[Melatonin as a marker of the grade of cardiac disorders during cachexia development in oncological patients of different ages].

We have examined 103 patients at the age from 28 to 78 with the newly diagnosed oncological disease at stages II-IV before the beginning of anticancer treatment. The identification of the signs of the cachexia syndrome and its stage (pre-cachexia, cachexia) were carried out in the accordance with the CASCO criteria (2011) and taking into the account the age of the patients. The cardiovascular infringements were found to be comorbid to the oncological disease significantly more often in patients with signs of cachexia syndrome on the pre-cachexia stage and the total index of cardiovascular disorders in oncological patients increases with the severity of cachexia. In the course of the cachexia symptoms development the significant decline of melatonin excretion level (evaluated by the excretion of its main metabolite 6-sulfatoximelatonin level - aMT6s) in oncological patients was noted. The lowest changes in aMT6s levels were observed in patients older than 60 years, referred to the group of pre-cachexia, which may indicate the heterogeneity of the investigated groups as a result of the combination of manifestations of geriatric syndromes and cancer pathology. The possibility of false-positive diagnosis of pre-cachexia due to a combination of polygenic metabolic and age-related changes in elderly patients should be taken into account. Therefore, evaluation of melatonin excretion can be recommended as an additional marker in diagnosis and differential diagnosis of cachexia syndrome particularly in geriatric patients. A significant correlation between the occurrence and/or worsening of cardiac disease in cancer patients, cachexia symptoms and reduced level of aMT6s were revealed.

[Cachexia syndrome: The present state of the problem and importance in clinical practice]. / Sindrom kakheksii: sovremennoe sostoianie problemy i znachenie v klinicheskoi praktike.

Available updates have changed our idea about cachexia as a terminal condition, which could consider it as a combined metabolic syndrome that gives rise to the worse course of the underlying disease, the lower efficiency of specific therapy, and higher death rates. Chronic inflammatory factors are recognized to be the main mechanisms for the development of cachexia syndrome (CS). In addition, diagnostic criteria for this pathological condition are well defined. These criteria are rather simple for use in clinical practice and they should be assessed by physicians at all stages of a follow-up of patients with severe chronic diseases, since cachexia may develop long before the appearance of the so-called extreme emaciation. The earlier the physician will anticipate the onset of CS, the more successful attempts to correct the latter and accordingly the better prognosis of the underlying disease will be. Available updates on the possibilities of correcting cachexia - anorexia are considered although there are no established standards for the management and treatment of patients with CS now. The elaboration of a step-by-step algorithm for following up the patients and a search for medications with proven clinical efficacy are relevant.

[CACHEXIA AS A COMPLEX METABOLIC SYNDROME AND OTHER CAUSES OF WEIGHT LOSS IN ELDERLY].

With a growing number of the elderly population, it is important to remember about the potential pathologic conditions, one of the main features of which is the weight loss (cachexia, anorexia, sarcopenia, hypermetabolism/hypercatabolism syndrome and etc.). These processes are interrelated and interdependent, especially in old age, and even modern medical literature does not clearly indicate the boundaries between this syndromes and pathological conditions. For instance, cachexia is a complex metabolic syndrome, resulting in the loss of muscle, but not always fat mass, arises in connection with the development of severe chronic systemic inflammation, which is especially inherent in the elderly, often accompanied by anorexia, and may also be part of another "old age syndrome"--sarcopenia. Sarcopenia is an age-related atrophic degenerative change in skeletal muscle, which occurs as a result of a long process with a very complex mechanism and is characterized by progressive and generalized decrease in muscle mass, its strength and by a risk of developing complications such as disturbance of mobility. Meanwhile, the earlier a physician suspects the onset of cachexia syndrome and/or other conditions involving abnormal weight loss, the more effective are going to be attempts to correct them with possible agents, which help to improve the prognosis and prolong life of the patient.

Structural aberrations of the X chromosome in man.

