Screening for vitamin B12 deficiency: caveat emptor.
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Gastrectomy↗
Biomedical subjects
R Green
Publications and source records attributed to R Green.
Pictorial review: Imaging of primary osteosarcoma of the spine.
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Adolescent↗
Inability of hyperglycemia to counter the ability of glucagon to increase net glucose output and activate glycogen phosphorylase in the perfused rat liver.
We examined the ability of hyperglycemia to alter the ability of glucagon to activate phosphorylase and stimulate glucose output in perfused rat livers. The livers were perfused with a Krebs-Henseleit buffer containing washed bovine erythrocytes and albumin at 37 degrees C for 90 or 120 minutes, In the first 60 minutes, the livers were perfused with insulin (10 microU/mL), glucagon (11 pg/mL), and glucose (105, 230, or 440 mg/dL). In the second 30 or 60 minutes, the glucagon concentration in the perfusate was elevated to 44, 88, 176 or 352 pg/mL or the infusion of glucagon was terminated. In the presence of glucose at 105 mg/dL, the termination of glucagon infusion decreased phosphorylase activity and glucose output. In contrast, the elevation of glucagon from 11 to 352 pg/mL activated phosphorylase and increased net glucose output in a dose-dependent manner. A linear correlation was observed between net glucose output and glycogen phosphorylase activity. An elevation of the glucose concentration from 105 to 230 or 440 mg/dL decreased net glucose output from 0.81 +/- 0.03 to 0.66 +/- 0.09 or -0.004 +/- 0.21 mg/min/100 g body weight, respectively, but did not cause significant change in phosphorylase-a activity (105 mg/dl, 50 +/- 11; 230 mg/dL, 40 +/- 2; 440 mg/dL, 69 +/ 3 mU/mg protein). The elevation of the glucagon concentration from 11 to 88 microU/mL in the presence of glucose at 105, 230, or 440 mg/dL increased net glucose output by 0.65 +/- 0.06, 0.61 +/- 0.08 or 0.64 +/- 0.26 mg/min 100 g body weight and raised phosphorylase-a activity by 65 +/- 5, 82 +/- 11, or 55 +/- 4 mU/mg protein, respectively. These results suggest that hyperglycemia decreases net hepatic glucose output without changing the activity of phosphory-lase-a. Further hyperglycemia does not alter the ability of glucagon to activate phosphorylase or to stimulate net hepatic glucose output.
Animals↗
Lipoprotein (a), homocysteine, and hypercoagulable states in young men with premature peripheral atherosclerosis: a prospective, controlled analysis.
PURPOSE: Elevated lipoprotein (a) (Lp[a]) lipoprotein, total homocysteine, and hypercoagulable states (HCS) have all been implicated as risk factors for premature-onset atherosclerosis. This study was performed to determine the prevalence of these abnormalities in young men with chronic lower extremity ischemia (peripheral vascular disease [PVD]) and to determine their relative strengths as risk factors for premature peripheral atherosclerosis. METHODS: We analyzed 50 young white men (aged 45 years or younger at onset of symptoms) and compared them with 45 age-matched white male control subjects. RESULTS: Atherosclerotic risk factors were similar in both groups. The mean (+/- SEM) Lp(a) lipoprotein level was 36 +/- 6 mg/dl among the study patients, compared with 14 +/- 2 mg/dl among control subjects (p = 0.02, Mann-Whitney). Twenty (40%) study patients and seven (16%) control subjects had Lp(a) lipoprotein levels of 30 mg/dl or greater (atherosclerotic risk threshold) (p = 0.01, odds ratio = 3.62, confidence interval (CI) 1.4 to 9.5). Positive HCS panels (antiphospholipid antibodies or deficiencies in antithrombin III, protein C, or protein S) were nearly twice as prevalent in study patients (n = 15, 30%) as in controls (n = 8, 18%), but this difference did not achieve statistical significance. The mean total plasma homocysteine level among the study patients was 15.9 +/- 0.9 mumol/L, which was not significantly different from the mean control value of 14.7 +/- 0.7 mumol/L. Lp(a) lipoprotein was related to risk of premature PVD through a linear logistic relationship (p = 0.003, odds ratio per each 1 mg/dl Lp(a) change was 1.03, CI 1.0 to 1.1). Multivariate analysis with stepwise logistic regression selected two variables: Lp(a) lipoprotein > or = 30 mg/dl (p = 0.01, odds ratio = 3.6, CI 1.3 to 9.9) and family history (p = 0.07, odds ratio = 2.2, CI 0.9 to 5.3). Tests of interaction demonstrated no effect between Lp(a) lipoprotein, HCS, and homocysteine. CONCLUSIONS: Lp(a) lipoprotein of 30 mg/dl or greater is an independent risk factor for premature peripheral atherosclerosis in men. None of the other examined variables exhibited a significant association with premature PVD.
