The Development of a Sex Pheromone Lure for the American Plum Borer, \u3ci\u3eEuzophera Semifuneralis\u3c/i\u3e (Lepidoptera: Pyralidae), a Major Pest of Cherry in Michigan.

Pheromone components of the American plum borer, Euzophera semifuneralis, were defined by use of the electroantennogram screening technique and capillary gas chromatographic retention times of sex pheromone gland constituents. Field studies showed that greatest attraction was achieved with a 1 mg load rate of a 4-component blend in a rubber septum. This blend consisted of a 2:1 ratio of Z,E-9,12-14:ALD and Z9-14:ALD and an equal amount of the corresponding alcohols in a 2:1 ratio, respectively. Commercial lures were used to compare the flight patterns of the American plum borer, peachtree borer (Synanthedon exitiosa), and lesser peachtree borer (Synanthedon pictipes) adults in Michigan in 1988

Reduced Intestinal Brain-Derived Neurotrophic Factor Increases Vagal Sensory Innervation of the Intestine and Enhances Satiation

Brain-derived neurotrophic factor (BDNF) is produced by developing and mature gastrointestinal (GI) tissues that are heavily innervated by autonomic neurons and may therefore control their development or function. To begin investigating this hypothesis, we compared the morphology, distribution, and density of intraganglionic laminar endings (IGLEs), the predominant vagal GI afferent, in mice with reduced intestinal BDNF (INT-BDNF_/_) and controls. Contrary to expectations of reduced development, IGLE density and longitudinal axon bundle number in the intestine of INT-BDNF_/_ mice were increased, but stomach IGLEs were normal. INT-BDNF_/_ mice also exhibited increased vagal sensory neuron numbers, suggesting that their survival was enhanced. To determine whether increased intestinal IGLE density or other changes to gut innervation in INT-BDNF_/_mice altered feeding behavior, meal pattern and microstructural analyses were performed. INT-BDNF_/_ mice ate meals of much shorter duration than controls, resulting in reduced meal size. Increased suppression of feeding in INT-BDNF_/_ mice during the late phase of a scheduled meal suggested that increased satiation signaling contributed to reduced meal duration and size. Furthermore, INT-BDNF_/_ mice demonstrated increases in total daily intermeal interval and satiety ratio, suggesting that satiety signaling was augmented. Compensatory responses maintained normal daily food intake and body weight in INT-BDNF_/_ mice. These findings suggest a target organ-derived neurotrophin suppresses development of that organ’s sensory innervation and sensory neuron survival and demonstrate a role for BDNF produced by peripheral tissues in short-term controls of feeding, likely through its regulation of development or function of gut innervation, possibly including augmented intestinal IGLE innervation

Risk-communication capability for public health emergencies varies by community diversity

<p>Abstract</p> <p>Background</p> <p>Public health emergencies heighten several challenges in risk-communication: providing trustworthy sources of information, reaching marginalized populations, and minimizing fear and public confusion. In emergencies, however, information may not diffuse equally among all social groups, and gaps in knowledge may increase. Such knowledge gaps vary by social structure and the size, socioeconomic status, and diversity of the population. This study explores the relationship between risk-communication capabilities, as perceived by public officials participating in emergency tabletop exercises, and community size and diversity.</p> <p>Findings</p> <p>For each of the three communication functions tested, risk-communication capabilities are perceived to be greater in communities with fewer then 10% of the population speaking a language other than English at home, decreasing as the percentage grows to 20% (ANOVA P ≤ 0.02). With respect to community size, however, we found an N-shaped relationship between perceived risk communication capabilities and population size. Capabilities are perceived highest in the largest communities and lowest in the smallest, but lower in communities with 20,000–49,999 inhabitants compared to those with 2,500–19,999.</p> <p>Conclusion</p> <p>The results of this study suggest the need to factor population diversity into risk communication plans and the need for improved state or regional risk-communication capabilities, especially for communities with limited local capacity.</p

Aortic dissection type I in a weightlifter with hypertension: A case report

Acute aortic dissection can occur at the time of intense physical exertion in strength-trained athletes like weightlifters, bodybuilders, throwers, and wrestlers

Naringenin Prevents Dyslipidemia, Apolipoprotein B Overproduction, and Hyperinsulinemia in LDL Receptor–Null Mice With Diet-Induced Insulin Resistance

