Cigarette smoking and risk of herpes zoster: a population-based cohort study in Taiwan.

The effects of cigarette smoking on the risk of herpes zoster (HZ) infection remain unclear. This study aimed to examine the association between cigarette smoking and HZ. Participants were collected from four rounds (2001, 2005, 2009 and 2013) of the Taiwan National Health Interview Survey. Incident cases of HZ were identified from the Taiwanese National Health Insurance database. Of the 57 641 participants, 3346 developed HZ during the observation period. After controlling for confounders, current smokers had a lower risk of incident HZ than never-smokers (adjusted hazard ratio 0.69; 95% CI 0.62-0.77). There was a trend toward a decreased risk of HZ with increasing numbers of cigarettes per day, years of smoking and cumulative pack-years of smoking among current smokers (Ptrend < 0.001). Former smoking was not associated with risk of HZ. In conclusion, current smoking was significantly associated with a decreased risk of developing HZ.

Cigarette smoking and risk of rosacea: a nationwide population-based cohort study.

BACKGROUND: Most evidence regarding the relationship between cigarette smoking and risk of rosacea is obtained from cross-sectional or case-control studies. OBJECTIVE: To examine the association between smoking and risk of developing rosacea. METHODS: Participants were collected from four rounds (2001, 2005, 2009 and 2013) of the Taiwan National Health Interview Survey. Incident cases of rosacea were identified from the National Health Insurance database. Cox proportional hazard model was used for the analyses. RESULTS: Of the 59 973 participants, 379 developed rosacea during a mean follow-up of 10.8 years. After adjustment for potential confounders, current smokers had a lower risk of rosacea than never smokers [adjusted hazard ratio (aHR) 0.60; 95% confidence interval (CI) 0.39-0.92]. An increase in smoking intensity was associated with a decreased risk of rosacea among current smokers (Ptrend  = 0.0101). Compared with never smokers, current smokers of >15 cigarettes/day had an aHR of 0.51 (95% CI: 0.26-0.99) for rosacea. For incident rosacea, the aHRs (95% CIs) of current smokers of ≤10 years of smoking and ≤10 pack-years of smoking were 0.44 (0.22-0.88) and 0.51 (0.29-0.89), respectively. Former smoking was not associated with rosacea risk. CONCLUSION: Current smoking was significantly associated with a decreased risk of rosacea.

Plasminogen activator inhibitor-1 is associated with leukocyte telomere length in American Indians: findings from the Strong Heart Family Study.

Essentials Plasminogen activator inhibitor-1 (PAI-1) advanced cellular senescence in experiment studies. No population study exists on the association between PAI-1 and biological aging in American Indians. We found cross-sectional and longitudinal associations between higher PAI-1 and shorter telomere length. Our findings suggest a pathway linking PAI-1 with biological aging beyond metabolic factors. SUMMARY: Background Plasminogen activator inhibitor-1 (PAI-1) promotes cellular aging both in vitro and in vivo. Telomere length is a marker of biological aging. Objectives To examine the cross-sectional and longitudinal associations between plasma PAI-1 and leukocyte telomere length in a large-scale epidemiological study of American Indians. Methods We measured leukocyte telomere length (LTL) and plasma PAI-1 in 2560 American Indians who were free of overt cardiovascular disease (CVD) and participated in the Strong Heart Family Study (SHFS) clinical examination in 2001-2003. LTL and PAI-1 were repeatedly measured in 475 participants who attended SHFS clinical visits in both 2001-2003 and 1998-1999. A generalized estimating equation model was used to examine the cross-sectional and longitudinal associations between PAI-1 and LTL, adjusting for known risk factors. Results A higher level of plasma PAI-1 was negatively associated with shorter age-adjusted LTL (ß = -0.023; 95% CI, -0.034 to -0.013). This association was attenuated (ß = -0.015; 95% CI, -0.029 to -0.002) after adjustments for demographics, study site, lifestyle (smoking, drinking and physical activity) and metabolic factors (obesity, blood pressure, fasting glucose, insulin, lipids and kidney function). Further adjustment for hsCRP did not change this association (ß = -0.015; 95% CI, -0.029 to -0.001). Longitudinal analysis revealed that change in plasma PAI-1 was also inversely associated with change in LTL after adjusting for demographics, follow-up years, lifestyle factors, changes in metabolic factors, baseline levels of PAI-1 and LTL (ß = -0.0005; 95% CI, -0.0009 to -0.0001). Conclusions A higher level of plasma PAI-1 was associated with shorter LTL in American Indians. This finding may suggest a potential role of PAI-1 in biological aging among American Indians.

