Objective To investigate changes in serum bilirubin and internal environment,etc.of neonatal hyperbilirubinemia that before and after the treatment of peripherally arteriovenous synchronous exchange transfusion. Methods In the strict monitoring of vital signs,hyperbilirubinemia peripheral vessels exchange transfusion was applied in five cases of neonatal,and the serum bilirubin,routine blood test,electrolytes before and after the exchange transfusion were detected.Results By comparing the data before and after the exchange transfusion,the total bilirubin and indirect bilirubin decreased obviously,respectively[(414.02 ±56.04)μmol/L,(225.72 ±53.54)μmol/L,t =5.433 P =0.01,(381.82 ±44.68)μmol/L,(199.22 ±57.37 )μmol/L,t =5.615 P =0.01 ],the difference was statistically significant,and also the platelet count were decreased obviously,respectively [(199.00 ± 42.01)×109 /L,(102.00 ±17.72)×109 /L,t =4.758,P =0.001],the difference was statistically significant.After the exchange transfusion,white blood cells,hemoglobin,potassium,sodium,chloride,calcium,glucose,blood pressure, heart rate and blood PH value had decreased or increased slightly,there was no significant difference P >0.05.Cere-bral palsy and other complications did not occur after 12 months of follow -up of the five cases.Conclusion The outer peripheral arteriovenous synchronous exchange transfusion therapy for neonatal severe hyperbilirubinemia can quickly reduce serum bilirubin,and has less impact on the body environment,it is an important and effective salvage treatment of neonatal hyperbilirubinemia,thereby reducing damage to the nervous system of bilirubin.

Objective To detect the expression intensity and distribution of minichromosome mainte-nance 2 protein (MCM-2) in normal skin and lesions of malignant and non-malignant hyperplasia. Methods Three groups of samples were collected, I.e., malignant group (including 15 cases of Bowen disease or highly differentiated squamous cell carcinoma of Grade Ⅰ or Ⅱ ), non-malignant group (including 4 cases of chro-momycosis, 2 cases of sporotrichosis, 5 cases of seborrheic keratosis, 4 cases of verruca vuigaris, 4 cases of chronic eczema, 4 cases of cutaneous fibroma), and normal group (10 cases of normal human control). The distribution and intensity of MCM-2 expression in the epidermis of these samples were assessed by immuno-histochemical SP method. Results The expression of MCM-2 was observed in basal and superbasal layer of epidermis in lesions of malignant and non-malignant hyperplasia, and only in epidermal basal layer in normal skin. A significant increment was observed in the density of MCM-2 positive cells in superbasal layer in malignant lesion compared with the non-malignant lesion. The epidermal expression level of MCM-2 in the non-malignant lesion was significantly lower than that in the malignant lesion, but higher than that in the normal skin (μ = -2.529, -3.705, respectively, both P < 0.05); the same was true for the proportion of MCM-2-postive basal cells. Conclusions The expression of MCM-2 protein varies with the proliferation status of epidermal cells, and may serve as an objective marker for epidermal cell proliferation.

Objective To detect the changes of cerebral perfusion in patients with MELAs syndrome by using MR perfusion technique.Methods Thirteen patients with MELAS syndrome and 13 controls with normal neurological conditions were scanned with the sequence of flow-sensitive alternating inversion recovery exempting separate T1 measurement(FAIREST).Their rCBF values were obtained in regions of bilateral basilar nuclei and thalami,as well as bilateral temporal lobes and occipital lobes.Regression analysis was carried out to determine the effect of location and side on the measurement of rCBF in controls.One-way ANOVA was conducted to compare rCBF values among the control group.the lesion ROIs and normal ROIs of the MELAS syndrome group.Results The values of rCBF were 0.83±0.23,1.17±0.30.0.93±0.28,and 1.11±0.25 for the left basilar ganglia,thalamus,temporal lobe,and occipital lobe respectively,while they were 0.77±0.15,1.03±0.34,1.06±0.23,and 1.09±0.23 for the right basilar ganglia,thalamus,temporal lobe.and occipital lobe respectively.Regression analysis revealed no effect of location and side on the rCBF (P＞0.05).The rCBF value for control group was 1.00±0.28,while it was 1.01±0.31 for the normal ROIs and 1.95±0.43 for the lesion ROIs in the MELAS syndrome group(F=54.99.P＜0.01).The rCBF of the lesion ROIs in the MELAS syndrome group was significantly higher than the normal ROIs and the control group.Conclusion CBF maps can reveal changes of cerebral blood flow in patients with ietal MELAS,which suggests increased perfusion in the stroke-like lesions.

