Biomedical subjects

M Mishima

Publications and source records attributed to M Mishima.

At least 37 records · Page 2Linked to original sources

PubMed2001

Quantification of tumor cell injury in vitro and in vivo using expression of green fluorescent protein under the control of the GADD153 promoter.

The GADD153 gene is strongly transcriptionally activated by many types of cellular injury and the magnitude of the change in GADD153 expression is proportional to the extent of damage. We developed a novel reporter system in which a chimeric gene containing the GADD153 promoter linked to the coding region of an enhanced green fluorescent protein (EGFP) gene was stably integrated into the genome of a clone of UMSCC10b head and neck carcinoma cells. Activation of the exogenous GADD153 promoter was quantified using flow cytometric measurement of EGFP expression following drug exposure. The exogenous GADD153 promoter in this clone was activated by N-methl-N'-nitro-N-nitrosoguanidine (MNNG) in a concentration-dependent manner with kinetics that closely paralleled perturbation of cell cycle phase distribution. EGFP expression was strongly activated by a variety of genotoxic agents including DNA cross-linking and methylating agents, oxygen free radicals, DNA intercalator, UV and gamma-radiation and hypoxia. When grown as a xenograft in nude mice, the stably transfected clone also demonstrated dose-dependent EGFP expression when measured 4 days after cisplatin treatment. The reporter system accurately categorized the relative potency of adducts produced by 6 related platinum-containing drugs. In conclusion, this reporter system can facilitate in vitro and in vivo screening for agents capable of producing cytotoxicity via a wide variety of different mechanisms, and can be utilized to investigate the relative potency of structurally related DNA adducts.

Animals↗

PubMed2001

P53 modulates the effect of loss of DNA mismatch repair on the sensitivity of human colon cancer cells to the cytotoxic and mutagenic effects of cisplatin.

This study examined how the DNA mismatch repair (MMR) system and p53 interact to maintain genomic integrity in the presence of the mutagenic stress induced by cisplatin (DDP). Sensitivity to the cytotoxic and mutagenic effect of DDP was assessed using a panel of sublines of the MMR-deficient HCT116 colon carcinoma cells in which MMR function had been restored by transfer of a copy of MLH1 on chromosome 3 or in which p53 function had been disabled by expression of HPV-16 E6. Loss of p53 function by expression of E6 in MMR-proficient HCT116+ ch3 cells conferred only 1.1-2.0-fold resistance to a panel of commonly used chemotherapeutic agents, whereas disruption of p53 in MMR-deficient HCT116 cells resulted in substantial levels of resistance to some agents (paclitaxel, 1.9-fold; gemcitabine, 2.7-fold; 6-thioguanine, 3.3-fold; and etoposide, 4.4-fold) but sensitization to other agents (topotecan, 2.5-fold; and DDP, 3.3-fold). Loss of MMR or p53 alone had only a minor effect on sensitivity to the mutagenic effect of DDP as measured by the appearance of variants resistant to 6-thioguanine, etoposide, topotecan, gemcitabine, and paclitaxel in the population 10 days later (1.0-2.4-fold), whereas loss of both p53 and MMR had a more profound effect (1.7-6.5-fold). Loss of both p53 and MMR increased the basal frequency insertion/deletion mutations detected by a shuttle vector-based assay to a greater extent than loss of either alone. In association with DDP-induced injury, loss of p53 or MMR alone resulted in 1.2- and 1.7-fold more mutations, whereas loss of both resulted in a 5.1-fold increase in mutant frequency. Examination of the impact of loss of p53 and/or MMR on the DDP-induced cell cycle checkpoint activation, p53 induction, ability of the cell to tolerate adducts in its DNA, and the rate of disappearance of platinum from genomic DNA indicated the effects of the loss of p53 and/or MMR on all of these parameters, suggesting a multifactorial etiology for the changes in sensitivity to the cytotoxic and mutagenic effects of DDP. These results indicate that p53 and MMR can cooperate to control sensitivity to the cytotoxic effect of DDP and to limit its mutagenic potential in the colon cancer cells.

Antineoplastic Agents↗

PubMed2001

Interferon-gamma-induced apoptosis in host cells infected with Neospora caninum.