Animal health policy principles for highly pathogenic avian influenza: shared experience from China and Canada.

Animal health policy for highly pathogenic avian influenza (HPAI) must, for the time being, be based on expert opinion and shared international experience. We used the intellectual capital and knowledge of experienced Chinese and Canadian practitioners and policy makers to inform policy options for China and find shared policy elements applicable to both countries. No peer-reviewed comprehensive evaluations or systematic regulatory impact assessments of animal health policies were found. Sixteen guiding policy principles emerged from our thematic analysis of Chinese and Canadian policies. We provide a list of shared policy goals, targets and elements for HPAI preparedness, response and recovery. Policy elements clustered in a manner consistent with core public health competencies. Complex situations like HPAI require complex and adaptive policies, yet policies that cross jurisdictions and are fully integrated across agencies are rare. We encourage countries to develop or deploy capacity to undertake and publish regulatory impact assessments and policy evaluation to identify policy needs and provide a basis for evidence-based policy development.

Targeted hepatocellular carcinoma proapoptotic BikDD gene therapy.

Hepatocellular carcinoma (HCC), the third leading cause of cancer death in the world, is the most general type of primary liver cancer. Although current treatment modalities, such as liver transplantation, resection, percutaneous ablation, transarterial embolization, chemotherapy and radiotherapy are potentially curative, these methods are not universally applicable to all of HCC patients, especially for those with poor prognosis in which no effective remedy is available. Therefore, development of novel therapeutic approach for the treatment of HCC is urgently needed. In the current study, we developed a promising HCC-targeted gene therapy vector driven by liver cancer-specific α-fetoprotein promoter/enhancer coupled to an established platform technology. The activity of this expression vector is comparable with or even higher than that of strong cytomegalovirus (CMV) promoter and exhibits strong promoter activity in liver cancer cells/tumors, but has nearly no or very low activity in normal cells/organs in vitro and in orthotopic animal models in vivo. Its cancer specificity exceeds that of the CMV promoter, which expresses non-specifically in both normal and tumor cells. In addition, targeted expression of a therapeutic BikDD, a mutant of proapoptotic gene Bik effectively and preferentially killed liver cancer cells, but not normal cells and significantly repressed growth of HCC tumors, and prolonged survival in multiple xenograft and syngeneic orthotopic mouse models of HCC through intravenous systemic gene delivery. Importantly, systemic administration of BikDD by our expression vector exerted no systemically acute toxicity compared with CMV-BikDD in mice. Taken together, this study elucidates a relatively safe and highly effective and specific systemic gene therapy strategy for liver cancer, and is worthy of further development for future clinical trials.

Tract-specific and region of interest analysis of corticospinal tract integrity in subcortical ischemic stroke: reliability and correlation with motor function of affected lower extremity.

BACKGROUND AND PURPOSE: TS analysis has been suggested as a useful method to evaluate the fiber integrity of white matter tracts. This study investigated the intrarater and interrater reliability and validity of a TS analysis for the CST and compared the results with those of a ROI-based analysis. MATERIALS AND METHODS: Diffusion spectrum imaging was performed on 7 patients with subcortical ischemic stroke on a 3T MR imaging system. For the TS analysis, seed regions were placed at the cerebral peduncle and the medial portion of the primary motor cortex to reconstruct the tracts of the CST for motor control of the lower extremity. The mean GFA was measured at the PLIC by calculating the weighted sum of the GFAs sampled by the CST tracts at this segment. For the ROI-based analysis, the posterior two-thirds of the PLIC were enclosed on the GFA maps, and the mean GFA in this ROI was calculated. RESULTS: The results showed good-to-excellent intrarater and interrater reliability on the seed region/ROI placement (mean kappa values >0.80) and mean GFA values (ICCs >0.90) for both the TS and ROI-based analyses. Both the GFA(PLIC-TS) and GFA(PLIC-ROI) values were highly correlated with the motor function of the affected lower extremity (r = 0.76 and 0.80, respectively; P < .05). CONCLUSIONS: We demonstrated good reliability and validity of the TS and ROI-based analyses of the CST corresponding to lower extremity motor control in patients with subcortical ischemic stroke.

Identification of quantitative trait loci (QTL) for oil and protein contents and their relationships with other seed quality traits in Brassica juncea.