Adult↗
Comparison of the deoxyuridine suppression test with serum levels of methylmalonic acid and homocysteine in mild cobalamin deficiency.
Both the deoxyuridine suppression test (dUST) and the cobalamin-dependent metabolites, methylmalonic acid (MMA) and homocysteine, are valuable tools for identifying clinical cobalamin deficiency. Examination of these metabolic changes in mild or marginal deficiency can provide useful comparisons of diagnostic frequencies and sensitivities and help define the sequence of metabolic changes in early deficiency. These tests were therefore compared directly with each other in 50 patients with low cobalamin levels and few or no obvious signs of deficiency. Serum homocysteine (P=0.0003) and MMA levels (P=0.0004) correlated with dUST results. However, the dUST results were abnormal significantly more often (38/50 patients) when matched against levels of homocysteine (25 abnormal results of 50; P=0.007) or MMA (20/50; P=0.008). Abnormalities of one or both serum metabolite levels (30/50 patients) occurred almost as often as dUST abnormalities (P=0.059). Metabolite levels, even when originally 'normal', fell with cobalamin therapy in many cases. The results indicate that both the dUST and serum metabolite levels become abnormal before macrocytic anaemia develops in mild cobalamin deficiency. The dUST appears to be most frequently abnormal of the tests; metabolite levels appear to rise almost concurrently but they do not become diagnostically abnormal as soon.
Bone Marrow↗
Hormone replacement therapy and cobalamin status in elderly women.
Serum cobalamin concentrations are frequently low in the elderly but the cause is often not apparent. Because oral contraceptives have been associated with low cobalamin concentrations in young women, we compared hormone use with cobalamin status in elderly women to determine whether it could account for their unexplained low cobalamin concentrations. Thirty-eight of the 111 women had abnormal cobalamin status (defined by low cobalamin, elevated methylmalonic acid, and/or elevated homocysteine concentrations) and 73 had normal status. There was no difference in hormone use between the two groups: 7 (18.4%) of the 38 cobalamin-deficient subjects used estrogens compared with 20 (27.4%) of the 73 control subjects. No differences in hormone use were apparent either when analysis was confined to abnormal serum cobalamin concentrations alone. Similarly, the 27 women taking hormones and the 84 women not taking hormones did not have significantly different serum cobalamin or serum total homocysteine concentrations. Indeed, hormone users had slightly, though not significantly, higher cobalamin concentrations and lower homocysteine concentrations than nonusers; furthermore, hormone users also had significantly lower serum methylmalonic acid concentrations. Thus, neither cobalamin concentrations nor cobalamin metabolic status were significantly worse in elderly women taking estrogen than in those not taking it (and, if anything, may have been slightly better). Hormone use does not appear to be a significant contributor to the low cobalamin concentrations or the mild metabolic evidence of cobalamin deficiency so often seen in the elderly.
Aged↗
Neutrophil nuclear segmentation in mild cobalamin deficiency: relation to metabolic tests of cobalamin status and observations on ethnic differences in neutrophil segmentation.
