Skipping breakfast has been considered a representative unhealthy behavior, but there is little information about the combined effects of breakfast skipping and other unhealthy health habits, especially smoking. First this cross-sectional study investigated unhealthy behaviors among breakfast skippers, and then examined the impact of the combined association of skipping breakfast and smoking on health. A total of 1,200 adults living in one Japanese community were sent questionnaires to elicit data on age, gender, breakfast-eating frequency, and other lifestyle habits. A total 603 of people returned their questionnaires (response rate: 50.3%), and 493 (230 men and 263 women) questionnaires were considered appropriate for analysis. Smoking rate in men (mean age, 53.7 years) and women (mean age, 50.4 years) was 41.3%, and 9.5%, respectively. Skipping breakfast was more prevalent in people under age 50 years (p < 0.001), and was related to other unhealthy behaviors. Binary logistic regression identified current smoking as the most significant factor related to breakfast skipping (3.10, 95%CI 1.50-6.39). Other factors included, age younger than 50 years (3.04, 95%CI 1.31-7.06) and poor sleeping quality (2.06, 95%CI 1.00-4.25). After examining the combined impact of skipping breakfast and smoking, the highest odds ratio for a diagnosis of diabetes mellitus was found among those who smoked and skipped breakfast (4.68, 95% CI: 1.46-15.05). Moreover, skipping breakfast among non-smokers showed a high association with perceived stress (2.83, 95% CI: 1.05-7.61). In conclusion, the combined unhealthy behaviors of skipping breakfast and smoking are associated with the prevalence of diabetes mellitus.
Ethnic differences in the pattern and trend of growth and weight have been described in studies of migrant populations. Our objective was to compare anthropometric parameters and overweight prevalence in third and fourth generation Japanese descendant preschoolers within the Peruvian preschool population. A total of 337 measurements of height and weight from 284 children, three to five years of age, were taken over three years in one Japanese-Peruvian preschool center in Lima, Peru. The data of each parameter were classified into three ethnic groups according to their parents' surnames: Japanese descendant children (n = 104), with both parents with Japanese surnames; Japanese-Peruvian descendant (n = 93), one parent with a Japanese surname and one with a non-Japanese surname; and Peruvian descendant (n = 140), both parents with non-Japanese surnames. We used the National Center for Health Statistics (NCHS) 2000 growth charts as reference values to obtain centiles, Z scores, and body mass index (BMI). In boys, the three groups differed significantly in height, weight, BMI, Z scores, and overweight prevalence. Peruvian descendant boys were taller and heavier than Japanese-Peruvian and Japanese descendants. Moreover, Japanese-Peruvian descendant boys were taller and heavier than Japanese descendant boys. In girls, there were no significant differences in height and weight and in overweight prevalence among the three ethnic groups. Japanese descendants in Peru have height, weight and BMI values similar to those of Japanese children in Japan but lesser than Peruvian children. These findings may be related to differences in ethnic background.
Tulobuterol, a sympathomimetic drug used as a transdermal patch, increases normal diaphragm muscle strength. Because diaphragm muscle weakness (i.e. decrease of contraction) is a feature of bronchial asthma and sepsis, we examined the in vitro and in vivo effects of tulobuterol on the contractility of diaphragm muscles prepared from mice treated with endotoxin. We measured contractile parameters of force-frequency curves and twitch kinetics using untreated or treated diaphragm muscles at 0 (E0) and 4 (E4) hours after E. coli endotoxin (20 mg/kg) administration. The force-frequency curve of E4 diaphragm muscle was decreased from that of E0 diaphragm muscle (p < 0.001). E4 diaphragm muscle was incubated in an organ buffer containing 10-7 or 10-5 M concentrations of tulobuterol for 1 h (in vitro). The force-frequency curves of both 10-7 (p < 0.01) or 10-5 M (p < 0.001) tulobuterol concentrations shifted significantly upward from those of no tulobuterol, indicating that tulobuterol can recover the diaphragm muscle contractility that was decreased by endotoxin. In the in vivo treatment, E0 and E4 diaphragm muscles were analyzed at 0, 12, and 24 h after transdermal tulobuterol treatment. The force-frequency curves of E0 and E4 diaphragm muscles at three time points were not significantly changed each other, indicating that tulobuterol patch restores the muscle contractility. Thus, diaphragm muscle contractility was maintained during 4 h of endotoxin administration with tulobuterol patch for over 24 h. We suggest that this treatment of bronchial asthma may protect against endotoxin contained in inhaled house dust.
