Kasabach-Merritt syndrome(KMS) is a massive haemangioma with thrombocytopenia and consumptive coagulopathy. The histopathology of KMS is thrombocytopenia and disseminated intravascular coagulation associated with massive haemangioma.A standard treatment regimen for KMS has not been established. Therapy includes surgery, embolism and medicine(steroids,α-interferon , immunosuppressant , etc).

Humans ; Infant ; Spasms, Infantile ; therapy

BACKGROUND:Carboxymethyl chitosan (CMCS),a chitin derivative,has a good application performance that makes it become a safe and effective hemostatic material.OBJECTIVE:To determine the hemostatic effect of CMCS and its biosecurity properties.METHODS:(1) CMCS powder was scattered on the caudal vein and liver wounds of Sprague-Dawley rats,and the hemostatic time was recorded as experimental group,while the time for natural haemostasis of the wound was recorded as control group.(2) CMCS powder was scattered on the tail,femoral artery and liver wounds of ICR mice,and the hemostatic time was recorded as experimental group,while the time for natural haemostasis of the wound was recorded as control group.(3) CMCS,Sodium dodecyl sulfate solution and distilled water were respectively applied on the skin of albino rabbits in a skin irritation test.(4) A delayed-type hypersensitivity test of CMCS was carried out by intradermal injection of CMCS in guinea pigs.(5) An intradermal irritation test was carried out by subcutaneous injection of normal saline containing CMCS and normal saline,respectively.Another intradermal irritation test was carried out by subcutaneous injection of the supernatant of CMCS olive oil extract and olive oil,respectively.RESULTS AND CONCLUSION:(1) Compared with the control group,the hemostatic time for caudal vein and liver wounds were significantly shortened in the Sprague-Dawley rats in the experimental group (P ＜ 0.01).(2) Compared with the control group,the time of hemostasis on the tail,femoral artery and liver wounds was significantly shortened in the ICR mice in the experimental group (P ＜ 0.05 or P ＜ 0.01).(3) The CMCS had no irritation to the skin of albino rabbits and no allergic reaction to the skin of guinea pigs.To conclude,the CMCS has good hemostatic effect on the wound in Sprague-Dawley rats and ICR mice,and has no skin irritation,allergic reactions and intradermal irritation reactions in albino rabbits and guinea pigs,which is a relatively safe hemostatic material.

Objective To explore the different influence of antiepileptic drugs(AEDs)at therapeutic levels to the maturation of brain.Methods 180 healthy Sprague-Dawley(SD)rats were divided into infant and adult group.Each age group was administered with PB,CNP,VPA,TPM or normal saline respectively in persistent 5 weeks.The steady-state plasma concentrations of AEDs at the experimental dosage were coincided with the range of clinical therapeutic concentrations.After AEDs withdrawed,the effects of AEDs on cognitive function were assessed by Morris water maze and two-way shuttle box at different time points.Body and brain weight were got immediately when the rats were sacrificed.Histological changes of brain were observed by HE staining,Nissl staining and transmission electron microscopy.Results(1) For immature rats,1 day or 14 days after AEDs withdrawed,there were significant differences between groups exposed to PB or CNP and control group in escape response latency(ERL)in the two-way shuttle box.Even after one month ERLs of immature rats receiving CNP((6.05?2.04)s)or PB((5.81? 1.75)s)were still longer than that of untreated controls((4.75?2.43)s,P

ObjectiveTo understand the characteristics of mutations in BCR-ABL1 kinase domain mutation,these chronic myeloid leukemia (CML) and Ph positive acute lymphoblastic leukemia (ALL)patients who got imatinib treatment had poor effect.MethodsTotally 177 CML patients and 33 Ph( + )ALL patients were selected at Beijing Dao-Pei Hospital from Sep.2007 to Dec.2010.All of them were Chinese patients.Totally 243 bone marrow or peripheral blood specimens were collected from the patients,who had early effect,then resistance emergenced,or for more than 3 months of poor efficacy.Extracted total RNA from the specimens' nuclear cells,reversed transcription to cDNA.Amplified the whole span of BCRABL1 fusion kinase gene by nest PCR (from 242 to 493 amino acid coding sequence),used the type AB3130XL gene sequencing instrument determinate the gene sequence of ABL1 kinase region and then used the Variant Reporter V1.0 software to analyze the results of gene mutations.ResultsThirty-two kinds of different mutations were detected of ABL1 gene mutations,accounting for 34.2％ (83/243 cases).Among them,the T315I was 12％ (10/83),mutation rate was the highest,followed by Y253H was 11％ (9/83),G250E was 7％ (6/83),E255K was 7％ (6/83),M351T was 6％ (5/83),E459K was 5％ (4/83) ;Q252H,D276G,F317L,E355G,F359V,H396R were all 4％ (3/83).Three cases of insertion mutations were found,including 2 cases of 357-358insk,1 case of V304RfsX17.Seven patients had found existence two or more point mutations.The multiple drug resistance mutations might exist in the same leukemia clone.The same individual was not only contain common resistance mutations,but also rare point mutations,insertion mutations.The mutations might be lead to loss of kinase activity.ConclusionsUnder the imatinib drugs pressure,the ABL1 gene mutation in leukemia cells appears randomly,and results in different resistant clones.Different resistant clones can coexist in the same patients in vivo; resistant clones not only contain point mutations,but also contain inserted deletion mutations.

