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We aimed to identify the minimum number of ambulatory blood pressure (ABP) measures to accurately determine daytime and nighttime systolic blood pressure (BP) averages and nocturnal dipping status (i.e., relative daytime:nighttime change). A total of 43 midlife participants wore an ABP monitor for 24 h with measurements every 20/30 min during the daytime/nighttime, as identified by a sleep diary. We calculated daytime/nighttime systolic BP average and dipping status from all available measurements per participant (i.e., normative data). We then calculated daytime and nighttime BP per participant based on a random selection of 8-20 and 4-10 measurements and replicated random selections 1,000 times. We calculated accuracy by checking the proportion from 1,000 different randomly selected samples for a particular number of measurements that systolic BP was ±5 mmHg of normative data, and dipping status remained unchanged for each participant compared with the normative value. The best fit for the regression model estimated the minimal number of measurements for an accuracy of 95% in BP averages. For a 95% accuracy in estimating daytime and nighttime systolic BP, 11 daytime and 8 nighttime measurements were required. The highest accuracy for dipping status was 91.6 ± 13.4% using 20 daytime and 10 nighttime measures, while the lowest was (83.4 ± 15.1%) using 8 daytime and 4 nighttime measures. In midlife adults, 11 daytime and 8 nighttime measurements are likely enough to calculate average systolic BPs accurately. However, no minimum number is suggested to accurately calculate dipping status.NEW & NOTEWORTHY We found that a minimum of 11 blood pressure (BP) measures are necessary to calculate an accurate average daytime BP, and 8 nighttime measures are necessary to calculate an accurate nighttime average if 95% accuracy is acceptable. Regarding BP dipping status, the current recommendations (20 daytime/7 nighttime) inaccurately classified the dipping status 10.5% of the time, suggesting that guidelines may need to be updated to classify patients as nocturnal dippers or nondippers correctly.
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Monitorização Ambulatorial da Pressão Arterial , Pressão Sanguínea , Ritmo Circadiano , Humanos , Monitorização Ambulatorial da Pressão Arterial/métodos , Pessoa de Meia-Idade , Pressão Sanguínea/fisiologia , Masculino , Feminino , Reprodutibilidade dos Testes , Adulto , Idoso , Fatores de Tempo , Valor Preditivo dos Testes , Sono/fisiologia , Hipertensão/fisiopatologia , Hipertensão/diagnósticoRESUMO
The time of day that we eat is increasingly recognized as contributing as importantly to overall health as the amount or quality of the food we eat. The endogenous circadian clock has evolved to promote intake at optimal times when an organism is intended to be awake and active; but electric lights and abundant food allow eating around the clock with deleterious health outcomes. In this review, we highlight literature pertaining to the effects of food timing on health, beginning with animal models and then translation into human experiments. We emphasize the pitfalls and opportunities that technological advances bring in bettering understanding of eating behaviors and their association with health and disease. There is great promise for restricting the timing of food intake both in clinical interventions and in public health campaigns for improving health via nonpharmacological therapies.
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Introduction: The research criteria for prodromal Parkinson disease (pPD) depends on prospectively validated clinical inputs with large effect sizes and/or high prevalence. Neither traumatic brain injury (TBI), post-traumatic stress disorder (PTSD), nor chronic pain are currently included in the calculator, despite recent evidence of association with pPD. These conditions are widely prevalent, co-occurring, and already known to confer risk of REM behavior disorder (RBD) and PD. Few studies have examined PD risk in the context of TBI and PTSD; none have examined chronic pain. This study aimed to measure the risk of pPD caused by TBI, PTSD, and chronic pain. Methods: 216 US Veterans were enrolled who had self-reported recurrent or persistent pain for at least three months. Of these, 44 met criteria for PTSD, 39 for TBI, and 41 for all three conditions. Several pain, sleep, affective, and trauma questionnaires were administered. Participants' history of RBD was determined via self-report, with a subset undergoing confirmatory video polysomnography. Results: A greater proportion of Veterans with chronic pain met criteria for RBD (36 % vs. 10 %) and pPD (18.0 % vs. 8.3 %) compared to controls. Proportions were increased in RBD (70 %) and pPD (27 %) when chronic pain co-occurred with TBI and PTSD. Partial effects were seen with just TBI or PTSD alone. When analyzed as continuous variables, polytrauma symptom severity correlated with pPD probability (r = 0.28, P = 0.03). Conclusion: These data demonstrate the potential utility of chronic pain, TBI, and PTSD in the prediction of pPD, and the importance of trauma-related factors in the pathogenesis of PD.
