Evaluation of Aphis glycines as an Alternative Host for Supporting Aphelinus albipodus Against Myzus persicae on Capsicum annuum cv. Ox Horn and Hejiao 13.

Bank plant systems provide effective biological control for pests infesting commercially important crops. Aphids cause physical damage to crops by feeding on the leaves, as well as transmitting damaging viral diseases. To develop a bank plant system to control aphids that damage vegetable crops, we initially reared the parasitoid Aphelinus albipodus (Hayat and Fatima) on the soybean aphid, Aphis glycines (Matsumura) reared on the soybean plant, Glycine max (L.) that was elected as the alternate host. Parasitoid adults that emerged from A. glycines were allowed to parasitize second instar nymphs of the aphid Myzus persicae (Sulzer) which were reared on sweet pepper and chili pepper leaves. The results showed that A. albipodus females feeding and parasitizing M. persicae nymphs reared on sweet pepper lived for 18.9 days, with an average fecundity of 337.3 progenies/female, while females feeding and parasitizing on M. persicae nymphs reared on chili pepper lived for 18.8 days, with an average fecundity of 356.2 progenies/female. There were no significant difference in the development time and reproduction of A. albipodus individuals parasitizing M. persicae nymphs reared on sweet pepper and chili pepper plants. The intrinsic rate of increase (r), net reproductive rate (R 0), net aphid killing rate (Z 0), and finite aphid killing rate (θ) of A. albipodus parasitizing sweet pepper and chili pepper M. persicae was 0.2258 days-1, 171.7 progeny adults, 222.6 aphids, and 0.4048 and 0.2295 days-1, 191.8 progeny adults, 243.3 aphids, and 0.4021, respectively. Our results suggested that A. glycines could serve as an effective alternative host for supporting A. albipodus against M. persicae infesting sweet pepper and chili pepper.

Activation of p38-mitogen-activated protein kinase contributes to ischemia reperfusion in rat brain.

Inflammation plays an important role in cerebral ischemia reperfusion, which can cause severe damage to the brain and may lead to cerebral hemorrhage transformation. p38-mitogen-activated protein kinase (p38mapk) has been implicated in the etiology of a number of diseases because it is a cause of inflammation, but comparatively little research has been carried out into its role in the etiology of ischemia reperfusion. We investigated the expression of p38mapk in cerebral ischemia reperfusion to gain a better understanding of its potential role in hemorrhagic transformation (HT). One hundred rats were randomly divided into three groups: an ischemia reperfusion group, an ischemia group, and a sham-operated group. We carried out neurological deficit assessments, infarct volume measurements, histopathological examinations, and immunohistochemistry analyses. p38mapk was overexpressed in the ischemia reperfusion group, which exhibited severe tissue damage and greater edema than the other two groups. These results suggest that p38mapk plays an important role in cerebral ischemia reperfusion, and may be one of the causes of HT.

A founder mutation in presenilin 1 causing early-onset Alzheimer disease in unrelated Caribbean Hispanic families.

CONTEXT: Genetic determinants of Alzheimer disease (AD) have not been comprehensively examined in Caribbean Hispanics, a population in the United States in whom the frequency of AD is higher compared with non-Hispanic whites. OBJECTIVE: To identify variant alleles in genes related to familial early-onset AD among Caribbean Hispanics. DESIGN AND SETTING: Family-based case series conducted in 1998-2001 at an AD research center in New York, NY, and clinics in the Dominican Republic. PATIENTS: Among 206 Caribbean Hispanic families with 2 or more living members with AD who were identified, 19 (9.2%) had at least 1 individual with onset of AD before the age of 55 years. MAIN OUTCOME MEASURE: The entire coding region of the presenilin 1 gene and exons 16 and 17 of the amyloid precursor protein gene were sequenced in probands from the 19 families and their living relatives. RESULTS: A G-to-C nucleotide change resulting in a glycine-alanine amino acid substitution at codon 206 (Gly206Ala) in exon 7 of presenilin 1 was observed in 23 individuals from 8 (42%) of the 19 families. A Caribbean Hispanic individual with the Gly206Ala mutation and early-onset familial disease was also found by sequencing the corresponding genes of 319 unrelated individuals in New York City. The Gly206Ala mutation was not found in public genetic databases but was reported in 5 individuals from 4 Hispanic families with AD referred for genetic testing. None of the members of these families were related to one another, yet all carriers of the Gly206Ala mutation tested shared a variant allele at 2 nearby microsatellite polymorphisms, indicating a common ancestor. No mutations were found in the amyloid precursor protein gene. CONCLUSIONS: The Gly206Ala mutation was found in 8 of 19 unrelated Caribbean Hispanic families with early-onset familial AD. This genetic change may be a prevalent cause of early-onset familial AD in the Caribbean Hispanic population.