Interferon-gamma (IFN-gamma) has a crucial role for host defence against parasite infection. It is not clear, however, how IFN-gamma affects the parasite-infected host cells. The effect of IFN-gamma on Neospora caninum-infected cells was investigated in murine fibroblasts and canine kidney cells in vitro. In the presence of IFN-gamma, the viability of the infected host cell was decreased and apoptotic cell death occurred, as analysed by DNA stainings with propidium iodide and a terminal deoxy-nucleotidyltransferase-mediated dUTP-biotin nick end labelling (TUNEL) and DNA fragmentation. The percentage of apoptotic cells depended on the dose of IFN-gamma. Flow cytometric analysis indicated a significant increase of FasL expression on the IFN-gamma treated cells following N. caninum infection. Moreover, IFN-gamma treatment down-regulated Bcl-2 expression in the cells cultured with N. caninum while parasite infection up-regulated Bcl-2 expression. The present study suggests that the IFN-gamma induced increases of FasL expression and down-regulated Bcl-2 expression in N. caninum-infected cells are associated with apoptosis in vitro.

3T3 Cells↗

PubMed2001

Culturally verified Mycoplasma pneumoniae pneumonia in Japan: a long-term observation from 1979-99.

We describe the prevalence of community-acquired M. pneumoniae pneumonia diagnosed by culture methods in a single institute in Japan from January 1979 to December 1999. Cultures were performed in 2971 pneumonia cases and yielded M. Pneumoniae in 508 cases. The epidemic peaks recurred regularly at 4-year intervals (1980, 84, 88 and 91-2). Although a large epidemic has not occurred since 1992, traces of epidemic periodicity have still persisted from 1992 to 1999 at 3-year intervals.

Adolescent↗

PubMed2001

Coronin forms a stable dimer through its C-terminal coiled coil region: an implicated role in its localization to cell periphery.

BACKGROUND: Coronin is an actin-binding protein, which contains WD (Trp-Asp) repeats and a coiled-coil motif, and plays a role in regulating organization of the actin cytoskeletal network. Coronin localizes to the cell periphery, is involved in lamellipodium extension, and has an implicated role in cytokinesis, cell motility and phagocytosis. RESULTS: Our experiments with two different tagged forms of Xenopus coronin (Xcoronin) have shown that Xcoronin forms an oligomer. This oligomer complex is stable, resistant to 2.4 M NaCl, 0.6 M KI or 2 M urea. Physiochemical analysis of endogenous Xcoronin and the protein expressed in COS7 cells or in bacteria has revealed that the oligomer complex is an Xcoronin dimer. A C-terminal coiled-coil motif of Xcoronin is necessary and sufficient for the dimerization. Mutations in the coiled-coil motif generated dimerization deficient mutants of Xcoronin. Moreover, these mutant forms of Xcoronin failed to localize to the cell periphery, suggesting that dimerization is important for the proper subcellular localization of Xcoronin. CONCLUSION: Xcoronin forms a stable dimer via its C-terminal coiled-coil region. We propose that coronin dimerization is necessary for its proper subcellular localization and function.

Actins↗

PubMed2001

Confirming the theoretical structure of the Japanese version of the McGill Pain Questionnaire in chronic pain.

OBJECTIVE: Based upon a tripartite theoretical model of pain, the Pain Rating Index of the McGill Pain Questionnaire continues to be one of the most frequently used instruments to measure clinical pain. However, differences in languages and cultural backgrounds have hindered its wide use and standardization in Japan. Although a number of exploratory factor analytic studies have failed to consistently support the theoretical structure of the instrument, a few previous confirmatory factor analytic studies did statistically support the a priori model. The purpose of this study was to test the theoretical structure of a Japanese version of the McGill Pain Questionnaire, which followed a format similar to the original questionnaire, through a confirmatory factor analysis. DESIGN: This study used confirmatory factor analysis on prospectively collected data from consecutive outpatients with chronic pain at a university hospital to test the hypothesis regarding the theoretical structure of the Japanese McGill Pain Questionnaire. RESULTS AND CONCLUSION: The first 16 Pain Rating Index subclass scores were subjected to confirmatory factor analysis procedures that yielded a well-fitting final model that explained 91% of the covariance in the observed data. The results approximately supported the hypothesis that the sensory, affective, and evaluative subscales of the Pain Rating Index are representative of the multidimensionality of the pain experience with minimal overlap but could not disregard relatively high intercorrelations among those subscales similar to the original McGill Pain Questionnaire. It is suggested that the theoretical structure of the McGill Pain Questionnaire is approximately kept in the Japanese McGill Pain Questionnaire used in this study. Therefore, the translation-based Japanese McGill Pain Questionnaire used in this study adequately permits comparison of studies from English-speaking and non-English-speaking populations, thus facilitating the first step toward international research exchange and communications.

