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Biomedical subjects

S A Miller

Publications and source records attributed to S A Miller.

At least 91 records · Page 5Linked to original sources
PubMed1994

Program management and health care informatics: defining relationships.

The program management (PM) structure is a relatively well-known organizational model for hospitals. A variation of the matrix structure, it allows for an interdisciplinary team of health care providers to facilitate patient care delivery. However, providing such focused care results in a complex, highly information-dependent operational environment. To meet the information needs of such an environment, careful planning in selecting and implementing technology is required. Along with supporting patient care, the technology will also help in managing costs, human resources, quality and utilization, as well as in monitoring performance and outcomes measurement. Focusing specifically on the information technology environment, this article addresses health care informatics (the diverse categories of information and systems) needed to support clinical program managers, executives and others in a PM organization. Examples from both a university-affiliated and a community-based program managed hospital illustrate their approach to PM and information technology.

Decision Support Systems, Management↗
PubMed1994

Anti-insulin antibodies are a cause of hypoglycemia following pancreas transplantation.

OBJECTIVE: Hypoglycemic symptoms have been reported by more than half of pancreas transplantation (PTX) recipients. To better understand the mechanism for the hypoglycemia documented in some of these patients, we studied the glucose and pancreatic hormone response to Sustacal in patients with and without hypoglycemia following PTX. RESEARCH DESIGN AND METHODS: Twelve patients with established, repeated episodes of hypoglycemia following PTX (hypo) were case-matched to PTX recipients without hypoglycemic symptoms (control; n = 7). On the day of the study, fasting glucose, free and total immunoreactive insulin (IRI), C-peptide, proinsulin, and glucagon were drawn (time 0); Sustacal was administered; and glucose, free and total IRI, and C-peptide were assayed at 15, 30, 45, 75, 120, 150, 180, and 240 min. Based on the glucose response to Sustacal, the hypo group was further divided into those whose glucose rose after Sustacal (hypo-high; n = 7) and those with no increase in glucose from baseline concentration (hypo-flat; n = 5). RESULTS: Before the administration of Sustacal, the hypo-high group had a lower fasting free/total IRI (0.26 +/- 0.06, mean +/- SE) than the hypo-flat (0.51 +/- 0.02) or control (0.52 +/- 0.04) groups (both P < 0.05 compared with hypo-high). The glucose response to Sustacal was greatest in the hypo-high group as defined. Area under the curve (AUC) for total IRI following Sustacal was also greatest in the hypo-high group (P < 0.05 compared with both control and hypo-flat groups), but there was no significant difference in free IRI AUC following Sustacal between the three groups. Two individuals developed hypoglycemia during the Sustacal challenge, both in the hypo-high group. CONCLUSIONS: The lower fasting free/total IRI ratio and greater increase in glucose and total IRI in response to Sustacal in the hypo-high group compared with either the hypo-flat or control groups are consistent with the presence of significant quantities of anti-insulin antibodies in the hypo-high group. Because anti-insulin antibodies are, in turn, an established cause of episodic hypoglycemia, this study provides the first data to support the hypothesis that significant quantities of anti-insulin antibodies are a cause of symptomatic hypoglycemia following PTX in some recipients.

Adult↗
PubMed1994

Immediate and delayed apoptotic cell death mechanisms: UVA versus UVB and UVC radiation.

The mechanism of cell death induced by the different waveband regions of ultraviolet radiation (UVR), i.e., UVA1 (340-400 nm), UVB (290-320 nm) and UVC (200-290 nm) was investigated, using equilethal doses (90% reproductive death) on L5178Y-R murine lymphoma cells. To distinguish between necrosis and apoptosis, the following endpoints were monitored over time using flow cytometry and transmission electron microscopy: percentage of remaining cells, membrane permeabilized cells, dead cells, apoptotic cells, and ultrastructural changes. All waveband regions of UVR were found to cause apoptosis as opposed to necrosis. However, UVA1-induced immediate (0-4 h) apoptosis, while UVB- or UVC-induced delayed apoptosis (<34 h). Moreover, the membrane permeability changes that only result from exposure to UVA1 radiation, especially to red blood cells, suggests that the immediate apoptotic mechanism involves membrane damage. Therefore, the results suggest that there are three death mechanisms available to one cell type: necrosis, immediate apoptosis, and delayed apoptosis (or programmed cell death).

Journal Article↗
PubMed1993

Role for differential cell proliferation in perforation and rupture of chick pharyngeal closing plates.

Patterns of cell proliferation show two distinct domains around avian pharyngeal closing plates as they form, perforate, and rupture. Pouch endoderm and groove ectoderm are in one domain showing 81-86% proliferation, which suggests relatively rapid growth. Cells in epithelia that comprise the pharyngeal closing plates contiguous with pouch and groove epithelia are vital but are dividing at a significantly lower percentage (62-64%). This phenomenon is similar to the lag in growth reported for cells in the oral membrane around the time of rupture (Miller and Olcott, 1989: Anat. Rec., 223:204-208), is consistent with Waterman's suggestion (1985: Anat. Rec., 211:450-457) that cellular reorganization, rather than massive degeneration, is a major mechanism of initial perforation, and suggests that differential growth is a contributor to performation and rupture of chick pharyngeal closing plates.

