Objective To investigate the clinical value of bronchofibroscope to the patients with respiratory failure treated by mechanical ventilation. Methods 44 patients with respiratory failure treated by mechanical venti-lation who were rescued with bronchofibroscope in EICU from January 2006 to June 2007 were compared the days of antibiotic application, the days of mechanical ventilation and mortality rate with 35 patients with respiratory failure treated by mechanical ventilation but not using bronchofibroscope during January 2005 to January 2006. Results Compared with the control group, the therapy group had fewer days of antibiotic application, fewer days of mechani-cal ventilation and lower mortality rate(P < 0.05). During absorbing expectoration with bronchofibroscope, compli-cation such as haemorrhage did not happen. Conclusion Bronchofibroscope application in the patients with respira-tory failure treated by mechanical ventilation can shorten the time of mechanical ventilation and cut down the mortal-ity rate,which was worth generalizing in clinical work.

OBJECTIVE To explore the incidence rate,pathogen distribution and characteristics of drug resistance of ventilator-associated pneumonia(VAP) patients due to acute lung injury and acute respiratory distress syndrome(ALI/ARDS) after severe injury,and analyze impact factors on VAP.METHODS All 183 cases with ALI/ARDS after severe injury from Jan 2004 to Mar 2008,were admiitted and given mechanic ventilation over 48 hours in our ICU and EICU.RESULTS VAP was found in 98 cases,accounted for 53.56%.Among them,42 were early-onset VAP and the other 56 were late-onset VAP.Altogether 276 pathogens were isolated,and most of them were Pseudomonas aeruginosa,Staphylococci aureus,Klebsiella pneumoniae,Acinetobacter baumannii and Escherichia coli.In 41 cases only one pathogen was isolated,the other 57 cases were with two or above pathogens.The revealed important risk factors were coma,prolonged mechanical ventilation,tracheotomy,antiacid treatment,use of antimicrobial agents and low albumin.CONCLUSIONS The incidence rate of VAP due to ALI/ARDS is high,and most of the isolated pathogens are drug resistant.Mixed infections are found commonly in these cases.

Objective To investigate the correlation between mucosal healing after treatment and prognosis of ulcerative colitis (UC).Methods UC patients who were remitted after treatment (n =82) were divided into MH group(A:DA1,0-1 ; Geboes,0-1) and non-MH group (B:DAI,0-1 ; Geboes,2-5) according to the assessment and were followed up for 2 years.The baseline characteristics,histological parameters,serologic indices (albumin,ESR,CRP,ANCA,IL-1 β,IL-6 and IL-15) at 0,12,24 months or recurrence and hospitalization,colon surgery,colon cancer were recorded.The correlation between mucosal healing and prognosis were assessed.Results There were no significant differences between group A and B in recurrence rate and recurrence time(P ＞ 0.05).The multivariate Cox regression analysis showed that gender (female),past recurrence,pANCA and basal plasmacytosis were independent risk factors for recurrence of UC (P ＜ 0.05).The rehospitalization rate [27.5％ (group A) VS 44.1％ (group B) ; P =0.018 ; OR=2.24,95％CI (1.11-3.98)] and colectomy rate [0％ (group A) VS 17.6％ (group B); P=0.035; OR =5.43,95％ CI (2.14-7.64)] between groups have significant differences,however,rates of cancer [0％ (group A) VS 2.7％ (group B) ; P=0.643; OR =3.43,95％CI (0.14-7.64)] were not significantly different.Conclusion Mucosal healing after treatment is associated with UC prognosis.

Objective To determine the evaluating prognostic value of plasma Nt-proBNP in patients with congestive heart failure.Methods 107 patients with congestive heart failure were included in this study,followed the degree of rehospitalization and mortality rate of the cured patients after left hospital.The plasma concentrations of Nt-proBNP were measured by enzymelinked immunozorbent assay(ELISA).Results Concentrations of Nt-proB-NP of Ⅱ,Ⅲ,Ⅳ classincation were(1129.8±383.2),(5849.7±567.6),(9506.3±492.4)ng/L in NYHA functional classification respectively(P＜0.01);the plasma level of Nt-proBNP had significant positive correlation with NYHA functional classification(r=0.759,P＜0.01).The degree of rehospitalization were(0.85±0.96),(1.98±0.86),(2.58±0.91)respectively(P＜0.01);mortality rate were 8.3%,12.5%,45.2%respectively(P＜0.01).Conclusion Plasma Nt-proBNP level may be the more important clinic value in evaluating prognosis in patients with congestive heart failure.

