Importance of self-weighing to avoid post-cessation weight gain: A secondary analysis of the fit and quit randomized trial.

Background: Smoking cessation is associated with weight gain, and the risk of weight gain is a common deterrent to quitting smoking. Thus, the identification of strategies for reducing post-smoking cessation weight gain is critical. Objective: Conduct secondary analysis of data from the Fit & Quit trial to determine if greater frequency of self-weighing is associated with less weight gain in the context of smoking cessation. Methods: Participants (N = 305) were randomized to one of three 2-month weight interventions (i.e., Stability, Loss, Bibliotherapy), followed by a smoking cessation intervention. Stability and Loss conditions received different types of self-weighing feedback. All participants received e-scales at baseline, to capture daily self-weighing data over 12 months. General linear models were applied to test the main objective. Results: Frequency of self-weighing was (mean ± SD) 2.67 ± 1.84 days/week. The Stability condition had significantly higher self-weighing frequency (3.18 ± 1.72 days/week) compared to the Loss (2.51 ± 1.99 days/week) and the Bibliotherapy conditions (2.22 ± 1.63 days/week). Adjusting for baseline weight and treatment condition, self-weighing 3-4 days/week was associated with weight stability (-0.77 kg, 95% CI: -2.2946, 0.7474, p = 0.3175), and self-weighing 5 or more days/week was associated with 2.26 kg weight loss (95% CI: -3.9249, -0.5953, p = 0.0080). Conclusions: Self-weighing may serve as a useful tool for weight gain prevention after smoking cessation. Feedback received about self-weighing behaviors and weight trajectory (similar to the feedback Stability participants received) might enhance adherence.

Disparities in functional recovery after dysvascular lower limb amputation are associated with employment status and self-efficacy.

PURPOSE: Employment status is considered a determinant of health, yet returning to work is frequently a challenge after lower limb amputation. No studies have documented if working after lower limb amputation is associated with functional recovery. The study's purpose was to examine the influence of full-time employment on functioning after lower limb amputation. METHODS: Multisite, cross-sectional study of 49 people with dysvascular lower limb amputation. Outcomes of interest included performance-based measures, the Component Timed-Up-and-Go test, the 2-min walk test, and self-reported measures of prosthetic mobility and activity participation. RESULTS: Average participant age was 62.1 ± 9.7 years, 39% were female and 45% were persons of color. Results indicated that 80% of participants were not employed full-time. Accounting for age, people lacking full-time employment exhibited significantly poorer outcomes of mobility and activity participation. Per regression analyses, primary contributors to better prosthetic mobility were working full-time (R2 ranging from 0.06 to 0.24) and greater self-efficacy (R2 ranging from 0.32 to 0.75). CONCLUSIONS: This study offers novel evidence of associations between employment and performance-based mobility outcomes after dysvascular lower limb amputation. Further research is required to determine cause-effect directionalities. These results provide the foundation for future patient-centered research into how work affects outcomes after lower limb amputation. IMPLICATIONS FOR REHABILITATIONLower limb amputation can pose barriers to employment and activity participation, potentially affecting the quality of life.This study found that the majority of people living with lower limb amputation due to dysvascular causes were not employed full-time and were exhibiting poorer prosthetic outcomes.Healthcare practitioners should consider the modifiable variable of employment when evaluating factors that may affect prosthetic mobility.The modifiable variable of self-efficacy should be assessed by healthcare professionals when evaluating factors that may affect prosthetic mobility.

Sync for Genes: Making Clinical Genomics Available for Precision Medicine at the Point-of-Care.

BACKGROUND: Making genomic data available at the point-of-care and for research is critical for the success of the Precision Medicine Initiative (PMI), a research initiative which seeks to change health care by "tak(ing) into account individual differences in people's genes, environments, and lifestyles." The Office of the National Coordinator for Health Information Technology (ONC) led Sync for Genes, a program to develop standards that make genomic data available when and where it matters most. This article discusses lessons learned from recent Sync for Genes activities. OBJECTIVES: The goals of Sync for Genes were to (1) demonstrate exchange of genomic data using health data standards, (2) provide feedback for refinement of health data standards, and (3) synthesize project experiences to support the integration of genomic data at the point-of-care and for research. METHODS: Four organizations participated in a program to test the Health Level Seven International (HL7®) Fast Healthcare Interoperability Resources (FHIR®) standard, which supports sharing genomic data. ONC provided access to subject matter experts, resources, tools, and technical guidance to support testing activities. Three of the four organizations participated in HL7 FHIR Connectathons to test FHIR's ability to exchange genomic diagnostic reports. RESULTS: The organizations successfully demonstrated exchange of genomic diagnostic reports using FHIR. The feedback and artifacts that resulted from these activities were shared with HL7 and made publicly available. Four areas were identified as important considerations for similar projects: (1) FHIR proficiency, (2) developer support, (3) project scope, and (4) bridging health information technology and genomic expertise. CONCLUSION: Precision medicine is a rapidly evolving field, and there is opportunity to continue maturing health data standards for the exchange of necessary genomic data, increasing the likelihood that the standard supports the needs of users.

