bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pilzsepsis – Therapeutische Strategie
Authors: Staubach K. H. 
Published: March 2005

ZusammenfassungDie Pilzsepsis stellt infolge der massiv angestiegenen systemischen Mykosen auch bei nicht neutropenischen Intensivpatienten ein nicht unerhebliches Problem dar. Aufgrund des großzügigen Einsatzes von Breitspektrumantibiotika erhält die physiologische Candida‐Besiedelung eine pathologische Bedeutung. Die Therapie der Pilzsepsis besteht aus kausalen, supportiven und adjunktiven Maßnahmen sowie einer so genannten Sepsisprophylaxe. Allein die sparsame und gezielte Applikation von Antibiotika könnte als Sepsisprophylaxe die Inzidenz und Letalität senken. Supportive und adjunktive Maßnahmen wie die zielorientierte Herz‐Kreislauf‐Therapie, die niedrig dosierte Kortikosteroid‐Therapie, die Applikation von aktiviertem Protein C und das Erreichen einer Normoglykämie können nach konsequenter Fokussanierung und Standardintensivtherapie das Outcome der Sepsispatienten signifikant verbessern.
SOLUBLE BIO‐MARKERS IN VASCULAR DISEASE: MUCH MORE THAN GAUGES OF DISEASE?
Authors: Woollard Kevin J 
Published: March 2005

SUMMARY1. In recent years demonstration of a direct association between slightly elevated serum levels of soluble proteins including the acute phase response proteins, selectins and intercellular adhesion molecules and the risk of developing vascular disease have been widely reported. These studies may provide the clinician with an insight into disease diagnosis, prognosis and disease activity.2. The simplest interpretation of this data is that soluble proteins are just sensitive markers of inflammation. However, they may in fact be modulating inflammation directly through interaction with circulating cells.3. Recent work has shown that these soluble proteins do indeed remain active and can bind to functional ligands expressed by circulating leucocytes. The current review focuses on the soluble proteins C‐reactive protein and soluble P‐selectin and describes previous studies characterizing their interaction with immune cells to modulate the pathogenesis of vascular disease.4. The current review focuses on the soluble proteins C‐reactive protein and soluble P‐selectin and describes previous studies characterizing their interaction with immune cells to modulate the pathogenesis of vascular disease.
RENAL DENERVATION CAUSES CHRONIC HYPOTENSION IN RATS: ROLE OF Β1‐ADRENOCEPTOR ACTIVITY
Authors: Jacob Frédéric , LaBine Brian G , Ariza Pilar , Katz Stephen A , Osborn John W 
Published: March 2005

SUMMARY1. Renal denervation (RDNX) chronically lowers mean arterial pressure (MAP) in normal rats but mechanisms leading to this hypotensive response remain unknown.2. We hypothesized that this sustained decrease in arterial pressure was because of a loss of β1‐adrenoceptor mediated renin secretion. Male Sprague‐Dawley rats were assigned to sham (SHAM; n = 9), unilateral (UniRDNX; n = 9), or bilateral (RDNX; n = 10) renal denervation groups and instrumented for telemetric MAP measurements, plasma renin concentration (PRC) measurements and intravenous infusion. Twenty‐four h MAP, heart rate, sodium and water balances were recorded 5 days before, 3 days during and 3 days after 1‐adrenoceptor blockade with atenolol.3. The 5‐day control MAP was significantly lower in RDNX (97 ± 1 mmHg) compared to SHAM (105 ± 2 mmHg) and UniRDNX (102 ± 2 mmHg) rats. No significant differences in basal PRC were observed between RDNX (2.2 ± 0.3 ngAng1/mL per h), UniRDNX (2.6 ± 0.4 ng/Ang1/mL per h) and SHAM (2.6 ± 0.4 ngAng1/mL per h) rats. By day 1 of atenolol, PRC was significantly lower in UniRDNX rats (1.8 ± 0.2 ngAg1/mL per h) compared to control values, but was unchanged during atenolol infusion in the other groups. By day 3 of atenolol, MAP was significantly decreased in all groups, but the absolute levels of MAP remained statistically different between RDNX (87 ± 1 mmHg) and SHAM (91 ± 1 mmHg) groups.4. We conclude that the arterial pressure lowering effect of RDNX is not solely dependent on the loss of neural control of renin release.
CARDIOVASCULAR ADAPTATIONS IN RATS SUBMITTED TO A RESISTANCE‐TRAINING MODEL
Authors: Barauna Valerio G , Junior Miguel Luis B , Costa Rosa Luis Fernando BP , Casarini Dulce E , Krieger José Eduardo , Oliveira Edilamar M 
Published: March 2005

