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Despite dietary factors being implicated in the pathogenesis of inflammatory bowel disease (IBD), nutritional therapy, outside of exclusive enteral nutrition (EEN), has not had a defined role within the treatment paradigm of pediatric IBD within IBD centers. Based on emerging data, Seattle Children's Hospital IBD Center has developed an integrated dietary program incorporating the specific carbohydrate diet (SCD) into its treatment paradigm. This treatment paradigm uses the SCD as primary therapy as well as adjunctive therapy for the treatment of IBD. The aim of this study was to evaluate the potential effects of the SCD on clinical outcomes and laboratory studies of pediatric patients with Crohn's disease (CD) and ulcerative colitis (UC). In this retrospective study, we reviewed the medical records of patients with IBD on SCD. We analyzed 26 children on the SCD: 20 with CD and 6 with UC. Duration of the dietary therapy ranged from 3 to 48 mo. In patients with active CD (Pediatric Crohn's Disease activity index [PCDAI] >10), PCDAI dropped from 32.8 ± 13.2 at baseline to 20.8 ± 16.6 by 4 ± 2 wk, and to 8.8 ± 8.5 by 6 mo. The mean Pediatric Ulcerative Colitis Activity Index for patients with active UC decreased from a baseline of 28.3 ± 10.3 to 20.0 ± 17.3 at 4 ± 2 wk, to 18.3 ± 31.7 at 6 mo. This retrospective review provides evidence that the SCD can be integrated into a tertiary care center and may improve clinical and laboratory parameters for pediatric patients with nonstructuring, nonpenetrating CD as well as UC. Further prospective studies are needed to fully assess the safety and efficacy of the SCD in pediatric patients with IBD.

Crohn's disease (CD) is a chronic idiopathic inflammatory intestinal disorder associated with fecal dysbiosis. Fecal microbial transplant (FMT) is a potential therapeutic option for individuals with CD based on the hypothesis that changing the fecal dysbiosis could promote less intestinal inflammation.MethodsNine patients, aged 12 to 19 years, with mild-to-moderate symptoms defined by Pediatric Crohn's Disease Activity Index (PCDAI of 10–29) were enrolled into a prospective open-label study of FMT in CD (FDA IND 14942). Patients received FMT by nasogastric tube with follow-up evaluations at 2, 6, and 12 weeks. PCDAI, C-reactive protein, and fecal calprotectin were evaluated at each study visit.ResultsAll reported adverse events were graded as mild except for 1 individual who reported moderate abdominal pain after FMT. All adverse events were self-limiting. Metagenomic evaluation of stool microbiome indicated evidence of FMT engraftment in 7 of 9 patients. The mean PCDAI score improved with patients having a baseline of 19.7 ± 7.2, with improvement at 2 weeks to 6.4 ± 6.6 and at 6 weeks to 8.6 ± 4.9. Based on PCDAI, 7 of 9 patients were in remission at 2 weeks and 5 of 9 patients who did not receive additional medical therapy were in remission at 6 and 12 weeks. No or modest improvement was seen in patients who did not engraft or whose microbiome was most similar to their donor.ConclusionsThis is the first study to demonstrate that FMT for CD may be a possible therapeutic option for CD. Further prospective studies are required to fully assess the safety and efficacy of the FMT in patients with CD.

This study examines the potential racial disparity in postpartum depression (PPD) symptoms among a cohort of non-Hispanic white and African American women after taking into consideration the influence of socioeconomic status (SES). Participants ( N  = 299) were recruited from maternity clinics serving rural counties, with oversampling of low SES and African Americans. The Edinburgh Postnatal Depression Scale (EPDS) was administered 1 and 6 months postpartum, and subjective SES scale at 6 months postpartum. Demographic information was collected during enrollment and 1 month postpartum, with updates at 6 months postpartum. Separate logistic regressions were conducted for 1 and 6 month time points for minor-major PPD (EPDS ≥ 10) and major PPD (EPDS > 12); with marital status, poverty, education, subjective SES, and race predictors entered in block sequence. After including all other predictors, race was not a significant predictor of minor-major or major PPD at 1 or 6 months postpartum. Subjective SES was the most consistent predictor of PPD, being significantly associated with minor-major PPD and major PPD at 6 months postpartum, with higher subjective SES indicating lower odds of PPD, even after accounting for all other predictors. This study shows that significant racial disparities were not observed for minor-major or major PPD criteria at 1 or 6 months postpartum. The most consistent and significant predictor of PPD was subjective SES. Implications of these findings for future research, as well as PPD screening and intervention are discussed.

