Russia’s Legal Transitions: Marxist Theory, Neoclassical Economics and the Rule of Law

We review the role of economic theory in shaping the process of legal change in Russia during the two transitions it experienced during the course of the twentieth century: the transition to a socialist economy organised along the lines of state ownership of the means of production in the 1920s, and the transition to a market economy which occurred after the fall of the Soviet Union in the 1990s. Despite differences in methodology and in policy implications, Marxist theory, dominant in the 1920s, and neoclassical economics, dominant in the 1990s, offered a similarly reductive account of law as subservient to wider economic forces. In both cases, the subordinate place accorded to law undermined the transition process. Although path dependence and history are frequently invoked to explain the limited development of the rule of law in Russia during the 1990s, policy choices driven by a deterministic conception of law and economics also played a role.This is the author accepted manuscript. The final version is available from Springer via http://dx.doi.org/10.1007/s40803-015-0012-

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

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 (≥ 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

Особливості гістоструктури підшлункової залози при аутоімунному панкреатиті I і II типів: зв’язок із рівнем IgG4-позитивних плазматичних клітин в органі

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 (≥ 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 (≥ 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 (≥ 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.Дифференциальная диагностика аутоиммунного панкреатита связана с различной степенью вовлеченности в патогенез иммуноглобулина G 4 субкласса. С целью изучения двух форм аутоиммунного панкреатита и их связи с уровнем IgG4-позитивных плазматических клеток в поджелудочной железе c помощью гистологических и иммуногистохимических методов обследовали 54 больных с хроническим панкреатитом, из них отобрано 15 случаев с аутоиммунным панкреатитом. При аутоиммунном панкреатите I типа наблюдали плотный лимфоплазмоцитарный перидуктальный инфильтрат, многоярусный фиброз, облитерирующий венулит и высокий уровень IgG4-ППК в поджелудочной железе (≥30 IgG4-ППК на большое поле зрения). Для аутоиммунного панкреатита II типа, кроме типичных патогистологических признаков аутоиммунного панкреатита, свойственно лейкоцитарное повреждение эпителия панкреатических протоков, низкий уровень IgG4-ППК в поджелудочной железе и очаговые поражения на I–III стадии заболевания (80% случаев).Диференційна діагностика аутоімунного панкреатиту пов’язана з різним ступенем залученості в патогенез імуноглобуліну G 4 субкласу. З метою вивчення двох форм аутоімунного панкреатиту та їх зв’язку з рівнем IgG4-позитивних плазматичних клітин у підшлунковій залозі за допомогою гістологічних та імуногістохімічних методів обстежили 54 хворих на хронічний панкреатит, із них відібрано 15 випадків з аутоімунним панкреатитом. При аутоімунному панкреатиті I типу спостерігали щільний лімфоплазмоцитарний перідуктальний інфільтрат, багатоярусний фіброз, облітеруючий венуліт і високий рівень IgG4-ППК у підшлунковій залозі (≥ 30 IgG4-ППК на велике поле зору). Для аутоімунного панкреатиту II типу, крім типових патогістологічних ознак аутоімунного панкреатиту, властиві лейкоцитарне ушкодження епітелію панкреатичних проток, низький рівень IgG4-ППК у підшлунковій залозі й осередкові ураження на I–III стадіях захворювання (80% випадків).

A Russian-Slovene conversation Yegor Gaidar and Ljubo Sirc discuss international economic co-operation and other topics

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