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Biomedical subjects

N Kalant

Publications and source records attributed to N Kalant.

At least 19 recordsLinked to original sources
PubMed2000

How valid are utilization review tools in assessing appropriate use of acute care beds?

BACKGROUND: Despite their widespread acceptance, utilization review tools, which were designed to assess the appropriateness of care in acute care hospitals, have not been well validated in Canada. The aim of this study was to assess the validity of 3 such tools--ISD (Intensity of service, Severity of illness, Discharge screens), AEP (Appropriateness Evaluation Protocol) and MCAP (Managed Care Appropriateness Protocol)--as determined by their agreement with the clinical judgement of a panel of experts. METHODS: The cases of 75 patients admitted to an acute cardiology service were reviewed retrospectively. The criteria of each utilization review tool were applied by trained reviewers to each day the patients spent in hospital. An abstract of each case prepared in a day-by-day format was evaluated independently by 3 cardiologists, using clinical judgement to decide the appropriateness of each day spent in hospital. RESULTS: The panel considered 92% of the admissions and 67% of the subsequent hospital days to be appropriate. The ISD underestimated the appropriateness rates of admission and subsequent days; the AEP and MCAP overestimated the appropriateness rate of subsequent days in hospital. The kappa statistic of overall agreement between tool and panel was 0.45 for ISD, 0.24 for MCAP and 0.25 for AEP, indicating poor to fair validity of the tools. INTERPRETATION: Published validation studies had average kappa values of 0.32-0.44 (i.e., poor to fair) for admission days and for subsequent days in hospital for the 3 tools. The tools have only a low level of validity when compared with a panel of experts, which raises serious doubts about their usefulness for utilization review.

Angina, Unstable↗
PubMed1998

Comparison of long-term care in an acute care institution and in a long-term care institution.

BACKGROUND: Acute care hospitals in Quebec are required to reserve 10% of their beds for patients receiving long-term care while awaiting transfer to a long-term care facility. It is widely believed that this is inefficient because it is more costly to provide long-term care in an acute care hospital than in one dedicated to long-term care. The purpose of this study was to compare the quality and cost of long-term care in an acute care hospital and in a long-term care facility. METHODS: A concurrent cross-sectional study was conducted of 101 patients at the acute care hospital and 102 patients at the long-term care hospital. The 2 groups were closely matched in terms of age, sex, nursing care requirements and major diagnoses. Several indicators were used to assess the quality of care: the number of medical specialist consultations, drugs, biochemical tests and radiographic examinations; the number of adverse events (reportable incidents, nosocomial infections and pressure ulcers); and anthropometric and biochemical indicators of nutritional status. Costs were determined for nursing personnel, drugs and biochemical tests. A longitudinal study was conducted of 45 patients who had been receiving long-term care at the acute care hospital for at least 5 months and were then transferred to the long-term care facility where they remained for at least 6 months. For each patient, the number of adverse events, the number of medical specialist consultations and the changes in activities of daily living status were assessed at the 2 institutions. RESULTS: In the concurrent study, no differences in the number of adverse events were observed; however, patients at the acute care hospital received more drugs (5.9 v. 4.7 for each patient, p < 0.01) and underwent more tests (299 v. 79 laboratory units/year for each patient, p < 0.001) and radiographic examinations (64 v. 46 per 1000 patient-weeks, p < 0.05). At both institutions, 36% of the patients showed anthropometric and biochemical evidence of protein-calorie undernutrition; 28% at the acute care hospital and 27% at the long-term care hospital had low serum iron and low transferrin saturation, compatible with iron deficiency. The longitudinal study showed that there were more consultations (61 v. 37 per 1000 patient-weeks, p < 0.02) and fewer pressure ulcers (18 v. 34 per 1000 patient-weeks, p < 0.05) at the acute care hospital than at the long-term care facility; other measures did not differ. The cost per patient-year was $7580 higher at the acute care hospital, attributable to the higher cost of drugs ($42), the greater use of laboratory tests ($189) and, primarily, the higher cost of nursing ($7349). For patients requiring 3.00 nursing hours/day, the acute care hospital provided more hours than the long-term care facility (3.59 v. 3.03 hours), with a higher percentage of hours from professional nurses rather than auxiliary nurses or nursing aides (62% v. 28%). The nurse staffing pattern at the acute care hospital was characteristic of university-affiliated acute care hospitals. INTERPRETATION: The long-term care provided in the acute care hospital involved a more interventionist medical approach and greater use of professional nurses (at a significantly higher cost) but without any overall difference in the quality of care.