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Adiponectin has vascular anti-inflammatory and protective effects. Although adiponectin protects against the development of albuminuria, historically, the focus has been on podocyte protection within the glomerular filtration barrier (GFB). The first barrier to albumin in the GFB is the endothelial glycocalyx (eGlx), a surface gel-like barrier covering glomerular endothelial cells (GEnCs). In diabetes, eGlx dysfunction occurs before podocyte damage; hence, we hypothesized that adiponectin could protect from eGlx damage to prevent early vascular damage in diabetic kidney disease (DKD). Globular adiponectin (gAd) activated AMPK signaling in human GEnCs through AdipoR1. It significantly reduced eGlx shedding and the tumor necrosis factor-α (TNF-α)-mediated increase in syndecan-4 (SDC4) and MMP2 mRNA expression in GEnCs in vitro. It protected against increased TNF-α mRNA expression in glomeruli isolated from db/db mice and against expression of genes associated with glycocalyx shedding (namely, SDC4, MMP2, and MMP9). In addition, gAd protected against increased glomerular albumin permeability (Ps'alb) in glomeruli isolated from db/db mice when administered intraperitoneally and when applied directly to glomeruli (ex vivo). Ps'alb was inversely correlated with eGlx depth in vivo. In summary, adiponectin restored eGlx depth, which was correlated with improved glomerular barrier function, in diabetes.
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Adiponectina , Diabetes Mellitus Tipo 2 , Glicocálix , Glomérulos Renais , Animais , Glicocálix/metabolismo , Glicocálix/efeitos dos fármacos , Adiponectina/metabolismo , Adiponectina/genética , Camundongos , Diabetes Mellitus Tipo 2/metabolismo , Glomérulos Renais/metabolismo , Glomérulos Renais/patologia , Glomérulos Renais/efeitos dos fármacos , Humanos , Nefropatias Diabéticas/metabolismo , Nefropatias Diabéticas/patologia , Células Endoteliais/metabolismo , Células Endoteliais/efeitos dos fármacos , Masculino , Barreira de Filtração Glomerular/metabolismo , Barreira de Filtração Glomerular/efeitos dos fármacos , Fator de Necrose Tumoral alfa/metabolismo , Sindecana-4/metabolismo , Sindecana-4/genética , Modelos Animais de Doenças , Camundongos Endogâmicos C57BLRESUMO
BACKGROUND: Diabetes mellitus is a chronic disease which is detrimental to cardiovascular health, often leading to secondary microvascular complications, with huge global health implications. Therapeutic interventions that can be applied to multiple vascular beds are urgently needed. Diabetic retinopathy (DR) and diabetic kidney disease (DKD) are characterised by early microvascular permeability changes which, if left untreated, lead to visual impairment and renal failure, respectively. The heparan sulphate cleaving enzyme, heparanase, has previously been shown to contribute to diabetic microvascular complications, but the common underlying mechanism which results in microvascular dysfunction in conditions such as DR and DKD has not been determined. METHODS: In this study, two mouse models of heparan sulphate depletion (enzymatic removal and genetic ablation by endothelial specific Exotosin-1 knock down) were utilized to investigate the impact of endothelial cell surface (i.e., endothelial glycocalyx) heparan sulphate loss on microvascular barrier function. Endothelial glycocalyx changes were measured using fluorescence microscopy or transmission electron microscopy. To measure the impact on barrier function, we used sodium fluorescein angiography in the eye and a glomerular albumin permeability assay in the kidney. A type 2 diabetic (T2D, db/db) mouse model was used to determine the therapeutic potential of preventing heparan sulphate damage using treatment with a novel heparanase inhibitor, OVZ/HS-1638. Endothelial glycocalyx changes were measured as above, and microvascular barrier function assessed by albumin extravasation in the eye and a glomerular permeability assay in the kidney. RESULTS: In both models of heparan sulphate depletion, endothelial glycocalyx depth was reduced and retinal solute flux and glomerular albumin permeability was increased. T2D mice treated with OVZ/HS-1638 had improved endothelial glycocalyx measurements compared to vehicle treated T2D mice and were simultaneously protected from microvascular permeability changes associated with DR and DKD. CONCLUSION: We demonstrate that endothelial glycocalyx heparan sulphate plays a common mechanistic role in microvascular barrier function in the eye and kidney. Protecting the endothelial glycocalyx damage in diabetes, using the novel heparanase inhibitor OVZ/HS-1638, effectively prevents microvascular permeability changes associated with DR and DKD, demonstrating a novel systemic approach to address diabetic microvascular complications.
