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Biomedical subjects

R M Pittilo

Publications and source records attributed to R M Pittilo.

At least 37 records · Page 2Linked to original sources

Repopulation of guinea-pig skin by melanocytes during wound healing: a morphometric study.

Epidermal keratinocytes and melanocytes have a close functional interrelationship. In order to study this relationship we used computer-assisted three-dimensional morphometry (CAM) to investigate the shape and size changes of the cutaneous melanocyte in healing guinea-pig skin. The combination of CAM with osmium iodide staining and resin embedding of tissue gave excellent results and allowed qualitative and quantitative morphometric assessment of melanocytes in vertical epidermal sections. The changes in melanocytes and keratinocytes during healing of a standard 1 cm full thickness wound in the guinea-pig were studied. After an initial decrease, more melanocytes per mm2 of epidermis were seen (from 36 days). These were smaller in volume with shorter, less branched dendrites compared to controls. An unexpected finding was a late phase of melanocyte proliferation, at the end of our study period (99 days). Clearly, the complex changes in the melanocyte-keratinocyte relationship during wound healing continue throughout and beyond the period of our study.

Animals↗

Effects of autologous mesothelial cell seeding on prostacyclin production within Dacron arterial prostheses.

Canine abdominal aortas have been replaced with Dacron arterial prostheses to assess the effects of mesothelial cell seeding on graft prostacyclin and thromboxane A2 release. At both 2 weeks and 6 weeks after surgery, three seeded and two unseeded control grafts were examined for prostacyclin release. In addition, thromboxane release was assessed in one seeded and one unseeded graft. Sections of aorta and graft were removed and incubated in PBS containing either 10 microM calcium ionophore A23187 or 20 microM arachidonic acid. The incubation mixture was sub-sampled at 5 min intervals over a 20 min period to assess the progressive release of prostacyclin and thromboxane A2 using a radioimmunoassay for 6-keto-prostaglandin F1 alpha and thromboxane B2 respectively. In seeded grafts, 6-keto-prostaglandin F1 alpha release averaged 15 per cent compared with aorta at 2 weeks and 45 per cent compared with aorta at 6 weeks. By contrast, release from unseeded grafts was undetectable at 2 weeks; however, by 6 weeks there was some release amounting to 15 per cent compared with aorta. There was a statistically significant increase in the release of 6-keto-prostaglandin F1 alpha from mesothelial cell seeded grafts at 6 weeks compared with unseeded grafts (P less than 0.01). Thromboxane release from the graft sections was variable and unrelated to whether the grafts had been seeded or not. These preliminary results, showing that grafts seeded with autologous peritoneal mesothelial cells release more prostacyclin than unseeded grafts, further highlight the role of the mesothelial cell as an alternative to the endothelial cell for improving the patency of arterial Dacron prostheses in the early postoperative days.

Animals↗

Ultrastructural observations of microgametogenesis in Eimeria bakuensis (Syn. E. ovina) of sheep.

The ultrastructure of microgametogenesis of Eimeria bakuensis was studied in the intestinal epithelium of an experimentally infected sheep. During development the nuclei became situated peripherally in the microgamont. Nuclear chromatin condensed into peripheral, dense portions that became the nuclei of the microgametes. The young microgamont was surrounded by a very narrow parasitophorous vacuole which widened during development and contained a few intravacuolar folds. Fissures and invaginations developed in the microgamont at the time the flagella began to grow. Polysaccharide granules were not present in the early and intermediate microgamonts but increased in number during the later stages and remained in the residual cytoplasm of the mature stage.

Animals↗

The effect of nicotine on human endothelial cell release of prostaglandins and ultrastructure.

The acute and sub-acute effects of nicotine at concentrations between 10(-9)M and 10(-2)M on human umbilical vein endothelial cell release of prostacyclin and prostaglandin E2 and the sub-acute effect on the endothelial cell ultrastructure have been examined. The acute effect of nicotine on prostaglandin release has been assessed by measuring release of prostacyclin and prostaglandin E2 following stimulation of confluent monolayers of endothelial cells with A23187 in the presence of nicotine. The sub-acute effect has been assessed by measuring A23187 stimulated release of prostacyclin and prostaglandin E2 from endothelial cells grown to confluence in the presence of nicotine. The cell monolayers were also examined for morphological and ultrastructural changes using light and electron microscopy. Nicotine treated and untreated cells released minimal amounts of prostaglandin E2. Concentrations of nicotine between 10(-9)M and 10(-4)M did not inhibit release of prostacyclin or induce morphological changes. Acute exposure to 10(-3)M nicotine resulted in a statistically significant inhibition of prostacyclin release, however, sub-acute exposure did not inhibit prostaglandin release or effect the cell morphology. Acute and sub-acute exposure to 10(-2)M nicotine resulted in a statistically significant inhibition of prostacyclin release. This was accompanied by the appearance of large translucent cytoplasmic inclusions which did not appear to be lipid rich as indicated by the negative uptake of oil-red-O and osmium tetroxide. This study shows that concentrations of nicotine comparable to the plasma levels of smokers (10(-9)-10(-6)M) do not induce morphological changes or effect the release of endothelial prostaglandins.

Calcimycin↗

Ultrastructural studies of the effects of amprolium and dinitolmide on Eimeria acervulina macrogametes.

Medication of chicks with 125 ppm amprolium or dinitolmide adversely affected oocyst sporulation of Eimeria acervulina (Weybridge strain). Dinitolmide delayed oocyst production and no oocyst wall formation was seen up to 168 h post infection. Both drugs caused large numbers of abnormally small wall-forming bodies to be produced in the macrogametes. In amprolium-fed chicks, abnormal oocyst wall formation was seen. It was concluded that the main drug action was against wall forming bodies of type 2.

Amprolium↗

The effects of nicotine on PGI2 production by rat aortic endothelium.

The production of prostacyclin by rat aortic rings was measured following administration of nicotine by a single subcutaneous injection and after continuous subcutaneous infusion over 7 days. Single subcutaneous injections of nicotine at 1, 5, 10 or 20 mg/kg had no effect on prostacyclin production by rat aortic rings in comparison with controls. However, aortic rings obtained after 7 days continuous subcutaneous infusion of 0.54 g/ml of nicotine at the rate of 1 microliter per hour produced significantly less prostacyclin than control animals.

Animals↗

Morphological effects of arprinocid on developmental stages of Eimeria tenella and E. brunetti.

Medication of chicks with 70 p.p.m. arprinocid in the food, starting 2 days prior to inoculation with Eimeria tenella, resulted in decreased oocyst production and oocyst sporulation. The main morphological alteration seen during the development of the second-generation schizont was a reduction in the number of second-generation merozoites due to incomplete merogony, resulting in large masses of vacuolated residual cytoplasm. In places around the developing macrogamete the integrity of the parasitophorous vacuole was lost by either the host cell limiting membrane making contact with the parasite pellicle, or the disruption of one or both of these surfaces apparently brought about by the intervention of the host cell mitochondria. Thirty p.p.m. arprinocid reduced sporulation of the oocysts of E. brunetti and caused enlargement of the perinuclear space in the late merozoites and swelling of the endoplasmic reticulum around wall-forming bodies II.

Adenine↗