Objective To review the clinical features,diagnostic work-up,classification,prognosis and treatment of systemic mastocytosis (SM).Methods The clinical data of 3 SM patients admitted to Peking Union Medical College Hospital (PUMCH) were retrospectively analyzed and the review of recent literatures was performed.Results All the 3 cases were pathologically diagnosed.According to WHO 2008 classification criteria,2 cases were diagnosed as aggressive SM (ASM) and the other one was diagnosed as indolent SM (ISM).Case 1 was a 60-year-old female patient who had overt mediator release syndrome manifesting as episodes of flushing,fever,vomiting,palpitation,hypotension and syncope.She was diagnosed as aggressive SM based on significantly increased number of abnormal mast cells (accounting for 6％ of all nucleated cells) in the bone marrow aspiration sample and biopsy specimen which accompanied with decreased other myeloid and erythroid elements.Her disease was refractory to the treatment of H2 antihistamines and led to a fatal outcome eventually.Case 2 was a 72-year-old male patient who underwent extended proximal gastrectomy with esophagogastric anastomosis due to endoscopically detected diffuse thickening of the gastric fundic mucosa.The diagnosis as indolent SM was established according to the dense infiltrate of abnormal mast cells in the surgically resected part of stomach and regional lymph nodes.He had been in complete remission for more than 6 years ever since then.Case 3 was a 41-year-old female patient who presented with fever,urticaria pigmentosa and diffuse bone lesions.A bone biopsy specimen demonstrated a dense infiltrate of mast cells while the assays for KIT-D816V mutation and FIP1L1-PDGFRα fusion gene yielded negative results.She was diagnosed as aggressive SM and a progression-free survival of more than 1 year had been achieved with the treatment of prednisone,interferon-α and pamidronate.Conclusions SM is a rare disease.Diagnosis is primarily dependent on histopathology.There is currently no curative therapy for systemic mastocytosis.Treatment is intended to reduce symptoms and improve quality of life.The prognosis of ISM is much better than that of ASM.

Objective To investigate the effects and probable mechanism ofShenfu injection on the oxidaitve damage of H2O2-induced PC12 cells.Methods PC12 cells were cultured and exposed to 100μmol/L H2O2 for 1 h to establish the oxidative damage model. The protective effect ofShenfu injection was observed by the cell survival rate measured by colorimetric MTT assay, and the leakage rate of lactic dehydrogense (LDH). Western blot methods were used to detect the expression of NF-κB signaling pathway.Results Compared with the model group,Shenfu injection at 5, 10, 20 ml/L could improve the PC12 cells survival rate (83.11% ± 2.59 %, 87.99% ± 0.59%, 85.26% ± 1.07%vs. 73.82% ± 1.82%;P<0.01 orP<0.05), decrease the LDH leakage rate (32.75% ± 4.10%, 28.52% ± 1.14%, 35.79% ± 1.62%vs. 64.34% ± 3.18%;P<0.01 or P<0.05). Western blot results showed thatShenfu injection could protect the PC12 cells from oxidaitve damage by suppressing the p-p65/p65 (1.30 ± 0.10, 1.17 ± 0.06, 1.37 ± 0.15 vs. 1.70 ± 0.10;P<0.01 orP<0.05), p-IκBα/IκBα (1.07 ± 0.12, 1.00 ± 0.10, 1.03 ± 0.06 vs. 1.17 ± 0.06; P<0.01 orP<0.05).ConclusionShenfu injection has a obvious antioxidant effect on PC12 cells in vitro.

Radiotherapy is an important therapy for uterine cervical cancer and plays a great role in improving the outcome in uterine cervical cancer patients. The high frequency subject headings/subheadings in papers on radio-therapy for uterine cervical cancer in the past 10 years were analyzed by co-occurrence clustering analysis to dis-play the hot spots and a strategic coordinate figure was plotted to show the developing tendency of its hot spots in studies on radiotherapy for uterine cervical cancer in order to provide reference for its-related studies.