Aged↗
PubMed1993

Non-enzymic glycation of collagen inhibits binding of oxidized low-density lipoprotein.

We have examined the effect of non-enzymic glycation of native soluble collagen, in solution or in gels, on binding of oxidized low-density lipoprotein (LDL). We found the following. (1) Glycation markedly inhibited binding of LDL. This is contrary to results previously reported; the difference may be attributable to the use of detergent- and heat-denatured collagen, covalently bound to agarose beads, in the earlier study. (2) With increased duration of glycation, collagen solution would not gel, and preformed gels dissolved. (3) [14C]Glucose bound to collagen gels dissociated slowly, even at pH 5, suggesting that it was not present as a Schiff's base; in addition, ketoamines, pentosidine and fluorescent advanced glycation products were not detectable in glycated collagen gels, although they accumulated in tendon collagen glycated under the same conditions. It is hypothesized that the difference in glycation effects between gel and tendon may be due to the strength of cross-linking before glycation: the increase in intermolecular distance in collagen fibrils which results from glycation disrupts the fibrils in gels, preventing binding of LDL and formation of glycation-dependent cross-links, whereas the extensive cross-linking in tendon maintains the intermolecular distances within a range which permits formation of glycation cross-links.

Animals↗
PubMed1993

More on cholesterol.

Explore the source record for details and available documents.

Anticholesteremic Agents↗
PubMed1992

Inhibition by serum components of oxidation and collagen-binding of low-density lipoprotein.

Low-density lipoprotein (LDL) is oxidized by cellular and noncellular mechanisms, both leading to an increased binding to collagen. We have investigated the effect of serum on lipid peroxidation, apoprotein oxidation and the binding of oxidized apoprotein to collagen. During noncellular oxidation, lipoprotein-deficient serum strongly inhibited all three processes. The serum fraction of M(r) > 100,000 was equally inhibitory; this effect was not due to alpha 1 or gamma globulins, alpha 2 macroglobulins, haptoglobins or ceruloplasmin. The serum fraction of M(r) 30,000-100,000 stimulated the binding of oxidized apoprotein but the albumin in this fraction inhibited lipid peroxidation and apoprotein oxidation. Serum ultrafiltrate (M(r) < 1000) inhibited lipid and protein oxidation, and binding; the inhibitory effect was abolished by deionization which removed histidine. The effects of lipoprotein-deficient serum and its fractions on cellular oxidation were similar but weaker than those on noncellular oxidation, HDL inhibited noncellular oxidation as well as binding of oxidized apoprotein. VLDL also inhibited oxidation; this could not be accounted for by its content of apo B. If present in vivo, these inhibitory effects would completely suppress both cellular and noncellular oxidation of LDL and its subsequent binding to collagen.

Apolipoproteins B↗
PubMed1989

Angiogenic activity of the atherosclerotic carotid artery plaque.