Knowledge of and Preparedness for Use of Environmental Assessments in Shelters During Disasters: Results of the 2013 State and Territorial Use of Shelter Assessments Survey.

OBJECTIVE: Environmental health assessments of disaster shelters are critical for monitoring the living conditions of the occupants. However, knowledge and levels of utilization of these assessments have never been estimated in the United States or its territories. We aimed to conduct a cross-sectional survey to ascertain knowledge and Utilization of environmental health disaster shelter assessments. METHODS: The State and Territorial Use of Shelter Assessments Survey (STUSA) of environmental health department directors (N=56) was carried out in 2013. RESULTS: Survey responses were received from 55 of 56 targeted jurisdictions. Of those respondents, 92% of state jurisdictions and 100% of territories reported having knowledge about shelter assessments. However, only 40% of states and 60% of territories reported receiving formal training, and 53% of states and 50% of territories reported having operational procedures for shelter assessments. High levels of knowledge and familiarity and low levels of training and processes for operationalizing assessments were assessed. CONCLUSIONS: Because environmental health assessments may provide useful information in disaster settings, we need to understand the barriers to their implementation. The results of these assessments may also help to validate their usefulness in protecting shelter occupants during disasters. (Disaster Med Public Health Preparedness. 2017;11:11-14).

Iron deficient and manganese supplemented diets alter metals and transporters in the developing rat brain.

Manganese (Mn) neurotoxicity in adults can result in psychological and neurological disturbances similar to Parkinson's disease, including extrapyramidal motor system defects and altered behaviors. Iron (Fe) deficiency is one of the most prevalent nutritional disorders in the world, affecting approximately 2 billion people, especially pregnant and lactating women, infants, toddlers, and adolescents. Fe deficiency can enhance brain Mn accumulation even in the absence of excess Mn in the environment or the diet. To assess the neurochemical interactions of dietary Fe deficiency and excess Mn during development, neonatal rats were exposed to either a control diet, a low-Fe diet (ID), or a low-Fe diet supplemented with Mn (IDMn) via maternal milk during the lactation period (postnatal days [PN] 4-21). In PN21 pups, both the ID and IDMn diets produced changes in blood parameters characteristic of Fe deficiency: decreased hemoglobin (Hb) and plasma Fe, increased plasma transferrin (Tf), and total iron binding capacity (TIBC). Treated ID and IDMn dams also had decreased Hb throughout lactation and ID dams had decreased plasma Fe and increased Tf and TIBC on PN21. Both ID and IDMn pups had decreased Fe and increased copper brain levels; in addition, IDMn pups also had increased brain levels of several other essential metals including Mn, chromium, zinc, cobalt, aluminum, molybdenum, and vanadium. Concurrent with altered concentrations of metals in the brain, transport proteins divalent metal transporter-1 and transferrin receptor were increased. No significant changes were determined for the neurotransmitters gamma aminobutyric acid and glutamate. The results of this study confirm that there is homeostatic relationship among several essential metals in the brain and not simply between Fe and Mn.

Brain accumulation of depleted uranium in rats following 3- or 6-month treatment with implanted depleted uranium pellets.

Depleted uranium (DU) is used to reinforce armor shielding and increase penetrability of military munitions. Although the data are conflicting, DU has been invoked as a potential etiological factor in Gulf War syndrome. We examined regional brain DU accumulation following surgical implantation of metal pellets in male Sprague-Dawley rats for 3 or 6 mo. Prior to surgery, rats were randomly divided into five groups: Nonsurgical control (NS Control); 0 DU pellets/20 tantalum (Ta) pellets (Sham); 4 DU pellets/16 Ta pellets (Low); 10 DU pellets/10 Ta pellets (Medium); 20 DU pellets/0 Ta pellets (High). Rats were weighed weekly as a measure of general health, with no statistically significant differences observed among groups in either cohort. At the conclusion of the respective studies, animals were perfused with phosphate-buffered saline, pH 7.4, to prevent contamination of brain tissue with DU from blood. Brains were removed and dissected into six regions: cerebellum, brainstem (pons and medulla), midbrain, hippocampus, striatum, and cortex. The uranium content was measured in digested samples as its 238U isotope by high-resolution inductively coupled plasma-mass spectrometry. After 3 mo postimplantation, DU significantly accumulated in all brain regions except the hippocampus in animals receiving the highest dose of DU (p < 0.05). By 6 mo, however, significant accumulation was measured only in the cortex, midbrain, and cerebellum (p < 0.01). Our data suggest that DU implanted in peripheral tissues can preferentially accumulate in specific brain regions.