SUMMARY1. The present study sought to evaluate cardiovascular adaptations, such as blood pressure (BP), heart rate (HR) and cardiac hypertrophy, to resistance training (RT) in a rat model.2. The training protocol consisted of four sets of 10–12 repetitions of the squat exercise performed at 65–75% of one repetition maximum (1RM) over 4 weeks. Animals were randomly divided into three groups: control (n = 8, CO), electrically stimulated (n = 8, ES) and trained (n = 8, TR; also electrically stimulated). Blood pressure and HR were measured by a direct method in conscious rats after the training period.3. All groups began with similar 1RM and 1RM/bodyweight (BW) ratio, however, at the end of the protocol only the TR group was different from the beginning (56% and 50%, respectively; both P < 0.01). The CO and ES groups had similar values for cardiac chambers weight/BW ratio, HR and diastolic, systolic and mean BP. Left ventricular hypertrophy (LVH) determined by the left ventricle (LV) weight/BW ratio was increased in the TR group (12%) when compared to CO (P < 0.01) or ES groups (P < 0.01). No changes were found in the weights of the atrium or right ventricle. Diastolic (14%) and mean BP (13%) were lower in the TR group (P < 0.05), whereas systolic BP and HR remained unchanged.4. Collectively these results demonstrate that the rat RT model used is associated with significant development of cardiac hypertrophy and lowering of resting BP. These cardiovascular adaptations seem to a result of the training exercise and not influenced by stress since circulating catecholamine levels and adrenal gland weights remained unchanged in all groups.
DIFFERENTIAL REGULATION OF ANGIOTENSIN II RECEPTORS DURING RENAL INJURY AND COMPENSATORY HYPERTROPHY IN THE RAT
Authors: Joly Emma , Nonclercq Denis , Caron Nathalie , Mertens Jeannine , Flamion Bruno , Toubeau Gerard , Kramp Ronald , Bouby Nadine 
Published: March 2005

SUMMARY1. The renin‐angiotensin system may be involved in the compensatory adaptations occurring after the reduction of renal mass and during the consecutive changes leading to chronic renal failure. We therefore investigated the regulation of angiotensin II receptors in two models of renal hypertrophy in the rat: hypertrophy following uninephrectomy (UNx) or subtotal nephrectomy (STNx). The level of angiotensin type 1 (AT1A‐R and AT1B‐R) and type 2 (AT2‐R) receptor mRNA was quantified by competitive reverse transcription‐polymerase chain reaction (RT‐PCR) in specific renal zones and the intrarenal distribution of angiotensin II receptors was analysed by immunohistochemistry.2. In the UNx rats, AT1‐R mRNA expression was not modified in the cortex or in the inner stripe of the outer medulla of the residual kidney at any time after the surgery (1, 4 and 12 weeks). In contrast, AT1‐R mRNA expression was significantly reduced in these zones in STNx rats (−33% and −40%, respectively). This downregulation was organ‐specific, as AT1‐R mRNA levels were not modified in the liver. The proportions of AT1‐R subtype (AT1A and AT1B) mRNA were unchanged by UNx or STNx. Very low levels of AT2‐R mRNA were found in the cortex of all groups. Immunostaining revealed a similar localization of AT1‐R in mesangial cells, proximal tubule, basolateral membrane of thick ascending limb, in both models of hypertrophy. AT1‐R labelling was also detected in the apical membrane of intercalated cells of cortical collecting ducts.3. This differential mRNA expression of angiotensin II receptors during compensatory hypertrophy and renal injury suggests that the development of renal hypertrophy is independent of AT1‐R and AT2‐R gene expression levels.
EFFECT OF ZINC SULPHATE AND ZINC METHIONINE ON GROWTH, PLASMA GROWTH HORMONE CONCENTRATION, GROWTH HORMONE RECEPTOR AND INSULIN‐LIKE GROWTH FACTOR‐I GENE EXPRESSION IN MICE
Authors: Yu Ze‐Peng , Le Guo‐Wei , Shi Yong‐Hui 
Published: March 2005

