RESUMEN
Background: Long Latency Reflex (LLR) is one of the late responses occurring after H reflex from a mixed nerve by submaximal stimulation. LLR has been found to be absent in patients with multiple sclerosis, spastic patients and in Huntington’s disease. A change in body temperature affects conduction velocity. It is a known fact that there is a change in body temperature during menstrual cycle. However, no studies are available to indicate changes in latency of LLR during the menstrual cycle. Aim: To determine the effect of menstrual cycle on Long Latency Reflex of Abductor Pollicis Brevis among healthy female volunteers. Material and Methods: A cross sectional study was carried out in 30 healthy female volunteers aged 20-30 yrs. The study was conducted between 9.00 a.m.-11.00 a.m using Digital Nerve Conduction/EMG/EP machine (Recorders Medicare system, India) in a laboratory maintained at 22º±3ºC. LLR was recorded during early follicular and mid-luteal phases by stimulation of median nerve while abducting the thumb and recording the EMG response of Abductor Pollicis Brevis. Body temperature was recorded. Latency of LLR obtained during two phases of menstrual cycle was compared. Result: The mean value of latency for LLR was 45.45±2.95 ms (mean±SD) in the mid luteal phase. It was significantly (Wilcoxon test, p<0.001) shorter than the value in the early follicular phase 47.10±2.51ms (mean±SD). This is possibly due to the higher body temperature in the mid luteal phase. Conclusion: Long Latency Reflex was found to be affected during the phases of the menstrual cycle in healthy female volunteers.
RESUMEN
Cadmium is one of the most toxic heavy metals and potential for human exposure has generally increased with increase in industrial usage of this element. The purpose of the present study was to determine anti-oxidative role of vitamin C against cadmium chloride induced oxidative stress on rat testis. Adult male rats(n=6/group) were divided into five groups ,one control (Gr.I- 0.9% Saline treated) & two untreated experimental & two pretreated experimental groups. The untreated groups were injected with single dose of 0.5 & 1 mg /kg bw cadmium chloride (Gr.II &Gr.III) intraperitoneally. Vitamin C (30mg/kg bw,ip) was orally administered for 30 days prior to the exposure to 0.5 and 1mg/kg bw(Gr,IIa &Gr.IIIA) of cadmium chloride. In all the groups, rats were sacrificed 15 days after the final cadmium chloride or saline administration and the changes in the testicular weight and testicular level of Melonaldehyde , glutathione & superoxide dismutase were studied. Exposure to cadmium chloride lead to significant decrease in the testicular weight& level of GSH & SOD and increase in the level of testicular MDA compared to normal control. Pretreatment with vitamin C (30mg/kg bw) significantly prevented the increase in MDA level of the testis & ameliorated the fall in GSH & SOD as well as testicular weight compared to 0.5mg/kg bw cadmium chloride group. But pretreatment with vitamin C did not show any beneficial effect with 1mg/kg bw cadmium treated group. The study reports the antioxidative role of vitamin C in ameliorating lower doses of cadmium chloride induced testicular damage.