A manganese-enhanced diet alters brain metals and transporters in the developing rat.

Manganese (Mn) neurotoxicity in adults can result in psychological and neurological disturbances similar to Parkinson's disease, including extrapyramidal motor system defects and altered behaviors. However, virtually nothing is known regarding excess Mn accumulation during central nervous system development. Developing rats were exposed to a diet high in Mn via maternal milk during lactation (PN4-21). The high Mn diet resulted in changes in hematological parameters similar to those seen with iron (Fe) deficiency in dams (decreased plasma Fe; increased plasma transferrin [Tf]) and pups (decreased hemoglobin [Hb] and plasma Fe; increased plasma Tf and total iron binding capacity). Mn-exposed pups showed an increase in brain Mn, chromium, and zinc concurrent with a decrease in brain Fe. In conjunction with the altered transport and distribution of essential metals within the brain, there was enhanced protein expression of the divalent metal transporter-1 (DMT-1) and transferrin receptor (TfR) overall in the brain; there was a general increase in each region analyzed (cerebellum, cortex, hippocampus, midbrain, and striatum). Neurochemical changes were observed as an increase in gamma-aminobutyric acid (GABA) and the ratio of GABA to glutamate, indicating enhanced inhibitory transmission in the brain. The results of this study demonstrate that developing rats undergo alterations in the transport and distribution of essential metals translating to neurochemical perturbations after maternal exposure to a diet supplemented with excess levels of Mn.

Developmental neurotoxicity of chlorpyrifos: targeting glial cells.

The pesticide chlorpyrifos (CPF) causes neurobehavioral damage, even at doses that do not elicit acute cholinergic toxicity. CPF disrupts the developing brain during glial proliferation and differentiation. Since glial cells play critical roles in brain development and function, we hypothesized that CPF neurotoxicity involves alteration of glial cell development. CPF effects in C6 glioma cells mirrored effects in the intact brain: inhibited DNA synthesis; interfered with adenylyl cyclase (AC) signaling; obstructed DNA binding to transcription factors involved in cell differentiation; and enhanced reactive oxygen species (ROS) formation. CPF was administered to prenatal and neonatal rats and examined for markers of astrocytes, oligodendrocytes, and neurons. Widespread effects were elicited by exposure during the peak period of gliogenesis. Males were preferentially targeted during postnatal exposures while females experienced delayed effects following gestational exposure, commensurate with behavioral outcomes. Alterations in glial cell development contribute to CPF neurotoxicity, extending vulnerability to myelination, synaptic plasticity, and architectural modeling, which continue into adolescence.

Synthesis of Pt(dpk)Cl(4) and the reversible hydration to Pt(dpk-O-OH)Cl(3).H-phenCl: X-ray, spectroscopic, and electrochemical characterization.

We report on the synthesis of a platinum(IV) compound containing a di-2-pyridyl ketone (dpk) ligand that is stable both in its anhydrous form [Pt(dpk)Cl(4)] (1) and in its hydrated form [Pt(dpk-O-OH)Cl(3)].H-phenCl (2). The crystal structure of the hydrated form shows that one of the hydroxide groups from the resulting gem-diol has undergone a cyclometalation/condensation reaction resulting in an oxygen atom directly coordinated to the Pt(IV) center and the formation of H-phenCl. We correlate our physical data with predictions made by molecular modeling, and we propose an explanation for the unusual activity found for this dpk ketone. Spectroscopic and solubility studies are presented here, as well. Electrochemical studies of 1 indicate that it undergoes a highly irreversible reduction at a potential of about -0.45 V vs Ag(+)/Ag in CH(3)CN and that the irreversibility is likely due to an EC mechanism, the nature of which is currently under further investigation. Another distinct redox pair, apparently reversible, appears at a potential of about -1.1 V vs Ag(+)/Ag.

Sex-selective hippocampal alterations after adolescent nicotine administration: effects on neurospecific proteins.

