Objective To investigate the influence factors of serum CA125 level in patients with ovarian chocolate cysts,and to study the effect on serum CA125 level of interventional therapy.Methods A total of 103 patients with single unilateral chocolate cyst of ovary underwent interventional treatment.According the serum CA125 level before interventional therapy,the patients were divided into normal group (CA125≤35 U/ml) and abnormal group (35 U/ml＜CA125≤200 U/ml).The clinical indexes of patients and ultrasound characteristics of cyst were compared between the two groups.The changes of serum CA125 levels before and after interventional therapy were analyzed.Results The difference of the course of diseases,dysmenorrhea history,diameter of cysts had statistical difference between the two groups (all P＜0.05).There were no statistical differences of age,history of dilivery,abortion history,history of pelvic surgery,cyst location between the two groups (all P＞0.05).In abnormal group,the mean serum level of CA125 reduced at 3 months (P＜0.000 1) and 6 months (P ＜0.000 1) after interventional therapy.In the normal group,there was no significant difference of the mean serum level of CA125 before and after interventional therapy (all P＞0.05).Conclusion Serum CA125 level is influenced by dysmenorrhea history,course of disease,diameter of cysts.Ultrasound-guided interventional therapy has intervention effect on patients with abnormal serum CA125 level before interventional therapy.

BACKGROUND: Some researches suggest that placenta is regarded as a new source of mesemchymal stem cells (MSCs). Adherent cells derived from placenta tissue have similar morphological characteristics and surface markers to MSCs; meanwhile, they can differentiate into osteoblasts and nerve cells.OBJECTIVE: To find a new source and way for MSCs separation.DESIGN: Observational study.SETTING: The Third People's Hospital of Wuxi.MATERIALS: Placenta was sourced from cesarean in our department of obstetrics and gynecology and provided confirmed consent from the relatives and ethics committee. The main reagents contained culture medium, sABC kit, DAB staining kit, caprine-anti-rat FITC, recombinant human basic fibroblast growth factor (rh-bFGF), rabbit-anti-human glial fibriliary acidic protein (GFAP).METHODS: The experiment was carried out in the Laboratory of Cells & Molecular Biology, the Third People's Hospital of Wuxi from May 2005 to August 2006. Placenta entity tissue was digested, adherent cells were cultured, morphological characteristics were observed, and growth curves of placenta-derived multipotent cells (PDMCs) in various generations were drawn. On the 1st and 7th days, supernatant was derived from cells in primary culture to measure content of β-glycerophosphate disodium (β-HCG) with chemiluminescence technique. In addition, expression of surface antigen and differentiating potency were detected at the same time. At 24 hours (at phase of nerve cells) and 2 weeks (at phase of osteoblasts) after inducible differentiation, cultured cells were dealt with routine immunocytochemical stain, and then they were observed under routine microscope or fluorescence microscope.MAIN OUTCOME MEASURES: ① Morphological indexes and growth curves of PDMCs; ② measurement of β-HCG in supernatant of PDMCs and expression of antigen of PDMCs with flow cytometer; ③ immunohistochemical analysis of PDMCs during and after inducible differentiation.RESULTS: ① Primary culture of PDMCs: After digestion of placenta tissue, a few of adherent cells were obtained and gradually formed thin and flat monolayer cells two weeks later. The monolayer cells grew like whirlpool or cluster. With the increase of cell density, soma was slenderer and slenderer and like fibroblast. ② Growth curves of PDMCs: Growth latency ranged from 2 to 8 days after cell inoculation. During this period, adherence was observed gradually but not obviously amplified. Eight days later, cells entered log growth phase. During this period, proliferation was active and cell process surrounding extended under phase contrast microscope. A lot of MSCs were observed in division phase between two nuclei. In addition, density was increased and cells connected to each other. Within 11-14 days, growth curve gradually entered platform phase. MSCs covered the bottom of bottle, cells slowly expanded, and primary culture stopped. ③ Measurement of β-HCG: Expression of β-HCG was not detected in supernatant at two time points. ④ Characteristics of surface antigen of PDMCs: PDMCs could express CD29, CD44 and CD105, but not CD34, CD45,CD19 and CD106. ⑤ Inducible differentiation of PDMCs: At 24 hours after inducing to nerve cells, form of PDMCs obviously changed, soma rebounded, refraction of nucleus was partially reinforced, structure was similar to dendrite and axis-cylinder, and positive neuro-specific enolase and GFAP were observed after staining.CONCLUSION:Placenta tissue contains PDMCs whose morphological function is similar to MSCs; in addition, placenta is regarded as an effective source of MSCs.

