Effect of iron deficiency without anaemia on days alive and out of hospital in patients undergoing valvular heart surgery.

Comprehensive evidence regarding the treatment of non-anaemic iron deficiency in patients undergoing valvular heart surgery is lacking. This study aimed to investigate the association between non-anaemic iron deficiency and postoperative outcomes in these patients. We retrospectively analysed 321 patients of which 180 (56%) had iron deficiency (defined as serum ferritin < 100 ng.ml-1 or < 300 ng.ml-1 with transferrin saturation < 20%). While the iron-deficient group had lower pre-operative haemoglobin levels than the non-iron deficient group (median (IQR [range]) 134 (127-141 [120-172]) g.l-1 , 143 (133-150 [120-179]) g.l-1 , p = 0.001), there was no between-group difference in allogeneic red blood cell transfusion. Median (IQR [range]) days alive and out of hospital at postoperative day 90 was 1 day shorter in the iron-deficient group (80 (77-82 [9-85]) days vs. 81 (79-83 [0-85]) days, p = 0.026). In multivariable analysis, only cardiopulmonary bypass duration (p = 0.032) and intra-operative allogeneic red blood cell transfusion (p = 0.011) were significantly associated with reduced days alive and out of hospital at postoperative day 90. Iron deficiency did not exert any adverse influence on secondary outcomes except length of hospital stay. Our findings indicate that non-anaemic iron deficiency alone is not associated with adverse effects in patients undergoing valvular heart surgery when it does not translate into an increased risk of allogeneic transfusion.

Association between intensive glycemic control and mortality in elderly diabetic patients in the primary care: A retrospective cohort study.

OBJECTIVE: To examine the association between the most recent HbA1c values and the mortality of elderly Type 2 Diabetic (T2DM) patients managed in the public primary care setting and to explore the associating risk factors. DESIGN: Retrospective cohort study. SUBJECTS: All T2DM patients aged 65 or above, who attended a public primary care clinic for regular follow up from 01/01/2012 to 31/12/2012 were included. Their follow up status till 31/12/2017 was reviewed. Those who were deceased on or before 31/12/2017 were matched randomly with controls that were alive in the same cohort for comparison. MAIN OUTCOME MEASURES: Patients' demographics, smoking status, duration of T2DM, biochemical parameters including the most recent HbA1c, lipid profile, renal function test, drug profile, co-morbidities and all-cause mortality were retrieved from Hospital Authority's CDARS and CMS systems. RESULTS: Both high (>8.0%) and low (<6.5%) HbA1c values were associated with increased odd ratio of all-cause mortality among T2DM elderly patients treated in the primary care. There was a 3-fold increase in odd ratio when the HbA1c reading was very low (<6.0%). Associated risk factors for all-cause mortality in elderly T2DM patients included smoker status, lower BMIs, and higher LDL levels and use of sulphonylureas. CONCLUSIONS: Glycemic target for elderly T2DM patients should be approached cautiously. Over-aggressive treatment may lead to increased mortality among elderly T2DM patients.

Russian Caucasians have a higher risk of erosive reflux disease compared with East Asians: A direct endoscopic comparison.

BACKGROUND: Erosive reflux disease (ERD) is prevalent in the West, and its incidence is increasing in the East. The differences between the West and East, especially in body composition, have not been investigated thoroughly. METHODS: Subjects who underwent esophagogastroduodenoscopy and body composition analysis during health screening were analyzed retrospectively. Russian Caucasians who visited Korea were propensity matched with native Koreans. Endoscopy results were analyzed to identify ERD and gastroesophageal flap valve (GEFV) status. Body composition and laboratory results were compared to identify risk factors for ERD. KEY RESULTS: 32 279 subjects underwent health screening with 1496 Russian Caucasians propensity matched with 1496 Koreans. ERD prevalence was 20.2% for Caucasians and 9.8% for Koreans (P<.001). Caucasians had significantly greater body mass index (BMI) and were more sarcopenic. Significant risk factors for ERD were Caucasian ethnicity (OR 1.629, 95% CI 1.265-2.099, P<.001), male gender (OR 2.374, 95% CI 1.883-2.993, P<.001), greater BMI (OR 1.067, 95% CI 1.041-1.093, P<.001), and abnormal GEFV (OR 2.730, 95% CI 2.194-3.397, P<.001). H. pylori seropositivity (OR 0.614, 95% CI 0.488-0.774, P<.001) and atrophic gastritis (OR 0.547, 95% CI 0.411-0.728, P<.001) were significantly preventive. CONCLUSIONS & INFERENCES: Caucasian ethnicity is a significant risk factor for ERD. Greater BMI, male gender and abnormal GEFV are associated with ERD, and H. pylori seropositivity and atrophic gastritis are preventive. Further studies are needed to assess the differences in ERD between Caucasians and East Asians.

