Infection risk in psoriatic patients receiving tumour necrosis factor inhibitors: a 20-year systematic review and meta-analysis of randomized controlled trials.

Tumour necrosis factor inhibitors (TNFis) are commonly used for treating psoriatic diseases; however, the risk of infection while receiving TNFis remains uncertain. The aim of this study was to investigate the infection risk in patients with psoriatic disease receiving TNFis. A prospectively registered systematic literature search was conducted in Medline (PubMed), Cochrane Central Register of Controlled Trials (CENTRAL), EMBASE and the ClinicalTrials.gov databases from inception to December 31, 2021. We included double-blind randomized controlled trials that compared TNFis or other biologics with placebo in adults with psoriasis or psoriatic arthritis. The primary outcomes included overall and serious infection risks, and secondary outcomes included upper respiratory infections and nasopharyngitis risks. The risk ratio of the dichotomous outcome was calculated using the Mantel-Haenszel method with random effects, and heterogeneity was assessed using Cochran's Q statistic and quantified using the I-squared statistic. A total of 48 studies with 15 464 patients with psoriatic diseases were included. The meta-analysis demonstrated a slightly increased overall infection risk (risk ratio = 1.09; 95% confidence interval, 1.02-1.15) but not serious infection risk (risk ratio = 0.95; 95% confidence interval, 0.61-1.49) among patients receiving TNFis. There were also no increased risks of upper respiratory infections (risk ratio = 1.10; 95% confidence interval, 0.94-1.28) or nasopharyngitis (risk ratio = 1.14; 95% confidence interval, 1.00-1.30). In subgroup analyses using the fixed effects model, only etanercept and certolizumab pegol were, respectively, associated with an increased risk of overall infection (RR = 1.14, 95% CI, 1.03-1.27) and upper respiratory infections (RR = 1.42, 95% CI, 1.02-1.98). In conclusion, evidence to date suggests an increased overall infection risk that is generally tolerable in patients with psoriatic diseases receiving TNFis. There are no increased risks of serious infections, upper respiratory infections or nasopharyngitis.

Association between sensorineural hearing loss and vitiligo: a nationwide population-based cohort study.

BACKGROUND: Vitiligo is an acquired depigmentation disease of the skin due to melanocyte destruction. A shared pathogenesis affecting melanocytes in the cochlea has been postulated. However, the association between vitiligo and sensorineural hearing loss (SNHL) is unclear. OBJECTIVE: To identify the association between vitiligo and SNHL. METHODS: This retrospective, nationwide cohort study included patients with vitiligo and age-, sex- and comorbidities-matched controls (propensity score matching; 1:4 ratio) from the National Health Insurance Research Database in Taiwan from 1 January 2000 to 31 December 2013. RESULTS: In total, 13 048 patients with vitiligo and 52 192 controls were included. SNHL developed in 0.61% patients with vitiligo and 0.29% controls. After adjusting for sex, age and comorbidities, a significant association between vitiligo and SNHL was found (adjusted hazard ratio, 2.18; 95% CI, 1.66-2.86). The other risk factors for developing SNHL included increased age, male sex, hyperlipidaemia, coronary artery disease and diffuse connective tissue diseases. In subgroup analysis, the association between vitiligo and SNHL remained significant in almost all the subgroups. CONCLUSION: A 2.2-fold increased risk of developing SNHL was found in patients with vitiligo. Proper referral to otologists for early screening and closer follow-up of SNHL should be considered for patients with vitiligo, especially for patients with older age.

Association between sodium-glucose co-transporter 2 inhibitors and risk of bullous pemphigoid in patients with type 2 diabetes: a nationwide population-based cohort study.