Objective: To study the expression of negative costimulatroy molecule B7-H4 in non-small cell lung cancer (NSCLC) tissues and its relationship with the clinical features of NSCLC. Methods: Fifty-two NSCLC specimens from pa-tients who were pathologically diagnosed in our hospital during January 2008 to April 2009 were included in the present study. B7-H4 expression and infiltration of CD3~+ T cells in NSCLC tissues were detected by immunohistochemistry. The correlation between B7-H4 expression, CD3~+ T infiltration, and the clinical features of NSCLC was studied. Results: The positive rate of B7-H4 in 52 NSCLC tissues was 48.08% (25/52), and B7-H4 expression in normal lung tissues was neg-ative or low (P <0.05). B7-H4 expression was positively correlated with the clinical tumor stages and lymph node metas-tasis of NSCLC (P < 0.05), and negatively correlated with tumor infiltration of CD3~+ T cells (P < 0.05), but had no re-lationship with clinicopathologie parameters of NSCLC (P > 0.05). Conclusion: Negative costimulatroy molecule B7-H4 may play important roles in the development of NSCLC. Positive expression of BT-H4 is correlated with the clinical tumor stages and lymph node metastasis of NSCLC, which provides a foundation for diagnosis and therapy of NSCLC.

With the further research of spinal cord injury treatment, a series of new drugs have been used in experiment and clinic. This article is to review the current developments of drugs combination in spinal cord injury.

OBJECTIVE:To evaluate the management of the free anti-TB drugs in He'nan province,and to analyze ex-periences and find out the gap.METHODS:Based on the requirements of the Chinese TB Control Program-Free anti-TB drug management manual,a questionnaire comprised of 17 items was developed and 20 TB drug storerooms at city or county level were randomly sampled for on the spot investigation.RESULTS:Of the total drug storerooms investigated,75% had yearly drug demand plan,but only 35% was up to the standard in inventory control,95% had no expired drug,90% had inventory/supply vouchers and detailed inventory records,only 25% achieved conformity between records and physical counts.The condition of drug storerooms and the storage of drugs were unable to meet the requirement.CONCLUSION:Tuberculosis Control Agency at different levels haven't paid due attention to the management of free anti-TB drugs.The personnel in this agency should raise their drug management responsibility from aspects of saving public belongings and ensuring patients' medication quality.

Aim Toinvestigatetheanalgesiceffectsof epidural osthole application on the mechanical allodyn-ia and the ERK/MAPK signaling pathway and the expression of COX-2 mRNA in the spinal dorsal horn.Methods 125adultmaleSDratswererandomizedin-to five groups( n=25 each) :Blank, Sham, NP, Ost and vehicle. At postoperative day 6, 1mg/rat osthole 50 μl was injected epidurally into group Ost and the same volume of vehicle was given into group vehicle. The mechanical pain threshold was measured by 50%MWT at 1 day before operation and the 3 rd,6 th,7 th, 14 th,21 st day after operation. After the measurement of pain threshold on postoperative day 14 , the L4-6 segment of spinal dorsal horn was removed for determi-nation of the expression of ERK, pERK and COX-2 mRNAbyWesternblotandRT-PCR.Results Com-pared with blank group, the mechanical pain threshold was only down-regulated at day 1 after operation in sham group, the expression of pERK and COX-2 mR-NA in sham group showed no significant difference ( P>0. 05 ); the mechanical pain threshold was signifi-cantly down-regulated after operation in NP, Ost and vehicle groups( P<0. 05 ) and the expression of pERK and COX-2 mRNA was significantly increased ( P <0. 05). Compared with vehicle group, the pain thresh-old in Ost group was significantly increased after drug administration( P<0. 05 ) and the expression of pERK and COX-2 mRNA was significantly reduced ( P <0. 05 ) . The expression of ERK showed no significant difference among each group(P>0. 05). The correla-tion analysis on pERK1/2 and COX-2 mRNA revealed the Pearson correlation coefficient was 0 . 878 and 0 . 910 , suggesting a strong positive correlation between pERKandCOX-2mRNA.Conclusions Ostholead-ministrated in the early stage after surgery can alleviate the nucleus pulposus-induced radicular inflammatory pain probably by inhibiting the expression of pERK and COX-2 mRNA in spinal dorsal horn.

