This case report presents an evaluation of the clinical effects of an allogeneic amniotic cell transplant for the treatment of type 1 diabetes mellitus. A 26-year-old man with type 1 diabetes was treated with stem cells isolated from his neonatal son's amniotic membrane, collected at birth (2 × 10(7) cells). The cells, which expressed high levels of cluster of differentiation (CD) 133 and CD34 as assessed by flow cytometry, were infused into the pancreatic dorsal artery through the left femoral artery. The main study outcome was the change in exogenous insulin requirements, which began to decrease 3 days after transplantation. At 3 months post-transplantation, the patient was insulin independent and remained so for 6.2 months. During a 36-month follow-up, the patient's blood glucose remained under control and insulin treatment was readjusted to a dosage of 8 IU/day. These preliminary data suggest that amniotic membrane stem cell transplantation can improve islet-cell function in response to glucose in vivo, although an alternative explanation (such as a honeymoon period due to reduced glucose toxicity) also has to be considered.
Mutations in the GABRG2 gene encoding the γ-aminobutyric acid (GABA) A receptor gamma 2 subunit are associated with genetic epilepsy with febrile seizures plus, febrile seizures plus, febrile seizures, and other symptoms of epilepsy. However, the mechanisms underlying Gabrg2-mediated febrile seizures are poorly understood. Here, we used the Cre/loxP system to generate conditional knockout (CKO) mice with deficient Gabrg2 in the hippocampus and neocortex. Heterozygous CKO mice (Gabrg2fl/wtCre+) exhibited temperature-dependent myoclonic jerks, generalised tonic-clonic seizures, increased anxiety-like symptoms, and a predisposition to induce seizures. Cortical electroencephalography showed the hyperexcitability in response to temperature elevation in Gabrg2fl/wtCre+ mice, but not in wild-type mice. Gabrg2fl/wtCre+ mice exhibited spontaneous seizures and susceptibility to temperature-induced seizures. Loss of neurons were observed in cortical layers V–VI and hippocampus of Gabrg2fl/wtCre+ mice. Furthermore, the latency of temperature- or pentylenetetrazol-induced seizures were significantly decreased in Gabrg2fl/wtCre+ mice compared with wild-type mice. In summary, Gabrg2fl/wtCre+ mice with Gabrg2 deletion in the neocortex and hippocampus reproduce many features of febrile seizures and therefore provide a novel model to further understand this syndrome at the cellular and molecular level.
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