A detailed RFLP-genomic map was used to study the genetics of oil, seed and meal protein and sum of oil and seed/meal protein contents in a recombinant doubled-haploid population developed by crossing black- and yellow-seeded Brassica juncea lines. Two yellow seed color genes (SC-B4, SC-A6) and one QTL for erucic acid content (E(1b)) showed pleiotropic effect for oil, protein and sum of oil and seed/meal protein contents. Six (O-A1, O-A6, O-A9, O-B3, O-B4, O-B5) and five (SP-A1, SP-A9, SP-B4, SP-B6, SP-C) QTLs were significant for oil and seed protein contents, respectively. Tight linkage of three of these QTLs (SP-A1, SP-A9, SP-B4, O-A1, O-A9, O-B4), with opposite effects, poses challenge to the plant breeders for simultaneous improvement of negatively correlated (r = -0.7**) oil and seed protein contents. However, one QTL for oil content (O-B3) and two for seed protein content (SP-B6, SP-C) were found to be unlinked, which offer the possibility for simultaneous improvement of these two traits. QTLs significant for meal protein (MP-A1, MP-A6, MP-A9, MP-B5, MP-B6) were significant at least for oil, seed protein or sum of oil and seed/meal protein contents (T-A6, T-A7, T-B4, T-B5). Sum of oil and seed protein contents and sum of oil and meal protein contents had a perfect correlation, as well as same epistatic interactions and QTLs with similar additive effect. This indicates that protein in seed or meal has practically the same meaning for breeding purposes. Epistatic interactions were significant for the quality traits, and their linkage reflected association among the traits.

Children who experience their first fracture at a young age have high rates of fracture.

Rate of fracture was examined according to age at first fracture in 313 New Zealand children (145 girls, 168 boys) under l3 years of age (95.4% of a consecutive series of children treated at one hospital for a recent confirmed fracture at any site). In their lifetimes they had experienced 468 separate fracture events, over half (54.7%) occurring in the 32.3% of children breaking bones on more than one occasion. Children experiencing a first fracture before 4 years of age had 36.7 (95%CI 30.7-44.1) fractures per l00 years of exposure: this was a significantly higher rate than that of children experiencing their first fracture later in life. Thus, using the <4.0 year age group as a reference, we found that rate ratios (adjusted for gender) for groups that had suffered the first fracture at later ages were: first fracture between 4.0 and 6.99 years, 0.77 (95%CI 0.58-1.03); first fracture between 7.0 and 9.99 years, 0.63 (95%CI 0.42-0.94); first fracture between 10.0 and 12.99 years, 0.48 (95% CI 0.32-0.72). Asthma was over-represented (31% seen, 25% expected), and a high proportion of the sample (32.9%) used corticosteroid medications; however, neither characteristic affected age at first fracture. In contrast, the large number (n= 42) of youngsters (13.4% of the sample) reporting adverse reactions to milk were younger at first fracture than children without reactions to milk (P<0.05). We conclude that children experiencing their first fracture at a young age have high rates of fracture and should be targeted for advice to improve their bone strength.

Molecular mapping of seed aliphatic glucosinolates in Brassica juncea.

An RFLP genomic map with 316 loci was used to study the inheritance of aliphatic glucosinolates in Brassica juncea using doubled-haploid (DH) populations developed from a cross between RLM-514, an agronomically superior non-canola quality B. juncea (high erucic acid and high glucosinolates), and an agronomically poor canola quality B. juncea breeding line. Two QTLs (GSL-A2a and GSL-A2b) associated with 3-butenyl were consistent across years and locations, and explained 75% of the phenotypic variance in the population. Three QTLs (GSL-A2a, GSL-F, GSL-B3) affected 2-propenyl and explained 78% of the phenotypic variance in the population. For total aliphatic glucosinolates, five QTLs explained 30% to 45% of the total phenotypic variance in the population in different environments. Several QTLs (GSL-A7 and GSL-A3) were highly inconsistent in different environments. Major QTLs (GSL-A2a and GSL-A2b) associated with individual glucosinolates were non-significant for total aliphatic glucosinolates. A marker-assisted selection strategy based on QTLs associated with individual glucosinolates rather than total aliphatic glucosinolates is proposed for B. juncea.

RFLP linkage analysis and mapping genes controlling the fatty acid profile of Brassica juncea using reciprocal DH populations.

