101 research outputs found
Π‘ΠΎΠ²Π΅ΡΡΠ΅Π½ΡΡΠ²ΠΎΠ²Π°Π½ΠΈΠ΅ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ² Π»Π΅ΡΠ΅Π½ΠΈΡ ΡΠΏΠΎΠ½ΡΠ°Π½Π½ΠΎΠ³ΠΎ ΠΏΠ½Π΅Π²ΠΌΠΎΡΠΎΡΠ°ΠΊΡΠ° Ρ ΠΏΠΎΠΌΠΎΡΡΡ Π²ΠΈΠ΄Π΅ΠΎΡΠΎΡΠ°ΠΊΠΎΡΠΊΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΡ ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΉ
Videothoracoscopic operations are more effective than standard open surgery. The number of recurrences of spontaneous pneumothorax after videothoracoscopic operations were 3.6%, and after open surgery β 2.6%. Method of choice for surgical treatment of spontaneous pneumothorax is videothoracoscopic operations. Videoassisted operations are more efficient and allow to perform low-impact operations using multiple-cross-linking domestic vehicles apparatuses.Π ΡΡΠ°ΡΡΠ΅ ΠΎΠ±ΠΎΠ±ΡΠ΅Π½ 15-Π»Π΅ΡΠ½ΠΈΠΉ ΠΎΠΏΡΡ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΡ Π²ΠΈΠ΄Π΅ΠΎΡΠΎΡΠ°ΠΊΠΎΡΠΊΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΉ ΠΏΡΠΈ Π»Π΅ΡΠ΅Π½ΠΈΠΈ 616 Π±ΠΎΠ»ΡΠ½ΡΡ
ΡΠΎ ΡΠΏΠΎΠ½ΡΠ°Π½Π½ΡΠΌ ΠΏΠ½Π΅Π²ΠΌΠΎΡΠΎΡΠ°ΠΊΡΠΎΠΌ. ΠΠΏΠΈΡΠ°Π½Ρ ΠΌΠ΅ΡΠΎΠ΄ΠΈΠΊΠΈ ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
Π²ΠΈΠ΄Π΅ΠΎΡΠΎΡΠ°ΠΊΠΎΡΠΊΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΉ Π² Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ ΠΎΠ±ΡΠ΅ΠΌΠ° ΠΈ Π»ΠΎΠΊΠ°Π»ΠΈΠ·Π°ΡΠΈΠΈ ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΏΡΠΎΡΠ΅ΡΡΠ° Π² Π»Π΅Π³ΠΎΡΠ½ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ. Π Π°ΡΡΠΌΠΎΡΡΠ΅Π½Ρ ΡΡΠ°ΠΏΡ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΌΠ΅ΡΠΎΠ΄ΠΈΠΊ ΡΠ½Π΄ΠΎΡΠΊΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Ρ
ΠΈΡΡΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π»Π΅ΡΠ΅Π½ΠΈΡ ΡΠΏΠΎΠ½ΡΠ°Π½Π½ΠΎΠ³ΠΎ ΠΏΠ½Π΅Π²ΠΌΠΎΡΠΎΡΠ°ΠΊΡΠ°. ΠΡΠΎΠ²Π΅Π΄Π΅Π½ Π°Π½Π°Π»ΠΈΠ· Π²ΡΠΏΠΎΠ»Π½Π΅Π½Π½ΡΡ
Π²ΠΈΠ΄Π΅ΠΎΡΠΎΡΠ°ΠΊΠΎΡΠΊΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΉ ΠΏΡΠΈ ΡΡΠΎΠΌ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΈ. Π Π΅ΡΠΈΠ΄ΠΈΠ²Ρ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ ΠΏΡΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠΈ Π΄Π°Π½Π½ΠΎΠ³ΠΎ ΠΌΠ΅ΡΠΎΠ΄Π° Ρ
ΠΈΡΡΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π»Π΅ΡΠ΅Π½ΠΈΡ ΡΠΎΡΡΠ°Π²ΠΈΠ»ΠΈ 3,6 %. ΠΠ΅ΡΠ°Π»ΡΠ½ΡΡ
ΠΈΡΡ
ΠΎΠ΄ΠΎΠ² Π½Π΅ Π±ΡΠ»ΠΎ
Π‘ΠΏΠΎΡΠΎΠ± ΠΏΠ°Π»Π»ΠΈΠ°ΡΠΈΠ²Π½ΠΎΠ³ΠΎ Π»Π΅ΡΠ΅Π½ΠΈΡ ΡΠ°ΡΠΏΡΠΎΡΡΡΠ°Π½Π΅Π½Π½ΡΡ ΡΠΎΡΠΌ ΡΠ°ΠΊΠ° Π»Π΅Π³ΠΊΠΎΠ³ΠΎ
We have proposed a palliative method for common forms of lung cancer, which combines the two previously mentioned methods. Using this method allows not only to stop the lung bleeding, but restore airway passage of the bronchi and then continue with the treatment of lung cancer (chemotherapy, radiotherapy). We used this method in 16 patients with age group from 54 to 76 years, with central lung cancer III AβIV stages, who had lung hemorrhage and atelectasis of bronchus. In the first step, rentgenendovascular