Hypertension and obesity are two disorders that are closely related; each occurs more frequently with the other than in an otherwise normal population. These two disorders, however, exert disparate effects on cardiovascular structure and function. The hallmark of essential hypertension is an increased total peripheral resistance, and hypertensive patients have a contracted intravascular volume and normal cardiac output but an increased left ventricular stroke work due to a high afterload. In contrast, obese patients have an increased intravascular volume, left ventricular filling pressure, cardiac output and a lower total peripheral and renal vascular resistance. Left ventricular adaptation will consist of eccentric hypertrophy in obesity regardless of the level of arterial pressure and concentric hypertrophy in lean hypertensive patients. Although obesity may mitigate the harmful effect of a chronically elevated total peripheral and renal vascular resistance and lessen target organ damage in essential hypertension, the combination of obesity and hypertension presents a double burden to the left ventricle and is associated with systolic and diastolic dysfunction and a propensity for high grade ventricular dysrhythmias. It is not surprising that congestive heart failure and sudden death are common sequelae of obesity hypertension. Weight reduction reduces arterial pressure by decreasing intravascular volume and cardiac output associated with a fall in sympathetic activity and reversal of cardiac hypertrophy. Therefore, weight loss unloads the heart from the two-fold burden caused by obesity and hypertension and should become a major goal in the prevention and treatment of heart disease.

Free radicals (and other toxic metabolites of oxygen) are generated in most cells as a consequence of normal metabolic processes, but cells are protected from injury by antioxidant mechanisms. Several forms of lung injury appear to result from generation of toxic metabolites of oxygen in quantities which exceed the antioxidant capacity of lung cells. Several manipulations which prevent free radical production or accumulation or enhance antioxidant capacity of lung tissue may prove to be useful therapeutically in acute and chronic diseases of the lungs.

Nonsurgical combined approaches of non-small cell lung cancer represent a concept that has only been investigated so far with chemotherapy and radiation therapy. Thoracic irradiation of locoregional disease is associated with a high rate of local control and a 5-10% long-term (5-year) survival; however, distant metastases remain the main cause of failure. This observation suggests that the tumor is often microscopically disseminated at the time of diagnosis. Systemic therapy therefore must be associated to radiation therapy to try to control both the undetectable metastases and the local disease. However, the results reported so far have been disappointing, probably because of the modest activity of the available chemotherapy. Further progress with the combined approach requires new developments in the chemotherapy of non-small cell lung cancer, particularly the introduction of new active drugs.