Neovascularization is observed in complicated atherosclerotic plaques associated with cellular proliferation, plaque hemorrhage, and thrombosis. The angiogenic activity of 278 plaque fragments was tested; the fragments were taken from 12 patients with cerebral ischemia who underwent carotid endarterectomy. Angiogenesis, determined by the sustained ingrowth of new vessels in the rabbit cornea, was induced in 125 (45%) of these fragments. By contrast, angiogenesis was found in only two (2.4%) of 80 control tissues (p less than 0.001): in none of 22 samples of boiled atherosclerotic plaque; in two of 26 samples of normal rabbit carotid artery; and in none of 32 samples of nonatherosclerotic human uterine artery. Histological evaluation revealed that the cellular zones (composed mainly of smooth-muscle cells) were highly angiogenic, with 97 (76%) of 127 samples showing angiogenesis compared with 23 (17%) of 132 acellular fragments that consisted of amorphic, necrotic, calcific, lipid-laden material (p less than 0.001). These results indicate that angiogenesis in vivo is a function of the cellular component of the advanced atherosclerotic plaque, and is not expressed in the normal, stable arterial wall. The fragile new vessels could promote the growth of the plaque or be a source of hemorrhages, microinfarcts, and plaque fissures that convert a stable, silent lesion to an expanding, ulcerated, thrombotic, symptomatic plaque.

Aged↗
PubMed1988

Enhancement of glycogen concentrations in primary cultures of rat hepatocytes exposed to glucose and fructose.

Glycogen synthesis in isolated hepatocytes can occur from glucose both by a direct mechanism and by an indirect process in which glucose is first metabolized to C3 intermediates before use for glycogenesis via gluconeogenesis. We studied the incorporation into glycogen of glucose and the gluconeogenic substrate, fructose, in primary cultures of hepatocytes from fasted rats. In the presence of insulin, both glucose and fructose promoted net deposition of glycogen; however, fructose carbon was incorporated into glycogen to a greater extent than that from glucose. When glucose and fructose were administered simultaneously, the glycogenic utilization of glucose was stimulated 2-3-fold, and that of fructose was increased by about 50%. At constant hexose concentrations, the total incorporation of carbon, and the total accumulation of glycogen mass, from glucose and fructose when present together exceeded that from either substrate alone. Fructose did not change the relative proportion of glucose carbon incorporated into glycogen via the indirect (gluconeogenic) mechanism. The synergism of glucose and fructose in glycogen synthesis in isolated rat hepatocytes in primary culture appears to result from a decrease in the rate of degradation of newly deposited glycogen, owing to (i) decreased amount of phosphorylase a mediated by glucose and (ii) noncovalent inhibition of residual phosphorylase activity by some intermediate arising from the metabolism of fructose, presumably fructose 1-phosphate.

Animals↗
PubMed1988

Effect of diet restriction on glucose metabolism and insulin responsiveness in aging rats.

The effect of age and of prolonged caloric restriction on glucose tolerance and insulin responsiveness has been studied in male Fischer 344 rats. Beginning at 1 month of age dietary intake of an experimental group (R) was limited to 60% of that of the control group (AL) which was allowed to eat ad libitum. Studies were carried out at intervals up to 24 months of age. In AL rats the oral glucose tolerance curve showed progressively higher peak levels of plasma glucose with age, and a decrease in the plasma insulin concentration at the time of the glucose peak. The R group did not show the increase in peak value with age and the corresponding insulin concentration was lower than that of the AL group. These results are compatible with a delay in the first phase of insulin secretion in aging AL rats. Insulin-stimulated glucose disposal was assessed by the method of Reaven et al. [Diabetes, 32 (1983) 175], at ages 4, 12, 18 and 24 months; using infusions of 2 mU of insulin and 1 mg of glucose/min per kg, the steady-state plasma glucose level (SSPG) was slightly lower in R than in AL rats, while the steady-state plasma insulin level was reduced by 40-60%. In rats aged 18-24 months the hepatic glucose output, measured with [3-3H]glucose, was the same for AL and R rats in the basal state and was reduced to the same extent by insulin. In the presence of epinephrine and propranolol, infusion of glucose and insulin at various rates demonstrated that the plasma glucose clearance rate increased linearly with increasing SSPI, and at comparable SSPI levels was lower in R than in AL rats. The ability of insulin to stimulate glycogenesis from glucose was measured in primary hepatocyte cultures. Insulin increased glycogenesis 3-fold in cells from AL rats and 4-6-fold in cells from R rats. There was no effect of age. The increased insulin responsiveness of R rats was not due to an increase in insulin binding or to a decrease in insulin degradation (measured with intact cells or as cytosolic insulinase activity).(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1988

Influence of collagen gel substratum on response to low-density lipoprotein by cultured human skin fibroblasts.

