bluuebunny/crossref_metadata_2025_split huggingface dataset:
Altered Ability of the Liver to Produce Glucose Following a Period of Glucagon Deficiency
Authors: Deri John J , Williams Phillip E , Steiner Kurt E , Cherrington Alan D 
Published: September 2013

It is known that the effectiveness of a physiologic increment in glucagon to stimulate glucose production wanes with time even when counterregulatory insulin secretion is prevented. The aim of the present study was to establish whether the converse is true: does glucagon become a more effective stimulus of glucose production following a period of acute hypoglu-cagonemia?
To determine this, somatostatin was infused along with basal replacement amounts of glucagon (0.65 ng/kg - min) and insulin (228 μU/kg · min) into five postabsorptive conscious dogs. After 1.5 h of basal hormone replacement, the glucagon infusion was terminated and a selective fall in the plasma glucagon level (75 ± 6 to 30 ± 4 pg/ml) occurred. This resulted in a drop in tracer (3H-glucose)-determined glucose production from 3.0 ± 0.4 to 1.5 ± 0.3 mg/kg min. The plasma insulin level remained unchanged at 10 ± 1 μU/ml throughout the experiment. Euglycemia (110 ± 4 mg/dl) was maintained by exogenous glucose infusion. After 3 h of glucagon lack, restoration of the glucagon infusion returned the IRG level to control values (78 ± 6 pg/ml) but restored glucose output only partially (42 ± 9%), necessitating continued glucose infusion to preserve euglycemia. Repetition of the experiment in dogs whose pancreatic glucoregulatory feedback loops were broken surgically (two-stage pancreatectomy) rather than pharmacologically resulted in similar findings. It is concluded that glucagon deficiency of 3-h duration leads to a decrease, rather than an increase, in hepatic sensitivity to glucagon.
Calcium–Calmodulin-Dependent Myosin Phosphorylation by Pancreatic Islets
Authors: MacDonald Michael J , Kowluru Anjaneyulu 
Published: September 2013

SUMMARY
Pancreatic islets contain enzyme activity which catalyzes the phosphorylation by MgATP of cardiac, skeletal, or smooth muscle myosin light chains. The enzyme is activated by calcium (Ka = 10 μM) and calmodulin (Ka = 2 μM) and inhibited by trifluoperazine (Ki = 10 μM), a known inhibitor of calmodulin and of insulin secretion. The enzyme binds to a calmodulin affinity column when Ca2+ is present and is eluted when Ca2+ is omitted. These are the properties of myosin light chain kinase. Since phosphorylation of smooth muscle myosin is necessary for its activation by actin, the kinase may have a key role in coupling stimuli that increase intracellular calcium to the contractile processes involved in insulin secretion.
Red Blood Cell Age, Pyruvate Kinase Activity, and Insulin Receptors: Evidence that Monocytes and RBCs May Behave Differently
Authors: Camagna Antonio , Pirro Roberto De , Tardella Laura , Rossetti Luciano , Lauro Renato , Caprari Patrizia , Samoggia Paola , Salvo Giuseppe 
Published: September 2013

Data emerging from insulin receptor studies performed on red blood cells (RBCs) and monocytes from the same subject are not always in agreement; dichotomy might occur since variations in mean RBC age are not taken into account or because insulin receptors on the two cell types behave differently.
In the present investigation RBCs from normal male subjects were separated into five populations of different mean age by means of centrifugation of RBCs on a discontinuous gradient of buffered Percoli for 10 min at 1000 x g. Insulin binding varied significantly depending upon the RBC population tested and was closely correlated to the activity of pyruvate kinase (r2 = 0.86), a well-known marker of RBC age.
These data suggested that pyruvate kinase assay might be helpful in studies of RBCs. To confirm this hypothesis, RBCs from 10 normal male subjects and 13 male patients with hemolytic anemia were studied; insulin binding was correlated to pyruvate kinase activity. By adjusting insulin binding to 2 x 109 RBCs/ml the range of data was abnormally high, but it became acceptable after adjusting insulin binding to pyruvate kinase activity (0.75 U/2 x 109 RBCs). The overalr2 = 0.82) but only slightly to reticulocyte number (r2 = 0.56) since not only reticulocytes but also erythrocytes lose receptors during maturation.
Pyruvate kinase activity was measured in RBCs from normal men and from normally menstruating women at the seventh and twenty-fourth days of the cycle; results demonstrated that adjustment of data, according to mean RBC age, broadens dichotomy of monocyte and RBC data.
In conclusion, this paper demonstrates that (1) insulin binding experiments may be carried out on RBCs separated into populations of different mean age; (2) by assaying the pyruvate kinase activity, it is possible to study RBC samples of different mean age and to reveal insulin binding variations provoked by changes in mean RBC age; (3) RBCs lose insulin receptors physiologically and continuously with age; (4) RBC insulin receptors of patients with hemolytic anemia are normal; and (5) monocyte and RBC insulin receptors may behave differently.
Diminished Production of Thromboxane B2 and Prostaglandin E by Stimulated Polymorphonuclear Leukocytes from Insulin-treated Diabetic Subjects
Authors: Qvist Rajes , Larkins Richard G 
Published: September 2013

