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    ΠžΡΠΎΠ±Π»ΠΈΠ²ΠΎΡΡ‚Ρ– гістоструктури ΠΏΡ–Π΄ΡˆΠ»ΡƒΠ½ΠΊΠΎΠ²ΠΎΡ— Π·Π°Π»ΠΎΠ·ΠΈ ΠΏΡ€ΠΈ Π°ΡƒΡ‚ΠΎΡ–ΠΌΡƒΠ½Π½ΠΎΠΌΡƒ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚Ρ– I Ρ– II Ρ‚ΠΈΠΏΡ–Π²: зв’язок Ρ–Π· Ρ€Ρ–Π²Π½Π΅ΠΌ IgG4-ΠΏΠΎΠ·ΠΈΡ‚ΠΈΠ²Π½ΠΈΡ… ΠΏΠ»Π°Π·ΠΌΠ°Ρ‚ΠΈΡ‡Π½ΠΈΡ… ΠΊΠ»Ρ–Ρ‚ΠΈΠ½ Π² ΠΎΡ€Π³Π°Π½Ρ–

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    Aims/hypothesis. The study was undertaken to examine the special aspects of pancreatic histopathology in patients with autoimmune pancreatitis (AIP) type I and II, in connection with the level of IgG4-positive plasma cells (PPC) in the tissue.Material and methods. The study was conducted on 54 patients with chronic pancreatitis, of whom15 cases with autoimmune pancreatitis were selected. Detailed histological evaluation in three topographical zones of the pancreas (head, body and tail) was carried out for each case.Results and interpretation. AIP type I was found in five cases. In all cases in pancreas (all three zones) stages III-IV of AIP were observed with characteristic dense lymphocytic and plasma cells infiltration, multilevel fibrosis and obliterating phlebitis. In the liver hepatitis was observed with a slight fibrosis and plasma cells infiltration (up to 5-PPC per high power field), IgG4-PPC were located in dilated portal tracts. The high level of IgG-PPC and IgG4-PPC in the pancreatic tissue (β‰₯ 30 IgG4-PPC per high power field) also confirmed the diagnosis of AIP type I, as IgG4-associated sclerosing disease. These patients had a diffuse damage of the pancreas at III (3 cases) and IV (2 cases) stages. All cases were marked by complicated disease course of AIP: in 60% (3 people) – a chronic fibrocystic pancreatitis, and 40% (2 people) – a chronic calculus pancreatopathy. In all the patients with AIP type I the dense plasma cells infiltrate around main and interlobular ducts and pancreatic lymph follicles was found with compact clusters of IgG4-PPC (β‰₯ 30 IgG4-PPC per high power field).AIP type II was found in other 10 cases. Two of them were characterized by diffuse, and eight – by the focal form of AIP. Stage IV of AIP was detected in one patient with the total damage of pancreas, and the AIP on II stage of development in another. AIP activity in these patients was minimal. Focal form of AIP type II which was located in the body of the pancreas (II-III stage AIP) was observed in three cases, in the