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Biomedical subjects

A C Sullivan

Publications and source records attributed to A C Sullivan.

At least 19 recordsLinked to original sources
PubMed2006

Electrohydrodynamic atomization: an approach to growing continuous self-supporting polymeric fibers.

The investigation presented in this paper illustrates a technique for growing in-situ polymerized networks, forming scaffold-like structures usually formed by means of electrospinning. The technique of jet atomization employing electrohydrodynamics is a manifestation of electrospinning. However, we show for the first time that using this technique where individual droplets are generated, a continuous self-supporting submicrometer web-like structure can be grown whereby fragments of the structure are delivered in the droplets and polymerize on the surface of the growing structure via polycondensation. The development of these growing fibers into web structures is a direct result of the processing route together with the excellent tailor-made cross-linking nature of the resin. An operational map is generated to identify a parametric space in which the stable cone-jet mode of electrohydrodynamic atomization prevails for generating the finest droplets. A statistical analysis on the formed fibers for a given time and electrospray condition is presented together with optical micrographs of the structure, which concludes the discussion in this paper.

Journal Article↗
PubMed1996

Purification and characterization of an insulin-stimulated insulin receptor serine kinase.

In cells, insulin stimulates autophosphorylation of the insulin receptor on tyrosine and its phosphorylation on serine and threonine by poorly characterized kinases. Here we describe methods for the purification of an insulin-stimulated insulin receptor serine kinase from human placenta and rat liver by sequential chromatography of solubilized membranes on wheat germ agglutinin-agarose, Mono Q, phenyl-Superose, and Superose 12. On silver-stained SDS-polyacrylamide gels, the resulting kinase was homogeneous (human) or near-homogeneous (rat) and had an apparent M(r) of 40000. The apparent M(r) determined by gel filtration was also 40000, suggesting that the kinase exists as a monomer. The kinase could be reconstituted back to the insulin receptor stripped of the kinase to yield a high stoichiometry of serine phosphorylation of the insulin receptor in the presence of insulin (0.75 +/- 0.15 mol/mol of beta-subunit, mean +/- SEM, n = 3). The activity of the reconstituted kinase toward the insulin receptor was insulin-regulated, being stimulated > 5-fold by insulin. Insulin increased the catalytic activity of the reconstituted kinase. The purified kinase specifically phosphorylated serine 1078 of the insulin receptor, a major site of insulin-stimulated serine phosphorylation in vivo, showing that the purified kinase phosphorylated a physiologically relevant site on the insulin receptor. Phosphorylation of serine 1078 of the insulin receptor to high stoichiometry by the kinase did not affect insulin-stimulated exogenous protein tyrosine kinase activity of the insulin receptor. Similarly, insulin receptor phosphorylated with or without the purified kinase exhibited the same levels of tyrosine autophosphorylation and of the tyrosine kinase-activating tris-phosphorylated kinase domain species. Properties of the kinase distinguished it from kinases known to act on the insulin receptor and other kinases that are insulin-stimulated, indicating that the kinase is a novel entity. The serine kinase underwent autophosphorylation on serine and immunoprecipitated with the insulin receptor. The availability of the purified kinase should facilitate cloning of the kinase, determination of the mechanism of activation of the kinase, and study of the wider potential role of the kinase in insulin signalling, and the ability to be able to phosphorylate serine 1078 to high stoichiometry should facilitate further studies into the function of this serine phosphorylation site.

Animals↗
PubMed1995

Transition from housestaff to nonphysicians as neonatal intensive care providers: cost, impact on revenue, and quality of care.

Nonphysician providers (NPP) increasingly fill roles traditionally performed by housestaff. Downsizing of a pediatric residency program prompted phased replacement of housestaff in a 26-bed neonatal intensive care unit (NICU). Subsidized education for neonatal nurse-practitioners, recruitment of physician assistants, and NPP leadership took place over 18 months, at which time all housestaff functions were assumed by NPP. Cost to establish the program, impact on hospital revenue under New York's prospective reimbursement system, and quality of care were evaluated. The net startup cost for the NPP program was $441,000 ($722,000 for education, salaries, staff replacement, and recruitment, partially offset by a New York State workforce demonstration project grant). Ongoing costs of the program are $1.2 million/yr (including salaries, off-hours medical backup, recruitment, administrative overhead, and loss of indirect and direct medical education reimbursement, partially offset by recaptured housestaff salaries and ancillary expense reductions). Access to care was maintained. Quality of care was assessed during the last 6 months of housestaff and the first 6 months of full NPP staffing, revealing similar weight-specific survival, and improvement in documentation and compliance with immunization and blood utilization guidelines during the NPP period. NPP are expensive in comparison to housestaff. Revenue is minimally adversely affected, but access to NICU services and quality of care was preserved and in some cases enhanced with NPP. In the context of graduate medical education reform, staffing problems such as ours will be encountered increasingly in inpatient subspecialty settings.

