A 42-year-old female with high fever and headache was admitted. Physical examination revealed hypertension, thrombocytosis with megakaryocytosis, hyperfibrinogenemia, and high level of serum noradrenaline. After operation of extrameduUary pheochromocytoma, all symptoms disappeared and findings became normal. The supernatant of tumor culture showed high levels of interleukin-6.
Diabetic polyneuropathy (DPN) is the most common complication of diabetes, yet its pathophysiology has not been established. Accumulating evidence suggests that long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays pivotal roles in the regulation of cell growth and survival during diabetic complications. This study aimed to investigate the impact of MALAT1 silencing in dorsal root ganglion (DRG) sensory neurons, using a α-tocopherol-conjugated DNA/RNA heteroduplex oligonucleotide (Toc-HDO), on the peripheral nervous system of diabetic mice. We identified MALAT1 upregulation in the DRG of chronic diabetic mice that suggested either a pathological change or one that might be protective and systemic intravenous injection of Toc-HDO effectively inhibited its gene expression. However we unexpectedly noted that this intervention paradoxically exacerbated disease with increased thermal and mechanical nociceptive thresholds indicating further sensory loss, greater sciatic-tibial nerve conduction slowing, and additional declines of intraepidermal nerve fiber density in the hindpaw footpads. Serine/arginine-rich splicing factors, which are involved in pre-mRNA splicing by interacting with MALAT1, reside in nuclear speckles in wild-type and diabetic DRG neurons; MALAT1 silencing was associated with their disruption. The findings provide evidence for an important role that MALAT1 plays in DPN, suggesting neuroprotection and regulation of pre-mRNA splicing in nuclear speckles. This is also the first example in which a systemically delivered nucleotide therapy had a direct impact on DRG diabetic neurons and their axons.
A 69-year-old man was admitted with neck muscle weakness, symmetric proximal muscle weakness, skin rash and elevated serum creatine kinase levels. Muscle biopsy showed perifascicular necrosis and perimysial alkaline phosphatase activity. Chest CT revealed interstitial lung disease and colorectal cancer was diagnosed on colonoscopy. He was serologically positive for anti-EJ antibody, leading to the diagnosis of antisynthetase syndrome (ASS). After laparoscopic low anterior resection of the rectum, he received intravenous methylprednisolone (1,000 mg/d for 3 days) followed by oral prednisolone (50 mg/d). Although his muscle weakness improved after corticosteroid therapy, he developed pericardial effusion with resultant asymptomatic hypotension and arrhythmia possibly due to pericarditis. Corticosteroid monotherapy was insufficient to control the disease, and, we decided to use oral cyclosporin concurrently. After this combined therapy started, pericardial effusion and arrhythmia were improved. We should keep in mind that pericarditis can occur in patients with anti-EJ antibody-positive ASS, and early combined therapy with corticosteroid and immunosuppressive drugs for ASS may improve the patient's prognosis.
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