SUMMARY1. The current experiment was conducted to investigate the effect of zinc sulphate (ZnSO4) and zinc methionine (Zn‐Met) on growth and their effect on plasma growth hormone (GH) concentration, growth hormone receptor (GHR) and insulin‐like growth factor I (IGF‐I) mRNA expression in mice.2. Ninety male KunMing (KM) mice were randomly divided into three treatments. The control group was fed on a basal diet containing 11.67 mg/kg of zinc. The ZnSO4 group and Zn‐Met group were fed on the diets supplemented with ZnSO4 or Zn‐Met at 30 mg/kg (containing zinc of 40.05 and 40.75 mg/kg, respectively). The mice were offered the test diets for 10 days. Weight gains and food intake were measured at the end of the experiment, zinc contents in liver and serum were determined using atomic absorption spectrophotometry; GH was determined by radioimmunoassay, the levels of GHR and IGF‐I mRNA were determined with reverse transcript polymerase chain reaction.3. Both ZnSO4 and Zn‐Met enhanced weight gain and food intake in the mice, Zn‐Met improved the growth and food intake more effectively than ZnSO4 did (P < 0.05). The both forms of zinc had no effect on GH and the level of GHR mRNA expression (P > 0.05) and they up‐regulated the expression of IGF‐I mRNA (P < 0.05). As compared to ZnSO4, Zn‐Met enhanced the level of IGF‐I mRNA significantly (P < 0.05).4. Both ZnSO4 and Zn‐Met had no effect on plasma GH and the expression of GHR mRNA, but they enhanced the expression of IGF‐I mRNA. Zinc methionine enhanced the weight gain and up‐regulated IGF‐I mRNA expression more effectively than ZnSO4.
RESISTANCE TO EXCESSIVE BODYWEIGHT GAIN IN RISPERIDONE‐INJECTED RATS
Authors: Ota Miyuki , Mori Keiji , Nakashima Akira , Kaneko Yoko S , Takahashi Hisahide , Ota Akira 
Published: March 2005

