Detection of Helicobacter pylori in nasal and maxillary sinus specimens from patients with chronic sinusitis

OBJECTIVES: In patients with chronic sinusitis, the colonization of nasal and maxillary sinus tissues by Helicobacter pylori (HP) was investigated using polymerase chain reaction, urease test (CLO test), culture, and immunohistochemical analysis. STUDY DESIGN: A prospective clinical study. METHODS: The subjects were 11 patients aged 20 to 72 years with chronic sinusitis who had undergone sinus surgery under local anesthesia. In 7 of 11 patients, the HP status of the stomach was also studied. Nasal and maxillary sinus tissues were studied using polymerase chain reaction, urease test, culture, and immunohistochemical analysis. Helicobacter pylori infection of nasal and maxillary sinus tissues was defined by at least two positive results of different tests. RESULTS: Three (16%) of 19 nasal and maxillary sinus specimens from two patients were shown to be HP-positive (positive by polymerase chain reaction and immunohistochemical analysis and weakly positive by the CLO test). In one of these two patients, HP infection of the stomach was confirmed. In the other, a positive findings on immunohistochemical analysis suggested HP infection of the stomach. Immunoreactive structures were seen by immunohistochemical analysis in the nasal, maxillary sinus, and gastric specimens of these two patients but were partially degraded. CONCLUSION: Helicobacter pylori may exist in the nasal and maxillary sinus tissue specimens of some patients with chronic sinusitis with gastric HP infection.     

Cholinergic nerves mediate acetaldehyde action in the gastrointestinal tract

The regulation mechanism of inhibition of intestinal ethanol absorption induced by high acetaldehyde (AcH) concentration in blood was investigated. We used atropine (AT), atropine methylbromide (ATMB), pirenzepine (PI), bethanechol (BE) and pilocarpine (PL) with or without cyanamide (CY; a potent inhibitor of aldehyde dehydrogenase, which induces high AcH concentration in blood). The K(a) (absorption rate constant) value after the CY-alone pretreatment was significantly lower than that in controls. In the high AcH-induced cases, the values of K(a) in AT and ATMB pretreatments were similar to controls, but the value of K(a) in PI pretreatment was lower than that in controls. The values of K(a) in the case of BE pretreatment with and without high AcH levels were lower than in controls. The K(a) value in the PL with CY was significantly lower than that with CY alone. However, its action was blocked by ATMB pretreatment. These results suggest that high blood AcH concentrations inhibit intestinal ethanol absorption through the peripheral cholinergic nerves via muscarinic receptors, except for the muscarinic M(1) receptor, compared to other subtypes of muscarinic receptors.     

Acetaldehyde, a metabolite of ethanol, activates the hypothalamic-pituitary-adrenal axis in the rat

Cyanamide is a potent inhibitor of aldehyde dehydrogenase (ALDH: EC 1.2.1.3) used in the treatment of alcoholics. In the presence of ethanol, cyanamide causes an accumulation of acetaldehyde, a highly toxic metabolite of ethanol, with unpleasant side-effects. A similar accumulation is seen in some Oriental people with low ALDH activity. We have investigated the effects of ethanol and cyanamide administration on the activation of the hypothalamic-pituitary-adrenal (HPA) axis using in situ hybridization histochemistry and radioimmunoassay. Ethanol plus cyanamide resulted in a significant increase in corticotrophin-releasing factor and arginine vasopressin mRNA in the paraventricular nucleus, and pro-opiomelanocortin mRNA in the anterior pituitary. Plasma corticosterone concentrations were also significantly elevated following ethanol plus cyanamide administration. The blood concentration of acetaldehyde in the ethanol plus cyanamide group increased significantly. These results suggest that acetaldehyde, induced by blocking ethanol metabolism, is able to activate the HPA axis operating through a central mechanism.     

