Three regulating systems, nervous, endocrine, and immune, are involved in the maintenance of homeostasis. The interactions between the nervous and endocrine systems are well studied and give rise to the development of an independent science — neuroendocrinology. The interactions between the neuroendocrine and immune systems are intensively studied and regarded as the most promising trend of research. Numerous data available up to date permit a new outlook at the bilateral exchange of signals in the interacting systems. The present review analyzes the information shedding light on the formation of a new integrative science in biology: neuroimmunoendocrinology. Special attention is paid to the regularities underling the integration of each system in the universal operating system. Recent information on the mechanisms of interaction between the neuroendocrine and immune systems is discussed from the same viewpoint.

Insulin-binding activity (IBA) of the peripheral blood mononuclears and T-lymphocytes was studied in children with type I diabetes mellitus of different duration and with a different degree of compensation. An increase of the m,ononuclear IBA was observed during the compensation phase in patients with initial diabetes and a reduction of receptor binding of insulin by mononuclears in those with a lingering disease. Changes in the IBA of T- lymphocytes and mononuclears were similar in initial diabetes and opposite in a lingering disease: an increase of mononuclear IBA and an appreciable decrease of T-cell IBA during decompensation and a decrease of mononuclear IBA andf a drop of hormone binding by T-cells during compensation. In initial diabetes the IBA of mononuclears was the lowest in children with ketoacidotic coma and ketoacidosis and in a protracted course of the disease without ketosis they were the lowest in patients in need of intensive insulin therapy with increased doses of the hormone. These data on the status of lymphocyte receptors in diabetics with type 1 disease will be useful for aessesing the disease severity and for developing differentiated approaches to adequate insulin therapy.

The efficacy of iodine prophylaxis in a large industrial city has been assessed. Screening of 4993 subjects revealed shifts in 31.6%. An appreciable share of the detected abnormalities were the initial (first or second) stages of diffuse and nodular goiter, which was to a certain measure due to improvement of the diagnostic methods. Assessment of iodine clearance with the urine in 205 subjects revealed iodine deficiency in 82.9%. The conditions for an outbreak of endemic goiter persist because of poor iodine prophylaxis. Testing of samples of "iodinated" salt revealed a low content of potassium iodide in virtually all the samples. The principal causes of a high incidence of goiter in the population is iodine deficiency combined with an increasing aggression of anthropogenic technogenic factors

In order to assess how lack of estrogens may influence the regulation of growth hormone (GH) secretion, we studied GH response to intravenous GHRH(1-29)NH2 in a dose of 1 mg/kg and standard oral clonidine and L-DOPA stimulation in 25 girls with Turner's syndrome (TS) aged 4 to 14. None of the patients had signs of spontaneous puberty or were administered any growth-promoting treatment before testing. Since gonadotrophin elevation is commonly observed in girls with TS at the age of 9 years, the patients were divided into 2 groups: those aged 4 to 9 (n=9, group A) and 9 to 14 (n=16, group B). Maximum GH level following clonidine stimulation was appreciably decreased in older girls (p<0.01). GHD (max level after standard provocation test no more than 7 ng/ml) was confirmed only in group В (67%). The peak GH responses to L-DOPA and GHRH did not vary much within groups A and В (mean ± SEM 12.9 ± 4.7 versus 8.5 ± 2.3 and 34.2 ± 8.0 versus 33.0 ± 9.7 ng/ml, respectively). In both groups, the weighed average for GH levels (AUC divided by time) after GHRH stimulation was higher than after L-DOPA, although the difference was less significant in group A (18.8 ± 2.6 versus 6.4 ± 2.6 ng/ml, p=0.17) than in group В (13.1 ± 5.1 versus 2.5 ± 0.6 ng/ml, p<0.05). To evaluate the effect of estrogen therapy on the GH axis, all girls in group В were tested again after 6 months of oral dihydrostilbestrol in a daily dose of 1.0 mg. Estrogen therapy resulted in an appreciable boosting of GH response to L-DOPA (GH AUC over 120 min, 1425.2 ± 444.6 versus 316.4 ± 77.3 ng/ml • min, p=0.03), but did not influence the response to GHRH (GH AUC over 90 min, 1219.8 ± 259.9 versus 1375.7 ± 636.6 ng/ml • min, p=0.5). Our results indicate that somatotroph response to exogenous GHRH stimulation in TS is not age-dependent. Replacement of estrogen did not influence GH secretion induced by GHRH but appreciably improved the response of GH to L-DOPA in older patients. Hence, we may conclude that pubertal-aged girls with TS may develop hypothalamic GH insufficiency of a certain degree due to primary ovarian failure.

The secretion of bioactive (LH_b) and immunoreactive (LHj) in response to gonadotropic hormone releasing factor (GHRF) was assessed in 8 women with pituitary macroadenoma (gonadotropinoma) and 6 patients with pituitary microadenoma combined with the polycystic ovaries syndrome. GHRF more intensively stimulated the secretion of LH_b in patients with macroadenoma than that of LHj. If the level of estrogens in the blood increases, the secretion of LH_b decreases in comparison with the production of LHi. In patients with pituitary microadenoma combined with the polycystic ovaries syndrome GHRF stimulated the secretion of LHj more intensively than that of LH_b.