SUMMARY1. The present study was carried out to explain the resistance of rats injected subcutaneously with risperidone, the atypical antipsychotic drug, for 21 consecutive days at 0.1 mg/kg per day (a dose equivalent to the one used for patients) to result in an excessive bodyweight despite the increase in diet‐uptake in rats against risperidone‐induced decrease in body temperature.2. Rectal temperature measurements were made in 8‐week‐old male Sprague‐Dawley rats maintained under standard laboratory conditions using a 12 h daylight cycle. A s.c. injection of risperidone (0.05 mg/kg) produced hypothermia in rats, which was observed during the daily injection for 21 consecutive days.3. Sera, white and brown adipose tissues, skeletal muscle and liver were extracted from 8‐week‐old male Sprague‐Dawley rats injected subcutaneously with risperidone (0.01 or 0.1 mg/kg per day) or a vehicle for 21 consecutive days. Serum levels of lipids, ketones and thyroid hormone were measured. The mRNA expression levels in these tissues and organs of the genes encoding the substances involved in heat production and/or lipid metabolism were investigated by using quantitative real‐time polymerase chain reaction amplification.4. Serum nonesterified fatty acid levels in risperidone 0.1 mg/kg per day s.c. injected rats were significantly lower than those in vehicle‐injected ones. Serum β‐hydroxybutyrate levels in risperidone‐injected rats tended to decrease compared with those in vehicle‐injected ones. The serum level of neither triiodothyronine nor thyroxine was affected by risperidone s.c. injection at the doses examined, although their values were within normal limits.5. Risperidone injection (0.1 mg/kg per day) for 21 consecutive days upregulated mRNA expressions in white adipose tissue of uncoupling protein 3 which dissipates energy as heat; peroxisome proliferator‐activated receptor (PPAR) γ coactivator 1α which activates mitochondrial biogenesis to expand the oxidative machinery; and PPARα which is necessary for the fat‐depletion of adipocytes for thermogenesis. The mRNA of lipogenic enzymes (acetyl‐CoA carboxylase α, fatty‐acid synthase and glycerol‐3‐phosphate acyltransferase), hormone sensitive lipase and β1‐adrenoceptor were also enhanced in white adipose tissue by the injection of 0.1 mg/kg per day risperidone.6. These findings suggest that the materials for heat generation in white adipose tissue would be readily supplied, which in turn would reduce a storage of lipids in white adipose tissue resulting in the lower rate of bodyweight gain of rats.
OPTICAL IMAGING OF RESPIRATORY NEURON ACTIVITY FROM THE DORSAL VIEW OF THE LOWER BRAINSTEM
Authors: Onimaru Hiroshi , Homma Ikuo 
Published: March 2005

SUMMARY1. We visualized respiratory‐related neuron network activity in the dorsal part of the pons and medulla of an in vitro preparation from newborn rats by optical recordings using a voltage‐sensitive dye. We measured optical signals from several seconds before to several seconds after the inspiratory phase using the inspiratory motor nerve discharge as the trigger signal and we averaged the optical signals of 20–50 respiratory cycles to obtain an optical image correlating specifically to inspiratory activity.2. Four areas that were excited or inhibited corresponding to the respiratory cycles were detected. (i) The most rostral activity was in the rostral and lateral parts of the pons, with activity mainly in the inspiratory phase, corresponding to the pontine‐respiratory group. (ii) In the midpontine level, inspiratory activity followed by long‐lasting hyperpolarization appeared in the midlateral parts. This part was presumed to reflect activity in the locus coeruleus. The hyperpolarization became almost negligible after treatment with the α‐adrenergic antagonist, phentolamine. (iii) In the dorsal medulla, the predominantly inspiratory activity was detected at the rostral level of the area postrema. This part was considered to reflect activity mainly of the hypoglossal nucleus. (iv) At a similar level, we also detected weak and disperse inspiratory activity extending more laterally and caudally than that of the hypoglossal nucleus activity. This might reflect activity of the dorsal respiratory group.3. In conclusion, the present optical recording study revealed that the dorsal part of the lower brainstem in the in vitro preparation is noticeably active as well as the ventral part shown in the previous study. This method is very useful for analysis of pharmacological properties, as well as the spatio‐temporal pattern of respiratory‐related network activity in the brainstem.
ACTIVE ROLE FOR THE VASCULATURE IN THE DELIVERY OF INSULIN TO SKELETAL MUSCLE
Authors: Vincent Michelle A , Clerk Lucy H , Rattigan Stephen , Clark Michael G , Barrett Eugene J 
Published: March 2005

