OBJECTIVE: To observe the characteristics of changes in non-invasive hemodynamic parameters in neonates with septic shock so as to provide clinical reference for diagnosis and treatment. METHODS: A observational study was conducted. The neonates with sepsis complicated with septic shock or not admitted to neonatal intensive care unit (NICU) of the First Affiliated Hospital of Shantou University Medical College were enrolled as the study subjects, who were divided into preterm infant (< 37 weeks) and full-term infant (≥ 37 weeks) according to the gestational age. Healthy full-term infants and hemodynamically stable preterm infants transferring to NICU after birth were enrolled as controls. Electronic cardiometry (EC) was used to measure hemodynamic parameters, including heart rate (HR), mean arterial pressure (MAP), stroke volume (SV), stroke volume index (SVI), cardiac output (CO), cardiac index (CI), systemic vascular resistance (SVR) and systemic vascular resistance index (SVRI), before treatment in the septic shock group, at the time of diagnosis of sepsis in the sepsis without shock group, and before the discharge from the obstetric department or on the day of transferring to NICU in the control group. RESULTS: Finally, 113 neonates with complete data and parental consent for non-invasive hemodynamic monitoring were enrolled, including 32 cases in the septic shock group, 25 cases in the sepsis without shock group and 56 cases in the control group. In the septic shock group, there were 17 cases at the compensated stage and 15 cases at the decompensated stage. There were 21 full-term infants (20 cured or improved and 1 died) and 11 premature infants (7 cured or improved and 4 died), with the mortality of 15.62% (5/32). There were 18 full-term infants and 7 premature infants in the sepsis without shock group and all cured or improved without death. The control group included 28 full-term infants and 28 premature infants transferring to NICU after birth. Non-invasive hemodynamic parameter analysis showed that SV, SVI, CO and CI of full-term infants in the septic shock group were significantly lower than those in the sepsis without shock group and control group [SV (mL): 3.52±0.99 vs. 5.79±1.32, 5.22±1.02, SVI (mL/m²): 16.80 (15.05, 19.65) vs. 27.00 (22.00, 32.00), 27.00 (23.00, 29.75), CO (L/min): 0.52±0.17 vs. 0.80±0.14, 0.72±0.12, CI (mL×s^-1×m^-2): 40.00 (36.67, 49.18) vs. 62.51 (56.34, 70.85), 60.01 (53.34, 69.68), all P < 0.05], while SVR and SVRI were significantly higher than those in the sepsis without shock group and control group [SVR (kPa×s×L^-1): 773.46±291.96 vs. 524.17±84.76, 549.38±72.36, SVRI (kPa×s×L^-1×m^-2): 149.27±51.76 vs. 108.12±12.66, 107.81±11.87, all P < 0.05]. MAP, SV, SVI, CO and CI of preterm infants in the septic shock group were significantly lower than those in the control group [MAP (mmHg, 1 mmHg ≈ 0.133 kPa): 38.55±10.48 vs. 47.46±2.85, SV (mL): 2.45 (1.36, 3.58) vs. 3.96 (3.56, 4.49), SVI (mL/m²): 17.60 (14.20, 25.00) vs. 25.50 (24.00, 29.00), CO (L/min): 0.32 (0.24, 0.63) vs. 0.56 (0.49, 0.63), CI (mL×s^-1×m^-2): 40.01 (33.34, 53.34) vs. 61.68 (56.68, 63.35), all P < 0.05], while SVR and SVRI were similar to the control group [SVR (kPa×s×L^-1): 1 082.88±689.39 vs. 656.63±118.83, SVRI (kPa×s×L^-1×m^-2): 126.00±61.50 vs. 102.37±11.68, both P > 0.05]. Further analysis showed that SV, SVI and CI of neonates at the compensation stage in the septic shock group were significantly lower than those in the control group [SV (mL): 3.60±1.29 vs. 4.73±1.15, SVI (mL/m²): 19.20±8.33 vs. 26.34±3.91, CI (mL×s^-1×m^-2): 46.51±20.34 vs. 61.01±7.67, all P < 0.05], while MAP, SVR and SVRI were significantly higher than those in the control group [MAP (mmHg): 52.06±8.61 vs. 48.54±3.21, SVR (kPa×s×L^-1): 874.95±318.70 vs. 603.01±111.49, SVRI (kPa×s×L^-1×m^-2): 165.07±54.90 vs. 105.09±11.99, all P < 0.05]; MAP, SV, SVI, CO and CI of neonates at the decompensated stage in the septic shock group were significantly lower than those in the control group [MAP (mmHg): 35.13±6.08 vs. 48.54±3.21, SV (mL): 2.89±1.17 vs. 4.73±1.15, SVI (mL/m²): 18.50±4.99 vs. 26.34±3.91, CO (L/min): 0.41±0.19 vs. 0.65±0.15, CI (mL×s^-1×m^-2): 43.34±14.17 vs. 61.01±7.67, all P < 0.05], while SVR and SVRI were similar to the control group [SVR (kPa×s×L^-1): 885.49±628.04 vs. 603.01±111.49, SVRI (kPa×s×L^-1×m^-2): 114.29±43.54 vs. 105.09±11.99, both P > 0.05]. CONCLUSIONS Full-term infant with septic shock exhibit a low cardiac output, high vascular resistance hemodynamic pattern, while preterm infant with septic shock show low cardiac output and normal vascular resistance. At the compensated stage the hemodynamic change is low output and high resistance type, while at the decompensated stage it is low output and normal resistance type. Non-invasive hemodynamic monitoring can assist in the identification of neonatal septic shock and provide basis for clinical diagnosis and treatment.
Humans ; Shock, Septic/physiopathology* ; Infant, Newborn ; Hemodynamics ; Female ; Male ; Case-Control Studies ; Infant, Premature