Background: The mechanisms underlying the relationship between particulate matter (PM) air pollution and cardiac disease are not fully understood. Objectives: We examined the effects and time course of exposure to fine PM [aerodynamic diameter < 2.5 μm (PM2.5)] on cardiac arrhythmia in 105 middle-age community-dwelling healthy nonsmokers in central Pennsylvania. Methods: The 24-hr beat-to-beat electrocardiography data were obtained using a high-resolution Holter system. After visually identifying and removing artifacts, we summarized the total number of premature ventricular contractions (PVCs) and premature atrial contractions (PACs) for each 30-min segment. A personal PM₂₄ nephelometer was used to measure individual-level real-time PM₂₄ exposures for 24 hr. We averaged these data to obtain 30-min average time— specific PM₂₄ exposures. Distributed lag models under the framework of negative binomial regression and generalized estimating equations were used to estimate the rate ratio between 10 μg/m³ increases in average PM₂₄ over 30-min intervals and ectopy counts. Results: The mean ± SD age of participants was 56 ± 8 years, with 40% male and 73% non-Hispanic white. The 30-min mean ± SD for PM₂.₄ exposure was 13 ± 22 μg/m³ , and PAC and PVC counts were 0.92 ± 4.94 and 1.22 ± 7.18. Increases of 10 μg/m³ in average PM₂₄ concentrations during the same 30 min or the previous 30 min were associated with 8% and 3% increases in average PVC counts, respectively. PM₂₄ was not significantly associated with PAC count. Conclusion: PM₂.₄ exposure within approximately 60 min was associated with increased PVC counts in healthy individuals.

IntroductionOral pirfenidone reduces lung function decline and mortality in patients with idiopathic pulmonary fibrosis (IPF). Systemic exposure can have significant side effects, including nausea, rash, photosensitivity, weight loss and fatigue. Reduced doses may be suboptimal in slowing disease progression.MethodsThis phase 1b, randomised, open-label, dose–response trial at 25 sites in six countries (Australian New Zealand Clinical Trials Registry (ANZCTR) registration number ACTRN12618001838202) assessed safety, tolerability and efficacy of inhaled pirfenidone (AP01) in IPF. Patients diagnosed within 5 years, with forced vital capacity (FVC) 40%–90% predicted, and intolerant, unwilling or ineligible for oral pirfenidone or nintedanib were randomly assigned 1:1 to nebulised AP01 50 mg once per day or 100 mg two times per day for up to 72 weeks.ResultsWe present results for week 24, the primary endpoint and week 48 for comparability with published trials of antifibrotics. Week 72 data will be reported as a separate analysis pooled with the ongoing open-label extension study. Ninety-one patients (50 mg once per day: n=46, 100 mg two times per day: n=45) were enrolled from May 2019 to April 2020. The most common treatment-related adverse events (frequency, % of patients) were all mild or moderate and included cough (14, 15.4%), rash (11, 12.1%), nausea (8, 8.8%), throat irritation (5, 5.5%), fatigue (4, 4.4%) and taste disorder, dizziness and dyspnoea (three each, 3.3%). Changes in FVC % predicted over 24 and 48 weeks, respectively, were −2.5 (95% CI −5.3 to 0.4, −88 mL) and −4.9 (−7.5 to −2.3,–188 mL) in the 50 mg once per day and 0.6 (−2.2 to 3.4, 10 mL) and −0.4 (−3.2 to 2.3, −34 mL) in the 100 mg two times per day group.DiscussionSide effects commonly associated with oral pirfenidone in other clinical trials were less frequent with AP01. Mean FVC % predicted remained stable in the 100 mg two times per day group. Further study of AP01 is warranted.Trial registration numberACTRN12618001838202 Australian New Zealand Clinical Trials Registry.

Background: The mechanisms for the relationship between particulate pollution and cardiac disease are not fully understood. Objective: We examined the effects and time course of exposure to fine particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) on ventricular repolarization of 106 nonsmoking adults who were living in communities in central Pennsylvania. Methods: The 24-hr beat-to-beat electrocardiogram (ECG) data were obtained using a high-resolution 12-lead Holter system. After visually identifying and removing artifacts and arrhythmic beats, we summarized normal beat-to-beat QTs from each 30-min segment as heart rate (HR)-corrected QT measures: QT prolongation index (QTI), Bazett's HR-corrected QT (QTcB), and Fridericia's HR-corrected QT (QTcF). A personal PM2.5 monitor was used to measure individual-level real-time PM2.5 exposures for 24 hr. We averaged these data and used 30-min time-specific average PM2.5 exposures. Results: The mean age of the participants was 56 ± 8 years, with 41% male and 74% white. The means ± SDs for QTI, QTcB, and QTcF were 111 ± 6.6, 438 ± 23 msec, and 422 ± 22 msec, respectively; and for PM2.5, the mean ± SD was 14 ± 22 μg/m3. We used distributed lag models under a framework of linear mixed-effects models to assess the autocorrelation-corrected regression coefficients (β) between 30-min PM2.5 and the HR-corrected QT measures. Most of the adverse ventricular repolarization effects from PM2.5 exposure occurred within 3–4 hr. The multivariable adjusted β (SE, p-value) due to a 10-μg/m3 increase in lag 7 PM2.5 on QTI, QTcB, and QTcF were 0.08 (0.04, p < 0.05), 0.22 (0.08, p < 0.01), and 0.09 (0.05, p < 0.05), respectively. Conclusions: Our results suggest a significant adverse effect of PM2.5 on ventricular repolarization. The time course of the effect is within 3–4 hr of elevated PM2.5.

