(-)-epicatechin treatment did not modify the thermogenic pathway in the gastrocnemius muscle of male rat offspring obeses by programming.

The aim of this study was to analyse the expression of genes related to the regulation of energy metabolism in skeletal muscle tissue by comparing male offspring in two age groups [at 110 and 245 postnatal days (pnd)] from a mother with obesity induced by a high-fat diet and (-)-epicatechin (Epi) administration. Four groups of six male offspring from different litters were randomly selected for the control groups [C and offspring of mothers with maternal obesity (MO)] or Epi intervention groups. We evaluated the effect of Epi on gastrocnemius tissue by analysing the mRNA and protein expression levels of Fndc5/irisin, Pgc-1α, Ucp3, and Sln. Epi significantly increased the Pgc-1α protein in the MO group of offspring at 110 pnd (p < 0.036, MO vs. MO+Epi), while at 245 pnd, Epi increased Fndc5/irisin mRNA expression in the MO+Epi group versus the MO group (p = 0.006).No differences were detected in Fndc5/irisin, Ucp3 or Sln mRNA or protein levels (including Pgc-1α mRNA) in the offspring at 110 pnd or in Pgc-1α, Ucp3, or Sln mRNA or protein levels (including Fndc5/irisin protein) at 245 pnd among the experimental groups. In conclusion, (-)-epicatechin treatment increased Fndc5/irisin mRNA expression and Pgc-α protein levels in the gastrocnemius muscle of offspring at postnatal days 110 and 245. Furthermore, it is suggested that the flavonoid effect in a model of obesity and its impact on thermogenesis in skeletal muscle are regulated by a different pathway than Fndc5/irisin.

Plural molecular and cellular mechanisms of pore domain KCNQ2 encephalopathy.

KCNQ2 variants in children with neurodevelopmental impairment are difficult to assess due to their heterogeneity and unclear pathogenic mechanisms. We describe a child with neonatal-onset epilepsy, developmental impairment of intermediate severity, and KCNQ2 G256W heterozygosity. Analyzing prior KCNQ2 channel cryoelectron microscopy models revealed G256 as a node of an arch-shaped non-covalent bond network linking S5, the pore turret, and the ion path. Co-expression with G256W dominantly suppressed conduction by wild-type subunits in heterologous cells. Ezogabine partly reversed this suppression. G256W/+ mice have epilepsy leading to premature deaths. Hippocampal CA1 pyramidal cells from G256W/+ brain slices showed hyperexcitability. G256W/+ pyramidal cell KCNQ2 and KCNQ3 immunolabeling was significantly shifted from axon initial segments to neuronal somata. Despite normal mRNA levels, G256W/+ mouse KCNQ2 protein levels were reduced by about 50%. Our findings indicate that G256W pathogenicity results from multiplicative effects, including reductions in intrinsic conduction, subcellular targeting, and protein stability. These studies provide evidence for an unexpected and novel role for the KCNQ2 pore turret and introduce a valid animal model of KCNQ2 encephalopathy. Our results, spanning structure to behavior, may be broadly applicable because the majority of KCNQ2 encephalopathy patients share variants near the selectivity filter.

Three Decades of Valproate: A Current Model for Studying Autism Spectrum Disorder.

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder with increased prevalence and incidence in recent decades. Its etiology remains largely unclear, but it seems to involve a strong genetic component and environmental factors that, in turn, induce epigenetic changes during embryonic and postnatal brain development. In recent decades, clinical studies have shown that inutero exposure to valproic acid (VPA), a commonly prescribed antiepileptic drug, is an environmental factor associated with an increased risk of ASD. Subsequently, prenatal VPA exposure in rodents has been established as a reliable translational model to study the pathophysiology of ASD, which has helped demonstrate neurobiological changes in rodents, non-human primates, and brain organoids from human pluripotent stem cells. This evidence supports the notion that prenatal VPA exposure is a valid and current model to replicate an idiopathic ASD-like disorder in experimental animals. This review summarizes and describes the current features reported with this animal model of autism and the main neurobiological findings and correlates that help elucidate the pathophysiology of ASD. Finally, we discuss the general framework of the VPA model in comparison to other environmental and genetic ASD models.

