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Berlin Brandenburg

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  • 1
    In: Environmental Entomology, 2019, Vol. 48(1), pp.12-21
    Description: To date, regulatory pesticide risk assessments have relied on the honey bee ( Apis mellifera L.) (Hymenoptera: Apidae) as a surrogate test species for estimating the risk of pesticide exposure to all bee species. However, honey bees and non- Apis bees may differ in their susceptibility and exposure to pesticides. In 2017, a workshop (‘Pesticide Exposure Assessment Paradigm for Non- Apis Bees’) was held to assess if honey bee risk assessment frameworks are reflective of non- Apis bee pesticide exposure. In this article, we summarize the workshop discussions on bumble bees ( Bombus spp.). We review the life history and foraging behavior of bumble bees and honey bees and discuss how these traits may influence routes and levels of exposure for both taxa. Overall, the major pesticide exposure routes for bumble bees and honey bees are similar; however, bumble bees face additional exposure routes (direct exposure of foraging queens and exposure of larvae and adults to soil residues). Furthermore, bumble bees may receive comparatively higher pesticide doses via contact or oral exposure. We conclude that honey bee pesticide risk assessments may not always be protective of bumble bees, especially queens, in terms of exposure. Data needed to reliably quantify pesticide exposure for bumble bees (e.g., food consumption rates, soil residue levels) are lacking. Addressing these knowledge gaps will be crucial before bumble bee exposure can be incorporated into the pesticide risk assessment process. Because bumble bees exhibit appreciable interspecific variation in colony and behavioral characteristics, data relevant to pesticide exposure should be generated for multiple species.
    Keywords: Bumble Bee ; Honey Bee ; Pesticide Exposure ; Risk Assessment
    ISSN: 0046-225X
    E-ISSN: 1938-2936
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  • 2
    Language: English
    In: Preventive Medicine, December 2015, Vol.81, pp.1-8
    Description: To evaluate the effectiveness of the parent- and early care education (ECE) center-based program on communication between parent, child, and their ECE center providers around fruits, vegetables and whole grain foods (FVWG). A total of n = 30 ECE center; 577 parent–child dyads participated in this group-randomized controlled trial conducted from 2011 to 2013 in Texas (n = 15 ECE center, 327 dyads intervention group; n = 15 ECE center, 250 dyads comparison group). Parent–child and parent-ECE center provider communication was measured using a parent-reported survey administered at baseline and end of the five-week intervention period. Multilevel linear regression analysis was used to compare the pre-to-post intervention changes in the parent–child and parent-ECE center provider communication scales. Significance was set at p 〈 0.05. At baseline, parent–child and parent-ECE center provider communication scores were low. There was a significant increase post-intervention in the parent-ECE center provider communication around vegetables (Adjusted β = 0.78, 95%CI: 0.13, 1.43, p = 0.002), and around fruit (Adjusted β = 0.62, 95%CI: 0.04, 0.20, p = 0.04) among the parents in the intervention group as compared to those in the comparison group. There were no significant intervention effects on parent–child communication. had significant positive effects on improving communication between the parents and ECE center providers around FVWG.
    Keywords: Preschool ; Parent–Child Communication ; Parent-Childcare Provider Communication ; Early Care Education ; Nutrition ; Fruits ; Vegetables ; Whole Grain Foods ; Medicine ; Public Health
    ISSN: 0091-7435
    E-ISSN: 1096-0260
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  • 3
    Language: English
    In: Maternal and child health journal, October 2016, Vol.20(10), pp.2030-6
    Description: Objectives Low gestational weight gain (GWG) in the second and third trimesters has been associated with increased risk of preterm delivery (PTD) among women with a body mass index (BMI) 〈 25 mg/m(2). However, few studies have examined whether this association differs by the assumptions made for first trimester gain or by the reason for PTD. Methods We examined singleton pregnancies during 2000-2008 among women with a BMI 〈 25 kg/m(2) who delivered a live-birth ≥28 weeks gestation (n = 12,526). Women received care within one integrated health care delivery system and began prenatal care ≤13 weeks. Using antenatal weights measured during clinic visits, we interpolated GWG at 13 weeks gestation then estimated rate of GWG (GWGrate) during the second and third trimesters of pregnancy. We also estimated GWGrate using the common assumption of a 2-kg gain for all women by 13 weeks. We examined the covariate-adjusted association between quartiles of GWGrate and PTD (28-36 weeks gestation) using logistic regression. We also examined associations by reason for PTD [premature rupture of membranes (PROM), spontaneous labor, or medically indicated]. Results Mean GWGrate did not differ among term and preterm pregnancies regardless of interpolated or assumed GWG at 13 weeks. However, only with GWGrate estimated from interpolated GWG at 13 weeks, we observed a U-shaped relationship where odds of PTD increased with GWGrate in the lowest (OR 1.36, 95 % CI 1.10, 1.69) or highest quartile (OR 1.49, 95 % CI 1.20, 1.85) compared to GWGrate within the second quartile. Further stratifying by reason, GWGrate in the lowest quartile was positively associated with spontaneous PTD while GWGrate in the highest quartile was positively associated with PROM and medically indicated PTD. Conclusions Accurate estimates of first trimester GWG are needed. Common assumptions applied to all pregnancies may obscure the association between GWGrate and PTD. Further research is needed to fully understand whether these associations are causal or related to common antecedents.
