Cholecystokinin is not a major regulator in the digestive system in the chicken

To find out whether physiological concentrations of cholecystokinin (CCK), a gastrointestinal hormone in mammals, are also active in chickens, the pancreatic amylase secretory response to CCK-8 was investigated in vitro. Rat pancreatic acini responded to the physiological concentration of CCK-8, but in chickens amylase release was induced at a concentration of CCK-8 1000 times higher than that observed in rats. In another experiment, biliary flow was tested with several doses of CCK-8. The bile flow was stimulated in a dose-dependent fashion, but a significant enhancement was not obtained at a concentration of 0.5 g CCK-8/kg body weight, which was considerably higher than physiological ones. It is concluded that endogeneous CCK does not have an important role in the digestive system in the chicken.     

Endocrine and exocrine pancreatic function after camostate-induced growth of the organ

It is well known that oral administration of camostate induces hyperplasia and hypertrophy of the rat pancreas. It is not clear, however, whether pancreatic hormone and enzyme secretion are affected by camostate treatment.In rats, daily administration of 200 mg camostate/kg b. wt for 14 days significantly increased pancreatic weight and pancreatic content of DNA, protein, amylase, lipase, trypsin and chymotrypsin, as well as the amount of insulin, glucagon and somatostatin. In the intact animal, blood glucose levels and serum concentrations of insulin and glucagon in response to an oral glucose load were not impaired after camostate treatment. In the isolated perfused pancreas, however, insulin and glucagon secretions were reduced, whereas somatostatin release was not affected. The volume of pancreatic juice produced by the unstimulated isolated perfused organ, as well as protein and enzyme secretion, were increased after camostate treatment. Likewise, the isolated perfused pancreas from camostate-treated rats secreted a larger volume of pancreatic juice and more protein in response to cholecystokinin (CCK), while enzyme secretion was affected in a non-parallel manner: amylase release was markedly reduced, lipase release was unchanged, and release of trypsin and chymotrypsin was increased.     

浅析操作系统微内核

阐述当前操作系统中流行的微内核体系结构。分析其具体功能结构，对比传统宏内核结构，总结出微内核在操作系统设计、实现及应用中的优势和劣势。针对微内核的低效率问题，结合当前较为成功的微内核设计思想和成型系统，给出了具体的性能改进方法。最后，在嵌入式操作系统广泛应用的背景下，给出了微内核实现嵌入式系统应用兼容性的基本思路。     

A novel exocrine gland inside the thoracic appendages (‘gemmae’) of the queenless antDiacamma australe

Summary In the queenless antDiacamma australe, all workers eclose with a pair of tiny thoracic appendages (gemmae). These are sac-like and exhibit a distinct cuticular sculpturing, with minute pores opening on the outer surface. These pores are connected to glandular cells which completely fill the appendages, and thus an exocrine stignal is likely to be released. We discuss the social context of this signal: only one worker in each colony retains the gemmae.     

The islet-acinar axis of the pancreas: Is there a role for glucagon or a glucagon-like peptide?

Intravenous glucagon inhibits exocrine pancreatic secretion in vivo, but exogenous glucagon does not affect exocrine secretion in vitro. Recent work, however, suggested that endogenous glucagon may be involved in the regulation of exocrine secretion even in vitro. We therefore investigated the effects of exogenous and endogenous glucagon on exocrine secretion by the isolated perfused rat pancreas in the presence of 1.8 mM glucose. Exogenous glucagon did not affect CCK-stimulated amylase output. 20 mM arginine stimulated glucagon release, but did not affect basal enzyme secretion. CCK-stimulated amylase output, however, was significantly inhibited in the presence of arginine. This inhibitory effect of arginine on exocrine pancreatic secretion could be blocked by glucagon antibodies, but not by nonspecific gammaglobulins. Thus exogenous glucagon failed to affect exocrine pancreatic secretion in vitro, but endogenously released glucagon or a glucagon-like peptide inhibited amylase release in the isolated perfused pancreas. We conclude that glucagon or a glucagon-like peptide may be a mediator in the islet-acinar axis.