多器官功能障碍综合征大鼠胰岛β细胞超微结构和功能的改变

Objective To explore the effect of multiple organ dysfunction syndrome (MODS) on the ultra-structure and function of pancreatic beta cells and to provide a theoretical basis for clinical treatment of high blood glucose in patients with MODS. Method This study was performed in the Animal Department of Fujian Provincial Hospital, the Key Laboratory of Fujian Provincial Cardiovascular Institute, the Pathology Department of Fujian Provincial Hospital and in the Electron Microscopic Department of Fujian Medical University. Sixteen pathogen-free male Sprague-Dawley rots weighing 180 ～ 220 g, were selected and randomly divided into MODS group and control group (8 rats per group). MODS was induced by intraperitoneal injection with bacterium c oli and cutting the left legs. Rats in the control group received an intraperitoneal injection of an equivalent volume of sodium chloride. The MODS model was considered successful when two or more organs showed dysfunction 48 h after the injection. The blood glucose and plasma insulin levels were measured in the fasting state and in response to a glucose load. All data were analyzed using t tests. The plasma insulin concentration was analyzed after logarithmic transforma-tion. The ultrastructure of the pancreatic beta cells was observed under an electron microscope. The expression of Bax was determined immunohistochemically. Results The blood glucose during fasting, the blood glucose level 30 min after a glucose load and the expression of Bax were significantly in the MODS group compared with the con-trol group (P <0.01). In addition, the plasma insulin concentration level was insignificantly increased 30 min af-ter the glucose load in the MODS group (P < 0.01). Pathological uhrastructural changes were found, as follows: most pancreatic beta cells in the MODS group exhibited vacuole degeneration, some were necrotized, the mitochen-dria had swollen and the rough endoplasmic reticulum had expanded. Conclusions The uhltrastructure of the pan-creatic beta cells in the MODS rats shewed significant pathologic changes, with increased expression of Bax. These pathological changes may he responsible for the decreased insulin secretion, which caused the increased blood glu-cose levels.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

阻塞性睡眠呼吸暂停低通气综合征患者血浆抵抗素和脂联素水平与胰岛素抵抗的相关研究

Objective To explore relationship between resistin'adipenectin and insulin resistance(IR) in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). Methods Based on polysomnography (PSG) and disease history ,68 patients were divided into three groups: mild ( L, n = 24 ), moderate ( M, n = 13 ), severe ( S, n = 31 ) OSAHS, and normal control ( n = 20 ). Fasting serum glucose, insulin, lipoids, resistin and adipanectin were measured. HOMA-IR was calculated, the correlation between HOMA-IR and resistin, adiponectin, lipoids, body mass index, waist-to-hip ratio, apnea-hypopnea index ( AHI), the lowest saturation of blood oxygen ( LSaO2) and the per-centage of total sleep time spent with an oxygen saturation less than 90% (T90) were analysed. Results The levels of serum resistins in each OSAHS group were (8.04 ±2. 14), ( 10.85±4.89 ), ( 13.34±3.52 )mg/L, and were sig-nificantly higher than those in control group ( 9.49 ± 2.40) mg/L ( P < 0.05 ), S were significantly higher than L (P<0.05) ;The levels of serum adiponectin of OSAHS groups were(6. 21 ± 1.74), (4. 19±1.80), (2.26± 1.17 ) mg/L, and were significantly lower than those in control group(9.49±2.40) mg/L (P < 0.05 ), and the inter-group differences were statistically significant (P <0. 05). HOMA-IR of M and S were(4.07±0.97), (5.61± 2.26) significantly higher than those of L and control group( 1.57 ±0. 58 ), (2.47 ±1.52 ) ( P < 0.05 ), and inter-group differences between M and S were statistical significant( P < 0.05 ). Spearman correlation analysis showed that HOMA-IR was significantly positive correlated with resistin, total cholesterol, triglyceride, body mass index,waist-hip rafio,AHI,T90( r =0. 794,0.438,0. 430,0. 351,0. 456,0.775,0.624 ,P <0.01 ) ,negative with adiponectin, LSaO2 (r=-0.563, -0.623 ,P <0.01 ). Partial correlation analysis showed that after the effect of adiponeetin and resis-tin were controlled,HOMA-IR was significant positive correlation with T90 and AHI(r =0.231,0.358 ,P <0.05 ). Multiple stepwise regression analysis showed that, to HOMA-IR, resistin and AHI were the most significant impact factors (R2 =0.613,F=69.810,P<0.01). Conclusions HOMA-IR is significantly positively correlated with the severity of OSAHS,independent of the blood lipids, body mass index, waist-hip ratio, resistin, adiponectin and other factors;the effects of blood lipids,body mass index,waist-hip ratio and other factors on HOMA-IR probably depend on resistin and adiponectin;AHI and plasma resistin level may determine the level of insulin resistance in patients with OSAHS.     