OBJECTIVE: The global epidemic of metabolic syndrome and its complications demands rapid evaluation of new and accessible interventions. Insulin resistance is the central biochemical disturbance in the metabolic syndrome. The citrus-derived flavonoid, naringenin, has lipid-lowering properties and inhibits VLDL secretion from cultured hepatocytes in a manner resembling insulin. We evaluated whether naringenin regulates lipoprotein production and insulin sensitivity in the context of insulin resistance in vivo. RESEARCH DESIGN AND METHODS: LDL receptor-null (Ldlr(-/-)) mice fed a high-fat (Western) diet (42% calories from fat and 0.05% cholesterol) become dyslipidemic, insulin and glucose intolerant, and obese. Four groups of mice (standard diet, Western, and Western plus 1% or 3% wt/wt naringenin) were fed ad libitum for 4 weeks. VLDL production and parameters of insulin and glucose tolerance were determined. RESULTS: We report that naringenin treatment of Ldlr(-/-) mice fed a Western diet corrected VLDL overproduction, ameliorated hepatic steatosis, and attenuated dyslipidemia without affecting caloric intake or fat absorption. Naringenin 1) increased hepatic fatty acid oxidation through a peroxisome proliferator-activated receptor (PPAR) gamma coactivator 1alpha/PPARalpha-mediated transcription program; 2) prevented sterol regulatory element-binding protein 1c-mediated lipogenesis in both liver and muscle by reducing fasting hyperinsulinemia; 3) decreased hepatic cholesterol and cholesterol ester synthesis; 4) reduced both VLDL-derived and endogenously synthesized fatty acids, preventing muscle triglyceride accumulation; and 5) improved overall insulin sensitivity and glucose tolerance. CONCLUSIONS: Thus, naringenin, through its correction of many of the metabolic disturbances linked to insulin resistance, represents a promising therapeutic approach for metabolic syndrome

Lipocalin-2 Deficiency Impairs Thermogenesis and Potentiates Diet-Induced Insulin Resistance in Mice

Lipocalin (LCN) 2 belongs to the lipocalin subfamily of low-molecular mass-secreted proteins that bind small hydrophobic molecules. LCN2 has been recently characterized as an adipose-derived cytokine, and its expression is upregulated in adipose tissue in genetically obese rodents. The objective of this study was to investigate the role of LCN2 in diet-induced insulin resistance and metabolic homeostasis in vivo. Systemic insulin sensitivity, adaptive thermogenesis, and serum metabolic and lipid profile were assessed in LCN2-deficient mice fed a high-fat diet (HFD) or regular chow diet. The molecular disruption of LCN2 in mice resulted in significantly potentiated diet-induced obesity, dyslipidemia, fatty liver disease, and insulin resistance. LCN2(-/-) mice exhibit impaired adaptive thermogenesis and cold intolerance. Gene expression patterns in white and brown adipose tissue, liver, and muscle indicate that LCN2(-/-) mice have increased hepatic gluconeogenesis, decreased mitochondrial oxidative capacity, impaired lipid metabolism, and increased inflammatory state under the HFD condition. LCN2 has a novel role in adaptive thermoregulation and diet-induced insulin resistanc

Adipocyte-specific protein tyrosine phosphatase 1B deletion increases lipogenesis, adipocyte cell size and is a minor regulator of glucose homeostasis

Peer reviewedPublisher PD

Hepatocyte ABCA1 Deletion Impairs Liver Insulin Signaling and Lipogenesis

Plasma membrane (PM) free cholesterol (FC) is emerging as an important modulator of signal transduction. Here, we show that hepatocyte-specific knockout (HSKO) of the cellular FC exporter, ATPbinding cassette transporter A1 (ABCA1), leads to decreased PM FC content and defective trafficking of lysosomal FC to the PM. Compared with controls, chow-fed HSKO mice had reduced hepatic (1) insulin- stimulated Akt phosphorylation, (2) activation of the lipogenic transcription factor Sterol Regulatory Element Binding Protein (SREBP)-1c, and (3) lipogenic gene expression. Consequently, Westerntype diet-fed HSKO mice were protected from steatosis. Surprisingly, HSKO mice had intact glucose metabolism; they showed normal gluconeogenic gene suppression in response to re-feeding and normal glucose and insulin tolerance. We conclude that: (1) ABCA1 maintains optimal hepatocyte PM FC, through intracellular FC trafficking, for efficient insulin signaling; and (2) hepatocyte ABCA1 deletion produces a form of selective insulin resistance so that lipogenesis is suppressed but glucose metabolism remains normal