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To understand the role of two Niemann-Pick type C2 (NPC2) transcripts, Vd40090 (NP1) and Vd74517 (NP5), in the chemosensing pathway of Varroa destructor, we evaluated the impact of NP5 silencing on mites behavior and compared the effect of silencing of either transcripts on the interaction between chemosensory transcripts. In contrast to silencing NP1, which reduced feeding and reproduction by the mite (Nganso et al., 2021), silencing of NP5 reduced significantly the host reaching ability, but it did not affect the feeding on nurse bee. However, silencing of either transcript changed dramatically the co-expression patterns among the putative chemosensory genes, binding proteins and receptors. The results suggest the role of gustatory receptors in the detection of long-range chemical cues in the chemosensory cascade of the Varroa mite.

ObjectivesTo explore magnitude and factors associated with non-urgent visits to the emergency department (ED) in a tertiary care centre, western Saudi Arabia.DesignA cross-sectional study.SettingED of a tertiary care hospital in western Saudi Arabia.Participants400 patients, both men and women.InterventionsAn interview-based questionnaire was administered to a consecutive sample of patients who visited the ED during morning shifts, where primary healthcare centres (PHCs) and outpatient clinics were available.Primary outcome measureED visits classified as non-urgent versus urgent (excluding life-threatening conditions) based on the Canadian Triage and Acuity Scale (CTAS). Levels IV and V were classified as non-urgent.ResultsMajority of the cases were adult (97.3%) and half of them were women (54.8%). Non-urgent visits represented 78.5% among non-life-threatening cases. One-third of the patients (33.8%) had three visits or more to the ED during the past year. Main reasons for visiting the ED were perception that the condition was urgent (42.0%), easy access (25.5%) and limited resources and services at the PHCs (17.8%). Patients 40–50 years old were more likely to have non-urgent visits (OR=3.21, 95% CI 1.15 to 8.98). However, likelihood of non-urgent visits was significantly lower among patients with cancer (OR=0.37, 95% CI 0.19 to 0.72) and cardiovascular disease (OR=0.43, 95% CI 0.23 to 0.83), and those who live near the hospital (OR=0.49, 95% CI 0.28 to 0.88).ConclusionsThe current study reported overuse of the ED. Enhancement of the primary care services, in concordance with community awareness, is an important component to reduce burden due to non-urgent use of the ED.

Do autoantibodies (Ab's) against glutamate/AMPA receptor subtype 3 affect the severity of seizures? Rats immunized with the GluR3B-peptide (amino acids (aa) 372-395) or with the control GluR3A-peptide (aa 245-274) produced the respective anti-GluR3B and anti-GluR3A Ab's (both types of Ab's found in some epilepsy patients). The GluR3B-immunized rats exhibited neuronal death and reactive gliosis in the brain, but not overt spontaneous seizures. Surprisingly, in response to the chemoconvulsant pentylenetetrazole, the GluR3B-immunized rats displayed fewer jerks, a lower percentage of generalized seizures, and a lower overall seizure-severity score than GluR3A-immunized, scrambled GluR3B-immunized or non-immunized control rats. These findings, combined with the previously demonstrated ability of anti-GluR3B Ab's to bind, activate, and kill neurons and glia, suggest that if these Ab's are present in the brain they may cause neuronal death, which by itself may be pro-epileptic, but they may also decrease the excitability of seizure-related neural circuits, thereby conferring partial protection from seizures induced by other exogenously applied epileptogenic stimuli. The present results could have clinical implications for epilepsy.

Genetic control has been studied of the response to the encephalitogenic nonapeptide (NP) determinant of myelin basic protein (BP) in inbred guinea pigs of strains resistant or susceptible to induction of experimental autoimmune encephalomyelitis (EAE). By studying bone marrow-reconstituted animals, we found that susceptibility to induction of EAE was a function of the genotype of the cells of the lymphohematopoietic system and not of the physiological environment or target organ. Analysis of the T cell response showed that susceptible strains 13 or (2 X 13)F1 hybrid guinea pigs recognized the NP determinant when injected with whole BP in adjuvant. Resistant strain 2 guinea pigs responded to undefined determinants on BP, but not to the NP moiety. We investigated the cells involved in regulating the response to the NP determinant by injecting susceptible F1 hybrids with BP-pulse macrophages of either parental strain. Susceptible strain 13 macrophages triggered a response to the NP determinant and induced clinical EAE. In contrast, F1 animals injected with resistant strain 2 macrophages failed to respond to the NP determinant, although the macrophages were capable of presenting other undefined determinants present on whole BP. Therefore, genetic control of the immune response to the NP determinant appears to be exerted at the level of antigen presentation by macrophages to T lymphocytes.