Fat body-derived juvenile hormone acid methyltransferase functions to maintain iron homeostasis in Drosophila melanogaster.

Iron homeostasis is of critical importance to living organisms. Drosophila melanogaster has emerged as an excellent model to study iron homeostasis, while the regulatory mechanism of iron metabolism remains poorly understood. Herein, we accidently found that knockdown of juvenile hormone (JH) acid methyltransferase (Jhamt) specifically in the fat body, a key rate-limiting enzyme for JH synthesis, led to iron accumulation locally, resulting in serious loss and dysfunction of fat body. Jhamt knockdown-induced phenotypes were mitigated by iron deprivation, antioxidant and Ferrostatin-1, a well-known inhibitor of ferroptosis, suggesting ferroptosis was involved in Jhamt knockdown-induced defects in the fat body. Further study demonstrated that upregulation of Tsf1 and Malvolio (Mvl, homolog of mammalian DMT1), two iron importers, accounted for Jhamt knockdown-induced iron accumulation and dysfunction of the fat body. Mechanistically, Kr-h1, a key transcription factor of JH, acts downstream of Jhamt inhibiting Tsf1 and Mvl transcriptionally. In summary, the findings indicated that fat body-derived Jhamt is required for the development of Drosophila by maintaining iron homeostasis in the fat body, providing unique insight into the regulatory mechanisms of iron metabolism in Drosophila.

Successful treatment of aortic dissection with pulmonary embolism: A case report.

BACKGROUND: Aortic dissection (AD) and pulmonary embolism (PE) are both life-threatening disorders. Because of their conflicting treatments, treatment becomes difficult when they occur together, and there is no standard treatment protocol. CASE SUMMARY: A 67-year-old man fell down the stairs due to syncope and was brought to our hospital as a confused and irritable patient who was uncooperative during the physical examination. Further examination of the head, chest and abdomen by computed tomography revealed a subdural hemorrhage, multiple rib fractures, a hemopneumothorax and a renal hematoma. He was admitted to the Emergency Intensive Care Unit and given a combination of oxygen therapy, external rib fixation, analgesia and enteral nutrition. The patient regained consciousness after 2 wk but complained of abdominal pain and dyspnea with an arterial partial pressure of oxygen of 8.66 kPa. Computed tomography angiograms confirmed that he had both AD and PE. We subsequently performed only nonsurgical treatment, including nasal high-flow oxygen therapy, nonsteroidal analgesia, amlodipine for blood pressure control, beta-blockers for heart rate control. Eight weeks after admission, the patient improved and was discharged from the hospital. CONCLUSION: Patients with AD should be alerted to the possibility of a combined PE, the development of which may be associated with aortic compression. In patients with type B AD combined with low-risk PE, a nonsurgical, nonanticoagulant treatment regimen may be feasible.