Mental health needs associated with COVID-19 on the diamond princess cruise ship: A case series recorded by the disaster psychiatric assistance team.

Coronavirus disease 2019 (COVID-19) infection prevention measures have led to a variety of mental health issues. Although several self-care methods have been recommended for those quarantined, evidence regarding how best to support quarantined people experiencing a mental health crisis is limited. In February 2020, the Diamond Princess cruise ship was quarantined in Yokohama port, Japan following a passenger testing positive for COVID-19. We were sent to address the mental health issues as the Disaster Psychiatric Assistance Team (DPAT). In the present study, we examined the acute mental health needs of the passengers and crew collected by the DPAT using the standard Emergency Medical Team daily reporting system. We assessed 206 cases (99 men and 107 women) with generic health issues and 127 cases (39 men and 88 women) with mental health issues. Mental health issues including disaster stress-related symptoms were as frequent as physical health events associated with COVID-19. The most significant mental health issue was anxiety, as an acute psychological reaction to the quarantine situation. Women and crews most frequently needed mental health support. Mental health improved in most clients after brief counseling. Although several passengers experienced suicidal ideation, there were no cases of actual suicide attempts during the quarantine period. This case has been regarded as a well-known public health event at the beginning of the COVID-19 era. In addition to physical health support, disaster mental health support was essential to save lives. Our findings may facilitate responses to future quarantines, accidents, and mental health crises.

Chronic exposure to valproic acid promotes insulin release, reduces KATP channel current and does not affect Ca (2+) signaling in mouse islets.

Hyperinsulinemia is one of the reported side effects of valproic acid (VPA), a medicine used to treat epilepsy. However, its underlying mechanism remains unknown. The present study was designed to investigate a direct effect of VPA on insulin secretion by using mouse pancreactic islets and ß-cells. VPA had no acute effect on insulin secretion from islets, or on cytosolic Ca(2+) ([Ca(2+)]i) in single ß-cells. However, following long-term exposure to VPA (48 h), both basal and glucose-stimulated insulin secretion were markedly elevated (5-fold), while the insulin gene expression level was unaltered. Following long-term exposure to VPA, ß-cells showed a decrease in whole cell KATP channel current. However, the increase in [Ca(2+)]i in response to the sulfonylurea drug, tolbutamide was attenuated. The present study shows that VPA has no acute effects, but long-term treatment results in enhancement of both basal and glucose-stimulated insulin secretion. This long-term effect may mediate the KATP channel, while VPA can also attenuate the effect of the KATP channel blocker tolbutamide.

Nesfatin-1 enhances glucose-induced insulin secretion by promoting Ca(2+) influx through L-type channels in mouse islet ß-cells.

Nucleobindin-2 (NUCB2)-derived nesfatin-1 located in the brain has been implicated in the satiety and control of energy metabolism. Nesfatin-1 is also produced in the periphery and present in the plasma. It has recently been reported that NUCB2/nesfatin-1 is localized in pancreatic islet ß-cells in mice and rats and released from islets. However, its function in islets remains largely unknown. This study examined direct effects of nesfatin-1 on insulin release from pancreatic islets and on cytosolic Ca(2+) concentration ([Ca(2+)](i)) in single ß-cells from ICR mice. In the presence of 8.3 mmol/L glucose, nesfatin-1 at 10(-10)-10(-9) mol/L tended to increase and at 10(-8) mol/L increased insulin release from isolated islets, while at 2.8 mmol/L glucose nesfatin-1 had no effect. Furthermore, nesfatin-1 at 10(-10)-10(-8) mol/L increased [Ca(2+)](i) in single ß-cells in the presence of 8.3 but not 2.8 mmol/L glucose. The nesfatin-1-induced [Ca(2+)](i) increase and insulin release were inhibited by removal of extracellular Ca(2+) and by addition of nitrendipine, a blocker of voltage-dependent L-type Ca(2+) channels. Unexpectedly, the [Ca(2+)](i) responses to nesfatin-1 were unaltered by inhibitors of protein kinase A (PKA) and phospholipase A(2) (PLA(2)). These results indicate that nesfain-1 potentiates glucose-induced insulin secretion by promoting Ca(2+) influx through L-type Ca(2+) channels independently of PKA and PLA(2) in mouse islet ß-cells.