Hepatitis E virus (HEV) is one of the causative agents of acute or fulminant hepatitis. Viral factors may play a role in the pathogenesis of fulminant hepatitis E. We aimed to investigate the nucleotide substitutions of the HEV genome affecting the severity of hepatitis E. The comparison of 28 reported full-length nucleotide sequences of genotype 4 HEV showed that the substitution of C at nucleotide 5907 (C5907) was most closely associated with fulminant hepatitis (fulminant hepatitis, 100%; acute hepatitis, 39.1%; p = 0.0204). Analyzing the full-length sequences of 28 genotype-4 and 11 genotype-3 HEV retrievable from DNA databases and 35 partial sequences recovered from patients with acute or fulminant hepatitis, we show that the presence of both U3148 and C5907 is associated with fulminant hepatitis in patients with HEV of genotype 4 (p = 0.0042) and genotype 3 or 4 (p = 0.0009), and that the prothrombin activity is significantly lower in patients infected with HEV carrying U3148 and C5907 than in those without the substitutions (p = 0.0069). U3148 and C5907 are silent substitutions that do not change amino acid. However, since U3148 is located at the RNA helicase domain and C5907 is located within the capsid gene, the secondary structure of the HEV RNA genome carrying U3148 and C5907 may be favorable for translation of the viral proteins. C5907 was associated with high HEV load (≥ 105 copies/ml) at initial examination (p = 0.0427). We propose that U3148 and C5907 are associated with the severity of hepatitis E.
In human immunodeficiency virus (HIV) infection, not only HIV itself but also systemic immune activation plays a role in the disease progression to acquired immune deficiency syndrome (AIDS). The systemic immune activation may be present even during highly active antiretroviral therapy (HAART). An increased expression of osteopontin, a proinflammatory cytokine, during HAART was reported in lymph nodes of HIV infected individuals. Osteopontin is also known to be involved in the pathogenesis of various HAART-induced diseases. Here, we measured osteopontin and other inflammatory markers such as neopterin and galectin-9 using serially collected plasma from patients with HIV/AIDS to find novel markers for immune activation. Four AIDS patients complicated with various opportunistic infections and one acute HIV patient were studied. Osteopontin levels (normal levels: < 820 ng/ml) were elevated in all the patients (1,178-2,450 ng/ml). Likewise, galectin-9 levels (normal levels: < 46 pg/ml) were elevated in all patients (> 130 pg/ml), with the exceptionally high level in the acute HIV patient (4,196 pg/ml). Neopterin levels (normal ranges: 2-8 pmol/L) were elevated in four patients (21-99 pmol/L). After HAART, the levels of galectin-9 and neopterin apparently decreased, whereas the levels of osteopontin did not decrease. Thus, the high levels of osteopontin were sustained despite the clinical improvement. Fisher exact probability test showed that the mode of the changes was different between osteopontin and galectin-9, and between osteopontin and neopteirn (p = 0.024). We therefore propose that the plasma osteopontin is a useful marker of immune activation during HAART and HAART-induced side effects.
