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Recent experimental and in-field evidence of the deleterious effects of insecticides on the domestic honey bee Apis mellifera have led to a tightening of the risk assessment requirements of these products, and now more attention is being paid to their sublethal effects on other bee species. In addition to traditional tests, in vitro and in silico approaches may become essential tools for a comprehensive understanding of the impact of insecticides on bee species. Here we present a study in which electrophysiology and a Markovian multi-state modelling of the voltage-gated sodium channel were used to measure the susceptibility of the antennal lobe neurons from Apis mellifera and Bombus terrestris, to the pyrethroids tetramethrin and esfenvalerate. Voltage-gated sodium channels from Apis mellifera and Bombus terrestris are differentially sensitive to pyrethroids. In both bee species, the level of neuronal activity played an important role in their relative sensitivity to pyrethroids. This work supports the notion that honey bees cannot unequivocally be considered as a surrogate for other bee species in assessing their neuronal susceptibility to insecticides.

Small RGK GTPases, Rad, Gem, Rem1, and Rem2, are potent inhibitors of high-voltage-activated (HVA) Ca 2+ channels expressed in heterologous expression systems. However, the role of this regulation has never been clearly demonstrated in the nervous system. Using transcriptional analysis, we show that peripheral nerve injury specifically upregulates Gem in mice dorsal root ganglia. Following nerve injury, protein expression was increased in ganglia and peripheral nerve, mostly under its phosphorylated form. This was confirmed in situ and in vitro in dorsal root ganglia sensory neurons. Knockdown of endogenous Gem, using specific small-interfering RNA (siRNA), increased the HVA Ca 2+ current only in the large-somatic-sized neurons. Combining pharmacological analysis of the HVA Ca 2+ currents together with Gem siRNA-transfection of larger sensory neurons, we demonstrate that only the P/Q-type Ca 2+ channels were enhanced. In vitro analysis of Gem affinity to various Ca V βx-Ca V 2.x complexes and immunocytochemical studies of Gem and Ca V β expression in sensory neurons suggest that the specific inhibition of the P/Q channels relies on both the regionalized upregulation of Gem and the higher sensitivity of the endogenous Ca V 2.1-Ca V β4 pair in a subset of sensory neurons including the proprioceptors. Finally, pharmacological inhibition of P/Q-type Ca 2+ current reduces neurite branching of regenerating axotomized neurons. Taken together, the present results indicate that a Gem-dependent P/Q-type Ca 2+ current inhibition may contribute to general homeostatic mechanisms following a peripheral nerve injury.

Small RGK GTPases, Rad, Gem, Rem1, and Rem2, are potent inhibitors of high-voltage-activated (HVA) Ca^sup 2+^ channels expressed in heterologous expression systems. However, the role of this regulation has never been clearly demonstrated in the nervous system. Using transcriptional analysis, we show that peripheral nerve injury specifically upregulates Gem in mice dorsal root ganglia. Following nerve injury, protein expression was increased in ganglia and peripheral nerve, mostly under its phosphorylated form. This was confirmed in situ and in vitro in dorsal root ganglia sensory neurons. Knockdown of endogenous Gem, using specific small-interfering RNA (siRNA), increased the HVA Ca^sup 2+^ current only in the large-somatic-sized neurons. Combining pharmacological analysis of the HVA Ca^sup 2+^ currents together with Gem siRNA-transfection of larger sensory neurons, we demonstrate that only the P/Q-type Ca^sup 2+^ channels were enhanced. In vitro analysis of Gem affinity to various Ca^sub V^[beta]x-Ca^sub V^2.x complexes and immunocytochemical studies of Gem and Ca^sub V^[beta] expression in sensory neurons suggest that the specific inhibition of the P/Q channels relies on both the regionalized upregulation of Gem and the higher sensitivity of the endogenous Ca^sub V^2.1-Ca^sub V^[beta]4 pair in a subset of sensory neurons including the proprioceptors. Finally, pharmacological inhibition of P/Q-type Ca^sup 2+^ current reduces neurite branching of regenerating axotomized neurons. Taken together, the present results indicate that a Gem-dependent P/Q-type Ca^sup 2+^ current inhibition may contribute to general homeostatic mechanisms following a peripheral nerve injury.

