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To assess whether a community water service is associated with the frequency of sugar-sweetened beverages (SSB) consumption, obesity, or perceived health status in rural Alaska.
We examined the cross-sectional associations between community water access and frequency of SSB consumption, body mass index categories, and perceived health status using data from the 2013 and 2015 Alaska Behavioral Risk Factor Surveillance System (BRFSS). Participants were categorized by zip code to ‘in-home piped water service’ or ‘no in-home piped water service’ based on water utility data. We evaluated the univariable and multivariable (adjusting for age, household income and education) associations between water service and outcomes using log-linear survey-weighted generalized linear models.
Rural Alaska, USA.
Eight hundred and eighty-seven adults, aged 25 years and older.
In unadjusted models, participants without in-home water reported consuming SSB more often than participants with in-home water (1·46, 95 % CI: 1·06, 2·00). After adjustment for potential confounders, the effect decreased but remained borderline significant (1·29, 95 % CI: 1·00, 1·67). Obesity was not significantly associated with water service but self-reported poor health was higher in those communities without in-home water (1·63, 95 % CI: 1·05, 2·54).
Not having access to in-home piped water could affect behaviours surrounding SSB consumption and general perception of health in rural Alaska.
The current study describes the results obtained from clinical examination of over 4700 suckling piglets from 19 individual herds in Germany. In this cohort the prevalence of inflammation and necrosis in the tails, ears, claw coronary bands, heels and teats was determined using a pre-defined scoring system. Results show that already in the 1st days of life, piglets were affected by inflammation and necrosis of the heels (80%), claw coronary bands (50%) and tail base (20%). The praevalences of these alterations in piglets were influenced by genetics (P <0.001) and age, decreasing gradually in the 2nd week of life (P <0.001). Moreover, a correlation between tail length after tail docking and the prevalence of tail necrosis (P⩽0.04) was found. Tail and ear biting as a behavioural trait was not detected during this study. The early onset, appearance and multiple locations of clinical signs of inflammation and the positive correlation with the genetic background of the piglets may suggest an impairment of the innate immune system by infectious and non-infectious agents. This is in contrast to previously described behavioural abnormalities seen in fattening pigs. Considering the obvious reduction of animal welfare due to the described lesions, there is a need to create awareness among pig farmers and to understand the multifactorial causality involved in this inflammation and necrosis syndrome in piglets.
To assess the prevalence of prediabetes and metabolic abnormalities among overweight or obese clozapine- or olanzapine-treated schizophrenia patients, and to identify characteristics of the schizophrenia group with prediabetes.
A cross-sectional study assessing the presence of prediabetes and metabolic abnormalities in schizophrenia clozapine- or olanzapine-treated patients with a body mass index (BMI) ≥27 kg/m2. Procedures were part of the screening process for a randomized, placebo-controlled trial evaluating liraglutide vs placebo for improving glucose tolerance. For comparison, an age-, sex-, and BMI-matched healthy control group without psychiatric illness and prediabetes was included. Prediabetes was defined as elevated fasting plasma glucose and/or impaired glucose tolerance and/or elevated glycated hemoglobin A1c.
Among 145 schizophrenia patients (age = 42.1 years; males = 59.3%) on clozapine or olanzapine (clozapine/olanzapine/both: 73.8%/24.1%/2.1%), prediabetes was present in 69.7% (101 out of 145). While schizophrenia patients with and without prediabetes did not differ regarding demographic, illness, or antipsychotic treatment variables, metabolic abnormalities (waist circumference: 116.7±13.7 vs 110.1±13.6 cm, P = 0.007; triglycerides: 2.3±1.4 vs 1.6±0.9 mmol/L, P = 0.0004) and metabolic syndrome (76.2% vs 40.9%, P<0.0001) were significantly more pronounced in schizophrenia patients with vs without prediabetes. The age-, sex-, and BMI-matched healthy controls had significantly better glucose tolerance compared to both groups of patients with schizophrenia. The healthy controls also had higher levels of high-density lipoprotein compared to patients with schizophrenia and prediabetes.
Prediabetes and metabolic abnormalities were highly prevalent among the clozapine- and olanzapine-treated patients with schizophrenia, putting these patients at great risk for later type 2 diabetes and cardiovascular disease. These results stress the importance of identifying and adequately treating prediabetes and metabolic abnormalities among clozapine- and olanzapine-treated patients with schizophrenia.