Autosomal dominant ApoA4 mutations present as tubulointerstitial kidney disease with medullary amyloidosis.

Sporadic cases of apolipoprotein A-IV medullary amyloidosis have been reported. Here we describe five families found to have autosomal dominant medullary amyloidosis due to two different pathogenic APOA4 variants. A large family with autosomal dominant chronic kidney disease (CKD) and bland urinary sediment underwent whole genome sequencing with identification of a chr11:116692578 G>C (hg19) variant encoding the missense mutation p.L66V of the ApoA4 protein. We identified two other distantly related families from our registry with the same variant and two other distantly related families with a chr11:116693454 C>T (hg19) variant encoding the missense mutation p.D33N. Both mutations are unique to affected families, evolutionarily conserved and predicted to expand the amyloidogenic hotspot in the ApoA4 structure. Clinically affected individuals suffered from CKD with a bland urinary sediment and a mean age for kidney failure of 64.5 years. Genotyping identified 48 genetically affected individuals; 44 individuals had an estimated glomerular filtration rate (eGFR) under 60 ml/min/1.73 m2, including all 25 individuals with kidney failure. Significantly, 11 of 14 genetically unaffected individuals had an eGFR over 60 ml/min/1.73 m2. Fifteen genetically affected individuals presented with higher plasma ApoA4 concentrations. Kidney pathologic specimens from four individuals revealed amyloid deposits limited to the medulla, with the mutated ApoA4 identified by mass-spectrometry as the predominant amyloid constituent in all three available biopsies. Thus, ApoA4 mutations can cause autosomal dominant medullary amyloidosis, with marked amyloid deposition limited to the kidney medulla and presenting with autosomal dominant CKD with a bland urinary sediment. Diagnosis relies on a careful family history, APOA4 sequencing and pathologic studies.

KCNQ2/3 Gain-of-Function Variants and Cell Excitability: Differential Effects in CA1 versus L2/3 Pyramidal Neurons.

Gain-of-function (GOF) pathogenic variants in the potassium channels KCNQ2 and KCNQ3 lead to hyperexcitability disorders such as epilepsy and autism spectrum disorders. However, the underlying cellular mechanisms of how these variants impair forebrain function are unclear. Here, we show that the R201C variant in KCNQ2 has opposite effects on the excitability of two types of mouse pyramidal neurons of either sex, causing hyperexcitability in layer 2/3 (L2/3) pyramidal neurons and hypoexcitability in CA1 pyramidal neurons. Similarly, the homologous R231C variant in KCNQ3 leads to hyperexcitability in L2/3 pyramidal neurons and hypoexcitability in CA1 pyramidal neurons. However, the effects of KCNQ3 gain-of-function on excitability are specific to superficial CA1 pyramidal neurons. These findings reveal a new level of complexity in the function of KCNQ2 and KCNQ3 channels in the forebrain and provide a framework for understanding the effects of gain-of-function variants and potassium channels in the brain.SIGNIFICANCE STATEMENT KCNQ2/3 gain-of-function (GOF) variants lead to severe forms of neurodevelopmental disorders, but the mechanisms by which these channels affect neuronal activity are poorly understood. In this study, using a series of transgenic mice we demonstrate that the same KCNQ2/3 GOF variants can lead to either hyperexcitability or hypoexcitability in different types of pyramidal neurons [CA1 vs layer (L)2/3]. Additionally, we show that expression of the recurrent KCNQ2 GOF variant R201C in forebrain pyramidal neurons could lead to seizures and SUDEP. Our data suggest that the effects of KCNQ2/3 GOF variants depend on specific cell types and brain regions, possibly accounting for the diverse range of phenotypes observed in individuals with KCNQ2/3 GOF variants.

Importance of multiplanar reformation angiographic images for the detection of carotid web: A case series.