The effect of low-density lipoprotein (LDL) on accumulation of glycosaminoglycans (GAG) was compared in cultures of human skin fibroblasts on a conventional plastic substratum and in a native type I collagen gel. The 24-h incorporation of [3H]glucosamine and Na2(35)SO4 into GAG secreted into the medium or associated with the substratum and cell surface (SCA) was measured in cells at subconfluent densities. When cells were grown on plastic, 13-25% of the labeled GAG was in the SCA pool. Cells cultured within a collagen gel matrix incorporated three times more [3H]glucosamine and up to five times more [35S]sulfate into this pool. The addition of LDL (300 micrograms protein/mL) to the medium increased the level of total GAG incorporation of [3H]glucosamine by 40-50% and of [35S]sulfate by 15-20% on both substrata. For cells on plastic the relative increase in the medium and SCA pool was similar, whereas for cells in collagen gel the response to LDL was twice as great in the SCA pool as in the medium. The distribution of GAG types was unaffected by LDL; hyaluronic acid remained the principal GAG in the media pools of both substrata, heparan sulfate remained the main SCA GAG in cultures on plastic, and dermatan sulfate remained the dominant GAG in the SCA pool of collagen gel cultures. LDL degradation was measured at intervals up to 48 h after the addition of 125I-labeled LDL. The rate of accumulation of degraded LDL products was lower in collagen gel cultures, but the final levels achieved were the same in the two substrata. Concentrations of total cell cholesterol were similar, although the increases in free cholesterol induced by LDL were 26% greater in cells within collagen gel than in those on plastic. We conclude that fibroblasts grown within a collagen gel, as compared with those on a plastic substratum, (i) accumulate more GAG that remain attached to the substratum and cell surface; (ii) respond to LDL with a similar degree of increase in GAG accumulation, but more of the increase is found in the substratum and cell surface compartment; and (iii) accumulate more intracellular free cholesterol in response to LDL.

Cells, Cultured↗
PubMed1988

Time-dependent alterations in the pathway of glucose incorporation into glycogen in primary cultures of rat hepatocytes following glucose starvation.

Isolated rat hepatocytes maintained in primary culture were able to use glucose for glycogen synthesis by both direct and indirect mechanisms. Cells that had been isolated from fed animals and then cultured in the absence of glucose, but in the presence of gluconeogenic substrates such as pyruvate and amino acids, had decreased glycogen contents compared with similar cells that had been cultured in the presence of glucose. Upon reexposure to glucose, the glucose-starved cells showed time-dependent changes in the preferred pathway for the use of glucose for glycogen synthesis. These changes were noted either in the absence or presence of insulin; however, net accumulation of glycogen was observed only in the presence of the hormone.

Animals↗
PubMed1988

The effects of acute and life-long food restriction on basal and stress-induced serum corticosterone levels in young and aged rats.

