The Worsening of Positional Mild Obstructive Sleep Apnea over Time Is Associated with an Increase in Body Weight: Impact on Blood Pressure and Autonomic Nervous System.

BACKGROUND: Most patients with mild obstructive sleep apnea (OSA) are positional dependent. Although mild OSA worsens over time, no study has assessed the natural course of positional mild OSA. OBJECTIVES: The aim of this study was to evaluate the natural course of positional mild OSA, its most valuable progression predictor, and its impact on blood pressure (BP) and the autonomic nervous system (ANS). METHODS: This retrospective observational cohort study enrolled 86 patients with positional mild OSA and 26 patients with nonpositional mild OSA, with a follow-up duration of 32.0 ± 27.6 months and 37.6 ± 27.8 months, respectively. Polysomnographic variables, BP, and ANS functions were compared between groups at baseline and after follow-up. RESULTS: In patients with positional mild OSA after follow-up, the apnea/hypopnea index (AHI) increased (9.1 ± 3.3/h vs. 22.0 ± 13.2/h, p = 0.000), as did the morning systolic BP (126.4 ± 13.3 mm Hg vs. 130.4 ± 15.9 mm Hg, p = 0.011), and the sympathetic activity (49.4 ± 12.3% vs. 55.3 ± 13.1%, p = 0.000), while the parasympathetic activity decreased (50.6 ± 12.3% vs. 44.7 ± 13.1%, p = 0.000). The body mass index changes were the most important factor associated with AHI changes among patients with positional mild OSA (Beta = 0.259, adjust R2 = 0.056, p = 0.016, 95% confidence interval 0.425 and 3.990). The positional dependency disappeared over time in 66.3% of patients with positional mild OSA while 69.2% of patients with nonpositional mild OSA retained nonpositional. CONCLUSIONS: In patients with positional mild OSA, disease severity, BP, and ANS regulation worse over time. Increased weight was the best predictor for its progression and the loss of positional dependency. Better treatments addressing weight control and consistent follow-up are needed for positional mild OSA.

Exploring the Factors Affecting Bitter Melon Peptide Intake Behavior: A Health Belief Model Perspective.

PURPOSE: Diabetes mellitus (DM) patients need to control their blood sugar level in order to achieve a good quality of life. This study was conducted using the health belief model (HBM), to explore the factors behind the bitter melon peptide (BMP) intake behavior and the role of self-efficacy in the model. MATERIALS AND METHODS: The subjects were type 2 diabetes mellitus patients in Taiwan. A structured questionnaire was adopted from the theory of health belief model and modified specifically for this study as an instrument to survey 292 DM patients, of whom 51.03% were female, 75.68% were married, and 49.32% were aged 40 to 64 years old. The data were analyzed using t-tests, one-way ANOVA and regression. RESULTS: Perceived susceptibility was the most sensitive in the response to the various demographic factors, whereas perceived barrier was the least sensitive. The HBM explained 38.0% of BMP intake behavior. Perceived benefits (ß= 0.357) and perceived susceptibility (ß= 0.348) were the major predictors. Self-efficacy mediated the relationship between perceived benefits and BMP intake behavior, as well as increased the variance explained to 51.30%. CONCLUSION: The perceived benefits of taking BMP and perceived susceptibility to DM complications were the two major drivers acting on BMP intake behavior. The power of perceived benefits was mediated by self-efficacy in driving DM patients to take BMP regularly. Several ways of affecting perceived susceptibility and perceived benefits were suggested.

Hand strength and dexterity in patients with Prader-Willi syndrome: a pilot intervention study.

OBJECTIVE: The study aim was to examine the hand function (hand strength and dexterity) and intervention effects of training in adults with Prader-Willi syndrome (PWS). METHODS: Six adults with PWS (two females; mean age 26.14 years) underwent hand muscle strength and dexterity training for 3 months (2 hours per week). The following hand function tests were performed pre- and post-intervention: (1) hand grip, lateral pinch, and tip pinch hand strength tests, (2) the Box and Block test (BBT) for gross manual dexterity and (3) the Purdue Pegboard test for finger dexterity. RESULTS: Before treatment, all subjects showed lower hand grip, lateral pinch, tip pinch strength, and poorer manual/finger dexterity relative to healthy adults. After training, hand function scores improved on many test items, but only the left hand tip pinch and the right hand BBT performance showed significant improvements. CONCLUSIONS: All subjects showed lower hand strength and poorer manual/finger dexterity compared with healthy adults; this should be considered during physical training programs. Owing to limitations in the intervention intensity and possible subject behavioral deficits, further research is needed to clarify the effects of this intervention on hand function in PWS patients.

Epidemiology and trend of pediatric adenoidectomy: a population-based study in Taiwan from 1997 to 2012.