Health Services Accessibility↗
PubMed1990

Light microscope study of the coexistence of GABA-like and glycine-like immunoreactivities in the spinal cord of the rat.

The distributions of GABA-like and glycine-like immunoreactivities in the rat spinal cord were compared by using postembedding immunohistochemistry on semithin sections. In laminae I, II, and III, the proportions of GABA immunoreactive cells were 28%, 31%, and 46%, respectively, whereas for glycine immunoreactive cells the proportions were 9%, 14%, and 30%. Nearly all of the glycine immunoreactive cells in this area were also immunoreactive with the anti-GABA antiserum. In lamina II, some Golgi-stained islet cells were glycine immunoreactive, whereas others were not. Immunoreactive cell bodies were also present in the remainder of the grey matter. Some of these reacted with anti-GABA or antiglycine antiserum; others showed immunoreactivity with both antisera. Immunoreactive axons were found in the ventral and lateral funiculi of the white matter. Many large axons reacted with antiglycine antiserum, whereas GABA-immunoreactive axons were mostly of small diameter. Some large and small axons showed both types of immunoreactivity. These results suggest that the inhibitory neurotransmitters GABA and glycine coexist within cell bodies and axons in the rat spinal cord.

Animals↗
PubMed1989

Differences in saccharin-induced cerebral glucose utilization between obesity-prone and -resistant rats.

Approximately half the male Sprague-Dawley rats fed a high energy diet develop diet-induced obesity (DIO). The remainder are diet-resistant (DR) and do not become obese. Resistance to DIO can be predicted before exposure to high energy diets by the presence of diminished norepinephrine (NE) release to an intravenous glucose load. Here chow-fed rats were prospectively placed in DR- or DIO-prone 'diet groups' by the areas under their glucose-induced (1 g/kg, i.v.) NE curves (DR rats less than 1200 pg/ml/60 min; DIO rats greater than 4500 pg/ml/60 min). To test the central pathways involved in the response to the intake of palatable foods, rats were first trained to drink 1 ml of 50% glucose within 1 min and then were tested for local cerebral glucose utilization using uptake of [14C]2-deoxy-D-glucose ([14C]2-DG) after receiving 0.15% sodium saccharin in place of glucose to avoid altering plasma glucose levels. Controls for basal cerebral metabolism (C) received no solution. DR-prone rats increased [14C]2-DG uptake by 60-190% in autonomic areas of the medulla (nucleus tractus solitarius, area postrema, dorsal motor nucleus X) and amygdala (central nucleus) in the S versus C conditions while DIO-prone rats had high basal levels of [14C]2-DG uptake in these areas and showed no increase after S. Also, DR-prone rats had 9-25% higher [14C]2-DG uptake in the ventromedial hypothalamic nucleus than DIO rats regardless of C or S conditions. Thus, pre-existing differences in the activation of autonomic areas of the brain in response to a food-related cue may be of etiological significance in the different patterns of food intake and weight gain seen in DR- and DIO-prone rats fed a high energy diet.

Animals↗
PubMed1989

Initiation and perpetuation of obesity and obesity resistance in rats.