The flavone eupatilin inhibits eotaxin expression in an NF-κB-dependent and STAT6-independent manner.

The CC chemokine eotaxin contributes to epithelium-induced inflammation in airway diseases such as asthma. Eupatilin (5,7-dihydroxy-3',4',6'-trimethoxyflavone), a bioactive component of Artemisia asiatica Nakai (Asteraceae), is reported to inhibit the adhesion of eosinophils to bronchial epithelial cells. However, little is known about the molecular mechanism of eupatilin-induced attenuation of bronchial epithelium-induced inflammation. In this study, we investigated the effect of eupatilin on expression of eotaxin-1 (CCL11), a potent chemoattractant for eosinophils. Eupatilin significantly inhibited eotaxin expression in bronchial epithelial cells stimulated with TNF-α, while NF-κB and IκBα kinase (IKK) activities declined concurrently. Eupatilin also inhibited mitogen-activated protein kinase (MAPK) activity; however, all of these anti-inflammatory activities were reversed by MAPK overexpression. In contrast, eupatilin did not affect the signal transducer and activator of transcription 6 (STAT6) signalling in bronchial epithelial cells stimulated with IL-4. Furthermore, eupatilin significantly attenuated TNF-α-induced eosinophil migration. These results suggest that the eupatilin inhibits the signalling of MAPK, IKK, NF-κB and eotaxin-1 in bronchial epithelial cells, leading to inhibition of eosinophil migration.

Resveratrol prevents renal lipotoxicity and inhibits mesangial cell glucotoxicity in a manner dependent on the AMPK-SIRT1-PGC1α axis in db/db mice.

AIMS/HYPOTHESIS: Many of the effects of resveratrol are consistent with the activation of AMP-activated protein kinase (AMPK), silent information regulator T1 (SIRT1) and peroxisome proliferator-activated receptor (PPAR)γ co-activator 1α (PGC-1α), which play key roles in the regulation of lipid and glucose homeostasis, and in the control of oxidative stress. We investigated whether resveratrol has protective effects on the kidney in type 2 diabetes. METHODS: Four groups of male C57BLKS/J db/m and db/db mice were used in this study. Resveratrol was administered via gavage to diabetic and non-diabetic mice, starting at 8 weeks of age, for 12 weeks. RESULTS: The db/db mice treated with resveratrol had decreased albuminuria. Resveratrol ameliorated glomerular matrix expansion and inflammation. Resveratrol also lowered the NEFA and triacylglycerol content of the kidney, and this action was related to increases in the phosphorylation of AMPK and the activation of SIRT1-PGC-1α signalling and of the key downstream effectors, the PPARα-oestrogen-related receptor (ERR)-1α-sterol regulatory element-binding protein 1 (SREBP1). Furthermore, resveratrol decreased the activity of phosphatidylinositol-3 kinase (PI3K)-Akt phosphorylation and class O forkhead box (FOXO)3a phosphorylation, which resulted in a decrease in B cell leukaemia/lymphoma 2 (BCL-2)-associated X protein (BAX) and increases in BCL-2, superoxide dismutase (SOD)1 and SOD2 production. Consequently, resveratrol reversed the increase in renal apoptotic cells and oxidative stress, as reflected by renal 8-hydroxy-deoxyguanosine (8-OH-dG), urinary 8-OH-dG and isoprostane concentrations. Resveratrol prevented high-glucose-induced oxidative stress and apoptosis in cultured mesangial cells through the phosphorylation of AMPK and activation of SIRT1-PGC-1α signalling and the downstream effectors, PPARα-ERR-1α-SREBP1. CONCLUSIONS/INTERPRETATION: The results suggest that resveratrol prevents diabetic nephropathy in db/db mice by the phosphorylation of AMPK and activation of SIRT1-PGC-1α signalling, which appear to prevent lipotoxicity-related apoptosis and oxidative stress in the kidney.

