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Bereavement is associated with many negative behavioural, psychological and physiological consequences and leads to an increased risk of mortality and morbidity. However, studies specifically examining neuroendocrine mechanisms of grief and bereavement have yet to be reviewed. This systematic review is a synthesis of the latest evidence in this field and aims to draw conclusions about the implications of neurobiological findings on the development of new interventions. PRISMA guidelines for systematic reviews were used to search for articles assessing neuroendocrine correlates of grief. Findings were qualitatively summarised. The National Heart, Lung, and Blood Institute Study Assessment Tool was used to assess the quality of the included studies. Out of 460 papers, 20 met the inclusion criteria. However, most were of fair quality only. As a neuroendocrine marker, the majority of the studies reported cortisol as the outcome measure and found elevated mean cortisol levels, flattened diurnal cortisol slopes and higher morning cortisol in bereaved subjects. Cortisol alterations were moderated by individual differences such as emotional reaction to grief, depressive symptoms, grief severity, closeness to the deceased and age or gender. Research on neuroendocrine mechanisms of grief is still in its early stages regarding grief measures and the use and timing of neuroendocrine assessments. Most of the studies focus on cortisol as outcome, and only limited data exist on other biomarkers such as oxytocin. Future research might consider assessing a broader range of neuroendocrine markers and use longitudinal designs with a focus on the psychobiological reactions to loss. Based on this, individually tailored psychosocial interventions, possibly in the palliative care context, might be developed to prevent prolonged grief disorder.

Women have a higher incidence of eating disorders than men. We investigated whether the effects of ghrelin on feeding are affected by sex and stress, and to elucidate the mechanisms that may cause sex differences in stress-mediated anorexia, focusing on ghrelin.

Acylated ghrelin was administered to naïve and psychologically stressed male and female C57BL/6J mice, followed by measurements of food intake and plasma hormone levels. Ovariectomy was performed to determine the effects of ovary-derived oestrogen on stress-induced eating disorders in female mice. The numbers of Agrp or c-Fos mRNA-positive cells and estrogen receptor α/c-Fos protein-double-positive cells were assessed.

Ghrelin administration to naïve female mice caused a higher increase in food intake, growth hormone secretion, Agrp mRNA expression in the arcuate nucleus and c-Fos expression in the nucleus tractus solitarius (NTS) than in male mice. In contrast, psychological stress caused a more sustained reduction in food intake in females than males. The high sensitivity of naïve females to exogenous ghrelin was attenuated by stress exposure. The stress-induced decline in food intake was not abolished by ovariectomy. Estrogen receptor-α but not -β antagonism prevented the decrease in food intake under stress. Estrogen receptor-α/c-Fos-double-positive cells in the NTS were significantly increased by stress only in females.

Stress-mediated eating disorders in females may be due to blockade of ghrelin signalling via estrogen receptor-α activation in the NTS. Targeting the ghrelin signal in the brain could be a new treatment strategy to prevent these disorders.

Stress-mediated eating disorders in females may be due to blockade of ghrelin signalling via estrogen receptor-α activation in the NTS. Targeting the ghrelin signal in the brain could be a new treatment strategy to prevent these disorders.The UK healthcare system, including skin cancer departments, has been profoundly affected by the COVID-19 pandemic. Despite service capacity and a worldwide increase in incidence, anecdotal reports suggest a decline in skin cancer diagnoses following COVID-19. click here To determine if there has been a decrease in skin cancer diagnosis in the UK in the COVID-19 era, we analysed data from the Northern Cancer Network from 23 March 2020 to 23 June 2020 and compared it with the same period in 2019 (pre-COVID). In the COVID period, there was a decrease of 68.61% in skin cancer diagnoses, from 3619 to 1136 (P less then 0.01). Surprisingly, skin cancer waiting times were also reduced in the COVID period compared to the pre-COVID period (median of 8 and 12 days, respectively; P less then 0.001). Collectively, these data highlight a statistically significant reduction in both skin cancer diagnoses and waiting times during the COVID period.Rh2 is a rare ginsenoside and there are few reports of its effect on cognition compared with other similar molecules. This study aimed to establish the impact of Rh2 treatment on improving scopolamine (Scop)-induced memory deficits in mice and illuminate the underlying mechanisms. First, memory-related behavior was evaluated using two approaches object location recognition (OLR), based on spontaneous activity, and a Morris water maze (MWM) task, based on an aversive stimulus. Our results suggested that Rh2 treatment effectively increased the discrimination index of the mice in the OLR test. In addition, Rh2 elevated the crossing numbers and decreased the escape latency during the MWM task. Moreover, Rh2 markedly upregulated the phosphorylation of the extracellular signal-regulated kinase (ERK)-cAMP response element binding (CREB)-brain derived neurotrophic factor (BDNF) pathway in the hippocampus. Meanwhile, the administration of Rh2 significantly promoted the cholinergic system and dramatically suppressed oxidative stress in the hippocampus. Taken together, Rh2 exhibited neuroprotective effects against Scop-induced memory dysfunction in mice. Rh2 activity might be ascribed to several underlying mechanisms, including its effects on modulating the cholinergic transmission, inhibiting oxidative stress and activating the ERK-CREB-BDNF signaling pathway. Consequently, the ginsenoside Rh2 might serve as a promising candidate compound for Alzheimer's disease.

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