Control of Black Vine Weevil larvae Otiorhynchus sulcatus (Fabricius) (Coleoptera:Curculionidae) in grow bags outdoors with nematodes

Abstract 1 Outdoor trials were carried out during 2001–02 on strawberries grown in commercial growing bags naturally infested with black vine weevil larvae (BVW) Otiorhynchus sulcatus in Co. Wexford, Ireland. 2 The two nematode isolates used in these trials were Heterorhabditis megidis (UK211) and Heterorhabditis downesi (K122), both laboratory cultured. Growing bags received nematodes either once (May 2001), twice (May and October 2001) or three times (May, October 2001 and May 2002). Ten days after each application date, nine blocks (of the total 27) were randomly selected, destructively assessed and discarded. 3 The single application (May 2001) resulted in a mortality of black vine weevil larvae, of 93.4% with H. megidis and 51.3% with H. downesi, compared with the control treatment at that date. Respective figures after the double application (May 2001 and October 2001) were 78.9 and 77.6% and after the triple application (May 2001, October 2001 and May 2002) the figures were 93.7 and 88.1%. 4 Results from these trials clearly indicate that entomopathogenic nematodes are good alternatives to chemical control of the black vine weevil on strawberries grown in growing bags in Ireland.     

Application of the comprehensive set of heterozygous yeast deletion mutants to elucidate the molecular basis of cellular chromium toxicity

Background  

The serious biological consequences of metal toxicity are well documented, but the key modes of action of most metals are unknown. To help unravel molecular mechanisms underlying the action of chromium, a metal of major toxicological importance, we grew over 6,000 heterozygous yeast mutants in competition in the presence of chromium. Microarray-based screens of these heterozygotes are truly genome-wide as they include both essential and non-essential genes.     

Glucocorticoid blockade reverses psychological stress-induced abnormalities in epidermal structure and function

Many cutaneous disorders are adversely affected by psychological stress (PS), but the responsible mechanisms are poorly understood. Recent studies have demonstrated that PS decreases epidermal proliferation and differentiation, impairs permeability barrier homeostasis, and decreases stratum corneum integrity. PS also increases the production of endogenous glucocorticoids (GC), and both systemic and topical GC cause adverse effects on epidermal structure and function similar to those observed with PS. We therefore hypothesized that increased endogenous GC in PS mediates its adverse cutaneous effects. To test this hypothesis, we used two independent approaches, administering either RU-486, a GC receptor antagonist that inhibits GC action, or antalarmin, a corticotropin-releasing hormone (CRH) receptor antagonist that prevents increased GC production in the face of PS. Inhibition of either GC action or production prevents the PS-induced decline in epidermal cell proliferation and differentiation, impairment in permeability barrier homeostasis, and decrease in stratum corneum (SC) integrity. Moreover, the pathophysiological basis for the abnormality in permeability barrier homeostasis; i.e., decreased lamellar body production and secretion, is restored toward normal by inhibition of GC action. Similarly, the mechanistic basis for the decrease in SC integrity, i.e., a reduction in corneodesmosomes, is also normalized by inhibition of GC action. Thus many of the adverse effects of PS on epidermal structure and function can be attributed to increased endogenous GC and conversely, approaches that either reduce GC production or action might benefit cutaneous disorders that are provoked or exacerbated by PS.     

Effect of the Novel Influenza A (H1N1) Virus in the Human Immune System

Background

The pandemic by the novel H1N1 virus has created the need to study any probable effects of that infection in the immune system of the host.

Methodology/Principal Findings

Blood was sampled within the first two days of the presentation of signs of infection from 10 healthy volunteers; from 18 cases of flu-like syndrome; and from 31 cases of infection by H1N1 confirmed by reverse RT-PCR. Absolute counts of subtypes of monocytes and of lymphocytes were determined after staining with monoclonal antibodies and analysis by flow cytometry. Peripheral blood mononuclear cells (PBMCs) were isolated from patients and stimulated with various bacterial stimuli. Concentrations of tumour necrosis factor-alpha, interleukin (IL)-1beta, IL-6, IL-18, interferon (FN)-alpha and of IFN-gamma were estimated in supernatants by an enzyme immunoassay. Infection by H1N1 was accompanied by an increase of monocytes. PBMCs of patients evoked strong cytokine production after stimulation with most of bacterial stimuli. Defective cytokine responses were shown in response to stimulation with phytohemagglutin and with heat-killed Streptococcus pneumoniae. Adaptive immune responses of H1N1-infected patients were characterized by decreases of CD4-lymphocytes and of B-lymphocytes and by increase of T-regulatory lymphocytes (Tregs).

