Mature plant and tissue resistance in the groundnut-peanut bud necrosis virus system

Leaves and plants of different ages of one susceptible (JL24) and two resistant (ICGV86031 and ICGV86388) groundnut genotypes were mechanically inoculated with peanut bud necrosis [tospo]virus, and the percentage of plants with systemic symptoms (incidence) and the incubation period were determined. The incidence decreased sharply in all three genotypes with the age of the inoculated leaves and plants. The incubation period increased with the age of leaves and plants. Apparently, only young tissue of young plants is susceptible, while mature tissue and plants are highly resistant. This mature tissue and plant resistance occurs irrespective of the susceptibility level of the genotype to peanut bud necrosis virus, however, it develops earlier in the resistant than in the susceptible genotype

The Cross-Cultural Dementia Screening (CCD):A new neuropsychological screening instrument for dementia in elderly immigrants

Objective: Currently, approximately 3.9% of the European population are non-EU citizens, and a large part of these people are from "non-Western" societies, such as Turkey and Morocco. For various reasons, the incidence of dementia in this group is expected to increase. However, cognitive testing is challenging due to language barriers and low education and/or illiteracy. The newly developed Cross-Cultural Dementia Screening (CCD) can be administered without an interpreter. It contains three subtests that assess memory, mental speed, and executive function. We hypothesized the CCD to be a culture-fair test that could discriminate between demented patients and cognitively healthy controls. Method: To test this hypothesis, 54 patients who had probable dementia were recruited via memory clinics. Controls (N = 1625) were recruited via their general practitioners. All patients and controls were aged 55 years and older and of six different self-defined ethnicities (Dutch, Turkish, Moroccan-Arabic, Moroccan-Berber, Surinamese-Creole, and Surinamese-Hindustani). Exclusion criteria included current or previous conditions that affect cognitive functioning. Results: There were performance differences between the ethnic groups, but these disappeared after correcting for age and education differences between the groups, which supports our central hypothesis that the CCD is a culture-fair test. Receiver-operating characteristic (ROC) and logistic regression analyses showed that the CCD has high predictive validity for dementia (sensitivity: 85%; specificity: 89%). Discussion: The CCD is a sensitive and culture-fair neuropsychological instrument for dementia screening in low-educated immigrant populations.</p

Recent Studies on Peanut Bud Necrosis Disease: Proceedings of a Meeting 20 Mar 1995

The current status of research on peanut bud necrosis disease caused by the peanut bud necrosis virus and transmitted by Thrips palmi is reviewed. Recent advances in the genome structure, host range, transmission, and spread of tospoviruses wi t h emphasis on the peanut bud necrosis virus are discussed. Epidemiology of the disease and resistance to both the vector and the virus are reviewed in detail. Agronomically acceptable varieties wi th resistance to either the vector or to the vector and the virus are now available

Pharmacological Modulation of Dopamine Receptor D2-Mediated Transmission Alters the Metabolic Phenotype of Diet Induced Obese and Diet Resistant C57Bl6 Mice

High fat feeding induces a variety of obese and lean phenotypes in inbred rodents. Compared to Diet Resistant (DR) rodents, Diet Induced Obese (DIO) rodents are insulin resistant and have a reduced dopamine receptor D2 (DRD2) mediated tone. We hypothesized that this differing dopaminergic tone contributes to the distinct metabolic profiles of these animals. C57Bl6 mice were classified as DIO or DR based on their weight gain during 10 weeks of high fat feeding. Subsequently DIO mice were treated with the DRD2 agonist bromocriptine and DR mice with the DRD2 antagonist haloperidol for 2 weeks. Compared to DR mice, the bodyweight of DIO mice was higher and their insulin sensitivity decreased. Haloperidol treatment reduced the voluntary activity and energy expenditure of DR mice and induced insulin resistance in these mice. Conversely, bromocriptine treatment tended to reduce bodyweight and voluntary activity, and reinforce insulin action in DIO mice. These results show that DRD2 activation partly redirects high fat diet induced metabolic anomalies in obesity-prone mice. Conversely, blocking DRD2 induces an adverse metabolic profile in mice that are inherently resistant to the deleterious effects of high fat food. This suggests that dopaminergic neurotransmission is involved in the control of metabolic phenotype

Effect of hosts on competition among clones and evidence of differential selection between pathogenic and saprophytic phases in experimental populations of the wheat pathogen Phaeosphaeria nodorum

<p>Abstract</p> <p>Background</p> <p>Monoculture, multi-cropping and wider use of highly resistant cultivars have been proposed as mechanisms to explain the elevated rate of evolution of plant pathogens in agricultural ecosystems. We used a mark-release-recapture experiment with the wheat pathogen <it>Phaeosphaeria nodorum </it>to evaluate the impact of two of these mechanisms on the evolution of a pathogen population. Nine <it>P. nodorum </it>isolates marked with ten microsatellite markers and one minisatellite were released onto five replicated host populations to initiate epidemics of Stagonospora nodorum leaf blotch. The experiment was carried out over two consecutive host growing seasons and two pathogen collections were made during each season.</p> <p>Results</p> <p>A total of 637 pathogen isolates matching the marked inoculants were recovered from inoculated plots over two years. Genetic diversity in the host populations affected the evolution of the corresponding <it>P. nodorum </it>populations. In the cultivar mixture the relative frequencies of inoculants did not change over the course of the experiment and the pathogen exhibited a low variation in selection coefficients.</p> <p>Conclusions</p> <p>Our results support the hypothesis that increasing genetic heterogeneity in host populations may retard the rate of evolution in associated pathogen populations. Our experiment also provides indirect evidence of fitness costs associated with host specialization in <it>P. nodorum </it>as indicated by differential selection during the pathogenic and saprophytic phases.</p