BACKGROUND: Certain anti-diabetic agents have been linked to the development of bullous pemphigoid (BP). However, the relationship between BP and sodium-glucose co-transporter 2 inhibitors (SGLT2is) remains inconclusive. OBJECTIVE: To investigate the association between SGLT2i usage and BP. METHODS: Participants were recruited from the Taiwan National Health Insurance Database between 2007 and 2018. A total of 149 060 patients with diabetes receiving SGLT2i were matched 1 : 2 with diabetic patients without SGLT2i usage. Factors such as age, sex, duration of diabetes condition, DPP4i usage, insulin usage and selected comorbidities were included in the multivariate analysis. RESULTS: Compared with the control, the 2-year-cumulative incidence was significantly low in patients using SGLT2i after adjustment for competing mortality. Patients with diabetes receiving SGLT2i had a low risk [adjusted hazard ratio (HR) 0.56, 95% confidence interval (CI), 0.33-0.96] for BP after adjustment for potential confounders. Age (HR, 1.06), renal disease (HR, 1.79), cerebrovascular disease (HR, 3.23), epilepsy (HR, 3.07), DPP4i users (HR: 2.55) and insulin users (HR: 2.56) were significant risk factors for BP. CONCLUSIONS: The risk of BP did not increase in patients receiving SGLT2i. Thus, SGLT2i could be a safe choice for patients with diabetes having additional risk factors or a history of BP.

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.

Increased risk of major depressive disorder among probands with psoriasis and unaffected siblings: a nationwide population-based study.

BACKGROUND: Previous studies have shown that patients with psoriasis have a higher risk of depression. However, the risk of major depressive disorder (MDD) among unaffected siblings of psoriasis probands remains unknown. This study aimed to investigate the risk of MDD among probands with psoriasis and unaffected siblings. METHODS: We selected subjects from the National Health Insurance Research Database (NHIRD) in Taiwan. Subjects were followed up from 01 January 1996 until a diagnosis of MDD, death or 31 December 2011. The Breslow-Cox model was used to calculate the adjusted relative risk (aRR). RESULTS: This study included 1094 probands with psoriasis, 1202 unaffected siblings and 4808 matched controls. Overall, 11.9% of the psoriasis probands (n = 130) and 2.5% of the unaffected siblings (n = 30) developed MDD, as compared with 1.1% of the controls (n = 52). Compared with controls, probands with psoriasis and unaffected siblings had aRRs of 10.60 [95% confidence interval (CI): 7.73-14.52] and 2.17 (95% CI: 1.44-3.28), respectively, for MDD. CONCLUSIONS: Probands with psoriasis and unaffected siblings have an increased risk of subsequently developing MDD. Further studies are needed to investigate the shared familial mechanisms underlying psoriasis and MDD.

Genetic interaction is associated with lower metabolic connectivity and memory impairment in clinically mild Alzheimer's disease.

Metabolic connectivity as showed by [18F] fluorodeoxyglucose (FDG) positron emission tomography (FDG-PET) reflects neuronal connectivity. The aim of this study was to investigate the genetic impact on metabolic connectivity in default mode subnetworks and its clinical-pathological relationships in patients with Alzheimer's disease (AD). We separately investigated the modulation of 2 default mode subnetworks, as identified with independent component analysis, by comparing APOE-ε4 carriers to noncarriers with AD. We further analyzed the interaction effects of APOE (APOE-ε4 carriers vs noncarriers) with PICALM (rs3851179-GG vs rs3851179-A-allele carriers) on episodic memory (EM) deficits, reduction in cerebral metabolic rate for glucose (CMRgl) and decreased metabolic connectivity in default mode subnetworks. The metabolic connectivity in the ventral default mode network (vDMN) was positively correlated with EM scores (ß =0.441, P < .001). The APOE-ε4 carriers had significantly lower metabolic connectivity in the vDMN than the APOE-ε4 carriers (t(96) = -2.233, P = .028). There was an effect of the APOE-PICALM (rs3851179) interactions on reduced CMRgl in regions of vDMN (P < .001), and on memory deficits (F3,93 =5.568, P = .020). This study identified that PICALM may modulates memory deficits, reduced CMRgl and decreased metabolic connectivity in the vDMN in APOE-ε4 carriers. [18F] FDG-PET-based metabolic connectivity may serve a useful tool to elucidate the neural networks underlying clinical-pathological relationships in AD.

Cancer is not a risk factor for bullous pemphigoid: 10-year population-based cohort study.