Journal Article↗

PubMed2001

The McGill Pain Questionnaire, Japanese version, reconsidered: confirming the theoretical structure.

BACKGROUND: Based on a tripartite theoretical model of pain, the Pain Rating Index (PRI) of the McGill Pain Questionnaire (MPQ) continues to be one of the most frequently used instruments to measure clinical pain. However, language and cultural barriers have hindered its wide use and standardization in Japan. Although a number of exploratory factor analysis studies have failed to support consistently the theoretical structure of the MPQ, a few previous confirmatory factor analysis studies did statistically support the a priori model. OBJECTIVE: To test, through confirmatory factor analysis (CFA), the theoretical structure of a Japanese version of the MPQ (JMPQ), which followed a format similar to that of the original MPQ. DESIGN: This study used CFA on prospectively collected data from 199 consecutive outpatients with chronic pain at a university hospital to test the theoretical structure of the JMPQ. RESULTS AND CONCLUSIONS: CFA was completed on the first 16 PRI subclass scores; this process yielded a well fitting final model that explained 92% of the covariance in the observed data. The results supported the hypothesis that the sensory, affective and evaluative subscales of the PRI are representative of the multidimensionality of the pain experience, with minimal overlap. It is suggested that the theoretical structure of the MPQ is maintained in the JMPQ used in this study. Therefore, this study is the first step toward standardization of the JMPQ, serving as a cultural bridge in the field of pain medicine between Japan and English-speaking nations such as Canada.

Adult↗

PubMed2001

Circadian variation of the onset of acute myocardial infarction in the Osaka area, 1998-1999: characterization of morning and nighttime peaks.

The onset of acute myocardial infarction (AMI) shows characteristic circadian variations; that is, a definite morning peak related to biologic rhythms and a vague nighttime peak related to socioeconomic factors. The recent economic recession in Japan may change the circadian variation, especially the nighttime peak. This study evaluated the recent circadian variation of AMI in Osaka and specified the patient subgroups showing either a morning or nighttime peak predominantly. Of 1,609 consecutive patients with AMI registered from April 1998 to January 2000, 1,252 whose onset of AMI was definitely identified were studied. The day was divided into six 4-h periods with a morning peak between 08.01 h and 12.00h, and nighttime peak between 20.01 h and 24.00h. When subgroup analysis was performed, female patients aged 65 years or more showed a morning peak alone and male patients aged less than 65 years with an occupation and the habits of cigarette smoking and alcohol intake showed a nighttime peak alone. Thus, in Osaka nighttime socioeconomic factors may currently be more potent triggers of AMI than the morning surges in younger male workers who smoke and drink.

Adult↗

PubMed2001

Modified protection against Toxoplasma gondii lethal infection and brain cyst formation by vaccination with SAG2 and SRS1.

Numerous studies have supported the importance of immunity to SAG1, the most predominant antigen of Toxoplasma tachyzoite, in protection against Toxoplasma gondii infection. Nevertheless, vaccination with SAGI provides insufficient protection when compared with that of Toxoplasma lysate (TL). In order to screen the Toxoplasma antigens for immunogenic potential shown by modified protection or induction of specific immune response after infection, recombinant antigens were prepared in Eschericha coli using DNA fragments corresponding to SAG1, SAG2, SAG3, SRS1 and P54 of T. gondii RH strain maintained in our laboratory. Each of the recombinant antigen products or a mixture of the five antigens (Mix) was used to vaccinate mice. Mice then received a lethal dose of T. gondii. Up to 25% of the mice vaccinated with SAG2, SRS1, P54 and Mix survived, whereas there were no survivors in gene 10- (negative control), SAG1- and SAG3- vaccinated groups. In all the survivors, brain cysts were not observed. Conversely, vaccination with TL almost completely protected mice in the acute phase but permitted brain cyst formation and resulted in gradual decrease of survivors to 33% during 4 months of experiments. Western blot analysis on convalescent sera showed an extensive IgG induction to a 30 kDa antigen in TL-vaccinated mice, a 22 kDa in SAG2-vaccinated mice and a 55 kDa in P54-vaccinated mice. The protection modified by boost in specific antibody is suggestive of the immunogenic potential of SAG2, SRS1 and possibly P54 against T. gondii infection.

