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Limited studies have explored the relationship between air pollution and rheumatoid arthritis (RA), with the results being somewhat inconsistent.This was a retrospective cohort study that included 322,301 subjects aged 30-50 years, selected from the National Health Insurance Research Database in Taiwan, were followed from 2001 to 2010. We used a time-dependent extended Cox model and incorporated time-dependent variables to estimate the associations between the annual mean concentrations of air pollutants with RA, including carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), particles with an aerodynamic diameter less than 10 μm (PM10), and sulfur dioxide (SO2), and reported the hazard ratio (HR) and 95% confidence interval (CI).Newly diagnosed RA was positively associated with a 100-ppb increase in CO (adjusted HR = 1.17 [95% CI = 1.16, 1.18]), a 10-ppb increase in NO2 (1.54 [1.45, 1.64]), a 10-ppb increase in O3 (1.37 [1.33, 1.41]), and a 1 ppb in SO2 (1.02 [1.00, 1.04]). There was no association between a 10-μg/m increase in PM10 and RA (1.02 [0.99, 1.05]).Our finding suggests that O3 and traffic-related air pollutants (CO and NO2) may be positively associated with incident RA. This is an important finding given that many individuals are exposed to similar levels of O3 and NO2 globally.

Purpose: The goal of this study was to describe the gender difference of grief experience and mood distress among caregivers who cared for terminal cancer patients residing in a hospice ward. Methods: This study recruited 432 caregivers who cared for terminal cancer patients in the hospice ward. Caregivers received telephone interviews 6 months after the patients had died. The Chinese versions of the Beck Depression Inventory (BDI), Beck Anxiety Inventory (BAI), and Inventory of Complicated Grief (ICG) developed in 1995 by Prigerson et al. were employed to assess the mood distress and grief status. Results: Total scores of BDI, BAI, and ICG were significantly higher in females. Six out of twenty-one items of BDI, lack of satisfaction, crying spells, sleep disturbance, fatigability, somatic preoccupation, and loss of libido, showed significantly higher scores in females. According to BAI, inability to relax, dizziness, fear of dying, fright, flushed face, and hot/cold sweats were significantly higher in females. After adjustment for potential confounders, the results show that female gender is associated with higher BDI (regression coefficient 3.24, 95% CI: 1.48–4.99), BAI (3.8; 1.11–6.50), and ICG (4.25, 1.09–7.40). Dichotomizing the BDI, BAI, and ICG into severe and nonsevere cases, the results showed that gender only contributes to severe anxiety status (BAI≧36), but not to severe depression (BDI≧29) or to prolonged grief (ICG≧25). Conclusions: Bereaved females had higher scores for depression and anxiety than males. Female gender is associated with severe anxiety; however, it is not associated with severe depression or prolonged grief. Copyright © 2010 John Wiley & Sons, Ltd.

Background This study assessed the symptom severity of patients with advanced cancer in a palliative care unit and explored the factors associated with symptom improvement. Methods This study was conducted in a palliative care unit in Taiwan between October 2004 and December 2009. Symptom intensity was measured by the “Symptom Reporting Form”, and graded on a scale of 0 to 4 (0 = none, and 4 = extreme). These measures were assessed on the 1st, 3rd, 5th, and 7th Day in the palliative care unit. The study data comprised routine clinical records and patients’ demographic data. Generalized estimating equation (GEE) was used to assess the symptom improvement, and investigate the factors associated with the symptom reporting form scores. Results Among the 824 recruited patients with advanced cancer, pain (78.4 %), anorexia (64.4 %) and constipation (63.5 %)were the most common and severe symptom. After controlling for other factors in the multivariate GEE model, the day of palliative care administration was a significant factor associated with all of the scales, except Days 7 on the dyspnoea and oedema scales and Day 5 on the anxiety scale. In addition, patients aged ≥ 65 years exhibited significantly lower scores on the pain, sleep disturbance, depression, and anxiety scales than did those aged