Carotid web (CW) is considered a variant of intimal fibromuscular dysplasia. CW represents between 9.4% and 37% of ischemic strokes that were initially misclassified as "cryptogenic." However, in Latin America, there is a lack of detection. We present 5 cases of ischemic stroke due to CW and discuss the usefulness of multiplanar reformatting (MPR) imaging in computed tomography angiography. The identification of CW with the use of tridimensional (3D) reconstructions and maximum intensity projection was 20%, the rest was misdiagnosed as atherosclerotic plaque. With the MPR, the identification of typical CW findings was improved, such as a thin septum, a shelf-like image, and a mountain shadow-like image. However, one must be alert to changes in the 3D disposition of the carotid bifurcation, as they may mask the typical CW findings. A good practice is to align the internal carotid artery exactly posterior to the external carotid artery in the sagittal plane.

Mechanistic Insights into the Oxidative Degradation of Formic and Oxalic Acids with Ozone and OH Radical. A Computational Rationale.

Gas-phase and aqueous oxidations of formic and oxalic acids with ozone and OH radicals have been thoroughly examined by DFT methods. Such acids are not only important feedstocks for the iterative construction of other organic compounds but also final products generated by mineralization and advanced oxidation of higher organics. Our computational simulation unravels both common and distinctive reaction channels, albeit consistent with known H atom abstraction pathways and formation of hydropolyoxide derivatives. Notably, reactions with neutral ozone and OH radical proceed through low-energy concerted mechanisms involving asynchronous transition structures. For formic acid, carbonylic H-abstraction appears to be more favorable than the dissociative abstraction of the acid proton. Formation of long oxygen chains does not cause a significant energy penalty and highly oxygenated products are stable enough, even if subsequent decomposition releases environmentally benign side substances like O2 and H2O.

Cellulase and chitinase activities and antagonism against Fusarium oxysporum f.sp. cubense race 1 of six Trichoderma strains isolated from Mexican maize cropping.

OBJECTIVE: To evaluate the enzymatic and biocontrol capacity of native Trichoderma strains isolated from corn crops in Irapuato (state of Guanajuato) and Napízaro (state of Michoacán), Mexico. RESULTS: Six native strains from Irapuato and Napízaro were tested, with five of them identified as T. harzianum and one as T. tomentosum. The six strains qualitatively and quantitatively showed enzyme activity for cellulase and chitinase. The best results were obtained for strains IrV6SIC7 and MichV6S2C2 with 878 IU L-1 of chitinase and 1323 IU L-1 of cellulase, respectively. All Trichoderma strains acted antagonistically toward Fusarium oxysporum f.sp. cubense race 1 (FocR1), with percentages of inhibition that ranged from 9 to 54%. In addition, the microscopic analysis allowed visualizing the mechanisms of mycoparasitism and antibiosis by either IrV6SIC7 or MichV6S2C2. The latter effects indicate that the tested native Trichoderma strains isolated from corn crops possessed enzymatic mechanisms as a strategy for biocontrolling FocR1 strains. CONCLUSION: The enzyme production by the Trichoderma strains represents a potential biotechnological utilization for either agricultural or industrial purposes.

Influence of maternal obesity on the skeletal muscle of offspring.

Maternal obesity has been described as a clinical entity associated with an increased incidence of metabolic diseases in the offspring, indicating a fetal programming phenomenon during this critical development period. Fetal exposure to an obesogenic environment affects multiple organs and tissues, including skeletal muscle, which is particularly susceptible to stressors from the external environment. Several studies have described alterations in the morphology and composition of skeletal muscle tissue secondary to obesogenic exposure in utero. In addition, modifications in signaling pathways related to the metabolism of energy substrates have been found in children born to mothers with obesity during pregnancy. This review addresses the current evidence describing the consequences of fetal exposure to an obesogenic maternal diet on skeletal muscle tissue, focusing on changes in tissue composition, alterations in signaling pathways related to glucose and fatty acid metabolism, mitochondrial biogenesis, and oxidative phosphorylation.