AIM: To observe the effect of mouse Sim2 (mSim2) eukaryotic expression vector transfection on the cell cycle in PC12 cells in vitro and to explore the role of Sim2 in the pathogenesis of Down syndrome. METHODS: The full open reading frame of mSim2 was amplified by reverse transcription-polymerase chain reaction (RT-PCR) and cloned into the vector pcDNA3. Then the constructed pcDNA3-Sim2 vectors were transiently transfected into PC12 with Lipofectamine~ TM . The expression of mSim2 was detected by RT-PCR. The effect of mSim2 on the cell cycle was observed by flow cytometry. RESULTS: The eukaryotic expression vector mSim2 was successfully constructed. There was notable expression of mSim2 in the cells transfected with pcDNA3-Sim2. There were more cells in G_0/G_1 phase in the pcDNA3-Sim2 transfected cells than that in the control (P

AIM: The effects of Yigu capsule on tartrate resistant acid phosphatase (TRAP) secretion and apoptosis in rat osteoclasts were investigated in order to further explore its mechanism of preventing and treating osteoporosis. METHODS: (1) Twenty-month-old Sprague-daweley rats were randomly divided into two groups(Yigu capsule group and saline group), and the drug-containing serum and control serum were prepared. (2) The newborn Sprague-daweley rat osteoclasts were cultured with different concentrations of Yigu capsule drug-containing serum. At different time point, TRAP activity was measured and the survival osteoclast was counted under reverse microscope.The percentage of osteoclast apoptosis was observed under fluorescence microscope after acridine orange staining. RESULTS: TRAP activity was lower and the percentage of osteoclast apoptosis was higher in drug-containing serum group than in control group at 24, 48 and 72 h( P

Objective To observe the effects of cyclic tensile strain (CTS) on in vitro expression of glycosaminoglycans (GAG) in rabbit chondrocytes of different ages.Methods Nine male New Zealand rabbits were grouped into juvenile (2 months), adult (8 months), and senior (31 months) groups. The bilateral knee joints were harvested using sterile technique from each rabbits. In each age group, rabbit articular chondrocytes were cultivated in vitro after randomization into a control group and a CTS group, with 6 specimens in each. In the next 3 days, CTS was applied (sin10％, 0. 5 Hz, 6 h/d) in the CTS group for 6 hours per day while no CTS was applied in the control group. After the first CTS treatment, the supernatant of cell culture was collected every 12 hours from each specimen in both groups to assess the GAG levels by Alcian blue assay.Results Expressions of GAG showed significant increases in both control and CTS groups in each age group ( P ＜ 0. 05) . Different age groups showed significant differences in the GAG secretion over different time points. Compared with the younger cells, the older ones showed the most significant difference in growth between the control and CTS groups at 12 hours, though the older cells produced less GAG than the younger ones in both groups at the end of the experiment (72 hours).Conclusions CTS can stimulate rabbit chondrocytes of different ages to secrete more GAG, and younger cells tend to produce more GAG than the older ones.

Objective To evaluate the impact of serum cystatin C (Cys C) level on short term prognosis in elderly patients with unstableangina (UA). Methods 167 patients with US were involved in this study. The serum Cys C level was measured by immunonephelometric assay.The patients were divided into normal group (Cys C<1.5 mg/L, n=102) and high Cys C group (Cys C≥1.5 mg/L, n=65) according totheir baseline of the first Cys C level within 24 hours. The clinical outcomes, including major cardiac events, mortality and readmission duringhospitalization and 6 months in the follow-up period were observed and evaluated. Results The major cardiac events, mortality and readmissionrate were higher in the high Cys C group than in the normal group (χ2=4.16, P=0.042). Conclusion The serum of Cys C level isclosely related to the short term prognosis of UA, it could be a risk factor to predict major cardiac events in patients with UA.