An RFLP linkage map, comprising 300 linked and 16 unlinked loci, was constructed using reciprocal DH populations of Brassica juncea. The linked loci were organized into 18 linkage groups and seven unlinked segments, covering a total map distance of 1,564 cM. The A and B genomes were identified. The chi(2) test showed that 96.1% of the common intervals in the two populations differed non-significantly for recombination fractions, thus strongly suggesting the absence of sex-based differences for recombination fractions in B. juncea. Two QTLs, E(1a) and E(1b), significantly affected erucic acid content, and individually explained 53.7% and 32.1%, respectively, and collectively 85.8% of the phenotypic variation in the population. The QTLs E(1a) and E(1b) showed epistasis, and the full model including epistasis explained nearly all of the phenotypic variation in the population. The QTLs E(1a) and E(1b) were also associated with contents of oleic, linoleic and linolenic acids. Three additional QTLs (LN(2), LN(3) and LN(4)) significantly influenced linolenic acid content. The QTL LN(2) accounted for 35.4% of the phenotypic variation in the population. Epistatic interactions were observed between the QTLs E1a and LN(2). The stability of the detected QTLs across years and locations, and breeding strategies for improving the fatty acid profile of B. juncea, are discussed.

Deficient transforming growth factor beta and interleukin-10 responses contribute to the septic death of burned patients.

In order to understand the roles of pro-inflammatory and anti-inflammatory cytokines in burn injury and sepsis post-burn, serial changes in serum levels of transforming growth factor beta-1 (TGF-beta-1) were determined and compared to those of IL-6 and IL-10 in 15 burned patients. Among these 15 patients, 8 recovered without sepsis. The other seven, who were septic, expired. Our results showed that an initial peak serum TGF-beta-1 response was detected within 1 day post-burn. Peak serum IL-6 and IL-10 responses were also detected within 4 days after the burn injury of these patients. Significant differences in peak serum IL-6, IL-10 and TGF-beta-1 levels were not found between patients with total body surface area (TBSA) of greater or less than 50% and between patients who survived or expired from burn injury. Afterwards, levels of circulating IL-6 and IL-10 remained low in the survivors. However, a second peak response in serum TGF-beta-1 levels was observed in all burned patients analyzed. The second peak serum TGF-beta-1 levels post-burn of the eight survivors and the seven non-survivors were from 28,542 to 76,554 pg/ml (a mean value of 51,256+/-14,264 pg/ml) and from 8616 to 40,851 pg/ml (a mean value of 24,079+/-10,399 pg/ml), respectively. A significant difference (P<0.01) in mean values of the second peak TGF-beta-1 responses between groups of survivors and non-survivors was detected. Levels of circulating IL-6 in the septic non-surviving patients showed a tendency to increase 1-2 weeks post-burn and reached high levels before the expiration of these patients. After an initial peak response, the serum IL-10 level remained low in one of the seven non-survivors, while it increased in the other six non-survivors. However, marked increases in circulating IL-10 levels were observed only just before the death of these non-survivors. In conclusion, an initial increase in serum levels of IL-6, IL-10 and TGF-beta-1 was detected post-burn. A marked increase in serum levels of IL-6 before death suggests its role in the pathophysiology of sepsis in burned patients. In addition, a low secondary TGF-beta-1 response and a lack and/or delay in the increase of circulating IL-10 in the non-survivors may all contribute to the pathophysiology of septic death in burned patients.

The effects of Ma-Xing-Gan-Shi-Tang on respiratory resistance and airway leukocyte infiltration in asthmatic guinea pigs.

Ma-Xing-Gan-Shi-Tang (MXGST), a traditional Chinese medicine, has been used in treatment of the bronchial asthma for several centuries. However, the therapeutic mechanisms of this Chinese medicine are still far from clear. To understand the mechanism of anti-asthmatic property of MXGST, a guinea pig model of allergic asthma was used to investigate the effects of MXGST on Dermatophagoides pteronyssinus-induced early and late asthmatic responses and airway inflammation, and examine direct beta2-adrenoceptor agonist activity in guinea-pig isolated trachea. Administration of MXGST (10 g/kg) extracts significantly inhibited the antigen induced immediate asthmatic responses (IAR) in actively sensitized guinea pig. MXGST caused concentration-dependent relaxation in strips of guinea pig trachea contracted with carbachol, and ICI-118551, a selective beta2-adrenoceptor antagonist, significantly inhibit the relaxation caused by MXGST. Furthermore, examination of bronchoalveolar lavage fluid (BALF) revealed that MXGST significantly inhibited the increase in neutrophil in the airway at 1, 6 and 24 hr after antigen challenge. Histopathologic examination results showed that MXGST suppressed the neutrophil infiltration into lung tissue. In conclusion, we suggest that the anti-asthmatic effects of MXGST are mainly due to its stimulation of beta2-adrenoceptors on bronchial smooth muscle and its anti-inflammatory ability to inhibit the neutrophil into the airway. The precise mechanism of action of MXGST in asthma remains to be elucidated.