AIM To examine the effects of the APP17-mer peptide against A? 25-35 -induced apoptosis and gain some insight into the neuroprotective mechanism of the APP17-mer peptide. METHODS Protective effects of APP17-mer peptide against A? 25-35 -induced apoptosis in SH-SY5Y cell was proved by cell morphology, LM-PCR DNA ladder assay and FCM assay. The antiapoptotic mechanism of APP17-mer peptide was investigated using the MTT assay to measure mitochondrial energy redox state, using the fluorescent probe DCF-DA?Rhodamine 123 to measure relative levels of cellular peroxides and mitochondrial membrane potential and using Western blot for AIF and NF-?B to detect the expression of AIF and NF-?B. RESULTS Damage of cell morphology was ameliorated by pretreating with APP17-mer peptide. The apoptotic rate of the SH-SY5Y cells exposed to A? 25-35 in the presence of APP17-mer peptide decreased from 63.75% to 28.25%. Exposure of SH-SY5Y to A? 25-35 for 48 h resulted in an increase in DCF-DA fluorescence,a decrease in Rhodamine 123 fluorescence and MTT reduction, the results were weakened by pre-incubating with APP17-mer peptide for 30 minutes. Treatment of cells with APP17-mer peptide resulted in a significant attenuation in the expression of AIF and a strong increase in the expression of NF-?B. CONCLUSION APP17-mer is protective against cell apoptosis induced by A? 25-35 by provoking and sustaining upregulation of a key antiapoptotic transcription factor NF-?B, by suppressing oxyradical production and by preserving mitochondrial function and inhibiting the release of apoptotic protein from mitochondria.

Objective To determine the MR phenotype of Leigh syndrome (IS) with SURF-1 gene mutation.Methods The cranial MR examination of eight patients with the diagnosis of Leigh syndrome associated with SURF-1 gene 604G→C mutations were reviewed retrospectively.Comparison was made with typical LS patients' MRI.Observation was made regarding lesions in basal ganglia,subthalamic nuclei,substantia nigra,and dentate nuclei,involvement of white matter,and brain atrophy.Results The MR findings of LS in the study included the following:3 cases exhibited involvement of brain stem and subthalamic nuclei,2 of these 3 cases also had basal ganglia abnormalities.3 cases showed abnormality in the white matter without any involvement of the deep nuclei.Cerebral atrophy was observed in all cases in the group,and was the only finding in two cases.Conclusion The imaging findings in LS with SURF-1 604G→C gene mutation were variable.

Objective To explore the effect of ectopic overexpression of Smac/DIABLO on the proliferation of pancreatic cancer cell line SW1990,and the sensitization to TRAIL and Gemcitabine induced apoptosis.Methods The Smac/DIABLO gene was transfected into the pancreatic cancer cell line SW1990 with the participation of Lipofectamine 2000 (SW1990/Smac).The cell line transfected with empty vector served as controls (SW1990/neo).The SW1990/neo and SW1990/Smac cells were assigned into the following treatment groups:TRAIL group,Gemcitabine group,TRAIL plus Gemcitabine group,and the control group.The SW1990 cells were treated with TRAIL and Gemcitabine in different concentrations and time.The cell growth inhibition rate (CGIR) was detected by MTT,the rate of apoptosis was measured by flow eytometry,the apoptosis morphous was observed by Heochst 33342 staining.The expressions of apoptosis-associated proteins such as Smas/DIABLO,XIAP,cytochrome C and caspase-3 were detected by Western blot.Results The cell growth of SW1990/Smac was significantly lower than growth of SW1990/ neo.The concentration of TRAIL were 200,500,1000 and 2500 ng/ml respectively.After 24 hours,the CGIR of SW1990/neo and SW1990/Smac were 11.11％,46.03％,67.08％,76.19％ and 22.11％,42.67％,56.63％,67.6％ respectively (P ＜ 0.05).The concentration of Gemcitabine were 10,20,40 and 60 μmol/L respectively.After 24 hours,the CGIR of SW1990/neo and SW1990/Smac were 15.2％,34.6％,55.16％,76.4％ and 22.65％,36.85％,55.11％,79.99％ respectively (P＜0.05).The cells of SW1990/neo and SW1990/Smac were treated by TRAIL(500 ng/ml),Gemcitabine (20 μmol/L) and combination group.The apoptosis rate were 5.64％,15.30％,27.27％ and 20.37％,23.27％,67.30％ (P ＜ 0.05) respectively.In combination group,the expressions of activators of caspase such as Smas/DIABLO,cytochrome C and caspase-3 increased significantly,while the expressions of inhibitor of apoptosis protein XIAP decreased.Conclusions Ectopic expression of Smac/DIABLO could induce the apoptosis of SW1990 cell,inhibit the cell proliferation,and enhence the sensitivity of SW1990 cell to TRAIL and Gemcitabine.The mechanism of apoptosis sensitization effect by Smac/DIABLO was associated with significant up-regulation of Smac/DIABLO,cytochrome C,down-regulation of XIAP,and the activation of caspase-3.