BACKGROUND: Bullous pemphigoid (BP) is the most common autoimmune bullous disease. Whether there is an increased risk for subsequent BP among patients with cancer is still unclear. OBJECTIVES: To evaluate the risk for subsequent BP in patients with cancer. METHODS: This nationwide population-based cohort study was based on data obtained from the Taiwan National Health Insurance Database between 2000 and 2011. A total of 36 838 patients with cancer and 147 352 age-, sex- and index-date-matched controls were recruited. The hazard ratio (HR) of subsequent BP in the patients with cancer was analysed using a Fine-Gray competing risk regression model with mortality as the competing event. RESULTS: The incidence of BP per 100 000 person-years was 17·2 in the patients with cancer and 19·8 in the controls; therefore, the crude incidence rate ratio was 0·87 [95% confidence interval (CI) 0·53-1·36]. The HR of subsequent BP in the patients with cancer was 0·47 (95% CI 0·23-0·94) using the Fine-Gray competing risk regression model. Age (HR 1·05, 95% CI 1·03-1·07), diabetes mellitus (HR 1·69, 95% CI 1·10-2·59) and cerebrovascular disease (HR 2·14, 95% CI 1·36-3·34) were independent risk factors for BP. CONCLUSIONS: The incidence of BP in patients with cancer was not higher than in the control group. Cancer is not a risk factor for BP.

Millimeter-wave system-on-chip advancement for fusion plasma diagnostics.

Recent advances in radio-frequency system-on-chip technology have provided mm-wave fusion plasma diagnostics with the capability to overcome major challenges such as space inefficiency, inflexible installation, sensitivity, susceptibility to EMI, and prohibitively high cost of conventional discrete component assemblies as higher imaging resolution and data accuracy are achieved by increasing the number of channels. Nowadays, shrinking transistor gate lengths on fabrication techniques have enabled hundreds of GHz operation, which is suitable for millimeter-wave diagnostics on current and future tokamaks. The Davis Millimeter Wave Research Center (DMRC) has successfully developed V-band (55-75 GHz) transmitter and receiver chips for Microwave Imaging Reflectometer (MIR) instruments. The transmitter can illuminate 8 different frequencies simultaneously within 55-75 GHz. Moreover, the receiver has the capability to amplify the reflected signal (>30 dB) while offering 10-30× reduction in noise temperature compared to current MIR instruments. Plasma diagnostics requires ultra-wideband (more than 20 GHz) operation which is approximately nine times wider bandwidth than the recent commercial impetus for communication systems. Current efforts are underway for gallium-arsenide monolithic microwave integrated circuit receiver chips at W-band (75-110 GHz) and F-band (90-140 GHz) permitting measurements at higher toroidal magnetic fields.

Measurement of the Dynamical Structure Factor of a 1D Interacting Fermi Gas.

We present measurements of the dynamical structure factor S(q,ω) of an interacting one-dimensional Fermi gas for small excitation energies. We use the two lowest hyperfine levels of the ^{6}Li atom to form a pseudospin-1/2 system whose s-wave interactions are tunable via a Feshbach resonance. The atoms are confined to one dimension by a two-dimensional optical lattice. Bragg spectroscopy is used to measure a response of the gas to density ("charge") mode excitations at a momentum q and frequency ω, as a function of the interaction strength. The spectrum is obtained by varying ω, while the angle between two laser beams determines q, which is fixed to be less than the Fermi momentum k_{F}. The measurements agree well with Tomonaga-Luttinger theory.

The symptom burden of autonomic dysfunction is positively associated with chronic rhinosinusitis status.

BACKGROUND: Dysregulation of the autonomic system can affect sinonasal physiological function and may exacerbate the symptom burden associated with rhinosinusitis. However, the association between autonomic dysfunction and chronic rhinosinusitis (CRS) has seldom been studied. Here, we investigated the relationship between autonomic dysfunction and CRS. METHODS: Patients with CRS who failed medical treatment were prospectively enrolled. All patients underwent pre-operative examinations and completed questionnaires, including the reflux symptom index (RSI) and the Sino-nasal Outcome Test-22 (SNOT-22). Autonomic dysfunction was scored using the 31-item Composite Autonomic Symptom Score (COMPASS 31), a validated simple instrument used to evaluate dysautonomia. RESULTS: We prospectively enrolled a total of 89 CRS patients, including 37 with polyps (CRSwNP) and 52 without polyps (CRSsNP). The most common dysautonomic symptoms were dry eye, dry mouth, postural dizziness, and a sensation of excessive fullness after meals. Significant positive correlations were evident between COMPASS 31 and SNOT-22 scores in CRSwNP patients. CRS-associated symptoms, including cough, post-nasal drip, sleep, and psychological dysfunction, were correlated with the level of autonomic dysfunction. CONCLUSIONS: We found a positive correlation between the symptom burdens of autonomic dysfunction and CRSwNP. The relationship between autonomic dysfunction and CRS is highly complex; further work is needed.

