Search

BACKGROUND Sexual function is a complex physiological process controlled by neurovascular and endocrine mechanisms that are affected by stressful events. The sexual response cycle consists of four main phases, which are sexual desire or libido, arousal or excitement, orgasm, and resolution. The COVID-19 outbreak is one of the most stressful events historically, causing several unpleasant consequences, including major physical and mental disorders, and sexual dysfunction and alteration in sexual behavior are possible anticipated consequences of the pandemic. Moreover, there are social taboos related to sexual behavior in Jordan, and the current knowledge on changes in Jordanian female sexual function during COVID-19 pandemic is limited. OBJECTIVE This study aims to evaluate the impact of COVID‐19 on women's sexual function during the early COVID-19 pandemic in Jordan. METHODS This is a cross-sectional study that employed a web-based survey to follow 200 female individuals from the general population in Jordan. The survey evaluated sexual function both during COVID-19 and 6 months prior to the pandemic. The primary outcomes investigated in this study were the changes in sexual intercourse frequency and sexual function aspects, including desire, arousal, satisfaction, orgasm, lubrication, and pain during sexual activity. Data were analyzed using paired t test, McNemar test, Pearson correlations, and multiple linear regression using SPSS 25. RESULTS During the COVID-19 pandemic, the participants’ sexual intercourse frequency increased while their sexual satisfaction was significantly changed. The proportion of participants who had 0-2 times per week of sexual intercourse was decreased during the COVID-19 pandemic compared with that before the pandemic (n=90, 45% vs n=103, 51.5%; P=.02). Conversely, the number of female individuals with 3-7 times per week of sexual intercourse increased after the pandemic compared with the prepandemic state (n=103, 51.5% vs n=91, 45.5%; P=.04). Female sexual satisfaction was significantly reduced after the COVID-19 pandemic compared with that before the pandemic (3.39 vs 3.30; P=.049). The other categories of sexual function, including desire, arousal, satisfaction, orgasm, lubrication, and dyspareunia showed no significant changes during the COVID-19 pandemic compared with the previous 6 months. There were no significant differences between the total sexual function mean scores during COVID-19 (15.73) compared with the prepandemic scores (15.85; P=.41). The total score of female sexual function during the pandemic was negatively associated with the participants’ age and education level. Correlations between various demographics and sexual function categories during the COVID-19 pandemic were identified. CONCLUSIONS This is the first study exploring female sexual function during the COVID-19 outbreak in Jordan. The results suggest that COVID-19–associated stress is influencing women's sexual function, necessitating the provision of adequate emotional and physiological well-being support for women during similar crises.

Insulin-induced hypoglycemia is a major barrier to the treatment of type-1 diabetes (T1D). Accordingly, it is important that we understand the mechanisms regulating the circulating levels of glucagon – the body’s principal blood glucose-elevating hormone which is secreted from alpha-cells of the pancreatic islets. Varying glucose over the range of concentrations that occur physiologically between the fed and fuel-deprived states (from 8 to 4 mM) has no significant effect on glucagon secretion in the perfused mouse pancreas or in isolated mouse islets (in vitro) and yet associates with dramatic changes in plasma glucagon in vivo. The identity of the systemic factor(s) that stimulates glucagon secretion remains unknown. Here, we show that arginine-vasopressin (AVP), secreted from the posterior pituitary, stimulates glucagon secretion. Glucagon-secreting alpha-cells express high levels of the vasopressin 1b receptor gene (Avpr1b). Activation of AVP neurons in vivo increased circulating copeptin (the C-terminal segment of the AVP precursor peptide, a stable surrogate marker of AVP) and increased blood glucose; effects blocked by pharmacological antagonism of either the glucagon receptor or vasopressin 1b receptor. AVP also mediates the stimulatory effects of hypoglycemia produced by exogenous insulin and 2-deoxy-D-glucose on glucagon secretion. We show that the A1/C1 neurons of the medulla oblongata drive AVP neuron activation in response to insulin-induced hypoglycemia. Exogenous injection of AVP in vivo increased cytoplasmic Ca2+ in alpha-cells (implanted into the anterior chamber of the eye) and glucagon release. Hypoglycemia also increases circulating levels of AVP in humans and this hormone stimulates glucagon secretion from isolated human islets. In patients with T1D, hypoglycemia failed to increase both plasma copeptin and glucagon levels. These findings suggest that AVP is a physiological systemic regulator of glucagon secretion and that this mechanism becomes impaired in T1D.

Understanding and accurately quantifying ion channel molecule gating in real time is vital for knowledge of cell membrane behaviour, drug discovery and toxicity screening. Doing this with single-molecule resolution first requires the detection of individual protein pore opening and closing transitions and construction of a so-called idealised record which indicates sample-point by sample-point whether a given molecule is open or closed. Creating this can be difficult, since patch-clamp electrophysiology data can be noisy or contain multiple ion channel molecules. We have recently developed a deep learning model to achieve this called Deep-Channel, but further development is limited by the massive datasets need to train and validate models. In the past, this problem has been tackled by simulation of single molecule activity from Markov models with the addition of pseudo-random noise. In the present report we develop a new method to synthesise raw data, based on generative adversarial networks (GANs). The limitation to direct application of a GAN with this method has been that whilst there are methods to generate classified output image by image, there has been no method to generate an entire timeseries with parallel idealisation, sample-point by sample-point. In this paper, we over-come this problem with DeepGANnel, a model that splits training data raw and parallel idealised data into different rows of image windows and passes these data through a progressive-GAN. This new methodology allows generation of realistic, idealisation synchronised single molecule patch-clamp data, without the biases inherent in pseudorandom simulation methods. This method will be useful for development of single molecule analysis methods and may in the future prove useful for generation of biological models including single molecule resolution stochastic data. The model is easily extendable to other timeseries data requiring parallel labelling, such as labelled ECG.

Insulin-induced hypoglycemia is a major barrier to the treatment of type-1 diabetes (T1D). Accordingly, it is important that we understand the mechanisms regulating the circulating levels of glucagon – the body’s principal blood glucose-elevating hormone which is secreted from alpha-cells of the pancreatic islets. Varying glucose over the range of concentrations that occur physiologically between the fed and fuel-deprived states (from 8 to 4 mM) has no significant effect on glucagon secretion in isolated islets (in vitro) and yet associates with dramatic changes in plasma glucagonin vivo. The identity of the systemic factor(s) that stimulates glucagon secretion remains unknown. Here, we show that arginine-vasopressin (AVP), secreted from the posterior pituitary, stimulates glucagon secretion. Glucagon-secreting alpha-cells express high levels of the vasopressin 1b receptor gene (Avpr1b). Activation of AVP neuronsin vivoincreased circulating copeptin (the C-terminal segment of the AVP precursor peptide, a stable surrogate marker of AVP) and increased blood glucose; effects blocked by pharmacological antagonism of either the glucagon receptor or vasopressin 1b receptor. AVP also mediates the stimulatory effects of hypoglycemia produced by exogenous insulin and 2-deoxy-D-glucose on glucagon secretion. We show that the A1/C1 neurons of the medulla oblongata drive AVP neuron activation in response to insulin-induced hypoglycemia. Exogenous injection of AVPin vivoincreased cytoplasmic Ca2+in alpha-cells (implanted into the anterior chamber of the eye) and glucagon release. Hypoglycemia also increases circulating levels of AVP in humans and this hormone stimulates glucagon secretion from isolated human islets. In patients with T1D, hypoglycemia failed to increase both plasma copeptin and glucagon levels. These findings suggest that AVP is a physiological systemic regulator of glucagon secretion and that this mechanism becomes impaired in T1D.