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Diabetes Mellitus Tipo 2 , Angiopatias Diabéticas , Nefropatias Diabéticas , Glucuronidase , Animais , Camundongos , Glicocálix/metabolismo , Nefropatias Diabéticas/etiologia , Nefropatias Diabéticas/prevenção & controle , Heparitina Sulfato/metabolismo , Heparitina Sulfato/farmacologia , Albuminas/farmacologia , Angiopatias Diabéticas/etiologia , Angiopatias Diabéticas/prevenção & controle , Angiopatias Diabéticas/metabolismo , Diabetes Mellitus Tipo 2/complicações , Diabetes Mellitus Tipo 2/tratamento farmacológico , Diabetes Mellitus Tipo 2/metabolismoRESUMO
Sleep fragmentation (SF) disrupts normal biological rhythms and has major impacts on cardiovascular health; however, it has never been shown to be a risk factor involved in the transition from cardiac hypertrophy to heart failure (HF). We now demonstrate devastating effects of SF on hypertrophic cardiomyopathy (HCM). We generated a transgenic mouse model harboring a patient-specific myosin binding protein C3 (MYBPC3) variant displaying HCM, and measured the progression of pathophysiology in the presence and absence of SF. SF induces mitochondrial damage, sarcomere disarray, and apoptosis in HCM mice; these changes result in a transition of hypertrophy to an HF phenotype by chiefly targeting redox metabolic pathways. Our findings for the first time show that SF is a risk factor for HF transition and have important implications in clinical settings where HCM patients with sleep disorders have worse prognosis, and strategic intervention with regularized sleep patterns might help such patients.
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PURPOSE: To understand the spectrum and volume of classical hematology (CH) referrals to hematology clinics at a National Cancer Institute (NCI)-designated cancer center (CC) to plan for the delivery of effective and equitable care for this population. METHODS: One referral office at the Academic CC located in Bexar County, TX, handles all adult hematology referrals. From October 1, 2021, to September 30, 2022, all nonmalignant hematology (MH) referrals were triaged daily to define the category of CH problem. Declined referrals (confirmed at triage that no CH problem was evident) are included as part of this analysis. Electronic consultation (opinion rendered without patient seen) at our CC is available and is not part of this analysis. RESULTS: One thousand nine hundred forty-five CH referrals were received in the 12-month period. Seventy-six referrals (3.9%) were declined. During the study period, there were 2,289 medical oncology referrals and 779 referrals for MH. CH referrals therefore comprise 39% of all hematology-oncology referrals and 71% of all hematology referrals at the CC. Anemia and thrombotic disorders were the most common categories of the accepted CH referrals at 487 (26%) and 393 (21%), respectively. Video visits were used for 447 of all CH referrals (23%), and the rest were in person. CONCLUSION: Nearly 40% of all referrals to hematology and medical oncology at our NCI-designated CC are for CH. Effective management of the CH population of patients will allow ideal care for CH problems and also allow cancer-focused care to improve.
