Entomological status of Anopheles sergentii and the first molecular investigation of its insecticide-resistant genes, kdr and ace-1 in Morocco.

BACKGROUND & OBJECTIVES: Prior to their elimination in 1974 and 2004, respectively, Plasmodium falciparum and P. vivax were the main native malaria parasites involved in disease transmission in Morocco. Imported cases of human malaria are still reported from the country. Anopheles labranchiae in northern Morocco and An. sergentii in the southern regions are the main malaria vectors. The bionomics and insecticide susceptibility of An. sergentii are poorly understood and need to be further studied to enhance the epidemiological surveillance of this important malaria vector. METHODS: The adults and larvae of Anopheles sergentii were collected during the mosquito breeding season in 2015 and 2016 and environmental characteristics of their breeding sites were recorded. Blood meals were analyzed using PCR-RFLP. Alongside, the WHO routine susceptibility tests with DDT (4%) and malathion (5%) were conducted and An. sergentii specimens were screened for knockdown resistance (kdr) and acetyl cholinesterase encoding (ace-1) gene mutations. RESULTS: Anopheles sergentii was observed during the summer and autumn seasons, feeding mainly on sheep, cows and also on humans. The WHO bioassays revealed complete susceptibility to DDT and malathion. Analysis of the sequences of the voltage-gated sodium channel gene revealed the absence of the kdr "Leu-Phe" mutation and PCR-RFLP revealed the absence of the G119S mutation in the ace-1. INTERPRETATION & CONCLUSION: With the increasing number of imported cases of human malaria in Morocco, the indiscriminate feeding behavior of this species may pose an infectious medical threat. Fortunately, the absence of insecticide resistance can ensure, for now, the efficiency of insecticides, as a part of the vector control program in controlling An. sergentii in Morocco.

Update of inflammatory proliferative retinopathy: Ischemia, hypoxia and angiogenesis.

Diabetic retinopathy (DR) and retinopathy of prematurity (ROP) present two examples of proliferative retinopathy, characterized by the same stages of progression; ischemia of the retinal vessels, leads to hypoxia and to correct the problem there is the setting up of uncontrolled angiogenesis, which subsequently causes blindness or even detachment of the retina. The difference is the following; that DR initiated by the metabolic complications that are due to hyperglycemia, and ROP is induced by overexposure of the neonatal retina to oxygen. In this review, we will demonstrate the physiopathological mechanism of the two forms of proliferative retinopathy DR and ROP, in particular the role of the CD40/CD40L axis and IL-1 on vascular complications and onset of inflammation of the retina, the implications of their effects on the onset of pathogenic angiogenesis, thus understanding the link between platelets and retinal ischemia. In addition, what are the therapeutic targets that could slow its progression?

Intra-familial phenotypic variability in a Moroccan family with hearing loss and palmoplantar keratoderma (PPK).

Mutations in the GJB2 gene encoding connexin 26 are the main cause of hereditary hearing impairment. These mutations generate mainly autosomal recessive and rarely autosomal dominant deafness. Dominant mutations in GJB2 can be responsible for isolated deafness as well as syndromic hearing loss associated with various skin abnormalities. Until now few papers discuss dominant mutations in the GJB2 gene. In this work we report a rare case about a Moroccan family with a compound heterozygous mutation (the dominant p.R75Q and the recessive c.35delG alleles) in the GJB2 gene with intra-familial phenotypic variability. This study reinforces the involvement of p.R75Q mutation of GJB2 in syndromic deafness associated with dermatological diseases the palmoplantar keratoderma.

Characterization of opioid peptides and opioid receptors in the brain of jerboa (Jaculus orientalis), a hibernating rodent.

The present study was undertaken to investigate the biochemical characteristics of the opioid receptors and opioid peptides in the jerboa (Jaculus orientalis) brain, a subdesert rodent of Morocco. We have demonstrated the presence of delta, mu, and kappa sites in the jerboa brain. The endogenous opioid peptides methionine-enkephalin, beta-endorphin, and dynorphin were evaluated in different physiological states of the animal (active and hibernating). The circulating methionine-enkephalin in different states of the animal (active, hibernating, exposure to cold conditions, and fasting) was evaluated in the plasma. Our results indicate that the hibernating state the opioid receptors level decreased, whereas the concentration of opioid peptides increased. These findings suggest that both opioid receptors and opioid peptides could be involved in the adaptation of the jerboa to survive under thermal stress.