Kalahari Group sediments accumulated in the Kalahari basin, which started forming during the breakup of Gondwana in the early Cretaceous. These sediments cover an extensive part of southern Africa and form a low-relief landscape. Current models assume that the Kalahari Group accumulated throughout the entire Cenozoic. However, chronology has been restricted to early–middle Cenozoic biostratigraphic correlations and to OSL dating of only the past ~ 300 ka. We present a new chronological framework that reveals a dynamic nature of sedimentation in the southern Kalahari. Cosmogenic burial ages obtained from a 55 m section of Kalahari Group sediments from the Mamatwan Mine, southern Kalahari, indicate that the majority of deposition at this location occurred rapidly at 1–1.2 Ma. This Pleistocene sequence overlies the Archaean basement, forming a significant hiatus that permits the possibility of many Phanerozoic cycles of deposition and erosion no longer preserved in the sedimentary record. Our data also establish the existence of a shallow early–middle Pleistocene water body that persisted for > 450 ka prior to this rapid period of deposition. Evidence from neighboring archeological excavations in southern Africa suggests an association of high-density hominin occupation with this water body.
Somatoform disorders are costly for society in terms of increased healthcare expenditure. Patients' illness perceptions have been found to play a role in somatoform disorders. However, it is unclear whether illness perceptions predict higher health costs in these patients.
A total of 1785 primary care patients presenting a new health complaint completed a questionnaire on their illness perceptions and emotional distress before the consultation. The physicians completed a questionnaire for each patient on diagnostics after the consultation. In a stratified subsample, physician interviewers established diagnoses of DSM-IV somatization and undifferentiated somatoform disorders (n = 144) using the Schedules for Clinical Assessment in Neuropsychiatry. Healthcare expenditure was obtained from Danish health registers for a 2-year follow-up period.
Patients had more negative perceptions of their well-defined physical health problems when they had a co-morbid somatoform disorder. A strong illness identity [β = 0.120, 95% confidence interval (CI) 0.029–0.212, p = 0.012], perceived negative consequences (β = 0.010, 95% CI 0.001–0.019, p = 0.024), a long timeline perspective (β = 0.013, 95% CI 0.005–0.021, p = 0.001), low personal control (β = − 0.009, 95% CI –0.015 to −0.002, p = 0.011) and negative emotional representations (β = 0.009, 95% CI 0.002–0.017, p = 0.020) predicted healthcare expenditure in somatoform disorders.
The results suggest that illness perceptions play a role in the perpetuation of symptoms in somatoform disorders and predict higher future healthcare expenditure among a subgroup of these patients.
Of the 13 US vancomycin-resistant Staphylococcus aureus (VRSA) cases, 8 were identified in southeastern Michigan, primarily in patients with chronic lower-extremity wounds. VRSA infections develop when the vanA gene from vancomycin-resistant enterococcus (VRE) transfers to S. aureus. Incl8-like plasmids in VRE and pSK41-like plasmids in S. aureus appear to be important precursors to this transfer.
Identify the prevalence of VRSA precursor organisms.
Prospective cohort with embedded case-control study.
Southeastern Michigan adults with chronic lower-extremity wounds.
Adults presenting to 3 southeastern Michigan medical centers during the period February 15 through March 4, 2011, with chronic lower-extremity wounds had wound, nares, and perirectal swab specimens cultured for S. aureus and VRE, which were tested for pSK41-like and Incl8-like plasmids by polymerase chain reaction. We interviewed participants and reviewed clinical records. Risk factors for pSK41-positive S. aureus were assessed among all study participants (cohort analysis) and among only S. aureus-colonized participants (case-control analysis).
Of 179 participants with wound cultures, 26% were colonized with methicillin-susceptible S. aureus, 27% were colonized with methicillin-resistant S. aureus, and 4% were colonized with VRE, although only 17% consented to perirectal culture. Six participants (3%) had pSK41-positive S. aureus, and none had Incl8-positive VRE. Having chronic wounds for over 2 years was associated with pSK41-positive S. aureus colonization in both analyses.
Colonization with VRSA precursor organisms was rare. Having long-standing chronic wounds was a risk factor for pSK41-positive S. aureus colonization. Additional investigation into the prevalence of VRSA precursors among a larger cohort of patients is warranted.