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Hematologia , Neoplasias , Adulto , Estados Unidos/epidemiologia , Humanos , National Cancer Institute (U.S.) , Encaminhamento e Consulta , Triagem , Oncologia , Neoplasias/complicações , Neoplasias/epidemiologia , Neoplasias/terapiaRESUMO
Podocin is a key membrane scaffolding protein of the kidney podocyte essential for intact glomerular filtration. Mutations in NPHS2, the podocin-encoding gene, represent the commonest form of inherited nephrotic syndrome (NS), with early, intractable kidney failure. The most frequent podocin gene mutation in European children is R138Q, causing retention of the misfolded protein in the endoplasmic reticulum. Here, we provide evidence that podocin R138Q (but not wild-type podocin) complexes with the intermediate filament protein keratin 8 (K8) thereby preventing its correct trafficking to the plasma membrane. We have also identified a small molecule (c407), a compound that corrects the Cystic Fibrosis Transmembrane Conductance Regulator protein defect, that interrupts this complex and rescues mutant protein mistrafficking. This results in both the correct localization of podocin at the plasma membrane and functional rescue in both human patient R138Q mutant podocyte cell lines, and in a mouse inducible knock-in model of the R138Q mutation. Importantly, complete rescue of proteinuria and histological changes was seen when c407 was administered both via osmotic minipumps or delivered orally prior to induction of disease or crucially via osmotic minipump two weeks after disease induction. Thus, our data constitute a therapeutic option for patients with NS bearing a podocin mutation, with implications for other misfolding protein disorders. Further studies are necessary to confirm our findings.
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Síndrome Nefrótica , Animais , Criança , Humanos , Camundongos , Peptídeos e Proteínas de Sinalização Intracelular/genética , Queratina-8/genética , Proteínas de Membrana/genética , Proteínas de Membrana/metabolismo , Chaperonas Moleculares/genética , Mutação , Síndrome Nefrótica/tratamento farmacológico , Síndrome Nefrótica/genética , Síndrome Nefrótica/patologiaRESUMO
OBJECTIVE: Given the complex interaction among the circadian system, energy metabolism, and obesity, the authors tested whether having obesity impacts the circadian variation in energy and glucose metabolism in humans. METHODS: Participants with BMI either in the healthy weight or obesity ranges were studied in a 5-day, in-laboratory protocol that equally distributed behaviors (i.e., sleep, eating, exercise) across 24 h. Energy metabolism was measured at rest and during a standardized exercise bout and blood was sampled before and after each identical study meal to assess glucose and insulin levels. RESULTS: In those with a healthy weight, the circadian nadir of energy expenditure, during both rest and exercise, occurred when participants would normally be asleep. However, in those with obesity, this nadir appears to occur during the habitual wake period. Differences in glucose regulation also depended on the circadian phase, such that individuals with obesity appeared to have relatively greater glucose intolerance during the circadian day and produced less insulin during the circadian night. CONCLUSIONS: Obesity is associated with altered circadian energy and glucose metabolism. Understanding and addressing these associations could lead to strategies that improve body weight and metabolic health in people with obesity.
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Ritmo Circadiano , Glucose , Humanos , Ritmo Circadiano/fisiologia , Glicemia/metabolismo , Obesidade/metabolismo , Insulina , Metabolismo Energético/fisiologiaRESUMO
STUDY OBJECTIVES: Averaged nighttime blood pressure (BP) is superior to daytime BP for cardiovascular risk stratification, and the relative change between daytime/nighttime BP (dipping%) significantly predicts cardiovascular risk. Newer reports suggest that 4 measurements at night may be enough for cardiovascular risk stratification. Since BP oscillates across the night, the temporal distribution of measurements across the night may impact nighttime BP and dipping%. Therefore, we compared average nighttime BP and dipping% when using measurements in the first half (1st-half), second (2nd-half), and a combination of both (combined). METHODS: Forty-three (17 females and twenty-six males) midlife adults aged 50±10 years old wore an ambulatory BP monitor for 24 hours at home, programmed to measure BP every 20 minutes when scheduled for daytime and every 30 minutes during a self-selected 8-hour nighttime for time-in-bed. We compared the nighttime BP averages and dipping% when using either the first four measurements from the 1st-half or 2nd-half of the nighttime and combined. RESULTS: Nighttime Systolic BP was significantly different across 1st-half, 2nd-half, and combined (111±9 vs.107±11 vs. 109±9 mmHg, p<0.01), respectively, with significant pairwise differences across all categories (p<0.01 for each). Systolic BP dipping% was significantly different across 1st-half, 2nd-half, and combined (9.9±5.5 vs.13.5±6.4 vs. 11.7±5.0 %, p<0.01), respectively, with significant pairwise differences across all categories (p<0.01 for each. Diastolic BP and diastolic dipping% were similar across the three different bins. CONCLUSION: In midlife adults, systolic nighttime BP and dipping% may depend upon when BP measurements are taken during the night.