La obesidad materna se ha descrito como una entidad clínica asociada con el aumento en la incidencia de enfermedades metabólicas en el producto de la gestación, lo que indica la existencia de un fenómeno de programación fetal que se lleva a cabo durante este periodo crítico del desarrollo. La exposición del feto a un ambiente obesogénico afecta múltiples órganos y tejidos, incluyendo el músculo esquelético, el cual es particularmente susceptible a estresores del ambiente externo. Diversos estudios han descrito alteraciones en la morfología y composición del tejido muscular esquelético secundarias a una exposición obesogénica in utero. Además, se han encontrado modificaciones en vías de señalización relacionadas al metabolismo de sustratos energéticos en los productos de madres con obesidad durante la gestación. En la presente revisión se aborda la evidencia actual que describe las consecuencias de la exposición fetal a una dieta materna obesogénica sobre el tejido muscular esquelético, con especial enfoque en los cambios en la composición del tejido, las alteraciones en las vías de señalización relacionadas con el metabolismo de la glucosa y los ácidos grasos, así como la biogénesis mitocondrial y la fosforilación oxidativa.

Influence of maternal obesity on the skeletal muscle of offspring / Influencia de la obesidad materna sobre el músculo esquelético de la progenie

Abstract Maternal obesity has been described as a clinical entity associated with an increased incidence of metabolic diseases in the offspring, indicating a fetal programming phenomenon during this critical development period. Fetal exposure to an obesogenic environment affects multiple organs and tissues, including skeletal muscle, which is particularly susceptible to stressors from the external environment. Several studies have described alterations in the morphology and composition of skeletal muscle tissue secondary to obesogenic exposure in utero. In addition, modifications in signaling pathways related to the metabolism of energy substrates have been found in children born to mothers with obesity during pregnancy. This review addresses the current evidence describing the consequences of fetal exposure to an obesogenic maternal diet on skeletal muscle tissue, focusing on changes in tissue composition, alterations in signaling pathways related to glucose and fatty acid metabolism, mitochondrial biogenesis, and oxidative phosphorylation.

Resumen La obesidad materna se ha descrito como una entidad clínica asociada con el aumento en la incidencia de enfermedades metabólicas en el producto de la gestación, lo que indica la existencia de un fenómeno de programación fetal que se lleva a cabo durante este periodo crítico del desarrollo. La exposición del feto a un ambiente obesogénico afecta múltiples órganos y tejidos, incluyendo el músculo esquelético, el cual es particularmente susceptible a estresores del ambiente externo. Diversos estudios han descrito alteraciones en la morfología y composición del tejido muscular esquelético secundarias a una exposición obesogénica in utero. Además, se han encontrado modificaciones en vías de señalización relacionadas al metabolismo de sustratos energéticos en los productos de madres con obesidad durante la gestación. En la presente revisión se aborda la evidencia actual que describe las consecuencias de la exposición fetal a una dieta materna obesogénica sobre el tejido muscular esquelético, con especial enfoque en los cambios en la composición del tejido, las alteraciones en las vías de señalización relacionadas con el metabolismo de la glucosa y los ácidos grasos, así como la biogénesis mitocondrial y la fosforilación oxidativa.

Implementation of a Fuzzy Inference System to Enhance the Measurement Range of Multilayer Interferometric Sensors.

This work presents a novel methodology to implement a fuzzy inference system (FIS) to overcome the measurement ambiguity that is typically observed in interferometric sensors. This ambiguity occurs when the measurand is determined by tracing the wavelength position of a peak or dip of a spectral fringe. Consequently, the sensor measurement range is typically limited to the equivalent of 1 free spectral range (FSR). Here, it is demonstrated that by using the proposed methodology, the measurement range of this type of sensor can be widened several times by overcoming the ambiguity over some FSR periods. Furthermore, in order to support the viability of the methodology, it was applied to a couple of temperature interferometric sensors. Finally, experimental results demonstrated that it was possible to quintuple the measurement range of one of the tested sensors with a mean absolute error of MAE = 0.0045 °C, while for the second sensor, the measurement range was doubled with an MAE = 0.0073 °C.