Several progenitor scenarios have been suggested for Type Ia supernovae. Here we discuss the consequences for the explosion mechanism and for observables of some of them, which are explored by means of multi-dimensional hydrodynamic and radiation transfer simulations. While the observables predicted from delayed detonations of Chandrasekhar-mass white dwarfs agree reasonably well with the data, the corresponding progenitor systems may be too rare to account for the observed rate of Type Ia supernovae. Several alternatives are investigated of which violent mergers of two white dwarfs and, perhaps, double detonations of sub-Chandrasekhar mass white dwarfs hold promise for reproducing the observables of normal Type Ia supernovae.
We argue that detonations of sub-Chandrasekhar mass white dwarfs can lead to bright explosions with light curves and spectra similar to those of observed Type Ia supernovae. Given that binary systems containing accreting sub-Chandrasekhar mass white dwarfs should be common, this suggests that a non-negligible fraction of the observed Type Ia supernova rate may arise from sub-Chandrasekhar mass explosions, if they can be ignited. We discuss aspects of how such explosions might be realized in nature and both merits and challenges associated with invoking sub-Chandrasekhar mass explosion models to account for observed Type Ia supernovae.
We present direct terrestrial evidence of ice volume change of the Darwin and Hatherton glaciers which channel ice from the Transantarctic Mountains into the Ross Ice Shelf. Combining glacial geomorphology with cosmogenic exposure ages from 25 erratics indicates a pre-LGM ice volume at least 600 m thicker than current Hatherton ice elevation was established at least 2.2 million years ago. In particular, five erratics spread across a drift deposit at intermediate elevations located below a prominent moraine feature mapped previously as demarcating the LGM ice advance limits, give a well-constrained single population with mean 10Be age of 37.0 ± 5.5 ka (1σ). At lower elevations of 50–100 m above the surface of Lake Wellman, a further five samples from within a younger drift deposit range in exposure age from 1 to 19 ka. Our preferred age model interpretation, which is partly dependent on the selection of a minimum or maximum age-elevation model, suggests that LGM ice volume was not as large as previously estimated and constrains LGM ice elevation to be within ± 50 m of the modern Hatherton Glacier ice surface, effectively little different from what is observed today.
Milk contains immunomodulatory compounds that may be important to protect the immature intestine in preterm neonates from harmful inflammatory reactions involved in disorders like necrotising enterocolitis (NEC). We hypothesised that bovine colostrum and milk formulas enriched with sialic acids (SL), gangliosides (Gang) or osteopontin (OPN) would improve gastrointestinal function and NEC resistance in preterm neonates. Forty-seven caesarean-delivered preterm pigs were given total parenteral nutrition for 2 d followed by 1·5 d of enteral feeding. In Expt 1, a control formula was compared with an OPN-enriched formula (n 13), while Expt 2 compared a control formula with bovine colostrum or formulas enriched with Gang or SL (n 4–6). OPN enrichment decreased NEC severity relative to control formula (P < 0·01), without any significant effects on NEC incidence, digestive enzyme activities and hexose absorption. Neither SL- nor Gang-enriched formulas improved NEC resistance or digestive functions, while all the intestinal functional parameters were significantly improved in pigs fed bovine colostrum, relative to formula. The effects in vivo were supported in vitro by bacteria- and dose-dependent modulation by colostrum whey of the cytokine response from bacteria-stimulated murine bone marrow-derived dendritic cells (DC). In conclusion, OPN had only moderate NEC-protective effects, while formulas enriched with Gang or SL were ineffective. The observed modulation of DC cytokine response by bovine colostrum whey in vitro may be due to a synergistic action of various milk bioactives, and it may explain its beneficial effects on NEC development and intestinal function in a piglet model of preterm infants.
The development of language and communication may play an important role in the emergence of behavioral problems in young children, but they are rarely included in predictive models of behavioral development. In this study, cross-sectional relationships between language, attention, and behavior problems were examined using parent report, videotaped observations, and performance measures in a sample of 116 severely and profoundly deaf and 69 normally hearing children ages 1.5 to 5 years. Secondary analyses were performed on data collected as part of the Childhood Development After Cochlear Implantation Study, funded by the National Institutes of Health. Hearing-impaired children showed more language, attention, and behavioral difficulties, and spent less time communicating with their parents than normally hearing children. Structural equation modeling indicated there were significant relationships between language, attention, and child behavior problems. Language was associated with behavior problems both directly and indirectly through effects on attention. Amount of parent–child communication was not related to behavior problems.
