Lower extremity deep venous thrombosis (LEDVT) is one of the common complications for postoperative patients with gynecologic oncology,which affect the prognosis of surgical patients seriously.LEDVT mainly caused by vein wall damage of pelvic surgical procedures and lower extremity infusion,slow venous blood flowing leading by anesthesia and bedridden,the hypercoagulability due to fasting before and after surgery and lack of fluid amount.

Background & Objective: The calcitonin gene-related peptide (CGRP) has a central role in the pathogenesis of migraine, but variations in CGRP-related genes, including the calcitonin gene-related polypeptide-alpha (CALCA) gene and the receptor activity modifying 1 (RAMP1) gene, have not been found to link with migraine in Australian population. The goals of this study were to determine whether variants in the two genes are related to migraine in Chinese population. Methods: Using a case-control approach, rs3781719 and rs145837941 in the CALCA gene and rs3754701 and rs7590387 at the RAMP1 locus was analyzed in a cohort of 504 migraine cases and 529 ethnically matched controls. Genotyping was performed using Sequenom MALDI-TOF mass spectrometry iPLEX platform. Results: The CALCA gene rs145837941 variant was not found in migraine or control group. No significant difference in genotypic and allelic distribution was observed in the other three polymorphisms between migraine cases and controls. All the three SNPs were also not selected as significant factors that independently contributed to susceptibility to migraine in multivariate analysis. In the subgroup analysis, the CALCA rs3781719 seemed to be a significant risk for migraine with aura, but was not statistically significant after FDR correction. Moreover, there was no synergistic relationship between the three SNPs in the multifactor dimensionality reduction analysis for explore locus–locus interactions. Conclusion: Our data suggested that variants in CALCA gene and RAMP1 gene were not associated with migraine in the Han-Chinese population.
Calcitonin Gene-Related Peptide ; Migraine Disorders

Forty five patients with acute cerebral infarction were randomized to two groups: in treatment group patients received local subhypothermia and conventional therapy, in control group patients received conventional therapy only. Clinical outcome was assessed by the National Institutes of Health Stroke Scale (NIHSS) on admission and at 7, 14 and 30 d after treatment. Serum neuron specific enolase (NSE), nitrogen monoxide ( NO ) , superoxide dismutase (SOD), interleukin-6 (IL-6 ) and intercellular adhesion molecule-1 (ICAM-1) were detected on admission and at 7,14 d after treatment The study showed that NIHSS scores of treatment group on 14, 30 d were lower than those of control group ( P ＜ 0. 05 ). Serum NSE, NO, IL-6 and ICAM-1 levels significantly decrease; while serum SOD levels increased (P ＜ 0. 05). In conclusion, local subhypothermia therapy can inhibit inflammatory reaction, reduce oxygen free radical formation and improve neurological function in patients with acute cerebral infarction.

Objective:To analyze the differentally expressed long non-coding RNA (lncRNA) among mice of different ages and explore the mechanism of kidney aging.Methods:Male C57BL/6 mice aged 3-month-old ( n=5), 12-month-old ( n=5) and 24-month-old ( n=5) (each weighting about 25 g) were randomly selected. PAS staining, Masson staining and senescence associated β-galactosidase (SA-β-gal) staining were used to detect the pathology and cell senescence of mice kidney. High throughput sequencing was performed to detect the differentially expressed lncRNA and their fragments per kilobase million. Real-time quantitative PCR was used to verify the differentially expressed lncRNA. Competitive endogenous RNA (ceRNA) network, which consisted of lncRNA, miRNA and mRNA was built. GO and KEGG enrichment analysis method were used to predict the biological function of differentially expressed lncRNA. Results:PAS staining and Masson staining showed the development of kidney fibrosis, and SA-β-gal staining positive region was increased significantly as age increased. There were 938 known lncRNA and 542 novel lncRNA differentially expressed among different ages' mouse kidney. Compared with 3-month-old mice, 33 lncRNA were up-regulated and 43 lncRNA were down-regulated in 12-month-old mice. Compared with 3-month-old mice, 130 lncRNA were up-regulated and 91 lncRNA were down-regulated in 24-month-old mice. Compared with 12-month-old mice, 36 lncRNA were up-regulated and 22 lncRNA were down-regulated in 24-month-old mice. The results of qRT-PCR about verified 10 lncRNAs with larger differential expression multiples and higer expression levels were consistent with the sequencing data. GO enrichment analysis showed that the target genes of lncRNA differentially expressed in the three groups were mostly located in the nucleus and cytoplasm, and might play a role by binding to proteins or participate in various protein phosphorylation, cell cycle, transcription, transcription regulation and other processes. KEGG enrichment analysis showed that the target genes of lncRNA differentially expressed in the three group were significantly enriched in Rap1 signaling pathway, FOXO signaling pathway and MAPK signaling pathway, which were closely related to kidney aging.Conclusion:There are significant differences in expression of lncRNA among the kidney of different ages mice, which are involved in the occurrence of renal senescence.