Neuropsychiatric symptoms in Alzheimer's disease: associations with caregiver burden and treatment outcomes.

BACKGROUND: Caregivers play a major role in providing care for patients with Alzheimer's disease (AD) and are themselves at higher risk of health comorbidities. AIM: To address the impact of neuropsychiatric symptoms of patients in different stages of AD on their caregivers' burden. DESIGN: This prospective study enrolled 260 AD patients with clinical dementia rating (CDR) of 0.5, 1 and 2 at a tertiary medical center. METHODS: All patients were tested using the mini-mental state examination (MMSE), the cognitive abilities screening instrument (CASI), the neuropsychiatric inventory (NPI) and the CDR scale. Data regarding therapeutic outcomes of anti-Alzheimer's drugs were also collected. Caregivers were tested using NPI. RESULTS: The mean follow-up interval was 25.0 ± 12.2 months, and two patients died during follow-up. NPI-burden was positively correlated with NPI-sum ( r = 0.822, P < 0.001) but negatively correlated with years of education ( r = -0.140, P = 0.024), CASI score ( r = -0.259, P < 0.001) and MMSE score ( r = -0.262, P <0.001). Multiple linear regression analysis showed that only NPI-sum was independently associated with mean NPI-burden. Both higher mean CASI and MMSE scores had better therapeutic outcome of anti-Alzheimer's drugs ( P = 0.001 and P = 0.005, respectively). CONCLUSIONS: The severity of neuropsychiatric symptoms in patients with AD was positively associated with caregiver's stress, and patients with better cognitive functions, under treatment with anti-Alzheimer's drugs, had better therapeutic outcomes. To reduce the impact of neuropsychiatric symptoms, it is crucial to detect dementia in its early phases and provide early intervention with anti-Alzheimer's drugs, which might help decrease the caregiver burden, thereby improving their quality of life.

Shared atypical brain anatomy and intrinsic functional architecture in male youth with autism spectrum disorder and their unaffected brothers.

BACKGROUND: Autism spectrum disorder (ASD) is a highly heritable neurodevelopmental disorder, yet the search for definite genetic etiologies remains elusive. Delineating ASD endophenotypes can boost the statistical power to identify the genetic etiologies and pathophysiology of ASD. We aimed to test for endophenotypes of neuroanatomy and associated intrinsic functional connectivity (iFC) via contrasting male youth with ASD, their unaffected brothers and typically developing (TD) males. METHOD: The 94 participants (aged 9-19 years) - 20 male youth with ASD, 20 unaffected brothers and 54 TD males - received clinical assessments, and undertook structural and resting-state functional magnetic resonance imaging scans. Voxel-based morphometry was performed to obtain regional gray and white matter volumes. A seed-based approach, with seeds defined by the regions demonstrating atypical neuroanatomy shared by youth with ASD and unaffected brothers, was implemented to derive iFC. General linear models were used to compare brain structures and iFC among the three groups. Assessment of familiality was investigated by permutation tests for variance of the within-family pair difference. RESULTS: We found that atypical gray matter volume in the mid-cingulate cortex was shared between male youth with ASD and their unaffected brothers as compared with TD males. Moreover, reduced iFC between the mid-cingulate cortex and the right inferior frontal gyrus, and increased iFC between the mid-cingulate cortex and bilateral middle occipital gyrus were the shared features of male ASD youth and unaffected brothers. CONCLUSIONS: Atypical neuroanatomy and iFC surrounding the mid-cingulate cortex may be a potential endophenotypic marker for ASD in males.

The High Mobility Group A1 (HMGA1) Transcriptome in Cancer and Development.