SUMMARY1. In the 80+ years since insulin's discovery, an enormous amount of literature has accumulated relating to its actions on body fat, glucose and protein metabolism. In particular, skeletal muscle has been extensively studied because of its major role as a site of insulin‐mediated glucose disposal. Liver and adipose tissue are two other extensively studied sites of insulin action. Much less investigation has been directed towards delineating insulin's actions on cells other than myocytes, adipocytes and hepatocytes.2. Over the past 5–10 years it has become increasingly evident that insulin exerts important actions on vascular cells. Here, we review evidence that insulin's action within muscle may be very much regulated by its ability to transit the vasculature to access the interstitial fluid (and hence the myocyte insulin receptor). Surprisingly little is known regarding the regulation of vascular events that first bring insulin to the capillary endothelium within muscle, whence presumably it transits from the vascular to the interstitial space. Recent studies suggest that insulin can increase blood flow and also influence the distribution of blood flow within skeletal muscle, potentially therefore regulating its own delivery to the capillary endothelium. Beyond insulin's ability to access the vascular lumen within skeletal muscle microvasculature lies the issue of its passing the endothelial barrier. Even less is known about the processes involved in insulin's actual transit across the endothelium. Available data do not clearly indicate whether this is a saturable, receptor‐mediated process or a passive‐diffusion pathway. Also, whether insulin in any manner regulates its own transit across the endothelium or its clearance via the lymphatic system is entirely unknown.3. The aim of the present review is to identify areas where knowledge is deficient and highlight hypotheses which may lead to a better understanding of the coordinated relationship between insulin's vascular actions within muscle and its metabolic actions in that tissue. Even so, there is now sufficient evidence to indicate that insulin's vascular action within skeletal muscle is a major regulatory locus for its insulin mediated glucose disposal.
USE OF GLUT‐4 NULL MICE TO STUDY SKELETAL MUSCLE GLUCOSE UPTAKE
Authors: Charron Maureen J , Gorovits Naira , Laidlaw J Skye , Ranalletta Mollie , Katz Ellen B 
Published: March 2005

SUMMARY1. The present review focuses on the effects of varying levels of GLUT‐4, the insulin‐senstive glucose transporter, on insulin sensitivity and whole body glucose homeostasis.2. Three mouse models are discussed including myosin light chain (MLC)‐GLUT‐4 mice which overexpress GLUT‐4 specifically in skeletal muscle, GLUT‐4 null mice which express no GLUT‐4 and the MLC‐GLUT‐4 null mice which express GLUT‐4 only in skeletal muscle. Overexpressing GLUT‐4 specifically in the skleletal muscle results in increased insulin sensitivity in the MLC‐GLUT‐4 mice. In contrast, the GLUT‐4 null mice exhibit insulin intolerance accompanied by abnormalities in glucose and lipid metabolism. Restoring GLUT‐4 expression in skeletal muscle in the MLC‐GLUT‐4 null mice results in normal glucose metabolism but continued abnormal lipid metabolism.3. The results of experiments using these mouse models demonstrates that modifying the expresssion of GLUT‐4 profoundly affects whole body insulin action and consequently glucose and lipid metabolism.
GLUCOSE PHOSPHORYLATION AS A BARRIER TO MUSCLE GLUCOSE UPTAKE
Authors: Fueger Patrick T 
Published: March 2005

SUMMARY1. Glucose phosphorylation is the first irreversible step of the muscle glucose uptake pathway and is catalysed by a hexokinase isozyme.2. While glucose transport is the primary barrier to muscle glucose uptake during basal conditions, glucose phosphorylation becomes an important barrier to muscle glucose uptake during stimulated conditions such as hyperinsulinaemia or exercise.3. High fat feeding markedly impairs insulin‐ and exercise‐stimulated muscle glucose uptake. As hexokinase II overexpression corrects this dietary‐induced deficit during exercise, glucose phosphorylation is a site of impairment following high fat feeding.4. Exercise is an important tool for diagnosing deficits in glucose phosphorylation.
INTERACTION OF PHYSIOLOGICAL MECHANISMS IN CONTROL OF MUSCLE GLUCOSE UPTAKE
Authors: Wasserman David H , Ayala Julio E 
Published: March 2005