Homocysteine, a sulfur-containing amino acid, is an intermediate during the conversion of methionine to cysteine. Homocysteine can cause vascular injury and atherosclerotic plaque instability. In addition, homocysteine may be directly correlated with hyperlipidemia and lipoprotein(a) and inversely with high-density lipoprotein cholesterol. However, the results regarding the association of homocysteine level with subtypes of stroke and traditional risk factors for stroke have been inconsistent, perhaps due to ethnic differences. The aim of this study was to evaluate the role of serum homocysteine levels in Turkish patients diagnosed with atherosclerotic stroke and those with cardioembolic stroke. We measured homocysteine levels, traditional risk factors for stroke (hypertension, diabetes mellitus, and smoking) and lipoprotein(a) levels in 103 patients with large-vessel atherosclerotic stroke, 37 patients with cardioembolic stroke, and 37 controls with normal cranial magnetic resonance imaging. Only hypertension was found to be a risk factor in all patient groups (p = 0.001). Hyperhomocysteinemia (homocysteine level ≥ 15.90 μmol/L) was more common in patients with large-vessel atherosclerotic stroke and cardioembolic stroke (p = 0.0435 and p = 0.007, respectively); nevertheless, it was found to be a risk factor only in patients with cardioembolic stroke (p = 0.023; odds ratio (OR): 5.745). Furthermore, in the patients with large-vessel atherosclerotic stroke, hyperhomocysteinemia was positively correlated with the lipoprotein(a) level (r = 0.227, p = 0.035). In conclusion, hyperhomocysteinemia is common in patients with large-vessel atherosclerotic stroke and cardioembolic stroke. More importantly, hyperhomocysteinemia is an independent risk factor only for cardioembolic stroke in the Turkish population.
Constraint-induced movement therapy (CIMT) has been extensively used for stroke rehabilitation. CIMT encourages use of the impaired limb along with restraint of the ipsilesional limb in daily life, and may promote behavioral recovery and induce structural changes in brain after stroke. The aim of this study was to investigate whether CIMT enhances neurogenesis in rat brain after stroke that was generated by middle cerebral artery occlusion. Adult rats were divided into sham group, ischemia group and ischemia treated with CIMT group. Rats of CIMT group were treated with a plaster cast to restrain the healthy forelimb for 14 days beginning 1 week after ischemia. The proliferation of neuronal cells labeled with bromodeoxyuridine (BrdU) and behavioral recovery were analyzed at day 29 after ischemia. We also measured the tissue level of stromal cell-derived factor 1 (SDF-1) by ELISA. SDF-1 might be involved in the regulation of neurogenesis following stroke. In the subventricular zone of the animals treated with CIMT, there was a significant increase in the number of BrdU-positive cells (135 ± 18, P < 0.05), compared with ischemia group (87 ± 12) or sham group (18 ± 3.6). Likewise, in the dentate gyrus, animals treated with CIMT showed a significant increase in BrdU-positive cells (296 ± 26, P < 0.05) compared with ischemia group (225 ± 18) or sham group (162 ± 11). CIMT treatment after stroke significantly improved behavioral performances and increased the SDF-1 protein levels in the cortex and dentate gyrus. In conclusion, CIMT treatment enhances neurogenesis and functional recovery after stroke.
Lamin A and C proteins, encoded by the lamin A/C gene (LMNA), are inner nuclear membrane proteins predominantly expressed in terminally differentiated cells. Mutations in LMNA can cause various forms of cardiomyopathy with arrhythmia in an autosomal dominant manner. We collected and evaluated the clinical characteristics of unclassified familial cardiomyopathy with advanced AV block and sporadic cases with advanced AV block. Mutation in LMNA was directly screened using the cycle sequencing method in 5 probands of the familial cardiomyopathy and 60 sporadic cases with advanced AV block. In four of the five familial cases (80%), we identified four distinct mutations: two protein-truncation mutations, R225X and 815_818delinsCCAGAC, and two missense mutations, Y259H and R166P. No sporadic cases carried LMNA mutation. Left ventricular end-diastolic diameter (LVEDD) was slightly enlarged in LMNA mutant carriers (123.5 ± 9.5%) as well as in non-carriers (125.1 ± 13.3%), while left ventricular fractional shortening (LVFS) was preserved in LMNA mutant carriers (32.3 ± 4.8%) and non-carriers (37.6 ± 6.8%). In LMNA mutation carriers, the average age at onset of advanced AV block is significantly lower than that in non-carriers (43.7 ± 9.5 vs. 65.3 ± 13 yr., p < 0.01). Ventricular tachycardia, sudden death, and poor prognosis were observed in LMNA mutation carriers. LMNA mutation could cause familial cardiomyopathy with insignificant LV remodeling, early-age onset of advanced AV block, and lethal ventricular arrhythmia. Screening of LMNA mutation might be beneficial for risk stratification and clinical management of this type of unclassified familial cardiomyopathy.