Bilateral Ischemic Strokes Secondary to Moyamoya Syndrome Associated With Graves Thyrotoxicosis in a Patient of Amerindian Descent From Peru: A Case Report.

Moyamoya disease (MMD) is characterized by progressive stenosis of the distal portion of the internal carotid artery and its two main branches, the middle cerebral artery, and the anterior cerebral artery. Clinically, MMD can present with ischemic or hemorrhagic cerebrovascular events. The term Moyamoya syndrome (MMS) is used when the characteristic Moyamoya vasculopathy presents in association with other conditions such as Graves' disease (GD). We report a case of a 34-year-old, right-handed male patient of Amerindian descent. He presented to the emergency room with a two-month history of palpitation, fatigue, and weight loss associated with sudden-onset left hemiparesis, facial asymmetry, and dysarthria. His workup was remarkable for elevated levels of thyroid hormones with the presence of autoantibodies and radiological findings typical of MMS. Moyamoya syndrome in association with Graves' disease has increasingly been noted in Latin American patients and should be considered in the differential diagnosis in the appropriate clinical context.

Removal of KCNQ2 from parvalbumin-expressing interneurons improves anti-seizure efficacy of retigabine.

Anti-seizure drug (ASD) targets are widely expressed in both excitatory and inhibitory neurons. It remains unknown if the action of an ASD upon inhibitory neurons could counteract its beneficial effects on excitatory neurons (or vice versa), thereby reducing the efficacy of the ASD. Here, we examine whether the efficacy of the ASD retigabine (RTG) is altered after removal of the Kv7 potassium channel subunit KCNQ2, one of its drug targets, from parvalbumin-expressing interneurons (PV-INs). Parvalbumin-Cre (PV-Cre) mice were crossed with Kcnq2-floxed (Kcnq2fl/fl) mice to conditionally delete Kcnq2 from PV-INs. In these conditional knockout mice (cKO, PV-Kcnq2fl/fl), RTG (10 mg/kg, i.p.) significantly delayed the onset of either picrotoxin (PTX, 10 mg/kg, i.p)- or kainic acid (KA, 30 mg/kg, i.p.)-induced convulsive seizures compared to vehicle, while RTG was not effective in wild-type littermates (WT). Immunostaining for KCNQ2 and KCNQ3 revealed that both subunits were enriched at axon initial segments (AISs) of hippocampal CA1 PV-INs, and their specific expression was selectively abolished in cKO mice. Accordingly, the M-currents recorded from CA1 PV-INs and their sensitivity to RTG were significantly reduced in cKO mice. While the ability of RTG to suppress CA1 excitatory neurons in hippocampal slices was unchanged in cKO mice, its suppressive effect on the spike activity of CA1 PV-INs was significantly reduced compared with WT mice. In addition, the RTG-induced suppression on intrinsic membrane excitability of PV-INs in WT mice was significantly reduced in cKO mice. These findings suggest that preventing RTG from suppressing PV-INs improves its anticonvulsant effect.

Addressing harmful alcohol use in primary care in Colombia: Understanding the sociocultural context.

Harmful alcohol use is a public health problem worldwide, contributing to an estimated 5.1% of the global burden of illness. Screening and addressing at-risk drinking in primary care settings is an empirically supported health care intervention strategy to help reduce the burden of alcohol-use problems. In preparation for introducing screening and treatment for at-risk drinking in primary care clinics in Colombia, we conducted interviews with clinicians, clinic administrators, patients, and participants in Alcoholics Anonymous. Interviews were conducted within the framework of the Detección y Atención Integral de Depresión y Abuso de Alcohol en Atención Primaria (DIADA, [Detection and Integrated Care for Depression and Alcohol Use in Primary Care] www.project-diada.org) research project, and its qualitative phase that consisted of the collection of data from 15 focus groups, 6 interviews and field observations in 5 regional settings. All participants provided informed consent to participate in this research. Findings revealed the association of harmful alcohol use with a culture of consumption, within which it is learned and socially accepted practice. Recognition of harmful alcohol consumption includes a social context that influences its screening, diagnosis and prevention. The discussion highlights how, despite the existence of institutional strategies in healthcare settings and the awareness of the importance of at-risk drinking among health personnel, the recognition of the harmful use of alcohol as a pathology should be embedded in an understanding of historical, social and cultural dimensions that may affect different identification and care scenarios.

