Scopolamine Treatment and Adaptation to Airsickness.

BACKGROUND: Airsickness is a clinical syndrome manifesting in a variety of symptoms, particularly nausea and vomiting during flight. Studies of habituation to motion sickness in humans treated by scopolamine have produced conflicting results. The drug accelerated habituation, but a rebound effect on symptom severity was observed after its withdrawal. The purpose of the present study was to investigate whether scopolamine affects the adaptation process. We also evaluated the relationship between initial symptom severity and adaptation to airsickness.METHODS: Aviator cadets in the first two stages of their training were divided into two groups, treated and not treated by scopolamine. Airsickness severity was evaluated using both simulator sickness and motion sickness questionnaires, and drug administration was recorded.RESULTS: A statistically significant higher rate of adaptation was observed among the scopolamine-treated group compared with the nontreated group. On the simulator sickness questionnaire, rate of adaptation for the two groups was -0.21 ± 0.53 and -0.1 ± 0.17, respectively, and for the motion sickness questionnaire -2.34 ± 1.54 and -0.91 ± 1.41, respectively. Examination of a possible connection between initial symptom severity and adaptation rate failed to reveal a significant relationship.CONCLUSIONS: We recommend the use of oral scopolamine to accelerate habituation and find it a relatively safe short-term treatment for airsickness. Our results support the notion that scopolamine accelerates the natural adaptation process.Doron O, Samuel O, Karfunkel-Doron D, Tal D. Scopolamine treatment and adaptation to airsickness. Aerosp Med Hum Perform. 2020; 91(4):313-317.

Intranasal gonadotropin-releasing hormone agonist (GnRHa) for luteal-phase support following GnRHa triggering, a novel approach to avoid ovarian hyperstimulation syndrome in high responders.

OBJECTIVE: To study whether intranasal GnRH agonist (GnRHa) can be effectively used for luteal support in high-responder patients undergoing fresh-embryo transfer after ovulation induction with the use of GnRHa. DESIGN: Retrospective cohort study. SETTING: Private fertility clinic. PATIENT(S): Forty-six high-responder patients were administered a GnRHa ovulation trigger to avoid ovarian hyperstimulation syndrome (OHSS), followed by 2 weeks of daily intranasal GnRHa (nafarelin) for luteal-phase support. No additional progesterone supplementation was administrated. INTERVENTION(S): Intranasal GnRHa for luteal-phase support. MAIN OUTCOME MEASURE(S): The primary outcome was ongoing clinical pregnancy rate. RESULT(S): High median progesterone levels were measured at midluteal phase and on the day of the first positive pregnancy test (190 nmol/L on both measures). We obtained 24 (52.1%) ongoing clinical pregnancies. None of the patients developed OHSS. CONCLUSION(S): Intranasal GnRHa is effective in achieving luteal-phase support in high-responder patients triggered with GnRHa and avoiding OHSS.

Novel myosin mutations for hereditary hearing loss revealed by targeted genomic capture and massively parallel sequencing.

Hereditary hearing loss is genetically heterogeneous, with a large number of genes and mutations contributing to this sensory, often monogenic, disease. This number, as well as large size, precludes comprehensive genetic diagnosis of all known deafness genes. A combination of targeted genomic capture and massively parallel sequencing (MPS), also referred to as next-generation sequencing, was applied to determine the deafness-causing genes in hearing-impaired individuals from Israeli Jewish and Palestinian Arab families. Among the mutations detected, we identified nine novel mutations in the genes encoding myosin VI, myosin VIIA and myosin XVA, doubling the number of myosin mutations in the Middle East. Myosin VI mutations were identified in this population for the first time. Modeling of the mutations provided predicted mechanisms for the damage they inflict in the molecular motors, leading to impaired function and thus deafness. The myosin mutations span all regions of these molecular motors, leading to a wide range of hearing phenotypes, reinforcing the key role of this family of proteins in auditory function. This study demonstrates that multiple mutations responsible for hearing loss can be identified in a relatively straightforward manner by targeted-gene MPS technology and concludes that this is the optimal genetic diagnostic approach for identification of mutations responsible for hearing loss.