A search was made for predisposing factors and sequelae of diet-induced obesity (DIO) or resistance to DIO (DR). During 3 mo on a high-energy (CM) diet, two-thirds of the male Sprague-Dawley rats ate 16% more calories over the first 30 days and developed DIO. The remaining one-third were DR, gaining the same amount of weight as chow-fed controls. Basal and norepinephrine (NE)-stimulated in vivo O2 consumption, performed before rats were placed on the CM diet, was the same in those rats that later became DR or DIO after 3 mo on the CM diet. DR rats were 4% lighter, whereas DIO rats were equal to chow-fed rats before their exposure to the CM diet. When CM-fed rats were switched to chow, DIO rats took 14 wk to reduce their body and retroperitoneal fat pad weights to those of chow-fed controls, whereas DR rats gained only 40% of the body weight, and fat pads were 34% lighter than controls. After 14 wk, DIO rats were neither hyperinsulinemic nor insulin resistant, whereas DR rats had 64% reduced areas under their insulin curves after intravenous glucose (1 g/kg) compared with controls. Unlike younger rats, animals here had inconsistent plasma NE responses to intravenous glucose. Therefore the CM diet produces DR and DIO states that tend to become self-perpetuating once established.

Animals↗
PubMed1989

Glucose-induced sympathetic activation in obesity-prone and resistant rats.

Half of the 3-month-old male Sprague-Dawley rats fed a diet enriched in calories, sucrose and fat (CM diet) for 3 months developed diet-induced obesity (DIO) while the remainder were diet resistant (DR), gaining the same amount of weight as chow-fed controls. DIO was associated with basal hyperinsulinemia and 196 percent heavier retroperitoneal fat pads than DR and chow-fed rats. Intravenous glucose infusion (lg/kg) also produced greater insulin release in DIO rats associated with a 25 percent reduction in glucose disposal rates; areas under the insulin curve were 273 and 51 percent higher than chow-fed and DR rats, respectively. DR rats, on the other hand, showed normal glucose disposal rates but increased insulin release to a glucose load (148 percent greater area under the curve than chow-fed rats). Glucose infusion produced activation of the sympathetic nervous system with release of norepinephrine (NE) into the plasma in chow-fed and DIO but not DR rats which had 40-50 percent lower areas under the NE curve. Also, the areas under the NE curve correlated with body weight gain (r = 0.632; P = 0.040) and retroperitoneal fat pad weight (r = 0.707; P = 0.030) in DR and DIO rats suggesting that glucose-induced sympathetic activation was in some way related to an underlying mechanism of body weight regulation in Sprague-Dawley rats.

Animals↗
PubMed1988

Effects of diet and obesity on brain alpha 1- and alpha 2-noradrenergic receptors in the rat.

The chronic feeding of a sweetened condensed milk/corn oil diet (CM diet) to adult male rats produced significant increases in body weight and levels of plasma insulin in 34% of the rats fed this diet with respect to chow-fed controls. Levels of alpha 1-noradrenergic receptor binding were lower (32%) in the hypothalamic ventromedial nucleus (VMN) of only those rats which became obese (DIO rats) with respect to both chow-fed controls and those rats which resisted the development of obesity on the CM diet (DR rats). Also, alpha 1-noradrenergic binding was inversely proportional to body weight gain in the VMN (r = -0.831). alpha 2-Noradrenergic receptors were 30-37% lower in both the DIO and DR rats in the dorsomedial nucleus and dorsal area of the hypothalamus, and the medial dorsal area and nucleus reuniens of the thalamus. The similar decreases in alpha 2-noradrenergic receptors in both the DIO and DR rats in these areas suggested that dietary factors alone were responsible for these changes. There were no significant differences from chow-fed rats for hypothalamic dopamine (D2) or beta-noradrenergic (beta 1- and beta 2-) receptors in either DR or DIO rats. These results indicate that VMN alpha 1-noradrenergic receptors co-vary with body weight and implicate a role for alpha 1-receptors in the VMN in the central neuronal regulation of body weight.

Animals↗
PubMed1987

Infusion of cholecystokinin between meals into free-feeding rats fails to prolong the intermeal interval.

The sulfated octapeptide of cholecystokinin (CCK-8) was infused intraperitoneally into 7 free-feeding male Sprague Dawley rats over a 6-day period. Infusions were given near the end of each free-feeding meal (1.87 microgram/meal/rat), and also during the intermeal interval in gradually increasing doses (0.10-0.63 microgram/5 min/rat). Food intake was continuously monitored and the infusions were controlled by microcomputer. Meal patterns, total food intake, and body weights during drug infusion were compared with data collected during a baseline period when only saline was infused. Meal-contingent CCK-8 infusion produced a significant 29.9% decrease in meal size which persisted throughout the drug-infusion period. Intermeal infusion of CCK-8 failed to prolong the intermeal interval (IMI) but it did initially prevent the compensatory decrease in IMI and increased feeding frequency expected after meal size was reduced. By the last day of drug infusion, total daily food intake recovered to baseline levels due to increased feeding frequency. Body weight was only transiently reduced by CCK-8 infusion. These findings show that tolerance does not develop to the action of CCK-8 to suppress meal size, and the administration of exogenous CCK-8 to free-feeding rats does not persistently prolong the intermeal interval.