Objective To explore the clinical characteristics of Pierre Robin syndrome and the experience of its diagnosis and therapy, and provide the accurate diagnosis and treatment of Pierre Robin syndrome .Methods Seventeen cases of Pierre Robin syn-drome from September 2008 to August 2013 were enrolled in this study .The clinical data were analyzed retrospectively to explore the clinical characteristics and treatment of Pierre Robin syndrome .Results Seventeen cases of Pierre Robin syndrome had typical clini-cal features, including micrognathia, cleft palate or high palatine arches, glossoptosis, and feeding difficulties.The babies were given corresponding treatment according to their clinical grading. Among those babies, three cases died , including one dying of severe pneu-monia in hospital, and the other two dying of severe pneumonia and malnutrition after giving up treatment .Among 14 survivors, 12 ba-bies were followed up , including 5 babies who achieved optimal growth and development when they were one year old , and the other 7 babies who had feeding difficulties in varying degrees after discharge , and lagged behind normal children in the growth and develop-ment.Conclusions Early diagnosis, accurate classification, and individualized treatment plan for Pierre Robin syndrome might im-prove the prognosis of children with this type of disease .

Objective To investigate the role of HMGB1 in the pathogenesis of organ injury of acute necrotizing pancreatitis (ANP).Methods Male ICR mice were randomly allocated into control group,ANP group and HMGB1 monoclonal antibody group.ANP model was induced by intraperitoneal injection of 20％ L-arginine.Mice in HMGB1 monoclonal antibody group were given intraperitoneal injection of 200 μg of HMGB1 monoclonal antibody immediately after the induction of the ANP model.All the mice were sacrificed at 12,24,and 48 h after ANP induction.Serum level of amylase and liver,renal function were determined,level of serum HMGB1 was measured by using enzyme-linked immunosorbent assay,and then the pathologic changes of pancreas and liver were routinely observed and scored.The HMGB1 mRNA levels in the liver and pancreas were studied by real time fluorescence quantitative PCR.Results The serum levels of HMGB1 at 12 h in control group,ANP group and HMGB 1 monoclonal antibody group were (9.09 ± 1.03),(25.04 ± 4.30),(16.84 ± 4.27) μg/L; and pathological scores of pancreatic tissue were (1.50 ± 0.55),(4.33 ± 0.52),(3.03 ± 0.32) points ; and HMGB1 mRNA expressions in pancreas were 0.48 ± 0.18,7.53 ± 2.71,3.26 ±2.33 ; HMGB1 mRNA expressions in liver were-1.23 ± 0.37,0.15 ± 0.65,－ 1.27 ± 0.72.The corresponding values in ANP group were significantly higher than those in control group (P ＜ 0.05).While the corresponding values in HMGB1 monoclonal antibody group were significantly lower than those in ANP group (P ＜0.05).There was a positive linear relationship between serum HMGB1 level and pancreatic pathological scores 24 h after ANP induction (r =0.768,P ＜ 0.05).In addition,the serum levels of AMY,AST,ALT,LDH,BUN,Cr showed a similar trend as that of serum level of HMGB1,and the serum level of HMGB1 was positively associated with serum levels of Cr,BUN and ALT (r =0.824,0.719,0.590,P＜0.05).Conclusions HMGB1 may be a key factor of inflammatory response and organ dysfunction of ANP in mice,and extrinsic supply of its monoclonal antibody may decrease the injuries of pancreas and other organs during ANP.

