რეგიონებიდან თბილისში სასწავლებლად მიგრირებული სტუდენტების სოციალიზაცია და ჯანმრთელობა

Introduction: In recent years, the migration of students from regions to the capital city has grown very much, the main reason of this is that most of the good universities are in Tbilisi. The goal of the research is to study the major problems that students face when they come to the city and it shows the impact of these factors on their psychological and physical condition. Methodology: For this research, one of the methods of qualitative research was conducted with the students from regions. We performed a focus group using semi-structured questionnaire. Results, Discussion: The research has shown that in the beginning, students from regions had difficulty adapting to the capital city. They rarely visited public places, were not involved in university life. Some were depressed by the high sense of independence; it was stressful to deal with domestic activities. In addition, the problem of adaptation has been revealed with regard to factors such as noise, transport, meals, etc. Because of this student complain of insomnia, irritability, weight gain, tiredness and various health problems. However, it should be noted that after 2-3 years of their arrival, the quality of adaptation has significantly increased, and therefore their physical and psychological condition has improved. Recommendations: It is necessary to conduct training sessions for students from regions and talk about their problems. We should create a positive and comfortable environment for them to involve in various activities in order to increase the quality of their socialization.შესავალი: ბოლო წლებში, რეგიონებიდან დედაქალაქში სტუდენტთა მიგრაციამ მაშტაბური ხასიათი მიიღო, ამის ძირითად მიზეზს კი თბილისში არსებული უამრავი უნივერსიტეტი წარმოადგენს. კვლევის მიზანია შეისწავლოს ის ძირითადი პრობლემები, რომელთაც სტუდენტები დედაქალაქში ჩამოსვლისას აწყდებიან და წარმოაჩინოს ამ ფაქტორების გავლენა მათ ჯანმრთელობის მდგომარეობაზე. მეთოდოლოგია: თვისებრივი კვლევის ფარგლებში ჩატარდა ფოკუს-ჯგუფი რეგიონებიდან თბილისში ჩამოსულ სტუდენტებთან ნახევრად სტრუქტურიზებული კითხვარის მეშვეობით. შედეგები, დისკუსია: კვლევამ აჩვენა, რომ სტუდენტებს პირველ წლებში ძალიან გაუჭირდათ ადაპტაცია ქალაქთან, ისინი ნაკლებად სტუმრობდნენ საზოგადოებრივ თავშეყრის ადგილებს, არ იყვნენ ჩართულნი საუნივერსიტეტო ცხოვრებაში, ზოგიერთს თრგუნავდათ დამოუკიდებლობის მაღალი მაჩვენებელი, ზოგიერთისთვის კი სტრესული აღმოჩნდა საოჯახო საქმეები. ამასთან, ადაპტაციის პრობლემა გამოიკვეთა ისეთ ფაქტორებთან დაკავშირებით, როგორიცაა ხმაური, გადაადგილება, ტრანსპორტი, კვება და ა.შ., რომელთა გამოც სტუდენტები უძილობას, გაღიზიანებას, წონაში მომატებას, დაღლასა და ჯამრთელობის სხვადასხვა პრობლემებს უჩივიან. თუმცა, უნდა აღინიშნოს, რომ ჩამოსვლიდან 2-3 წლის შემდეგ ადაპტაციის ხარისხი საგრძნობლად გაიზარდა, შესაბამისად შემსუბუქდა მათი ფიზიკური და ფსიქოლოგიური მდგომარეობაც. რეკომენდაციები: მიზანშეწონილია რეგიონებიდან ჩამოსული სტუდენტებისთვის გარკვეული ტრენინგების ჩატარება და საუბრები მათი პრობლემების შესახებ. ამასთან, მათთვის უფრო მოქნილი და მორგებული გარემოს შექმნა, აქტიური ჩართვა სხვადასხვა აქტივობებში, რათა გაიზარდოს მათი სოციალიზაციის ხარისხი

A new fasciocutaneous flap model identifies a critical role for endothelial Notch signaling in wound healing and flap survival.

