J Formos Med Assoc
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Pressure ulcers are a common problem in hospital care and long-term care. Pressure ulcers are caused by prolonged compression of soft tissues, which can cause local tissue damage and even lead to serious infections. This study uses a deep learning algorithm to construct a system that diagnoses pressure ulcers and assists in making treatment decisions, thus providing additional reference for first-line caregivers. ⋯ Our CNN model, which was based on Inception-ResNet-v2, achieved high accuracy when classifying different types of pressure ulcers, making it applicable in clinical circumstances.
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Epstein-Barr virus-related hemophagocytic lymphohistiocytosis (EBV-HLH) is a life-threatening hyperinflammatory syndrome. Although etoposide-based immunochemotherapy has improved survival rates, consensus regarding the appropriate salvage therapy for patients with refractory or relapsed EBV-HLH is lacking. We performed a retrospective study to examine the efficacy of a lymphoma-based treatment regimen for children with refractory or relapsed EBV-HLH. ⋯ Four patients (67%) were disease free for a median of 10 years without undergoing allogeneic hematopoietic stem cell transplantation. No grade 3 or 4 nonhematologic adverse events occurred. Lymphoma-based chemotherapy is a potential curative treatment for some subgroups of children with refractory or relapsed EBV-HLH.
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Hereditary cerebral cavernous malformations (CCMs) are characterized by clustered dilated capillary-like vessels in the brain. Autosomal dominant polycystic kidney disease (PKD) is characterized by renal cysts and extra-renal abnormalities. We report a Taiwanese family in which the index case exhibited coexisting phenotypes of both CCMs and PKD. ⋯ Segregation analysis revealed that four siblings were affected by either isolated aforementioned PKD2 or CCM2 variant. Notably, radiological CCMs were exclusively found in siblings who had this CCM2 variant, and bilateral internal carotid artery aneurysms were restricted to one sibling who had the PKD2 variant but not the CCM2 variant. Our study expands the genetic spectrum of CCM2 and demonstrates unambiguous cosegregation of CCM2 and PKD2 variants with their respective phenotypes.