Conclusions/Significance

Infection by the H1N1 virus is accompanied by a characteristic impairment of the innate immune responses characterized by defective cytokine responses to S.pneumoniae. Alterations of the adaptive immune responses are predominated by increase of Tregs. These findings signify a predisposition for pneumococcal infections after infection by H1N1 influenza.     

Differential white blood cell count and type 2 diabetes: systematic review and meta-analysis of cross-sectional and prospective studies

Objective

Biological evidence suggests that inflammation might induce type 2 diabetes (T2D), and epidemiological studies have shown an association between higher white blood cell count (WBC) and T2D. However, the association has not been systematically investigated.

Research Design and Methods

Studies were identified through computer-based and manual searches. Previously unreported studies were sought through correspondence. 20 studies were identified (8,647 T2D cases and 85,040 non-cases). Estimates of the association of WBC with T2D were combined using random effects meta-analysis; sources of heterogeneity as well as presence of publication bias were explored.

Results

The combined relative risk (RR) comparing the top to bottom tertile of the WBC count was 1.61 (95% CI: 1.45; 1.79, p = 1.5*10⁻¹⁸). Substantial heterogeneity was present (I² = 83%). For granulocytes the RR was 1.38 (95% CI: 1.17; 1.64, p = 1.5*10⁻⁴), for lymphocytes 1.26 (95% CI: 1.02; 1.56, p = 0.029), and for monocytes 0.93 (95% CI: 0.68; 1.28, p = 0.67) comparing top to bottom tertile. In cross-sectional studies, RR was 1.74 (95% CI: 1.49; 2.02, p = 7.7*10⁻¹³), while in cohort studies it was 1.48 (95% CI: 1.22; 1.79, p = 7.7*10⁻⁵). We assessed the impact of confounding in EPIC-Norfolk study and found that the age and sex adjusted HR of 2.19 (95% CI: 1.74; 2.75) was attenuated to 1.82 (95% CI: 1.45; 2.29) after further accounting for smoking, T2D family history, physical activity, education, BMI and waist circumference.

Conclusions

A raised WBC is associated with higher risk of T2D. The presence of publication bias and failure to control for all potential confounders in all studies means the observed association is likely an overestimate.     

The growth of children in relation to the timing of obesity development

Objective: To examine whether there is an association between the timing of the development of obesity and children's growth. Research Methods and Procedures: This study investigated 141 prepubertal obese children (76 girls) and 72 healthy non‐obese children (39 girls). The target height standard deviation score (SDS), the percentage weight for height, and the height SDS (H‐SDS) at presentation and at the age of 2 years were calculated. Patients were classified, according to whether obesity developed before or after the age of 3 years, as presenting with early‐onset or late‐onset obesity, respectively. Results: Mean age (±SD) at presentation was 9.4 (2.1) years. At the age of 2 years, the H‐SDS of the children with early‐onset obesity was 1.3 (1.0) vs. 0.9 (1.3) for the late‐onset obese (p > 0.5) and 0.4 (1.0) for controls (p < 0.001), and the children with late‐onset obesity were also significantly taller than controls (p < 0.005). At presentation, children with early‐onset obesity were significantly taller than children with late‐onset obesity [1.1 (0.8) vs. 0.6 (1.0); p < 0.001] and controls [0.2 (0.8); p < 0.001]. There was no increase in H‐SDS after the age of 2 years in the late‐onset obese children (p > 0.05). H‐SDS values were below average in 21% of the children with late‐onset obesity and in only 4% of the children with early‐onset obesity. Discussion: These findings indicate that late development of obesity is not associated with increased stature in prepubertal children; however, it may be preceded by growth acceleration in the early years of life. Growth acceleration in early life may be a predictor for future obesity.