Flap surgery is a common treatment for severe wounds and a major determinant of surgical outcome. Flap survival and healing depends on adaptation of the local flap vasculature. Using a novel and defined model of fasciocutaneous flap surgery, we demonstrate that the Notch ligand Delta-like 1 (Dll1), expressed in vascular endothelial cells, regulates flap arteriogenesis, inflammation and flap survival. Utilizing the stereotyped anatomy of dorsal skin arteries, ligation of the major vascular pedicle induced strong collateral vessel development by end-to-end anastomosis in wildtype mice, which supported flap perfusion recovery over time. In mice with heterozygous deletion of Dll1, collateral vessel formation was strongly impaired, resulting in aberrant vascularization and subsequent necrosis of the tissue. Furthermore, Dll1 deficient mice showed severe inflammation in the flap dominated by monocytes and macrophages. This process is controlled by endothelial Dll1 in vivo, since the results were recapitulated in mice with endothelial-specific deletion of Dll1. Thus, our model provides a platform to study vascular adaptation to flap surgery and molecular and cellular regulators influencing flap healing and survival

CSF-1 and Notch signaling cooperate in macrophage instruction and tissue repair during peripheral limb ischemia

Ischemia causes an inflammatory response featuring monocyte-derived macrophages (MF) involved in angiogenesis and tissue repair. Angiogenesis and ischemic macrophage differentiation are regulated by Notch signaling via Notch ligand Delta-like 1 (Dll1). Colony stimulating factor 1 (CSF-1) is an essential MF lineage factor, but its role in ischemic macrophage development and the interaction with Notch signaling is so far unclear. Using a mouse model of hind limb ischemia with CSF-1 inhibitor studies and Dll1 heterozygous mice we show that CSF-1 is induced in the ischemic niche by a subpopulation of stromal cells expressing podoplanin, which was paralleled by the development of ischemic macrophages. Inhibition of CSF-1 signaling with small molecules or blocking antibodies impaired macrophage differentiation but prolonged the inflammatory response, resulting in impaired perfusion recovery and tissue regeneration. Yet, despite high levels of CSF-1, macrophage maturation and perfusion recovery were impaired in mice with Dll1 haploinsufficiency, while inflammation was exaggerated. In vitro, CSF-1 was not sufficient to induce full MF differentiation from donor monocytes in the absence of recombinant DLL1, while the presence of DLL1 in a dose-dependent manner stimulated MF differentiation in combination with CSF-1. Thus, CSF-1 is an ischemic niche factor that cooperates with Notch signaling in a non-redundant fashion to instruct macrophage cell fate and maturation, which is required for ischemic perfusion recovery and tissue repair

Regulation of monocyte cell fate by blood vessels mediated by Notch signalling

A population of monocytes, known as Ly6Clo monocytes, patrol blood vessels by crawling along the vascular endothelium. Here we show that endothelial cells control their origin through Notch signalling. Using combinations of conditional genetic deletion strategies and cell-fate tracking experiments we show that Notch2 regulates conversion of Ly6Chi monocytes into Ly6Clo monocytes in vivo and in vitro, thereby regulating monocyte cell fate under steady-state conditions. This process is controlled by Notch ligand delta-like 1 (Dll1) expressed by a population of endothelial cells that constitute distinct vascular niches in the bone marrow and spleen in vivo, while culture on recombinant DLL1 induces monocyte conversion in vitro. Thus, blood vessels regulate monocyte conversion, a form of committed myeloid cell fate regulation

Regulation of monocyte cell fate by blood vessels mediated by Notch signalling

A population of monocytes, known as Ly6C(lo) monocytes, patrol blood vessels by crawling along the vascular endothelium. Here we show that endothelial cells control their origin through Notch signalling. Using combinations of conditional genetic deletion strategies and cell-fate tracking experiments we show that Notch2 regulates conversion of Ly6C(hi) monocytes into Ly6C(lo) monocytes in vivo and in vitro, thereby regulating monocyte cell fate under steady-state conditions. This process is controlled by Notch ligand delta-like 1 (Dll1) expressed by a population of endothelial cells that constitute distinct vascular niches in the bone marrow and spleen in vivo, while culture on recombinant DLL1 induces monocyte conversion in vitro. Thus, blood vessels regulate monocyte conversion, a form of committed myeloid cell fate regulation