George J. Brewer, Department of Human Genetics, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA,
Fred Askari, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA,
Matthew T. Lorincz, Department of Neurology, University of Michigan, Ann Arbor, MI, USA,
Martha Carlson, Department of Pediatrics-Neurology, University of Michigan, Ann Arbor, MI, USA,
Michael Schilsky, Department of Internal Medicine, Cornell University, New York, NY, USA,
Karen J. Kluin, Department of Neurology, Department of Speech Pathology, University of Michigan, Ann Arbor, MI, USA,
Peter Hedera, Department of Neurology, Vanderbilt University, Nashville, TN, USA,
Paolo Moretti, Departments of Neurology and Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA,
John K. Fink, Department of Neurology, University of Michigan, Ann Arbor, MI, USA,
Roberta Tankanow, College of Pharmacy, University of Michigan, Ann Arbor, MI, USA,
Robert B. Dick, Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA,
Julia Sitterly, Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA
Background: The initial treatment of the neurologic presentation of Wilson's disease is problematic. Penicillamine, used for years on most patients, causes neurologic worsening in up to half of such patients, and half of those who worsen never recover. Zinc, ideal for maintenance therapy, is too slow for these acutely ill patients. We have developed tetrathiomolybdate (TM) for this type of patient, and it has worked well in open label studies. Trientine, another anticopper drug on the market approved for penicillamine intolerant patients, had not been tried in this type of patient. Here, we report on a double blind trial of TM versus trientine in the neurologically presenting Wilson's disease patient. Design and Methods: The study was a double blind design in which patients received either TM plus zinc, or trientine plus zinc, for 8 weeks. Patients were accepted if they presented with neurologic symptoms from Wilson's disease, if they had not been treated longer than 4 weeks with penicillamine or trientine. Patients were followed in the hospital for the 8 weeks of treatment with weekly semiquantitative neurologic and speech examinations, to evaluate possible neurologic worsening. They also had blood and urine studies done weekly. At discharge from hospital they were continued on zinc maintenance therapy, and returned at yearly intervals for 3 years for further evaluation. Results: Twenty-three patients were entered into the trientine arm and 6 reached criteria for neurologic deterioration, while 25 patients were entered into the TM arm and only 1 deteriorated (p < 0.05).
Background: The initial treatment of the neurologic presentation of Wilson's disease is problematic. Penicillamine, used for years on most patients, causes neurologic worsening in up to half of such patients, and half of those who worsen never recover. Zinc, ideal for maintenance therapy, is too slow for these acutely ill patients. We have developed tetrathiomolybdate (TM) for this type of patient, and it has worked well in open label studies. Trientine, another anticopper drug on the market approved for penicillamine intolerant patients, had not been tried in this type of patient. Here, we report on a double blind trial of TM versus trientine in the neurologically presenting Wilson's disease patient. Design and Methods: The study was a double blind design in which patients received either TM plus zinc, or trientine plus zinc, for 8 weeksThis study was originally published in reference 1. Patients were accepted if they presented with neurologic symptoms from Wilson's disease, if they had not been treated longer than 4 weeks with penicillamine or trientine. Patients were followed in the hospital for the 8 weeks of treatment with weekly semiquantitative neurologic and speech examinations, to evaluate possible neurologic worsening. They also had blood and urine studies done weekly. At discharge from hospital they were continued on zinc maintenance therapy, and returned at yearly intervals for 3 years for further evaluation. Results: Twenty-three patients were entered into the trientine arm and 6 reached criteria for neurologic deterioration, while 25 patients were entered into the TM arm and only 1 deteriorated (p < 0.05). One patient on trientine had an adverse event while 7 on TM had adverse events. All adverse events were mild. Four patients in the trientine arm died during follow-up, 3 having shown initial neurologic deterioration, 2 patients in the TM arm died. In those patients who did not deteriorate or die, neurologic and speech recovery over 3 years was good. Interpretation: TM is a superior choice to trientine for the initial therapy of neurologic Wilson's disease.