tail (I and II Stage AIP) – in two cases, and in the head – in one case (I stage AIP). Another two cases showed conjoined destruction of the body and tail (II stage).In the focal form of AIP type II in epithelium of main pancreatic duct, collecting ducts and acini single and multiple neutrophilic leukocytes were observed, including the formation of microabscesses. Areas of desquamation, epithelial mitotic figures were observed in ductal epithelium. Suchlike high activity of AIP type II was observed in half of the cases. Lymphocytic and plasma cells infiltration was located not only in the ducts area but also in the stroma and lobules. For AIP type II at stages III-IV obliterating phlebitis located in the fibrous tissue was typical. In periductal fibrous tissue clusters of IgG PPC were identified. All cases show focal compact clusters of IgG4-PPC in periductal, perilobular and fibrotic tissue. IgG4-PPC were counted to the limit of 5-10 per high power field.Conclusions. Autoimmune pancreatitis type I is marked by dense lymphocytic and plasma cells infiltrate in periductal zone, multilevel fibrosis, obliterating venulitis and a high level of IgG4-PPC in the pancreas (β‰₯ 30 IgG4-PPC per high power field). Autoimmune pancreatitis type II, in addition to the known histopathologic features of AIP, was defined by neutrophilic leukocyte epithelial damage of pancreatic ducts and low level of IgG4-PPC in the pancreas. For AIP type II in 80% of cases focal damage of the pancreas at stage I-III was typical. In perspective those findings will lead to developing of simple and affordable diagnostic for AIP type I and II.Π”ΠΈΡ„Ρ„Π΅Ρ€Π΅Π½Ρ†ΠΈΠ°Π»ΡŒΠ½Π°Ρ диагностика Π°ΡƒΡ‚ΠΎΠΈΠΌΠΌΡƒΠ½Π½ΠΎΠ³ΠΎ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚Π° связана с Ρ€Π°Π·Π»ΠΈΡ‡Π½ΠΎΠΉ ΡΡ‚Π΅ΠΏΠ΅Π½ΡŒΡŽ вовлСчСнности Π² ΠΏΠ°Ρ‚ΠΎΠ³Π΅Π½Π΅Π· ΠΈΠΌΠΌΡƒΠ½ΠΎΠ³Π»ΠΎΠ±ΡƒΠ»ΠΈΠ½Π° G 4 субкласса. Π‘ Ρ†Π΅Π»ΡŒΡŽ изучСния Π΄Π²ΡƒΡ… Ρ„ΠΎΡ€ΠΌ Π°ΡƒΡ‚ΠΎΠΈΠΌΠΌΡƒΠ½Π½ΠΎΠ³ΠΎ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚Π° ΠΈ ΠΈΡ… связи с ΡƒΡ€ΠΎΠ²Π½Π΅ΠΌ IgG4-ΠΏΠΎΠ·ΠΈΡ‚ΠΈΠ²Π½Ρ‹Ρ… плазматичСских ΠΊΠ»Π΅Ρ‚ΠΎΠΊ Π² ΠΏΠΎΠ΄ΠΆΠ΅Π»ΡƒΠ΄ΠΎΡ‡Π½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Π΅ c ΠΏΠΎΠΌΠΎΡ‰ΡŒΡŽ гистологичСских ΠΈ иммуногистохимичСских ΠΌΠ΅Ρ‚ΠΎΠ΄ΠΎΠ² обслСдовали 54 Π±ΠΎΠ»ΡŒΠ½Ρ‹Ρ… с хроничСским ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚ΠΎΠΌ, ΠΈΠ· Π½ΠΈΡ… ΠΎΡ‚ΠΎΠ±Ρ€Π°Π½ΠΎ 15 случаСв с Π°ΡƒΡ‚ΠΎΠΈΠΌΠΌΡƒΠ½Π½Ρ‹ΠΌ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚ΠΎΠΌ. ΠŸΡ€ΠΈ Π°ΡƒΡ‚ΠΎΠΈΠΌΠΌΡƒΠ½Π½ΠΎΠΌ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚Π΅ I Ρ‚ΠΈΠΏΠ° наблюдали ΠΏΠ»ΠΎΡ‚Π½Ρ‹ΠΉ Π»ΠΈΠΌΡ„ΠΎΠΏΠ»Π°Π·ΠΌΠΎΡ†ΠΈΡ‚Π°Ρ€Π½Ρ‹ΠΉ ΠΏΠ΅Ρ€ΠΈΠ΄ΡƒΠΊΡ‚Π°Π»ΡŒΠ½Ρ‹ΠΉ ΠΈΠ½Ρ„ΠΈΠ»ΡŒΡ‚Ρ€Π°Ρ‚, многоярусный Ρ„ΠΈΠ±Ρ€ΠΎΠ·, ΠΎΠ±Π»ΠΈΡ‚Π΅Ρ€ΠΈΡ€ΡƒΡŽΡ‰ΠΈΠΉ Π²Π΅Π½ΡƒΠ»ΠΈΡ‚ ΠΈ высокий ΡƒΡ€ΠΎΠ²Π΅Π½ΡŒ IgG4-ППК Π² ΠΏΠΎΠ΄ΠΆΠ΅Π»ΡƒΠ΄ΠΎΡ‡Π½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Π΅ (β‰₯30 IgG4-ППК Π½Π° большоС ΠΏΠΎΠ»Π΅ зрСния). Для Π°ΡƒΡ‚ΠΎΠΈΠΌΠΌΡƒΠ½Π½ΠΎΠ³ΠΎ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚Π° II Ρ‚ΠΈΠΏΠ°, ΠΊΡ€ΠΎΠΌΠ΅ Ρ‚ΠΈΠΏΠΈΡ‡Π½Ρ‹Ρ… патогистологичСских ΠΏΡ€ΠΈΠ·Π½Π°ΠΊΠΎΠ² Π°ΡƒΡ‚ΠΎΠΈΠΌΠΌΡƒΠ½Π½ΠΎΠ³ΠΎ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚Π°, свойствСнно Π»Π΅ΠΉΠΊΠΎΡ†ΠΈΡ‚Π°Ρ€Π½ΠΎΠ΅ ΠΏΠΎΠ²Ρ€Π΅ΠΆΠ΄Π΅Π½ΠΈΠ΅ эпитСлия панкрСатичСских ΠΏΡ€ΠΎΡ‚ΠΎΠΊΠΎΠ², Π½ΠΈΠ·ΠΊΠΈΠΉ ΡƒΡ€ΠΎΠ²Π΅Π½ΡŒ IgG4-ППК Π² ΠΏΠΎΠ΄ΠΆΠ΅Π»ΡƒΠ΄ΠΎΡ‡Π½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Π΅ ΠΈ ΠΎΡ‡Π°Π³ΠΎΠ²Ρ‹Π΅ пораТСния Π½Π° I–III стадии заболСвания (80% случаСв).Π”ΠΈΡ„Π΅Ρ€Π΅Π½Ρ†Ρ–ΠΉΠ½Π° діагностика Π°ΡƒΡ‚ΠΎΡ–ΠΌΡƒΠ½Π½ΠΎΠ³ΠΎ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚Ρƒ пов’язана Π· Ρ€Ρ–Π·Π½ΠΈΠΌ ступСнСм залучСності Π² ΠΏΠ°Ρ‚ΠΎΠ³Π΅Π½Π΅Π· Ρ–ΠΌΡƒΠ½ΠΎΠ³Π»ΠΎΠ±ΡƒΠ»Ρ–Π½Ρƒ G 4 субкласу. Π— ΠΌΠ΅Ρ‚ΠΎΡŽ вивчСння Π΄Π²ΠΎΡ… Ρ„ΠΎΡ€ΠΌ Π°ΡƒΡ‚ΠΎΡ–ΠΌΡƒΠ½Π½ΠΎΠ³ΠΎ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚Ρƒ Ρ‚Π° Ρ—Ρ… зв’язку Π· Ρ€Ρ–Π²Π½Π΅ΠΌ IgG4-ΠΏΠΎΠ·ΠΈΡ‚ΠΈΠ²Π½ΠΈΡ… ΠΏΠ»Π°Π·ΠΌΠ°Ρ‚ΠΈΡ‡Π½ΠΈΡ… ΠΊΠ»Ρ–Ρ‚ΠΈΠ½ Ρƒ ΠΏΡ–Π΄ΡˆΠ»ΡƒΠ½ΠΊΠΎΠ²Ρ–ΠΉ Π·Π°Π»ΠΎΠ·Ρ– Π·Π° допомогою гістологічних Ρ‚Π° імуногістохімічних ΠΌΠ΅Ρ‚ΠΎΠ΄Ρ–Π² обстСТили 54 Ρ…Π²ΠΎΡ€ΠΈΡ… Π½Π° Ρ…Ρ€ΠΎΠ½Ρ–Ρ‡Π½ΠΈΠΉ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚, Ρ–Π· Π½ΠΈΡ… Π²Ρ–Π΄Ρ–Π±Ρ€Π°Π½ΠΎ 15 Π²ΠΈΠΏΠ°Π΄ΠΊΡ–Π² Π· Π°ΡƒΡ‚ΠΎΡ–ΠΌΡƒΠ½Π½ΠΈΠΌ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚ΠΎΠΌ. ΠŸΡ€ΠΈ Π°ΡƒΡ‚ΠΎΡ–ΠΌΡƒΠ½Π½ΠΎΠΌΡƒ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚Ρ– I Ρ‚ΠΈΠΏΡƒ спостСрігали Ρ‰Ρ–Π»ΡŒΠ½ΠΈΠΉ Π»Ρ–ΠΌΡ„ΠΎΠΏΠ»Π°Π·ΠΌΠΎΡ†ΠΈΡ‚Π°Ρ€Π½ΠΈΠΉ ΠΏΠ΅Ρ€Ρ–Π΄ΡƒΠΊΡ‚Π°Π»ΡŒΠ½ΠΈΠΉ Ρ–Π½Ρ„Ρ–Π»ΡŒΡ‚Ρ€Π°Ρ‚, багатоярусний Ρ„Ρ–Π±Ρ€ΠΎΠ·, ΠΎΠ±Π»Ρ–Ρ‚Π΅Ρ€ΡƒΡŽΡ‡ΠΈΠΉ Π²Π΅Π½ΡƒΠ»Ρ–Ρ‚ Ρ– високий Ρ€Ρ–Π²Π΅Π½ΡŒ IgG4-ППК Ρƒ ΠΏΡ–Π΄ΡˆΠ»ΡƒΠ½ΠΊΠΎΠ²Ρ–ΠΉ Π·Π°Π»ΠΎΠ·Ρ– (β‰₯ 30 IgG4-ППК Π½Π° Π²Π΅Π»ΠΈΠΊΠ΅ ΠΏΠΎΠ»Π΅ Π·ΠΎΡ€Ρƒ). Для Π°ΡƒΡ‚ΠΎΡ–ΠΌΡƒΠ½Π½ΠΎΠ³ΠΎ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚Ρƒ II Ρ‚ΠΈΠΏΡƒ, ΠΊΡ€Ρ–ΠΌ Ρ‚ΠΈΠΏΠΎΠ²ΠΈΡ… патогістологічних ΠΎΠ·Π½Π°ΠΊ Π°ΡƒΡ‚ΠΎΡ–ΠΌΡƒΠ½Π½ΠΎΠ³ΠΎ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‚Ρƒ, властиві Π»Π΅ΠΉΠΊΠΎΡ†ΠΈΡ‚Π°Ρ€Π½Π΅ ΡƒΡˆΠΊΠΎΠ΄ΠΆΠ΅Π½Π½Ρ Π΅ΠΏΡ–Ρ‚Π΅Π»Ρ–ΡŽ ΠΏΠ°Π½ΠΊΡ€Π΅Π°Ρ‚ΠΈΡ‡Π½ΠΈΡ… ΠΏΡ€ΠΎΡ‚ΠΎΠΊ, низький Ρ€Ρ–Π²Π΅Π½ΡŒ IgG4-ППК Ρƒ ΠΏΡ–Π΄ΡˆΠ»ΡƒΠ½ΠΊΠΎΠ²Ρ–ΠΉ Π·Π°Π»ΠΎΠ·Ρ– ΠΉ осСрСдкові ураТСння Π½Π° I–III стадіях Π·Π°Ρ…Π²ΠΎΡ€ΡŽΠ²Π°Π½Π½Ρ (80% Π²ΠΈΠΏΠ°Π΄ΠΊΡ–Π²).