Among 209 patients with Shereshevsky-Turner syndrome, 69 women with structural aberrations of X chromosome were detected: 46,X,i(Xq) - 11; 45,X/46,X,i(Xq) - 24; 45,X/46,X,r(X) - 14; 45,X/46,X,f(X or Y) - 10; 45,X/46,X,del(Xq) - 4; 45,X/46,X,del(Xp) - 2; 45,X/46,X,idic(X) - 2; 46,X,idic(X) - 1; and 46,X,t(X,2) - 1. All the patients with structural abnormalities of X chromosome were short in stature, but in no group was it as low on the average as in 45,X cases. Somatic signs were noticed in all structural changes of X, but they were less frequent and less pronounced. In some patients with r(X) and i(Xq), spontaneous menstrual bleeding and breast development was found. The structurally abnormal X chromosome appears to be functionally inactive, the phenotype of patients with structural rearrangements being close to the phenotype of patients with X monosomy. At the same time, the abnormal X might have certain effects in early embryogenesis which mitigated the further development of the Shereshevsky-Turner syndrome.

[Human isodicentric X-chromosomes]. / Izoditsentricheskie X-khromosomy u cheloveka.

The large submetacentric abnormal late replicating X-chromosomes were found in three patients under karyological studies of 168 patients with Turner's syndrome. G- and C-banding revealed that abnormal chromosomes are three variants of isodicentric chromosomes resulting from the junction of the short arms of two X-chromosomes. The patients' karyotypes are respectively: 45,X/46,X,dic (X)(qter leads to p22: :p22 leads to qter); 46X,dic(X)(qter leads to p21: :p21 leads to qter); 46,X/46,X,dic(X)(qter leads to p11: :p11 leads to qter). All the three patients had different size deficiencies of the short arm of the X-chromosome. Partial X-monosomy caused the appearance of features of the Turner syndrome, which was less expressed in our patients compared to those with the entire X-monosomy.

[Double autosomal aberration: trisomy 21 and familial reciprocal translocation t(10;12)(p14;q21)]. / Dvoinaia autosomnaia aberratsiia: trisomiia 21 i semeinaia retsiproknaia translokatsiia t(10;12)(p14;q21).

A child with the Down syndrome revealed besides a regular trisomy 21, an enlargment of the short arm of chromosome 10, and the deletion of the long arm of chromosome 12. The proband's mother, who was phenothypically normal woman, appeared to be a carrier of the reciprocal translocation, her karyotype being: 46, XX, rep (10;12) (10qter leads to leads to 10p14; 12q21 leads to 12qter; 12pter leads to 12q21 : 10p14 leads to 10pter). Hence, the proband had double chromosomal aberration 47, XX, +21, rcp (10; 12) (10qter leads to 10p14 : 12q21 leads to leads to 12qter; 12pter leads to 12q21 : 10p14 leads to 10pter) mat. There is no reason to relate hard manifistation of the Down syndrome with the detected translocation. The influence of the mathernal non-devision in the meiosis and the rise of the trisomy 21 is discussed. In the following pregnancies it is advisable to amniocentesis.

[Familial X-autosomal translocation t (X, 2)]. / Semeinaia X-autosomnaia translokatsiia t (X, 2)

A loss of part of the short arm of the X-chromosome and a partial trisomy of chromosome 2 were detected in a girl with the Shereshevsky--Turner syndrome; her karyotype was 46, Xt (X,2) (Xqter leads to Xp11 : : 2q36 leads to 2q ter). The patient's mother had a balanced X-autosomal translocation 46, X,t, (X,2) (Xq ter leads to Xp11 : : 2q36 leads to 2q ter; 2p ter leads to 2q36 : : Xp11 leads to Xp ter). The daughter's abnormal X-chromosome was a late labelling one, while her mother had the late label in the normal X-chromosome.

[Identification of several chromosome aberrations in man by the fluorescent method using quinacrine yprite]. / Identifikatsiia nekotorykh khromosomnykh perestroek u cheloveka fluorestensentnym metodom s ispol'zovaniem akrikhi-iprita

The applications of the fluorescent staining of chromosomes with quinacrine mustard allowed to identify a dicentric Y-chromosome in two patients with defected external gynaetalies: a boy of 15 years old and a girl of 2 years old. Both the patients had mosaicism of sex chromosomes: 45, x/46, x dic (Y). The dicentric Y-chromosome, resembling chromosome, 16, had bright luminescence of the thelomeric regions characteristic of the normal Y-chromosome. Besides, a balanced autosomic translocation t (1, 14) (q 31, q 3) was found in the girl identified also with quinacrine mustard fluorescent staining.