Neutrophil hypersegmentation is considered the most sensitive peripheral blood cell marker of cobalamin deficiency. However, its diagnostic value in the mild deficiency states that accompany most low cobalamin levels and its relation to metabolic test of cobalamin status are unknown. The authors compared neutrophil lobe averages and percent neutrophils with 5 or more lobes (%5+ lobes) in 169 subjects with their mean corpuscular volume (MCV) and serum cobalamin, methylmalonic acid (MMA), homocysteine, and folate levels and, in 65 cases, with the deoxyuridine suppression test (dUST). Only 9 subjects had hypersegmentation by lobe average and 20 subjects by %5+ lobes. They were not more often cobalamin-deficient than subjects without hypersegmentation. Moreover, only one of 34 subjects with dUST results diagnostic for cobalamin deficiency had neutrophil hypersegmentation. Both indices of neutrophil segmentation in the 169 subjects correlated significantly with homocysteine levels. They also showed weak inverse correlation with cobalamin levels, but did not correlate with MMA, folate, or MCV values. Cobalamin therapy for 6 months did not significantly change neutrophil lobe averages in 35 subjects with mild deficiency, compared with 8 nondeficient controls, and only marginally improved the %5+ lobes. A surprising, incidental observation was that blacks had significantly greater neutrophil segmentation by both criteria than did whites and others. This difference was unrelated to cobalamin or folate status. Our results indicate that dUST abnormalities precede all morphologic changes of deficiency, including hypersegmentation. Although a tendency exists for neutrophil segmentation to increase very slightly as some serum values, especially homocysteine, start to worsen in mild cobalamin deficiency, the metabolic changes precede overt hypersegmentation. Neutrophil nuclear segmentation is insufficiently sensitive in relation to metabolic evidence of deficiency to be used as a clinical tool in the diagnosis of mild cobalamin deficiency.
Asian People↗
Establishing outreach health services for homeless persons: an emerging role for nurse managers.
Nurse-managed clinics can be an effective strategy for addressing the health care needs of homeless and indigent populations. The role of the nurse manager in the establishment of a clinic involves community leadership--specifically, it involves addressing strategic planning, financial and manpower issues. The collaborative relationship of nurse managers, educators, and the community laid the groundwork for accessible and affordable health care for the homeless and indigent of one northwest Georgia community. Specific tools and strategies are presented.
Ambulatory Care Facilities↗
G. Rainey Williams, MD. The importance of doing it right.
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Faculty↗
Analysis of paediatric prescribing profiles in two health-funding systems.
OBJECTIVE: To investigate the adequacy of two large South African medical administrative databases in providing prescribing profiles for paediatricians and general practitioners (GPs) respectively. DESIGN: Statistical analysis of data captured during 1994. Data were analysed retrospectively with frequency analysis and non-parametric tests. SETTING: Two industry databases, one covering a prepaid health maintenance organisation (HMO), the other providing a chronic medication programme for medical schemes and their members. MAIN OUTCOME MEASURES: Comparison of prescribing profiles of specialists and GPs. MAIN RESULTS: Data from the HMO revealed that referrals to paediatricians were mainly for gastro-intestinal and respiratory problems. Paediatricians' prescriptions for treatment of gastro-oesophageal reflux and/or abdominal pain represented 15.5% of all items prescribed and accounted for 40.7% of total paediatric medicine costs. GPs used formulary items more frequently, and cost per prescription was two-thirds that of specialists. Data from the chronic medication programme were used to compare treatment of asthma by the two provider groups. There were significant differences in the prescribing profiles of the two groups, with specialists using more in the way of "third-line agents' and newer, expensive products. Significant numbers of prescriptions did not conform to national guidelines for treatment of asthma. CONCLUSIONS: Industry databases provide a viable and valuable source of information; however, some problems were experienced in extracting the required data. Prescribing profiles revealed certain practices that require review, in particular the relatively low use of generic products, the early resorting to drug therapy for gastrooesophageal reflux, and non-conformity with national guidelines for management of childhood asthma.
Asthma↗
In vitro complementation analysis localizes 23S rRNA posttranscriptional modifications that are required for Escherichia coli 50S ribosomal subunit assembly and function.
In vitro transcripts of Escherichia coli 23S rRNA are compromised severely (at least five orders of magnitude below natural 23S rRNA) in their ability to reconstitute into catalytically active, correctly assembled 50S subunits in a standard reconstitution procedure. Denaturation experiments suggest that this deficiency is the result of missing posttranscriptional modifications present in natural 23S rRNA. An in vitro complementation analysis was performed where partial natural 23S rRNA fragments prepared by RNase H digestion or hammerhead ribozyme cleavage were combined with the remaining RNA as a partial in vitro transcript in a standard reconstitution reaction and the peptidyl transferase activity was measured. This approach has identified a ca. 80-nt region in 23S rRNA (extending from position 2445 to 2523) containing the natural RNA element essential for E. coli 50S subunit assembly and has excluded the requirement for all but six of the known posttranscriptional modifications in 23S rRNA for 50S subunit assembly or peptidyl transferase activity. Importantly, this chimeric reconstitution approach provides a system for the analysis of pure mutant populations of 23S rRNA reconstituted into 50S subunits.
