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Background:Due to inappropriate diet, smoking, alcohol consumption, regular use of drugs like NSAIDs and sedentary lifestyle, one may feel upper abdominal pain which may be the predictor of the gastrointestinal disorder called Peptic Ulcer. When an imbalance occurs between the defensive factor and aggressive factor of the stomach, ulcer formation in the esophageal lining, stomach, or duodenum takes place. This leads to the formation of small sores that cause pain. Another condition that synergizes the abdominal pain is vomiting materials which look like coffee grounds, blood in the stool, black or tarry stools. This pain may increase after lunch or dinner. This problem persists, that often leads to the gastroenterologist's consultation.Objective:There are many antiulcer screening models present for the determination of antiulcer activity of the drug molecule. The main objective of this study is to find which model is best for the determination of antiulcer activity.Methods:A literature search was conducted on the databases namely Science direct and PubMed with the help of different keywords such as "Anti-ulcer", "In-vitro models" and "In-vivo models". The search was customized by applying the appropriate filters so as to get the most relevant articles to meet the objective of this review article.Result:There are different research and review papers based on the antiulcer screening models for the determination of antiulcer activity of new drug molecules.Conclusion:On the basis of our study, we found some useful models for the antiulcer activity of drugs and suggested that, if we use in-vitro and in-vivo methods together, then we may obtain the most relevant result in our research area.

The authors describe the case of a 39-year-old man who presented to our hospital with easy fatigability and malaise. On physical examination, hypertension was noted without any cushingoid appearance. Laboratory testing revealed normochromic-normocytic anaemia with positive results of occult blood in the stool, hyperglycaemia and hypokalemia. Upper endoscopy revealed active gastric ulcer with Helicobacter pylori infection, likely causing gastrointestinal bleeding. Endocrine examinations showed that both serum adrenocorticotropic hormone and cortisol were elevated with loss of diurnal variation. A diagnosis of Cushing’s disease secondary to pituitary adenoma was made as results of brain MRI and blood sampling from inferior petrosal sinus. In a patient with peptic ulcer disease, physician should be alert to the possible endocrine background.

Traumatic brain injury (TBI) remains a complicated and urgent disease in our modernized cities. It becomes now a public health disease. We have got more and more patients in Neurosurgery Intensive Care Unit following motor vehicle accidents and others causes. TBI brings multiple disorders, from the primary injury to secondary injury. The body received the disturbances in the brain, in the hypothalamo-pituitary-adrenocortical (HPA) axis, in the gastric mucosa, in the immune and neuroendocrine systems. The mortality of TBI is more than 50 000 deaths / year, the third of the mortality of all injuries. Cushing ulcer is one of the severe complications of TBI and its mortality rate is more than 50%. Many studies have improved the management of TBI and the associated complications to give patients a better outcome. Furthers studies need to be done based on the similar methodology to clarify the different steps of the HPA axis and the neuroendocrine change associated. The aim of the present review is to assess the clinical and endocrinal features of hypopituitarism and stress ulcer following TBI.

Dr Harvey Cushing. Illustration by Venita Jay, MD, FRCPC. I is a formidable task for any biographer to record all of the achievements of Harvey William Cushing, commonly known as the Father of American Neurosurgery. Regarded as the leading neurosurgeon of the 20th century, Cushing was a tireless investigator, dedicated teacher, prolific writer, gifted artist, and ardent bibliophile. His name is known to every medical student and is immortalized in the well-known Cushing syndrome, Cushing disease, Cushing reflex, and Cushing ulcer. Cushing also left a lasting legacy in pathology with his work on the pituitary gland and brain tumors. Cushing launched neurosurgery as a distinct discipline and firmly established it as a separate specialty. Every phase of Cushing’s career has been the subject of intense scrutiny, with extensive biographies detailing his college days at Yale, medical training at Harvard, surgical residency at Johns Hopkins, and the years at Peter Bent Brigham and Yale. There are also several well-known biographies of Cushing, including those written by John F. Fulton, Elizabeth H. Thomson, and Justin F. Denzel. Born on April 8, 1869, in Cleveland, Ohio, Cushing was the youngest of 10 children, 7 of whom survived to maturity. His great-grandfather, grandfather, father, and older brother Ned were physicians. Cushing attended Yale College in New Haven, Conn, and graduated from that institution in 1891. While at Yale, Russell Chittenden encouraged in Cushing an interest in physiological chemistry. Cushing greatly admired his father and his brother Ned. He followed in the family tradition and embarked on a medial career, joining Harvard Medical School in Boston, Mass. Cushing attended Harvard from 1891 to 1896 and received his medical degree in 1895. He completed his internship at Massachusetts General Hospital. During his medical school years, Cushing was a keen and observant student, who was able to recognize the importance of new developments. Ether anesthesia had come into vogue, and medical students were called upon to administer it. One patient anesthetized by Cushing died, which disturbed Cushing so much that he wanted to quit medicine. Brooding over the tragedy and hoping that such deaths could be prevented if vital signs were monitored, he embarked on a new venture with fellow student Ernest Amory Codman. Together, they developed a record of an

Similar to adults, children under physiologic stress can develop an imbalance in defensive (mucosal layer, motility) and aggressive (gastric acid, bile salts, enzymes) factors responsible for maintaining a healthy gastrointestinal tract. Hypoxia in the gastrointestinal tract likely disrupts the defensive factors, thereby permitting damage by aggressive factors to upper gastrointestinal epithelium that may progress to stress ulceration and acute upper gastrointestinal tract bleeding (UGIB). The basic pathophysiology may be similar in children and adults; however, differences in the time to developing ulceration, ulcer location, and number of ulcers have been reported. Functional development of the gastrointestinal tract is influenced by disease, gestational and postnatal age, and exposure to and type of enteral feedings, thereby confounding the development and prophylaxis of UGIB in neonates and infants. In addition, pharmacotherapy decisions are often complicated by drug administration issues and adverse effects.