Status of Grey Leaf Spot Disease In Kenyan Maize Production Ecosystems

Grey leaf spot disease (GLS), Cercospora zeae-maydis, which has previously been attributed to diverse pathogen species in other countries, has become a serious biotic constraint to production of maize ( Zea mays L.) in Kenya. It is necessary to determine the distribution and aetiology of the disease across all the maize production agro-ecologies in order to inform the development of appropriate management strategies against the disease. Samples were collected from maize growing areas in Kenya with GLS symptoms on maize crops and other plants. On the basis of cultural and morphological examinations, and restricted fragment length polymorphism and taxon-specific PCR analyses, Cercospora zeae-maydis group II and C. sorghi var. maydis were identified from typical GLS lesions on maize, with the former being predominant (>96% of the cases) and distributed throughout the country. The latter exhibited minor incidence (<4%) in western Kenya. Nucleotide sequence analyses further provided evidence that C. zeae-maydis group II and C. sorghi var. maydis were distinct fungi.La maladie de t\ue2che grise de la feuille (GLS), Cercospora zeae-maydis, attribu\ue9e aux esp\ue8ces de pathogens diverses dans d'autres pays, est devenue une s\ue9rieuse contrainte biotique \ue0 la production de ma\uefs ( Zea mays L.) au Kenya. Il est n\ue9cessaire de d\ue9terminer la distribution et l'\ue9tiologie de la maladie \ue0 travers toutes les r\ue9gions agro-\ue9cologques productrices de ma\uefs pour mieux d\ue9velopper des strat\ue9gies appropri\ue9es de gestion contre la maladie. Des \ue9chantillons \ue9taient recueillis dans des r\ue9gions producteurs du ma\uefs au Kenya tenant compte de la pr\ue9sence des sympt\uf4mes GLS sur les ma\uefs et autres cultures. Sur base des examens culturales et morphologiques ainsi que du polymorphisme de la longueur du fragment isol\ue9 et les analyses PCR du taxon sp\ue9cifique, Cercospora zeae-maydis le groupe II de Cercospora zeae-maydis et C. sorghi var. maydis \ue9taient identifi\ue9s par des l\ue9sions typiques de GLS sur le ma\uefs, ce dernier \ue9tant le plus pr\ue9dominant (> 96 % de tous les cas) et distribu\ue9 \ue0 travers tout le pays avec une incidence mineur de 4 % dans l'ouest du Kenya. L'analyse de s\ue9quences de nucl\ue9otides avait par la suite montr\ue9 avec evidence que le C. zeae-maydis group II et C. sorghi var. maydis \ue9taient de champignons distincts

Exact analytical expression for magnetoresistance using quantum groups

We obtain an exact analytical expression for magnetoresistance using noncommutative geometry and quantum groups.Then we will show that there is a deep relationship between magnetoresistance and the quantum group $su_{q}(2)$, from which we understand the quantum interpretation of the quantum corrections to the conductivity.Comment: 8 pages, 3 figures, replaced with the version published in Physics Letters

Propofol for endotracheal intubation in neonates: A dose-finding trial

Objective: To find propofol doses providing effective sedation without side effects in neonates of different gestational ages (GA) and postnatal ages (PNA). Design and setting: Prospective multicentere dose-finding study in 3 neonatal intensive care units. Patients: Neonates with a PNA <28 days requiring non-emergency endotracheal intubation. Interventions: Neonates were stratified into 8 groups based on GA and PNA. The first 5 neonates in every group received a dose of 1.0 mg/kg propofol. Based on sedative effect and side effects, the dose was increased or decreased in the next 5 patients until the optimal dose was found. Main outcome measures: The primary outcome was the optimal single propofol starting dose that provides effective sedation without side effects in each age group. Results: After inclusion of 91 patients, the study was prematurely terminated because the primary outcome was only reached in 13% of patients. Dose-finding was completed in 2 groups, but no optimal propofol dose was found. Effective sedation without side effects was achieved more often after a starting dose of 2.0 mg/kg (28%) than after 1.0 mg/kg (3%) and 1.5 mg/kg (9%). Propofol-induced hypotens

MARCH1 protects the lipid raft and tetraspanin web from MHCII proteotoxicity in dendritic cells

Dendritic cells (DCs) produce major histocompatibility complex II (MHCII) in large amounts to function as professional antigen presenting cells. Paradoxically, DCs also ubiquitinate and degrade MHCII in a constitutive manner. Mice deficient in the MHCII-ubiquitinating enzyme membrane-anchored RING-CH1, or the ubiquitin-acceptor lysine of MHCII, exhibit a substantial reduction in the number of regulatory T (Treg) cells, but the underlying mechanism was unclear. Here we report that ubiquitin-dependent MHCII turnover is critical to maintain homeostasis of lipid rafts and the tetraspanin web in DCs. Lack of MHCII ubiquitination results in the accumulation of excessive quantities of MHCII in the plasma membrane, and the resulting disruption to lipid rafts and the tetraspanin web leads to significant impairment in the ability of DCs to engage and activate thymocytes for Treg cell differentiation. Thus, ubiquitin-dependent MHCII turnover represents a novel quality-control mechanism by which DCs maintain homeostasis of membrane domains that support DC's Treg cell-selecting function