OBJECTIVETo observe the efficacy on primary osteoporosis treated with spreading moxibustion for warming yang and activating blood circulation so as to provide the effective clinical therapeutic methods for osteoporosis.

METHODSSixty cases of primary osteoporosis were randomized into a spreading moxibustion group (30 cases) and a calcium tablet group (30 cases). In the calcium tablet group, caltrate was prescribed for oral administration, 600 mg per day. In the spreading moxibustion group, on the basis of the treatment as the calcium tablet group, the spreading moxibustion was applied at Dazhui (GV 14) to Yaoshu (GV 2) for warming yang and activating blood circulation. The duration of treatment was 12 weeks. Visual analogue scale (VAS) score, TCM clinical symptom score and bone mineral density (BMD) were observed and compared before and after treatment in the patients between the two groups.

RESULTSVAS scores were reduced apparently after treatment in the two groups (both P < 0.01) and the results in the spreading moxibustion group were obviously superior to that in the calcium tablet group (2.36 +/- 0.43 vs 4.52 +/- 0.35, P < 0.01). BMD were all increased in the two groups (P < 0.05, P < 0.01) and the results in the spreading moxibustion group were superior to those in the calcium tablet group (both P < 0.05). The total clinical effective rate was 86.67% (26/30) in the spreading moxibustion group, apparently better than 63.33% (19/30) in the calcium tablet group (P < 0.05). TCM clinical symptom scores after treatment were all reduced apparently in the two groups (both P < 0.01), and the result in the spreading moxibustion group was obviously superior to that in the calcium tablet group (4.72 +/- 1.90 vs 6.82 +/- 2.30, P < 0.01). The total effective rate of TCM symptoms was 93.33% (28/30) in the spreading moxibustion group, apparently better than 70.00% (21/30) in the calcium tablet group (P < 0.05).

CONCLUSIONThe combined therapy of spreading moxibustion for warming yang and activating blood circulation and the oral administration of caltrate apparently relieves pain and TCM clinical symptoms, improves BMD in the patients of osteoporosis and achieves definite clinical efficacy in the patients of osteoporosis.

Aged ; Blood Circulation ; Bone Density ; Female ; Humans ; Male ; Middle Aged ; Moxibustion ; Osteoporosis ; physiopathology ; therapy ; Yang Deficiency ; physiopathology ; therapy

BACKGROUND: Hippocampus is an important region involved in learning and memory. Some methods for freshly isolated hippocampal pyramidal neurons have been described. These methods need multiple enzymes or the procedure is complex.OBJECTIVE: To acquire large quantities of hippocampal neurons from rats suitable for patch clamp study.DESIGN: An animal experimental observation.SETTING: Department of Physiology and Pathophysiology, School of Medicine, Xi'an Jiao Tong University.MATERIALS: The experiments were carried out in the Medical Experimental Center, School of Medicine, Xi'an Jiao Tong University between March and October 2004. The animals were the 10-15-day-old SpragueDawley rats, bothmale and female.METHODS: Hippocampal pyramidal neurons were freshly isolated. Delayed rectifier potassium current and voltage-gated Ca2 + currents were recorded by whole-cell patch clamp configuration.MAIN OUTCOME MEASURES: Acute isolated neurons were observed with a Leica microscope. Recordings of delayed rectifier potassium currents and voltage-gated Ca2+ currents were obtained.RESULTS: ① Under the inverted microscope, the acute isolated neurons had a smooth and glassy surface, a three-dimensional contour, a pyramidal shape with a longer apical dendrite and several basal dendrites. ② After the whole cell recording configuration was formed, voltage-gated barium currents through calcium channels were elicited by 200 ms depolarizing potential from -70 mV to +20 mV, with an increment of 10 mV, a holding potential was -90 mV. Delayed rectifier potassium current (Ikd) was elicited by a protocol consisting of a multiple depolarizing pulses (-60 mV to +50 mV),preceded by a single prepulse step to -50 rmV, with inactivated transient outward potassium currents from a holding potential of -80 mV.CONCLUSION: This method is simple and ideal for the dissociation of neurons from rat hippocampus, and offers a powerful tool for functional analysis of ion channels by patch clamp.