Necrotizing fasciitis of the head and neck: an analysis of 47 cases.

Necrotizing fasciitis is an overwhelming infection common to the perineum, abdominal wall, and extremities. It is a surgical emergency related to a high mortality rate that is more often seen in elderly and immunocompromised patients. Necrotizing fasciitis occurs uncommonly in the head and neck region. Over a 12-year period, 47 cases of necrotizing fasciitis of the head and neck region were collected at this hospital. The demographics, predisposing factors, clinical presentation and courses, management, complications, and outcomes were analyzed. The cases were divided into two groups: survivors and nonsurvivors. Statistical comparisons were made of the parameters age, gender, smoking or drinking habit, underlying medical problems, laboratory data, and treatments used. Forty-two patients (89.4 percent) had associated systemic disease; most of these patients had diabetes (72.3 percent). The clinical manifestations are nonspecific but are often typical for diagnosis. The necessity of computed tomographic scans is not conclusive in this study. Presentation of septic shock (p = 0.004) and association with underlying malignancy (p = 0.03) were the only statistically significant factors that led to a poor prognosis. The cornerstones of proper management include early diagnosis, aggressive surgical debridement, broad-spectrum antibiotics, and intensive supportive care.

Dislocation-controlled perforated layer phase in a PEO- b-PS diblock copolymer.

Small angle x-ray analyses show that the shear-induced hexagonal perforated layer phase in a poly(ethylene oxide)- b-polystyrene diblock copolymer consists of trigonal (R3;m) twins and a hexagonal (P6(3)/mmc) structure, with trigonal twins being majority components. Transmission electron microscopy reveals that the hexagonal structure is generated through sequential intrinsic stacking faults on the second layer from a previous edge dislocation line, while the trigonal twins are formed by successive intrinsic stacking faults on neighboring layers due to the plastic deformation under mechanical shear.

Luteolin-inhibited arylamine N-acetyltransferase activity and DNA-2-aminofluorene adduct in human and mouse leukemia cells.

N-Acetyltransferase enzyme is an important enzyme in the first step of arylamine compounds metabolism. Luteolin has been shown to exit antibacterial and antineoplastic activity. The purpose of this present study is to evaluate the question of whether luteolin could affect arylamine N-acetyltransferase (NAT) activity and DNA-2-aminofluorene adduct formation in human (HL-60) and mouse (L1210) leukemia cells. By using HPLC, N-acetylation of 2-aminofluorene was determined. Luteolin displayed a dose-dependent inhibition to cytosolic NAT activity and intact human and mice leukemia cells. Time-course experiments showed that N-acetylation of 2-aminofluorene measured from intact human and mice leukemia cells were inhibited by luteolin for up to 24 hours. Using standard steady-state kinetic analysis, it was demonstrated that luteolin was a possible uncompetitive inhibitor to NAT activity in cytosols. The DNA-2-aminofluorene adduct formation in human and mouse leukemia cells were inhibited by luteolin. This report is the first demonstration to show that luteolin affects human and mice leukemia cells NAT activity and DNA-2-aminofluorene on adduct formation.

Construction of a framework map in Pinus contorta subsp. latifolia using random amplified polymorphic DNA markers.

We report on the construction of the first random amplified polymorphic DNA (RAPD) framework map in Pinus contorta subsp. latifolia. Genomic DNA of haploid megagametophytes from 90 open-pollinated seeds originating from a single tree were amplified with 840 random decamer oligonucleotide primers by the polymerase chain reaction. Three-hundred twenty-eight RAPD markers with fragment sizes that ranged between 260 and 3080 base pairs were found segregating at 110 random decamer oligonucleotide primers. Of these 328 RAPD markers, 148 were mapped to 16 framework linkage groups and 77 were mapped as accessory markers onto the framework linkage groups, on a support interval of minimal LOD score of 3. The 16 framework maps cover a distance of 2287 cM. The estimate of genome size was 2407 cM with a 95% confidence interval of 2304-2459 cM.