Stimulation of dendritic cells with Helicobacter pylori vacuolating cytotoxin negatively regulates their maturation via the restoration of E2F1.

Helicobacter pylori induces an infiltration of dendritic cells (DCs) into the infected gastric mucosa. Although DCs play an important role in the regulation of inflammation, the effects of H. pylori vacuolating cytotoxin (VacA) on DC maturation process have not yet been elucidated. The role of VacA in DC maturation following co-exposure to Escherichia coli lipopolysaccharide (LPS) was investigated. The treatment of immature DCs with LPS up-regulated the expression of surface molecules [e.g. CD40, CD80, CD86 and major histocompatibility complex (MHC) class II], as well as the production of cytokines [e.g. interleukin (IL)-1ß, IL-12p70 and tumour necrosis gactor (TNF)-α] compared with those of unstimulated controls. Co-stimulation with H. pylori VacA significantly reduced the up-regulated DC maturation markers induced by LPS. In addition, VacA sustained the immature state of DCs with high endocytosis and low migratory capacity. The LPS-induced down-regulation of E2F1 expression in DCs was recovered by co-stimulation with VacA. Moreover, suppression of E2F1 by small interfering RNA resulted in a significant recovery of the inhibited DC maturation by VacA. In contrast, VacA did not affect nuclear factor (NF)-κB responses to LPS and the NF-κB signal was not associated with VacA-induced inhibition of DC maturation. These results suggest that the exposure of DCs to H. pylori VacA negatively regulates DC maturation via the restoration of E2F1. The immunomodulatory action of VacA on DCs may contribute to the ability of VacA-producing H. pylori to establish a persistent infection in the gastric mucosa.

Reducing ammonia emissions and volatile fatty acids in poultry litter with liquid aluminum chloride.

This study was a pen trial in which the effects of adding different rates of liquid aluminum chloride (AlCl(3)) on litter pH, total volatile fatty acids (VFAs), and ammonia (NH(3)) fluxes was evaluated. Liquid AlCl(3) treatments used in this study were sprayed on the rice hull surface at rates of 100 g, 200 g, and 300 g liquid AlCl(3)/kg rice hulls; untreated rice hulls served as controls. Litter pH, total VFAs, and NH(3) fluxes were all lowered (P< 0.05) by all of the liquid AlCl(3) treatments compared with controls during certain times of the 5 week study. However, there were no significant differences among treatments on litter pH at the end of the study (from 3 to 5 weeks) or NH(3) fluxes at beginning of the study (0 to 3 weeks). Total VFAs were reduced 16 %, 29 %, and 53 % by 100 g liquid AlCl(3)/kg rice hulls, 200 g liquid AlCl(3)/kg rice hulls, and 300 g liquid AlCl(3)/kg rice hulls, respectively. Liquid AlCl(3)additions reduced NH(3) fluxes by 35 %, 57 % and 67 %, respectively, at the low, medium and high rates. In summary, these results indicate that adding liquid aluminum chloride to rice hulls would be a useful tool in reducing the negative environmental impact of poultry litter. It should be noted that the decreased VFA production and NH(3) volatilization was chiefly associated with reduction in litter pH.

Upregulation of rat Ccnd1 gene by exendin-4 in pancreatic beta cell line INS-1: interaction of early growth response-1 with cis-regulatory element.