Objective To study the establishment of rat model of asphyxia-cardiac arrest and efficacy of CPR in order to find the length of optimum time of asphyxia to cause injury.Methods One hundred and twenty-six male Sprague-Dawley rats were randomly (random number) divided into sham operation group and experimental groups.Cardiac arrest was induced by asphyxiation after intravenous injection of vecuronium bromide.The experimental groups were assigned into AP4 (four-minute asphyxia period),AP6 and AP8 subgroups in accordance with different lengths of time of asphyxia subjected to.In these groups,CPR,including pre-cordial compression and synchronized mechanical ventilation,was initiated 4,6 and 8 min after asphyxia-induced cardiac arrest,respectively.The successful ratio of resuscitation and hemodynamic variables were recorded.Brain water content,neural deficit scores (NDS),imaging changes on MR,pathological changes of brain tissue and neuronal apoptosis were evaluated at 1 d,3 d and 7 days after ROSC.All the data were analyzed by single-factor analysis of variance or Chi-square test.P ＜ 0.05 was considered statistically significant.Result The lowest NDS occurred at 1 d after ROSC,brain water content and imaging changes on MR were most obvious at 3 d after ROSC,while pathological changes of brain tissue and neuronal apoptosis increased and reached the peak at 7d after ROSC.The survival rates after 24 hours of AP4,AP6 and AP8 groups were 85％,75％ and 45％,respectively.The rate of ROSC and survival rate of AP8 group were significantly lower than those of other groups (P ＜0.01).The longer time of asphyxia the severer pathological changes of brain tissue,brain edema,neural deficit,and magnetic resonance imaging changes in all experimental groups.As compared to other groups,the brain damage index of AP8 group was most serious,while that of AP6 group was moderate.Conclusions The rat model following asphyxia-induced cardiac arrest and cardiopulmonary resuscitation was established successfully.From the evidence of survival rate and damage grade of brain tissue,asphyxia for 6 min may be the rational length of ischemic time in this model.

Objective To determine the value of using B-type natriuretic peptide (BNP) and D-dimer in preliminary recognition of cardioembolic stroke patients.Methods A mutilple-center study was conducted in Foshan Hospital of traditional Chinese Medicine (TCM) and its affiliated hospitals from July 2015 to July 2016.In the emergency departments (EDs),emergency physicians prospectively assessed consecutive adult patients with acute cardioembolic stroke and measured plasma BNP by POCT platform on admission,then followed up.Stroke neurologists evaluated patients' functional outcome at hospital discharge and also made discharge diagnosis and stroke etiologic subtypes according to the TOAST criteria.Results In this study,290 acute ischemic stroke patients met the study criteria [mean age (68.41 ± 12.06) years;53.8％ female].Of the enrolled patients,28.3％ were diagnosed with LAA at discharge,17.9％ with CE,42.8％ with SAO,11.0％ with SOE or SUE.And the mean BNP concentration was significantly higher in the CE group than that in other three subtypes (P ＜ 0.001).After adjustment for multiple clinical predictors like gender,age,coronary artery disease,atrial fibrillation and renal function,BNP and D-dimer were associated with CE [BNP OR:1.044 (95％ CI 1.025,1.064),P ＜ 0.001;D-dimer OR:1.511(95％ CI 1.020,2.238),P =0.039,respectively].Conclusion Through POCT technique in the EDs,cardioembolic stroke patients can be differentiated from other TOAST subtypes.BNP with/without D-dimer has good but different corresponding diagnostic performance in preliminary recognition of cardioembolic stroke patients.

OBJECTIVE: To carry out phenotypic and genotypic analysis for two Chinese pedigrees affected with coagulation factor XII (F XII) deficiency. METHODS: Plasma prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (FIB), thrombin time (TT), and blood coagulation factor VIII, IX, XI, XII activity (FVIII:C, FIX:C, FXI:C, FXII:C) were determined with one stage clotting assay on a STAGO coagulation analyzer. FXII antigen was determined with an enzyme linked immunosorbent assay (ELISA). The 14 exons and their flanking sequences of the F12 gene were subjected to PCR amplification and Sanger sequencing. The conservation and structure of mutant protein were analyzed with MegAlign software and PYMOL software. RESULTS: The APTT of the probands was significantly prolonged, while their FXII:C and FXII:Ag were significantly reduced. Genetic analysis of the proband has revealed three novel mutations in the F12 gene, including g.5972G>A splice site mutation in intron 5, g.8810_8814delGTCTA in exon 14, and g.6259G>A (p.Pro182Leu) in exon 7. In addition, a previously known mutation IVS13-1G>A has been found. CONCLUSION Four mutations have been identified in the two Chinese pedigrees, among which three were novel. Above mutations probably played a role in the defect of FXII in the two pedigrees.
Exons ; Factor XII ; genetics ; Factor XII Deficiency ; genetics ; Genetic Testing ; Humans ; Pedigree