BACKGROUND & OBJECTIVES: Chromatin structure is the single most important feature that distinguishes a cancer cell from a normal cell histologically. Chromatin remodeling proteins regulate chromatin structure and high mobility group A (HMGA1) proteins are among the most abundant, nonhistone chromatin remodeling proteins found in cancer cells. These proteins include HMGA1a/HMGA1b isoforms, which result from alternatively spliced mRNA. The HMGA1 gene is overexpressed in cancer and high levels portend a poor prognosis in diverse tumors. HMGA1 is also highly expressed during embryogenesis and postnatally in adult stem cells. Overexpression of HMGA1 drives neoplastic transformation in cultured cells, while inhibiting HMGA1 blocks oncogenic and cancer stem cell properties. Hmga1 transgenic mice succumb to aggressive tumors, demonstrating that dysregulated expression of HMGA1 causes cancer in vivo. HMGA1 is also required for reprogramming somatic cells into induced pluripotent stem cells. HMGA1 proteins function as ancillary transcription factors that bend chromatin and recruit other transcription factors to DNA. They induce oncogenic transformation by activating or repressing specific genes involved in this process and an HMGA1 "transcriptome" is emerging. Although prior studies reveal potent oncogenic properties of HMGA1, we are only beginning to understand the molecular mechanisms through which HMGA1 functions. In this review, we summarize the list of putative downstream transcriptional targets regulated by HMGA1. We also briefly discuss studies linking HMGA1 to Alzheimer's disease and type-2 diabetes. CONCLUSION: Further elucidation of HMGA1 function should lead to novel therapeutic strategies for cancer and possibly for other diseases associated with aberrant HMGA1 expression.

Hes1 Increases the Invasion Ability of Colorectal Cancer Cells via the STAT3-MMP14 Pathway.

The Notch pathway contributes to self-renewal of tumor-initiating cell and inhibition of normal colonic epithelial cell differentiation. Deregulated expression of Notch1 and Jagged1 is observed in colorectal cancer. Hairy/enhancer of split (HES) family, the most characterized targets of Notch, involved in the development of many cancers. In this study, we explored the role of Hes1 in the tumorigenesis of colorectal cancer. Knocking down Hes1 induced CRC cell senescence and decreased the invasion ability, whereas over-expression of Hes1 increased STAT3 phosphorylation activity and up-regulated MMP14 protein level. We further explored the expression of Hes1 in human colorectal cancer and found high Hes1 mRNA expression is associated with poor prognosis in CRC patients. These findings suggest that Hes1 regulates the invasion ability through the STAT3-MMP14 pathway in CRC cells and high Hes1 expression is a predictor of poor prognosis of CRC.

Protective effects of morphine preconditioning in delayed phase on myocardial ischemia-reperfusion injury in rabbits.

The aim of this study was to investigate the protective mechanisms of delayed-phase morphine preconditioning on myocardial ischemia-reperfusion injury. Thirty healthy male New Zealand white rabbits were randomly divided into three groups: a sham operation group (C), ischemia-reperfusion group (I/R), and delayed-phase morphine preconditioning group (M) (N = 10/group). Rabbits in the C group received thoracotomy for 160 min. Rabbits in the I/R group received left artery blockage for 40 min and reperfusion for 120 min. Rabbits in the M group received 1.0 mg/kg intravenous morphine 24 h prior to the identical treatment as the rabbits in the I/R group. In each group, the interleukin (IL)-10 and tumor necrosis factor (TNF)-α levels were detected at five time points: 20 min before the left coronary artery blockage (T1), 20 and 40 min after the left coronary artery blockage (T2 and T3, respectively), and 1 and 2 h after the myocardial reperfusion (T4 and T5, respectively). After reperfusion, the infarction size was measured with Evans blue and 2,3,5-triphenyltetrazolium chloride (TTC) staining. Compared with the C group, serum IL-10 and TNF-α concentrations increased in the I/R and M groups; the difference was significant (P < 0.05). When compared with the I/R group, the IL-10 concentrations in the M group were significantly increased (P < 0.05), but the infarction size and TNF-α concentrations were significantly decreased (P < 0.05). These results suggested that delayed-phase morphine preconditioning might achieve myocardial protection through the regulation and balance of inflammatory cytokines.

Effect of morphine preconditioning in the delayed phase on the expression of p38 mitogen-activated protein kinase in a rabbit model of myocardial ischemia-reperfusion injury.