AIMS/HYPOTHESIS: The aim of this study was to investigate the effect of exendin-4 on the expression of cyclin D1 gene (Ccnd1), which is critical in regulating the progression of the cell cycle in INS-1 cells. MATERIALS AND METHODS: INS-1 cells were stimulated with exendin-4 (10 nmol/l). Transient transfection and luciferase reporter assays were performed to measure promoter activities of rat Ccnd1. Electrophoretic mobility shift and chromatin immunoprecipitation assays were used to examine the binding of transcription factors to sites responsive to exendin-4 in vitro and in vivo, respectively. RESULTS: Exendin-4 increased both Ccnd1 mRNA and its protein levels in a time-dependent manner. The region from -174 to +130 of the promoter was found to contain cis-regulatory elements responsible for exendin-4-mediated gene induction. Early growth response-1 (EGR1) protein was bound to the region from -153 to -134, which includes the putative EGR1 binding site (5'-CACCCCCGC-3'). Moreover, exendin-4 recruited EGR1 protein to the promoter in vivo. CONCLUSIONS/INTERPRETATION: These findings suggest that exendin-4 activates Ccnd1 transcription through induction of EGR1 binding to a cis-regulatory element between -153 and -134 on the rat Ccnd1 promoter. These results provide an important indication that exendin-4 is a growth factor regulating beta cell proliferation.

Exendin-4 induction of cyclin D1 expression in INS-1 beta-cells: involvement of cAMP-responsive element.

Glucagon-like peptide-1 (GLP-1) and its analog exendin-4 (EX) have been considered as a growth factor implicated in pancreatic islet mass increase and beta-cell proliferation. This study aimed to investigate the effect of EX on cyclin D1 expression, a key regulator of the cell cycle, in the pancreatic beta-cell line INS-1. We demonstrated that EX significantly increased cyclin D1 mRNA and subsequently its protein levels. Although EX induced phosphorylation of Raf-1 and extracellular-signal-regulated kinase (ERK), both PD98059 and exogenous ERK1 had no effect on the cyclin D1 induction by EX. Instead, the cAMP-elevating agent forskolin induced cyclin D1 expression remarkably and this response was inhibited by pretreatment with H-89, a protein kinase A (PKA) inhibitor. Promoter analyses revealed that the cAMP-responsive element (CRE) site (at position -48; 5'-TAACGTCA-3') of cyclin D1 gene was required for both basal and EX-induced activation of the cyclin D1 promoter, which was confirmed by site-directed mutagenesis study. For EX to activate the cyclin D1 promoter effectively, CRE-binding protein (CREB) should be phosphorylated and bound to the putative CRE site, according to the results of electrophoretic mobility shift and chromatin immunoprecipitation assays. Lastly, a transfection assay employing constitutively active or dominant-negative CREB expression plasmids clearly demonstrated that CREB was largely involved in both basal and EX-induced cyclin D1 promoter activities. Taken together, EX-induced cyclin D1 expression is largely dependent on the cAMP/PKA signaling pathway, and EX increases the level of phosphorylated CREB and more potently trans-activates cyclin D1 gene through binding of the CREB to the putative CRE site, implicating a potential mechanism underlying beta-cell proliferation by EX.

Dexamethasone suppresses the expansion and transdifferentiation of transplanted porcine neonatal pancreas cell clusters (NPCCs) into beta-cells in normal nude mice.

OBJECTIVES: This study was performed to investigate the effect of dexamethasone on the expansion and transdifferentiation of transplanted neonatal pancreas cell clusters (NPCCs) in vivo. METHODS: Porcine NPCCs were generated from 1 to 3-day-old neonatal pigs. After transplantation (Tx) of 4000 islet equivalents (IEqs) of NPCCs beneath the renal subcapsular space of normoglycemic nude mice, dexamethasone (Dx, 1 mg/kg) or vehicles were injected daily. Intraperitoneal glucose tolerance testing (ip-GTT) was performed at 4 weeks (n = 4) and 10 weeks (n = 7) after Tx. After harvesting the grafts, total graft and beta-cell graft mass were determined by morphometric analysis. RESULTS: Although the mean value of AUCg was elevated in the Dx-treated group at 10 weeks after Tx, the glucose levels of all the animals by ip-GTT were within the normal range. At 10 weeks after Tx, the relative volume, absolute mass of beta-cells in the graft, and total graft mass were significantly lower in the Dx-treated group (relative volume of beta-cells: 22.0% versus 35.3%, P < 0.05; beta-cells mass: 1.0 +/- 1.2 mg versus 2.2 +/- 5.6 mg, P < 0.05, total graft mass: 4.4 +/- 5.4 mg versus 6.3 +/- 1.3 mg, P < 0.05, Dx-treated versus control), but there was no difference at 4 weeks. Morphologically prominent cystic structures were observed in the Dx group at 10 weeks. CONCLUSION: Our results suggest that dexamethasone suppresses the expansion and transdifferentiation of transplanted porcine NPCCs into beta-cells in normal nude mice.