Towards an Optimal Methodology for Basidiomes Production of Naturally Occurring Species of the Genus Oudemansiella (Basidiomycetes).

Oudemansiella species are worldwide distributed and they are characterized for having attractive appearance, a soft fleshy context and mild taste and odor, what makes them interesting for mushroom intensive production. However, studies on their cultivation are scarce and there is no information regarding productive and morphological parameters of fruiting bodies obtained in culture. Here, we propose a methodology to determine the best production technique for the cultivation of not only Oudemansiella species but also of other xylophagous species assaying five different mushroom cultivation systems. Also, the optimal temperature of vegetative growth, the optimal lignocellulosic substrates and the nutritional properties of two naturally occurring Oudemansiella species were determined. As a result, bags with holes-system proved to be the most appropriate technique for the production of fruiting bodies, 25 °C was determined as the optimal temperature for mycelial growth and wheat straw as the best substrate. The evaluated species showed a higher content of fats and fiber and a lower content of proteins and carbohydrates compared to other mushrooms. Furthermore, this is the first report of the cultivation of O. cubensis on agricultural wastes in the world.

Arsenic Stress-Related F-Box (ASRF) gene regulates arsenic stress tolerance in Arabidopsis thaliana.

Arsenic (As), a non-biodegradable contaminant, is extremely toxic to plants and animals in its inorganic form. As negatively affects plant growth and development, primarily by inducing oxidative stress through redox imbalance. Here we characterized the Arabidopsis F-box protein gene AT2G16220 (Arsenic Stress-Related F-box (ASRF)) that we identified in the genome-wide association study. The asrf mutant seedlings showed high sensitivity to arsenate (AsV) stress. AsV significantly affected asrf seedling growth when germinated on or exposed to AsV-supplemented growth regimes. AsV stress significantly induced production of reactive oxygen species and proline accumulation in asrf, so the asrf maintained high proline content, possibly for cellular protection and redox homeostasis. Heterozygous seedlings (Col-0 x asrf, F1 progeny) were relatively less affected by AsV stress than asrf mutant but showed slightly reduced growth compared with the Col-0 wild type, which suggests that the homozygous ASRF locus is important for AsV stress resistance. Transcriptome analysis involving the mutant and wild type revealed altered phosphate homeostasis in asrf seedlings, which implies that ASRF is required for maintaining phosphate and cellular- homeostasis under excess AsV. Our findings confirm the roles of ASRF in As stress tolerance in plants, for a novel way to mitigate arsenic stress.

Role of Oligodendrocytes and Myelin in the Pathophysiology of Autism Spectrum Disorder.

Autism Spectrum Disorder (ASD) is an early neurodevelopmental disorder that involves deficits in interpersonal communication, social interaction, and repetitive behaviors. Although ASD pathophysiology is still uncertain, alterations in the abnormal development of the frontal lobe, limbic areas, and putamen generate an imbalance between inhibition and excitation of neuronal activity. Interestingly, recent findings suggest that a disruption in neuronal connectivity is associated with neural alterations in white matter production and myelination in diverse brain regions of patients with ASD. This review is aimed to summarize the most recent evidence that supports the notion that abnormalities in the oligodendrocyte generation and axonal myelination in specific brain regions are involved in the pathophysiology of ASD. Fundamental molecular mediators of these pathological processes are also examined. Determining the role of alterations in oligodendrogenesis and myelination is a fundamental step to understand the pathophysiology of ASD and identify possible therapeutic targets.

Peroxymonosulfate/solar radiation process for the removal of aqueous microcontaminants. Kinetic modeling, influence of variables and matrix constituents.