embolization of bronchial artery (REVEBA) and their branches approaching to the tumor is performed. In the next stage, the patients underwent laser recanalization of tumor stenosis of the segmental or main bronchi. We were able to achieve a positive hemostatic effect in 15 patients, which was seen throughout first 5 months. Recanalization and restoration of the bronchial airway was achieved in all the patients. All these factors allowed the patients undergo subsequent radiation and chemotherapy. Tumor relapse, recurrence of stenosis and pulmonary bleeding have not been observed during the first 5 months. Possibilities of using the adove mentioned methods in the treatment of common forms of lung cancer have been shown.ΠΠ°ΠΌΠΈ ΠΏΡΠ΅Π΄Π»ΠΎΠΆΠ΅Π½ ΡΠΏΠΎΡΠΎΠ± ΠΏΠ°Π»Π»ΠΈΠ°ΡΠΈΠ²Π½ΠΎΠ³ΠΎ Π»Π΅ΡΠ΅Π½ΠΈΡ ΡΠ°ΡΠΏΡΠΎΡΡΡΠ°Π½Π΅Π½Π½ΡΡ
ΡΠΎΡΠΌ ΡΠ°ΠΊΠ° Π»ΡΠ³ΠΊΠΎΠ³ΠΎ, ΠΊΠΎΡΠΎΡΡΠΉ ΠΎΠ±ΡΠ΅Π΄ΠΈΠ½ΡΠ΅Ρ Π΄Π²Π΅ ΡΠ°Π½Π΅Π΅ ΡΠΊΠ°Π·Π°Π½Π½ΡΠ΅ ΠΌΠ΅ΡΠΎΠ΄ΠΈΠΊΠΈ. ΠΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ Π΄Π°Π½Π½ΠΎΠ³ΠΎ ΡΠΏΠΎΡΠΎΠ±Π° ΠΏΠΎΠ·Π²ΠΎΠ»ΡΠ΅Ρ Π½Π΅ ΡΠΎΠ»ΡΠΊΠΎ ΠΎΡΡΠ°Π½ΠΎΠ²ΠΈΡΡ Π»Π΅Π³ΠΎΡΠ½ΠΎΠ΅ ΠΊΡΠΎΠ²ΠΎΡΠ΅ΡΠ΅Π½ΠΈΠ΅ ΠΈ Π²ΠΎΡΡΡΠ°Π½ΠΎΠ²ΠΈΡΡ ΠΏΡΠΎΡ
ΠΎΠ΄ΠΈΠΌΠΎΡΡΡ Π±ΡΠΎΠ½Ρ
Π°, Π½ΠΎ ΠΈ Π² Π΄Π°Π»ΡΠ½Π΅ΠΉΡΠ΅ΠΌ ΠΏΡΠΎΠ΄ΠΎΠ»ΠΆΠΈΡΡ Π»Π΅ΡΠ΅Π½ΠΈΠ΅ ΡΠ°ΠΊΠ° Π»Π΅Π³ΠΊΠΎΠ³ΠΎ (Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΡ, Π»ΡΡΠ΅Π²Π°Ρ ΡΠ΅ΡΠ°ΠΏΠΈΡ). ΠΠ°Π½Π½ΡΠΉ ΡΠΏΠΎΡΠΎΠ± ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ Π½Π°ΠΌΠΈ Ρ 16 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΡΠ΅Π½ΡΡΠ°Π»ΡΠ½ΡΠΌ ΡΠ°ΠΊΠΎΠΌ Π»Π΅Π³ΠΊΠΎΠ³ΠΎ III AβIV ΡΡ., Ρ ΠΊΠΎΡΠΎΡΡΡ
Π±ΡΠ»ΠΎ Π»Π΅Π³ΠΎΡΠ½ΠΎΠ΅ ΠΊΡΠΎΠ²ΠΎΡΠ΅ΡΠ΅Π½ΠΈΠ΅ ΠΈ Π°ΡΠ΅Π»Π΅ΠΊΡΠ°Π· Π±ΡΠΎΠ½Ρ
Π°. ΠΠ΅ΡΠ²ΡΠΌ ΡΡΠ°ΠΏΠΎΠΌ Π²ΡΠΏΠΎΠ»Π½ΡΠ»Π°ΡΡ ΡΠ΅Π½ΡΠ³Π΅Π½ΡΠ½Π΄ΠΎΠ²Π°ΡΠΊΡΠ»ΡΡΠ½Π°Ρ ΡΠΌΠ±ΠΎΠ»ΠΈΠ·Π°ΡΠΈΡ Π±ΡΠΎΠ½Ρ
ΠΈΠ°Π»ΡΠ½ΡΡ
Π°ΡΡΠ΅ΡΠΈΠΉ ΠΈ ΠΈΡ
Π²Π΅ΡΠ²Π΅ΠΉ, ΠΏΠΎΠ΄Ρ
ΠΎΠ΄ΡΡΠΈΡ
ΠΊ ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ. Π‘Π»Π΅Π΄ΡΡΡΠΈΠΌ ΡΡΠ°ΠΏΠΎΠΌ Π±ΡΠ»Π° Π»Π°Π·Π΅ΡΠ½Π°Ρ ΡΠ΅ΠΊΠ°Π½Π°Π»ΠΈΠ·Π°ΡΠΈΡ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΡ
ΡΡΠ΅Π½ΠΎΠ·ΠΎΠ² Π±ΡΠΎΠ½Ρ
ΠΎΠ². ΠΠ°ΠΌ ΡΠ΄Π°Π»ΠΎΡΡ Π΄ΠΎΠ±ΠΈΡΡΡΡ ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ Π³Π΅ΠΌΠΎΡΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΡΡΡΠ΅ΠΊΡΠ° Ρ 15 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² (ΡΡΠΎΠΉΠΊΠΈΠΉ Π³Π΅ΠΌΠΎΡΡΠ°Π· ΠΎΡΠΌΠ΅ΡΠ°Π»ΡΡ Π½Π° ΠΏΡΠΎΡΡΠΆΠ΅Π½ΠΈΠΈ 5 ΠΌΠ΅Ρ.), Π° ΡΠ°ΠΊΠΆΠ΅ ΡΠ΅ΠΊΠ°Π½Π°Π»ΠΈΠ·Π°ΡΠΈΠΈ Π±ΡΠΎΠ½Ρ
ΠΎΠ² Ρ Π²ΡΠ΅Ρ
ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ². ΠΡΠ΅ ΡΡΠΎ ΠΏΠΎΠ·Π²ΠΎΠ»ΠΈΠ»ΠΎ Π½Π°ΡΠΈΠΌ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ°ΠΌ Π² ΠΏΠΎΡΠ»Π΅Π΄ΡΡΡΠ΅ΠΌ ΠΏΡΠΎΠΉΡΠΈ Π»ΡΡΠ΅Π²ΡΡ Π»ΠΈΠ±ΠΎ Ρ