OBJECTIVETo evaluate variations in the plasma tissue factor (TF) and urokinase type plasminogen activator (u-PA) system and their relationship with clinical cancer type, pathological classification and metastatic status in cancer patients.

METHODSPlasma levels of TF and its inhibitor (TFPI), as well as u-PA and its receptor (u-PAR) were measured using ELISA in 76 patients with malignant tumors and 24 patients with benign tumors.

RESULTSPlasma levels of TF and u-PAR in the malignant tumor group were significantly higher than those of the benign tumor group and the normal control. U-PA and u-PAR increased significantly in patients with esophageal and gastric cancer. However, most of these parameters except TFPI did not vary according to pathological classification. A significant elevation was evident in patients with local infiltration, lymph node involvement and distal metastasis, while u-PAR only increased in the latter two categories.

CONCLUSIONSBoth the TF and u-PA systems are activated in cancer patients. U-PA and its receptor might prove to be a clinically useful marker for disease progression.

Adult ; Aged ; Aged, 80 and over ; Female ; Humans ; Lipoproteins ; blood ; Male ; Middle Aged ; Neoplasm Metastasis ; Neoplasms ; blood ; pathology ; Receptors, Cell Surface ; blood ; Receptors, Urokinase Plasminogen Activator ; Thromboplastin ; metabolism ; Urokinase-Type Plasminogen Activator ; blood

Ectopic pregnancy is a common gynecological acute abdomen disease. Once the pregnant tissue is ruptured, it will rapidly develop into hemorrhagic shock or even death. In recent years, blood transfusion from the body is widely used in the rescue of intra-abdominal hemorrhage of ectopic pregnancy, which can reduce the time of cross matching and blood collection, reduce the risk of allogeneic blood transfusion, and enable patients with hemorrhagic shock to receive timely and effective treatment. Hemolysis caused by autologous blood transfusion is rarely reported. Once hemolysis occurs, if it is not handled in time, severe cases can occur acute renal injury, hyperkalemia, or cardiac arrest or even sudden death. We retrospectively analyzed the diagnosis and treatment of a patient with hemolysis after autologous blood transfusion, suggesting that the adverse reactions of blood transfusion occur not only in allogeneic blood transfusion, but also in autologous blood transfusion. It should be handled reasonably in clinical work to reduce the occurrence of similar complications.

OBJECTIVETo investigate the plasma levels of coagulation factor VII (FVII) and polymorphisms of FVII gene in patients with coronary heart disease (CHD), and evaluate the effect of plasma FVII levels and FVII gene polymorphisms on CHD.

METHODSPlasma FVIIa, FVII: Ag and FVIIc were measured and polymorphisms of FVII gene were analyzed in 149 control cases and 60 CHD cases, including 33 acute myocardial infarction (AMI) cases by a combination of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and agarose gel electrophoresis.

RESULTSFVIIa, FVIIc in AMI group were significantly higher than that in control group, but FVII: Ag wasn't. There were no significant difference in plasma FVIIa, FVII: Ag and FVIIc between CHD and control group. The IVS7 genotypic frequency in AMI group was significantly different from that in control group. There was no significant difference in genotypic frequencies and allelic frequencies in other polymphism sites. FVII: Ag was significantly higher in -402A homozygote than that in -402G homozygote.

CONCLUSIONSIncreased FVII levels, especially FVIIa and FVIIc in plasma, may contribute to coronary artery thrombosis. There was significant difference in IVS7 genotype frequency between control and AMI groups, but the rest weren't significantly different. FVII: Ag was significantly higher in -402A homozygote than that in -402G homozygote. Polymorphism of -402 G/A may play an indirect role in AMI by regulating plasma FVII levels.

Coronary Disease ; blood ; genetics ; Factor VII ; analysis ; genetics ; Female ; Genotype ; Humans ; Male ; Middle Aged ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length

OBJECTIVETo accomplish a kind of therapeutic gene for hemophilia A, and observe the expression of human factor VIII (hF VIII) in vivo.