Objective To compare the real-time dissolutions of 3 kinds of Simvastatin tablets used in our hospital, and provide reference information for clinical applications. Methods The dissolution rate of simvastatin tablets was deter-mined by the Chinese Pharmacopoeia 2010, and the HPLC method was used to determine the simvastatin content at the wavelength of 238 nm and the Weibull’s equation was adopted to fit the dissolution curves. The shape parameters (m) were performed statistical analysis; Using the similarity f2 as the index, compared the dissolution curve between tablets and the preparation. Results The dissolution of simvastatin tablets manufactured by the 3 manufaccturer was no less than 90% in 30 min, which comply with the national specifications. Compared with the dissolution curve of 6 tablets from the same batch, the homogenicity of samples from A was better, with poor homogenicity of tablets from B or C. There’s significant difference in the shape parameter m of tablets from B and C (P< 0.05), and there’s no significant difference in m of tablets from C and A(P>0.05). Conclusion The in vitro dissolution of the simvastatin tablets are de-termined with single point test procedures. The dissolution of the tablets from 3 manufactures comply with national specifications. However, there’s significant difference in real time dissolution of national tablets. It’s necessary to im-prove the quality of national tablets. Cautions should be taken while use in clinical practices.

AIM:To investigate whether crocin alleviates right ventricular injury induced by monocrotaline(MCT)in rats with pulmonary arterial hypertension(PAH),and to explore the underlying mechanisms.METHODS:Forty male SD rats were randomly divided into 4 groups:normal group,PAH group,crocin group and sildenafil group,with 10 rats in each group.The rats in PAH,crocin and sildenafil groups received subcutaneous injection of MCT(50 mg/kg)to establish the PAH model.Starting from the day of MCT injection,the rats in crocin group received crocin(200 mg/kg),the rats in sildenafil group received sildenafil(30 mg/kg),and those in PAH and normal groups were orally gavaged with an equal volume of saline once daily.After 4 weeks,measurements of right ventricular systolic pressure(RVSP),mean pulmonary artery pressure(mPAP),right ventricular hypertrophy index(RVHI)and right ventricular mass index(RVMI)were taken for the rats in each group.Tissue staining was conducted to observe pathological changes in the right ventricle,and the expression levels of inflammatory factors(IL-1β,IL-6 and TNF-α),the p38 MAPK/NF-κB inflammato-ry pathway,CCL2,CCR2,and the macrophage marker CD68 were assessed.RESULTS:Compared with PAH group,the rats in crocin and sildenafil groups exhibited significant reductions in RVSP,mPAP,RVHI and RVMI(P＜0.05).Right ventricular tissue displayed no evident infiltration of inflammatory cells or proliferation of collagen fibers.The down-regulation of the p38 MAPK/NF-κB pathway and inflammatory factors(IL-1β,IL-6 and TNF-α)was significant(P＜0.05).Additionally,the CCL2/CCR2 pathway and the infiltration of CD68+ macrophages were markedly decreased(P＜0.05).CONCLUSION:Crocin effectively mitigates right ventricular damage in MCT-induced PAH rats,with its effica-cy comparable to that of sildenafil at the dosage utilized in this experiment.Some protective mechanisms of crocin may be attributed to its regulatory effects on inflammation.