Nicotine is a neuroteratogen that targets cell development and synaptic function into adolescence, when smoking typically commences. We used a rat model of adolescent nicotine exposure to characterize the types of cells involved in hippocampal alterations. Nicotine was given to adolescent rats by minipump infusions from postnatal day (PN) 30 to PN47.5, using a dose rate (6 mg/kg/day) that replicates the plasma nicotine levels found in smokers. We examined specific neuronal and astrocyte proteins in the posttreatment period (PN50, PN60), when deficits in neurotransmission first appear: glial fibrillary acidic protein (GFAP), a marker for astrocytes; neurofilament 68-kDa protein (NF68), which is concentrated in the neuronal perikaryon and proximal neurites; and neurofilament 200-kDa protein (NF200), which is found in axonal projections distal to the perikaryon. Adolescent nicotine treatment evoked a significant decrease across all three markers, with the effect restricted to females and showing intensification between PN50 and PN60. These changes correspond to the sex-selectivity and temporal course over which other biomarkers indicate hippocampal cell damage and alterations in synaptic function. We conclude that administration of nicotine to adolescent rats alters neuroproteins in the female hippocampus during withdrawal, effects that could contribute to neurobehavioral deficits.

Developmental neurotoxicity elicited by prenatal or postnatal chlorpyrifos exposure: effects on neurospecific proteins indicate changing vulnerabilities.

The developmental neurotoxicity of the organophosphate pesticide chlorpyrifos (CPF) is thought to involve both neurons and glia, thus producing a prolonged window of vulnerability. To characterize the cell types and brain regions involved in these effects, we administered CPF to developing rats and examined neuroprotein markers for oligodendrocytes (myelin basic protein, MBP), for neuronal cell bodies (neurofilament 68 kDa, NF68), and for developing axons (neurofilament 200 kDa, NF200). Prenatal CPF administration on gestational days (GDs) 17-20 elicited an immediate (GD21) enhancement of MBP and NF68; by postnatal day (PN) 30, however, there were deficits in all three biomarkers, with the effect restricted to females. Exposure in the early postnatal period, PN1-4, did not evoke significant short-term or long-term changes in the neuroproteins. However, with treatment on PN11-14, we found reductions in MBP in the immediate posttreatment period (PN15, PN20) throughout the brain, and deficiencies across all three proteins emerged by PN30. With this regimen, males were targeted preferentially. The sex-selective effects seen here for the GD17-20 and PN11-14 regimens match those reported earlier for subsequent behavioral performance. These results indicate a shift in the populations of neural cells targeted by CPF, dependent upon the period of exposure. Similarly, developmental differences in the sex selectivity of the biochemical mechanisms underlying neurotoxicant actions are likely to contribute to discrete behavioral outcomes.

Methyl parathion: a review of health effects.

Methyl parathion is an organophosphorus (OP) insecticide with insecticidal properties derived from acetylcholinesterase (AChE) inhibition; this same property is also the root of its toxicity in humans. Poisoning with methyl parathion leads to cholinergic overstimulation with signs of toxicity including sweating, dizziness, vomiting, diarrhea, convulsions, cardiac arrest, respiratory arrest, and, in extreme cases, death. Reports of methyl parathion intoxication, usually seen only in field pesticide applicators, have increased throughout the United States as a result of unauthorized application of methyl parathion inside homes. The health concerns of the use of methyl parathion have resulted in cancellation of its use in most food crops in the United States. This review examines the well-documented neurotoxicity of methyl parathion as well as effects on other organ systems.

Chlorpyrifos targets developing glia: effects on glial fibrillary acidic protein.

The organophosphate pesticide, chlorpyrifos (CPF), is a developmental neurotoxicant. In cell cultures, CPF affects gliotypic cells to a greater extent than neuronotypic cells, suggesting that glial development is a specific target. We administered CPF to developing rats and examined the levels of glial fibrillary acidic protein (GFAP), an astrocytic marker. Prenatal CPF exposure (gestational days 17-20) elicited an increase in GFAP levels in fetal brain, but the effect was seen only at high doses that elicited maternal and fetal systemic toxicity. Early postnatal (PN) CPF treatment (PN1-4) elicited effects only in the cerebellum of male rats; GFAP was suppressed initially (PN5) and showed a rebound elevation (PN10) before returning to normal values by PN30. In contrast, when we administered CPF during the peak of gliogenesis and glial cell differentiation (PN11-14), GFAP was initially decreased across all brain regions and in both sexes; in males, subsequent elevations were seen on PN30, with the largest effect in the striatum; females also showed an increase in striatal GFAP. Our results indicate that CPF disrupts the pattern of glial development in vivo, with the maximum effect corresponding to the peak period of gliogenesis and glial cell differentiation. As glia are responsible for axonal guidance, synaptogenesis and neuronal nutrition, glial targeting suggests that these late-occurring developmental processes are vulnerable to CPF, extending the critical period for susceptibility into stages of synaptic plasticity, myelination, and architectural modeling of the developing brain.