OBJECTIVE: To analyze the phenotype and genotype of a pedigree affected with congenital dysfibrinogenemia. METHODS: Liver and kidney functions of the proband and her relatives were determined. Coagulation tests including prothrombin time (PT), activated partial thromboplastin time (APTT) and thrombin time(TT), fibrin(ogen) degradation products (FDPs), D-dimer(D-D) and the calibration experiment of protamine sulfate of against plasma TT were detected in the proband and her predigree members. The activity and antigen of fibrinogen (Fg) in plasma were measured by Clauss method and immunonephelometry method, respectively. All of the exons and exons-intron boundaries of the three fibrinogen genes (FGA, FGB and FGG) were subjected to PCR amplification and Sanger sequencing. Potential influence of the suspected mutations were analyzed with bioinformatics software including PolyPhen-2, SIFT and Mutation Taster. RESULTS: The proband had normal PT, APTT, FDPs, D-D and prolonged TT (31.8 s). The activity of fibrinogen (Fg) in plasma was significantly decreased but the antigen was normal. Genetic analysis revealed a heterozygous c.92G>A (p.Gly31Glu) mutation in exon 2 of the FGA gene. Family studies revealed that the mother carried the same mutation. Bioinformatic analysis suggested that the mutation may affect the function of Fg Protein. CONCLUSION The dysfibrinogenemia was probably caused by the novel Gly31Glu mutation of the FGA gene.
Afibrinogenemia ; congenital ; genetics ; DNA Mutational Analysis ; Female ; Fibrinogen ; genetics ; Humans ; Mutation ; Pedigree ; Phenotype

Objective: To analyze the phenotype and genotype of a pedigree affected with congenital dysfibrinogenemia. Methods: Liver and kidney functions of the proband and her relatives were determined. Coagulation tests including prothrombin time (PT), activated partial thromboplastin time (APTT) and thrombin time(TT), fibrin(ogen) degradation products (FDPs), D-dimer(D-D) and the calibration experiment of protamine sulfate of against plasma TT were detected in the proband and her predigree members. The activity and antigen of fibrinogen (Fg) in plasma were measured by Clauss method and immunonephelometry method, respectively. All of the exons and exons-intron boundaries of the three fibrinogen genes (FGA, FGB and FGG) were subjected to PCR amplification and Sanger sequencing. Potential influence of the suspected mutations were analyzed with bioinformatics software including PolyPhen-2, SIFT and Mutation Taster. Results: The proband had normal PT, APTT, FDPs, D-D and prolonged TT (31.8 s). The activity of fibrinogen (Fg) in plasma was significantly decreased but the antigen was normal. Genetic analysis revealed a heterozygous c. 92G>A (p.Gly31Glu) mutation in exon 2 of the FGA gene. Family studies revealed that the mother carried the same mutation. Bioinformatic analysis suggested that the mutation may affect the function of Fg Protein. Conclusion The dysfibrinogenemia was probably caused by the novel Gly31Glu mutation of the FGA gene.

OBJECTIVETo analyze clinical manifestation and genetic mutations in 8 Chinese pedigrees featuring hereditary dysfibrinogenemia.

METHODSProthrombin time(PT), activated partial thromboplastin time(APTT), thrombin time(TT), calibration of plasma protamine sulfate against TT, fibrinogen (Fg) activity, coagulation factors II, V, VII, VIII, IX, X, XI and XII of all probands and their family members were detected with an automatic blood coagulation analyzer; D-dimer(D-D) and fibrin(ogen) degradation products(FDPs) were also dtected by automatic blood coagulation analyzer, Fg antigen were detected with an immunoturbidimetry method. Exons of fibrinogen genes FGA, FGB and FGG and flanking sequences were amplified by polymerase chain reaction(PCR) and sequenced.

RESULTSAll of the probands showed normal levels of FDPs, D-dimer(D-D) and activity of coagulation factor II,V,VII, VIII, IX,X,XI, XII. Plasma PT and APTT were normal or slightly prolonged. Prolonged TT was found in all of the probands, whilst TT was not significantly shortened by protamine sulfate. Fg antigen was within the normal range, but Fg activity was significantly decreased. The Fg antigen/activity ratio was greater than 2. One proband has carried a heterozygous variant of the FGA gene g.1233G>A(p.A α Arg35His). Four have carried a heterozygous mutation of the FGB gene g.9692A>G(p.Bβ Asn190Ser). The remaining 3 had heterozygous substitution of FGG gene g.10819G>A(p.γ Arg301His). In addition, 2 polymorphisms (p.A α Thr331Ala) and p.B β Arg478Lys) were identified in FGA and FGB genes.

CONCLUSIONp.A α Arg35His, p.B β Asn190Ser and p. γ Arg301His are responsible for the inherited dysfibrinogenemia in the 8 Chinese pedigrees. p.B β Asn190Ser is firstly reported in China. p.B β Asn190Ser and p. γ Arg301His may be mutation hot spot in the Chinese population.

Afibrinogenemia ; blood ; genetics ; Fibrin Fibrinogen Degradation Products ; analysis ; Fibrinogen ; analysis ; genetics ; Humans ; Pedigree