Differential effects on T-cell function following exposure to serum from schizophrenia smokers.

Cigarette smoking is more prevalent in subjects with schizophrenia compared to those with other psychiatric disorders or the general population and could therefore affect molecular pathways that impact the pathophysiology of this disorder. As smoking is also known to suppress immune responses, we investigated the effects of 'smoking-conditioned' serum obtained from schizophrenia and control subjects on healthy T cell in vitro. We found that T-cell proliferation was significantly increased following exposure to serum from smoking schizophrenia patients whereas no effect was observed when using serum from smoking control subjects or non-smoking patients and controls. We eliminated the possibility that these effects were due to quantitative differences in cigarette consumption as serum levels of the stable nicotine metabolite cotinine were similar in schizophrenic and control smokers. Molecular characterization showed that serum from patient smokers increased expression of T-cell activation markers CD69(high), CD25(high), co-stimulatory molecules CD26+, CD27+ and CD28+, and decreased T-cell receptor complex components TCRalpha/beta and CD3. Moreover, analysis of supernatants collected after T-cell exposure to serum from smoking patients showed a time-dependent decline in interleukin (IL)-2 levels, suggesting that the proliferation effect is promoted by enhanced IL-2 processing. These results suggest that cigarette smoking has selective effects on serum components that, in turn, lead to altered immune function in schizophrenia patients relative to healthy subjects. Further studies aimed at characterizing these components could result in a better understanding of the onset and aetiology of schizophrenia and potentially lead to novel therapeutic strategies.

Artifacts in recording immediate mandibular translation: a laboratory investigation.

STATEMENT OF PROBLEM: Even though immediate mandibular translation has been extensively studied and analyzed, and its clinical significance emphasized, there is controversy as to whether it actually exists or whether it is just an artifact of the pantograph. PURPOSE: The aim of this study was to determine whether what appears to be pantographic evidence of immediate mandibular translation can actually be an artifact and, if so, to find a method to avoid it. MATERIAL AND METHODS: The first part of this article explains geometrically with computer vector graphics how pure rotation can produce a pantographic tracing on the horizontal plate that is identical to what would be seen for immediate mandibular translation. The second part of the article presents a technique that uses a modified pantograph that eliminates the rotational artifact and thus permits proper interpretation of true immediate mandibular translation. RESULTS: This study shows that pure rotation about the sagittal axis mimics immediate mandibular translation on a pantographic tracing when the plates are inferior to the transverse horizontal axis, produces scribings in an opposite direction for plates in a superior position, and produces no scribing when the plates are level with it. By modifying the pantograph so the tip of the scribing pin of the horizontal plate is level with the transverse horizontal axis, true immediate mandibular translation can most easily be differentiated from rotational artifact. CONCLUSIONS AND CLINICAL SIGNIFICANCE: Rotation can cause artifacts that mimic immediate mandibular translation. A technique to avoid this problem is presented. This technique provides the foundation for a valid evaluation of patients to determine whether true immediate mandibular translation exists and whether it is clinically important.