Objective To observe the serum levels of high mobility group box-1 protein (HMGB1)in patients with acute cholangitis (AC) and to investigate contributions of HMGB1 in AC.Methods Serum HMGB1 concentrations were determined by an enzyme-linked immunosorbent assay in 30 patients with AC of severe type (ACST) and 42 patients with mild acute cholangitis at the time of admission (within 72 h after the onset).A total of 50 healthy subjects were recruited as the control group.Fluorescent quantitative PCR (FQPCR) was used to detect the HMGB1 mRNA expression and the relationship between serum HMGB1 levels and clinical factors was analyzed.Results The serum HMGB1 levels in healthy control group,mild group and ACST group were (1.82 ± 0.64) μg/L,(10.46 ± 3.75) μg/L,(18.89 ± 6.86) μg/L,respectively.The mean value of serum HMGB1 level in mild group was significantly higher than that in control group,while significantly lower than that in ACST group (P ＜ 0.05).Compared to the control group,the HMGB1 mRNA level in patients of AC increased significantly and the level of ACST group was higher than that of mild group.The serum HMGB1 levels of patients with positive bile or/and blood cultures were higher than that of negative.After emergency endoscopic nasal biliary drainage,the serum HMGB1 levels of patients significantly decreased compared to preoperational (P ＜ 0.05).The HMGB1 levels were significantly positively correlated with white cell counts,C-reactive protein (CRP),total serum bilirubin,direct bilirubin and alkaline phosphatase (ALP).By logistic regression analysis,serum HMGB1 levels had correlation with severity of disease.Conclusion Serum HMGB1 levels significantly increased in patients with AC and the serum concentrations of ACST group were higher than those of mild group.Serum HMGB1 level has a correlation with sepsis.ENBD could lower its serum levels.Serum HMGB1 has predictive value to severity of disease.

Objective To observe the clinical effect of modified Zhisou powder and Symbicort Turbuhaler simultaneously on patients with Cough Variant Asthma. Methods 120 patients with Cough Variant Asthma were randomly recurited into two groups. 60 patients in the treatment group were treated with modified Zhisou powder and Symbicort Turbuhaler; 60 patients in the control group were treated with Symbicort Turbuhaler. 4 weeks was a therapeutic course in both group. Results The markedly controlled rate (MCR) (clinical control+excenence)of the treatment group was 83.3%, obviously surpassed the control group (70.0%) (P＜0.05); There was obvious improvement of cough, expectoration, breath lessness and throaty pruritus after the therapy in both groups, but it was much better in the treatment group than the control group(P＜0.05). The pulmonary function was significantly improved after treatment in both groups(FEV1, FEV1% and PEF, P＜0.05). The improvement showed significant difference between the two groups(P＜0.05). There was obvious decrease of EOS, IL-5 and ECP in both groups. The decrease of ECP and IL-5 in the treatment group was greater than the control group(P＜0.01). Conclusion The therapy of modified Zhisou powder and Symbicort Turbuhaler has advantage over pure western therapy.

Objective To explore the diagnostic effect of serum level of cystatin C (CysC) on the renal function after neonatal asphyxia by detection of serum level of CysC, blood urea nitrogen (BUN) and serum creatinine (SCr) and calculation of glomerular filtration rate (GFR) in neonatal asphyxia. Methods The clinical data of 86 neonates with asphyxia (46 cases in mild asphyxia group,40 cases in severe asphyxia group) and 30 neonates without asphyxia (control group) were collected and the serum level of CysC, BUN and SCr were detected at 24 h to 72 h after birth. Results Serum levels of CysC, BUN and SCr were (1.97 ±0.33) mg/L, (4.97 ±2.15) mmol/L, (90.41 ±24.32) μmol/L in mild asphyxia group, (2.65 ±0.41) mg/L, (10.88 ± 3.31) mmol/L, (125.82 ± 45.44) μ mol/L in severe asphyxia group and (1.24 ± 0.35)mg/L, (4.25 ± 2.04) mmol/L, (58.41 ± 19.22) μmol/L in control group, respectively. The differences were significant among three groups and those values in mild and severe asphyxia groups were higher than those in control group. The sensitivity of CysC level to evaluate renal function in mild asphyxia group was better than BUN and SCr level (P＜ 0.05). In neonata] asphyxia, the serum level of CysC had negative correlation with GFR (P ＜ 0.01). Conclusions Serum level of CysC can be adopted to evaluate the renal function after neonatal asphyxia, which is better than BUN and SCr. With a higer level of CysC, the renal function injury may be worse.

