Type 2 diabetes represents a progressive disease, primarily characterised by impairment of glycoregulation, despite the application of various therapy modalities. The main problem with type 2 diabetes, is progressive impairment of betacell functioning, and impairment of insulin resistance. There is an ongoing pursuit after adequate therapy modalities aiming at preservation of beta-cell function followed by loss of weight and assurance of good glycoregulation. For mentioned reasons, research has been done recently on the functioning of enteropancreatic axis in type 2 diabetes. It has been noted that oral intake of food or glucose leads to higher increase in secretion of insulin in comparison to the intake of the same quantity of glucose intravenously, resulting in assumption that hormone signals from endocrine cells of intestine released by the intake of food represent potent stimulators of insulin secretion. Such role is played by GLP-1 and GIP, GIT peptide hormons which stimulate secretion of insulin and release themselves into blood when stomach himus penetrates into duodenum, that is before glucose from himus is absorbed into internal body media. Persons with type 2 diabetes have got low level of secreted GLP-1 after meal. Chronic administration of GLP-1 agonists leads to reducing glycemia and HbA1c. The potential of GLP-1 agonists to decelerate progressive decay of beta-cells at diabetics is alluring, but insufficiently documented. DPP-IV inhibitors represent complementary approach for provoking incretin effects, by oral intake of pills.

Alkaptonuria is one of 4 disorders originally defined as an inborn error of metabolism. The hallmark of the disease is passage of urine that becomes black when left standing. There is a familial pattern of inheritance. The defect lies in the catabolic pathway of tyrosine. The product, homogentisic acid, in deficiency of the hepatic enzyme homogentisate 1,2- dioxygenase (HGO) accumulates in the blood, but is rapidly cleared in the kidney and excreted. Upon contact with air, homogentisic acid is oxidized to form a pigmentlike polymeric material responsible for the black color of standing urine. Although homogentisic acid blood levels are kept very low through rapid kidney clearance, over time homogentisic acid is deposited in cartilage throughout the body and is converted to the pigmentlike polymer through an enzyme-mediated reaction that occurs chiefly in collagenous tissues. As the polymer accumulates within cartilage, a process that takes many years, the normally transparent tissues become slate blue, an effect ordinarily not seen until adulthood. The earliest sign of the disorder is the tendency for diapers to stain black.. but in most cases desease is hardly diagnosed before the fourth decade of life, external signs of pigment deposition, called ochronosis, begin to appear. The slate blue, gray, or black discoloration of sclerae and ear cartilage is indicative of widespread staining of the body tissues, particularly cartilage. The hips, knees, and intervertebral joints are affected most commonly and show clinical symptoms resembling rheumatoid arthritis. Because of calcifications that occur in these sites, however, the radiologic picture is more consistent with osteoarthritis.

Beside great improvement in diagnostical ant therapeutic aproach in curement of brain tumors, gliomas still have
bad prognosis. Better results could be obtained only in early tumor discavery. Alpha pheto protein (AFP) and carcinoembrionic antigen (CEA) are markers specific for certain carcinomas (hepatocelular, nonseminated testicular, colorectal). Thieir specifity for gliomas still has not been stated. The aim of tis study was to determine tissue or sera levels of AFP, and CEAin experimentaly induced gliomas, and teir poential use in human gliomas diagnosis. For analyses , tissue supernatant homogenate C6 of rat glioma and sera were used during different phases of development (days 0,7,14,21 and 31). Tumor markers were also determened as well as in tissue of human brain tumors (two anaplastic astrocitomas an one glioblastoma). Techique applied was immunoenzyme type Mein method. Obtained results showed no signs of AFPeither in sera, or in rat brain tissue or human glioma tissue. CEA however, showed statisticlly, important specifity, for glioma tissue. During tumorgenesis tissue concentracion of CEA showed statisticly higher levels in comparasion with controls , starting from day 7, reachin peak of tumorgenesis on day 21, (p < 0.001). CEAwas not detectable in control animal group sera, and also during the period of tumor development. CEA concentracion obtained from animal brain were similar to those in human
brain tissue tumors. Further investigation need to be caried out, in order to determine the potential role of this marker in
diagnosis and treatment establishment course.

Specific immunotherapy (SIT) has been used for almost a century but its form of administration is still a matter of
debate. At present curative SIThas only demonstrated its efficiancy, under the conditions that an appropriate allergen extract
is used, and patients are careffuly selected. However, many alergic patients likely to respond to immunotherapy are not
treated specificaly, due to the prevaling opinion that immunotherapy is ineffective, and has more uneffectable side effects
than drug treatment. Direct comparison of efficiancy between immunotherapy and drugs is problematic as this implies a
comparison between a treatment aiming at interfering with the pathophysiological mechanisms of the alergic inflammation
with potential for long term effect, or even cure (immunotherapy), and a treatment abolishing symptoms whi-le being
administered, but without long term preventive capacity (drugs). In most patients the situation is not an either but ra-ther
both and. The advantages of combinig immunotherapy and drugs are related to a higher likelihood of increasing effi-ciancy,
reducing side effects, and improving patient compliance by combining a treatment having an immediate effect with one
functioning more slowly