Antineoplastic Agents, Hormonal ; therapeutic use ; Antineoplastic Agents, Phytogenic ; therapeutic use ; Breast Neoplasms ; drug therapy ; prevention & control ; secondary ; surgery ; Chemotherapy, Adjuvant ; methods ; Early Detection of Cancer ; methods ; Female ; Humans ; Tamoxifen ; therapeutic use ; Taxoids ; therapeutic use

Anthracyclines ; pharmacology ; therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Breast Neoplasms ; drug therapy ; metabolism ; Cisplatin ; administration & dosage ; Deoxycytidine ; administration & dosage ; analogs & derivatives ; Drug Resistance, Neoplasm ; Female ; Humans ; Taxoids ; administration & dosage ; Vinblastine ; administration & dosage ; analogs & derivatives

Aged ; Aged, 80 and over ; Breast Neoplasms ; epidemiology ; pathology ; physiopathology ; therapy ; China ; epidemiology ; Female ; Humans ; Middle Aged ; Treatment Outcome

Breast Neoplasms ; diagnosis ; therapy ; Chemotherapy, Adjuvant ; Combined Modality Therapy ; Female ; Humans ; Neoadjuvant Therapy

Antibodies, Monoclonal ; therapeutic use ; Antibodies, Monoclonal, Humanized ; therapeutic use ; Antineoplastic Agents ; therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Breast Neoplasms ; classification ; metabolism ; pathology ; surgery ; therapy ; Carcinoma ; classification ; metabolism ; pathology ; surgery ; therapy ; Cetuximab ; Chemotherapy, Adjuvant ; Cyclophosphamide ; therapeutic use ; Female ; Fluorouracil ; therapeutic use ; Humans ; Lymphatic Metastasis ; Methotrexate ; therapeutic use ; Neoplasm Staging ; Receptor, ErbB-2 ; metabolism ; Receptors, Estrogen ; metabolism ; Receptors, Progesterone ; metabolism ; Trastuzumab

240 ?g/L group(P

OBJECTIVE: To improve the accuracy of diagnosis and treatment efficacy of hemangiopericytoma in nasal cavity and paranasal sinuses. METHOD: The clinical and pathological data of 5 cases with hemangiopericytoma in nasal cavity and paranasal sinuses verified by pathology were analyzed retrospectively. RESULT: Computed tomography scan revealed vascular in 5 cases. On CT scan, hemangiopericytoma generally appeared to be a uniform high density mass with obvious enhancement upon injection of contrast material. In pathological examination, there were plentiful capillaries which were like tree branch. The normal endocytes were in the inner wall of the vessel. The round, oval and spear-like pericytes scattered around the vessel. The split phase of the nucleus could be found in the tumor cell. All cases underwent surgical resection and were proved by pathological examination. The clinical data showed that the prognosis of sinonasal hemangiopericytoma was closely related to its histological grade. The recur rate in highly malignant hemangiopericytoma was obviously higher than that in middle and low malignant tumor. The rate of misdiagnosis was 80%. CONCLUSION Hemangiopericytoma is a potentially malignant tumor. Medical imaging can help to demonstrate the site, configuration, and characteristics of the tumors and contribute to the treatment. But there are not characteristic medical features. The final diagnosis must depend on the closely related to its pathological grade. The doctor should pay attention to the description of histological pathology. All the patients must be followed up carefully.
Adult ; Aged ; Female ; Follow-Up Studies ; Hemangiopericytoma ; diagnosis ; pathology ; Humans ; Male ; Middle Aged ; Nasal Cavity ; pathology ; Paranasal Sinus Neoplasms ; diagnosis ; pathology ; Retrospective Studies ; Young Adult

Antineoplastic Agents, Hormonal ; therapeutic use ; Bone Neoplasms ; secondary ; Breast Neoplasms ; chemistry ; drug therapy ; pathology ; Disease Progression ; Female ; Humans ; Menopause ; Neoplasm Recurrence, Local ; Receptors, Estrogen ; analysis ; Receptors, Progesterone ; analysis ; Tamoxifen ; therapeutic use

Adolescent ; Adult ; Child ; Female ; Humans ; Male ; Nasal Septum ; injuries ; Skull Fractures ; diagnostic imaging ; Tomography, Spiral Computed ; Young Adult

Aim To illustrate the actions and molecular mechanisms of interventions taken to convert the metabolism pathways of cellular apoptosis caused by hypoxia and hypoxia-reperfusion in hypertrophic cardiomyocytes.Methods Angiotensin Ⅱ(0.1 ?mol?L-1)was applied to induce the hypertrophy of mice cardiomyocytes.The cardiomyocytes received the treatment of hypoxia-reperfusion in a tri-gas incubator to simulate the conditions of hypoxia-reperfusion.Before hypoxia/reperfusion,no drug intervention and pre-treatments of DCA(1 mmol?L-1),TMZ(5 ?mol?L-1),LC(50 ?mol?L-1)and AA(10 ?mol?L-1)were given respectively.The glucose and fatty acid oxidative metabolism rates were measured with radioactive counting methods.RT-PCR and Western blot methods were employed respectively to measure the mRNA and protein expression levels of cytochrome C and apoptosis inducers.The spectrophotometry method was used to measure the activity of Caspase-3 and Hoechst 33258 staining to quantify the percentage of cellular apoptosis.Results At post-hypoxia 12 h and post-reperfusion 4 h,the glucose oxidative metabolism rates in hypertrophic cardiomyocytes all decreased while the fatty acid oxidative metabolism rates increased.DCA,TMZ and LC all could inhibit both the reduction of glucose oxidative metabolism after hypoxia-reperfusion and the elevation of fatty acid oxidative metabolism after hypoxia-reperfusion.AA drove the reduction of glucose oxidative metabolism rate even lower and the fatty acid oxidative metabolism rate even higher in hypertrophic cardiomyocytes after ischemia/reperfusion.At the same time,DCA,TMZ and LC could inhibit the expression levels of mitochondrial cytochrome C and AIF mRNA and proteins,the nuclear translocation of cytochrome c and AIF proteins and the activity of caspase-3.And with the opposing actions to AA,DCA,TMZ and LC could inhibit the apoptotic rate of hypertrophic cardiomyocytes after hypoxia-reperfusion.And AA had the opposite effect.Conclusion Intervening in the metabolism pathway of hypertrophic cardiomyocytes was an effective way to prevent and control their programmed death through inhibiting the expression of mitochondrial apoptotic proteins.