As an initial step to investigate the possibility that abnormal polymorphonuclear leukocyte (PMNL) function in diabetes might be related to abnormalities of arachidonic acid metabolism, products of the cyclooxygenase pathway were assayed in PMNL from 27 insulintreated diabetic subjects and 27 age- and sex-matched nondiabetic subjects. It was found that the major prostanoid products formed were thromboxane B2 (TxB2) and prostaglandin E (PGE). Production of both these substances was greatly enhanced in PMNL from control and diabetic subjects by exposure to a killed preparation of Staphylococcus aureus (S. aureus) or to zymosan.
There was a marked reduction in the production of TxB2 by PMNL from diabetic subjects in response to stimulation by both S. aureus [670 ± 98 (SE) versus 1010 ± 76 pg/106 PMNL/90 min, P &lt; 0.01] and zymosan (583 ± 53 versus 1034 ± 46 pg/106 PMNL/90 min, P &lt; 0.001). Similarly, production of PGE was significantly reduced in diabetics in response to both S. aureus (145 ± 29 versus 232 ± 16 pg/106 PMNL/90 min, P &lt; 0.05) and zymosan (181 ± 21 versus 271 ± 27 pg/ 106 PMNL/90 min, P &lt; 0.01). There was no relation between the plasma glucose at the time of the test and the production of either prostanoid.
Diminished production of cyclooxygenase products of arachidonic acid metabolism should be added to the known abnormalities of PMNL in diabetes. In view of the demonstrated or inferred effects of cyclooxygenase products on aspects of PMNL function, this observation may be important in understanding the pathogenesis of PMNL dysfunction in diabetes.
Effects of Long-Term Optimization and Short-Term Deterioration of Glycemic Control on Glucose Counterregulation in Type I Diabetes Mellitus
Authors: Bolli Geremia , Feo Pierpaolo De , Cosmo Salvatore De , Perriello Gabriele , Angeletti Gabriella , Ventura Maria Rosa , Santeusanio Fausto , Brunetti Paolo , Gerich John E 
Published: September 2013

To assess the effects of glycemie control on glucose counterregulation, rates of plasma glucose recovery from hypoglycemia and counterregulatory hormonal responses were studied in 18 C-peptide-negative patients with insulin-dependent diabetes mellitus (IDDM) before and after either improvement, no change, or deterioration in glycemic control. Hypoglycemia was induced by an i.v. insulin infusion (30 mU/m2 · min for 1 h) after maintenance of euglycemia overnight with i.v. insulin.
In 13 patients with long duration of IDDM (9 ± 0.5 yr, mean ± SEM) and initially poor glycemic control (mean diurnal blood glucose, MBG 199 ± 8 mg/dl, ketoamine-HbA1 12.4 ± 0.2%; nondiabetic subjects 104 ± 4 mg/dl and 6.8 ± 0.09%, respectively), rates of plasma glucose recovery from hypoglycemia (0.30 ± 0.01 versus 0.60 ± 0.01 mg/dl · min in nondiabetic subjects, P &lt; 0.001) and plasma glucagon (AUC 0.56 ± 0.09 versus 6.3 ± 0.50 ng/ml ·150 min in non-diabetic subjects, P &lt; 0.01) and epinephrine (AUC 16.9 ± 0.2 versus 25.7 ± 0.2 ng/ml 150 min in nondiabetic subjects, P &lt; 0.001) responses to hypoglycemia were impaired. Intensive therapy (three daily injections of insulin) instituted in 7 out of 13 IDDM patients for up to 9 mo improved MBG (124 ± 6 mg/dl, P &lt; 0.01) and ketoamine-HbA1 (7.9 ± 0.02%, P &lt; 0.01) but not rates of plasma glucose recovery (0.31 ± 0.01 mg/dl · min) and plasma glucagon (AUC 0.69 ± 0.07 ng/ml · 150 min) and epinephrine (AUC 14.9 ± 0.17 ng/ml ·150 min) responses. Similarly, no changes in glucose counterregulation were observed in the six IDDM patients in whom glycemic control was poorly maintained for 6–8 mo (MBG 201 ± 7 mg/dl, ketoamine-HbA112.3 ± 0.2%).
In five patients with short duration of IDDM (11 ± 0.5 mo) and optimized glycemic control (MBG 131 ± 8 mg/dl, ketoamine-HbA1 7.9 ± 0.2%), rates of plasma glucose recovery, as well as counterregulatory responses of plasma glucagon and epinephrine, were normal. Neither deterioration of glycemic control for 2 wk (MBG 229 ± 12 mg/dl, ketoamine-HbA1 9.1 ± 0.2%) nor its improvement over the 2 subsequent wk (MBG 120 ± 8 mg/dl, ketoamine-HbA1 8.5 ± 0.2%) resulted in any significant change in glucose counterregulation. It is concluded that near-normalization of glycemic control for up to 9 mo is insufficient to reverse the impairment in glucose counterregulation found in long-term IDDM. Short-term deterioration in glycemic control, when not accompanied by alterations in counterregulatory hormone secretion, does not impair glucose counterregulation.
Effect of Insulin Antibodies on Insulin Pharmacokinetics and Glucose Utilization in Insulin-dependent Diabetic Patients
Authors: Waldhäusl Werner K , Bratusch-Marrain Paul , Kruse Viggo , Jensen Ivan , Nowotny Peter , Vierhapper Heinrich 
Published: September 2013