ΠΈΠΌΠΈΠΎΡΠ΅ΡΠ°ΠΏΠΈΡ. ΠΠ° 5-ΠΌΠ΅ΡΡΡΠ½ΡΠΉ ΠΏΠ΅ΡΠΈΠΎΠ΄ Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΡ ΡΠ΅ΡΠΈΠ΄ΠΈΠ² ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠ³ΠΎ ΡΡΠ΅Π½ΠΎΠ·Π° ΠΈ ΠΏΠΎΠ²ΡΠΎΡΠ½ΡΠ΅ Π»Π΅Π³ΠΎΡΠ½ΡΠ΅ ΠΊΡΠΎΠ²ΠΎΡΠ΅ΡΠ΅Π½ΠΈΡ Π½Π°ΠΌΠΈ Π½Π΅ Π½Π°Π±Π»ΡΠ΄Π°Π»ΠΈΡΡ. ΠΠΎΠΊΠ°Π·Π°Π½Π° Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΡ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΡ ΠΌΠ΅ΡΠΎΠ΄Π° Π² Π»Π΅ΡΠ΅Π½ΠΈΠΈ ΠΎΡΠ»ΠΎΠΆΠ½Π΅Π½Π½ΡΡ
ΡΠΎΡΠΌ Π·Π»ΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΠΎΠΏΡΡ
ΠΎΠ»Π΅ΠΉ Π»Π΅Π³ΠΊΠΎΠ³ΠΎ
Cytokines and HIF-1Ξ± as dysregulation factors of migration and differentiation of monocyte progenitor cells of endotheliocytes in the pathogenesis of ischemic cardiomyopathy
Background. Angiogenic endothelial dysfunction and progenitor endothelial cells (EPCs) in ischemic cardiomyopathy (ICMP) have not been studied enough.The aim. To establish the nature of changes in the cytokine profile and HIF-1Ξ± in blood and bone marrow associated with impaired differentiation of monocytic progenitor cells of endotheliocytes (CD14+VEGFR2+) in the bone marrow and their migration into the blood in patients with coronary heart disease (CHD), suffering and not suffering from ICMP.Materials and methods. A single-stage, single-centre, observational case-control study was conducted involving 74 patients with CHD, suffering and not suffering from ICMP (30 and 44 people, respectively), and 25 healthy donors. In patients with CHD, bone marrow was obtained during coronary bypass surgery, peripheral blood β before surgery. Healthy donors were taken peripheral blood. The number of CD14+VEGFR2+ in bone marrow and blood was determined by flow cytometry; the concentration of IL-6, TNF-Ξ±, M-CSF, GM-CSF, MCP-1 and HIF-1Ξ± β by the method of enzyme immunoassay.Results. A high content of CD14+VEGFR2+ cells in the blood of patients with CHD without cardiomyopathy was established relative to patients with ICMP against the background of a comparable number of these cells in myeloid tissue. Regardless of the presence of ICMP in the blood, patients with CHD showed an excess of TNF-Ξ±, a normal concentration of IL-6, GM-CSF, HIF-1Ξ± and a deficiency of M-CSF, and in the bone marrow supernatant, the concentration of IL-6 and TNF-Ξ± exceeded that in the blood plasma (the level of GM-CSF β only in patients without cardiomyopathy). With ICMP, the normal concentration of MCP-1 was determined in the blood plasma, and with CHD without cardiomyopathy, its elevated content was determined.Conclusion. The formation of ICMP is accompanied by insufficient activation of EPCs migration with the CD14+VEGFR2+ phenotype in blood without disruption of their differentiation in the bone marrow, which associated with the absence of an increase in the concentration of MCP-1 in blood plasma and not associated with the plasma content of M-CSF, GM-CSF, HIF-1Ξ±, IL-6 and TNF-Ξ±
Genetic Biomarkers of Antipsychotic-Induced Prolongation of the QT Interval in Patients with Schizophrenia.
