A daily body temperature rhythm (BTR) is critical for the maintenance of homeostasis in mammals. While mammals use internal energy to regulate body temperature, ectotherms typically regulate body temperature behaviorally [1]. Some ectotherms maintain homeostasis via a daily temperature preference rhythm (TPR) [2], but the underlying mechanisms are largely unknown. Here, we show that Drosophila exhibit a daily circadian clock dependent TPR that resembles mammalian BTR. Pacemaker neurons critical for locomotor activity are not necessary for TPR; instead, the dorsal neuron 2s (DN2s), whose function was previously unknown, is sufficient. This indicates that TPR, like BTR, is controlled independently from locomotor activity. Therefore, the mechanisms controlling temperature fluctuations in fly TPR and mammalian BTR may share parallel features. Taken together, our results reveal the existence of a novel DN2- based circadian neural circuit that specifically regulates TPR; thus, understanding the mechanisms of TPR will shed new light on the function and neural control of circadian rhythms.

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Background Peritoneal dialysis (PD) is associated with various complications, some of which may result in its discontinuation. Pleuroperitoneal communication (PPC) is commonly recognized by the presence of a diaphragmatic defect and pressure elevation in the abdominal cavity due to the dialysate. PPC is unpredictable and its presence prevents the continuation of PD. We present the clinical course and pathological findings of PPC in a PD patient after bacterial peritonitis and total gastrectomy for gastric neuroendocrine tumors. We provide a brief review of PD-related complications that develop due to a non-infectious pathology, including those related to catheter use and an elevated intra-abdominal pressure. Case presentation A 65-year-old Japanese man, who had been receiving PD treatment for 1 year, visited our hospital owing to a cloudy dialysate. Bacteria were detected in the dialysate. He had been previously diagnosed with gastric neuroendocrine tumors and gastrectomy had been planned. On admission, we started a 14-day antibiotic treatment for PD-related peritonitis. The patient showed a good clinical course. Gastrectomy was performed as planned, and the postoperative course was uneventful. During the perioperative period, PD was temporally changed to hemodialysis. Five weeks after the gastrectomy, PD treatment was resumed with gradual increase in the exchange volume. After returning to PD overnight, using an automated peritoneal dialysis machine, the patient complained of breathing difficulty and he gained weight. Right-sided pleural effusion was observed on a chest radiograph, and PPC was confirmed by scintigraphy when a mixture of technetium-99m and dialysate was seen entering the right hemithorax within 120 min. The patient did not consent to surgery for the PPC and he hoped to continue to receive PD treatment conservatively. We advised the patient to undergo dialysate exchange in a semi-seated position, and he was prohibited from lying down during the daytime. He continued PD treatment without signs of pleural effusion and over-volume. Conclusions This case of PPC occurring after bacterial peritonitis and total gastrectomy for gastric neuroendocrine tumors in a PD patient demonstrates the necessity of recognizing the PPC pathology in PD management and establishing methods for preventing PPC development after bacterial peritonitis or surgical procedures.