New technologies to address the presence of pharmaceutical and personal care products (PPCPs) in wastewater are needed, especially in those cases in which water will be reused. In this work, the activation of peroxymonosulfate (PMS) with simulated solar radiation has been applied to the oxidation of a mixture of six PPCPs, i.e. caffeine, primidone, N,N-diethyl-3-methylbenzamide (DEET), methylparaben, clofibric acid and ibuprofen. The sole application of solar radiation, i.e. solar photolysis, only led to the oxidation of clofibric acid (complete degradation in 90 min). The combination of PMS and solar radiation resulted in the degradation of all target micropollutants. The complete degradation of this mixture at initial 100 ppb was achieved with 0.5 mM of initial PMS after 90 min. A kinetic study that acceptably simulates the experimental data under different conditions has been proposed. The effects of initial PPCP concentration (1 mg L-1-100 µg L-1), PMS dose (0.1-5 mM), and pH (3-9) were tested and kinetically simulated. Finally, the PPCPs removal study was carried out in two real water matrices (river and a secondary effluent of an urban wastewater treatment plant). A higher dose of PMS, ten times higher, was required to achieve complete degradation of the micropollutants if compared to ultrapure water.

Assessing the Impact of Patient-Facing Mobile Health Technology on Patient Outcomes: Retrospective Observational Cohort Study.

BACKGROUND: Despite the growth of and media hype about mobile health (mHealth), there is a paucity of literature supporting the effectiveness of widespread implementation of mHealth technologies. OBJECTIVE: This study aimed to assess whether an innovative mHealth technology system with several overlapping purposes can impact (1) clinical outcomes (ie, readmission rates, revisit rates, and length of stay) and (2) patient-centered care outcomes (ie, patient engagement, patient experience, and patient satisfaction). METHODS: We compared all patients (2059 patients) of participating orthopedic surgeons using mHealth technology with all patients of nonparticipating orthopedic surgeons (2554 patients). The analyses included Wilcoxon rank-sum tests, Kruskal-Wallis tests for continuous variables, and chi-square tests for categorical variables. Logistic regression models were performed on categorical outcomes and a gamma-distributed model for continuous variables. All models were adjusted for patient demographics and comorbidities. RESULTS: The inpatient readmission rates for the nonparticipating group when compared with the participating group were higher and demonstrated higher odds ratios (ORs) for 30-day inpatient readmissions (nonparticipating group 106/2636, 4.02% and participating group 54/2048, 2.64%; OR 1.48, 95% CI 1.03 to 2.13; P=.04), 60-day inpatient readmissions (nonparticipating group 194/2636, 7.36% and participating group 85/2048, 4.15%; OR 1.79, 95% CI 1.32 to 2.39; P<.001), and 90-day inpatient readmissions (nonparticipating group 261/2636, 9.90% and participating group 115/2048, 5.62%; OR 1.81, 95% CI 1.40 to 2.34; P<.001). The length of stay for the nonparticipating cohort was longer at 1.90 days, whereas the length of stay for the participating cohort was 1.50 days (mean 1.87, SD 2 vs mean 1.50, SD 1.37; P<.001). Patients treated by participating surgeons received and read text messages using mHealth 83% of the time and read emails 84% of the time. Patients responded to 60% of the text messages and 53% of the email surveys. Patients were least responsive to digital monitoring questions when the hospital asked them to do something, and they were most engaged with emails that did not require action, including informational content. A total of 96% (558/580) of patients indicated high satisfaction with using mHealth technology to support their care. Only 0.40% (75/2059) patients opted-out of the mHealth technology program after enrollment. CONCLUSIONS: A novel, multicomponent, pathway-driven, patient-facing mHealth technology can positively impact patient outcomes and patient-reported experiences. These technologies can empower patients to play a more active and meaningful role in improving their outcomes. There is a deep need, however, for a better understanding of the interactions between patients, technology, and health care providers. Future research is needed to (1) help identify, address, and improve technology usability and effectiveness; (2) understand patient and provider attributes that support adoption, uptake, and sustainability; and (3) understand the factors that contribute to barriers of technology adoption and how best to overcome them.