Expression of the intermediate filament vimentin in proliferating duct cells as a marker of pancreatic precursor cells.

OBJECTIVES: The expression of the intermediate filament (IF) vimentin, usually considered a marker of mesenchymal cells, has been observed in the epithelial cells during embryogenesis, carcinogenesis, and dedifferentiation, suggesting that it might be useful as a marker of proliferating precursor cells in the pancreas. METHODS: Rat pancreata at E18 and at different time points after partial pancreatectomy (Px) and human and neonatal pig pancreatic tissue sections and monolayer cultured pancreatic duct cells were observed. All tissues were simultaneously immunostained with pancytokeratin and vimentin antibodies. In costained duct cells, PDX-1 or PCNA expression was also analyzed using confocal microscope images. RESULTS: In the rat embryonic pancreas at E18, all epithelial cells that formed ductlike structures expressed both cytokeratin and vimentin IF, whereas no duct cells costained for IF in the adult rat or neonatal pig pancreas. Such costaining reappeared in the following order: common pancreatic duct, main ducts, foci of regeneration and then disappeared completely at 30 days after Px. In humans, costaining was found in only 1 diabetic patient's pancreatic section, which was accompanied by massive duct cell proliferation. In monolayer culture, most of the duct cells of human and neonatal pigs coexpressed both IF proteins. Only a few costained duct cells also expressed PDX-1, and most of those cells were also stained with PCNA in rat embryonic pancreas and regenerating foci after partial Px. CONCLUSIONS: Vimentin IF expression might be a useful marker for pancreatic precursor cells and could be used to investigate the concept of the dedifferentiation of fully matured duct cells during the process of the beta-cell neogenesis.

Magnesium sulfate does not reduce postoperative analgesic requirements.

BACKGROUND: Because magnesium blocks the N-methyl-D-aspartate receptor and its associated ion channels, it can prevent central sensitization caused by peripheral nociceptive stimulation. However, transport of magnesium from blood to cerebrospinal fluid (CSF) across the blood-brain barrier is limited in normal humans. The current study was designed to evaluate whether perioperative intravenous magnesium sulfate infusion affects postoperative pain. METHODS: Sixty patients undergoing abdominal hysterectomy received 50 mg/kg intravenous magnesium sulfate as a bolus dose followed by a continuous infusion of 15 mg x kg(-1) x h(-1) for 6 h (magnesium group) or the same volume of isotonic saline (control group). At the end of surgery, serum and CSF magnesium concentration were measured in both groups. The cumulative postoperative analgesic consumption was measured to assess the analgesic effect using a patient-controlled epidural analgesia device. Pain intensities at rest and during forced expiration were evaluated at 6, 24, 48, and 72 h postoperatively. RESULTS: At the end of surgery, patients in the magnesium group had significantly greater postoperative serum magnesium concentrations compared with both preoperative and control group values (P < 0.001). Despite significantly higher serum magnesium concentrations in the magnesium group, there was no significant difference in magnesium concentration measured in postoperative CSF. Cumulative postoperative analgesic doses were similar in both groups. However, there was observed an inverse relation between cumulative postoperative analgesic consumption and the CSF magnesium concentration in both groups. Visual analog pain scores at rest and during forced expiration were similar and less than 4 in both groups. CONCLUSIONS: Perioperative intravenous administration of magnesium sulfate did not increase CSF magnesium concentration and had no effects on postoperative pain. However, an inverse relation between cumulative postoperative analgesic consumption and the CSF magnesium concentration was observed. These results suggest that perioperative intravenous magnesium infusion may not be useful for preventing postoperative pain.