Trends in the gentamicin and arbekacin susceptibility of methicillin-resistant <Emphasis Type="Italic">Staphylococcus aureus</Emphasis> and the genes encoding aminoglycoside-modifying enzymes

It is generally accepted that methicillin-resistant Staphylococcus aureus (MRSA) is also resistant to aminoglycoside antibiotics. We investigated trends of gentamicin and arbekacin susceptibilities and the prevalence of the genes encoding aminoglycoside-modifying enzymes (AMEs) for a total of 218 strains of MRSA isolated from blood specimens obtained from 1978 through 2002 in one hospital. The minimum inhibitory concentrations of gentamicin at which 50% of the strains were inhibited (MIC₅₀) were ≥128 and 32 μg/ml for isolates obtained from 1978 to 1984 and from 1985 to 1989, respectively, and 0.5 μg/ml for isolates obtained from 1990 to 2002. The MIC₉₀ of gentamicin was consistently ≥128 μg/ml. Investigation of the occurrence of AME revealed that the MIC₅₀ of gentamicin was highly correlated with the presence of aac(6′)/aph(2″) encoding aminoglycoside acetyl/phosphotransferase. The MIC₅₀ of arbekacin was 2 μg/ml for strains isolated in 1978–1984 and ≤0.5 μg/ml for strains isolated from 1985 to 2002. The MIC₉₀ of arbekacin was 8 μg/ml for the strains isolated in 1978–1989 and 1 to 2 μg/ml for strains isolated in 1990–2002. Though it has been established that AAC(6′)/APH(2″) modifies arbekacin, the trend of arbekacin resistance was not necessarily consistent with the presence of this enzyme. However, the prevalence of both aac(6′)/aph(2″) and aph(3′)-III in the strains isolated from 1978 through 2002 was correlated with the MIC₉₀ values of arbekacin. Thus, it is most likely that APH(3′)-III, in addition to AAC(6′)/APH(2″), is somehow involved in arbekacin resistance in S. aureus. Our results imply that gentamicin- and arbekacin-resistant MRSAs have consistently decreased for the past 25 years and that this finding is, most likely, attributable to the declining prevalence of genes encoding for AMEs.     

Bactericidal activities of parenteral antibiotics and genotype of penicillin-binding protein in Streptococcus pneumoniae and Haemophilus influenzae isolated from children's blood

A total of 16 isolates of Streptococcus pneumoniae and 18 isolates of Haemophilus influenzae were obtained from the blood of children admitted to the pediatric wards of hospitals in Hokkaido Kamikawa subprefecture between January 2003 and December 2005. The ages of the patients with S. pneumoniae or H. influenzae infection ranged from 2 months to 9 years and from 1 month to 4 years, respectively. The diagnoses of S. pneumoniae infection were as follows: pneumonia in 8 patients, occult bacteremia in 5 patients, and meningitis in 3 patients. The diagnoses of H. influenzae were: meningitis in 6 patients, pneumonia in 4 patients, occult bacteremia in 4 patients, epiglotitis in 2 patients, and facial cellulitis in 2 patients. Out of 16 S. pneumoniae isolates, penicillin-resistant strains with a mutation of 3 genes were observed in 7 children, and penicillin intermediate-resistant strains with a mutation of 1 or 2 genes were observed in 8 children. Out of 18 H. influenzae isolates, the β-lactamase-negative ampicillin-resistant strain with a substitution of 2 points in the ftsI gene was revealed in 2 children, the β-lactamase-negative ampicillin-resistant strain with a substitution of 1 point in the ftsI gene was observed in 4 children, the β-lactamase-positive amoxicillin/clavulanic acid-resistant strain with blaTEM-1 and ftsI with 2 substitutions in the ftsI gene was observed in 3 children, and the β-lactamase-positive ampicillin-resistant strain with blaTEM-1was not observed. The MBC90s of ampicillin, ceftriaxone, cefotaxime, meropenem, panipenem, and vancomycin against S. pneumoniae were 8 μg/ml, 1 μg/ml, 1 μg/ml 1 μg/ml, 0.25 μg/ml, and 0.5 μg/ml, respectively. Those of ampicillin, piperacillin, ceftriaxone, cefotaxime, meropenem, and panipenem against H. influenzae were >128 μg/ml, >128 μg/ml, 0.25 μg/mL, 1 μg/ml, 0.12 μg/ml, and 0.5 g/ml, respectively. It is suggest that the minimum bactricidal concentration (MBC) was dissociated from the minimum inhibitory concentration (MIC) in S. pneumoniae and H. influenzae with abnormal pbp genes.     