The Eustachian tube is normally closed, but it opens upon swallowing for only less than one second to equalize the middle ear pressure with the atmospheric pressure, and immediately closes again. Patients with patulous Eustachian tube (PET) suffer from annoying symptoms, such as aural fullness (sensation of fullness in the ear), autophonia (abnormally loud audition of own voice), audition of breathing sound, and fluctuating sensation of the tympanic membrane upon respiration. The diagnosis of PET is not difficult when patients complain of such typical symptoms. However, there is an unexpected pitfall, in which the symptoms of PET are masked by the presence of conductive hearing loss and obvious middle ear pathology. Here, we propose that this condition be termed ‘masked patulous Eustachian tube’ to promote correct diagnosis prior to planning the middle ear surgery. Four representative patients with ‘masked patulous Eustachian tube’ are presented: two exhibited symptoms after repair of chronic perforation of the tympanic membrane, one after stapes surgery for otosclerosis, and one after cholesteatoma surgery. In these patients, the symptoms of PET became evident only after surgery due to the improvement of hearing. The degree of hearing improvement varied among the patients from 15 to 40 dB in average hearing level. It is therefore important to examine the presence of ‘masked patulous Eustachian tube’, in addition to a middle ear disease for which surgery is planned. The surgeon should inform the patient of the possibility of ‘masked patulous Eustachian tube’ to avoid the postoperative disappointment.
Recent studies have shown the remarkable gender differences in the susceptibility or expression of many diseases. The mechanism underlying the gender differences is unclear. In the present study, we evaluated the effects of gender differences and different ischemia time on the renal ischemia-reperfusion injury (IRI). The IRI was induced in the bilateral kidneys of 156 male and 30 female BALB/c mice. Renal function, serum creatinine and blood urea nitrogen, and pathology of the kidneys were examined at 24 hr after IRI. Renal IRI was generated successfully in 182 of 186 mice with a 97.85% success rate. The levels of serum creatinine and blood urea nitrogen were significantly increased in male mice subjected to 30 min, 35 min, or 45 min of renal ischemia and in female mice subjected to 75 min of renal ischemia, compared to the control group at 24 hr after operation. In males following 35 min or 45 min of ischemia and in females following 75 min of ischemia, typical acute tubular necrosis was found in the areas of corticomedullary junction and the histopathologic scores, which represent the degree of renal tissue injuries, were significantly increased. In view of our data, the kidneys of male are much more susceptible to IRI than those of female. The optimal ischemia time of kidney is 35 - 45 min in males and 75 min in females for generating a stable model of IRI in mice. Investigation of the gender differences might provide a new area for mechanistic study of renal IRI.
Alcohol consumption is associated with a decreased risk of type II diabetes and cardiovascular diseases. However, there is a great deal of controversy concerning the relationship between alcohol consumption and insulin resistance. This association may be further confounded by an increase in body weight levels. The aim of this study was to determine whether alcohol consumption promotes insulin resistance according to body weight levels in community-dwelling men. Study participants without a clinical history of stroke, transient ischemic attack, myocardial infarction, angina or diabetes were randomly recruited from a single community at the time of their annual health examination (678 men aged 59 ± 14 years). They were classified into never drinkers, light drinkers [< 1 unit (22.9 g ethanol)/day], moderate drinkers (1-1.9 unit/day), and heavy drinkers (≥ 2 unit/day), and further divided into underweight [body mass index (BMI) < 23 kg/m2] or overweight (BMI ≥ 23.0 kg/m2). Insulin resistance was estimated on the basis of the homeostasis model assessment of insulin resistance (HOMA-IR), and HOMA-IR and potential confounders were compared between the groups. The confounders included age, BMI, smoking status, serum gamma glutamyltransferase, and high molecular-weight adiponectin. In the overall, HOMA-IR is significantly correlated with age, BMI, serum gamma glutamyltransferase, and high molecular-weight adiponectin. After adjustment for potential confounders, mean log HOMA-IR is significantly lower in the heavy drinkers irrespective of BMI categories. In conclusion, alcohol consumption is associated with decreased insulin resistance independent of BMI in Japanese community-dwelling men.