Small RGK GTPases, Rad, Gem, Rem1, and Rem2, are potent inhibitors of high-voltage-activated (HVA) Ca super(2+) channels expressed in heterologous expression systems. However, the role of this regulation has never been clearly demonstrated in the nervous system. Using transcriptional analysis, we show that peripheral nerve injury specifically upregulates Gem in mice dorsal root ganglia. Following nerve injury, protein expression was increased in ganglia and peripheral nerve, mostly under its phosphorylated form. This was confirmed in situ and in vitro in dorsal root ganglia sensory neurons. Knockdown of endogenous Gem, using specific small-interfering RNA (siRNA), increased the HVA Ca super(2+) current only in the large-somatic-sized neurons. Combining pharmacological analysis of the HVA Ca super(2+) currents together with Gem siRNA-transfection of larger sensory neurons, we demonstrate that only the P/Q-type Ca super(2+) channels were enhanced. In vitro analysis of Gem affinity to various Ca sub(V) beta x-Ca sub(V)2.x complexes and immunocytochemical studies of Gem and Ca sub(V) beta expression in sensory neurons suggest that the specific inhibition of the P/Q channels relies on both the regionalized upregulation of Gem and the higher sensitivity of the endogenous Ca sub(V)2.1-Ca sub(V) beta 4 pair in a subset of sensory neurons including the proprioceptors. Finally, pharmacological inhibition of P/Q-type Ca super(2+) current reduces neurite branching of regenerating axotomized neurons. Taken together, the present results indicate that a Gem-dependent P/Q-type Ca super(2+) current inhibition may contribute to general homeostatic mechanisms following a peripheral nerve injury.

We have identified previously a repressor element in the transcription start site region of the cyclin E1 promoter that periodically associates with an atypical, high molecular weight E2F complex, termed CERC. Purification of native CERC reveals the presence of the type II arginine methyltransferase PRMT5, which can mono- or symetrically dimethylate arginine residues in proteins. Chromatin immunoprecipitations (ChIPs) show that PRMT5 is associated specifically with the transcription start site region of the cyclin El promoter. ChIP analyses also show that this correlates with the presence on the same promoter region of arginine-methylated proteins including histone H4, an in vitro substrate of PRMT5. Consistent with its presence within the repressor complex, forced expression of PRMT5 negatively affects cyclin E1 promoter activity and cellular proliferation, effects that require its methyltransferase activity. These data provide the first direct experimental evidence that a type II arginine methylase is involved in the control of transcription and proliferation.

Zika virus was recently linked to birth defects, especially microcephaly. In this report from French territories in the Americas, the rate of birth defects possibly associated with intrapartum Zika virus infection was found to be 7%.

An outbreak of severe acute respiratory syndrome coronavirus 2 caused by the Gamma variant of concern infected 24/44 (55%) employees of a gold mine in French Guiana (87% symptomatic, no severe forms). The attack rate was 60% (15/25) among fully vaccinated miners and 75% (3/4) among unvaccinated miners without a history of infection.

French Guiana (FG) was the first country in South America to declare chikungunya virus infection (CHIKV). The outbreak affected about 16,000 persons between February 2014 and October 2015, with several atypical cases, but only two fatal cases. We aimed to describe the clinical presentation of patients hospitalized for CHIKV infection, to estimate and identify risk factors of unusual and severe forms in adult patients. A monocentric retrospective study was conducted in Cayenne hospital, the main city and the main hospital in FG, from March 1st 2014 to August 31st 2015. All patients admitted for at least one night with a biological diagnosis of CHIKV infection during the 2014/2015 outbreak were included, except pregnant women and children under 15 years. During the study period, 285 patients with a diagnosis of CHIKV infection were hospitalized in Cayenne hospital, among whom 96 nonpregnant adults were studied. Five were classified as severe forms (5.2%) and 23 as unusual forms (23.9%). The most frequent atypical and/or severe form was neurological (n = 20), followed by cardio-respiratory failure (acute respiratory failure n = 4, acute heart failure n = 2), digestive and hepatic disorders (acute hepatitis n = 3, acute pancreatitis n = 2), renal disorders (acute renal failure n = 5) and muscular impairment (rhabdomyolysis n = 3). During the outbreak, hospitalizations were frequent, particularly for common forms, driven by algic clinical presentations and concerns due to the novelty of this infection. Despite atypical neurological and liver forms of CHIKV infection, case-fatality was low in French Guiana. No specific risk factor of atypical and/or severe forms was found in our study.

Oropouche fever is a zoonotic dengue-like syndrome caused by Oropouche virus. In August-September 2020, dengue-like syndrome developed in 41 patients in a remote rainforest village in French Guiana. By PCR or microneutralization, 23 (82.1%) of 28 tested patients were positive for Oropouche virus, documenting its emergence in French Guiana.

While some clinical signs may point to COVID-19 or dengue in case series, at the individual patient scale, the imperfect positive predictive value and clinical variability do not guarantee a diagnosis of certainty (Table 1). [...]some studies report 25% of patients with confirmed dengue having a cough and 20% with upper respiratory tract symptoms [14]. Because of this great disruption in the organization of care, until recently it was only after receiving the results (24–48 hours for negative results) that further explorations were performed, which for a while led to potentially dangerous diagnostic delays in patients with dengue. According to the context and clinical presentation, physicians may prescribe a malaria test, blood and urine cultures, serologies, or molecular diagnosis of differential diagnoses. The extinction of the dengue virus epidemic is less likely when increased human movement enhances the rescue effect. [...]modeling suggests that infection hubs and reservoirs can be locations people