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Biomedical subjects

D C Morris

Publications and source records attributed to D C Morris.

At least 91 records · Page 5Linked to original sources

Impaired gastric acid secretion in mast cell-deficient mice.

Gastric acid secretion in normal (+/+) C57B1/6J mice and congeneic, mast cell-deficient (mi/mi) C57B1/6J mice was examined. The mast cell-deficient animals had approximately 50% of the normal quantity of gastric histamine and a blunted basal acid level and secretory response. These observations were noted despite the presence of parietal cells, which were normal in number and morphology. The H2-antagonist ranitidine inhibited basal acid secretion in both groups of animals. Exogenous histamine induced a significant secretory response in normal and mast cell-deficient groups, but only the secretory response in normal animals could be blocked by the H2-antagonist. Treatment of mast cell-deficient animals with histamine for seven consecutive days before stimulation did not restore the histamine response to the normal (+/+) levels. The normal animals demonstrated an acid secretory response to pentagastrin. Mast cell-deficient mice also responded to pentagastrin, but the response was less than that observed in the normal animals, and a significant difference was not evident in all experiments. Furthermore, simultaneous injection of mast cell-deficient animals with histamine and pentagastrin did not restore pentagastrin responsiveness to normal levels, although the histamine concentration used was sufficient to raise acid secretion to basal levels of normal mice. These results support the conclusion that non-mast cell histamine only partially contributes to basal gastric acid secretion and is insufficient to facilitate full parietal cell responsiveness. Furthermore, pentagastrin requires the presence of mast cells to elicit a maximal secretory response but can use non-mast cell histamine to activate the parietal cells for acid secretion.

Animals↗

Failed elective percutaneous transluminal coronary angioplasty requiring coronary artery bypass surgery. In-hospital and late clinical outcome at 5 years.

This study was performed to define the in-hospital and late clinical outcome at 5 years in 430 patients who had a failed elective percutaneous transluminal coronary angioplasty (PTCA) and underwent coronary artery bypass graft (CABG) surgery during their hospitalization. This group comprised 5.9% of 7,246 patients undergoing elective PTCA. CABG surgery was performed in 346 patients with ongoing myocardial ischemia (80.5%) and in 84 patients without ischemia (19.5%). Their mean age was 56 +/- 9 years, and 76.3% were male. One-vessel disease was present in 72.3%, and the mean left ventricular ejection fraction was 59 +/- 11%. Overall, 1.9 +/- 0.9 bypass grafts were placed. There was increased use of the internal thoracic artery in the nonischemic group. A new nonfatal postprocedural Q wave myocardial infarction occurred in 21.2% and occurred more frequently in the ischemic (25.4%) than in the nonischemic (3.6%) group (p less than 0.0001). There were six in-hospital deaths (1.4%), an incidence that did not differ between the two groups. Follow-up was 99.8% complete. There were 25 deaths (93.2 +/- 1.5%, 5-year survival), including 16 of cardiac cause (95.3 +/- 1.3%, 5-year cardiac survival). Q wave myocardial infarction occurred in 111 patients (91 in-hospital), and freedom from cardiac death or nonfatal myocardial infarction at 5 years was 71 +/- 3%. In the group going to CABG surgery with ongoing ischemia, the 5-year cardiac survival was 94.9 +/- 1.6%, and in the group without ischemia, the corresponding survival was 96.2 +/- 2.2%. By multivariate analysis, the presence of preoperative myocardial ischemia, pre-PTCA diameter stenosis less than 90%, and the presence of multiple-vessel disease correlated with the occurrence of cardiac death or nonfatal myocardial infarction at 5 years. At this large-volume center with extensive PTCA operator and surgical experience, the excellent survival and low event rates over 5 years support the concept that despite the failed elective PTCA procedure, there was little effect on long-term survival provided the patient underwent prompt successful surgical revascularization.

Aged↗

It could never happen here!

Any disaster represents a reactive situation. The key in disaster recovery is to limit this reactive period by quickly evaluating the damage and then implementing the contingency plan. All action should be known and planned. In this way, management can deal with the crisis, and operations can be restored efficiently and effectively.

Disaster Planning↗

Laser-assisted transluminal angioplasty of the superficial femoral and popliteal arteries.

