We found higher levels of serum glutamate in subjects with ASD and this might reflect altered glutamatergic neurotransmission which may aid early ASD detection. Further investigations are needed with a large number of participants to further clarify the possibility of using glutamate as a biomarker for ASD.
While animal models for schizophrenia, ranging from pharmacological models to lesions and genetic models, are available, they usually mimic only the positive symptoms of this disorder. Identifying a feasible model of chronic schizophrenia would be valuable for studying the possible underlying mechanism and to investigate emerging treatments. Our hypothesis starts from the observation that combining ketamine with isolation could result in long-lasting neuro-psychological deficits and schizophrenia-like features; thus, it could probably be used as the first model of chronic schizophrenia that emphasizes the characteristic of having a multifactorial etiology. By the means of this study, we investigated the effects of ketamine administration combined with isolation in inducing schizophrenia-like symptoms in male albino rats and the brain reactive oxygen species levels. Our results showed that the number of lines crossings in the open field test, the number of open arm entries in the elevated plus maze, and the spontaneous alternations percentage in the Y-maze were significantly lower in the ketamine + isolation group compared to both the control and ketamine + social housing group (p < 0.05). Furthermore, the ketamine + isolation intervention significantly increased the MDA levels and decreased the GPx levels both in the hippocampus and the cortex of the rats. In addition, our premise of creating a model capable of exhibiting both positive and negative symptoms of schizophrenia was also based on adding the aripiprazole treatment to a group of rats. Therefore, we compared the ketamine + social isolation group with the ketamine + social isolation + aripiprazole group in order to attempt to discover if the antipsychotic drug would significantly decrease the potential positive schizophrenia-like symptoms induced by social isolation and ketamine. Given that we obtained significant results, we cautiously presume that this might be an important step in developing our animal model capable of illustrating both positive and negative symptoms of schizophrenia. This study could be a first step towards the creation of a complex animal model capable of exhibiting the multifactorial origin and manifestation of schizophrenia.
Prospective studies of patients with SLE have reported a prevalence of clinically apparent coronary artery disease (CAD) of up to 20%, a marked increase compared with the estimated CAD prevalence rate of 3.5% among healthy females 20–35 years (AHA 1997 Heart and Stroke Statistical Update). Nitric oxide is an important mediator of inflammation associated with vascular damage. We measured nitric oxide production by cultures of peripheral blood monocytes (N= 26) from patients with SLE and determined serum immunoglobulin concentrations (N=19). Elevated immunoglobulin concentrations were observed in sera from 8 patients (42%), and 4 individuals had a selective increase in IgE (>100 IU/ml), with other immunoglobulin isotypes in the normal range. Nitric oxide (NO) production by adherent monocyte cultures from patients with SLE was determined on day 7 using a modified colorimetric Griess reaction to measure nitrite, the stable NO metabolite. The results showed activation in 31% of the patients, with nitrite concentrations exceeding the baseline of 2.8μM more than threefold, reaching 8.8 μM. The mechanism of this in vivo activation of blood monocytes among some patients with SLE remains to be established. Activated monocyte-derived nitric oxide may contribute to the development of atherosclerosis and cardiovascular complications seen in many patients with SLE.
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