Disrupting the impact of socio-contextual disadvantage on school readiness skill attainment among preschool children: The role of Head Start attendance

Created in 1965, Head Start is the longest running national school readiness program in the United States. Head Start was developed to improve children\u27s social and academic readiness for kindergarten and to reduce the academic achievement gap between impoverished and more affluent children. However, questions about the effectiveness of Head Start have trouble the program since its inception. Head Start children often experience considerably more sociocontextual risk, specifically in the form of more economic disadvantage, maternal psychological distress, and dangerous neighborhoods. The goal of the present study was to evaluate the extent to which attending Head Start buffers children from some of the harmful effects of sociocontextual risk on their acquisition of academic and social school readiness skills. Socio-contextual risk factors were largely unrelated to the school readiness skills. Only mothers\u27 reports of anxiety were significantly associated with slower rates of increase in children\u27s PPVT scores, suggesting that mothers who are more anxious have children who are not developing receptive vocabulary scores as quickly as children whose mothers have fewer anxiety symptoms. Head Start did not buffer the impact of socio-contextual risk on children\u27s attainment of school readiness skills. A secondary goal of the present study was to validate mothers\u27 reports of neighborhood danger with interviewer impressions of neighborhood safety and objective crime reports. Interviewer impressions correlated significantly with mothers\u27 reports of neighborhood danger and official crime statistics. Interestingly, official crime statistics were not correlated with mothers\u27 reports of neighborhood danger, but were correlated with interviewer impressions. Interviewers may provide a valuable objective perspective of characteristics of the neighborhood. This sample was not intended to explore the effects of natural disasters on household structures, maternal psychopathology, or children\u27s academic development. However, results clearly highlighted the need to empirically consider the specific challenges associated with lowincome families after a natural disaster. Study implications and promising directions for future research are discussed

Disrupting the impact of socio-contextual disadvantage on school readiness skill attainment among preschool children: The role of Head Start attendance

Created in 1965, Head Start is the longest running national school readiness program in the United States. Head Start was developed to improve children\u27s social and academic readiness for kindergarten and to reduce the academic achievement gap between impoverished and more affluent children. However, questions about the effectiveness of Head Start have trouble the program since its inception. Head Start children often experience considerably more sociocontextual risk, specifically in the form of more economic disadvantage, maternal psychological distress, and dangerous neighborhoods. The goal of the present study was to evaluate the extent to which attending Head Start buffers children from some of the harmful effects of sociocontextual risk on their acquisition of academic and social school readiness skills. Socio-contextual risk factors were largely unrelated to the school readiness skills. Only mothers\u27 reports of anxiety were significantly associated with slower rates of increase in children\u27s PPVT scores, suggesting that mothers who are more anxious have children who are not developing receptive vocabulary scores as quickly as children whose mothers have fewer anxiety symptoms. Head Start did not buffer the impact of socio-contextual risk on children\u27s attainment of school readiness skills. A secondary goal of the present study was to validate mothers\u27 reports of neighborhood danger with interviewer impressions of neighborhood safety and objective crime reports. Interviewer impressions correlated significantly with mothers\u27 reports of neighborhood danger and official crime statistics. Interestingly, official crime statistics were not correlated with mothers\u27 reports of neighborhood danger, but were correlated with interviewer impressions. Interviewers may provide a valuable objective perspective of characteristics of the neighborhood. This sample was not intended to explore the effects of natural disasters on household structures, maternal psychopathology, or children\u27s academic development. However, results clearly highlighted the need to empirically consider the specific challenges associated with lowincome families after a natural disaster. Study implications and promising directions for future research are discussed

Diaphragm weakness and mechanical ventilation – what\u27s the critical issue?

While animal studies indicate that controlled mechanical ventilation (MV) induces diaphragm weakness and myofiber atrophy, there are no data in humans that confirm MV per se produces diaphragm weakness. Whether or not diaphragm weakness results from MV, sepsis, corticosteroids, hyperglycemia, or a combination of these factors, however, is not the most important issue raised by the recent study from Hermans and colleagues. This study makes an important contribution by providing additional evidence that many critically ill patients have profound diaphragm weakness. If diaphragm weakness of this magnitude is present in most mechanically ventilated patients, a strong argument can be made that respiratory muscle weakness is a major contributor to respiratory failure