Animals↗
PubMed1987

Glucose, insulin and sympathoadrenal activation.

Selective activation of the two components of the sympatho-adrenal system (SAS) was produced by infusing male Sprague-Dawley rats with glucose or insulin. Intravenous glucose (0.5, 1 or 2 g/kg) raised plasma levels of glucose and insulin associated with a predominant activation of the sympathetic nervous system (SNS) as indicated by increased plasma norepinephrine (NE) levels. Glucose-induced release of NE was still seen in hypoinsulinemic, streptozotocin-treated rats but was absent after ganglionic blockade with chlorisondamine or following mannitol or saline infusions which failed to alter glucose or insulin levels. Insulin-induced (10 or 20 U/kg) hyperinsulinemia with its associated hypoglycemia produced predominant activation of the adrenal medulla producing increased plasma epinephrine (E) levels. But significant SNS activation also occurred with a concomitant increase in NE levels (14-22% of E) which appeared to be primarily from sympathetic nerves since increases still occurred following adrenal demedullectomy. Therefore, changes in plasma glucose levels alone and possibly altered intracellular concentrations or rates of glucose utilization can act as an important determinant of the pattern SAS activation although this may require pathological changes in plasma glucose levels to occur.

Adrenal Medulla↗
PubMed1987

Resistance to diet-induced obesity: food intake, pancreatic sympathetic tone, and insulin.

After 15 wk on a moderately high-calorie high-fat (CM) diet, 43% of 40 3-mo-old male Sprague-Dawley rats developed diet-induced obesity (DIO) (29% more weight gain), whereas 57% of diet-resistant (DR) rats gained no more weight than 20 chow-fed controls. When switched to chow for another 7 wk, DR rats ate 13% less, gained 55% less weight, and had 49% lower food efficiency, whereas DIO rats ate 4% less but had comparable weight gain and efficiency to controls. DIO rats had 29% more carcass lipid (percent of carcass weight). DIO rat retroperitoneal white adipose pads had 65% more cells that were the same size as those in chow-fed pads; DR rat cells were similar to controls. Both DR and DIO rats increased norepinephrine turnover in their interscapular brown adipose pads by greater than 90%. DIO rats also had 40% lower pancreatic turnover; their plasma insulin levels were 327% of controls after 15 wk on the CM diet and 188% after 7 wk on chow. DR levels were the same as controls at both times. Therefore, regulation of caloric intake, pancreatic sympathetic tone, and plasma insulin levels were three important differences between rats that resisted and those that developed DIO on high-energy diets.

Adipose Tissue, Brown↗
PubMed1987

Glucose-induced norepinephrine levels and obesity resistance.

The value of glucose-stimulated sympathetic activation in differentiating rats that would subsequently resist or develop diet-induced obesity (DIO) when chronically fed a high-calorie diet (CM) enriched in fat and sucrose was tested in 3-mo-old male Sprague-Dawley rats. While the rats were on chow the areas under the curve for plasma glucose, insulin, and norepinephrine (NE) levels were measured for 60 min after an intravenous glucose load (1 g/kg). Half of the rats then switched to the CM diet for 14 wk developed DIO with 54% more weight gain and 205% heavier retroperitoneal fat pads; half [diet resistant (DR)] had weight gain and pad weights comparable to chow-fed controls. Caloric intake was comparable in all animals. NE areas after intravenous glucose loads were 54% lower in DR than DIO rats, and there was a positive correlation (r = 0.63) between these NE areas and subsequent weight gain on the CM diet. Areas under the insulin curve correlated with subsequent weight gain on chow (r = 0.71) but not the CM diet. These results suggest that rats predisposed to become DR on the CM diet have dampened sympathetic activation after a glucose load, possibly because of heightened end-organ responsiveness to NE.

Adipose Tissue↗