Background and objectives: Diabetes is a complex metabolic disorder affecting the glucose status of the human body. Immune system activation is highly related to type 2 diabetes incidence, progression, adaptive and innate immunity is involved in the inflammation. Vitamin D insufficiency causes insulin resistance as well as glucose intolerance, which are symptoms of significant vitamin D deficiency. Increased inflammatory biomarkers and insulin resistance are prominent symptoms of this illness. Materials and methods: Serum specimens were taken from 120 people, with 70 patients (35 males and 35 females) with type 2 diabetic individuals and 50 healthy controls (25 males and 25 females) divided into two groups. Patients in the study population ranged from (18-50) years old and were hospitalized at Ballad and Salah Aldeen General Hospitals in Salah Aldeen province from August 2019 to February 2020. Results: Vitamin D levels were considerably reduced in females and male diabetic patients compared to controls, while leptin levels were elevated with ALP levels that were slightly diminished in diabetic males compared to controls but higher in diabetic females. Both C-reactive protein and serum uric acid levels were significantly higher in male and female diabetic patients compared to controls. In addition, these were increased in male diabetic individuals when compared to female diabetic individuals. Conclusion: In type 2 diabetes individuals, severe vitamin D deficiency and increased leptin cause inflammation and complicate bone metabolic illness.

Vascular tone is generally controlled by both the humoral component and the neuro-vegetative component. Regarding the second one, catecholaminergic sympathetic innervation of blood vessels is almost a rule in the body[1,2].
It is known that the iris is sympathetically inner-vated, both at the level of the iris dilator muscle[1,2] and at the level of iris blood vessels[3]. Cathecolamines are responsible for vasoconstriction and, in some vascular beds, vasodilation. [...]

Histamine and serotonin (5-hydroxytryptamine) are two amino acid derivatives with important biological functions [1]. Histamine, an endogenous monoamine, is synthesized from the histidine and is stored in most tissues and degraded in liver by histaminase. The most important roles of histamine are: mediation of type I allergic reactions, stimulation of stomach secretion of hydrochloric acid and pepsin (as autacoid), and functioning as a neurotransmitter (especially in the central nervous system)[2]. Regarding the vascular effects of histamine in non-ocular territories, there have not been many published literature reviews, for example, there are data reviewed for pulmonary artery[3], brain territory[4], but these data are not recent.

Current knowledge based on large randomized con-trolled trials documented so far that early protein intake from milk products, in the first six months of life, is associated with various changes in later outcomes regarding body weight or body composition [1,2]. Beyond the exclusive milk nutrition period, complementary fe-eding practices are less investigated in terms of obesity appearance [3]. Macronutrients supply in early life, such as carbohydrates and fats, do not seem to be implicated in later childhood obesity [4], whereas protein supply is much more studied in the present [5]. Due to rapid weight gain and body size evolution in first 3 years of life, nutritional requirements are high, but exceeding some normal ranges leads to future disturbances. [...]

Environmental lead sources are represented by air, soil, food, water. Lead distribution in the environment continues to be a worrying public health issue considering its potential cumulative effects in the body due to various routes of exposure. Once exposed to lead, individuals have persistent elevated blood levels because of redistribution from bones sanctuaries, even years after cessation of exposure. Oxidative stress seems to play an important part regarding lead adverse effects, because the metal is responsible for reactive oxygen species (ROS) production and it also might inhibit antioxidants levels [...]

Lupus erythematosus is an autoimmune disease with multiple symptoms and each patient presents a particular clinical and immunological-biological profile. The cause of the disease remains unknown. Lupus erythematosus embraces three clinical forms: chronic, subacute and systemic. Events in the three clinical forms range from skin involvement (chronic form) to serious systemic implications, affecting patient's health and life (as a systemic disease).
The systemic form - systemic lupus erythematosus - has a wide range of immunological abnormalities that cause inflammation in various organs and systems. The inflammation occurs as a result of excessive production of autoantibodies, that are directed against self structures that are no longer recognized. In systemic lupus, cutaneous manifestations are often accompanied by renal, cardiac, osteoarticular, neuropsychiatric disorders.

Prostatic pathology represents one of the most common causes of dermato-urological addressability, because of the varied age interval, but also because of the symptoms that decrease rapidly and visibly the patients’ quality of life. Benign prostatic hypertrophy (BPH) is represented by increased volume of the prostate, which generates an obstructive and irritative symptomathology in the pelvic urinary tract. The hormonal influence presents a certain contribution in the development and evolution of BPH, by the imbalance occurred between androgens and estrogens, revealed by the significant decrease of the ratio androgens/estrogens hormones and by the inflammatory factors (1,2,3,4).