The effects of V2 antagonist (OPC-31260) on endolymphatic hydrops

In the present study, two experiments were performed to investigate the influence of OPC-31260 on experimentally induced endolymphatic hydrops in guinea pigs and the regulation of aquaporin-2 (AQP2) mRNA expression in the rat inner ear. In morphological studies, the increases in the ratios of the length of Reissner's membrane (IR-L) and the cross-sectional area of the scala media (IR-S) were quantitatively assessed among normal guinea pigs (normal ears) and three groups with hydropic ears: hydropic ears with no infusion (non-infusion hydropic ears), hydropic ears with an infusion of physiological saline into the scala tympani (saline-infused hydropic ears) and hydropic ears with infusion of 0.3% OPC-31260 into the scala tympani (OPC-infused hydropic ears). IR-Ls in the experimental groups were markedly larger than in the normal ear group, but there was no significant difference among the groups of non-infusion hydropic ears, saline-infused hydropic ears and OPC-infused hydropic ears. The IR-Ss of non-infusion hydropic ears and saline-infused hydropic ears (48.8-49.3%) were statistically different from that of normal ears (6.5%) (Dunnet multiple comparison test, P<0.01). However, IR-S of the OPC-infused hydropic ears (-14.8%) was significantly smaller than those of non-infusion hydropic ears and saline-infused hydropic ears (one-way ANOVA, P<0.01). In the quantitative polymerase chain reaction study, a comparison of the ratio of AQP2 and beta-actin mRNA (MAQP2/Mbeta-actin) was made between water-injected and OPC-31260-injected rats. An intravenous injection of OPC-31260 resulted in a significant decrease in MAQP2/Mbeta-actin both in the cochlea and in the endolymphatic sac (t-test, P<0.001). These results indicate that water homeostasis in the inner ear is regulated via the vasopressin-AQP2 system, and that the vasopressin type-2 antagonist OPC-31260 is a promising drug in the treatment of Meniere's disease.     

Personal stigma and coping strategies in families of patients with schizophrenia: Comparison between Japan and Korea

Introduction: It has been extensively documented that caregivers of persons who have serious and persistent mental disorders must successfully cope with many challenging problems in order to provide good care. However, little is known about the relationship between family stigma and strategies for coping with patients with schizophrenia. Therefore, the present study compared the personal stigma and coping strategies of families of patients with schizophrenia by examining the socio‐cultural factors that affect the care experience of families in Northeast Asian countries. Methods: Two self‐rating scales were used to compare personal stigma and coping strategies regarding family members of patients with schizophrenia in 47 Japanese and 92 Korean families. Respondents reported their personal attitudes (personal stigma) with respect to a case vignette that described a person with chronic schizophrenia. Results: Analysis revealed the following: 1) although no differences in coping strategies were observed between the countries, the personal stigma of families was significantly higher in Korea than in Japan; 2) coping strategies, such as positive communication, coercion, and avoidance, were significantly associated with personal stigma in Korean families; however, in Japanese families, resignation was significantly associated with personal stigma. Discussion: The present findings suggest that personal family stigma was higher in Korea than Japan, and the features associated with coping strategies differ between countries. It is important to determine the features of personal stigma that are associated with schizophrenia. Furthermore, education and support programs for families with schizophrenia based on trans‐cultural considerations must be emphasized in both countries.     

In vitro drug-drug interactions with perospirone and concomitantly administered drugs in human liver microsomes.

In vitro metabolism studies were conducted to assess drug-drug interactions between perospirone, an antipsychotic agent, and concomitantly administered drugs--biperiden, flunitrazepam, haloperidol, and diazepam--using human liver microsomes. The metabolism of perospirone in the presence of 100 microg/ml drugs was decreased to 45-73% of that in their absence, whereas no effects were observed with any of the drugs at 1 microg/ml or lower. The effects of perospirone on the metabolism of concomitantly administered drugs were also assessed, and no inhibitory effect was observed. Thus, the metabolism of perospirone and concomitantly administered drugs did not demonstrate any marked mutual inhibition in the human liver microsomes. On the other hand, the perospirone metabolism was markedly reduced by ketoconazole indicating a major role for CYP 3A4. Based on the inhibition constant (Ki) for perospirone metabolism and the plasma unbound concentration of ketoconazole, in vivo perospirone clearance was estimated to be reduced to 64-90% of the control level. Thus careful attention should be paid to the possibility of increase in unchanged perospirone concentration when perospirone is co-administered with drugs that are known as CYP3A4 inhibitors, including macrolide antibiotics and other imidazole antifungals.     