In vitro synergistic effects of double combinations of β-lactams and azithromycin against clinical isolates of Neisseria gonorrhoeae

In Japan, Neisseria gonorrhoeae, a sexually transmitted pathogen, has recently shown significant resistance to various antimicrobial agents. In this study, a checkerboard method was utilized to investigate the in vitro activities of cefixime (CFIX), cefteram (CFTM), or amoxicillin (AMPC) in combination with azithromycin (AZM) against 25 clinical isolates of N. gonorrhoeae. Synergy, defined as a fractional inhibitory concentration (FIC) index of less than or equal to 0.50, was observed in 32% of isolates with CFIX+AZM, 12% of isolates with CFTM+AZM, and 4% of isolates with AMPC+AZM. Moreover, partial synergy, defined as an FIC index of greater than 0.50 and less than 1, was observed in 44% of isolates with CFIX+AZM, 68% of isolates with CFTM+AZM, and 52% of isolates with AMPC+AZM. In particular, as a result of the combination of CFIX and AZM, for all isolates, significant reductions were observed in the median CFIX minimum inhibitory concentration (MIC; from 0.25 to 0.008 μg/ml; P < 0.0001) and the median AZM MIC (from 0.12 to 0.03 μg/ml; P < 0.0001). However, antagonism, defined as an FIC index of greater than 1, was observed in only 4% of the isolates with both CFIX+AZM and CFTM+AZM, while it was seen in 12% of the isolates with AMPC+AZM. To our knowledge, this is the first study to demonstrate that the in vitro activity of CFIX against N. gonorrhoeae can be significantly enhanced in combination with AZM.     

Antimicrobial activities of tosufloxacin against Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella branhamella catarrhalis isolated from otolaryngological infectious diseases

In 2003, the Japan Society for Infectious Diseases in Otolaryngology conducted its third nationwide survey of clinical isolates from otolaryngological infectious diseases. We selected three primary causative organisms of otolaryngological infectious diseases, Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella Branhamella catarrhalis, and evaluated their sensitivities to tosufloxacin (TFLX), a new oral quinolone, because the survey revealed a rise in drug-resistant strains, suggesting potential problems with the antibiotics commonly used against these organisms. The minimum inhibitory concentration (MIC)₉₀ values of TFLX against S. pneumoniae, H. influenzae, and M. catarrhalis were 0.25 μg/ml, ≤0.06 μg/ml, and ≤0.06 μg/ml respectively, and TFLX was shown to be as effective as or superior to other new quinolones. In addition, TFLX showed sufficient antimicrobial effects against frequently detected drug-resistant bacteria such as penicillin-resistant S. pneumoniae (PRSP) and β-lactamase-negative, ampicillin-resistant strains of H. influenzae (BLNAR). Furthermore, only a few strains of bacteria showed resistance to TFLX.     

Clinical and bacteriological evaluation of the efficacy of piperacillin in children with pneumonia

We aimed to prospectively evaluate the clinical and bacteriological effects of piperacillin in children with pneumonia. Twenty-eight patients (6 months to 5 years of age) with pneumonia were treated with piperacillin. In the same period, 95 strains of Haemophilus influenzae and 41 strains of Streptococcus pneumoniae were isolated in our department and the minimum inhibitory concentration (MIC) of piperacillin was determined. The clinical efficacy of piperacillin was excellent in 4 cases, good in 23, and fair in 1; the response rate was 96.4% (27/28). Among the isolates from our department, there were 4 strains (9.8%) of penicillin-susceptible S. pneumoniae (PSSP), 32 strains (78.0%) of penicillin-intermediate-resistant S. pneumoniae (PISP), and 5 strains (12.2%) of penicillin-resistant S. pneumoniae (PRSP). Against S. pneumoniae, the MIC₅₀ and MIC₉₀ for piperacillin were 0.5 μg/ml and 2 μg/ml, respectively. Panipenem showed the best results, followed by piperacillin, ampicillin, and flomoxef. Among the isolates from our department, there were 51 strains (53.7%) of β-lactamase-negative ampicillin-susceptible H. influenzae, 42 strains (44.2%) of β-lactamase-negative ampicillin-resistant H. influenzae, 1 strain (1.1%) of β-lactamase-positive ampicillin-resistant H. influenzae, and 1 strain (1.1%) of β-lactamase-positive amoxicillin-clavulanic acid-resistant H. influenzae. The MIC₅₀ and MIC₉₀ for piperacillin against H. influenzae were 0.0625 μg/ml and 0.125 μg/ml, respectively. Tazobactam/piperacillin and piperacillin showed the best results, followed by panipenem, ampicillin, and flomoxef. Piperacillin proved to be very useful for the treatment of pneumonia in children.     