Objective To compare the efficacy of dexmedetomidine versus remifentanil in combination with sevoflurane for gynecological laparoscopy. Methods Forty ASA Ⅰ or Ⅱ patients aged 18-64 yr with body mass index of 18-30 kg/m2 undergoing gynecological laparoscopy were randomly assigned to one of two groups ( n =20 each): dexmedetomidine group (group D) and remifentanil group (group R). Starting from 5 min before induction of anesthesia, dexmedetomidine was infused at 0.05 μg · kg - 1 · min- 1 in group D and remifentanil at 0.1 μg· kg- 1· min-1 in group R for 10 min, then dexmedetomidine infusion rate was increased to 0. 3 μg· kg-1 · h-1 and remifentanil infusion rate was increased to 0.15 μg· kg-1 · min-1 . Anesthesia was induced with propofol 1.5-2.0 mg/kg and fentanyl 2 μg/kg. Tracheal intubation was facilitated with cis-atracurium 0.15 mg/kg. Anesthesia was maintained with sevoflurane and fentanyl 1 μg/kg and intermittent iv boluses of cis-atracurium. Narcotrend index was maintained at 40-50. Blood sample was taken from external jugular vein for blood gas analysis and determination of serum concentrations of corticosteroid, norepinephrine and epinephrine before administration, at 5 min after intubation, at 10 min of aeroperitoneum and at 5 min after extubation. The pH value and concentrations of lactic acid and glucose were recorded. The time for recovery of spontaneous breathing, eye-opening time, extubation time, orientation time and perioperative side-effects were recorded. Numeric rating scale was used to assess the intensity of pain during 2 h after operation. The analgesics used were also recorded. Results The serum concentrations of norepinephrine and epinephrine were significanfly lower at 10 min of aeroperitoneum, the time for recovery of spontaneous breathing was shorter, eye-opening time longer and the incidence of shivering and nausea and vomiting lower, the percentage of patients requiring rescue opioids lower in group D than in group R ( P ＜ 0.05). Conclusion The efficacy of dexmedetomidine combined with sevoflurane anesthesia is better than remifentanil combined with sevoflurane anesthesia for gynecological laparoscopy.

Objective To investigate the clinical phenotype and genotype in three probands with antithmmbin(AT)deficiency and their families,and to identify the molecular mechanism of AT deficiency.Methods Chromogenic substrate method and immunoturbidimetry assay was used to detect the plasma levels of AT:A and AT:Ag,respectively.Genomic DNA was extracted from the peripheral blood.All 7 exons and the flanking sequences were amplified by PCR.and the abnormal mutant genes were analyzed by direct sequencing.Western blot was used to detect the AT levels and thrombin generation tests were used to detect coagulation status.Results The plasma levels of AT:A and AT:Ag of the three probands declined by 50%.G7386C(Trp225Cys)mutation in exon 4,C2591G(Ser36stop)in exon 2 and C9819T(Arg359stop)in exon 5 were characterized in the three prebands and they could result in W(Trp)225C(Cys)missense mutation,S(Set)36X(stop)nonsense mutation and R(Arg)359X(stop)nonsense mutation respectively,The testing results of phenotype and genotype from some of their family members showed consistent with results from the probands.Western blot results indicated that the Icyels of PC:Ag were lower compared with the normal pooled plasma.The hypercoagulative status was present in the probands using thrombin generation tests.Conclusions Type Ⅰ hereditary AT deficiency was found in these three families.The 3 heterozygous mutations.W225C,S36X and R359X are genetic defects of hereditary AT deficiency.W225C and S36X have not been described before.