Antimicrobial resistance of Staphylococcus aureus isolated from impetigo patients between 1994 and 2000

BACKGROUND: The incidence of strains of Staphylococcus aureus resistant to the antimicrobial agents used in treating impetigo has been increasing. AIM: To determine the antimicrobial susceptibility of S. aureus in impetigo. METHODS: We measured the antimicrobial susceptibility of Staphylococcus aureus isolated from impetigo patients between 1994 and 2000. RESULTS: The MIC50 of gentamicin was always higher than that of other antimicrobial agents until 1999. In isolates obtained since 1996, the MIC90 of gentamicin was over 12.5 micro g/mL, which is markedly higher than that found for other skin infections (folliculitis, furuncles, paronychia, phlegmone, secondary infection of eczema, dermatitis, ulcer and decubitus). There were no strains of S. aureus resistant to vancomycin and fusidic acid. After 2000, we could find only one strain resistant to minocycline and ofloxacin. CONCLUSION: Clindamycin has shown excellent activity against most S. aureus isolates between 1994 and 2000. The incidence of methicillin-resistant S. aureus was always below 20%.     

Effects of perinatal exposure to flutamide on sex hormones and androgen-dependent organs in F1 male rats

Flutamide, which has antiandrogenic properties, was administered to pregnant rats, and effects on male offspring were examined. Crj: CD (SD) IGS (SPF) females were administered flutamide (0.15, 0.6, 2.5, 10.0, 100 mg/kg, p.o.) from gestation Day 14 to post parturition Day 3. The number of pups, body weights, clinical features, anogenital distance (AGD), nipple retention, testicular descent, and urogenital malformation in F1 males were examined. Hormone measurement, necropsy and histopathological examination were carried out at post-neonatal Day 4 (PND 4) and PND 60. Sperm analysis was also carried out at PND 60. Decrease in body weight was seen in the 100 mg/kg group and the AGD was decreased at 2.5 mg/kg and above. Retention of nipples, hypospadia, vaginal pouches, penis malformation, unilateral ectopic testis, and decrease of organ weights (prostate, seminal vesicles, levator ani muscle plus bulbocavernosus muscle, testis) were observed at 10 mg/kg and above. Testicular testosterone (T) was increased significantly with 100 mg/kg at PND 4 and tendencies for increase were observed in serum T, LH and FSH at 10 mg/kg and more at the same time point. In contrast, elevated levels of LH and FSH were seen with 100 mg/kg at PND 60. Histopathological examination revealed defects or hypoplastic changes of genital organs (> or = 10 mg/kg), squamous metaplasia (10 mg/kg) or mucification (100 mg/kg) of the urethral diverticulum epithelium and inflammation of genital organs (100 mg/kg). Though only undescended testes lacked spermatogenesis at 10 mg/kg, atrophic change of seminiferous tubules and azoospermia were observed in the 100 mg/kg group, despite testicular descent. Perinatal administration of flutamide affected F1 male rats at 2.5 mg/kg and above. In addition to urogenital malformation, 100 mg/kg flutamide caused high LH and FSH levels at PND 60. This study indicates that the most sensitive parameter is AGD, whereby reduction was observed at 2.5 mg/kg. A clear no-effect level (NOEL: 0.6 mg/kg) was obtained in this perinatal study of an antiandrogenic chemical.     

Effect of an orally active Na+/H+ exchange inhibitor, SMP-300, on experimental angina and myocardial infarction models in rats.

The effects of SMP-300, an orally active, potent, and selective Na+/H+ exchange inhibitor, were evaluated and compared with those of nifedipine, propranolol, and nicorandil on three experimental angina models and on myocardial infarction in rats. SMP-300 (0.1-1 mg/kg, p.o.) reduced isoproterenol-induced ST segment depression in a dose-dependent manner. Its maximal effect was comparable to that reported for propranolol and greater than that of nifedipine. SMP-300 (0.3-1 mg/kg) reduced vasopressin-induced ST segment depression in a dose-dependent manner, and its maximal effect was comparable to those of nifedipine and nicorandil. SMP-300 (0.3-1 mg/kg, p.o.) and propranolol (100 mg/kg, p.o.) inhibited coronary artery occlusion-induced T-wave elevation, but nifedipine (3 mg/kg, p.o.) did not. SMP-300 (1 mg/kg, p.o.) reduced myocardial infarct size after 40 min of coronary artery occlusion followed by 24 h of reperfusion, but nifedipine (3 mg/kg, p.o.) or propranolol (100 mg/kg, p.o.) did not. This study provides support for the future use of a Na+/H+ exchange inhibitor as an anti-anginal drug with a novel mode of action.