Accidental plant poisoning and identification of Datura seed

Recently an accidental plant poisoning occurred in Niigata. In order to identify the actual cause of poisoning, we analyzed the remaining sample, which caused the poisoning. Based on the patient\u27s symptoms such as a dilatation of the pupil, thirst, and others, the poisoning was recognized as being caused by an anticholinergic substance. Furthermore, compressed-reniform shape and the buff color of the sample suggested the origin to be derived from the seeds of Datura (Solanaceae) . The studies were carried out by comparing the external features and anatomical characteristics of the seeds with four comparative materials, namely D. innoxia, D. metel, D. stramonium, and D. stramonium f. inermis. These four materials could be distinguished from each other externally based on the differences in the color and texture, and anatomically by the structure of the sclerenchymatous epidermal cells. In conclusion, the poisoning was confirmed to be caused by an accidental intake of the seeds of D. innoxia. 新潟で中毒事故が発生した。この中毒の真の原因を明らかにするため,我々は患者が摂取した残りの食物試料を分析した。患者の諸症状,即ち,瞳孔散大,口渇等から,この中毒は抗コリン性物質により引き起こされたものと考えられた。また,患者が摂取した残りの試料は,扁平かつ腎臓形で黄土色を呈していたことから,ナス科 Datura 属の種子が原因と考えられた。そこで,比較材料4種即ち,D.inoxia ,D.metal ,D.sramonium f.inermis とともに,組織形態を含む比較形態学的研究を行った。これら4分類群(taxa)の種子は外部形態的には色と質感,内部形態的には表皮の構造の違いによって区別しえた。結論として,この中毒はD.inoxia の種子の誤摂取によって引き起こされたものと確証した

Post-intervention Status in Patients With Refractory Myasthenia Gravis Treated With Eculizumab During REGAIN and Its Open-Label Extension

OBJECTIVE: To evaluate whether eculizumab helps patients with anti-acetylcholine receptor-positive (AChR+) refractory generalized myasthenia gravis (gMG) achieve the Myasthenia Gravis Foundation of America (MGFA) post-intervention status of minimal manifestations (MM), we assessed patients' status throughout REGAIN (Safety and Efficacy of Eculizumab in AChR+ Refractory Generalized Myasthenia Gravis) and its open-label extension. METHODS: Patients who completed the REGAIN randomized controlled trial and continued into the open-label extension were included in this tertiary endpoint analysis. Patients were assessed for the MGFA post-intervention status of improved, unchanged, worse, MM, and pharmacologic remission at defined time points during REGAIN and through week 130 of the open-label study. RESULTS: A total of 117 patients completed REGAIN and continued into the open-label study (eculizumab/eculizumab: 56; placebo/eculizumab: 61). At week 26 of REGAIN, more eculizumab-treated patients than placebo-treated patients achieved a status of improved (60.7% vs 41.7%) or MM (25.0% vs 13.3%; common OR: 2.3; 95% CI: 1.1-4.5). After 130 weeks of eculizumab treatment, 88.0% of patients achieved improved status and 57.3% of patients achieved MM status. The safety profile of eculizumab was consistent with its known profile and no new safety signals were detected. CONCLUSION: Eculizumab led to rapid and sustained achievement of MM in patients with AChR+ refractory gMG. These findings support the use of eculizumab in this previously difficult-to-treat patient population. CLINICALTRIALSGOV IDENTIFIER: REGAIN, NCT01997229; REGAIN open-label extension, NCT02301624. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that, after 26 weeks of eculizumab treatment, 25.0% of adults with AChR+ refractory gMG achieved MM, compared with 13.3% who received placebo

Minimal Symptom Expression' in Patients With Acetylcholine Receptor Antibody-Positive Refractory Generalized Myasthenia Gravis Treated With Eculizumab

The efficacy and tolerability of eculizumab were assessed in REGAIN, a 26-week, phase 3, randomized, double-blind, placebo-controlled study in anti-acetylcholine receptor antibody-positive (AChR+) refractory generalized myasthenia gravis (gMG), and its open-label extension

Peripheral Neuropathy: Clinical Pearls for Making the Diagnosis

Peripheral neuropathy can be encountered by clinicians in a multitude of clinical settings: the patient with Guillain-Barré syndrome who presents to the ED, the patient with suspected carpal tunnel syndrome being referred to orthopedic surgery, the patient with diabetes seeing a primary care provider for new-onset paresthesias in the feet, or the patient following up with the oncology team about adverse medication reactions to chemotherapy. Given the number of systemic conditions with which peripheral neuropathy is associated, clinicians in all specialties need to understand the basic diagnostic principles of the condition

Calpain inhibition as a possible new therapeutic target in multiple sclerosis

Multiple sclerosis (MS), the most common chronic autoimmune inflammatory disease of the central nervous system (CNS), is characterized by demyelination and neurodegeneration. In particular, neurodegeneration is a major factor in disease progression with neuronal death and irreversible axonal damage leading to disability. MS is manageable with current therapies that are directed towards immunomodulation but there are no available therapies for neuroprotection. The complex pathophysiology and heterogeneity of MS indicate that therapeutic agents should be directed to both the inflammatory and neurodegenerative arms of the disease. Activity of the Ca2+ activated protease calpain has been previously implicated in progression of MS and its primary animal model, experimental autoimmune encephalomyelitis (EAE). The effects of calpain inhibitors in EAE involve downregulation of Th1/Th17 inflammatory responses and promotion of regulatory T cells, overall leading to decreased inflammatory cell infiltration in CNS tissues. Furthermore, analysis of brains, spinal cords and optic nerves from EAE animals revealed decreases in axon degeneration, motor neuron and retinal ganglion cell death. This resulted in improved severity of paralysis and preservation of visual function. Taken together, the studies presented in this brief review suggest that use of calpain inhibitors in combination with an immunomodulatory agent may be a potential therapeutic strategy for MS and optic neuritis