Prevalence of β-lactamase-nonproducing ampicillin-resistant <Emphasis Type="Italic">Haemophilus influenzae</Emphasis> and <Emphasis Type="Italic">Haemophilus influenzae</Emphasis> type b strains obtained from children with lower respiratory tract infections

The prevalence of strains with ampicillin (ABPC) resistance among Haemophilus influenzae strains isolated from the nasopharynx of children with lower respiratory tract infections has increased significantly during the 6 years from 2000, when it was 41.9%, to 2005, when it reached 60.1%. From 2002, the prevalence exceeded 50%, and the prevalence of β-lactamase-nonproducing ABPC-resistant (BLNAR) strains with a minimum inhibitory concentration (MIC) of ABPC of over 4 μg/ml doubled, from 28.2% in 2002 to 54.7% in 2005. In H. influenzae strains obtained from the nasopharynx of children with lower respiratory tract infections between April 2004 and March 2006, identification of serotype b was defined, using the slide agglutination method. The frequency of isolation of H. influenzae type b (Hib) strains was then measured and the ABPC resistance conditions of the Hib strains were also evaluated. The frequency of the Hib strains was found to be 30 out of 479 strains, 6.3%. Of these 30 strains, BLNAR accounted for 53.3% (16 strains), approximately the same frequency of isolation as that of the BLNAR isolated from all H. influenzae strains during the same period. In Japan, the prevalence of BLNAR strains among clinically isolated H. influenzae strains has continued to increase, and the frequency of isolation of BLNAR strains among Hib strains has also continued to rise. As a countermeasure, attempts at improving resistance have been made through judicious antibiotic use, but concern that the choice of antibiotics for Hib meningitis may become complicated has sparked a keen interest in the introduction of Hib conjugate vaccine. Part of this report was presented at the fifty-fourth general meeting of the Japanese Society of Chemotherapy (Kyoto, May 2006).     

卡维地洛与美托洛尔治疗高原慢性充血性心力衰竭疗效的对比研究

目的 比较卡维地洛与美托洛尔治疗高原慢性心力衰竭(CHF)的疗效.方法 90例CHF患者随机分成3组:常规治疗组(20例)给予血管紧张素转化酶抑制剂、利尿剂、地高辛等常规心力衰竭治疗.美托洛尔组(34例)、卡维地洛组(36例)在上述治疗基础上分别给予美托洛尔50 mg,2次/d;卡维地洛25 mg,2次/d口服.随访半年,治疗前、后采用超声心动图测定患者心功能并进行疗效观察.结果 治疗后美托洛尔组、卡维地洛组左心室舒张末期内径(LVEDD)[分别为(57.3±6.5)、(57.2±6.9)mm]和左心室收缩末期内径(LVSED)[分别为(46.6±7.0)、(44.0±6.9)mm]显著低于常规治疗组[分别为(64.7±9.1)、(53.4±9.8)mm],左心室射血分数(LVEF)显著高于常规治疗组[分别为(47.5±8.1)%、(52.9±8.5)%、(42.8±9.2)%](P均＜0.05).卡维地洛组LVEF改善优于美托洛尔组(P＜0.05).死亡情况:常规治疗组4例,美托洛尔组1例,卡维地洛组无死亡.美托洛尔组、卡维地洛组病死率均明显低于常规治疗组(P均＜0.05).结论 美托洛尔、卡维地洛均可明显改善高原CHF患者心功能.卡维地洛疗效及耐受性略优于美托洛尔.