In 106 community-dwelling middle-aged non-smokers we examined the time-course and the acute effects of fine particles (PM 2.5 ) on heart rate variability (HRV), which measures cardiac autonomic modulation (CAM). Twenty-four hours beat-to-beat ECG data were visually examined. Artifacts and arrhythmic beats were removed. Normal beat-to-beat RR data were used to calculate HRV indices. Personal PM 2.5 nephelometry was used to estimate 24-h individual-level real-time PM 2.5 exposures. We use linear mixed-effects models to assess autocorrelation- and other major confounder-adjusted regression coefficients between 1–6 h moving averages of PM 2.5 and HRV indices. The increases in preceding 1–6 h moving averages of PM 2.5 was significantly associated with lower HF, LF, and SDNN, with the largest effect size at 4–6 h moving averages and smallest effects size at 1 h moving average. For example, a 10  μ g/m 3 increase in 1 and 6-h moving averages was associated with 0.027 and 0.068 ms 2 decrease in log-HF, respectively, and with 0.024 and 0.071 ms 2 decrease in log-LF, respectively, and with 0.81 and 1.75 ms decrease in SDNN, respectively (all P -values <0.05). PM 2.5 exposures are associated with immediate impairment of CAM. With a time-course of within 6 h after elevated PM 2.5 exposure, with the largest effects around 4–6 h.

To describe preloss and postloss grief symptoms among family members of nursing home (NH) residents with advanced dementia, and to identify predictors of greater postloss grief symptoms. Prospective cohort study. 22 NHs in the greater Boston area. 123 family members of NH residents who died with advanced dementia. Preloss grief was measured at baseline, and postloss grief was measured 2 and 7 months postloss using the Prolonged Grief Disorder Scale. Independent variables included resident and family member sociodemographic characteristics, resident comfort, acute illness, acute care prior to death, family member depression, and family member understanding of dementia and of resident's prognosis. Levels of preloss and postloss grief were relatively stable from baseline to 7 months postloss. Feelings of separation and yearning were the most prominent grief symptoms. After multivariable adjustment, greater preloss grief and the family member having lived with the resident prior to NH admission were the only factors independently associated with greater postloss grief 7 months after resident death. The pattern of grieving for some family members of NH residents with advanced dementia is prolonged and begins before resident death. Identification of family members at risk for postloss grief during the preloss period may help guide interventions aimed at lessening postloss grief.

This study examined mortality among patients with advanced dementia who resided in nursing homes. More than half the patients died in 6 months. Pneumonia, febrile episodes, and eating problems were frequent harbingers of death. This study examined mortality among patients with advanced dementia who resided in nursing homes. More than half the patients died in 6 months. Pneumonia, febrile episodes, and eating problems were frequent harbingers of death. A growing number of Americans are dying with dementia. 1 Prior work suggests that patients with advanced dementia are under-recognized as being at high risk for death and receive suboptimal palliative care. 2 – 4 The lack of information characterizing the final stage of dementia may impede the quality of care provided to these patients. Our current understanding of end-stage dementia is based on findings from retrospective studies, 3 – 7 cross-sectional studies, 8 or investigations of hospitalized patients. 9 – 12 The clinical course of advanced dementia has not been described in a rigorous, prospective manner. The incidence of clinical complications, the extent of physical suffering, and . . .

The occurrence of Parkinson's disease (PD) is known to be associated both with increased nigrostriatal iron content and with low serum cholesterol and PD, but there has been no study to determine a potential relationship between these two factors. High-resolution MRI (T1-, T2, and multiple echo T2*-weighted imaging) and fasting lipid levels were obtained from 40 patients with PD and 29 healthy controls. Iron content was estimated from mean R2* values (R2* = 1/T2*) calculated for each nigrostriatal structure including substantia nigra, caudate, putamen, and globus pallidus. This was correlated with serum cholesterol levels after controlling for age, gender, and statin use. In patients with PD, higher serum cholesterol levels were associated with lower iron content in the substantia nigra (R = -0.43, p = 0.011 for total-cholesterol, R = -0.31, p = 0.080 for low-density lipoprotein) and globus pallidus (R = -0.38, p = 0.028 for total-cholesterol, R = -0.27, p = 0.127 for low-density lipoprotein), but only a trend toward significant association of higher total-cholesterol with lower iron content in the striatum (R = -0.34, p = 0.052 for caudate; R = -0.32, p = 0.061 for putamen). After adjusting for clinical measures, the cholesterol-iron relationships held or became even stronger in the substantia nigra and globus pallidus, but weaker in the caudate and putamen. There was no significant association between serum cholesterol levels and nigrostriatal iron content for controls. The data show that higher serum total-cholesterol concentration is associated with lower iron content in substantia nigra and globus pallidus in Parkinson's disease patients. Further studies should investigate whether this is mechanistic or epiphenomenological relationship.