Francisella tularensis was identified as the cause of a die-off which occurred among a colony of semi-free-living common marmosets (Callithrix jacchus). During the outbreak 5 out of 62 animals died of tularaemia in a research facility located in the district of Goettingen, Germany. All animals had been born at the facility suggesting an endemic infection. A total of five culture isolates were recovered and characterized as F. tularensis holarctica, biovar I. These cultures represent the first isolates obtained in the Federal Republic of Germany for more than 45 years. The outbreak area shows several geographical and ecological characteristics known to favour long-term presence of F. tularensis. Persistence of the pathogen in the remote region along the former German–German border, continuous re-introduction from eastern European countries after destruction of the ‘Iron curtain’ or introduction through migrating birds are testable hypotheses which could explain the emergence of tularaemia in this particular region.
Background and objective: Proinflammatory cytokines as well as nitric oxide (NO) play a major role in mediating the response to lipopolysaccharide (LPS). The present study tested the hypothesis that LPS induces proinflammatory cytokines in the lung via the Toll-like receptor 4 (TLR4)/CD14 signalling cascade. Methods: Control mice and TLR4-deficient (TLR4-D) mice were used to test TLR4-mediated effects of LPS. Both strains received either Escherichia coli LPS (20 mg kg−1 intraperitoneal) or saline and their lungs were collected at different time points. Pulmonary nuclear factor κB (NFκB) activation was investigated with electromobility shift assay. mRNA expression of inflammatory mediators and their corresponding receptors were detected with Ribonuclease Protection Assay. Protein expression was detected by ELISA and western blotting. Inducible NO synthase (iNOS) expression was monitored by RT-PCR and iNOS activity by conversion of l-arginine to citrulline. Immune cells were sampled by bronchoalveolar lavage (BAL) and classified. Results: LPS application induced CD14-, but not TLR4 protein expression in control mice. Activation of pulmonary NFκB was observed within 60 min in control, but not in TLR4-D mice. Six hours of LPS administration induced a significant increase in pulmonary tumour necrosis factor α-, interleukin-1β- and interleukin-6 mRNA and protein expression in control mice compared to TLR4-D mice. Furthermore, LPS induced a significantly higher increase of the iNOS expression and catalytic activity in control mice than in TLR4-D mice. BAL revealed an increase in total cell count in all LPS treated mice. Conclusion: Our findings suggest that TLR4 plays a key role for regulating the expression of relevant cytokines within the lung during endotoxic shock.
Inherited disorders in which the predominant clinical syndrome is gait disturbance due to lower extremity spastic weakness are referred to collectively as the hereditary spastic paraplegias (HSPs). The various types of HSP are classified clinically according to the mode of inheritance (dominant, recessive, and X-linked); and whether lower extremity spasticity and weakness and often urinary urgency and subtle dorsal column impairment occur alone (“uncomplicated HSP”), or are accompanied by additional neurologic or systemic symptoms for which alternative causes are excluded (“complicated HSP”) (Harding, 1983).
There are at least 20 genetically distinct types of HSP (Table 53.1) including ten dominant, seven recessive, and three X-linked HSP syndromes. Eight of these HSP syndromes are “uncomplicated;” eight of these are “complicated” by the presence of additional neurologic signs; and four of these may present as either “uncomplicated” or “complicated” HSP syndromes. For some of these latter syndromes, both “uncomplicated” and “complicated” HSP phenotypes may coexist even in the same family (Table 53.1).
It is important to recognize that the HSPs are classified clinically, rather than on the basis of subclinical involvement or neuropathologic findings. Certainly, lower extremity spastic weakness may be an important feature of many other disorders, both inherited and apparently sporadic including such diverse disorders as amyotrophic lateral sclerosis, Friedreich's ataxia (Berciano et al., 2002; Ragno et al., 1977), Machado Joseph disease (spinocerebellar ataxia type 3), Charlevoix–Sanguenay syndrome (Engert et al., 2000), primary lateral sclerosis, and familial Alzheimer's disease due to presenilin 1 mutation (Brooks et al., 2003; Assini et al., 2003; Tabira et al., 2002).
This paper reports the fabrication of large diameter pores (> 150 nm) in anodic aumina that can be used to create wire arrays with significant surface effects, but without significant quantum confinement. These wires, therefore, allow us to distinguish between optica absorption spectra features originating from quantum effects and those from surface effects. The paper presents techniques towards fabricating these bismuth wire arrays, and presents optical absorption data from two bismuth nanowire arrays in the semimeta-semiconductor transition diameter regime. The results from previous publications are summarized and future directions are outlines.