To determine the impact of insulin-binding antibodies on total (TIRI) and free insulin (FIRI) as well as on insulin sensitivity, 10 insulin-dependent diabetic patients (IDDM) with poststimulatory C-peptide &lt;100 pmol/L and an insulin binding capacity (IBC) between &lt;1 and 294 μg/L serum were studied during and after a 1-h nonprimed, constant-rate insulin infusion (study 1: 0.057 U/kg body wt, study 2: 0.286 U/kg body wt). Euglycemia was maintained by variable glucose infusion. Control studies were performed in 5 healthy subjects.
Basal TIRI (mU/L) was lowest in healthy subjects (16 ± 1 [SE]) and elevated in diabetic patients (IBC &lt;25 μg/L: 72 ± 11, IBC &gt;25 μg/L: 1772 ± 842), whereas serum concentrations of FIRI were considerably smaller but still two- to threefold greater (P &lt; 0.01) in the patients than in healthy subjects (13 ± 1). After intravenous (i.v.) insulin administration, almost identical increments in serum TIRI were seen in healthy subjects and in diabetic patients with low IBC (&lt;25 μg/L), whereas those with high IBC (&lt;25 μg/L) had a heterogeneous response.
The increments of free serum insulin induced by the infusion of 0.057 and 0.286 U of insulin/kg body wt were almost identical for healthy subjects and diabetic patients, whereas overall glucose utilization, as estimated by the glucose infusion rate necessary to maintain euglycemia, was mostly lower in the diabetic patients (low IBC: study 1: 3.2 ± 0.4 mg/kg min, study 2: 4.0 ± 0.3; high IBC: study 1: 1.2 ± 0.1, study 2: 3.8 ± 0.3) than in healthy subjects (study 1: 3.9 ± 0.6, study 2: 6.1 ± 0.5). Insulin clearance remained constantly within the normal range, but tended to be elevated in diabetic patients with high IBC, who also displayed a 50–100% rise in apparent insulin half-life.
We conclude that elevated insulin-binding capacity: (1) increases serum total insulin, but affects serum free insulin only to a minor extent, and (2) is associated with a rise in apparent free insulin half-life in diabetic patients with high IBC only. (3) Insulin sensitivity is significantly impaired in IDDM and is not improved by short-term normal glycemia; and (4) the relative contribution of insulin antibodies and nonimmunologic factors to impaired insulin action in IDDM cannot be separated by the euglycemic clamp technique.
Slow Component-a of Axonal Transport, Nerve myo-Inositol, and Aldose Reductase Inhibition in Streptozocin-Diabetic Rats
Authors: Tomlinson David R , Sidenius Per , Larsen Jørn Rolighed 
Published: September 2013