Osteoclastogenesis is enhanced by activated B cells but suppressed by activated CD8(+) T cells.

Host immune response is known to contribute to the progression of periodontitis, and alveolar bone destruction in periodontitis is associated with enhanced osteoclast activity. Therefore, we evaluated the roles of activated lymphocyte subsets in osteoclastogenesis. Osteoclast precursors were co-cultured with activated lymphocytes (B, CD4(+) T, CD8(+) T) in the presence of either macrophage colony-stimulating factor (M-CSF) alone or M-CSF plus soluble receptor activator of NF-kappaB ligand (sRANKL), and subsequent differentiation into active osteoclasts was evaluated by a resorption assay. The activated B and CD4(+) cells, but not CD8(+) T cells, induced osteoclast differentiation in the presence of M-CSF alone. In the presence of M-CSF and sRANKL, B cells induced the formation of small but highly active osteoclasts and increased resorption, while CD8(+) T cells profoundly suppressed osteoclastogenesis. Co-culture using an insert well or supernatant suggested that both B and CD8(+) T cells acted on osteoclasts mostly via soluble proteins. Activated B cells expressed many osteoclastogenic factors including RANKL, TNF-alpha, IL-6, MIP-1alpha, and MCP-3. CD8(+) T cells expressed a substantial amount of osteoprotegerin (OPG) along with RANKL. However, blocking antibody to OPG did not reverse the suppression by CD8(+) T cells, suggesting that other factor(s) are involved. Taken together, activated B cells promoted osteoclastogenesis, while CD8(+) T cells inhibited the osteoclast formation via direct interaction. The results imply the importance of lymphocyte subpopulations in the development of periodontitis.

Role of skin prick test and serological measurement of specific IgE in the diagnosis of occupational asthma resulting from exposure to vinyl sulphone reactive dyes.

OBJECTIVES: Some patients with occupational asthma resulting from exposure to reactive dyes have skin reactivity to the causative dyes and specific IgE to reactive dyes have been found in these patients. However, the usefulness of skin prick tests (SPTs) and serological measurement of specific IgE in screening, diagnosis, and monitoring the occupational asthma resulting from exposure to reactive dyes have not yet been assessed. In this study, the clinical validation of SPTs and measurement of specific IgE to vinyl sulphone reactive dyes by enzyme linked immunosorbent assay (ELISA) was evaluated. METHODS: 42 Patients with occupational asthma from reactive dyes (true positive group) were enrolled. In these the causative reactive dye was confirmed by bronchial challenge test. 93 Asymptomatic factory workers with negative challenge to the reactive dye (true negative group) and 16 unexposed controls with negative challenge to the reactive dye were also enrolled. Skin prick tests were done with 10 mg/ml reactive dye in 0.4% phenol/0.9% saline. IgE specific to reactive dye conjugated to human serum albumin (HSA) was measured with enzyme linked immunosorbent assays (ELISAs). RESULTS: None of the unexposed controls had a positive response to SPTs. The sensitivity (76.2% v 53.7%), specificity (91.4% v 86.0%), positive predictive value (80.0% v 62.9%), and negative predictive value (89.5% v 80.8%) of SPTs were higher than those of ELISAs. The mean weal size of reaction to reactive dye was weakly correlated with the ELISA optical density of IgE to reactive dye conjugate in patients with occupational asthma from reactive dyes (n=41, r=0.337, p<0.05). In four patients with occupational asthma from reactive dyes and eight control subjects exposed to reactive dye, IgE specific to reactive dye conjugated to HSA was detected with ELISA even though they showed negative skin reactivity. Six patients completely avoided the reactive dye for a mean (SD) 27.8 (10.3) months, IgE specific to reactive dyes decreased in all six patients (p<0.05) during this time. CONCLUSIONS: Both SPTs and detection of IgE specific to reactive dye in serum samples could be valuable for screening, diagnosis, and monitoring occupational asthma resulting from exposure to reactive dyes. These two tests would complement each other.