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BACKGROUND: Shiga toxin (Stx)-producing Escherichia coli hemolytic uremic syndrome (STEC-HUS) is the leading cause of acute kidney injury in children, with an associated mortality of up to 5%. The mechanisms underlying STEC-HUS and why the glomerular microvasculature is so susceptible to injury following systemic Stx infection are unclear. METHODS: Transgenic mice were engineered to express the Stx receptor (Gb3) exclusively in their kidney podocytes (Pod-Gb3) and challenged with systemic Stx. Human glomerular cell models and kidney biopsies from patients with STEC-HUS were also studied. FINDINGS: Stx-challenged Pod-Gb3 mice developed STEC-HUS. This was mediated by a reduction in podocyte vascular endothelial growth factor A (VEGF-A), which led to loss of glomerular endothelial cell (GEnC) glycocalyx, a reduction in GEnC inhibitory complement factor H binding, and local activation of the complement pathway. Early therapeutic inhibition of the terminal complement pathway with a C5 inhibitor rescued this podocyte-driven, Stx-induced HUS phenotype. CONCLUSIONS: This study potentially explains why systemic Stx exposure targets the glomerulus and supports the early use of terminal complement pathway inhibition in this devastating disease. FUNDING: This work was supported by the UK Medical Research Council (MRC) (grant nos. G0901987 and MR/K010492/1) and Kidney Research UK (grant nos. TF_007_20151127, RP42/2012, and SP/FSGS1/2013). The Mary Lyon Center is part of the MRC Harwell Institute and is funded by the MRC (A410).
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Infecções por Escherichia coli , Síndrome Hemolítico-Urêmica , Nefropatias , Podócitos , Escherichia coli Shiga Toxigênica , Criança , Humanos , Camundongos , Animais , Podócitos/metabolismo , Podócitos/patologia , Toxina Shiga/genética , Toxina Shiga/metabolismo , Toxina Shiga/uso terapêutico , Fator A de Crescimento do Endotélio Vascular/metabolismo , Fator A de Crescimento do Endotélio Vascular/uso terapêutico , Infecções por Escherichia coli/complicações , Infecções por Escherichia coli/tratamento farmacológico , Infecções por Escherichia coli/metabolismo , Síndrome Hemolítico-Urêmica/tratamento farmacológico , Síndrome Hemolítico-Urêmica/metabolismo , Síndrome Hemolítico-Urêmica/patologia , Escherichia coli Shiga Toxigênica/metabolismo , Ativação do Complemento , Nefropatias/patologiaRESUMO
[This corrects the article DOI: 10.3389/fpsyt.2021.687615.].
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Aim: To investigate potential pharmacokinetic interactions between atogepant and esomeprazole. Methods: Atogepant, esomeprazole, or both were administered to 32 healthy adults in an open-label, nonrandomized, crossover study. Systemic exposure (area under the plasma concentration-time curve [AUC] and peak plasma concentration [Cmax]) for atogepant administered in combination versus alone were compared using a linear mixed effects model. Results: Coadministration with esomeprazole delayed atogepant time to Cmax by â¼1.5 h and reduced Cmax by â¼23% with no statistically significant change in AUC compared with atogepant alone. Administration of atogepant 60 mg alone or in combination with esomeprazole 40 mg was well tolerated in healthy adults. Conclusion: Esomeprazole had no clinically meaningful effect on atogepant pharmacokinetics. Clinical Trial Registration: unregistered phase I study.