This study measured sugars and polyols, weight/unit length, and slow component-a of axonal transport (SCa) in dorsal root afferents of the sciatic nerves of control rats and rats with streptozocin (STZ)-induced diabetes of 4-wk duration. The effects of two treatments—aldose reductase inhibition ‘Statil (“Static” is a trademark; the property of Imperial Chemical Industries PLC.) ICI 128436 at 25 mg/kg/day, p.o.’ and myo-inositol supplementation (650 mg/kg/day, p.o.)—were studied in control and diabetic groups. Inclusion of untreated controls and diabetics gave a total of six groups for the study. The treatments were begun on the day after injection of STZ and were maintained throughout the protocol.
The sciatic nerves of the diabetic (untreated) rats showed accumulation of sorbitol and fructose, depletion of myo-inositol, and an 8% increase in weight/unit length. All of these abnormalities were prevented by treatment with Statil. Treatment of diabetic rats with myo-inositol prevented its depletion in the sciatic nerve, but did not affect the accumulation of sorbitol and fructose nor the increase in weight/unit length. Neither treatment exerted any apparent effect on body weight, blood glucose, nerve weight, or nerve sugars and polyols in the control rats.
The diabetic rats showed a retardation of the wave of transported-labeled protein (shown as increased leftward skewness of the wave) and a reduction in mean transport velocity (calculated as the mean velocity for all segments contributing to the transport wave: 0.96 ± 0.09 mm/day in diabetics versus 1.15 ± 0.07mm/day in controls). These abnormalities were not affected significantly in the diabetic groups by treatment with either Statil or with myo-inositol.
Quelques aspects généraux de l'évolution économique et monétaire mondiale en 1956
Authors: Hérouville Hubert d' 
Published: September 2013

L'expansion économique se poursuit, mais à un rythme ralenti en Europe occidentale et orientale ainsi qu'en U.R.S.S. Aux États-Unis, la reprise amorcée à l'automne dernier reste très peu sensible et au Canada on s'attend également à une augmentation de l'activité moindre qu'il n'était prévu.
Cependant, les tensions inflationnistes se maintiennent ; elles se renforcent même parfois. Il y a un climat général de hausse des prix (prix de gros, coût de la vie, salaires...), à peine tempéré, en fin d'année, par une baisse des cours de certaines matières premières.
Les pouvoirs publics poursuivent leur politique de restriction de crédit (en l'assouplissant dans quelques cas), et plus généralement de limitation de la demande globale. L'épargne continue à se développer.
Dans l'ensemble, les plus grandes difficultés ont été éprouvées pour tenter de maintenir l'expansion sans inflation.
Les transformations des réserves monétaires mondiales et l'évolution des balances extérieures des États-Unis
Authors: Silz Édouard 
Published: September 2013

La présente étude est consacrée aux changements les plus notables que l'on a observés en ces dernières années dans les réserves en or et en devises et à la recherche des causes qui les expliquent.
Mais les notions de réserves et de devises prêtent à autant de définitions, et répondent à autant de concepts différents que le concept même de monnaie. Aussi, a-t-il fallu recourir pour les recouper les unes par les autres à des statistiques de conception et d'inspiration différentes — d'où les tentatives de rapprochement et de critique statistique qui ont été faites au début de l'article.
Pour juger de la signification économique des transformations survenues, il a fallu ensuite examiner ce qu'il était possible d'entendre par «adéquation» des réserves aux besoins. A la lumière de l'analyse théorique qui en a été donnée, il est apparu qu'un exposé pleinement exhaustif n'était pas possible et que la meilleure approche consistait à examiner distinctement l'évolution des comptes des principaux composants de l'économie internationale et au premier chef des États-Unis. En effet, ce sont directement ou indirectement les relations des U.S.A. avec les autres pays qui, en définitive, déterminent les transformations dans les réserves d'or et devises. D'où la deuxième partie consacrée aux balances extérieures des États-Unis : l'exposé des balances extérieures de l'Allemagne et de la Grande-Bretagne étant réservé à un numéro ultérieur.
Les balances américaines ont été examinées à la lumière de l'évolution de toute la période d'après-guerre en reprenant successivement : la balance des règlements courants, l'aide gouvernementale et les mouvements de capitaux privés. C'est leur combinaison qui explique, en définitive, l'apport de devises qu'elles ont dû fournir au reste du monde. L'étude qui en a été faite dans leur ensemble et distinctement aussi avec les principaux pays et zones monétaires fait apparaître que les transformations intervenues dans l'économie des balances au cours des dix dernières années sont aussi essentielles que les traits communs qui s'y retrouvent.
Après le retour progressif à l'équilibre encore assez précaire qui s'était opéré à partir de la fin de la récession américaine et de la guerre de Corée, il semble que l'on soit entré, depuis peu, dans une nouvelle phase qui paraît témoigner d'une accentuation du poids spécifique des États-Unis dans l'économie internationale. Un gonflement général de la valeur des transactions, le retour à un excédent croissant de la balance américaine des règlements courants, des transformations de la technique et de la répartition de l'aide américaine, des exportations de capitaux privés plus importants caractérisent cette nouvelle phase qui a été particulièrement étudiée.
Systemic treatment with 4-211At - phenylalanine enhances survival of rats with intracranial glioblastoma
Authors: Borrmann N. , Friedrich S. , Schwabe K. , Hedrich H. J. , Krauss J. K. , Knapp W. H. , Nakamura M. , Meyer G.-J. , Walte A. 
Published: September 2013