Animals↗

PubMed2000

Effects of nasal continuous positive airway pressure on soluble cell adhesion molecules in patients with obstructive sleep apnea syndrome.

PURPOSE: Obstructive sleep apnea syndrome is common in middle-aged men and may be associated with an increased risk of cardiovascular disease. We investigated the effect of nasal continuous positive airway pressure (CPAP) treatment on levels of soluble cell adhesion molecules-which have been shown to be associated with the development of atherosclerosis-in these patients. SUBJECTS AND METHODS: We studied 23 patients with obstructive sleep apnea syndrome diagnosed by polysomnography who were treated with nasal CPAP. Serum soluble intercellular adhesion molecule-1, E-selectin, and vascular cell adhesion molecule-1 levels were measured before nasal CPAP was started, and after 3 or 4 days (n = 19), 1 month (n = 23), or 6 months (n = 11) of treatment. RESULTS: After 3 to 4 days of nasal CPAP therapy, the mean (+/- SD) soluble E-selectin level had decreased from 89 +/- 44 ng/mL to 69 +/- 28 ng/mL (P = 0.002). After 1 month, the soluble intercellular adhesion molecule-1 level had decreased from 311 +/- 116 ng/mL to 249 +/- 74 ng/mL (P = 0.02). After 6 months, soluble vascular cell adhesion molecule-1 levels had not changed significantly, while the mean soluble intercellular adhesion molecule-1 level (212 +/- 59 ng/mL) had decreased further (P = 0.02). Before treatment, soluble intercellular adhesion molecule-1 levels and the apnea and hypopnea index were correlated (r = 0.43, P = 0.04). CONCLUSIONS: Obstructive sleep apnea and hypopnea have a significant adverse effect on serum soluble cell adhesion molecule-1 levels that may be reduced by nasal CPAP treatment.

Adult↗

PubMed2000

Effect of pre-reperfusion residual flow on recovery from myocardial stunning: a myocardial contrast echocardiography study.

BACKGROUND: Myocardial contrast echocardiography (MCE) may be used to assess coronary microvasculature in patients with myocardial infarction. Myocardial contrast echocardiography-no reflow suggests poor functional outcome; however, MCE with reflow does not necessarily indicate good myocardial salvage or sufficient functional recovery from myocardial stunning. In this study, MCE was performed to assess the effect of pre-reperfusion residual flow (PRF) on the recovery from myocardial stunning. METHODS AND RESULTS: The size of the occluded bed, an area supplied with an infarct-related artery, was determined by comparing pre- and post-reperfusion MCE images in 40 patients with first acute myocardial infarction. Myocardial contrast echocardiography-no reflow was observed after reperfusion in 8 patients. Significant PRF was not recognizable in any of the 8 patients. The other patients with MCE reflow were subdivided into 2 groups on the basis of the ratio of the area perfused by PRF to that of the occluded bed: 14 patients with the ratio of more than 10% (PRF[+]), and the other 18 patients (PRF[-]). The wall motion score (0, normal to 4, dyskinetic) was obtained in the convalescent stage. RESULTS: (1) Wall motion of the infarct area after day 3 was better in patients with PRF than in patients without PRF. (2) Left ventricular functional improvement in the long term was remarkable in patients with good reflow and PRF(+), modest in patients with good reflow but PRF(-), and not detectable in patients with MCE-no reflow. No significant correlation was found between angiographic collateral grades and PRF. CONCLUSIONS: The presence of residual flow within the infarct area before reperfusion results in not only good myocardial salvage but also rapid functional recovery from myocardial stunning.

Coronary Circulation↗

PubMed2000

p53 interacts with the DNA mismatch repair system to modulate the cytotoxicity and mutagenicity of hydrogen peroxide.