    Keywords: Gestational Weight Gain ; Pregnancy ; Preterm Delivery ; Weight Gain Measures ; Body Weight ; Weight Gain ; Fetal Membranes, Premature Rupture -- Epidemiology ; Premature Birth -- Epidemiology
    ISSN: 10927875
    E-ISSN: 1573-6628
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  • 4
    Language: English
    In: Maternal and Child Health Journal, 2015, Vol.19(9), pp.2066-2073
    Description: Studies report increased risk of preterm birth (PTB) among underweight and normal weight women with low gestational weight gain (GWG). However, most studies examined GWG over gestational periods that differ by term and preterm which may have biased associations because GWG rate changes over the course of pregnancy. Furthermore, few studies have specifically examined the amount and pattern of GWG early in pregnancy as a predictor of PTB. Within one integrated health care delivery system, we examined 12,526 singleton pregnancies between 2000 and 2008 among women with a body mass index 〈25 kg/m 2 , who began prenatal care in the first trimester and delivered a live-birth 〉28 weeks gestation. Using self-reported pregravid weight and serial measured antenatal weights, we estimated GWG and the area under the GWG curve (AUC; an index of pattern of GWG) during the first and second trimesters of pregnancy (≤28 weeks). Using logistic regression adjusted for covariates, we examined associations between each GWG measure, categorized into quartiles, and PTB (〈37 weeks gestation). We additionally examined associations according to the reason for PTB by developing a novel algorithm using diagnoses and procedure codes. Low GWG in the first and second trimesters was not associated with PTB [aOR 1.11, (95 % CI 0.90, 1.38) with GWG 〈8.2 kg by 28 weeks compared to pregnancies with GWG 〉12.9]. Similarly, pattern of GWG was not associated with PTB. Our findings do not support an association between GWG in the first and second trimester and PTB among underweight and normal weight women.
    Keywords: Pregnancy ; Gestational weight gain ; Weight gain measures ; Preterm birth
    ISSN: 1092-7875
    E-ISSN: 1573-6628
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  • 5
    Language: English
    In: The Annals of Thoracic Surgery, December 2016, Vol.102(6), pp.1845-1853
    Description: Despite the critical need for donor lungs, logistic and geographic barriers hinder lung utilization. We hypothesized that lungs donated after circulatory death subjected to 6 hours of cold preservation after ex vivo lung perfusion (EVLP) would have similar outcomes after transplantation as lungs transplanted immediately after EVLP, and that both would perform superiorly compared with lungs transplanted immediately after procurement. Donor porcine lungs were procured after circulatory death and 15 minutes of warm ischemia. Three groups (n = 5 per group) were randomized: immediate left lung transplantation (Immediate group), EVLP for 4 hours followed by transplantation (EVLP group), or EVLP for 4 hours followed by 6 hours of cold preservation followed by transplantation (EVLP+Cold group). Lungs were reperfused for 2 hours before obtaining pulmonary vein samples for partial pressure of oxygen/fraction of inspired oxygen ratio calculations, airway pressures for compliance measurements, and wet/dry weight ratios. The partial pressure of oxygen/fraction of inspired oxygen ratios in the EVLP and EVLP+Cold groups were significantly improved compared with those in the Immediate group (429.7 ± 51.8 and 436.7 ± 48.2 versus 117.4 ± 22.9 mm Hg, respectively). In addition, dynamic compliance was significantly improved in the EVLP and EVLP+Cold groups compared with immediate group (26.2 ± 4.2 and 27.9 ± 3.5 versus 11.1 ± 2.4 mL/cmH O, respectively). There were no differences in oxygenation capacity or dynamic compliance between the EVLP and EVLP+Cold groups. Inflammatory cytokine levels were significantly lower in the EVLP and EVLP+Cold groups. Lungs donated after circulatory death can be successfully transplanted as much as 6 hours after EVLP. Cold preservation of lungs after ex vivo assessment and rehabilitation may improve organ allocation, even to distant recipients, without compromising allograft function.