Antipsychotics (AP) induced prolongation of the QT interval in patients with schizophrenia (Sch) is an actual interdisciplinary problem as it increases the risk of sudden death syndrome. Long QT syndrome (LQTS) as a cardiac adverse drug reaction is a multifactorial symptomatic disorder, the development of which is influenced by modifying factors (APs' dose, duration of APs therapy, APs polytherapy, and monotherapy, etc.) and non-modifying factors (genetic predisposition, gender, age, etc.). The genetic predisposition to AP-induced LQTS may be due to several causes, including causal mutations in the genes responsible for monoheme forms of LQTS, single nucleotide variants (SNVs) of the candidate genes encoding voltage-dependent ion channels expressed both in the brain and in the heart, and SNVs of candidate genes encoding key enzymes of APs metabolism. This narrative review summarizes the results of genetic studies on AP-induced LQTS and proposes a new personalized approach to assessing the risk of its development (low, moderate, high). We recommend implementation in protocols of primary diagnosis of AP-induced LQTS and medication dispensary additional observations of the risk category of patients receiving APs, deoxyribonucleic acid profiling, regular electrocardiogram monitoring, and regular therapeutic drug monitoring of the blood APs levels
The Use of Sutureless Electrosurgical and Ultrasound Technologies in Lung Surgeries β Literature Review
ΠΠ° ΡΠΎΠ²ΡΠ΅ΠΌΠ΅Π½Π½ΠΎΠΌ ΡΡΠΎΠ²Π½Π΅ ΡΠ°Π·Π²ΠΈΡΠΈΡ Π²ΠΈΠ΄Π΅ΠΎΡΠΎΡΠ°ΠΊΠΎΡΠΊΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠΉ Ρ
ΠΈΡΡΡΠ³ΠΈΠΈ Π»Π΅Π³ΠΊΠΈΡ
ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ Π²ΡΠ±ΠΎΡΠ° ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠ΅ ΡΠ½Π΄ΠΎΡΡΠ΅ΠΏΠ»Π΅ΡΠΎΠ² (ΠΠ‘), ΠΎΡΡΡΠ΅ΡΡΠ²Π»ΡΡΡΠΈΡ
ΠΎΠ΄Π½ΠΎΠ²ΡΠ΅ΠΌΠ΅Π½Π½ΠΎΠ΅ ΠΏΡΠΎΡΠΈΠ²Π°Π½ΠΈΠ΅ ΠΈ ΡΠ°ΡΡΠ΅ΡΠ΅Π½ΠΈΠ΅ Π»Π΅Π³ΠΎΡΠ½ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ ΠΌΠ΅ΠΆΠ΄Ρ Π½Π°Π»ΠΎΠΆΠ΅Π½Π½ΡΠΌ ΡΡΠ΄ΠΎΠΌ ΡΠ°Π½ΡΠ°Π»ΠΎΠ²ΡΡ
ΡΠΊΠΎΠ±ΠΎΠΊ. ΠΠ΄Π½Π°ΠΊΠΎ ΡΠΈΡΠΎΠΊΠΎΠ΅ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ ΠΠ‘ ΠΏΠΎΠΊΠ°Π·Π°Π»ΠΎ, ΡΡΠΎ ΠΌΠ΅Ρ
Π°Π½ΠΈΡΠ΅ΡΠΊΠΈΠΉ ΡΠΎΠ² Π½Π΅ Π²ΡΠ΅Π³Π΄Π° ΠΎΠ±Π΅ΡΠΏΠ΅ΡΠΈΠ²Π°Π΅Ρ Π½Π°Π΄Π΅ΠΆΠ½ΡΠΉ Π°ΡΡΠΎΡΡΠ°Π·, ΡΡΠΎ Π·Π°ΡΡΠ°Π²Π»ΡΠ΅Ρ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°ΡΡ Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΡΠ΅ ΡΠΈΠ½ΡΠ΅ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΌΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ. ΠΡΠΎΠΌΠ΅ ΡΠΎΠ³ΠΎ, Π½Π΅Π΄ΠΎΡΡΠ°ΡΠΊΠ°ΠΌΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΡ ΠΠ‘ ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΈΡ
Π²ΡΡΠΎΠΊΠ°Ρ ΡΠ΅Π½Π°, ΠΏΠΎΡΡΠ΅Π±Π½ΠΎΡΡΡ Π² ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠΈ Π½Π΅ΡΠΊΠΎΠ»ΡΠΊΠΈΡ
ΠΊΠ°ΡΡΡΠΈΠ΄ΠΆΠ΅ΠΉ, ΠΏΠΎΡΡΡΠ΅Π·Π΅ΠΊΡΠΈΠΎΠ½Π½ΠΎΠ΅ Π²ΡΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅ ΠΈΠ· Π΄ΡΡ
Π°Π½ΠΈΡ Π½Π΅ΠΈΠ·ΠΌΠ΅Π½Π΅Π½Π½ΡΡ
ΡΡΠ°ΡΡΠΊΠΎΠ² Π»Π΅Π³ΠΎΡΠ½ΠΎΠΉ ΠΏΠ°ΡΠ΅Π½Ρ
ΠΈΠΌΡ, Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΡΠ΅ ΡΡΡΠ΄Π½ΠΎΡΡΠΈ Π² ΡΠ°Π·ΠΌΠ΅ΡΠ΅Π½ΠΈΠΈ ΡΠ°Π±ΠΎΡΠ΅ΠΉ ΡΠ°ΡΡΠΈ Π°ΠΏΠΏΠ°ΡΠ°ΡΠ° Π² ΠΏΠ»Π΅Π²ΡΠ°Π»ΡΠ½ΠΎΠΉ ΠΏΠΎΠ»ΠΎΡΡΠΈ, Π±ΠΎΠ»ΡΡΠΎΠΉ Π΄ΠΈΠ°ΠΌΠ΅ΡΡ ΡΠΎΡΠ°ΠΊΠΎΠΏΠΎΡΡΠ° (Π’), Π½Π΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΡΠΉ Π΄Π»Ρ Π²Π²Π΅Π΄Π΅Π½ΠΈΡ ΠΠ‘.The review presents data of the use of electric seal and ultrasonic technology in the performance of open and videothoracoscopic lung resections. The possibility of seamless resection of the lung tissue by using bipolar electric seal (LigaSure) and ultrasonic (Harmonic) scalpel with tolerable aerohemostasis shown. The advantages and possible drawbacks of these methods displayed
Interleukins 4 and 6 as factors of modulation of subpopulation composition of blood monocytes in patients with ischemic cardiomyopathy
Aim. To evaluate the ratio of the fractions of classical, intermediate, non-classical and transitional monocytes in correlation with the concentration of interleukins 4 and 6 in the blood of patients with ischemic cardiomyopathy.