Accurate prognostication in advanced cancer may facilitate better palliative care. An objective marker may be more applicable and appropriate than a subjective evaluation by physicians. The aim of this study was to evaluate liver function tests as useful prognostic factors for survival in patients with advanced cancer. We recruited advanced cancer patients from January 2007 to December 2009. Data on age, sex, cancer diagnosis, site of metastases, clinical symptoms, and performance status were collected at the time of admission to the palliative care unit. Analyzed laboratory data were obtained on the Day 1 of admission to the palliative care unit. A total of 522 patients were enrolled; 322 (61.7%) of them were males. The mean age was 60.6 ± 13.2 years. Multiple logistic regression analysis adjusting for age and sex demonstrated aspartate transaminase (AST) > 80 IU/L [odds ratio (OR) = 2.01, p = 0.010] and alanine transaminase > 80 IU/L (OR = 1.89, p = 0.047) were independently significant prognostic factors of death within 14 days. AST > 80 IU/L (OR = 3.67, p = 0.017) and albumin

Hypertension leads to structural and functional changes at baroreceptor synapses in the medial nucleus tractus solitarius (NTS), but the underlying molecular mechanisms remain unknown. Our previous studies show that brain-derived neurotrophic factor (BDNF) is abundantly expressed by rat nodose ganglion (NG) neurons, including baroreceptor afferents and their central terminals in the medial NTS. We hypothesized that hypertension leads to upregulation of BDNF expression in NG neurons. To test this hypothesis, we used two mechanistically distinct models of hypertension, the spontaneously hypertensive rat (SHR) and the deoxycorticosterone acetate (DOCA)-salt rat. Young adult SHRs, whose blood pressure was significantly elevated compared with age-matched Wistar-Kyoto (WKY) control rats, exhibited dramatic upregulation of BDNF mRNA and protein in the NG. BDNF transcripts from exon 4, known to be regulated by activity, and exon 9 (protein-coding region) showed the largest increases. Electrical stimulation of dispersed NG neurons with patterns that mimic baroreceptor activity during blood pressure elevations led to increases in BDNF mRNA that were also mediated through promoter 4. The increase in BDNF content of the NG in vivo was associated with a significant increase in the percentage of BDNF-immunoreactive NG neurons. Moreover, upregulation of BDNF in cell bodies of NG neurons was accompanied by a significant increase in BDNF in the NTS region, the primary central target of NG afferents. A dramatic increase in BDNF in the NG was also detected in DOCA-salt hypertensive rats. Together, our study identifies BDNF as a candidate molecular mediator of activity-dependent changes at baroafferent synapses during hypertension.

Activity of arterial baroreceptors is modulated by neurohumoral factors, including nitric oxide (NO), released from endothelial cells. Baroreceptor reflex responses can also be modulated by NO signaling in the brainstem nucleus tractus solitarius (NTS), the primary central target of cardiovascular afferents. Our recent studies indicate that brain-derived neurotrophic factor (BDNF) is abundantly expressed by developing and adult baroreceptor afferents in vivo, and released from cultured nodose ganglion (NG) neurons by patterns of baroreceptor activity. Using electrical field stimulation and ELISA in situ, we show that exogenous NO nearly abolishes BDNF release from newborn rat NG neurons in vitro stimulated with single pulses delivered at 6 Hz, but not 2-pulse bursts delivered at the same 6-Hz frequency, that corresponds to a rat heart rate. Application of L-NAME, a specific inhibitor of endogenous NO synthases, does not have any significant effect on activity-dependent BDNF release, but leads to upregulation of BDNF expression in an activity-dependent manner. The latter effect suggests a novel mechanism of homeostatic regulation of activity-dependent BDNF expression with endogenous NO as a key player. The exogenous NO-mediated effect does not involve the cGMP-protein kinase G (PKG) pathway, but is largely inhibited by N-ethylmaleimide and TEMPOL that are known to prevent S-nitrosylation. Together, our current data identify previously unknown mechanisms regulating BDNF availability, and point to NO as a likely regulator of BDNF at baroafferent synapses in the NTS.