Aim To investigate the effect of indirubin derivative PHⅡ-7 and TRAIL on proliferation in breast cancer cell MCF-7 and its MDR counterpart MCF-7/ADR and the mechanism.Methods Growth inhibition rate was examined respectively by MTT assay under treatment with TRAIL or PHⅡ-7 or in combination. Cell apoptosis and ROS production were examined by flow cytometry.The change of TRAIL receptors(DR4/DR5 )in mRNA was analysed by realtime PCR.Re-sults IC50 of PHⅡ-7 on MCF-7 and MCF-7/ADR was (4.49 ±1.55 ),(3.44 ±0.90 )μmol · L-1 respec-tively;MDA-MB-231 was TRAIL sensitive cell line, and apparently TRAIL induced apoptosis in MDA-MB-23 1 .Low concentration of PHⅡ-7 in combination with TRAIL could augment TRAIL-induced cytotoxic effect including apoptosis while TRAIL or PHⅡ-7 treatment alone had limited cytotoxity to those cells.Besides, PHⅡ-7 at this concentration had little toxicity to hu-man peripheral blood mononuclear cells even if in com-bination with TRAIL.PHⅡ-7 generated ROS produc-tion inside MCF-7 and MCF-7/ADR cells and up-regu-lated DR4/DR5 expression concentration dependently. Once upon ROS scavenger NAC involved,the effect of TRAIL receptors up-regualtion by expression was abro-gated.Conclusions PHⅡ-7 at low concentration could improve the sensitivities of breast cancer cell MCF-7 and MCF-7/ADR to TRAIL,the mechanism of which may be the ability of ROS production by PHⅡ-7 help up-regulated TRAIL receptor DR4,DR5 .Our re-search set a solid foundation for PHⅡ-7 in combination with TRAIL in future clinical application.

Objective To explore whether ginsenoside Rg1 can attenuate ?-amyloid peptide 25-35-induced Tau hyperphosporylation in rat embryo cortical neurons by regulating the activity of GSK-3? and PP2A. Methods Primary cultures of cortical neurons were prepared from the embryonic day 18?2 in Sprague-Dawley rats. The experimental groups were designed as follows:1.Neurons culture (control group); 2. Neurons exposed to 20?mol/L A?_ 25-35 for 12 hours (A?-model group); 3.Neurons exposed to 20?mol/L A?_ 25-35 and 10 mmol/L lithium chloride (LiCl), a specific inhibitor of glycogen synthase kinase-3?(GSK-3?), for 12 hours (LiCl group); 4.Neurons exposed to 20?mol/L A?_ 25-35 for 12 hours in the presence of 24-hour pretreatment with ginsenoside Rg1 (Rg1 pretreatment group) . Western blotting and immunocytochemical staining were used to detect the levels of Tau phosphorylation,total Tau and GSK-3? in cortical neurons. Non-radioimmunoassay was introduced to detect the activity of protein phosphatase 2A (PP2A). Results In A?-model group, the levels of Tau protein phosphorylation in the sites of Ser 396 ,Ser 199/202 ,Thr 231 and total Tau were enhanced. Meanwhile, the expression of GSK-3? was also increased, but the activity of PP2A was unchanged. In LiCl group and Rg1 pretreatment group , the hyperposphorylations of Tau protein and total Tau and the expression of GSK-3? were markedly reduced compared to those of the A?-model group (P

Objective To investigate the correlation of insulin resistance (IR) and benign prostate hyperplasia (BPH). Methods The 200 health examination men were divided into three groups according to the prostate volume (PV). There were 100 healthy subjects as control group (PV≤20 ml), 50 cases in BPH1 group (20 ml＜PV＜50 ml) and 50 cases in BPH2 group (PV≥50 ml).The fasting blood glucose (FBG) and fasting serum insulin (FSI) were determined using hexokinase method and radioimmunoassy, respectively. The IR index (IRI) and body mass index (BMI) were calculated according to the formula in HOMA model. Results There were no statistical differences between BPHl group and healthy control group in IRI (1.10±0. 18 vs. 1.18±0.21) and BMI (22. 0±3.0vs. 21.8±2.7) (t=0.74, 0.18, both P＞0. 05), but the IRI (1.31±0.19) and BMI (24. 8±3.29) increased in BPH2 group (P=0. 01, 0.03). The percentage of hyperglycosemia was higher in BPH patients than in normal controls (25% vs. 5%, P = 0. 00). Of them, the percentage of hyperglycosemia was the highest in BPH2 group (36%, P = 0. 01 ), their IRI ( 1.47 ± 0.21 ) was higher than in euglycemia patients (t=3.92, P=0.00), but the BM1 was unchanged compared with the control group ( 25.8 ± 4.3 vs. 24.3 ± 2.71, P = 0. 95 ). Conclusions There is a positive correlation of IR and hyperglycosemia with severe BPH, and the IR in severe BPH is independent of BMI.