This study aimed to investigate the protective effects of delayed morphine preconditioning on myocardial ischemia-reperfusion injury. We randomly divided 30 rabbits into three groups with 10 rab-bits in each group as follows: sham operation group (C group), isch-emia-reperfusion group (I/R group), and morphine pretreatment group (M group). Rabbits in C Group received left coronary without blocking for 160 min. The left descending artery of rabbits in the I/R group was blocked for 40 min and reperfused for 120 min. Rabbits in the M group received intravenous administration of 1.0 mg/kg morphine; after 24 h, rabbits in this group received the same treatment as that administered to the I/R group. We determined tumor necrosis factor alpha (TNF-α) levels in blood samples from the internal carotid artery of rabbits in each group 20 min before occlusion of the left descending coronary artery, 20 and 40 min after occlusion of the left descending coronary artery, and 1 and 2 h after myocardial reperfusion. After 120 min of reperfusion, immunoblotting was used to measure the activity levels of myocardial p38 mitogen-activated protein kinase (MAPK); in addition, the infarct size was measured. Compared to the I/R group, the M group showed a significant decrease in TNF-α levels, p38 MAPK activity, and the myocardial infarct size (I/R group 37.8% ± 1.7% vs 21.5% ± 2.4%; P < 0.05). Thus, morphine preconditioning in the delayed phase may exert protective effects on myocardial I/R injury by inhibiting myocar-dial p38 MAPK activity and decreasing TNF-α production.

Effects of isoflurane preconditioning in the delayed phase on myocardial tumor necrosis factor alpha levels and caspase-3 protein expression in a rabbit model of ischemia-reperfusion injury.

This study aimed to investigate the protective effects and the mechanisms underlying these effects of isoflurane preconditioning in the delayed phase of myocardial ischemia-reperfusion injury. We randomly divided 30 healthy male New Zealand white rabbits into three groups with 10 rabbits in each group as follows: sham operation group (C group), ischemia-reperfusion group (I/R group), and 2.0% isoflurane preconditioning group (S group). Rabbits in the C group received thoracotomy for 160 min. Rabbits in the I/R group underwent left coronary artery occlusion for 40 min and reperfusion for 120 min. Rabbits in the S group received inhalation of 2.0% isoflurane and 100% oxygen for 2 h; after 24 h, rabbits in this group received the same treatment as that administered to rabbits in the I/R group. We examined the tumor necrosis factor alpha (TNF-α) levels in each group 20 min before occlusion of the left coronary, 20 and 40 min after occlusion of the left coronary artery, and 1 and 2 h after myocardial reperfusion. After reperfusion, immunoblotting was used to measure the myocardial caspase-3 expression levels, and the infarct size was measured using Evans blue and tetrazolium chloride staining. The levels of TNF-α and caspase-3 were lower in the S group than in the I/R group, and the myocardial infarct size decreased in the S group. Thus, isoflurane preconditioning in the delayed phase exerted protective effects by decreasing the myocardial caspase-3 expression and TNF-α production in a rabbit model of ischemia-reperfusion injury.

Comorbidity profiles in association with vitiligo: a nationwide population-based study in Taiwan.

BACKGROUND: The previous literature has demonstrated the association of autoimmune and atopic diseases with vitiligo, but there has been no large-scale nationwide study conducted to confirm this. OBJECTIVES: The present study was conducted to clarify the comorbid profiles in vitiligo patients and thereby better understand their clinical scenarios and underlying pathogenesis. METHODS: This was a retrospective population-based study conducted from 1996 to 2011 via the National Health Insurance Research Database in Taiwan. The differences in the prevalence of multiple autoimmune and atopic diseases between case subjects and controls were analysed by multiple logistic regression method. RESULTS: A total of 14883 vitiligo patients and 59532 controls were enroled. The prevalence of vitiligo was 0.064% and the peak of onset age was 40-59 years old. The non-stratified analysis evidenced a significant association between vitiligo and several comorbid diseases, including alopecia areata, Hashimoto thyroiditis, myasthenia gravis, psoriasis, Graves' disease, Sjögren's syndrome, systemic lupus erythematosus and atopic dermatitis. Vitiligo patients also had higher prevalence of multiple comorbidities than controls. In the age- and gender-stratified analysis, increased risks of systemic lupus erythematosus and Sjögren's syndrome were observed only in subjects aged 60-79. The association of vitiligo with myasthenia gravis and rheumatoid arthritis was identified only in the subgroup aged 20-39 and in females aged 60-79 respectively. CONCLUSION: Our study not only confirmed the significant association of vitiligo with multiple autoimmune and atopic diseases in Taiwan but also disclosed several unique findings, including the much lower prevalence of vitiligo, delayed onset of vitiligo by three decades, different associated comorbidity profiles comparing to westerners and the age- and gender-specific approach for the vitiligo-associated comorbidities.