Pro-inflammatory activation following demyelination is required for myelin clearance and oligodendrogenesis

Remyelination requires innate immune system function, but how exactly microglia and macrophages clear myelin debris after injury and tailor a specific regenerative response is unclear. Here, we asked whether pro-inflammatory microglial/macrophage activation is required for this process. We established a novel toxin-based spinal cord model of de- and remyelination in zebrafish and showed that pro-inflammatory NF-κB-dependent activation in phagocytes occurs rapidly after myelin injury. We found that the pro-inflammatory response depends on myeloid differentiation primary response 88 (MyD88). MyD88-deficient mice and zebrafish were not only impaired in the degradation of myelin debris, but also in initiating the generation of new oligodendrocytes for myelin repair. We identified reduced generation of TNF-α in lesions of MyD88-deficient animals, a pro-inflammatory molecule that was able to induce the generation of new premyelinating oligodendrocytes. Our study shows that pro-inflammatory phagocytic signaling is required for myelin debris degradation, for inflammation resolution, and for initiating the generation of new oligodendrocytes

Mechanisms underlying a thalamocortical transformation during active tactile sensation

During active somatosensation, neural signals expected from movement of the sensors are suppressed in the cortex, whereas information related to touch is enhanced. This tactile suppression underlies low-noise encoding of relevant tactile features and the brain’s ability to make fine tactile discriminations. Layer (L) 4 excitatory neurons in the barrel cortex, the major target of the somatosensory thalamus (VPM), respond to touch, but have low spike rates and low sensitivity to the movement of whiskers. Most neurons in VPM respond to touch and also show an increase in spike rate with whisker movement. Therefore, signals related to self-movement are suppressed in L4. Fast-spiking (FS) interneurons in L4 show similar dynamics to VPM neurons. Stimulation of halorhodopsin in FS interneurons causes a reduction in FS neuron activity and an increase in L4 excitatory neuron activity. This decrease of activity of L4 FS neurons contradicts the "paradoxical effect" predicted in networks stabilized by inhibition and in strongly-coupled networks. To explain these observations, we constructed a model of the L4 circuit, with connectivity constrained by in vitro measurements. The model explores the various synaptic conductance strengths for which L4 FS neurons actively suppress baseline and movement-related activity in layer 4 excitatory neurons. Feedforward inhibition, in concert with recurrent intracortical circuitry, produces tactile suppression. Synaptic delays in feedforward inhibition allow transmission of temporally brief volleys of activity associated with touch. Our model provides a mechanistic explanation of a behavior-related computation implemented by the thalamocortical circuit

Epstein-Barr virus: clinical and epidemiological revisits and genetic basis of oncogenesis

Epstein-Barr virus (EBV) is classified as a member in the order herpesvirales, family herpesviridae, subfamily gammaherpesvirinae and the genus lymphocytovirus. The virus is an exclusively human pathogen and thus also termed as human herpesvirus 4 (HHV4). It was the first oncogenic virus recognized and has been incriminated in the causation of tumors of both lymphatic and epithelial nature. It was reported in some previous studies that 95% of the population worldwide are serologically positive to the virus. Clinically, EBV primary infection is almost silent, persisting as a life-long asymptomatic latent infection in B cells although it may be responsible for a transient clinical syndrome called infectious mononucleosis. Following reactivation of the virus from latency due to immunocompromised status, EBV was found to be associated with several tumors. EBV linked to oncogenesis as detected in lymphoid tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), post-transplant lymphoproliferative disorders (PTLD) and T-cell lymphomas (e.g. Peripheral T-cell lymphomas; PTCL and Anaplastic large cell lymphomas; ALCL). It is also linked to epithelial tumors such as nasopharyngeal carcinoma (NPC), gastric carcinomas and oral hairy leukoplakia (OHL). In vitro, EBV many studies have demonstrated its ability to transform B cells into lymphoblastoid cell lines (LCLs). Despite these malignancies showing different clinical and epidemiological patterns when studied, genetic studies have suggested that these EBV- associated transformations were characterized generally by low level of virus gene expression with only the latent virus proteins (LVPs) upregulated in both tumors and LCLs. In this review, we summarize some clinical and epidemiological features of EBV- associated tumors. We also discuss how EBV latent genes may lead to oncogenesis in the different clinical malignancie