    Keywords: Animals–Methods ; Extracorporeal Circulation–Methods ; Female–Methods ; Lung Transplantation–Methods ; Male–Methods ; Organ Preservation–Methods ; Shock–Methods ; Swine–Methods ; Time Factors–Methods ; Tissue and Organ Harvesting–Methods ; Warm Ischemia–Methods ; Abridged;
    ISSN: 0003-4975
    E-ISSN: 1552-6259
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  • 6
    In: American Journal of Gastroenterology, 2015, Vol.110(1), pp.170-179
    Description: OBJECTIVES:: METHODS:: RESULTS:: Seventy-five patients had both computer-generated and physician-documented HPIs. The mean overall impression score for computer-generated HPIs was higher than physician HPIs (3.68 vs. 2.80; P〈0.001), even after adjusting for physician and visit type, location, mode of transcription, and demographics. Computer-generated HPIs were also judged more complete (3.70 vs. 2.73; P〈0.001), more useful (3.82 vs. 3.04; P〈0.001), better organized (3.66 vs. 2.80; P〈0.001), more succinct (3.55 vs. 3.17; P〈0.001), and more comprehensible (3.66 vs. 2.97; P〈0.001). CONCLUSIONS::
    Keywords: Medicine;
    ISSN: 0002-9270
    E-ISSN: 15720241
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  • 7
    In: American Journal of Gastroenterology, 2016, Vol.111(11), pp.1546-1556
    Description: OBJECTIVES:: METHODS:: RESULTS:: There were 217 and 154 patients in the GI PROMIS and control arms, respectively. Patient satisfaction was similar between groups (P〉0.05). Intervention patients had similar assessments of their providers’ interpersonal skills (DISQ 89.4±11.7 vs. 89.8±16.0, P=0.79) and shared decision-making (SDM-Q-9 79.3±12.4 vs. 79.0±22.0, P=0.85) vs. controls. CONCLUSIONS::
    Keywords: Medicine;
    ISSN: 0002-9270
    E-ISSN: 15720241
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  • 8
    Language: English
    In: Endocrine-related cancer, August 2011, Vol.18(4), pp.413-28
    Description: Obese breast cancer patients exhibit a higher risk for larger tumor burden and an increased likelyhood of metastasis. The molecular effects of obesity on carcinogenesis are mediated by the autocrine and paracrine effects of the adipocytokine leptin. Leptin participates in the tumor progression and metastasis of human breast. We show that leptin induces clonogenicity and increases the migration potential of breast cancer cells. We found that survivin expression is induced in response to leptin. In this study, we examine the role and leptin-mediated regulation of survivin. Leptin treatment leads to survivin upregulation, due in part to the activation of Notch1 and the release of a transcriptionally active Notch1 intracellular domain (NICD). Chromatin immunoprecipitation analysis shows that NICD gets recruited to the survivin promoter at the CSL (CBF1/RBP-Jk, Su(H), Lag-1) binding site in response to leptin treatment. Inhibition of Notch1 activity inhibits leptin-induced survivin upregulation. Leptin-induced transactivation of epidermal growth factor receptor (EGFR) is involved in leptin-mediated Notch1 and survivin upregulation, demonstrating a novel upstream role of leptin-EGFR-Notch1 axis. We further show that leptin-induced migration of breast cancer cells requires survivin, as overexpression of survivin further increases, whereas silencing survivin abrogates leptin-induced migration. Using a pharmacological approach to inhibit survivin, we show that 3-hydroxy-3-methylglutaryl-coenzyme-A-reductase inhibitors, such as lovastatin, can effectively inhibit leptin-induced survivin expression and migration. Importantly, leptin increased breast tumor growth in nude mice. These data show a novel role for survivin in leptin-induced migration and put forth pharmacological survivin inhibition as a potential novel therapeutic strategy. This conclusion is supported by in vivo data showing the overexpression of leptin and survivin in epithelial cells of high-grade ductal carcinomas in situ and in high-grade invasive carcinomas.