Ⅺ deficiency in Chinese Han population. Conclusion The 13 mutations of the F Ⅺ gene which were found in this study may unravel the molecular pathogenesis of the F Ⅺ deficiency in Chinese Han population.

Objective To investigate the genetic diagnosis and molecular pathogenesis of four patients with combined deficiency of coagulation factor Ⅴ and Ⅷ and their family members. Methods The APPT, FT, FⅤ: C, FⅧ: C were detected for phenotypic diagnosis. Thrombin generation assay was applied to determine the generation condition of thrombin in patients and healthy controls. Cenomic DNA was extracted from peripheral blood using the TianGen RelaxCene Blood DNA System;amniotic fluid DNA was extracted with phenol-ethyl ether method. The LMAN1 and MCFD2 genes were analyzed by PCR. Gene mutations were detected with nucleotid sequences by using end-labeling dideoxy method. Results The APTT of Proband 1 was significantly prolonged to 88. 2s and her PT was prolonged to 19. 6 s. The combined deficiency was identified with FⅧ (FⅧ: C 24. 2% ) and FV(FⅤ: C 9. 1% ). Proband 2 and 3 were sisters. The coagulation studies revealed that both of them had prolonged APTT (71.6 s and 74.6 s respectively) and PT (22. 1 s and 18. 3 s respectively). The combined deficiency of FⅤ (FⅤ: C 7. 6% and 14. 5% respectively) and FⅧ( FⅧ: C 25% and 19.6% respectively) were identified. Proband 4 was detected to have the prolonged APTT (70.3 s),PT (18.2 s) and the deficiency of FⅤ(FⅤ: C 9. 4% ) and FⅧ (15. 7% ). The remaining phenotype indicators test of the 4 probands were normal. The diagnosis for the 4 probands was combined deficiency of factor Ⅴ and Ⅷ. The proband 1 was detected to have compound heterozygous mutations in LMAN1 gene while having the LMAN1 and MCFD2 direct gene sequencing. One mutation was a small insertion located on exon 8 [ nt912insA (X71661. 1)] that resulted in p. 305frameshiftX20 and her mother was detected to have the same heterozygous mutation on the the locus. The other mutation was located on exon 11: nt1366C > CT ( X71661. 1 ) , p. 456Arg > Stop which was inherited from her father. Amniocyte DNA was detected to have only one heterozygous mutaion [nt1366C > CT (X71661. 1) , 456Arg > Stop] inherited from the father. No mutation in MCFD2 gene was found in proband 1 and her parents. The analysis of the MCFD2 gene in proband 2 and 3 revealed a novel homozygous single base substitution (nt411T>C) in exon 4, which results in the exchange of the amino acid isoleucine by the amino acid threonine at amino acid position 136 (p. Ile136Thr). Sequencing of the whole LMAN1 gene showed that the proband 4 had one homozygous nonsence mutation in the exon 5 of the LMAN1 ( nt615C >T,p. 202 Arg> Stop). All of the 4 probands with combined deficiency of FⅤ and FⅧ showed declined endogenous thrombin potential in the thrombin generation tests. Conclusion The combined deficiency of FⅤ and FⅧ in the proband 1 results from the compound heterozygous mutations ( nt1366C > CT and nt912insA) in LMAN1 gene, which are inherited from her parents respectively. The prenatal genetic investigation for the patient mother with preganency indicates that the fetus is a female carrier with one mutation (nt1366C > CT) inherited from the father. The homozygous missence mutation ( nt411T > C, p. Ile136Thr) in the MCFD2 gene accounts for the proband 2 and 3. The daughter of the proband 2 is a carrier with a heterozygous mutation inherited from her mother. The homozygous nonsence mutation in the LMAN1 gene of the proband 4 results in the deficency of F Ⅴ and FⅧ.