During an initial 1-year experience with percutaneous laser-assisted balloon angioplasty at the Vancouver General Hospital, 9 of 61 patients considered suitable for intervention because of arterial occlusive disease were selected for laser treatment. The neodymium-YAG laser with a contact sapphire tip was chosen because the probes and tips are reusable, thereby reducing the cost per patient. The patients had either severe limiting claudication or pain at rest, involving the superficial femoral or popliteal artery. One of the patients had lesions in both legs, making a total of 10 lesions. In 8 of the 10 lesions, treatment initially was successful. In the other two instances, the laser perforated the arterial wall, but the patients suffered no ill effects; repair by bypass surgery was uncomplicated. Another patient had distal thrombosis at the time of angioplasty of the popliteal artery; this responded to fibrinolytic therapy and subsequent balloon angioplasty of the peroneal artery. The initial 80% success rate was reasonable, considering that all these patients would otherwise have undergone bypass surgery. One patient had recurrent stenosis 5 months after the procedure. The other seven had good results with relief of symptoms. However, follow-up has been short (mean 4.9 months), the longest being only 11 months.

Aged↗

Matrix vesicle biogenesis in vitro by rachitic and normal rat chondrocytes.

Calcifying matrix vesicles (MVs) are released from chondrocytes and osteoblasts in monolayer culture. In the present studies, we tested the ability of rachitic versus normal rat growth plate chondrocytes in micromass or monolayer primary cultures to produce MVs. Unlike earlier reports of in vitro MV biogenesis by chicken chondrocytes in which most MVs were released into the medium, we found that most of the released rat matrix vesicles were entrapped in a newly formed cartilaginous matrix enveloping the cells. These matrix-associated MVs could be isolated by mild collagenase treatment and concentrated by differential centrifugation. Vesicle production slowed in the older 2- to 4-week-old cultures and, unlike vesicle release from cultured chicken chondrocytes, active vesicle production did not show a second burst of activity at 3 to 4 weeks. Alkaline phosphatase (ALP) activity diminished with time in culture in cells and matrix vesicles, suggesting a decrease in differentiative expression. Protein profiles on SDS polyacrylamide gels of native matrix vesicles and culture-derived MVs from rachitic and normal cells were quite similar and showed a typical simplified protein pattern as compared to chondrocyte plasma membrane proteins. There were distinctive proteins migrating at 130, 80 to 95, 66, 43, 20, and 14 kd. Culture-derived MVs showed vigorous in vitro calcifying activity that was ALP related. We conclude that 1) rachitic chondrocytes are essentially normal in their matrix vesicle production; 2) matrix entrapment of MVs is a characteristic of rat chondrocyte cultures; and 3) culture-produced MVs are similar to native MVs in protein profile and calcifiability, and thus can be studied as a model for normal MV composition and calcification.

Animals↗

Heterotopic ossification: a case report and immunohistochemical observations.

This report describes the case of a 69-year-old man with adenocarcinoma of the transverse colon who developed heterotopic ossification in a metastatic axillary lymph node. The areas of pathologic bone formation were characterized by the appearance of osteoblast-like cells at the surfaces of the mineral deposits. Immunostaining for alkaline phosphatase revealed a significant concentration of this enzyme in these cells and, to a lesser degree, on the apical membrane of the glandular cells of the adenocarcinoma adjacent to the ossification centers. Proliferating mesenchymal cells in close proximity to the areas of osteogenesis also showed significant immunolabeling. We conclude that metastatic colonic carcinoma can promote heterotopic ossification, and that alkaline phosphatase is intimately associated with bone formation under these pathologic conditions.

Adenocarcinoma↗

Pacemaker electrode repositioning using the loop-snare technique.

Using a percutaneous femoral vein approach under fluoroscopic control, a malpositioned ventricular pacemaker electrode was released from the right ventricular wall by hooking the lead with a deflecting wire inserted into a RIM catheter. A closed loop was formed by tightening the handle of the wire allowing the electrode to be dislodged and pulled into the inferior vena cava. The electrode was then snared using a loop formed by an exchange wire advanced through an 8 French catheter with a J-curve steamed at its tip. The electrode was advanced to the right ventricular apex and released by advancing one end of the snare wire while pulling the other end to open the loop.

Aged↗

Presence and activity of alkaline phosphatase in two human osteosarcoma cell lines.

The presence and activity of alkaline phosphatase in SAOS-2 and TE-85 human osteosarcoma cells grown in culture were examined at the ultrastructural level. A monoclonal antibody raised against purified human bone osteosarcoma alkaline phosphatase was used to localize the enzyme in cultures of the osteosarcoma cells. Similar cultures were analyzed for alkaline phosphatase activity using an enzyme cytochemical method with cerium as the capture agent. Alkaline phosphatase was immunolocalized at the light microscopic level in an osteogenic sarcoma and ultrastructurally on the SAOS-2 cell membrane and the enclosing membrane of extracellular vesicular structures close to the cells. In contrast, the TE-85 cells were characterized by the absence of all but a few traces of immunolabeling at the cell surface. Enzyme cytochemical studies revealed strong alkaline phosphatase activity on the outer surface of the SAOS-2 cell membrane. Much lower enzyme activity was observed in the TE-85 cells. The results support biochemical data from previous studies and confirm that SAOS-2 cells have a significantly greater concentration of alkaline phosphatase at the plasma membrane.