Methods. 18 patients with ischemic cardiomyopathy (17 men and 1 woman) aged 47-66 years with circulatory insufficiency of functional class II-III according to the classification of heart failure of the New York Heart Association, were examined. The control group included 14 healthy donors matched by gender and age to patients with ischemic cardiomyopathy without any diseases of cardiovascular system and other systems in an exacerbation stage. In blood of the patients with ischemic cardiomyopathy, the relative content of classical (CD14++CD16-), intermediate (CD14++CD16+), non-classical (CD14+CD16+) and transitional (CD14+CD16-) monocytes was assessed by flow cytometry and the concentration of interleukins 4 and 6 by enzyme-linked immunosorbent assay (ELISA).
Results. It was shown that the number of non-classical monocytes in the blood of patients with ischemic cardiomyopathy was 2 times lower than normal (5.05 % [4.08; 6.58] and 10.07 % [9.34; 13.84], respectively, p < 0.01), as well as the concentration of interleukin-4 (0.02 pg/ml [0; 0.04] and 0.15 pg/ml [0.05; 0.65], respectively, p < 0.05). The number of classical monocytes in the blood of patients had a tendency to decrease, and the proportion of intermediate monocytes and the concentration of interleukin-6, on the contrary, were slightly higher than in healthy individuals, and were interdependent (r = 0.61; p < 0.05). The relative content of transitional monocytes in the blood was comparable with that of healthy donors.
Conclusions. The subpopulation composition of blood monocytes in patients with ischemic cardiomyopathy is characterized by a deficiency of the fraction of non-classical monocytes with protective properties against endothelium, and interleukin-4 in the blood with a certain increase in the content of interleukin-6 and the number of intermediate cells with ability to cooperate with T-lymphocytes, which predisposes to diffuse atheromatosis of small coronary arteries and diffuse hypoxic myocardial damage in ischemic cardiomyopathy
ΠΠΠΠΠΠ’ΠΠ ΠΠΠΠ‘ΠΠΠΠΠ§ΠΠ‘ΠΠΠ― Π ΠΠΠΠΠ¦ΠΠ― ΠΠΠΠΠΠ₯ Π‘ ΠΠ‘ΠΠΠΠ¬ΠΠΠΠΠΠΠΠ ΠΠΠΠΠ’Π ΠΠ‘ΠΠΠ ΠΠ§ΠΠ«Π₯ Π’ΠΠ₯ΠΠΠΠΠΠΠ
ΠΠ±ΠΎΠ±ΡΠ΅Π½ ΠΎΠΏΡΡ Π²ΡΠΏΠΎΠ»Π½Π΅Π½ΠΈΡ Ρ 113 Π±ΠΎΠ»ΡΠ½ΡΡ
Π²ΠΈΠ΄Π΅ΠΎΡΠΎΡΠ°ΠΊΠΎΡΠΊΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠΉ (ΠΠ’Π‘) ΡΠ΅Π·Π΅ΠΊΡΠΈΠΈ Π»Π΅Π³ΠΊΠΈΡ
(Π Π) Ρ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ ΡΠ»Π΅ΠΊΡΡΠΎΡΠ²Π°ΡΠΎΡΠ½ΡΡ
ΡΠ΅Ρ
Π½ΠΎΠ»ΠΎΠ³ΠΈΠΉ (ΠΠ‘Π’). ΠΡΠΈΠ²Π΅Π΄Π΅Π½Π° ΠΎΡΠ΅Π½ΠΊΠ° ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
ΠΌΠ΅ΡΠΎΠ΄ΠΈΠΊ ΡΠ½Π΄ΠΎΡΠΎΡΠ°ΠΊΠ°Π»ΡΠ½ΡΡ
ΡΠ»Π΅ΠΊΡΡΠΎΡΠ²Π°ΡΠΎΡΠ½ΡΡ
ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΉ, Π² ΡΠΎΠΌ ΡΠΈΡΠ»Π΅ Π² ΡΠΎΡΠ΅ΡΠ°Π½ΠΈΠΈ Ρ Π½Π°Π»ΠΎΠΆΠ΅Π½ΠΈΠ΅ΠΌ ΠΌΠ΅Ρ
Π°Π½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΡΠ²Π°, ΡΡΠ°Π²Π½ΠΈΡΠ΅Π»ΡΠ½Π°Ρ ΠΎΡΠ΅Π½ΠΊΠ° ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΡΡΠΈ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΡ ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
ΡΠ»Π΅ΠΊΡΡΠΎΡΠ²Π°ΡΠΎΡΠ½ΡΡ
ΠΊΠΎΠΌΠΏΠ»Π΅ΠΊΡΠΎΠ² Π² ΠΠ’Π‘ Ρ
ΠΈΡΡΡΠ³ΠΈΠΈ Π»Π΅Π³ΠΊΠΈΡ
.
ΠΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ ΠΠ‘Π’ ΠΏΠΎΠ·Π²ΠΎΠ»ΠΈΠ»ΠΎ ΡΠΌΠ΅Π½ΡΡΠΈΡΡ ΠΏΡΠΎΠ΄ΠΎΠ»ΠΆΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΡ ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΈ, ΡΡΠΆΠ΅ΡΡΡ ΠΊΡΠΎΠ²ΠΎΠΏΠΎΡΠ΅ΡΠΈ, Π΄Π»ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΡ Π»Π΅ΡΠ΅Π½ΠΈΡ Π±ΠΎΠ»ΡΠ½ΡΡ
Π² ΡΡΠ°ΡΠΈΠΎΠ½Π°ΡΠ΅ Π΄ΠΎ 7,3 Π΄Π½Ρ. ΠΠ°ΠΈΠ±ΠΎΠ»Π΅Π΅ ΡΠ°ΡΡΡΠΌ ΠΎΡΠ»ΠΎΠΆΠ½Π΅Π½ΠΈΠ΅ΠΌ Π±ΡΠ»Π° Π½Π΅Π³Π΅ΡΠΌΠ΅ΡΠΈΡΠ½ΠΎΡΡΡ ΡΠ²Π° Π»Π΅Π³ΠΊΠΈΡ
(7%), Π»Π΅Π³ΠΊΠΎ ΡΡΡΡΠ°Π½ΠΈΠΌΠ°Ρ ΠΊΠΎΠ½ΡΠ΅ΡΠ²Π°ΡΠΈΠ²Π½ΡΠΌΠΈ ΠΌΠ΅ΡΠΎΠ΄Π°ΠΌΠΈ
Possibilities of improving of videothoracoscopic operations, performed for spontaneous pneumothorax
ΠΠ±ΠΎΠ±ΡΠ΅Π½ 15βΠ»Π΅ΡΠ½ΠΈΠΉ ΠΎΠΏΡΡ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΡ Π²ΠΈΠ΄Π΅ΠΎΡΠΎΡΠ°ΡΠΊΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΉ (ΠΠ’Π) ΠΏΡΠΈ Π»Π΅ΡΠ΅Π½ΠΈΠΈ 616 Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΏΠΎ ΠΏΠΎΠ²ΠΎΠ΄Ρ ΡΠΏΠΎΠ½ΡΠ°Π½Π½ΠΎΠ³ΠΎ ΠΏΠ½Π΅Π²ΠΌΠΎΡΠΎΡΠ°ΠΊΡΠ° (Π‘Π). ΠΠΏΠΈΡΠ°Π½Ρ ΠΌΠ΅ΡΠΎΠ΄Ρ Π²ΡΠΏΠΎΠ»Π½Π΅Π½ΠΈΡ ΠΠ’Π Π² Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ ΠΎΠ±ΡΠ΅ΠΌΠ° ΠΈ Π»ΠΎΠΊΠ°Π»ΠΈΠ·Π°ΡΠΈΠΈ ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΏΡΠΎΡΠ΅ΡΡΠ° Π² ΡΠΊΠ°Π½ΠΈ Π»Π΅Π³ΠΊΠΈΡ
. Π Π°ΡΡΠΌΠΎΡΡΠ΅Π½Ρ ΡΡΠ°ΠΏΡ ΡΠ½Π΄ΠΎΡΠΊΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Ρ
ΠΈΡΡΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π²ΠΌΠ΅ΡΠ°ΡΠ΅Π»ΡΡΡΠ²Π° ΠΏΠΎ ΠΏΠΎΠ²ΠΎΠ΄Ρ Π‘Π. Π Π΅ΡΠΈΠ΄ΠΈΠ²Ρ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ ΠΏΡΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠΈ ΠΠ’Π Π²ΠΎΠ·Π½ΠΈΠΊΠ»ΠΈ Ρ 3, 6 Π±ΠΎΠ»ΡΠ½ΡΡ
. ΠΡΠ΅ ΠΏΠ°ΡΠΈΠ΅Π½ΡΡ ΠΆΠΈΠ²Ρ.A 15βyears experience of videothoracoscopic operations in the treatment of 616 patients, suffering spontaneous pneumothorax, was summarized. The methods of videothoracoscopic operations, depending on the volume and localization of pathological process in pulmonary tissues, were depicted. The stages of endoscopic surgical intervention for spontaneous pneumothorax were analyzed. The disease recurrence, while using videothoracoscopic operations, have occurred in 3.6% of patients. All the patients are alive
ΠΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°ΡΠΈΡ ΠΈ ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΎΠ½Π½ΡΠΉ ΡΠΎΡΡΠ°Π² VEGFR2+ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΊΡΠΎΠ²ΠΈ ΠΈ ΠΊΠΎΡΡΠ½ΠΎΠ³ΠΎ ΠΌΠΎΠ·Π³Π° ΠΏΡΠΈ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ
Aim. To identify disturbances of differentiation and subpopulation composition of VEGFR2+ cells in the blood and bone marrow associated with the features of the cytokine profile in the blood and bone marrow in patients with coronary artery disease (CAD) with and without ischemic cardiomyopathy (ICM).Materials and methods. The study included 74 patients with Π‘AD with and without ICM (30 and 44 people, respectively) and 18 healthy donors. In all patients with Π‘AD, peripheral blood sampling was performed immediately before coronary artery bypass grafting, and bone marrow samples were taken during the surgery via a sternal incision. In the healthy donors, only peripheral blood sampling was performed. In the bone marrow and blood samples, the number of VEGFR2+ cells (CD14+VEGFR2+ cells) and their immunophenotypes CD14++CD16-VEGFR2+, CD14++CD16+VEGFR2+, CD14+CD16++VEGFR2+, and CD14+CD16-VEGFR2+ was determined by flow cytometry. Using enzyme-linked immunosorbent assay, the levels of VΠGF-Π, TNFΞ±, M-CSF, and IL-13, as well as the content of MCP-1 (only in the blood) and the M-CSF / IL-13 ratio (only in the bone marrow) were determined.Results. The content of CD14+VEGFR2+ cells in the blood of CAD patients with and without ICM was higher than normal values due to the greater number of CD14++CD16-VEGFR2+, CD14++CD16+VEGFR2+, and CD14+CD16++VEGFR2+. In the bone marrow of the patients with ICM, the content of CD14++CD16-VEGFR2+, CD14+CD16++VEGFR2+, and CD14+CD16-VEGFR2+ was lower than in patients with CAD without ICM, and the number of CD14++CD16+VEGFR2+ cells corresponded to that in the controls. Regardless of the presence of ICM in CAD, a high concentration of TNFΞ± and normal levels of VEGF-A and IL-13 were observed in the blood. In CAD without ICM, an excess of MCP-1 and deficiency of M-CSF were revealed in the blood. In the bone marrow, the levels of VEGF-A, TNFΞ±, M-CSF, and IL-13 were comparable between the groups of patients against the background of a decrease in the M-CSF / IL-13 ratio in the patients with ICM.Conclusion. Unlike CAD without cardiomyopathy, in ICM, no excess of VEGFR2+ cells and MCP-1 in the blood is observed, which hinders active migration of CD14+CD16++VEGFR2+ cells from the myeloid tissue, and a decrease in the M-CSF / IL-13 ratio in the bone marrow disrupts differentiation of other forms of VEGFR2+ cells, preventing vascular repair.Π¦Π΅Π»Ρ: ΡΡΡΠ°Π½ΠΎΠ²ΠΈΡΡ Π½Π°ΡΡΡΠ΅Π½ΠΈΡ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΠΎΠ²ΠΊΠΈ ΠΈ ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΎΠ½Π½ΠΎΠ³ΠΎ ΡΠΎΡΡΠ°Π²Π° VEGFR2+ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² Π² ΠΊΡΠΎΠ²ΠΈ ΠΈ ΠΊΠΎΡΡΠ½ΠΎΠΌ ΠΌΠΎΠ·Π³Π΅ Π²ΠΎ Π²Π·Π°ΠΈΠΌΠΎΡΠ²ΡΠ·ΠΈ Ρ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΡΠΌΠΈ ΡΠΈΡΠΎΠΊΠΈΠ½ΠΎΠ²ΠΎΠ³ΠΎ ΠΏΡΠΎΡΠΈΠ»Ρ ΠΊΡΠΎΠ²ΠΈ ΠΈ ΠΊΠΎΡΡΠ½ΠΎΠ³ΠΎ ΠΌΠΎΠ·Π³Π° Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΡΡ ΡΠ΅ΡΠ΄ΡΠ° (ΠΠΠ‘), ΡΡΡΠ°Π΄Π°ΡΡΠΈΡ
ΠΈ Π½Π΅ ΡΡΡΠ°Π΄Π°ΡΡΠΈΡ
ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠ΅ΠΉ (ΠΠΠΠ).ΠΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. Π ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ Π²ΠΎΡΠ»ΠΈ 74 Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΠΠ‘, ΡΡΡΠ°Π΄Π°ΡΡΠΈΡ
ΠΈ Π½Π΅ ΡΡΡΠ°Π΄Π°ΡΡΠΈΡ
ΠΠΠΠ (30 ΠΈ 44 ΡΠ΅Π»ΠΎΠ²Π΅ΠΊΠ° ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²Π΅Π½Π½ΠΎ), ΠΈ 18 Π·Π΄ΠΎΡΠΎΠ²ΡΡ
Π΄ΠΎΠ½ΠΎΡΠΎΠ². Π£ Π²ΡΠ΅Ρ
Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΠΠ‘ Π·Π°Π±ΠΎΡ ΠΏΠ΅ΡΠΈΡΠ΅ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΡΠΎΠ²ΠΈ ΠΏΡΠΎΠΈΠ·Π²ΠΎΠ΄ΠΈΠ»ΡΡ Π½Π΅ΠΏΠΎΡΡΠ΅Π΄ΡΡΠ²Π΅Π½Π½ΠΎ ΠΏΠ΅ΡΠ΅Π΄ ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠ΅ΠΉ ΠΊΠΎΡΠΎΠ½Π°ΡΠ½ΠΎΠ³ΠΎ ΡΡΠ½ΡΠΈΡΠΎΠ²Π°Π½ΠΈΡ, Π° ΠΊΠΎΡΡΠ½ΠΎΠ³ΠΎ ΠΌΠΎΠ·Π³Π° β ΠΈΠ· ΡΠ°Π·ΡΠ΅Π·Π° Π³ΡΡΠ΄ΠΈΠ½Ρ Π²ΠΎ Π²ΡΠ΅ΠΌΡ ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΈ. Π£ Π·Π΄ΠΎΡΠΎΠ²ΡΡ
