[Mycosis of the maxillary sinus]. / Mikoz verkhnechelyustnoi pazukhi.

In the structure of morbidity and mortality has significantly increased the role of mycoses. The increase in their spread is due not only to the improvement of the quality of diagnosis, but also the emergence of new strains resistant to previously used antifungal drugs, a significant change in the immune status of the population. In addition to environmental factors, it is important to introduce modern methods of treatment that increase survival in the whole spectrum of diseases. This situation can't affect the structure of diseases of ENT organs: the number of mycoses has increased significantly in recent decades. The issues of diagnosis and treatment of mycoses of the paranasal sinuses continue to be an urgent problem of otorhinolaryngology. The reason for this is a number of difficulties associated with the diagnosis: the absence of specific symptoms of the disease, the possible secondary nature of the attachment of fungal infection against the background of bacterial lesions, transient carrier of infection, technical difficulties and errors in the study of biomaterial with insufficient standardization of microbiological methods. Our report is devoted to the clinical case of aspergillosis of the maxillary sinus and a review of the literature on this issue, which in our opinion can be very interesting to the medical community.

Investigation of Taurine Derivative Magnesium-Bis-(2-Aminoethanesulfonic)-Butadioateon Alleviation of Neurological Defects in Simulated Hemorrhagic Stroke in Rats.

Stroke or ischemia is caused by a blockage in a specific blood vessel that partially or completely reduces the blood flow to the brain. Nutritional factors such as antioxidants and healthy eating patterns are important variables in preventing stroke. Molecular composition properties such as molecular binding and screening can be used to evaluate the specific activity and morphological changes. The present study aimed to evaluate the effectiveness of pharmacological correction of the consequences of a hemorrhagic stroke in rats with a new derivative of taurine magnesium-bis-(2-aminoethanesulfonic)-butadioate. The animals (n=170) were divided into four groups as follows: 1) control group (n=20), 2) group 2 suffered a hemorrhagic stroke without pharmacological correction (n=50), 3) group 3 (n=50) underwent simulation of hemorrhagic stroke received Taurine at the dose of 50 mg/kg, 4) Group 4 underwent simulation of hemorrhagic stroke with correction of hemorrhagic stroke with magnesium-bis-(2-aminoethanesulfonic)-butadioate at the dose of 150 mg/kg (LKHT 3-17) (n=50). Hemorrhagic stroke was induced by transfusing autologous blood into the parietal lobe of the right hemisphere of the brain. Lethality, neurological status, locomotor, and exploratory behavior, as well as the morphological pattern of the brain damage, were assessed on the 1st, 3rd, and 7th days after the pathology simulation. Neurological deficit was determined in animals by the McGrow stroke index scale. The locomotor and exploratory behavior was evaluated using the Acti-track software and hardware complex. Two criteria were considered when assessing morphological changes in the brain: the average thickness of the cerebral cortex (in micrometers) and the number of neurons without degenerative changes. LKHT 3-17 (150 mg/kg) and taurine (50 mg/kg) reduced lethality by 1.7 and 1.36 times, respectively, on the 3rd day after stroke compared to that of the control (p<0.05). In parallel, a neurological deficit was effectively corrected LKHT 3-17 and taurine to 5.3±0.8 and 6.5±0.9, respectively, on the 1st day in contrast to the control of 8.1±0.7 points. The locomotor and exploratory behavior was significantly different on the 7th day and was accompanied by a significant increase in total activity under the influence of LKHT 3-17 to 491 conventional units (CU) compared to the control of 110 conventional units. On the 1st day, the thickness of the cortex was 1943.7±44.08 µm, and 1491.0±38.61 µm in the control and LKHT 3-17 groups, respectively. The number of neurons without neurodegenerative changes prevailed in LKHT 3-17 group (18.7±4.32), and the lowest number was observed in the group without pharmacological correction of the pathology (14.3±3.78). The taurine derivative magnesium-bis-(2-aminoethanesulfonic)-butadioate, which is a combination of the amino acid, magnesium ion, and succinic acid, decreases the neurological deficits, lethality, and enhances the locomotor and exploratory behavior in experimental hemorrhagic stroke in rats. The effect of the studied medication on the dynamics of molecular pathophysiological mechanisms occurring in the cell requires additional research.

Evaluation of the Neuroprotective Effect of Magnesium-Bis-(2-Aminoethanesulfonic)-Butanedioate in Simulated Ischemic Stroke in Rats.

Sudden loss of blood flow to an area of the brain causes ischemic stroke, which leads to the loss of nerve function in the brain. The brain tissue leads to the death of brain cells in less than a few minutes due to the lack of oxygen and nutrients. This study aimed to evaluate the effectiveness of pharmacological correction of the consequences of ischemic stroke with a new derivative of taurine magnesium-bis-(2-aminoethanesulfonic)-butanedioate under laboratory code LKHT 3-17 in rats. The ischemic stroke was simulated by electrocoagulation of the right middle cerebral artery. The assessment of lethality, neurological status, locomotor, exploratory behavior, and morphological pattern of the brain damage was carried out on the 1st, 3rd, and 7th day after the pathology simulation. Neurological deficit was determined by the McGrow stroke index scale. The locomotor and exploratory behavior was evaluated using the Acti-track software and hardware complex. When assessing the morphological changes in the brain, attention was paid to two criteria, including the average thickness of the brain cortex and the number of neurons without degenerative changes. The substances were administered 60 minutes before the start of surgery. The animals were divided into an intact group (n=20); ischemic stroke simulation group without pharmacological correction (n=50); a group with correction of the ischemic stroke with taurine at the dose of 50 mg/kg (n=50); and a group with correction of ischemic stroke with magnesium-bis-(2-aminoethanesulfonic)-butadioate (LKHT 3-17) at the dose of 150 mg/kg (n=50).LHT 3-17 (150 mg/kg) and taurine (50 mg/kg) reduced lethality by 1.55 and 1.47 times, respectively, on the 7th day after stroke, compared to the control group (P<0.05). In parallel, an effective correction of neurological deficit was found for LKHT 3-17 and taurine to 4.0±0.8 and 7.6±0.9, respectively, on the 3rd day in contrast to the control of 8.1±0.8 points. The locomotor and exploratory behavior was most significantly different on the 1st and 7th days and was accompanied by a significant increase in the speed of movement under the influence of LKHT3-17 to 20 and 20 conventional units, compared to the control of 7 and 5 cu. On the 1st day, the thickness of the cortex was 1877.3±43.3 µm in the control group, and 1531.8±39.1 µm in the LKHT 3-17 group. The number of neurons without neurodegenerative changes prevailed in the group administered with LHT 3-17 (19.3±4.3), and the lowest number was observed in the group without pharmacological correction of the pathology (14.3±3.7).LKHT 3-17 at a dose of 150 mg/kg is more effective than taurine 50 mg/kg in protecting nerve activity in experimental ischemic stroke and reducing lethality, minimizing nerve defects, reducing volume, accelerating the process of tissue repair, helping stroke, and activating the regenerative processes.