Escherichia coli↗
Rayburne W. Goen, MD: looking to the future.
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History, 20th Century↗
New mattresses: how fast do they become a significant source of exposure to house dust mite allergens?
BACKGROUND: Sensitization and exposure to mite allergens is a major risk factor for asthma. Little is known about the rate of build-up of allergens in the mite micro-habitats. OBJECTIVES: To investigate the rate of increase in mite allergen levels in new mattresses. METHODS: Der p 1 was measured in the dust samples collected from six identical new single mattresses over a period of 2 years. RESULTS: Der p 1 increased significantly at 4 months as compared with baseline level (P < 0.01), but no difference was found between the concentrations at 4, 8, 12 and 24 months. There was a significant correlation between Der p 1 concentration in mattresses at 4, 8, 12 and 24 months and Der p 1 levels in the bedroom carpet at the beginning of the study. CONCLUSIONS: New mattresses can become a significant source of exposure to mite allergens after a short period of time (< 4 months). There is little justification for advising mite sensitive patients to replace their mattresses as a part of avoidance regime.
Allergens↗
Domestic allergens in public places. II: Dog (Can f1) and cockroach (Bla g 2) allergens in dust and mite, cat, dog and cockroach allergens in the air in public buildings.
BACKGROUND: Sensitization and exposure to indoor allergens are the major risk factors for asthma. It is possible that significant exposure to domestic allergens occurs outside the home. OBJECTIVES: To investigate the levels of Can f 1 and Bla g 2 in the dust from carpeted floors and upholstered seats in public buildings and public transport and the airborne concentrations of Der p 1, Fel d 1, Can f 1 and Bla g 2 in schools and offices. METHODS: Can f 1 and Bla g 2 were measured in the dust collected by vacuuming a 1 m2 area of carpet, as well as upholstered seats in five schools, six hotels, four cinemas, six pubs, three buses and two trains. Dust was also collected from the bedroom carpet, living room carpet, mattress and sofa in 20 homes with and 20 homes without a dog in the same area. Personal airborne sampling (2 L/min) was conducted for 8 h in offices (n = 16) and classrooms (n = 9). In addition, airborne samples in schools were collected using a high volume pump (60 L/min) for 1 h in three classrooms immediately after the children vacated the school. Can f 1, Bla g 2, Der p 1 and Fel d 1 were assayed using a two-site monoclonal antibody-based ELISA. RESULTS: Can f 1 was detected in all dust samples from public places, ranging from 0.2 to 52.5 micrograms/g. Significantly higher levels were found in upholstered seats (geometric mean--GM 9.4 micrograms/g) than in carpets (GM 1.5 micrograms/g; P < 0.001), and levels of Can f 1 > 10 micrograms/g were found in 40% of upholstered seats in public places. Can f 1 was significantly higher in upholstered seats in public places than in sofas in homes without a dog (GM 1.8 micrograms/g; P < 0.001). Detectable levels of Bla g 2 were found in all of the schools (GM 2.4 U/g, range 0.8-4.4 U/g). Bla g 2 concentration greater than 2U/g (provisional threshold level representing risk of sensitization) was measured in 65% of the classrooms sampled. Der p 1 and Bla g 2 were below the detection limit in all airborne samples. However, airborne Fel d 1 and Can f 1 were detected in schools and offices, albeit in low concentrations. CONCLUSIONS: Upholstered seats from public places constitute a reservoir for the accumulation of dog allergen, and a source of exposure to Can f 1 inside public buildings or on public transport. Exposure to cockroach allergens in schools may be important for cockroach sensitized asthmatic children.
Air Pollution, Indoor↗
Hyperhomocysteinemia and low pyridoxal phosphate. Common and independent reversible risk factors for coronary artery disease.