OBJECTIVETo study the chemical constituents of Iodes cirrhosa and evaluate their bioactivity.

METHODThe compounds were isolated and purified by various kinds of column chromatography methods and their structures were determined by spectroscopic data analysis. Neuroprotective assay against serum deprivation induced SH-SYSY-JNK3 cell apoptosis was evaluated by MTr method while potassium channel-blocking activity was assayed in both non-specific and specific K+ channel-regulator screening models.

RESULTTwenty-one compounds were obtained from an EtOAc portion of an ethanolic extract of the root of I. cirrhosa. Their structures were elucidated as 1beta, 3beta-dihydroxyurs-9(11),12-diene(1), bauerenyl acetate(2),3beta-hydroxy-11-oxo-olean-12-enyl palmitate(3), 3beta-acetoxy-urs-12-ene-11-one(4), betulinic acid(5), stigmasta-5, 22-diene-3beta-ol(6), 7beta-hydroxystigmasterol(7), stigmasta-5, 22diene-3beta-ol3-O-beta-D-glucopyranoside(8),scopoletin(9),scopolin(10),clovamide(11),methyl 3,5-di-O-caffeoylquinate(12),3,5-dicaffeoylquinic acid(13),2,6-dimethoxy-1,4-benzoquinone(14), protocatechualdehyde(15), vanillin(16), protocatechuic acid(17), vanillic acid(18),caffeic acid(19),azelaic acid(20),and succinic acid(21). Compound 3,4,6,9,10,14,15,18 and 20 showed neuroprotective activities against serum deprivation induced SH-SYSY-JNK3 cell apoptosis at a concentration of 1.0 x 10(6) mol x L(1) with relative protection rates of 177%, 144%, 137%, 137%, 143%, 145%, 137%, 189%, 130%, respectivley. Compound 16 could increase DiBAC4(3) fluorescence response in both non-specific and specific K+ channel-regulator screening models at the concentration of 1.0 x 10(-5) mol x L(-1).

CONCLUSIONCompound 1 was a new compound and all compounds were isolated from this genus for the first time. Compounds 3,4,6,9,10,14,15,18 and 20 showed neuroprotective activities while 16 exhibited K+ channel-blocking activity.

Apoptosis ; drug effects ; Cell Line, Tumor ; Humans ; Magnoliopsida ; chemistry ; Neuroprotective Agents ; chemistry ; pharmacology ; Plant Extracts ; chemistry ; pharmacology ; Potassium Channels ; drug effects

Background: In China, secondary cytoreductive surgery (SCR) has been widely used in ovarian cancer (OC) over the past two decades. Although Gynecologic Oncology Group-0213 trial did not show its overall survival benefit in first relapsed patients, the questions on patient selection and effect of subsequent targeting therapy are still open. The preliminary data from our pre-SOC1 phase II study showed that selected patients with second relapse who never received SCR at recurrence may still benefit from surgery. Moreover, poly(ADP-ribose) polymerase inhibitors (PARPi) maintenance now has been a standard care for platinum sensitive relapsed OC. To our knowledge, no published or ongoing trial is trying to answer the question if patient can benefit from a potentially complete resection combined with PARPi maintenance in OC patients with secondary recurrence. Methods SOC-3 is a multi-center, open, randomized, controlled, phase II trial of SCR followed by chemotherapy and niraparib maintenance vs chemotherapy and niraparib maintenance in patients with platinum-sensitive second relapsed OC who never received SCR at recurrence. To guarantee surgical quality, if the sites had no experience of participating in any OC-related surgical trials, the number of recurrent lesions evaluated by central-reviewed positron emission tomography–computed tomography image shouldn't be more than 3. Eligible patients are randomly assigned in a 1:1 ratio to receive either SCR followed by 6 cyclesof platinum-based chemotherapy and niraparib maintenance or 6 cycles of platinum-based chemotherapy and niraparib maintenance alone. Patients who undergo at least 4 cycles of chemotherapy and must be, in the opinion of the investigator, without disease progression, will be assigned niraparib maintenance. Major inclusion criteria are secondary relapsed OC with a platinum-free interval of no less than 6 months and a possibly complete resection. Major exclusion criteria are borderline tumors and non-epithelial ovarian malignancies, received debulking surgery at recurrence and impossible to complete resection. The sample size is 96 patients. Primary endpoint is 12-month non-progression rate.