To find a new preventive strategy for the infection of Schistosoma japonica, plasmid pIRES-Sj97-Sj14-Sj26 that contains fatty binding protein (Sj14), GST (Sj26) and paramyocin (Sj97) that are expressed on the membrane, was constructed. RT-PCR was used to detect the expression of Sj14 mRNA, Sj26 mRNA and Sj97 mRNA in the Hela cells, the indirect immunofluorescent test was employed for the detection of the expression of trans-membrane Sj26 after the plasmid was trans-fected into Hela cells. Fifty BALB/c mice were randomly divided into 5 groups and pIRES-Sj97-Sj14-Sj26 plasmid DNA, pIRES-Sj14-Sj26 plasmid DNA, plRES-Sj26 plasmid DNA,plRES blank vector and normal saline were respectively injected into the quadriceps muscles of thigh.Eight weeks after the immunization the mice were killed and significantly higher level of IgG was detected in the pIRES-Sj97-Sj14-Sj26 group as compared with the plRES blank vector, normal saline and pIRES-Sj26 groups (P<0.01) and the pIRES-Sj14-Sj26(P<0.05). Single splenocyte suspension was prepared to detected the level of IFN-γ by ELISA and the lymphocyte stimulating index (SI) by MTT SI was significantly higher of in the pIRES-Sj97-Sj14-Sj26 group than in other groups (P<0.01), while the IFN-γ, level was significantly higher the pIRES-Sj97-Sj14-Sj26 group than in pIRES blank vector and normal saline groups (P<0.01), but no significant differences were found when compared with pIRES-Sj14-Sj26 and pIRES-Sj26 groups. Flow cytometery showed that the percent-ages of CD4+ and CD8+ T cells were much higher in the pIRES-Sj97-Sj14-Sj26 group (P<0.01,P<0.05). It was concluded that pIRES-Sj97-Sj14-Sj26 vaccine may induce stronger immune response in BALB/c mice.

In order to construct a eukaryotic co-expression plasmid containing membrane-anchored Sjcl4FABP and Sjc26GST genes and identify their expression in vitro, Sj14 and Sj26 genes were obtained by RT-PCR with total RNA of Schistosoma japonicum adult worms as the template and cloned into eukaryotic expression plasmid pVAC to construct recombinant plasmids pVAC-Sj14 and pVAC-Sj26. Then a 23 amino-acid signal peptide of human interleukin-2 (IL-2) upstream Sj14 or Sj26 gene and a membrane-anchored sequence containing 32 amino-acids of carboxyl-terminal of human placental alkaline phosphatase (PLAP) downstream were amplified by PCR as the template of plasmid pVAC-Sj14 or pVAC-Sj26 only to get two gene fragments including Sj14 gene and Sj26 gene. The two modified genes were altogether cloned into a eukaryotic co-expression plasmid pIRES, resulting in another new recombinant plasmid pIRES-Sj26-Sj14. The expression of Sj14 and Sj26 genes was detected by RT-PCR and indirect immunofluorescent assays (IFA) when the plasmid pIRES-Sj26-Sj14 was transfected into eukaryotic Hela cells. Restriction enzyme analysis, PCR and sequencing results revealed that the recombinant plasmids pVAC-Sj14, pVAC-Sj26 and plRES-Sj26-Sj14 were successfully constructed and the expression of modified Sj14 and Sj26 genes could be detected by RT-PCR and IFA. A bivalent membrane-anchored DNA vaccine encoding Sj14 and Sj26 genes was acquired and expressed proteins were proved to be mostly anchored in cellular membranes.

In order to construct a eukaryotic co-expression plasmid containing membrane-anchored Sjcl4FABP and Sjc26GST genes and identify their expression in vitro, Sj14 and Sj26 genes were obtained by RT-PCR with total RNA of Schistosoma japonicum adult worms as the template and cloned into eukaryotic expression plasmid pVAC to construct recombinant plasmids pVAC-Sj14 and pVAC-Sj26. Then a 23 amino-acid signal peptide of human interleukin-2 (IL-2) upstream Sj14 or Sj26 gene and a membrane-anchored sequence containing 32 amino-acids of carboxyl-terminal of human placental alkaline phosphatase (PLAP) downstream were amplified by PCR as the template of plasmid pVAC-Sjl4 or pVAC-Sj26 only to get two gene fragments including Sjl4 gene and Sj26 gene. The two modified genes were altogether cloned into a eukaryotic co-expression plasmid pIRES,resulting in another new recombinant plasmid pIRES-Sj26-Sj 14. The expression of Sj14 and Sj26genes was detected by RT-PCR and indirect immunofluorescent assays (IFA) when the plasmid pIRES-Sj26-Sj 14 was transfected into eukaryotic Hela cells. Restriction enzyme analysis, PCR and sequencing results revealed that the recombinant plasmids pVAC-Sj14, pVAC-Sj26 and pIRES-Sj26-Sj14 were successfully constructed and the expression of modified Sj 14 and Sj26 genes could be detected by RT-PCR and IFA. A bivalent membrane-anchored DNA vaccine encoding Sj14 and Sj26 genes was acquired and expressed proteins were proved to be mostly anchored in cellular membranes.