Hyperglycemia-Induced Diaphragm Weakness is Mediated by Oxidative Stress

INTRODUCTION: A major consequence of ICU-acquired weakness (ICUAW) is diaphragm weakness, which prolongs the duration of mechanical ventilation. Hyperglycemia (HG) is a risk factor for ICUAW. However, the mechanisms underlying HG-induced respiratory muscle weakness are not known. Excessive reactive oxygen species (ROS) injure multiple tissues during HG, but only one study suggests that excessive ROS generation may be linked to HG-induced diaphragm weakness. We hypothesized that HG-induced diaphragm dysfunction is mediated by excessive superoxide generation and that administration of a specific superoxide scavenger, polyethylene glycol superoxide dismutase (PEG-SOD), would ameliorate these effects. METHODS: HG was induced in rats using streptozotocin (60 mg/kg intravenously) and the following groups assessed at two weeks: controls, HG, HG + PEG-SOD (2,000U/kg/d intraperitoneally for seven days), and HG + denatured (dn)PEG-SOD (2000U/kg/d intraperitoneally for seven days). PEG-SOD and dnPEG-SOD were administered on day 8, we measured diaphragm specific force generation in muscle strips, force-pCa relationships in single permeabilized fibers, contractile protein content and indices of oxidative stress. RESULTS: HG reduced diaphragm specific force generation, altered single fiber force-pCa relationships, depleted troponin T, and increased oxidative stress. PEG-SOD prevented HG-induced reductions in diaphragm specific force generation (for example 80 Hz force was 26.4 ± 0.9, 15.4 ± 0.9, 24.0 ± 1.5 and 14.9 ± 0.9 N/cm2 for control, HG, HG + PEG-SOD, and HG + dnPEG-SOD groups, respectively, P \u3c0.001). PEG-SOD also restored HG-induced reductions in diaphragm single fiber force generation (for example, Fmax was 182.9 ± 1.8, 85.7 ± 2.0, 148.6 ± 2.4 and 90.9 ± 1.5 kPa in control, HG, HG + PEG-SOD, and HG + dnPEG-SOD groups, respectively, P \u3c0.001). HG-induced troponin T depletion, protein nitrotyrosine formation, and carbonyl modifications were largely prevented by PEG-SOD. CONCLUSIONS: HG-induced reductions in diaphragm force generation occur largely at the level of the contractile proteins, are associated with depletion of troponin T and increased indices of oxidative stress, findings not previously reported. Importantly, administration of PEG-SOD largely ablated these derangements, indicating that superoxide generation plays a major role in hyperglycemia-induced diaphragm dysfunction. This new mechanistic information could explain how HG alters diaphragm function during critical illness

Diaphragm weakness in mechanically ventilated critically ill patients

INTRODUCTION: Studies indicate that mechanically ventilated patients develop significant diaphragm muscle weakness, but the etiology of weakness and its clinical impact remain incompletely understood. We assessed diaphragm strength in mechanically ventilated medical ICU patients, correlated the development of diaphragm weakness with multiple clinical parameters, and examined the relationship between the level of diaphragm weakness and patient outcomes. METHODS: Transdiaphragmatic twitch pressure (PdiTw) in response to bilateral magnetic stimulation of the phrenic nerves was measured. Diaphragm weakness was correlated with the presence of infection, blood urea nitrogen, albumin, and glucose levels. The relationship of diaphragm strength to patient outcomes, including mortality and the duration of mechanical ventilation for successfully weaned patients, was also assessed. RESULTS: We found that infection is a major risk factor for diaphragm weakness in mechanically ventilated medical ICU patients. Outcomes for patients with severe diaphragm weakness (PdiTw \u3c10 \u3ecmH2O) were poor, with a markedly increased mortality (49%) compared to patients with PdiTw ≥10 cmH2O (7% mortality, P = 0.022). In addition, survivors with PdiTw(12.3 ± 1.7 days) than those with PdiTw ≥10 cmH2O (5.5 ± 2.0 days, P = 0.016). CONCLUSIONS: Infection is a major cause of severe diaphragm weakness in mechanically ventilated patients. Moreover, diaphragm weakness is an important determinant of poor outcomes in this patient population

Diaphragm weakness and mechanical ventilation - what's the critical issue?