Abstract：

Objective To compare the effect of carvedilol and motoprolol on high altitude chronic congestive heart failure (CHF). Methods Ninety patients with high altitude chronic CHF were divided into three groups randomly:Twenty patients in the regular treatment group treated with angiotensin-converting enzyme inhibitor (ACEI) ,diuretics and digoxin; motoprolol (50 mg twice daily) was given in the motoprolol group( 34cases) additional to regular treatment; carvedilol (25 mg twice daily) was given in the carvedilol group(36cases ) additional to regular treatment. All the patients were followed up for six months and measured the changes of cardiac function by echocardiography. Results Left ventricular end-diastolic dimension (LVEDD) was ( 57. 3 ± 6. 5 ) mm and (57.2 ± 6. 9) mm in the carvedilol group and the motoprolol group respectively, and left ventricular end-systolic dimension (LVESD) was (46. 6 ± 7.0) mm and (44. 0 ± 6. 9 ) mm in the carvedilol group and the motoprolol group respectively, which were all significantly smaller than that in the regular treatment group ([64.7 ±9. 1]mm and [53.4 ±9.8]mm for LVEDD and LVESD,respectively) (Ps ＜0.05). Left ventricular ejection fraction (LVEF) in the carvedilol group and the motoprolol group ( [47.5 ± 8. 1] % and [52. 9 ±8.5] % ,respectively) was higher than that in regular treatment group( [42. 8 ±9. 2]% ) (Ps ＜0. 05).The improvement of LVEF in the carvedilol group was better than that in the motoprolol group (P ＜ 0. 05 ). One case died in the motoprolol group and no death in the carvedilol group,4 cases died in the regular treatment group,the mortality in the motoprolol group and the carvedilol group was significantly lower than that in the regular treatment group. Conclusion Carvedilol and motoprolol significantly improved cardiac function in high latitude CHF patients,and the effect of Carvedilol is slightly better than that of motoprolol.     

Spectral Entropy as a Monitor of Depth of Propofol Induced Sedation

Objective The aim of this prospective, observational study was to evaluate State and Response entropy (Entropy^TM Monitor, GE Healthcare, Finland), indices as measures of moderate (“conscious”) sedation in healthy adult patients receiving a low dose propofol infusion. Sedation was evaluated using: (I) the responsiveness component of the OAA/S scale␣(Observer’s Assessment of Alertness/Sedation scale) and (II) multi-channel electroencephalogram (EEG) interpretation by a clinical expert. Methods 12 ASA I patients were recruited. A target-controlled infusion of propofol was administered (using Schnider’s pharmacokinetic model) with␣an initial effect site concentration set to 0.5 μg ml⁻¹. A␣4 minute equilibrium period was allowed. This concentration was increased at 4 minute intervals by 0.5 μg ml⁻¹ to a maximum of 2.0 μg ml⁻¹. State (SE) and Response (RE), entropy values were recorded for each 4 minute epoch together with clinical sedation scores (OAA/S) and continuous multi-channel EEG. The multi-channel EEG recorded during the final minute of each 4 minute epoch or “patient/time unit” was presented to a neurophysiologist who assigned a label “sedated/not sedated”. SE/RE values were compared in patient/time units with clinical or EEG evidence of sedation versus those without. Results Mean SE and RE values were less in patient/time units when clinical evidence of sedation was present, [mean = 86.8 (95% CI, 84.0–88.3) and 94.3 (95%CI, 92–96.1)], P = 0.002 and P = 0.001, respectively. In patient/time units assigned the label “sedated” by the clinical neurophysiologist assessing the multi-channel EEG, SE and RE values were less [mean = 87.5 (95% CI, 86.3–88.4) and 95.0 (95% CI, 93.8–96.1)] P = 0.001 and P < 0.001, respectively. Conclusions A statistically significant decrease in SE and RE values was demonstrated in patient/time units in which clinical or EEG evidence of sedation was present. We conclude that spectral entropy offers potential as a monitor of propofol induced sedation Mahon P, Kowalski RG, Fitzgerald AP, Lynch EM, Boylan GB, McNamara B, Shorten GD. Spectral entropy as a monitor of depth of propofol induced sedation. Ethical Approval The Clinical Research Ethics Committee of the Cork Teaching Hospitals, Cork, Ireland approved the study protocol on 1st March 2005. The Clinical Research Ethics Committee of the Cork Teaching Hospitals, is a recognised Ethics Committee under regulation 7 of the European Communities (Clinical Trials on Medicinal Products for Human Use) regulations 2004, and is authorised to carry out the ethical review of clinical trials of investigational medicinal products. Presentation This work was presented in part (poster format) at the European Society of Anaesthesia, Annual Congress, Munich, Germany, June 9–12 2007. (Monitoring: equipment and computers poster section).Abstract reference: 3AP9-9. European Journal of Anaesthesia 2007(24) Suppl. 39 p 37.