Global Prevalence of Young-Onset Dementia: A Systematic Review and Meta-analysis

Importance: Reliable prevalence estimates are lacking for young-onset dementia (YOD), in which symptoms of dementia start before the age of 65 years. Such estimates are needed for policy makers to organize appropriate health care. Objective: To determine the global prevalence of YOD. Data sources: The PubMed, Embase, CINAHL, and PsycInfo databases were systematically searched for population-based studies on the prevalence of YOD published between January 1, 1990, and March 31, 2020. Study selection: Studies containing data on the prevalence of dementia in individuals younger than 65 years were screened by 2 researchers for inclusion in a systematic review and meta-analysis. Data extraction and synthesis: Prevalence estimates on 5-year age bands, from 30 to 34 years to 60 to 64 years, were extracted. Random-effects meta-analyses were conducted to pool prevalence estimates. Results were age standardized for the World Standard Population. Heterogeneity was assessed by subgroup analyses for sex, dementia subtype, study design, and economic status based on the World Bank classification and by meta-regression. Main outcomes and measures: Prevalence estimates of YOD for 5-year age bands. Results: A total of 95 unique studies were included in this systematic review, of which 74 with 2 760 379 unique patients were also included in 5-year age band meta-analyses. Studies were mostly conducted in Europe and in older groups in Asia, North America, and Oceania. Age-standardized prevalence estimates increased from 1.1 per 100 000 population in the group aged 30 to 34 years to 77.4 per 100 000 population in the group aged 60 to 64 years. This gives an overall global age-standardized prevalence of 119.0 per 100 000 population in the age range of 30 to 64 years, corresponding to 3.9 million people aged 30 to 64 years living with YOD in the world. Subgroup analyses showed prevalence between men and women to be similar (crude estimates for men, 216.5 per 100 000 population; for women, 293.1 per 100 000 population), whereas prevalence was lower in high-income countries (crude estimate, 663.9 per 100 000 population) compared with upper-middle-income (crude estimate, 1873.6 per 100 000 population) and lower-middle-income (crude estimate, 764.2 per 100 000 population) countries. Meta-regression showed that age range (P < .001), sample size (P < .001), and study methodology (P = .02) significantly influenced heterogeneity between studies. Conclusions and relevance: This systematic review and meta-analysis found an age-standardized prevalence of YOD of 119.0 per 100 000 population, although estimates of the prevalence in low-income countries and younger age ranges remain scarce. These results should help policy makers organize sufficient health care for this subgroup of individuals with dementia. Study registration: PROSPERO CRD42019119288This study was supported by the Gieskes-Strijbis Foundation, Alzheimer Netherlands, and the Dutch Young-Onset Dementia Knowledge Centre

A randomised clinical trial on a comprehensive geriatric assessment and intensive home follow-up after hospital discharge: the Transitional Care Bridge

<p>Abstract</p> <p>Background</p> <p>Older patients are at high risk for poor outcomes after acute hospital admission. The mortality rate in these patients is approximately 20%, whereas 30% of the survivors decline in their level of activities of daily living (ADL) functioning three months after hospital discharge. Most diseases and geriatric conditions that contribute to poor outcomes could be subject to pro-active intervention; not only during hospitalization, but also after discharge. This paper presents the design of a randomised controlled clinical trial concerning the effect of a pro-active, multi-component, nurse-led transitional care program following patients for six months after hospital admission.</p> <p>Methods/Design</p> <p>Three hospitals in the Netherlands will participate in the multi-centre, double-blind, randomised clinical trial comparing a pro-active multi-component nurse-led transitional care program to usual care after discharge. All patients acutely admitted to the Department of Internal Medicine who are 65 years and older, hospitalised for at least 48 hours and are at risk for functional decline are invited to participate in the study. All patients will receive integrated geriatric care by a geriatric consultation team during hospital admission. Randomization, which will be stratified by study site and cognitive impairment, will be conducted during admission. The intervention group will receive the transitional care bridge program, consisting of a handover moment with a community care Care Nurse (CN) during hospital admission and five home visits after discharge. The control group will receive 'care as usual' after discharge. The main outcome is the level of ADL functioning six months after discharge compared to premorbid functioning measured with the Katz ADL index. Secondary outcomes include; survival, cognitive functioning, quality of life, and health care utilization, satisfaction of the patient and primary care giver with the transitional care bridge program. All outcomes will be measured at three, six and twelve months after discharge. Approximately 674 patients will be enrolled to either the intervention or control group.</p> <p>Discussion</p> <p>The study will provide new knowledge on a combined intervention of integrated care during hospital admission, a proactive handover moment before discharge and intensive home visits after discharge.</p> <p>Trial registration</p> <p><b>Trial registration number: NTR 2384</b></p