SUMMARY1. Control of glucose uptake is distributed between three steps. These are the rate that glucose is delivered to cells, the rate of transport into cells, and the rate that glucose is phosphorylated within these same cells. The functional limitations to each one of these individual steps has been difficult to assess because they are so closely coupled to each other. Studies have been performed in recent years using complex isotopic techniques or transgenic mouse models to shed new light on the role that each step plays in overall control of muscle glucose uptake.2. Membrane glucose transport is a major barrier and glucose delivery and glucose phosphorylation are minor barriers to muscle glucose uptake in the fasted, sedentary state. GLUT‐4 is translocated to the muscle membrane during exercise and insulin‐stimulation. The result of this is that it can become so permeable to glucose that it is only a minor barrier to glucose uptake.3. In addition to increasing glucose transport, exercise and insulin‐stimulation also increase muscle blood flow and capillary recruitment. This effectively increases muscle glucose delivery and by doing so, works to enhance muscle glucose uptake.4. There is a growing body of data that suggests that insulin resistance to muscle glucose uptake can be because of impairments in any one or more of the three steps that comprise the process.
GANGLION BLOCKADE DOES NOT PREVENT CORTISOL‐INDUCED HYPERTENSION IN MAN
Authors: Williamson Paula M , Tam Sim Hom , Kelly John J , Whitworth Judith A 
Published: March 2005

SUMMARY1. The aim of the present study was to assess the effect of ganglion blockade on blood pressure in cortisol treated human subjects.2. Four healthy male subjects were treated with cortisol 80 mg/day for a 5‐day period. Ganglion blockade was achieved by intravenous trimethaphan.3. Ganglion blockade did not significantly alter blood pressure in the pretreatment phase or on the last day of cortisol treatment.4. Taken together with our previous observations that sympathetic activity is unaltered or reduced by cortisol, these results suggest that cortisol induced hypertension in humans is not a result of overactivity of the autonomic nervous system.
Comparison of inhaled corticosteroid combined with theophylline and double‐dose inhaled corticosteroid in moderate to severe asthma
Authors: WANG Yan , WANG Chang‐Zheng , LIN Ke‐Xiong , QIAN Gui‐Sheng , ZHUO Wen‐Lei , LI Shu‐Ping , ZHAO Zhi‐Qiang , LIAO Xiu‐Qing , SONG Yun‐Xi 
Published: March 2005

Objective:  Recent studies have found that theophylline exerts anti‐inflammatory and immunomodulatory effects. This study was performed to compare the efficacy of inhaled corticosteroids (ICS) combined with slow‐release theophylline (SRT) with that of double‐dose ICS in asthma control, anti‐inflammatory activity and safety.Methodology:  In a randomized, open, parallel, control trial, 41 patients with asthma were randomly treated with either beclomethasone dipropionate 500 µg b.i.d. (BDP group) or a combination of BDP 250 µg b.i.d and SRT 0.2 g b.i.d. (SRT/BDP group) for 6 weeks. At the start and at the end of treatment, lung function testing and sputum induction were performed, and plasma cortisol levels were measured. Sputum was analyzed for cell differential counts and the interleukin (IL)‐5 level. Patients kept a record of peak expiratory flow (PEF), symptom score, and β2‐agonist use.Results:  Significant increases in the morning and the evening PEF and FEV1 were observed (P < 0.05), together with an obvious reduction in symptom score and β2‐agonist use (P < 0.01). Significant decreases in the percentage eosinophils and IL‐5 level in induced sputum also occurred (P < 0.05). However, there was no difference between the two groups for all these parameters. There was no significant change in the plasma cortisol level for either group.Conclusions:  Both ICS combined with SRT and double‐dose ICS had the same effect on asthma control, improving symptoms and ameliorating lung function. Both therapies had similar anti‐airway inflammatory effects and therapeutic safety. Combining SRT with ICS may allow a reduction in ICS dose when treating asthma.