Опыт исследования палеопатологии позвоночника с помощью компьютерной томографии и рентгенографии

In this paper, an interesting case of spinal pathology is considered. In 2015, under the supervision of V.V. Cherevko, archaeological excavations were carried out on the territory of a cemetery near the village of Vaskovi-chi, Glubokoye district, Vitebsk region (Republic of Belarus). In the course of the archaeological excavations, two burials were discovered, which date back to the end of the 19th century. The remains from the burial 2 belonged to a relatively young male, lying on his back with his hands stretched down and the spine unnaturally curved in the lumbar region. To diagnose the pathological change, computer tomography and radiography of the spine of the man, who lived about 150 years ago in the countryside of Belarus, were applied. The scanning of the object under study was carried out at the Resource Center for Nuclear Physics Research Methods using X-rays on a 40-slice PET-CT tomograph. Radiography was carried out at the Research Institute of Medical Primatology. The most likely cause of this pathology was tuberculous spondylosis — unstable compression fractures of the bodies of the ninth through to the twelfth thoracic vertebrae and fusion of the resulting bone mass with the body of the first lumbar vertebra. As a result, a kyphotic bone conglomerate was formed in the area of transition of the tho-racic to the lumbar spine. There was osteomalacia of the bodies of the corresponding thoracic vertebrae. The torso became bent. When the person was standing, his head should have been at the level of his pelvis. It is hard to imagine how this person could move around, care for himself, and have a normal life. The disease proceeded, most likely, without serious neurological disorder. The fact of the chronic course of the deformity indirectly testifies in favor of the latter, and, accordingly, for the gradual progression of the deformity it is necessary that the spine was in an upright position, that is that the person could walk a little, at least sit, not being bed-ridden or paralyzed

Metabolic changes in rat brain histaminergic neurons during subhepatic cholestasis

brain, histaminergic neurons, histochemistry, subhepatic cholestasis.The aim of the present work was to assess metabolic changes in histaminergic neurons in the rat brain during subhepatic cholestasis. Studies were performed on male Wistar rats using quantitative histochemical methods. The results showed that in cholestasis, histaminergic neurons in the rat hypothalamus developed significant changes in succinate dehydrogenase, lactate dehydrogenase, and glucose-6-phosphate dehydrogenase activity, in NADH and NADPH, and in acid phosphatase and monoamine oxidase B. These changes depended on the duration of cholestasis and had a dynamic, wave-like nature. The changes were apparent after five days of cholestasis, reached a maximum at 10-20 days, decreased at 45 days, and completely disappeared at 90 days

Structural-metabolic changes in histaminergic neurons of the rat hypothalamus in conditions of loss of bile

brain, histaminergic neurons, morphometry, histochemistry, bile.The aim of the present work was to evaluate structural and metabolic changes in histaminergic neurons in hypothalamic nucleus E2 in rats in conditions of complete external drainage of bile. Studies were performed on male Wistar rats (n = 45). Controls consisted of animals subjected to sham surgery with preservation of physiological bile flow throughout the experiment. Quantitative histological and histochemical methods were used. Serial frontal cryostat sections cut from the posterior hypothalamus were used for detection of the activity of the following enzymes: monoamine oxidase B, succinate dehydrogenase. NADH dehydrogenase, NADPH dehydrogenase, glucose-6-phosphate dehydrogenase, lactate dehydrogenase, and acid phosphatase. Morphological studies of histaminergic neurons were performed on preparations stained with thionine. These studies showed that complete external drainage of bile led to transient size reductions and rounding of cell perikarya. Metabolic changes were seen within a day of bile loss and subsequently progressed. All energy metabolic pathways were suppressed and acid phosphatase activity was increased on day 5

Basic therapy efficacy in children with pulmonary hypertension related to congenital heart defects: place of endothelial dysfunction and systemic inflammation markers

Aim. To evaluate efficacy of the specific therapy by results of 4-year observation of patients with pulmonary arterial hypertension associated with congenital heart defects (PH-CHD)Material and methods. The evaluation is provided, of endotheliumcondition dynamics during one year (baseline, in 6 and 12 months) by the level of endothelium dysfunction markers, cells reparation and proinflammatory factor — interleukin-1. Dynamics of clinical status of patients and of the condition of the right heart chambers by echocardiography with Doppler study, was monitored during 4 years.Results. In severe PH patients under bosentan complex therapy the clinical improvement was marked as exercise tolerance improvement, decreased rate of pulmonary crises and decreased functional class of the disease, tendency to increase life duration. In bosentan group, there was 10-time reduction of vascular endothelial growth factor level, double decrease of sPECAM-1 and by 70% — of proinflammatory cytokine interleukin-1. In moderate and severe PH without bosentan therapy there was statistically significant increase of sPECAM-1, increase of vascular endothelial growth factor by 5 and 2 times, respectively, and progression of the disease.Conclusion. For infants with PH-CHD, complex bosentan therapy makes it for clear clinical improvement related to antiproliferative and antiaggregant effects, which are mediated by non-selective inhibition of endothelin-1 receptors. Absence of PH-specific therapy determines the progression of disease, irrelevant to functional class

Diagnostics of myocardial damage in premature newborns with transient heart disease in the early neonatal period

Purpose. To assess frequency and severity of myocardial damage in premature infants with transient myocardial ischemia in the early neonatal period.Materials and methods. The study includes 73 newborns of a gestational age of 31–36 weeks with respiratory failure and oxygen dependence in the first 2 hours of life. Newborns are divided into groups: Group 1: classic electrocardiographic criteria of transient myocardial ischemia and an increase in the level of troponin I in the blood; Group 2: electrocardiographic criteria for transient myocardial ischemia and a normal level of troponin I; Group 3: no ECG changes and normal troponin I level. We assessed blood gases, conducted electrocardiography, determined troponin I in the blood on the 1st and 7th day of life, assesses duration of oxygen therapy in all the children.Results. Group I: troponin I concentration on the 7th day of life – 0.415 [0.222; 0.639] ng/ml, Group II – 0.073 [0.051; 0.104] ng/ml and Group III – 0.017 [0.006; 0.051] ng/ml. Transient myocardial ischemia was detected in 41% of examined patients, and destructive myocardial changes – in 21.9%. An analysis of the gas composition of blood in the first 2 hours demonstrated that there was a significant predominance of the level of bases in the children of Group I. The duration of artificial ventilation in children of Group I was 56 [3; 96] hours, exceeding the indicators of children of Group II (9 [8; 11]) by 5 times, and Group III (20.5 [13; 72]) – by 2.5 times. Also newborns in Group I experienced a maximum need for oxygen therapy through a mask.Conclusion. 21.9% of premature infants experience destructive myocardial changes against the background of transient myocardial ischemia; newborns with transient myocardial ischemia and destructive changes have a significantly more pronounced metabolic acidosis in the first hours of life and a longer need for oxygen therapy

Right chambers of the heart in children with pulmonary circulation hypervolemia

The ultrasound and angiographic parameters of the right chambers of the heart were analyzed in children with pulmonary arterial hypertension (PAH) associated with congenital heart defects. The investigation was conducted in relation to the functional class (degree) of PAH. Right cardiac remodeling was found to depend to a greater extent on afterload (pulmonary artery systolic pressure and pulmonary vascular resistance); moreover, diastolic dysfunction developed just in moderate (Functional Class II) PAH. It was ascertained that there was a prompter development of PAH with myocardial systolic and diastolic dysfunction in the presence of congenital malformations with arterial hypoxemia