A clinical study was conducted in 32 healthy adults to evaluate the possibility of interactions between atogepant, a new drug for the prevention of migraine, and esomeprazole, a drug used to reduce stomach acid. The participants of the study were given each drug alone and together to understand the effect they had on the body's ability to absorb, distribute, and excrete each drug alone and together. The results of this study show that there are no clinically important changes in how atogepant is processed by the body when administered with esomeprazole, and they can be safely taken together.
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Esomeprazol , Adulto , Humanos , Esomeprazol/efeitos adversos , Esomeprazol/farmacocinética , Estudos Cross-Over , Área Sob a Curva , Administração Oral , Interações MedicamentosasRESUMO
The renin angiotensin aldosterone system is a key regulator of blood pressure. Aldosterone is the final effector of this pathway, acting predominantly via mineralocorticoid receptors. Aldosterone facilitates the conservation of sodium and, with it, water and acts as a powerful stimulus for potassium excretion. However, evidence for the pathological impact of excess mineralocorticoid receptor stimulation is increasing. Here, we discussed how in the heart, hyperaldosteronism is associated with fibrosis, cardiac dysfunction, and maladaptive hypertrophy. In the kidney, aldosterone was shown to cause proteinuria and fibrosis and may contribute to the progression of kidney disease. More recently, studies suggested that aldosterone excess damaged endothelial cells. Here, we reviewed how damage to the endothelial glycocalyx may contribute to this process. The endothelial glycocalyx is a heterogenous, negatively charged layer on the luminal surface of cells. Aldosterone exposure alters this layer. The resulting structural changes reduced endothelial reactivity in response to protective shear stress, altered permeability, and increased immune cell trafficking. Finally, we reviewed current therapeutic strategies for limiting endothelial damage and suggested that preventing glycocalyx remodelling in response to aldosterone exposure may provide a novel strategy, free from the serious adverse effect of hyperkalaemia seen in response to mineralocorticoid blockade.
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Aldosterona , Endotélio Vascular , Humanos , Aldosterona/metabolismo , Endotélio Vascular/metabolismo , Células Endoteliais/metabolismo , Antagonistas de Receptores de Mineralocorticoides/uso terapêutico , FibroseRESUMO
The glomerular endothelial glycocalyx (GEnGlx) forms the first part of the glomerular filtration barrier. Previously, we showed that mineralocorticoid receptor (MR) activation caused GEnGlx damage and albuminuria. In this study, we investigated whether MR antagonism could limit albuminuria in diabetes and studied the site of action. Streptozotocin-induced diabetic Wistar rats developed albuminuria, increased glomerular albumin permeability (Ps'alb), and increased glomerular matrix metalloproteinase (MMP) activity with corresponding GEnGlx loss. MR antagonism prevented albuminuria progression, restored Ps'alb, preserved GEnGlx, and reduced MMP activity. Enzymatic degradation of the GEnGlx negated the benefits of MR antagonism, confirming their dependence on GEnGlx integrity. Exposing human glomerular endothelial cells (GEnC) to diabetic conditions in vitro increased MMPs and caused glycocalyx damage. Amelioration of these effects confirmed a direct effect of MR antagonism on GEnC. To confirm relevance to human disease, we used a potentially novel confocal imaging method to show loss of GEnGlx in renal biopsy specimens from patients with diabetic nephropathy (DN). In addition, patients with DN randomized to receive an MR antagonist had reduced urinary MMP2 activity and albuminuria compared with placebo and baseline levels. Taken together, our work suggests that MR antagonists reduce MMP activity and thereby preserve GEnGlx, resulting in reduced glomerular permeability and albuminuria in diabetes.
