α2‐Antiplasmin and its deficiency: fibrinolysis out of balance

Summary. Fibrinolysis serves an important role in the process of coagulation, ensuring that clots that are formed in response to injury resolve after the injured tissue is repaired. Fibrinolysis occurs because the protein plasminogen is converted to the active serine protease plasmin by its activating molecules (primarily tissue plasminogen activator). One of the inhibitors of fibrinolysis is α₂‐antiplasmin, which acts as the primary inhibitor of plasmin(ogen). Congenital deficiency of α₂‐antiplasmin causes a rare bleeding disorder because of increased fibrinolysis. Despite the rare nature of this disorder, understanding of the actions of α₂‐antiplasmin and the results of its deficiency has provided the opportunity for better understanding of the fibrinolytic system in both how it affects the risk of bleeding and its impact on other bodily systems. Here, we review the history of the discovery of α₂‐antiplasmin, our understanding of its genetics and function, and our current knowledge of its congenital deficiency. We also discuss some of the current avenues of investigation into its impact on other diseases and physiological states.     

The teaching of behavioural sciences

Summary. Medical science over the last few decades has undergone vast changes. Technologically it has advanced at a rapid pace. There has been a realization as well that the behaviour of individuals and communities also influences the occurrence of disease. Medical schools around the globe have realized the need for incorporating behavioural sciences as an integral part of the basic sciences taught to medical students.
This paper presents the experience of Christian Medical College, Veilore in teaching behavioural sciences. Students are taught sociology, psychology and medical anthropology through a community-based, problem-oriented teaching programme. The students have first-hand experience of living in a community and learn by observation and interaction. Pre- and post-assessment has shown a significant improvement of their knowledge and attitude. Feedback from students also indicates that they find this programme relevant and interesting.     

Quantitative analysis of macrophages and perisinusoidal cells in primary biliary cirrhosis

Immunohistochemistry and image analysis were used to quantify alterations in the Kupffer cell and 'activated' perisinusoidal cell populations in the different stages of primary biliary cirrhosis. Anti-CD68 macrophage antibodies were used to detect Kupffer cells, and anti-α-smooth muscle actin (α-SMA), PR 2D3 and anti-desmin antibodies to detect perisinusoidal cells. Liver biopsy material was available from 26 patients with primary biliary cirrhosis and 23 patients with histologically normal liver. Increased Kupffer cell numbers were observed in periportal/periseptal zones of stage 3 primary biliary cirrhosis ( n = 9), and in random parenchymal areas of stage 3 and stage 4 cases. Significantly increased 'activated' perisinusoidal cell numbers were seen only in periportal/periseptal zones of stage 3 and stage 4 primary biliary cirrhosis. Neither Kupffer cell nor perisinusoidal cell numbers altered significantly in stage 1 and 2 primary biliary cirrhosis ( n = 6). PR 2D3 positivity and increased α-SMA immunoreactivity by perisinusoidal cells in primary biliary cirrhosis support myofibroblastic differentiation of these cells. Human perisinusoidal cells, unlike their rodent counterparts, did not express desmin in primary biliary cirrhosis or control liver. Kupffer cell and 'activated' perisinusoidal cell accumulation in periportal/periseptal zones of the precirrhotic and cirrhotic primary biliary cirrhosis liver support the concept of Kupffer cell-mediated stimulation of perisinusoidal cells. Furthermore, these findings indicate that Kupffer cell–perisinusoidal interactions play an important role in the development of liver fibrosis and cirrhosis in primary biliary cirrhosis.     

Clinicopathological correlates of CD56 expression in multiple myeloma: a unique entity?

Summary. Prior studies have suggested that loss of plasma cell CD 5 6 expression in multiple myeloma defines a unique patient subset and that CD56 expression reliably discriminates between monoclonal gammopathy of undetermined significance (MGUS) and multiple myeloma (MM). We conducted a study of 68 untreated patients with MM from a single institution to define the clinicopathological correlates of CD56 expression. We find CD56 expression in 55% of MM. Lack of CD56 expression does not define a unique clinicopathological or prognostic entity in MM. Strong CD 5 6 expression can also be found in MGUS and does not help to distinguish from MM.