Luteolin inhibits the growth and arylamine N-acetyl-transferase activity in Neisseria gonorrhoeae.

Growth inhibition and arylamine N-acetyltransferase (NAT) activity in Neisseria gonorrhoeae were inhibited by luteolin, a drug which originated from herbs. The growth inhibition was based on changes in optical density (OD) using a spectrophotometer, and arylamine NAT activity with 2-aminofluorene (2-AF) was determined using high pressure liquid chromatography. The inhibition of growth in N. gonorrhoeae demonstrated that luteolin elicited a dose-dependent growth inhibition in the N. gonorrhoeae cultures. Suspensions of N. gonorrhoeae with or without specific concentrations of luteolin cotreatment showed different percentages of 2-AF acetylation. The data indicated that there was reduced NAT activity associated with increased levels of luteolin in N. gonorrhoeae suspensions. Time-course experiments showed that NAT activity measured from intact N. gonorrhoeae cells was inhibited by luteolin for at least 4 h. Using standard steady-state kinetic analysis, it was demonstrated that luteolin was a possible uncompetitive inhibitor to NAT activity in N. gonorrhoeae. This report is the first to show that luteolin can inhibit N. gonorrhoeae NAT activity.

Random amplified polymorphic DNA diversity of marginal and central populations in Pinus contorta subsp. latifolia.

Fifteen populations of lodgepole pine (Pinus contorta subsp. latifolia) were surveyed for diversity across 52 random amplified polymorphic DNAs (RAPDs). The objective was to compare single-locus and multilocus structures in four marginal, three intermediate, and eight central populations. Single-locus estimates indicated average observed and expected heterozygosity to be 0.19 and 0.17, respectively. When these estimates were split into population categories, a clear trend of increasing diversity was detected in the direction of marginal to central populations. F-statistics indicated an excess of heterozygotes, with F(IS) ranging from -0.08 for marginal populations to -0.15 for central populations and averaging -0.12 over 15 populations. The estimates of F(ST) decreased towards the margins of the species range, indicating increased population differentiation. Forty-nine of 52 RAPDs tested neutral in the Ewens-Watterson analysis. Multilocus analysis showed significant two-locus and high-order gametic disequilibria in all 15 populations. The most prominent components of the two-locus analysis were the variance of disequilibrium (VD, 46.2%) and the multilocus Wahlund effect (31.9%). This high value for VD indicated that founder effects could explain much of the observed multilocus associations. When analyzed by population categories, the VD showed a decreasing trend indicating that variation due to founder effects was more prominent in marginal populations. The two-locus Wahlund effect (WC) that is characteristic of strong population subdivision was highest in the central populations. This indicated significant levels of gene flow between populations with different allelic combinations.

Anti-inflammatory and neuroprotective effects of magnolol in chemical hypoxia in rat cultured cortical cells in hypoglycemic media.

Our previous studies demonstrated that magnolol protects neurons against chemical hypoxia by KCN in cortical neuron-astrocyte mixed cultures (14). In the present study, we examined whether the neuroprotective effect of magnolol involve modulating inflammatory mediators, prostaglandin E2 (PGE2) and nitric oxide (NO), induced by KCN (hypoxia) or KCN plus lipopolysaccharide (LPS). In glucose-absent (hypoglycemia) media, KCN or KCN plus LPS induced increases in lactate dehydrogenase (LDH) activity by 32% and 34%, and PGE2 production by 12% and 32%, respectively. Both LDH and PGE2 increases were suppressed by 100 microM magnolol. In addition, although KCN or LPS alone did not increase NO generation, KCN plus LPS increased NO generation. This increase was reduced by 100 microM magnolol or 10 microM L-NAME, but the LDH increase and PGE2 production were not reduced by L-NAME. These findings suggest that the protective effects of magnolol against brain damage by KCN or KCN plus LPS in hypoglycemic media may involve inhibition of PGE2 production, but inhibition of NO generation may not be important.

Temporary hearing impairment after general anesthesia--a case report.

The incidence of hearing impairment after anesthesia is rare. We report a case who received left total knee and hip replacement and developed severe hearing impairment of the left ear after general anesthesia. Examination of the left ear by an otolaryngologist showed that there was no noticeable abnormality. The hearing acuity recovered gradually and returned to normal 3 days later. The use of nitrous oxide during anesthesia was incriminated as the possible cause.