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Diabetes Mellitus , Nefropatias Diabéticas , Ratos , Animais , Humanos , Antagonistas de Receptores de Mineralocorticoides/farmacologia , Antagonistas de Receptores de Mineralocorticoides/uso terapêutico , Antagonistas de Receptores de Mineralocorticoides/metabolismo , Albuminúria/tratamento farmacológico , Células Endoteliais/metabolismo , Receptores de Mineralocorticoides/metabolismo , Receptores de Mineralocorticoides/uso terapêutico , Glicocálix/metabolismo , Ratos Wistar , Nefropatias Diabéticas/metabolismo , Diabetes Mellitus/metabolismoRESUMO
OBJECTIVES: We aimed to examine trial feasibility plus physiological and psychological effects of a guided meditation practice, Yoga Nidra, in adults with self-reported insomnia. METHODS: Twenty-two adults with self-reported insomnia were recruited to attend two visits at our research center. At Visit 1 (V1), participants were asked to lie quietly for ninety minutes. The primary outcome was change in electroencephalography (EEG). Heart rate variability (HRV), respiratory rate and self-reported mood and anxiety were also measured. At Visit 2 (V2), the same protocol was followed, except half of participants were randomized to practice Yoga Nidra for the first 30-min. RESULTS: There were no between-group changes (V1-V2) in alpha EEG power at O1 (Intervention: 13 ± 70%; Control: -20 ± 40%), HRV or sleep onset latency in response to Yoga Nidra. Respiratory rate, however, showed statistically significant difference between groups (Yoga Nidra -1.4 breaths per minute (bpm) change during and - 2.1 bpm afterwards vs. Control +0.2 bpm during and + 0.4 bpm after; p = .03 for both during and after). The intervention displayed good acceptability (well-tolerated) and credibility (perceived benefit ratings) with implementation success (target sample size reached; 5% dropout rate). CONCLUSIONS: This preliminary clinical trial provides early evidence that Yoga Nidra is a well-tolerated, feasible intervention for adults reporting insomnia. Decreased respiratory rate in response to Yoga Nidra needs to be confirmed in more definitive studies. TRIAL REGISTRATION INFORMATION: This trial was registered on ClinicalTrials.gov as "A Closer Look at Yoga Nidra: Sleep Lab Analyses" (NCT#03685227).
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Meditação , Distúrbios do Início e da Manutenção do Sono , Yoga , Adulto , Humanos , Yoga/psicologia , Meditação/psicologia , Distúrbios do Início e da Manutenção do Sono/terapia , Sono , AnsiedadeRESUMO
BACKGROUND: Community pharmacies in the United States are beginning to serve as patient care service destinations addressing both clinical and health-related social needs (HRSN). Although there is support for integrating social determinant of health (SDoH) activities into community pharmacy practice, the literature remains sparse on optimal pharmacy roles and practice models. OBJECTIVE: To assess the feasibility of a community pharmacy HRSN screening and referral program adapted from a community health worker (CHW) model and evaluate participant perceptions and attitudes toward the program. METHODS: This feasibility study was conducted from January 2022 to April 2022 at an independent pharmacy in Buffalo, NY. Collaborative relationships were developed with 3 community-based organizations including one experienced in implementing CHW programs. An HRSN screening and referral intervention was developed and implemented applying a CHW practice model. Pharmacy staff screened subjects for social needs and referred to an embedded CHW, who assessed and referred subjects to community resources with as-needed follow-up. Post intervention, subjects completed a survey regarding their program experience. Descriptive statistics were used to report demographics, screening form, and survey responses. RESULTS: Eighty-six subjects completed screening and 21 (24.4%) an intervention and referral. Most participants utilized Medicaid (57%) and lived within a ZIP Code associated with the lowest estimated quartile for median household income (66%). Eighty-seven social needs were identified among the intervention subjects, with neighborhood and built environment (31%) and economic stability challenges (30%) being the most common SDoH domains. The CHW spent an average of 33 minutes per patient from initial case review through follow-up. All respondents had a positive perception of the program, and the majority agreed that community pharmacies should help patients with their social needs (70%). CONCLUSIONS: This feasibility study demonstrated that embedding a CHW into a community pharmacy setting can successfully address HRSN and that participants have a positive perception toward these activities.