This study has shown once more that celiac disease is associated with some psychiatric signs/diagnoses, and that it decreased quality of life. Further studies are needed to determine the factors that could reduce the psychiatric signs. It is apparent that those studies would contribute new approaches to improve diagnosis, treatment, and quality of life.

We evaluated the electrophysiological and histopathological effects of low-energy gallium arsenide (904 nm) laser irradiation on the intact skin injured rat sciatic nerve. Twenty-four male Wistar rats were divided into three groups ( n=8 each). At the level of proximal third of the femur the sciatic nerve was crushed bilaterally with an aneurysm clip (Aesculap FE 751, Tuttingen, Germany) for half a second. A gallium arsenide laser (wavelength 904 nm, pulse duration 220 ns, peak power per pulse 27 W, spot size 0.28 cm2, pulse repetition rate 16, 128 and 1000 Hz; total applied energy density 0.31, 2.48 and 19 J/cm2) was applied to the right sciatic nerve for 15 min daily at the same time on 7 consecutive days. The same procedure was performed on the left sciatic nerve of same animal, but without radiation emission, and this was accepted as control. Compound muscle action potentials were recorded from right and left sides in all three groups before surgery, just at the end of injury, at the 24th hour and on the 14th and 21st days of injury in all rats using a BIOPAC MP 100 Acquisition System Version 3.5.7 (Santa Barbara, USA). BIOPAC Acknowledge Analysis Software (ACK 100 W) was used to measure CMAP amplitude, area, proximal and distal latency, total duration and conduction velocity. Twenty-one days after injury, the rats were sacrificed. The sciatic nerves of the operated parts were harvested from the right and left sides. Histopathological evaluation was performed by light microscopy. Statistical evaluation was done using analysis of variance for two factors (right and left sides) repeated-measures (CMAP variables within groups) and the Tukey-Kramer Honestly Significant Difference test (CMAP variables between laser groups). The significance was set at p < 0.05. No statistically significant difference (p > 0.05) was found regarding the amplitude, area, duration and conduction velocity of CMAP for each applied dose (0.31, 2.48 and 19 J/cm2) on the irradiated (right) side and the control (left) side, or between irradiated groups. Twenty-one days after injury there were no qualitative differences in the morphological pattern of the regenerated nerve fibres in either irradiated (0.31, 2.48 and 19 J/cm2) or control nerves when evaluated by light microscopy. This study showed that low-energy GaAs irradiation did not have any effect on the injured rat sciatic nerve.

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Background: Alcohol-induced lung damage may be associated with increased oxidative stress. Objective: Our aim was to investigate alcohol-induced changes in the biochemistry and histopathology of the lung. Methods: Rats were divided into two groups, a control group and an ethanol group. The ethanol group received 2 g/kg ethanol (total: 3 ml) intraperitoneally. The controls were given the same amount of saline via the same route. Three hours later, the rats were sacrificed, and blood and lung tissue samples were obtained. Oxidative stress was assessed by measuring the levels of erythrocyte reduced glutathione (GSH), tissue malondialdehyde (MDA), myeloperoxidase (MPO) and Na⁺-K⁺ ATPase. Histopathologic evaluation of the lung tissues was also performed. Results: In the ethanol group, serum and tissue MDA levels and MPO activities were increased (p = 0.007, p = 0.001 and p = 0.000), and lung tissue Na⁺-K⁺ ATPase activities and erythrocyte GSH were decreased (p = 0.001 and p = 0.000) compared to the controls. Histopathologic examination demonstrated alveolocapillary thickening, alveolar degeneration, leukocyte infiltration and erythrocyte extravasation in the lungs of the ethanol group (p < 0.05). Conclusion: These results suggest that high-doseacute alcohol administration aggravates systemic and local oxidative stress leading to acute lung injury, ranging from mild pulmonary dysfunction to severe lung injury. It should be borne in mind that rapid onset of the acute respiratory distress syndrome (ARDS) may also be due to increased oxidative stress following alcohol abuse, especially when ischemic disturbances, e.g. coronary heart disease, acute ischemia of the extremities and traumatic accidents, are concomitantly present. Therefore, precautions against ARDS may prevent morbidity and mortality in alcohol-induced lung damage in at-risk patients.

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