Objective To explore the radiosensitivity of berberine on esophageal cancer cells under hypoxia condition.Methods MTT assay and clonogenic survival assay were used to evaluate the effect of berberine on proliferation inhibition and radiosensitivity of esophageal cancer cells,respectively.Immunofluorescence was employed to examine the expression of HIF-1.The change of cell cycle distribution and cell apoptosis was assayed by flow cytometry.The expression of HIF-1 was measured by Western blot.DNA damage was detected by γ-H2AX Foci counting.Results With a clear dose and time effect,berberine inhibited cell proliferation and enhanced cell radiosensitivity(t =3.69,P＜0.05)with a sensitizing enhancement ratio(SER)of 1.42.Berberine caused a dose-dependent decrease in HIF-1 protein expression and also significantly increased the cell apoptosis in ECA-109 population(t=4.74,P＜0.05).Compared with the radiation alone group,berberine enhanced X-ray induced DNA double chain breaks(DSB).Conclusions Berberine can increase the radiosensitivity of esophageal cell line ECA-109,which may be associated with decrease of HIF-1 expression and induction of apoptosis in ECA-109 cells.

Objective To investigate the anti-tumor effect of the recombined adeno-associated virus encoding melanoma differentiation -associated gene-7 (MDA-7) regulated by progression-elevated gene (PEG) promotor on human hepatocellular carcinoma (HCC) in nude mice. Methods A nude mouse model of subcutaneously implanted HCC cell line HepG2 tumor was established. AAV-PEG-MDA-7 was injected from the tail vain after tumor cell innoculation. RT-PCR, Western blot and immunohistochemical analysis were employed to detect MDA-7 expression in mice; MDA-7 plasma concentration was detected by ELISA assay. Tumor growth was observed, tumor cell apoptosis and angiogenesis in tumor tissues were measured by TUNEL and immunohistochemical analysis. Results Seven days after tumor cell innoculation RT-PCR, Western blot, and immunohistochemistry showed that MDA-7 was only expressed in the liver. ELISA assay showed that the concentration of MDA-7 in plasma was gradually increased to reach the plateau (200 ng/ml). Tumor growth was significantly inhibited in mice injected with rAAV-PEG-MDA-7, and the tumor growth-inhibiting rate was 62%. TUNEL and immunohistochemical analysis demonstrated significant induction of tumor cell specific apoptosis and reduction of vascular formation in tumor tissues. Conclusions rAAV-PEG-MDA-7 exhibits tumor-specific cytotoxicity and liver tendency, inhibiting tumor growth possibly by tumor cell apoptosis-induciug effect and antiangiogenesis.

Purpose To investigate whether FoxM1 participate in inhibitory effect of cisplatin (CDP) in resistant osteosarcoma cell lines by down-regulation of Rad51.Methods The resistant osteosarcoma cell lines were induced by gradually increasing dose intermittent action,and were named MG-63/R and HOS-MNNG/R respectively.The mRNA and protein level of FoxMl and Rad51 were detected by qRT-PCR and Western blot analysis in resistant cells and parental cells.The mRNA and protein level of FoxM1 and Rad51 were detected by qRT-PCR and Western blot analysis in resistant cells after treatment of 4 μmol/L Thiostrepton.The effect of single or combined treated of 4 tμmol/L Thiostrepton or 2 tμg/mL CDP on the rate of cell proliferation in resistant cells was examed by cell counting.Results Resistant osteosarcoma cell lines MG-63/R and HOSMNNG/R were established and stablely growthed in the concentration of 2 μg/mL CDP,and the resistance index was 30.52 and 37.87 respectively (severe CDP resistance).The mRNA and protein level of FoxM1 and Rad51 were significantly increaced in resistant cells compared with parental cells.The proliferation rate of resistant cells in conbination of 4 μmol/L Thiostrepton and 2 μg/mL CDP treated group was significantly lower than these two drugs single treated group.The level of mRNA and protein of FoxM1 and Rad51 were significantly decreased after 4 μmol/L Thiostrepton treatment in CDP resistant cells.Conclusion The results suggest that FoxM1 and Rad51 may participate in the resistant osteosarcoma cells to CDP.FoxM1 inhibitor Thiostrepton may strengthen the inhibitory effect of CDP in the resistant cells by down-regulation of Rad51.