctional epidermolysis bullosa(JEB). This is the first case report in China. Methods The clinical, histologic, electron microscopic, and immunofluorescence changes of the disease were evaluated. Results Besides the symptom of inherited epidermolysis bullosa, the patient had special clinical manifestations such as atrophic alopecia and dental dysplasia. The disease was inherited in an autosomal recessive mode in this pedigree. Electron－ microscopy found the fissure in lamina lucida, accompaning with dysplasia and sparse hemidesmosome. Immunofluorescence study did not show BPAg2 in the basement membrane zone, indicating that mutation in the gene encoding BPAg2 leading to the disease in this family. Conclusions The case is diagnosed as GABEB, a special type of JEB. Although GABEB has its characteristic, clinical manifestations, electron microscopy and immunofluorescence study are important for confirmative diagnosis and classification, and will guide the study of mutation detection.

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.

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.