    Histostructure of pancreas in patients with autoimmune pancreatitis type I and II: connection with the level of IgG4-positive plasma cells

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    Differential diagnosis of autoimmune pancreatitis apart from everything else is based on specifi cs of immunoglobulin G4 involvement into the pathogenesis. Aims: to analyze two forms of autoimmune pancreatitis and their relation to the level of IgG4-positive plasma cells. Methods and results. The present study was conducted on 54 patients with chronic pancreatitis, from which 15 cases with autoimmune pancreatitis were selected by using morphological and immunohistochemical methods. Conclusion. It has been established that for autoimmune pancreatitis type I dense lymphocytic periductal infi ltrate, multilevel fi brosis, obliterating venulitis and high IgG4-positive plasma cells in the pancreas (β‰₯ 30 per high power fi eld) were typical. In the cases of autoimmune pancreatitis type II, besides the specifi c histopathological signs of AIP, signifi cantly epithelial damage of pancreatic ducts by leukocytes, low levels of IgG4-PPC in the pancreas and focal lesions on stages I-III of disease (80%) were observed

    International Student Voice(s) – Where and What are They?

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    International students come from diverse contexts and countries. In spite of the multiplicity in their educational values and cultures, these students are often viewed as a homogenous group and perceived as having similar voices and needs. This chapter engages in an in-depth statistical examination to highlight this diversity in international student voices. Further, it draws attention to the dominance of particular international student groups in the research discourse and the challenges faced by international students. Finally, the chapter considers the consequences of ignoring this heterogeneity and proposes recommendations for an inclusive higher education sector that meaningfully engages with these multiple international student voices
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