Π΄ΠΎΠ½ΠΎΡΠΎΠ² Π·Π°Π±ΠΈΡΠ°Π»ΠΈ ΡΠΎΠ»ΡΠΊΠΎ ΠΏΠ΅ΡΠΈΡΠ΅ΡΠΈΡΠ΅ΡΠΊΡΡ ΠΊΡΠΎΠ²Ρ.Β Π ΠΊΠΎΡΡΠ½ΠΎΠΌ ΠΌΠΎΠ·Π³Π΅ ΠΈ ΠΊΡΠΎΠ²ΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΏΡΠΎΡΠΎΡΠ½ΠΎΠΉ ΡΠΈΡΠΎΡΠ»ΡΠΎΡΠΈΠΌΠ΅ΡΡΠΈΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ ΡΠΈΡΠ»Π΅Π½Π½ΠΎΡΡΡ VEGFR2+ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² (CD14+VΠGFR2+ ΠΊΠ»Π΅ΡΠΎΠΊ) ΠΈ ΠΈΡ
ΠΈΠΌΠΌΡΠ½ΠΎΡΠ΅Π½ΠΎΡΠΈΠΏΠΎΠ² CD14++CD16-VEGFR2+, CD14++CD16+VEGFR2+, CD14+CD16++VEGFR2+, CD14+CD16-VEGFR2+, ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΈΠΌΠΌΡΠ½ΠΎΡΠ΅ΡΠΌΠ΅Π½ΡΠ½ΠΎΠ³ΠΎ Π°Π½Π°Π»ΠΈΠ·Π° ΡΠ΅Π³ΠΈΡΡΡΠΈΡΠΎΠ²Π°Π»ΠΈ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΡ VΠGF-Π, TNFΞ±, M-CSF, IL-13, Π° ΡΠ°ΠΊΠΆΠ΅ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ MCP-1 (ΡΠΎΠ»ΡΠΊΠΎ Π² ΠΊΡΠΎΠ²ΠΈ) ΠΈ ΡΠΎΠΎΡΠ½ΠΎΡΠ΅Π½ΠΈΠ΅ M-CSF/IL-13 (ΡΠΎΠ»ΡΠΊΠΎ Π² ΠΊΠΎΡΡΠ½ΠΎΠΌ ΠΌΠΎΠ·Π³Π΅).Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. Π‘ΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ CD14+VEGFR2+ ΠΊΠ»Π΅ΡΠΎΠΊ Π² ΠΊΡΠΎΠ²ΠΈ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΠΠ‘ Π±Π΅Π· ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ ΠΈ Ρ ΠΠΠΠ Π±ΡΠ»ΠΎ Π²ΡΡΠ΅ Π½ΠΎΡΠΌΡ ΠΈΠ·-Π·Π° Π±ΠΎΠ»ΡΡΠ΅ΠΉ ΡΠΈΡΠ»Π΅Π½Π½ΠΎΡΡΠΈ CD14++CD16-VEGFR2+, CD14++CD16+VEGFR2+ ΠΈ CD14+CD16++VEGFR2+ ΡΠΎΡΠΌ. Π ΠΊΠΎΡΡΠ½ΠΎΠΌ ΠΌΠΎΠ·Π³Π΅ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΠΠΠ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ CD14++CD16-VEGFR2+, CD14+CD16++VEGFR2+ ΠΈ CD14+CD16-VEGFR2+ ΡΠΎΡΠΌ Π±ΡΠ»ΠΎ Π½ΠΈΠΆΠ΅, ΡΠ΅ΠΌ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΠΠ‘ Π±Π΅Π· ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ, Π° ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²ΠΎ CD14++CD16+VEGFR2+ ΠΊΠ»Π΅ΡΠΎΠΊ ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²ΠΎΠ²Π°Π»ΠΎ ΠΈΡ
ΡΠΈΡΠ»Ρ Π² Π³ΡΡΠΏΠΏΠ΅ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ. ΠΠ½Π΅ Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ Π½Π°Π»ΠΈΡΠΈΡ ΠΠΠΠ ΠΏΡΠΈ ΠΠΠ‘ Π² ΠΊΡΠΎΠ²ΠΈ ΠΎΡΠΌΠ΅ΡΠ°Π»Π°ΡΡ Π²ΡΡΠΎΠΊΠ°Ρ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΡ TNFΞ±, Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΠΉ ΡΡΠΎΠ²Π΅Π½Ρ VEGF-Π ΠΈ IL-13; ΠΏΡΠΈ ΠΠΠ‘ Π±Π΅Π· ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ β ΠΈΠ·Π±ΡΡΠΎΠΊ ΠΠ‘Π -1 ΠΈ Π΄Π΅ΡΠΈΡΠΈΡ M-CSF Π² ΠΊΡΠΎΠ²ΠΈ. Π ΠΊΠΎΡΡΠ½ΠΎΠΌ ΠΌΠΎΠ·Π³Π΅ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΡ VΠGF-Π, TNFΞ±, M-CSF, IL-13 Π±ΡΠ»Π° ΡΠΎΠΏΠΎΡΡΠ°Π²ΠΈΠΌΠΎΠΉ ΠΌΠ΅ΠΆΠ΄Ρ Π³ΡΡΠΏΠΏΠ°ΠΌΠΈ Π±ΠΎΠ»ΡΠ½ΡΡ
Π½Π° ΡΠΎΠ½Π΅ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΡ M-CSF/IL-13 Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΠΠΠ.ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. Π ΠΎΡΠ»ΠΈΡΠΈΠ΅ ΠΎΡ ΠΠΠ‘ Π±Π΅Π· ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ ΠΏΡΠΈ ΠΠΠΠ Π½Π΅ ΡΠΎΡΠΌΠΈΡΡΠ΅ΡΡΡ ΠΈΠ·Π±ΡΡΠΎΠΊ VEGFR2+ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΈ ΠΠ‘Π -1 Π² ΠΊΡΠΎΠ²ΠΈ, ΡΡΠΎ Π·Π°ΡΡΡΠ΄Π½ΡΠ΅Ρ Π°ΠΊΡΠΈΠ²Π½ΡΡ ΠΌΠΈΠ³ΡΠ°ΡΠΈΡ CD14+CD16++VEGFR2+ ΠΊΠ»Π΅ΡΠΎΠΊ ΠΈΠ· ΠΌΠΈΠ΅Π»ΠΎΠΈΠ΄Π½ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ, Π° ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ M-CSF/IL-13 Π² ΠΊΠΎΡΡΠ½ΠΎΠΌ ΠΌΠΎΠ·Π³Π΅ Π½Π°ΡΡΡΠ°Π΅Ρ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΠΎΠ²ΠΊΡ ΠΎΡΡΠ°Π»ΡΠ½ΡΡ
ΡΠΎΡΠΌ VEGFR2+ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ², ΠΏΡΠ΅ΠΏΡΡΡΡΠ²ΡΡ ΡΠ΅ΠΏΠ°ΡΠ°ΡΠΈΠΈ ΡΠΎΡΡΠ΄ΠΎΠ²
- β¦