Animals↗
PubMed1993

Efficacy of physostigmine as a pretreatment for organophosphate poisoning.

Continuous administration of the carbamate physostigmine, producing approximately 40% serum cholinesterase (ChE) inhibition, provides significant protection against the lethal effects of the organophosphorous nerve agent pinacolyl methylphosphonofluoridate (soman). Rats pretreated with physostigmine were also protected against the development of cholinergic symptoms and loss of body weight. Soman and physostigmine both inhibit ChE, yet animals pretreated with physostigmine exhibited less ChE inhibition in serum and brain than did animals exposed to soman alone. In addition, there did not appear to be any additive effect of presenting both anticholinesterases simultaneously. To further examine the effectiveness of physostigmine, we compared the results of this study with previously collected pyridostigmine data from our laboratory. This comparison indicates that physostigmine is more effective than pyridostigmine in protecting against the detrimental effects of soman.

Animals↗
PubMed1993

Behavioral toxicity of anticholinesterases in primates: chronic physostigmine and soman interactions.

Dose rates for continuous infusion of physostigmine salicylate required to inhibit 30 and 60% of normal serum cholinesterase activity in rhesus monkeys were determined. The effects of continuous physostigmine infusion at these dose rates on the behavioral toxicity of daily repeated low-dose soman were determined not to be deleterious; in fact, they were slightly (and variably) protective.

Animals↗
PubMed1993

A comparative analysis of results and morbidity in type I diabetics undergoing preemptive versus postdialysis combined pancreas-kidney transplantation.

Although combined pancreas-kidney transplantation (PKT) has become a valid treatment option for selected type I diabetics, the timing of PKT relative to the degree of nephropathy remains controversial. We analyzed results and morbidity in 30 type I diabetics undergoing PKT after starting dialysis (PKT:D) versus 31 type I diabetics undergoing PKT prior to dialysis (PKT:ND). The two groups were similar with the respect to age, duration and severity of diabetes, gender, race, preservation time, retransplants, sensitization, HLA-matching, and CMV status. The mean preoperative serum creatinine was higher in the PKT:D group (9.9 +/- 3.4 vs. 3.9 +/- 1.9 mg/dl PKT:ND, P < 0.01). All patients were managed with quadruple immunosuppression with OKT3 induction. Actuarial patient survival is 100% (PKT:D) and 96.8% (PKT:ND). Renal and pancreas allograft survival are 97% and 93%, respectively, in both groups. The incidence of rejection, infection, operative complications, reflux pancreatitis, and total hospital days was similar in both groups. Long-term renal and pancreas allograft function and quality of life were like-wise comparable. No adverse coagulation or immunologic effects were noted in the PKT:ND group. Rehabilitation potential favored the PKT:ND group. PKT can be performed safely and effectively in the absence of uremia. In selected type I diabetics with significant nephropathy, we believe that PKT is the best treatment option and need not be considered as preemptive, especially in view of increasing waiting times and the variable progressive nature of diabetic complications.

Adult↗
PubMed1993

Long-wavelength UVA radiation induces oxidative stress, cytoskeletal damage and hemolysis.

We investigated the ability of the different wavelength regions of UV radiation, UVA (320-400 nm), UVB (290-320 nm) and UVC (200-290 nm), to induce hemolysis. Sheep erythrocytes were exposed to radiation from either a UVA1 (> 340 nm) sunlamp, a UVB sunlamp, or a UVC germicidal lamp. The doses used for the three wavelength regions were approximately equilethal to the survival of L5178Y murine lymphoma cells. Following exposure, negligible hemolysis was observed in the UVB- and UVC-irradiated erythrocytes, whereas a decrease in the relative cell number (RCN), indicative of hemolysis, was observed in the UVA1-exposed samples. The decrease in RCN was dependent on dose (0-1625 kJ/m2), time (0-78 h postirradiation) and cell density (10(6)-10(7) cells/mL).. Hemolysis decreased with increasing concentration of glutathione, hemoglobin or cell number, while the presence of pyruvate drastically enhanced it. Because scanning spectroscopy (200-700 nm) showed that hemoproteins and nicotinamide adenine dinucleotides were oxidized, cytoplasmic oxidative stress was implicated in the lytic mechanism. Further evidence of oxidation was obtained from electron micrographs, which revealed the formation of Heinz bodies near the plasma membrane. The data demonstrate that exposure of erythrocytes to UVA1, but not UVB or UVC, radiation causes oxidation of cytoplasmic components, which results in cytoskeletal damage and hemolysis.

Animals↗
PubMed1993

Non-nuclear damage and cell lysis are induced by UVA, but not UVB or UVC, radiation in three strains of L5178Y cells.