3,3'-Diaminobenzidine↗

LANs today.

Comparing long lists of functions, argue these authors, is not the best way to choose a LAN. Instead, the key is that the LAN must support your hospital's environment. You must dictate that environment's characteristics, and then select the LAN that best suits your specific needs.

Computer Systems↗

Matrix vesicles and calcification of rachitic rat osteoid.

Tibiae from rachitic weanling rats were studied during healing to examine the mechanism of bone mineralization. Rickets was induced by feeding the animals a low phosphate, low vitamin D diet for five weeks. Calcification was reinstituted in three ways; group I animals received 1.0 ml of NaH2PO4 i.p. and the rachitogenic diet in a darkened room; group II animals were placed in a lighted room and given standard laboratory chow; group III animals were placed in lighted room, given standard laboratory chow and received 1.0 ml of 0.1M NaH2PO4 i.p. Group I healed slowly while II and III were found to heal rapidly and at nearly identical rates. Groups II and III revealed a significantly elevated serum alkaline phosphatase activity and became hyperphosphatemic as the rickets healed suggesting a more vigorous recovery. Ultrastructurally, numerous matrix vesicles were noted in unhealed rachitic bone matrix and these structures acquired mineral upon initiation of healing. Vesicle-associated mineral aggregates increased in size penetrating through and beyond the vesicle membrane and were incorporated into the advancing mineralization front. By 48 hrs. post-healing initiation, the osteoid borders were almost completely mineralized in groups II and III. These observations suggest that in addition to pre-existing mineral, matrix vesicles can also serve as nucleating sites in the osteoid of post-fetal bone.

Alkaline Phosphatase↗

Early noninvasive detection of successful reperfusion in patients with acute myocardial infarction.

Myoglobin (Mb) is a protein that enters rapidly and is rapidly cleared from plasma after coronary reperfusion. We sought to determine the accuracy with which a rapid rise in plasma [Mb] could predict successful coronary artery reopening in patients undergoing coronary arteriography in conjunction with attempted reperfusion in acute myocardial infarction. In 42 patients, plasma Mb levels were measured before and for at least 4 hours after attempted reperfusion. Thirty-five patients were successfully reperfused. In each, the plasma Mb level rose rapidly with peak [Mb] occurring at 111 +/- 8.1 (+/- SEM) minutes after application of therapy. In contrast, Mb levels rose more slowly in the seven patients who were not reperfused, with peak [Mb] occurring 360 +/- 61.4 minutes after attempted reperfusion. T25-100 (the time required for [Mb] to rise from 25% to 100% of peak value) was shorter in patients successfully reperfused (71 +/- 7.9 minutes) and longer (341 +/- 35.3 minutes) in patients in whom therapy was unsuccessful. A rapid rise in [Mb] after successful reperfusion was also evident by a more than 4.6-fold rise in [Mb] over the first 2 hours after reperfusion in all but five patients; in contrast, [Mb] rose by less than 4.6-fold over this same interval in every patient not successfully reperfused (sensitivity, 85%; specificity, 100%; predictive accuracy, 88%). We conclude that a rapid rise in plasma Mb level over the initial 2 hours after attempted reperfusion in acute myocardial infarction provides a useful index of successful reperfusion.

Adult↗

Light microscopic localization of alkaline phosphatase in fetal bovine bone using immunoperoxidase and immunogold-silver staining procedures.

We localized alkaline phosphatase in the metaphyses of fetal bovine tibial bone by use of avidin-biotin-immunoperoxidase and immunogold-silver staining procedures. Low melting-point, paraffin-embedded sections of periodate lysine-paraformaldehyde-fixed undecalcified bone were used for immunostaining. We suggest that the combination of intact embryonic bone with this fixative and the immunohistochemical procedures used in this study may have helped to preserve antigenicity and thus to improve the efficiency of immunolabeling. Similar patterns of alkaline phosphatase localization were produced by the immunoperoxidase and immunogold-silver staining methods. The latter, although free of immunoreagents such as diaminobenzidine, must be monitored closely to avoid nonspecific staining during the silver enhancement procedure. Both methods revealed a concentration of the enzyme in osteoblasts and in areas of osteoid that lined the bone trabeculae. The results support the findings of earlier enzyme cytochemical studies in which osteoblasts were shown to have significant alkaline phosphatase activity.

Alkaline Phosphatase↗

A quiet evolution.

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Hospital Information Systems↗