BACKGROUND: High plasma homocysteine is associated with premature coronary artery disease in men, but the threshold concentration defining this risk and its importance in women and the elderly are unknown. Furthermore, although low B vitamin status increases homocysteine, the link between these vitamins and coronary disease is unclear. METHODS AND RESULTS: We compared 304 patients with coronary disease with 231 control subjects. Risk factors and concentrations of plasma homocysteine, folate, vitamin B12, and pyridoxal 5'-phosphate were documented. A homocysteine concentration of 14 mumol/L conferred an odds ratio of coronary disease of 4.8 (P < .001), and 5-mumol/L increments across the range of homocysteine conferred an odds ratio of 2.4 (P < .001). Odds ratios of 3.5 in women and of 2.9 in those 65 years or older were seen (P < .05). Homocysteine correlated negatively with all vitamins. Low pyridoxal 5'-phosphate (< 20 nmol/L) was seen in 10% of patients but in only 2% of control subjects (P < .01), yielding an odds ratio of coronary disease adjusted for all risk factors, including high homocysteine, of 4.3 (P < .05). CONCLUSIONS: Within the range currently considered to be normal, the risk for coronary disease rises with increasing plasma homocysteine regardless of age and sex, with no threshold effect. In addition to a link with homocysteine, low pyridoxal-5'-phosphate confers an independent risk for coronary artery disease.
Age Factors↗
Analytical magnetapheresis of ferritin-labeled lymphocytes.
Analytical magnetapheresis is a technique for analyzing magnetic particles in suspension. The magnetically susceptible particles form a deposition pattern from the suspending medium under carefully controlled flow and magnetic field conditions. This technique was used to determine the effective magnetic volumetric susceptibility, delta chi, of human lymphocytes labeled with an iron-rich protein, ferritin. Dynabeads M450, monodisperse polymeric beads doped with magnetite, of a diameter 4.5 microns, close to that of human lymphocytes, were used as a reference. The experiment showed an almost complete deposition of ferritin-labeled lymphocytes at an average flow velocity of 0.28 mm/s, a representative magnetic field of 1.67 T, and a magnetic field gradient of 2.57 T/mm. The calculated delta chi was (2.92 +/- 0.24) x 10(-6)[SI] (ferritin-labeled lymphocytes), and the corresponding number of ferritin molecules per lymphocyte was (1.75 +/- 0.44) x 10(7). In comparison, an almost complete deposition of the Dynabeads was observed at a much higher average flow velocity, 15 mm/s, a much lower field, 0.164 T, and a much lower field gradient, 0.025 T/mm. These results corresponded to a much higher delta chi = 0.245[SI] (Dynabeads M450). These results offer important guidelines in evaluating the use of ferritin as a soluble magnetic cell label.
Calibration↗
Estimated potassium reflection coefficient in perfused proximal convoluted tubules of the anaesthetized rat in vivo.
1. As yet there is no definitive description of the mechanism and route by which K+ reabsorption is achieved in the proximal convoluted tubule (PCT). We have assessed the contribution of convective K+ transport to net potassium ion flux (JK) by estimating the reflection coefficient of K+ (sigma K) in the proximal tubule of anaesthetized rats previously prepared for in vivo microperfusion. 2. Alterations in the luminal concentration of the impermeant solute raffinose in single-perfused (lumen only) and double-perfused (lumen and capillaries) PCTs were found to change fluid reabsorption in a predictable fashion. 3. Net potassium ion flux (JK) in single- and double-perfused tubules was significantly correlated with net fluid flux (Jv), suggesting that convective K+ transport may be a significant factor in overall K+ transport by the PCT. 4. Estimates of sigma K in single- and double-perfused tubules were very similar (0.14 +/- 0.06 and 0.13 +/- 0.05, respectively), even though K+ diffusion was not strictly controlled in the former group. The maximum effect of 'pseudo-solvent' drag in double-perfused tubules was estimated to give a sigma K of 0.40. This low value for sigma K suggests that true convection/solvent drag may be an important driving force for the reabsorption of K+ from the PCT of the rat.
Anesthesia↗
A base pair between tRNA and 23S rRNA in the peptidyl transferase centre of the ribosome.
Interaction of the conserved CCA terminus of tRNA with rRNA in the peptidyl transferase P site has been studied by in vitro genetics. A watson-Crick G-C pair between G2252 in a conserved hairpin loop of 23S rRNA and C74 at the acceptor end of tRNA is required for proper functional interaction of the CCA end of tRNA with the ribosomal P site. These findings establish a direct role for 23S rRNA in protein synthesis.
Base Composition↗