    Keywords: Cell Movement ; Breast Neoplasms -- Metabolism ; Erbb Receptors -- Metabolism ; Inhibitor of Apoptosis Proteins -- Metabolism ; Leptin -- Metabolism ; Receptor, Notch1 -- Metabolism
    ISSN: 13510088
    E-ISSN: 1479-6821
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  • 9
    In: Neurology, 2017, Vol.89(11), pp.1152-1161
    Description: OBJECTIVE:: To determine whether providing remote neurologic care into the homes of people with Parkinson disease (PD) is feasible, beneficial, and valuable. METHODS:: In a 1-year randomized controlled trial, we compared usual care to usual care supplemented by 4 virtual visits via video conferencing from a remote specialist into patientsʼ homes. Primary outcome measures were feasibility, as measured by the proportion who completed at least one virtual visit and the proportion of virtual visits completed on time; and efficacy, as measured by the change in the Parkinsonʼs Disease Questionnaire–39, a quality of life scale. Secondary outcomes included quality of care, caregiver burden, and time and travel savings. RESULTS:: A total of 927 individuals indicated interest, 210 were enrolled, and 195 were randomized. Participants had recently seen a specialist (73%) and were largely college-educated (73%) and white (96%). Ninety-five (98% of the intervention group) completed at least one virtual visit, and 91% of 388 virtual visits were completed. Quality of life did not improve in those receiving virtual house calls (0.3 points worse on a 100-point scale; 95% confidence interval [CI] −2.0 to 2.7 points; p = 0.78) nor did quality of care or caregiver burden. Each virtual house call saved patients a median of 88 minutes (95% CI 70–120; p 〈 0.0001) and 38 miles per visit (95% CI 36–56; p 〈 0.0001). CONCLUSIONS:: Providing remote neurologic care directly into the homes of people with PD was feasible and was neither more nor less efficacious than usual in-person care. Virtual house calls generated great interest and provided substantial convenience. CLINICALTRIALS.GOV IDENTIFIER:: NCT02038959. CLASSIFICATION OF EVIDENCE:: This study provides Class III evidence that for patients with PD, virtual house calls from a neurologist are feasible and do not significantly change quality of life compared to in-person visits. The study is rated Class III because it was not possible to mask patients to visit type.
    Keywords: Medicine;
    ISSN: 0028-3878
    ISSN: 1526632X
    E-ISSN: 1526632X
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  • 10
    Language: English
    In: The Lancet Psychiatry, April 2018, Vol.5(4), pp.339-347
    Description: People with major depressive disorder frequently exhibit increasing persistence of major depressive episodes. However, evidence for neuroprogression (ie, increasing brain pathology with longer duration of illness) is scarce. Microglial activation, which is an important component of neuroinflammation, is implicated in neuroprogression. We examined the relationship of translocator protein (TSPO) total distribution volume (V ), a marker of microglial activation, with duration of untreated major depressive disorder, and with total illness duration and antidepressant exposure. In this cross-sectional study, we recruited participants aged 18–75 years from the Toronto area and the Centre for Addiction and Mental Health (Toronto, ON, Canada). Participants either had major depressive episodes secondary to major depressive disorder or were healthy, as confirmed with a structured clinical interview and consultation with a study psychiatrist. To be enrolled, participants with major depressive episodes had to score a minimum of 17 on the 17-item Hamilton Depression Rating Scale, and had to be medication free or taking a stable dose of medication for at least 4 weeks before PET scanning. Eligible participants were non-smokers; had no history of or concurrent alcohol or substance dependence, neurological illness, autoimmune disorder, or severe medical problems; and were free from acute medical illnesses for the previous 2 weeks before PET scanning. Participants were excluded if they had used brain stimulation treatments within the 6 months before scanning, had used anti-inflammatory drugs lasting at least 1 week within the past month, were taking hormone replacement therapy, had psychotic symptoms, had bipolar disorder (type I or II) or borderline antisocial personality disorder, or were pregnant or breastfeeding. We scanned three primary grey-matter regions of interest (prefrontal cortex, anterior cingulate cortex, and insula) and 12 additional regions and subregions using F-FEPPA PET to measure TSPO V . We investigated the duration of untreated major depressive disorder, and the combination of total duration of disease and duration of antidepressant treatment, as predictor variables of TSPO V , assessing their significance. Between Sept 1, 2009, and July 6, 2017, we screened 134 participants for eligibility, of whom 81 were included in the study (current major depressive episode n=51, healthy n=30). We excluded one participant with a major depressive episode from the analysis because of unreliable information about previous medication use. Duration of untreated major depressive disorder was a strong predictor of TSPO V (p〈0·0001), as were total illness duration (p=0·0021) and duration of antidepressant exposure (p=0·037). The combination of these predictors accounted for about 50% of variance in TSPO V in the prefrontal cortex, anterior cingulate cortex, and insula. In participants who had untreated major depressive disorder for 10 years or longer, TSPO V was 29–33% greater in the prefrontal cortex, anterior cingulate cortex, and insula than in participants who were untreated for 9 years or less. TSPO V was also 31–39% greater in the three primary grey-matter regions of participants with long duration of untreated major depressive disorder compared with healthy participants (p=0·00047). Microglial activation, as shown by TSPO V , is greater in patients with chronologically advanced major depressive disorder with long periods of no antidepressant treatment than in patients with major depressive disorder with short periods of no antidepressant treatment, which is strongly suggestive of a different illness phase. Consistent with this, the yearly increase in microglial activation is no longer evident when antidepressant treatment is given. Canadian Institutes of Health Research and Neuroscience Catalyst Fund.
    Keywords: Medicine
    ISSN: 2215-0366
    E-ISSN: 2215-0374
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