SummaryObjective: Increased amino acid transport in brain tumours is used for diagnostic purposes. It has been shown that the α-emitting radionuclide astatine-211 labeled to L-phenylalanine is taken up by glioblastoma cells. We here tested, if systemic treatment with 4-[211At] astatine-phenylalanine (At-Phe) has a beneficial effect on survival of rats with intracranial glioblastoma. Animals, methods: The rat glioblastoma cell line BT4Ca was implanted into the prefrontal cortex of female BDIX rats by stereotaxic microinjection (10 000 cells/3 μl; n = 83). 3 days after implantation At-Phe or phosphate buffered saline were injected intravenously. A third group was treated twice, i.e., on day 3 and 10. Health condition was assessed each day by using a score system. Rats were sacrificed on days 6, 10, 13 and 17 after implantation, or when showing premortal health condition to measure tumour volume and necrosis. The proliferation index (PI) was assessed after immunohistochemical staining of Ki-67. Results: Survival time of rats treated twice with At-Phe was significantly prolonged. Additionally, both At-Phe-treated groups remained significantly longer in a better health condition. Rats with poor health status had larger tumours than rats with fair health condition. Overall, irrespective of treatment the PI was reduced in rats with poor health condition. Necrosis was larger in rats treated twice with At-Phe. Conclusion: Intravenous treatment with At-Phe enhanced survival time of rats with intracranial glioblastomas and improved health condition. These results encourage studies using local treatment of intracranial glioblastoma with At-Phe, either by repeated local injection or by intracavital application after tumour resection.
Low Bone Density in Systemic Sclerosis. A Systematic Review
Authors: Omair Mohammed A. , Pagnoux Christian , McDonald-Blumer Heather , Johnson Sindhu R. 
Published: September 2013

Objective.The effect of systemic sclerosis (SSc) on bone density is not well understood. Through systematic review of the literature, the objectives of this study were to synthesize data about the prevalence of low bone mineral density (BMD), risk factors for low BMD, and occurrence of fracture and fracture-related mortality in SSc.Methods.A search was conducted of MEDLINE (1948–2012), Evidence Based Medicine Reviews (1991–2012), EMBASE (1980–2012), and CINAHL (1981–2012). Abstracts were screened to identify studies that evaluated low BMD in patients with SSc. Two investigators independently used a standardized form to abstract prevalence of osteopenia and osteoporosis (OP); risk factors for low BMD, BMD measurements, frequency of fracture, and fracture-related mortality.Results.Screening of 1032 citations identified 19 articles. Fifteen studies compared patients with SSc to controls. Most patients were white, female (prevalence 74%–100%), and postmenopausal (prevalence 45.9%–100%). The prevalence of low BMD and OP was 27%–53.3% and 3%–51.1%, respectively. Ten studies reported a lower BMD in patients with SSc compared to matched controls, whereas 2 studies reported no difference. Candidate risk factors for low BMD in SSc include family history of OP, age, menopause, diffuse subtype, presence of internal organ involvement, low vitamin D levels, and calcinosis. However, the studies supporting these factors were conflicting. Fracture rate ranged between 0% and 38%. No study reported OP-related fracture mortality.Conclusion.The data suggest that patients with SSc are at risk of low BMD and fracture, especially when other risk factors for OP are present. The interaction of SSc manifestations, traditional OP risk factors, and clinically relevant outcomes is complex and warrants further research.
Syrian field hospitals: A creative solution in urban military conflict combat in Syria
Authors: Sankari Abdulghani , Atassi Basel , Sahloul Mohammed Zaher 
Published: September 2013

AbstractSince the war started in Syria nearly two years ago several independent organizations reported the use of medicine as a weapon by the Syrian authorities, killing of doctors and arresting patients who were admitted to the hospitals for treatment. In year 2012 the World Health Organization (WHO) found nearly 50% of hospitals are not functioning due to lack of staff, equipment and medicine. This report highlights how the doctors in Syria are creative and courageous to risk their own lives to save thousands of innocent lives.