Tumor Induced Hepatic Myeloid Derived Suppressor Cells Can Cause Moderate Liver Damage

<div><p>Subcutaneous tumors induce the accumulation of myeloid derived suppressor cells (MDSC) not only in blood and spleens, but also in livers of these animals. Unexpectedly, we observed a moderate increase in serum transaminases in mice with EL4 subcutaneous tumors, which prompted us to study the relationship of hepatic MDSC accumulation and liver injury. MDSC were the predominant immune cell population expanding in livers of all subcutaneous tumor models investigated (RIL175, B16, EL4, CT26 and BNL), while liver injury was only observed in EL4 and B16 tumor-bearing mice. Elimination of hepatic MDSC in EL4 tumor-bearing mice using low dose 5-fluorouracil (5-FU) treatment reversed transaminase elevation and adoptive transfer of hepatic MDSC from B16 tumor-bearing mice caused transaminase elevation indicating a direct MDSC mediated effect. Surprisingly, hepatic MDSC from B16 tumor-bearing mice partially lost their damage-inducing potency when transferred into mice bearing non damage-inducing RIL175 tumors. Furthermore, MDSC expansion and MDSC-mediated liver injury further increased with growing tumor burden and was associated with different cytokines including GM-CSF, VEGF, interleukin-6, CCL2 and KC, depending on the tumor model used. In contrast to previous findings, which have implicated MDSC only in protection from T cell-mediated hepatitis, we show that tumor-induced hepatic MDSC themselves can cause moderate liver damage.</p></div

The chemokine receptor CX3CR1 coordinates monocyte recruitment and endothelial regeneration after arterial injury

Abstract Regeneration of arterial endothelium after injury is critical for the maintenance of normal blood flow, cell trafficking, and vascular function. Using mouse models of carotid injury, we show that the transition from a static to a dynamic phase of endothelial regeneration is marked by a strong increase in endothelial proliferation, which is accompanied by induction of the chemokine CX3CL1 in endothelial cells near the wound edge, leading to progressive recruitment of Ly6Clo monocytes expressing high levels of the cognate CX3CR1 chemokine receptor. In Cx3cr1‐deficient mice recruitment of Ly6Clo monocytes, endothelial proliferation and regeneration of the endothelial monolayer after carotid injury are impaired, which is rescued by acute transfer of normal Ly6Clo monocytes. Furthermore, human non‐classical monocytes induce proliferation of endothelial cells in co‐culture experiments in a VEGFA‐dependent manner, and monocyte transfer following carotid injury promotes endothelial wound closure in a hybrid mouse model in vivo. Thus, CX3CR1 coordinates recruitment of specific monocyte subsets to sites of endothelial regeneration, which promote endothelial proliferation and arterial regeneration

Melanoma and lymphoma subcutaneous tumor-bearing mice suffer from mild liver damage.

<p>C57BL/6 and BALB/c mice bearing indicated subcutaneous tumors were sacrificed, when tumor diameter reached 15 mm. ALT (A) and AST (B) levels were analyzed in mouse serum (N≥8 mice per tumor, N≥6 naïve mice, 3 independent experiments). Naïve C57BL/6 mice (C, left image) or mice bearing B16 subcutaneous tumors (C, right image) were sacrificed, when tumor diameter reached 20 mm. TUNEL assays were performed on liver specimen (C; scale bar  = 100 µm; N = 2 mice per group, total of 5 TUNEL assays per group) and TUNEL positive cells were counted in 20 non-overlapping visual fields. Means of TUNEL positive cells per liver section were plotted (D). C, Representative examples of visual fields are shown. Data are expressed as mean ±SEM. *<i>p</i><0.05, ***<i>p</i><0.001, ****<i>p</i><0.0001 (by One-way ANOVA).</p

Human remain from a new Upper Pleistocene sequence in Bondi cave (Western Georgia)

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