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The researcher concluded that there is a high risk of periodontal disease among patients with schizophrenia, and there is an even higher risk of periodontal disease induced by medication that increased SFR. Preventive dental protocol should be increased during the dental health care of this disadvantaged patient group.

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The aim of the present study was to investigate the association between various clinical aspects of schizophrenia and seropositivity against Toxoplasma gondii (Nicolle et Manceaux, 1908). We selected 94 patients with schizophrenia and investigated the seropositivity rate for anti-T. gondii IgG antibodies by ELISA. Clinical parameters of schizophrenic patients such as illness type and status, clinical course, awareness of the illness and need for electroconvulsive therapy (ECT) were compared with their serological status. Anti-T. gondii IgG antibodies were detected in 43 (46%) of schizophrenic patients. Chronic patients had a rate of 34 (72%) seropositivity, whereas 9 (22%) of the patients with partial remission showed evidence of latent toxoplasmosis. Of continuous patients, 35 (81%) were found to be seropositive and this rate was significantly more than in the other groups. The rate of latent toxoplasmosis was detected significantly higher in patients who lack awareness of schizophrenia (36, i.e. 72%) than the patients who were aware of their illnesses (7, i.e. 16%). Anti-T. gondii IgG antibodies were detected in 38 (70%) of ECT performed patients while this percentage was 13% in the ones who had never been treated with ECT. This difference was also statistically significant. We showed that Toxoplasma-infected subjects had 15× higher probability of having continuous course of disease than Toxoplasma-free subjects. Our results put forth the possibility of latent toxoplasmosis to have a negative impact on the course of schizophrenia and treatment response of schizophrenic patients.

The negative effect of the disorder on the biological and functional status and daily living activities in BD patients also influences the patients' sexual experiences and satisfaction. The negative effects of chronic diseases such as BD should therefore be defined and the disorder evaluated from a wide perspective during the treatment process.

It is shown that ECT, while increasing the anti-inflammatory response such as the levels of IL-4 and TGF-β, it did not affect the levels of MPO and NF-κB activation in this study.

BackgroundStuttering is defined as a disruption in the rhythm of speech and language articulation, where the subject knows what he/she wants to say, but is unable to utter the intended word or phrase fluently. The effect of sex on development and chronicity of stuttering is well known; it is more common and chronic in males. We aimed to investigate the relationship between developmental stuttering and serum testosterone levels in this study.Materials and methodsIn this study, we evaluated a total of 50 children (7–12 years of age); eight (16%) were female and 42 (84%) were male. Twenty-five children who stutter and 25 typically fluent peers with the same demographic properties (ages between 7 years and 12 years) were included in this study. The testosterone levels of the two groups were determined in terms of nanogram per milliliter (ng/mL) by enzyme-linked immunosorbent assay. The difference between the means of the two groups was analyzed.ResultsThe medians of the testosterone levels of the stutterer and control groups were determined as 20 ng/mL (range =12–184 ng/mL) and 5 ng/mL (range =2–30 ng/mL), respectively. Testosterone levels of the stutterer group were significantly higher than in the control group (P=0.001). Besides, there was a significant correlation between the severity of the stuttering and testosterone levels in the stutterer group (P=0.0001).ConclusionThe findings of this study show that testosterone may have an effect on the severity of developmental stuttering and on the clinical differences between sexes. However, further investigations are needed to show that testosterone may play a role in the etiology of developmental stuttering.

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