The relationship between fat distribution and arterial pressure (AP) in women of a reproductive age revealed that AP was reliably higher in women with the abdominal distribution of fat than in the control and directly correlated with the waist circumference and the waist/hips ratio. It is noteworthy that the waist and waist/hips ratio are prognostically significant and simple factors for assessing the possible level of AP in obese women. The level of IRI and the IRI/glucose ratio in this population are also reliably higher than in the control, and directly correlate with the waist/hips ratio. The authors hypothesize that hyperinsulinism and insulin resistance, observed in cases with the abdominal distribution of fat, contribute to the pathogenesis of hypertension in obesity. Hence, abdominal distribution of fat is a factor promoting an increase of AP in obesity. We believe that timely treatment of obesity followed by maintenance of body weight within the norm is a method of preventing and treating hypertension in women of a reproductive age with the abdominal accumulation of fat.

Since 1940, radioactive iodine therapy has become the most common treatment for thyrotoxicosis in adults in the United States. In Europe, a similar trend is observed, although thyreostatic drugs are more often used as the main treatment method. In many ways, radioactive iodine is an ideal treatment for thyrotoxicosis; the economic efficiency and safety of the method are well known.

This lecture is an extended commentary on the document published above, “Prospects for the treatment of thyrotoxicosis 13 * 1 by 2000,” prepared by a group of experts of the European Thyroid Association (ETA) and published in 1995.

This document, briefly referred to as the report below, has been approved by the ETA Assembly and agreed with the views of its members.

By the end of the 1st decade after the Chernobyl accident, an increase in the incidence of thyroid cancer in the affected population of Russia was recorded [3], including in children [1]. The oncological alertness of doctors to any nodular formations of this organ has reasonably increased. Special observation is required by those who incorporated radioactive iodine in utero and in the first 3 years of life, when the radiosensitivity of thyroid tissue is maximum [2]. Nevertheless, voluminous thyroid formations after exposure to ionizing radiation, like non-irradiated ones, can be non-tumorous in nature, moreover, proceed not from thyroid tissue and simulate nodular goiter.

Experimental studies of the regenerative processes in the resected thyroid were carried out 30 days after the operation in 30 albino rats with different volumes of tissue left. Qualitative methods were used: organometry and histometry. After moderate (40-65%) resection the regenerate was characterized by the development of quantitative signs of increased functional activity and by sufficiently high compensatory potential. More radical resection was associated with the development of structural signs of functional overstrain of the regenerating portion of the thyroid, manifesting by an increase in the content of thyrocytes, disappearance of colloid, and development of perivascular edema and dystrophy of an appreciable portion of epitheliocytes.

The authors present the findings confirming the contribution of uric acid (UA) to the etiology and pathogenesis of diabetes mellitus. Experiments were carried out on 90 albino rats. It has been shown on the models of prediabetes and latent and mani- fest diabetes mellitus that hyperuricaemia (HU) is not only a sign, characterizing the severity of carbohydrate disorders, but a factor promoting the progress of these shifts as well. The diabetogenic effect of HU is the more significant, the more manifest are the background carbohydrate disorders. Preinjection of UA to animals markedly potentiated the diabetogenic effect of alloxane.

GC rats bred from Wistar stock for genetic predisposition to cataleptic reaction are characterized by a slightly lower blood testosterone level than the control Wistar rats. This difference becomes significant after immobilization stress when the level of testosterone increases by 14% in GC and by 61% in Wistar rats (p<0.05). Stress brought about a 68% increase in DOC production by the adrenal tissue in Wistar but caused no changes in GS animals. Stress-induced decrease in aldosterone production was greater in GC and resulted in a significant difference between the two strains (0.77 ± 0.09 and 0.46 ± 0.06 mg/100 mg tissue, p<0.05). The detected endocrine characteristics of GC rats resemble the picture of chronic stress and are similar to those known about male schizophrenics.

To date, a large number of original studies and review articles have appeared on the so-called metabolic syndrome, or Syndrome X, which includes obesity, arterial hypertension (AH), coronary heart disease (IHD), and non-insulin-dependent diabetes mellitus (NIDDM) [19, 62 , 69]. According to modern concepts, the factor of tissue sensitivity decrease to insulin takes part in the mechanisms of the development of this syndrome and related diseases [19, 26, 62], therefore it has another name - insulin resistance syndrome (IR) [19]. The idea of ​​the involvement of IR in the pathogenesis of the above diseases opens up additional opportunities for their prevention and treatment. However, a wide range of issues of principle remains unclear at present. In this regard, it seems interesting to us to analyze the current state of the problem, to highlight the mechanisms that bind IR and each of the syndrome-forming diseases, and to formulate issues that are essential for the development of pathogenetically substantiated schemes for the prevention and treatment of syndrome X.

Primary glycosylation undergoes not only albumin, but also other plasma proteins. Glycosylation of apolipoproteins, which are part of low density lipoproteins (LDL), leads to an increase in electrophoretic mobility and a slowdown in the degradation of the latter using fibroblasts, which can contribute to the development of atherosclerosis [51]. Glycosylated LDL are actively subjected to secondary oxidation, as a result of which they acquire atherogenic properties [32].

Significant changes were found in the exchange of very low density glycosylated lipoproteins [35]. The triglycerides contained in them are less likely to be cleaved by lipoprotein lipase. This is one of the factors in maintaining hypertriglyceridemia in diabetes.