The potential to induce non-nuclear changes in mammalian cells has been examined for (1) UVA1 radiation (340-400 nm, UVASUN 2000 lamp), (2) UVA+UVB (peak at 313 nm) radiation (FS20 lamp), and (3) UVC (254 nm) radiation (G15T8 lamp). The effects of irradiation were monitored in vitro using three strains of L5178Y (LY) mouse lymphoma cells that markedly differ in sensitivity to UV radiation. Comparisons were made for the effects of approximately equitoxic fluences that reduced cell survival to 1-15%. Depending on the cell strain, the fluences ranged from 830 to 1600 kJ/m2 for the UVASUN lamp, 75 to 390 J/m2 for the FS20 lamp and 3.8 to 17.2 J/m2 for the G15T8 lamp. At the exposure level used in this study, irradiation with the UVASUN, but not the FS20 or G15T8, lamp induced a variety of non-nuclear changes including damage to cytoplasmic organelles and increased plasma membrane permeability and cell lysis. Cell lysis and membrane permeabilization were induced by the UVA1 emission of the UVASUN lamp, but not by its visible+IR components (> 400 nm). The results show that the plasma membrane and other organelles of LY cells are highly sensitive to UVA1 but not to UVB or UVC radiation. Also UVA1, but not UVB or UVC radiation, causes rapid and extensive lysis of LY cells. In conclusion, non-nuclear damage contributes substantially to UVA cytotoxicity in all three strains of LY cells.

Animals↗
PubMed1993

Activation of the human immunodeficiency virus promoter by UVA radiation in combination with psoralens or angelicins.

The effects of mono- and bifunctional furocoumarins plus UVA radiation (PUVA and related treatments) on the human immunodeficiency virus-1 (HIV-1) promoter were studied using HeLa cells stably transfected with the chloramphenicol acetyl transferase gene under the control of the HIV-1 promoter. The experiments were performed with three psoralens (5-methoxypsoralen, 5-MOP; 8-methoxypsoralen, 8-MOP; and 4'-aminomethyl-4,8,5'-trimethylpsoralen, AMT) and four angelicins (angelicin; 4,5'-dimethylangelicin, 4,5'-DMA; 6,4'-dimethylangelicin, 6,4'-DMA; and 4,6,4'-trimethylangelicin, TMA). The drugs alone and UVA radiation alone showed no effect on the HIV promoter. However, when the cells were incubated with the furocoumarins at 0.1-40 micrograms/mL and then irradiated, the HIV promoter was activated in distinct fluence ranges, i.e. (1) no promoter activity was discernible at low fluences (e.g. at 0.1 microgram/mL of 8-MOP up to 100 kJ/m2), (2) as the fluence was increased, the promoter activity increased to reach a maximum (10-50-fold with respect to the unexposed samples), and (3) as the fluence was further increased, the promoter activity decreased. Similar (although shifted on the fluence scale) patterns were observed with either > 340-nm UVA radiation or with UVA radiation contaminated with a small amount of UVB radiation (typical for PUVA lamps). The effective fluences were inversely related to the drug concentration. Experiments with 5-MOP and 8-MOP indicated reciprocity of the drug concentration and radiation fluence. The HIV promoter response patterns were similar for monofunctional angelicins and bifunctional psoralens.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Survival↗
PubMed1993

The analysis of benefit and risk of combined pancreatic and renal transplantation versus renal transplantation alone.

Currently, diabetes mellitus is the most common cause of renal failure in adults. However, combined pancreatic and renal transplantation (PRT) remains controversial when compared with renal transplantation alone (RTA) in diabetic recipients. We analyzed the results and morbidity in four age-matched groups--31 patients with Type I diabetes undergoing PRT before dialysis, 30 patients with diabetes who are dependent of dialysis undergoing PRT, 31 concurrent and historic patients with Type I diabetes undergoing RTA and 31 concurrent patients without diabetes undergoing RTA. All patients received cadaver donor organs and were managed with cyclosporine and prednisone immunosuppression with selective OKT3 induction. The four groups were comparable with respect to age, weight, gender, duration and severity of diabetes, dialysis type, number of retransplants, degree of sensitization, preservation time and matching. The groups differed with regard to duration of dialysis and period of follow-up evaluation, pretransplant blood transfusions, racial distribution and OKT3 induction therapy. PRT was associated with a greater morbidity rate as evidenced by a slightly higher incidence of rejection, infections and reoperations. The number of readmissions and hospitalization period during the first 12 months was also greater after PRT versus RTA. However, none of these differences were significant. No detrimental effect was noted on renal allograft function at one year; patient and graft survival was actually higher in the PRT groups. Quality of life was improved in nearly 90 percent of PRT recipients. Although the improved results after PRT may be attributed to selection bias, only lesser differences were noted among the four study groups. The aforementioned data suggest that appropriate patient selection can overcome the morbidity associated with PRT, resulting in excellent patient and graft survival with the potential for complete rehabilitation.

Actuarial Analysis↗