OBJECTIVES: To assess population-level data for pediatric adenoidectomy. METHODS: Using data from the Taiwan National Health Insurance Research Database for the 1997-2012 period, all inpatients <18 years who received adenoidectomies were identified by codes from the International Classification of Diseases, 9th Revision. RESULTS: A total of 20,599 children underwent adenoidectomy (mean age, 7.4 years; 67% boys). The overall incidence rate was 24.5 per 100,000 children. The highest incidence was observed for the ages of 3-5 years in both genders (p < .001). Boys exhibited higher incidence rates than did girls (p < .001). Longitudinal data revealed an increase in the incidence rates from 1997 (14.8/100,000) to 2012 (26.9/100,000) (p trend < .001). The proportion of adenoidectomies performed at medical centers decreased from 60.5 to 46.9%, whereas those performed at regional hospitals increased from 36.4 to 47.2% (all p trend < .001). The proportion of pediatric adenoidectomies performed for sleep-disordered breathing (SDB) increased significantly from 10.1 to 35.6%, whereas those for infections decreased from 32.3 to 8.0% (all p trend < .001). CONCLUSIONS: This study revealed an increasing trend of pediatric inpatient adenoidectomy incidence rates during 1997-2012 in Taiwan. Moreover, surgical indications have shifted from infections to SDB.

Revision adenoidectomy in children: a population-based cohort study in Taiwan.

There is a lack of population-level analysis of revision adenoidectomy in children. This study reveals the revision rates and factors associated with paediatric revision adenoidectomy in Taiwan. From the Taiwan National Health Insurance Research Database, we identified all in-hospital children (age <18 years) who underwent adenoidectomy between 2000 and 2007. All children had received at least 5 years of follow-up from the index date, and the clinical records until 2012 were examined. Factors affecting the paediatric revision adenoidectomy were analysed using the multivariable Cox proportional hazards model. A total of 10,396 children were enrolled (mean age 7.3 years; 66% boys; mean follow-up period 8.7 years). Two hundred and seventy-five children underwent revision adenoidectomy, and the mean interval between primary adenoidectomy and revision surgery was 2.97 years. Only 58.5% of children underwent revision surgery at the initial hospital. The incidence of revision surgery was highest in the second year (0.69%), followed by the third year (0.53%) after primary adenoidectomy. The multivariable Cox proportional hazards model revealed that young age [hazard ratio (HR) = 0.8], male gender (HR = 1.57), surgery at an eastern hospital (HR = 2.08), surgical indication of adenoid hypertrophy (HR = 1.51), and concurrent ventilation tube insertion (HR = 2.61) or nasal surgeries (HR = 4.84) were associated with revision adenoidectomy. The incidence of revision adenoidectomy in Taiwan was 2.6%. Male gender, young age, concurrent nasal or ventilation tube insertion, and surgery at an eastern hospital increased the risk of revision.

Altered expression of carbonic anhydrase-related protein XI in neuronal cells expressing mutant ataxin-3.

Spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD) is a late-onset neurodegenerative disorder caused by the expansion of a polyglutamine tract within the gene product, ataxin-3. Microarray analysis revealed a dramatic differential expression of carbonic anhydrase-related protein XI (CA-RPXI/CA11) in the presence or absence of mutant ataxin-3. Therefore, we examined the expression and distribution of all three CA-RPs (CA8, 10, and 11) in human neuronal cells that stably express mutant ataxin-3. Compared with the cells containing normal ataxin-3, protein expression of CA8 and CA11 is significantly increased in human neuroblastoma cells harboring mutant ataxin-3. Semi-quantitative RT-PCR demonstrated that all three CA-RPs exhibited significantly higher transcript levels in neuronal cells expressing mutant ataxin-3. Interestingly, CA11 is distributed not only in the cytoplasm but also within the nuclei of the stably transfected mutant cells when compared with the sole cytoplasmic distribution in cells containing normal ataxin-3. In addition, results from transient transfection assays in SK-N-SH and Neuro2a (N2a) cells also confirmed the nuclear localization of CA11 in the presence of truncated ataxin-3. Most importantly, immunohistochemical staining of the MJD transgenic mouse and post-mortem MJD human brain also revealed that CA11 is highly expressed in both cytoplasm and nuclei of the brain cells. Recruitment of CA11 into nuclear inclusions containing mutant ataxin-3 revealed a possible correlation between CA11 and disease progression. Although the exact function of CA-RPs is still undefined in the central nervous system, our findings suggest that CA-RPs, especially CA11, may play specific roles in the pathogenesis of Machado-Joseph disease.

Static balance function in children with cochlear implants.

OBJECTIVE: This study aimed to assess the static balance function in deaf adolescents with cochlear implants. METHODS: We included 24 adolescents who had received unilateral cochlear implantation for at least 5 years. Each subject underwent stabilometry testing under 4 different conditions: (A) firm surface with eyes open; (B) firm surface with eyes closed; (C) foam pad with eyes open; and (D) foam pad with eyes closed. All of them received tests with their cochlear implant turned on and off. Another 24 age- and sex-matched adolescents with normal hearing were tested in the same way for comparison. Sway velocity and circular area were measured and analyzed. RESULTS: The mean sway velocity of the cochlear implant group under conditions A-D was 1.68, 1.98, 2.36, and 5.25 cm/s, respectively, and the mean circular area of the cochlear implant group under conditions A-D was 7.39, 6.68, 12.21, and 34.27 cm(2), respectively. Both of the parameters showed statistical significance between the cochlear implant group and the normal hearing group for conditions A, C and D (p<0.05). Furthermore, there was no significant balance function change among cochlear implant group with their implant "on" and "off". CONCLUSIONS: This study showed that the static balance function in adolescents with long-term use of cochlear implants was worse than those of normal hearing peers. The difference between the cochlear implant group and normal hearing group was the highest when both visual and somatosensory inputs were disrupted. The postural stability was similar whether or not the cochlear implant was activated.

