A primary cilium was frequently observed in the endocrine alpha, beta and delta cells, as well as in the excretory duct cells of the pancreas of normal mice and rats. The characteristic components of the cilium including the basal body, axoneme (shaft), and terminal part were clearly recognizable. The basal body or distal centriole surrounded by Golgi vesicles was perpendicularly oriented to the proximal centriole, and a dense striated band was seen filling the gap between them. The microtubules of the basal body consisted of nine peripheral triplets exhibiting a 9 + 0 pattern, an appearance similar to that of the proximal centriole. Rootlets, basal feet and alar sheets associated with the basal body were occasionally seen. The axoneme usually consisted of a 9 + 0 pattern of microtubule doublets, but other irregular patterns of 7 + 2, 7 + 3, and 8 + 1 were also seen. The microtubules in the terminal part of the cilium became fewer in number and had no peculiar arrangement. The cilium of the endocrine cells always projected into the intercellular canaliculus and was covered by the ciliary sheath, and occasionally, double cilia were visualized in the vicinity of beta cells. In the excretory duct cells, the cilium showed similar features, but it was slightly longer and always projected into the dense secretory content of duct lumen. On the other hand, no primary cilium was ever observed in the acinar cells of mouse and rat pancreas. In conclusion, the present study describes the morphology of primary cilia and its associated components in the endocrine and excretory duct cells of the pancreas of mice and rats. The findings suggest that the primary cilium should be considered as a constant intracellular organelle though its function and significance remain speculative.

The ultrastructural changes in the morphology of the islets of Langerhans in response to streptozotocin were studied in the mice pancreas. Male white albino CSI mice were given a single intravenous injection of 75 mg kg(-1) body weight streptozotocin, and were sacrificed at different time intervals up to 48 h following the treatment. Their pancreases were excised and randomly processed for electron microscopic examination. Hyperglycaemia and glucosuria were detected 8 h after treatment, became remarkably high at 24 h and persisted then after. Light and electron microscopic examination of the islets of Langerhans from treated mice revealed an early chromatin aggregation and cytoplasmic vesiculation in the central B cells during the first 2 h of treatment. Nuclear shrinkage and pyknosis with swelling of mitochondria and endoplasmic reticulum were evident 8 h later, and lysis of B cells occurred 12 h after treatment. The morphology of A and D cells at the margin of the islets and in between B cell debris looked perfectly unaltered. Macrophage infiltration among lytic B cells was seen 24 h after drug administration, which contained clear and large phagocytic vacuoles. The necrobiotic and phagocytic figures disappeared from the pancreatic sections of 48 h treated mice, and the islets were smaller in size and consisted entirely of intact A and D cells with occasional degranulated B cells. No features of apoptosis were ever recorded, and the exocrine pancreatic tissue was protected from the effect of streptozotocin. In conclusion, the present study illustrates the sequence of morphological changes that occurs in the islets of Langerhans of mice after streptozotocin administration. It also confirms that streptozotocin at a high single dose in mice produces a specific necrosis of B cells with no evidence of apoptotic figures as another mechanism of cell death.

The efficacy of daily versus twice weekly and once weekly oral iron therapy was analyzed to optimize a protocol for treatment of IDM among Jordanian children. One hundred and forty-eight children aged between 6 and 60 months with Hb estimate less than 11 gm/dl were screened. They were randomly divided into three regimens of oral iron therapy for a period of 12 weeks; a group was supplemented with a single weekly dose of iron; a second group received two doses weekly; and a third group had a daily dose of iron. Hb was assayed 3 and 12 weeks after therapy, while ferritin was assayed after 12 weeks of treatment. A significant rise in Hb concentration was observed which was most significant 12 weeks after treatment. Iron supplementation after 3 weeks was similar in all treated groups, and no significant difference in Hb concentration among the three groups was noticed. By the end of the third week, the anemia had respectively resolved by 18, 11.8 and 23.4% in the daily, twice weekly, and once weekly groups. On the other hand, the percentage of recovery of anemia respectively was 78, 90.2 and 74.5% at the end of 12 weeks of iron therapy. Hb recovery percentage was comparable in the three treated groups, and no significant difference was reported between them either at 3 or at 12 weeks of therapy. Ferritin levels in the daily and twice weekly treated groups were similar after 12 weeks of iron therapy and were significantly higher than the ferritin levels of weekly treated group. Although the anemia in the three treated groups was resolved after 3 and 12 weeks of oral iron therapy, we conclude that the regimen of two doses per week is the most effective in resolving anemia with less cost and fewer side effects.

The size, number and volume per cell of secretion granules in rat exocrine pancreas have been measured using stereological techniques. The changes which occur as a result of feeding starved animals (90 min) or stimulating lobular fragments in vitro with carbachol are documented. In fasted animals mean acinar cell volume was estimated as 1670 micron 3 and the cells contained an average of around 450 secretion granules with a corrected mean diameter of 0.70 micron. They occupied around 7% of cell volume. After feeding mean cell volume was about 1300 micron 3 and the cells contained an average of about 190 granules per cell with a mean diameter of 0.58 micron. They occupied 3% of cell volume. A shift in the size frequency distribution of granule diameters occurred as a result of feeding. In vitro experiments in which lobules were induced to secrete with carbachol (10 microM, 3 h, 37 degrees C) had a similar effect. Mean cell volume was reduced from around 1760 micron 3 to 1360 micron 3, mean granule number from around 420 per cell to 180 per cell and the volume density of granules was reduced from about 8% to 3% of cell volume. There was no significant change in mean granule diameter or shift in the size-frequency distribution of granule diameters. Incubation of tissues with cycloheximide (1 mM, 3 h, 37 degrees C) did not prevent secretion by carbachol but it prevented replacement of granules. As a consequence, depletion by carbachol was greater in the presence of cycloheximide, the granules being reduced to around 110 per cell and to only 2.5% of cell volume. We conclude that feeding causes a preferential loss of larger granules and that during secretion replacement of granules occurs. Some of these granules are smaller than those evident in the glands of starved animals.

The number, volume, and size of zymogen granules in pancreatic acinar cells of normal and streptozotocin-diabetic rats were measured using stereological techniques. These morphometric data were then correlated with the amylase activity of the acinar cells. In the normal rats, the acinar cells had a mean volume of 1,253.5 Km' and contained 343 zymogen granules, which occupied a volume of 103 pm' of the cell (8.28%). In the diabetic rats, the mean acinar cell volume was estimated as 1,017 km3 and the cell contained 220 zymogen granules, which occupied a volume of 55.8 pm' (5.38%). The cell volume and zymogen granule number and volume were 19, 36, and 46%. respectively, more in normal rat pancreas, while no difference in the size of zymogen granules