METHODSHuman clotting factor VIII cDNA with B-domain deleted (Delta760aa approximately 1639aa) was inserted into vector pRC/RSV to form pRC/RSV-hF VIII BD, which conjugated with in vivo liposome transfection reagent (DOTAP-Cholesterol) to accomplish a kind of therapeutic gene, pRC/RSV-hF VIII BD-DOTAP-Cholesterol. Mice were injected with pRC/RSV-hF VIII BD-DOTAP-Cholesterol i.m. and sacrificed 48 hours, 10 days, 20 days, 30 days, 40 days and 50 days later, respectively. Tissues such as heart, liver, spleen, lung, kidney and muscle were harvested, the distribution and transcription as well as expression of hF VIII BD cDNA were detected by means of PCR, RT-PCR and immunohistochemistry techniques. In addition, the antigen and antibody of hF VIII in plasma were measured.

RESULTSThere was high expression of hF VIII in plasma and tissues at the 48(th) hour after injection. On day 10, antigen level of hF VIII in plasma reached its peak, 17.55 ng/ml, and gradually reduced later. The antibody of hF VIII in plasma emerged on day 10 after injection, and increased and gradually reached 37.06 U/ml on day 50 after injection. PCR, RT-PCR and immunohistochemistry showed that hF VIII BD cDNA and its transcription as well as expression existed in all kinds of tissues, and lasted longer in spleen, lungs and kidneys than in heart, liver and muscle.

CONCLUSIONTherapeutic gene, pRC/RSV-hF VIII BD-DOTAP-Cholesterol, produced by combination of pRC/RSV-hF VIII BD and DOTAP-Cholesterol liposome can express human F VIII successfully in vivo, which lays an experimental foundation for curing hemophilia A by gene-drug in clinic.

Animals ; DNA, Complementary ; Disease Models, Animal ; Factor VIII ; biosynthesis ; genetics ; therapeutic use ; Gene Expression ; Genetic Therapy ; Genetic Vectors ; Hemophilia A ; therapy ; Humans ; Liposomes ; Mice ; Mice, Inbred BALB C ; Tissue Distribution ; Transfection

OBJECTIVETo identify the mutation of coagulation factor VII (F VII) gene in two pedigrees with hereditary F VII deficiency.

METHODSF VII gene mutations were analysed in two propositi and their family members by direct DNA sequencing. Allele specific PCR and PCR combined with restricted enzyme digestion were used to confirm the detected mutations.

RESULTSTwo gene mutations were detected in the propositus of pedigree A: G to C transition at position 6390 resulting in Trp40Cys and G to A at 11496 resulting in Arg353Gln, both are heterozygotes. The heterozygosity for polymorphism Arg353Gln was confirmed with the restriction enzyme Msp I digestion in his mother. In the propositus of pedigree B, there was a T to G transition at position 11482 resulting in His348Gln, heterozygosity of which was confirmed with Nsp I digestion in the propositus and his daughter. G to T transition at position 11514 resulting in Thr359Met was also found in the propositus of pedigree B, and the heterozygosity for Thr359Met was confirmed with allele specific PCR in the propositus and his son.

CONCLUSIONThree missense mutations were found in two pedigrees with hereditary F VII deficiency. A novel Trp40Cys mutation was reported for the first time.

Factor VII ; genetics ; Factor VII Deficiency ; genetics ; Female ; Heterozygote ; Humans ; Male ; Mutation, Missense ; Pedigree ; Point Mutation ; Polymerase Chain Reaction ; methods

OBJECTIVETo explore gene defect of hereditary coagulation factor XIII deficiency.

METHODSPCR and gene sequencing or ARMS-PCR were used to detect the FXIIIA gene of peripheral white blood cell (PBC) from two Chinese hereditary coagulation factor XIII deficiency family members and 60 normal subjects respectively. The level of FXIIIA gene mRNA was tested by RT-PCR.

RESULTS(1) Nucleotide sequence analysis of the two probands' and their family members' DNA revealed that all of the three patients had homozygous missense mutation in FXIII A subunit gene. Proband 1 had a C to G transition at nucleotide (nt) 1 241 in exon 10 and proband 2 and his sister a C to T transition at nt 232 in exon 3 of FXIII A gene, which resulted in the substitution of Ser413 with Trp and Arg 77 with Cys, respectively. Family study showed that the two mutations were inherited from the parents who were correspondingly heterozygotes at nt 1 241 or nt 232. (2) The two mutations were not found in the normal subjects. (3) The FXIIIA gene mRNA level in the two probands was a little decreasing.

CONCLUSIONIt is the two novel mutations that results in FXIIIA deficiency. The two mutations of FXIIIA gene may affect its function or alter protein folding. The defective FXIII which is unstable and degraded rapidly in cytoplasm may be the main cause of FXIII deficiency.

Blood Coagulation Disorders, Inherited ; genetics ; Child ; Exons ; genetics ; Factor XIII ; genetics ; Factor XIII Deficiency ; genetics ; Female ; Heterozygote ; Humans ; Pedigree ; Point Mutation ; Polymerase Chain Reaction ; methods