Decreased protein synthesis of Hsp27 associated with cellular toxicity in a cell model of Machado-Joseph disease.

Machado-Joseph disease is an autosomal dominant spinocerebellar degeneration caused by the expansion of a polyglutamine tract within the gene product, ataxin-3. We have previously shown that increased oxidative stress and decreased expression of Hsp27 may be contributory factors to the disease progression. In this study, we utilized neuroblastoma SK-N-SH cells stably transfected with full-length expanded ataxin-3 to further investigate the mechanism(s) resulting in the decreased expression of Hsp27. Results from 35S-methionine pulse-chase labeling and protein degradation assays revealed that decreased Hsp27 in mutant MJD cells is due to defects in protein synthesis. Our results further demonstrated that Hsp27 degradation is independent of the proteasome degradation pathway. In addition, we showed that overexpression of Hsp27 desensitizes mutant MJD cells to apoptotic stress. Taken together, these findings provide the first evidence that expanded ataxin-3 interferes with Hsp27 synthesis, which may contribute to the impairment of the cells' ability to respond to stresses and trigger the progression of this late-onset disease.

Measurement of hearing aid outcome in the elderly: comparison between young and old elderly.

OBJECTIVE: To evaluate speech performance and subjective outcomes for older individuals who have hearing impairment and use digital hearing aids. The outcomes between young and old elderly users were compared. STUDY DESIGN: Prospective. SUBJECTS AND METHODS: Fifty-nine patients with hearing loss fitted with digital hearing aids were included. They were divided into two groups. Group A consisted of 32 subjects aged 65 to 80 years, whereas group B had 27 subjects older than 80 years. Speech performance and subjective outcomes were measured 4 months after fitting of hearing aids. Hearing Handicap Inventory for the Elderly-Screening Version (HHIE-S), Client Oriented Scale of Improvement (COSI), satisfaction, and usage questionnaires were used as subjective assessments. RESULTS: Improvements in speech performance were not significantly different between these two groups. There were no statistical differences in terms of HHIE-S score reduction, satisfaction rate, daily usage time, and COSI scores between both groups. CONCLUSION: Age by itself is not a limiting factor for older patients with hearing impairment to benefit from digital hearing aids.

Dynamic expression of Hsp27 in the presence of mutant ataxin-3.

Machado-Joseph disease (MJD)/spinocerebellar ataxia type 3 (SCA3) is an autosomal dominant spinocerebellar degeneration characterized by a wide range of clinical manifestations. The molecular mechanisms underlying the selective neuronal death typical of MJD/SCA3 are unknown. In this study, human SK-N-SH neuroblastoma cells stably transfected with full-length MJD with 78 CAG repeats were assayed for the dynamic expression of Hsp27, known as a suppressor of poly-Q mediated cell death, in the presence of mutant ataxin-3 in different passages of cultured cells. A dramatic decrease of Hsp27 expression was observed in the earlier passage of cultured SK-N-SH-MJD78 cells, however, the later passage of cells showed a significant increase of Hsp27 to almost the same level of the parental cells. Furthermore, immunohistochemical analysis of MJD transgenic mice and post-mortem human brain tissues showed increased expression of Hsp27 compared to normal control brain, suggesting an up-regulation of Hsp27 in the end stage of MJD. However, mutant cells of earlier passages were more susceptible to serum deprivation than mutant cells of later passages, indicating weak tolerance toward stress in cells with reduced Hsp27. While heat shock was used to assess the stress response, cells expressing mutant ataxin-3 displayed normal response upon heat shock stimuli when compared to the parental cells. Taken together, we proposed that during the early disease stage, the reduction of Hsp27 synthesis mitigated the ability of neuron cells to cope with cytotoxicity induced by mutant ataxin-3, triggering the cell death process during the disease progress. In the late stage of disease, after prolonged stressful conditions of polyglutamine cytotoxicity, the increased level of Hsp27 may reflect a dynamic process of the survived cells to unfold and remove mutant ataxin-3. However, this increased Hsp27 still cannot reverse the global dysfunction of cellular proteins due to accumulation of cytotoxic effects.

HSP27 and cell death in spinocerebellar ataxia type 3.

Spinocerebellar ataxia type 3 (SCA3) is an autosomal dominant spinocerebellar degeneration characterized by a wide range of clinical manifestations. In this review, we discuss the role(s) that heat shock protein 27 (HSP27) may play in the cell death process of spinocerebellar ataxia type 3.