This study focused on the question of how the DNA mismatch repair (MMR) system and p53 interact to maintain genomic integrity in the presence of the mutagenic stress induced by hydrogen peroxide (H(2)O(2)). The cytotoxic and mutagenic effects of H(2)O(2) were compared in four colon carcinoma sublines: HCT116, HCT116/E6, HCT116+ch3, and HCT116+ch3/E6, representing MMR(-)/p53(+), MMR(-)/p53(-), MMR(+)/p53(+), and MMR(+)/p53(-) phenotypes, respectively. Loss of p53 in MMR-proficient cells did not significantly alter cellular sensitivity to H(2)O(2), but disruption of p53 in MMR-deficient cells resulted in substantial resistance to H(2)O(2) (IC(50) values of 203.8 and 66.2 microM for MMR(-)/p53(-) and MMR(-)/p53(+) cells, respectively). The effect of loss of p53 and MMR function on sensitivity to the mutagenic effect of H(2)O(2) paralleled the effects on cytotoxic sensitivity. In MMR-deficient cells, loss of p53 resulted in a 3.5- and 2.2-fold increase in the generation of 6-thiogunaine and ouabain-resistant clones, respectively. Loss of MMR in combination with loss of p53 synergistically increased the frequency of frameshift mutations in the CA repeat tracts of the out-of-frame shuttle vector pZCA29 and further promoted instability of microsatellite sequences under H(2)O(2) stress. Flow cytometric analysis showed that H(2)O(2) treatment produced a G(l) and G(2)/M phase arrest in MMR(+)/p53(+) cells. Loss of MMR did not alter the ability of H(2)O(2) to activate either checkpoint; loss of p53 in either the MMR-proficient or deficient cells resulted in impairment of the G(l) arrest and a more pronounced G(2)/M arrest. H(2)O(2) caused a greater and more longed increase in p53 protein levels in MMR-proficient than in the MMR-deficient cells. The results demonstrate that the effect of disabling p53 function is modulated by the proficiency of the MMR system (and vice versa) and that there is an overlap between the functions of p53 and the MMR system with respect to the activation of apoptosis and mutagenesis after an oxidative stress.

Base Pair Mismatch↗

PubMed2000

Distorted trachea in patients with chronic obstructive pulmonary disease.

BACKGROUND AND OBJECTIVES: We evaluated the size and configuration of the trachea in patients with chronic obstructive pulmonary disease (COPD; n = 35) on high-resolution computed tomography (HRCT) images and compared them with those of healthy volunteers (n = 24). METHODS: Using a newly developed computed method for analyzing the digital data of HRCT, the size and configuration of the trachea were automatically evaluated. RESULTS: The size of the trachea of the COPD subjects was the same as that of the control subjects; however, the configuration was more distorted in the COPD patients. There was no difference in the tracheal index (TI), which is the ratio of the coronal to the sagittal length, between these two groups; however, the ratio of the short to the long radius (SR/LR) was significantly smaller in the COPD group than in the control group. There was a significant correlation between SR/LR and airflow limitation as assessed by pulmonary function tests in the COPD group. CONCLUSIONS: The SR/LR is a better index of tracheal deformity than the classical TI. This deformity is not a consequence secondary to hyperinflation or emphysematous change of the lung, because the low attenuation area of the lung was not correlated with SR/LR.

Aged↗

PubMed2000

Computed tomographic measurements of airway dimensions and emphysema in smokers. Correlation with lung function.

Chronic obstructive pulmonary disease (COPD) is characterized by the presence of airflow obstruction caused by emphysema or airway narrowing, or both. Low attenuation areas (LAA) on computed tomography (CT) have been shown to represent macroscopic or microscopic emphysema, or both. However CT has not been used to quantify the airway abnormalities in smokers with or without airflow obstruction. In this study, we used CT to evaluate both emphysema and airway wall thickening in 114 smokers. The CT measurements revealed that a decreased FEV(1) (%predicted) is associated with an increase of airway wall area and an increase of emphysema. Although both airway wall thickening and emphysema (LAA) correlated with measurements of lung function, stepwise multiple regression analysis showed that the combination of airway and emphysema measurements improved the estimate of pulmonary function test abnormalities. We conclude that both CT measurements of airway dimensions and emphysema are useful and complementary in the evaluation of the lung of smokers.

Adult↗

PubMed2000

Airway wall thickness in asthma assessed by computed tomography. Relation to clinical indices.

