ABSTRACT
Morphine is one of the most potent alkaloid in opium, which has substantial medical uses and needs and it is the first active principle purified from herbal source. Morphine has commonly been used for relief of moderate to severe pain as it acts directly on the central nervous system; nonetheless, its chronic abuse increases tolerance and physical dependence, which is commonly known as opiate addiction. Morphine withdrawal syndrome is physiological and behavioral symptoms that stem from prolonged exposure to morphine. A majority of brain regions are hypofunctional over prolonged abstinence and acute morphine withdrawal. Furthermore, several neural mechanisms are likely to contribute to morphine withdrawal. The present review summarizes the literature pertaining to neural mechanisms underlying morphine withdrawal. Despite the fact that morphine withdrawal is a complex process, it is suggested that neural mechanisms play key roles in morphine withdrawal
ABSTRACT
Various substances in cigarette smoke including nicotine have been shown to promote/induce cancer cell proliferation. Since cotinine has a longer half life and stability in the blood, it has become the preferred biomarker for cigarette smoking exposure. Seventy-three gastric cancer patients were included in this study. The tumor tissues were stained with H and E for pathological evaluation. The cotinine levels were measured in urine using a competitive ELISA. Tumors were 90% adenocarcinoma with 63% intestinal and 37% diffuse subtypes. Tumors were poorly [45.2%] or moderately differentiated [41.1%] and localized mainly [77%] in the upper part of stomach. The levels of cotinine were significantly different between smoker [283.83 +/- 178.10 ng/mL] and non-smoker [39.28 +/- 113.34 ng/mL] groups [p < 0.001]. However, there is no-significant correlation between tumor characteristics and cotinine level in smoker patients. Cotinine level correlates with smoking in gastric patients, however, correlation with the tumor features has not been observed