Comparison of allergenic components between German cockroach whole body and fecal extracts.

BACKGROUND: Cockroaches have been demonstrated to be an etiologic factor in allergic diseases. Further, sensitivity to cockroach places patients with asthma at risk for exacerbations that require emergency medical care. OBJECTIVE: This study compared the differences in allergenic components between German cockroach whole body and German cockroach fecal extracts (GWBE and GFE). METHODS: Patients with asthma and/or allergic rhinitis were skin prick tested with German cockroach extract (Bayer Corporation, West Haven, CT). Serum specimens from these patients, 25 with positive skin tests and 8 with negative tests, were used for the ELISA and immunoblot experiments. RESULTS: By ELISA, 72% (18 of 25) and 60% (15 of 25) of positive responders' sera showed IgE antibodies to GWBE and GFE, respectively, and the IgE levels to GWBE were highly correlated with those to GFE (r = .84, P < .01). In inhibition ELISA experiments, extensive cross-reactivity was observed between GWBE and GFE, slight cross-reactivity between GWBE and Dermatophagoides farinae, and no cross-reactivity between GFE and D. farinae. The two-site monoclonal antibody ELISA detected more of the German cockroach major allergens in GFE compared with GWBE; 6.2 times (2420 vs 390 U/mL) for Bla g 1 and 3 times (15.32 vs 5.07 microg/mL) for Bla g 2. In the immunoblot comparison of patients' sera, the IgE antibodies binding to GWBE were apparently different from those binding to GFE in all the positive responders' sera; eg, 50% or more of the 25 positive responders' sera reacted to 43- to 67-kDa proteins in GWBE and to 28- to 30-kDa proteins in GFE, respectively. No IgE antibodies bound to components in GWBE and GFE in the 8 negative responders' sera. CONCLUSIONS: There are major differences between the allergenic components of GWBE and GFE. Based on the amounts of major allergens (Bla g 1, Bla g 2), German cockroach feces are a more important source of allergen than the whole body in respiratory allergic diseases.

Hahella chejuensis gen. nov., sp. nov., an extracellular-polysaccharide-producing marine bacterium.

A bacterial strain, designated 96CJ10356T, which produced abundant extracellular polysaccharides and red pigment was isolated from marine sediment collected from Marado, Cheju Island, Republic of Korea. The organism is Gram-negative, aerobic, rod-shaped and motile. Growth was not observed in the absence of NaCl, and was optimal at an NaCl concentration of 2%. The strain contained oxidase and catalase, and was able to hydrolyse aesculin and gelatin. The major cellular fatty acids were saturated or monounsaturated straight-chain fatty acids. An almost complete 16S rDNA sequence of the test strain was determined. Phylogenetic analysis based on the neighbour-joining and Fitch-Margoliash methods indicated that the organism formed a distinct phyletic line within the gamma Proteobacteria. This relationship was also supported by sequence comparison, as no valid bacterial species showed more than 90% sequence homology with the isolate. It is clear from polyphasic evidence that the isolate merits the status of genus in the gamma subclass of the Proteobacteria, and the name Hahella chejuensis gen. nov., sp. nov. is proposed for the marine isolate 96CJ10356T (= KCTC 2396T = IMSNU 11157T).

Epidural verapamil reduces analgesic consumption after lower abdominal surgery.