Postmortem studies have shown that airway wall thickening is present in asthmatic patients and may play a pathophysiologic role. We investigated the presence and characteristics of airway wall thickening in patients with asthma, using helical computed tomography. Eighty-one asthmatic patients and 28 healthy control subjects were studied cross-sectionally. Airway wall thickness was assessed by a validated method on the basis of wall area (WA), WA corrected by body surface area (WA/BSA), and WA%, defined as (WA/total area) x 100 at the apical bronchus of the right upper lobe. Airway luminal area (Ai) and Ai/BSA were also examined. Asthma duration and severity, pulmonary function, and serum eosinophil cationic protein levels were evaluated. Intraobserver and interobserver reproducibility of WA, WA%, and Ai measurements were good. As compared with control, WA, WA/BSA, and WA% were significantly increased in patients with mild (n = 13), moderate (39), and severe persistent (22) asthma but not in patients with intermittent asthma (7). Comparison of the four asthmatic subgroups demonstrated thicker airways in more severe disease, but no difference in Ai or Ai/BSA. When all asthmatic patients were analyzed together, WA and WA/BSA correlated with the duration, although weakly, and severity of asthma. WA and WA/BSA negatively correlated with FEV(1) (percentage of predicted), FEV(1)/FVC (%), and FEF(25-75%) (percentage of predicted), whereas WA% negatively correlated with only FEV(1). We conclude that airway wall thickening occurs in patients with asthma and is not limited to those with severe disease. The degree of airway wall thickening may relate to the duration and severity of disease and the degree of airflow obstruction.

Adult↗

PubMed2000

[Sudden cardiac arrest after induction of general anesthesia: a case report].

We experienced sudden cardiac arrest after induction of general anesthesia using isoflurane. The patient had had paroxysmal atrial fibrillation for one year and had been treated with digoxin and cibenzoline succinate. Sinus rhythm appeared soon after the start of closed chest compression. However cardiac arrest recurred, and we inserted a temporary pacemaker catheter to stabilize the circulatory status. She awoke from anesthesia without any complications. The diagnosis of sick sinus syndrome (SSS) was made postoperatively and she had a permanent pacemaker implanted. We thought that the hidden SSS had been the cause of this sudden cardiac arrest.

Aged↗

PubMed2000

[Postoperative pancreatitis after total hip replacement under general anesthesia].

A 61 year old male patient developed postoperative pancreatitis after total hip replacement under general anesthesia with sevoflurane. The patient had chronic renal failure and was receiving hemodialysis. The estimated intraoperative blood loss was 1500 ml, and 1200 ml of blood was administered. The intraoperative mean blood pressure was 60 to 70 mmHg and the central venous pressure at the end of anesthesia was 0 mmHg. Postoperatively he complained of severe upper abdominal pain. On the 1st postoperative day serum amylase level increased to fifteen times of the normal level. He complained again of severe abdominal pain on hemodialysis. From these episodes, we estimate that the circulatory disturbance of pancreas is the cause of this postoperative pancreatitis.

Acute Disease↗

PubMed1999

Changes in intra-abdominal visceral fat and serum leptin levels in patients with obstructive sleep apnea syndrome following nasal continuous positive airway pressure therapy.

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) is a common disorder in obese subjects. Visceral fat accumulation (VFA) is a better predictor of coronary heart disease than body mass index. Leptin is a hormone involved in the control of body weight and fat distribution. The effect of nasal continuous positive airway pressure (NCPAP) treatment on VFA and serum leptin levels in OSAS patients has not been known. METHODS AND RESULTS: VFA and subcutaneous fat accumulation (SFA) were assessed by CT before and after NCPAP treatment in 22 OSAS patients (mean apnea and hypopnea index >50 episodes/h). Serum leptin levels of another 21 OSAS patients were measured before and after 3 to 4 days of NCPAP to gain insight into the mechanism by which NCPAP affects fat distribution. VFA and SFA decreased significantly after 6 months of NCPAP treatment (236+/-16 to 182+/-14cm(2), P=0.0003 and 215+/-21 to 189+/-18 cm(2), P=0.003, respectively). VFA decreased significantly in the body weight reduction group (n=9, P<0.01) and the no body weight reduction group (n=13, P<0.03). In contrast, SFA changed significantly in the body weight reduction group only (P<0.01). Leptin levels decreased significantly following 3 to 4 days of NCPAP (P<0.01), whereas body weight, fasting insulin, and cortisol levels did not change significantly. CONCLUSIONS: Correction of sleep disordered breathing by NCPAP may be used to reduce VFA in OSAS patients. OSAS may have significant effects on the serum leptin levels.

Adipose Tissue↗