While animal studies indicate that controlled mechanical ventilation (MV) induces diaphragm weakness and myofiber atrophy, there are no data in humans that confirm MV per se produces diaphragm weakness. Whether or not diaphragm weakness results from MV, sepsis, corticosteroids, hyperglycemia, or a combination of these factors, however, is not the most important issue raised by the recent study from Hermans and colleagues. This study makes an important contribution by providing additional evidence that many critically ill patients have profound diaphragm weakness. If diaphragm weakness of this magnitude is present in most mechanically ventilated patients, a strong argument can be made that respiratory muscle weakness is a major contributor to respiratory failure

Hyperglycemia and acquired weakness in critically ill patients: potential mechanisms

Critical illness polyneuropathy/critical illness myopathy (CIP/CIM) is a major cause of mortality and long-term morbidity in critically ill patients, but the true incidence and prevalence of these syndromes are not known. Hermans and colleagues show that when intensive insulin therapy is used as part of routine clinical practice in the intensive care unit, the incidence of CIP/CIM as determined by electrophysiologic testing is reduced. Our understanding of the mechanisms responsible for inducing prolonged weakness in intensive care unit patients is limited, and the role of hyperglycemia in modulating these processes is unknown. Intensive insulin therapy currently remains the only effective therapeutic intervention that has been shown to reduce the incidence of CIP/CIM

Individual and community socioeconomic status : impact on mental health in individuals with arthritis

Peer reviewedPublisher PD

Eicosapentaenoic acid preserves diaphragm force generation following endotoxin administration

INTRODUCTION: Infections produce severe respiratory muscle weakness, which contributes to the development of respiratory failure. An effective, safe therapy to prevent respiratory muscle dysfunction in infected patients has not been defined. This study examined the effect of eicosapentaenoic acid (EPA), an immunomodulator that can be safely administered to patients, on diaphragm force generation following endotoxin administration. METHODS: Rats were administered the following (n = 5/group): (a) saline, (b) endotoxin, 12 mg/kg IP, (c) endotoxin + EPA (1.0 g/kg/d), and (d) EPA alone. Diaphragms were removed and measurements made of the diaphragm force-frequency curve, calpain activation, caspase activation, and protein carbonyl levels. RESULTS: Endotoxin elicited large reductions in diaphragm specific force generation (P \u3c 0.001), and increased diaphragm caspase activation (P \u3c 0.01), calpain activation (P \u3c 0.001) and protein carbonyl levels (P \u3c 0.01). EPA administration attenuated endotoxin-induced reductions in diaphragm specific force, with maximum specific force levels of 27 +/- 1, 14 +/- 1, 23 +/- 1, and 24 +/- 1 N/cm2, respectively, for control, endotoxin, endotoxin + EPA, and EPA treated groups (P \u3c 0.001). EPA did not prevent endotoxin induced caspase activation or protein carbonyl formation but significantly reduced calpain activation (P \u3c 0.02). CONCLUSIONS: These data indicate that endotoxin-induced reductions in diaphragm specific force generation can be partially prevented by administration of EPA, a nontoxic biopharmaceutical that can be safely given to patients. We speculate that it may be possible to reduce infection-induced skeletal muscle weakness in critically ill patients by administration of EPA

Clinical relevance of Tai Chi on pain and physical function in adults with knee osteoarthritis: An ancillary meta-analysis of randomized controlled trials

The clinical relevance of Tai Chi on pain, stiffness, and physical function in adults with knee osteoarthritis (KOA) has not been established. Therefore, the purpose of the current study was to address this gap. Eight randomized controlled trials from a recent meta-analysis representing 407 participants (216 Tai Chi, 191 control) in adults ≥18 years of age with KOA and included the assessment of pain, stiffness, and physical function using the Western Ontario and McMaster Universities Arthritis Index (WOMAC) were assessed. The inverse variance heterogeneity model (IVhet) was first used to pool standardized mean difference effect sizes (ES) for each outcome. Clinical relevance, i.e., number-needed-to treat (NNT) ≤10 and relative risk reduction (RRR) ≥25% was calculated across assumed controlled risks (ACR) ranging from 0.01 to 0.99. Statistically significant improvements were found for pain (ES, −0.75, 95% CI, −0.99, −0.51; Q = 8.9, p = 0.26; I2 = 21%), stiffness (ES, −0.70, 95% CI, −0.95, −0.46; Q = 9.6, p = 0.21; I2 = 27%), and physical function (ES, −0.91, 95% CI, −1.12, −0.70; Q = 7.2, p = 0.40; I2 = 3%). The intersection of results for a NNT ≤10 and RRR ≥25% yielded high evidence and clinically relevant improvements across a wide range of ACR for pain (0.15 to 0.88), stiffness (0.15 to 0.87), and physical function (0.13 to 0.97). These findings suggest that Tai Chi results in statistically significant as well as clinically important improvements in pain, stiffness, and physical function across a wide range of ACR in adults with KOA