UNLABELLED: In this double-blind study, we administered lumbar epidural bupivacaine or bupivacaine plus verapamil to investigate the possible role of the calcium channel blocker, verapamil, in postoperative pain. One hundred patients (ASA physical class I or II) scheduled for lower abdominal surgery were randomly assigned to one of four groups. Group 1 received 10 mL of 0.5% epidural bupivacaine injected 15 min before incision, followed by 10 mL of epidural normal saline 30 min after incision. Group 2 received 10 mL of epidural normal saline injected before incision, followed by 10 mL of 0.5% epidural bupivacaine 30 min after incision. Group 3 received 10 mL of 0.5% epidural bupivacaine plus 5 mg of verapamil injected before incision, followed by 10 mL of epidural normal saline 30 min after incision. Group 4 received the same drugs as Group 3, in the reverse order. Pain and mood numeric rating scores, sedation scores, Prince Henry scores, patient-controlled cumulative postoperative analgesic consumption, and the incidence of side effects were assessed 2, 6, 12, 24, and 48 h after the operation in each group. Cumulative postoperative analgesic consumption in Groups 3 and 4 was significantly lower (P < 0.05) than that in Groups 1 and 2 24 and 48 h after surgery. There were no differences in the pain, mood, and sedation scores and the incidence of side effects among the four groups. We conclude that epidural verapamil decreases postoperative pain, possibly by interfering with normal sensory processing and by preventing the establishment of central sensitization. IMPLICATIONS: Calcium plays an important role in pain physiology at the spinal cord level. We examined the effect of bupivacaine plus verapamil (calcium channel blocker) and of bupivacaine alone. We demonstrated that the combination, administered epidurally, resulted in less postoperative analgesic consumption than bupivacaine alone.

Blockade of myocardial ATP-sensitive potassium channels by ketamine.

BACKGROUND: The adenosine triphosphate (ATP)-sensitive potassium (KATP) channel underlies the increase in potassium permeability during hypoxia and ischemia. The increased outward potassium current during ischemia may be an endogenous cardioprotective mechanism. This study was designed to determine the effects of ketamine on KATP channel in rat hearts. METHODS: Inside-out and cell-attached configurations of patch-clamp techniques and 3 M potassium chloride-filled conventional microelectrodes were used to investigate the effect of ketamine on KATP channel currents in single rat ventricular myocytes and on the action potential duration of rat papillary muscles, respectively. RESULTS: Ketamine inhibited KATP channel activity in rat ventricular myocytes in a concentration-dependent manner. In the inside-out patches, the concentration of ketamine for half-maximal inhibition and the Hill coefficient were 62.9 microM and 0.54, respectively. In a concentration-dependent manner, ketamine inhibited pinacidil- and 2,4-dinitrophenol-activated KATP channels in cell-attached patches. The application of ketamine to the intracellular side of membrane patches did not affect the conduction of single-channel currents of KATP channels. Ketamine increased the action potential duration, which was then shortened by pinacidil in a concentration-dependent manner. CONCLUSIONS: Ketamine inhibited KATP channel activity in a concentration-dependent manner. These results suggest that ketamine may attenuate the cardioprotective effects of the KATP channel during ischemia and reperfusion in the rat myocardium.

Epidural morphine plus ketamine for upper abdominal surgery: improved analgesia from preincisional versus postincisional administration.

Increased postoperative pain may be caused by central nervous system plasticity, which may be related to actions of N-methyl-D-aspartic acid (NMDA) receptors on neurons in the dorsal horn of the spinal cord. Opioids act mainly on presynaptic receptors and reduce neurotransmitter release, while ketamine antagonizes NMDA receptors and prevents wind-up and long-term potentiation. Thus, we postulated that central nervous system sensitization would be prevented more effectively by the preoperative use of these two drugs simultaneously, and the effect of preemptive analgesia would be demonstrated. Ketamine, 60 mg, and morphine, 2 mg, were injected epidurally through an indwelling catheter that was inserted at the T7-8 interspace in 60 ASA physical status class 1-2 patients. The drugs were injected before induction of anesthesia (Group 1; n = 30) or immediately after removal of a surgical specimen (Group 2; n = 30). An additional 2 mg of morphine was injected when the patients complained of resting pain. The analgesic effect was assessed by the time from first analgesic injection to second dose and the number of patients who needed supplemental injections. Complications were also noted. The duration of analgesia was longer (P < 0.01) in Group 1 (31.1 +/- 16.0 h) than in Group 2 (21.1 +/- 12.0 h), and the proportion of patients who needed supplemental injections was decreased (P < 0.05) in Group 1 (56.7%) compared with Group 2 (90.0%). The incidence of adverse effects was not different between the two groups. In conclusion, preoperative administration of morphine and ketamine is more effective in reducing postoperative pain than it is when given during the operation.