The effects of short term (1-month) and life-long 60% ad libitum food restriction on the adrenocortical response to restraint stress were compared in young and aged Fischer 344 rats. In rats restricted for 1 month (study 1), the adrenocortical response differed as a function of age. In 8-month-old animals, the initial steep rise in corticosterone in response to stress was of similar magnitude in ad libitum and restricted animals. In 23-month-old animals the corticosterone response was severely blunted in restricted animals. In life-long restricted animals (study 2), the corticosterone response to restraint stress was tested at 8, 16, and 24 months of age. The general pattern of response to stress in these animals was similar to that in study 1. The 16- and 24-month-old animals showed the same blunted response to stress found in the 23-month-old animals restricted for only 1 month, suggesting that the severe restriction per se and not life-long food restriction blunted the response to stress in aged animals. The similarity between the response to stress in study 1 and study 2 was evident even though animals were tested in one case before feeding when corticosterone levels were high, and in the other 4-5 h after feeding when corticosterone levels were lower. In study 3 it was found that in food-restricted young rats, the mean corticosterone level over a 24-h period was significantly elevated above that in ad libitum fed young rats. In aged rats, however, except before daily feeding, corticosterone levels of food-restricted rats remained significantly below those of ad libitum fed animals, whose levels were, in turn, significantly elevated compared to those of ad libitum fed young rats. These findings suggest that in aged animals severe food restriction reduces basal corticosterone levels, adrenal responsiveness to stress, and adrenal size and has the potential to protect against the consequences of high corticosterone levels in aging.

Adrenal Cortex↗
PubMed1987

Compartmentation of glucose 6-phosphate in hepatocytes.

Rat hepatocytes were incubated with 14C-labelled hexoses, and the specific radioactivities of glucose 6-phosphate, glucose 1-phosphate and fructose 6-phosphate were determined. (1) When suspensions of freshly isolated hepatocytes were incubated with [14C]glucose, the specific radioactivities of glucose 1-phosphate and fructose 6-phosphate were severalfold higher than that of glucose 6-phosphate. The ratios of the specific radioactivities decreased with time of incubation. These relationships were also found when incubations were carried out with primary cultures of rat hepatocytes or with crude homogenates of hepatocytes, but not with isolated nuclei. (2) When cells were incubated with [14C]fructose, the ratios of the specific radioactivities were higher than with [14C]glucose, and also decreased with time. (3) Paired incubations were carried out with a mixture of galactose and fructose, with one or other sugar being labelled with 14C. The specific radioactivity of glucose released into the medium was greater than that of glucose 6-phosphate when fructose was labelled, but not when galactose was labelled. Furthermore, glucose 6-phosphate and glucose in the medium differed with regard to the distribution of 14C between C-1 and C-6. These results are interpreted as evidence that glucose 6-phosphate in hepatocytes does not exist as a homogeneous pool, but that subcompartments exist which are associated with glucose phosphorylation, gluconeogenesis and glycogenolysis.

Animals↗
PubMed1987

Hepatic glucose extraction in normal and diabetic man.

Fractional hepatic extraction of glucose was determined from the appearance in the systemic circulation of ingested 3-[3H]glucose. Using the glucose clamp technique, studies were done under steady-state conditions of basal glycemia and insulinemia, normoglycemia (0.8 mg/mL) and mild hyperinsulinemia (approximately 40 microU/mL), hyperglycemia (2 mg/mL-1) and hyperinsulinemia (approximately 100 microU/mL). Based on previous results in the dog, an oral glucose load of 2 g was used to label the portal vein glucose; this amount was chosen so as to minimize disturbance of the portal steady state but still avoid excessive loss during absorption. Additional subjects with hyperglycemia and hyperinsulinemia received an oral load of 50 g of glucose. Fractional extraction in normal subjects under near-basal conditions of glycemia and insulinemia was 19% in normal subjects and in patients with noninsulin-dependent diabetes mellitus (NIDDM) elevation of serum insulin, with or without hyperglycemia, which led to an average extraction rate of 32% of the ingested glucose. Absolute hepatic glucose uptake, calculated from the fractional extraction the plasma glucose concentration, and hepatic plasma flow accounted for 50% to 72% of total glucose use during the various steady states and following ingestion of 50 g of glucose. It is concluded that hepatic uptake or extraction, as opposed to net uptake, proceeds actively even when plasma glucose and insulin are within the normal basal range; it is increased in the presence of hyperinsulinemia, with or without hyperglycemia; and it is unaltered in NIDDM.

Adult↗