bluuebunny/crossref_metadata_2025_split huggingface dataset:
Semi‐starvation alters myofibrillar mRNA concentrations to expedite rapid recovery of muscle protein stores following feeding
Authors: Svanberg  , Kiri  , Isgaard  , Goldspink  
Published: March 2003

BackgroundProtein synthesis in skeletal muscle is reduced following starvation and restored by feeding. The mediators and mechanisms are incompletely understood. The aim of this study was to evaluate whether prolongation of undernutrition induced changes in muscle gene expression at the level of mRNA and protein.Materials and methodsThe changes in myosin heavy‐chain 2X mRNA in adult partially starved (50% of ad libitum standard rodent chow intake for 4 or 7 days) C57BL mice or subsequently refed mice were studied. Ad libitum‐fed mice were used as controls. Protein synthesis, total RNA and myosin heavy‐chain 2X mRNA concentrations were determined. Plasma concentrations of amino acids were measured by high‐performance liquid chromatography.ResultsPartial starvation of 4 and 7 days reduced body weight by 15.6 ± 1% and 17.1 ± 2.1% (P ≤ 0.05) vs. ad libitum fed controls. Protein synthesis was reduced by 32 ± 9% and protein content by 20 ± 4% (P ≤ 0.05) following 7 days of partial starvation. Plasma amino acid concentrations were increased (6297 ± 853) in refed animals vs. ad libitum‐fed controls (3057 ± 141, P ≤ 0.05). Total RNA concentration (μg RNA μg−1 DNA) in skeletal muscle was unchanged. Myosin heavy‐chain 2X mRNA concentration did not change following 4 days of partial starvation but increased by 24 ± 5% (P ≤ 0.05) following 7 days of partial starvation, hence suggesting that expression of myosin mRNA was nutritionally altered.ConclusionPostprandial stimulation of protein synthesis following starvation may thus be a combination of increased mRNA availability and increased translation. This effect may be activated by peak concentrations of amino acids in plasma following feeding.
Protein sgp 120 as a marker of an acquired angioedema
Authors: Paranos S. , Nikolic G. 
Published: March 2003

BackgroundAngioedema is not an event peculiar to an acute‐phase response. We registered the appearance of angioedema in four nonatopic patients suffering from diverse inflammatory stimuli.Materials and methodsSerum concentrations of C‐reactive protein (CRP), haptoglobin, α1‐antitrypsin, α2‐macroglobulin, C3, C4, C1INH and protein sgp 120 (classified as a regulatory protein of the complement system) were assessed over 7 consecutive days, beginning with the onset of angioedema in these four patients.ResultsInstead of returning to the normal level, CRP peaked again on the 4th day (A‐test, P < 0.05) and declined significantly by the 7th day (A‐test, P < 0.05). Serum levels of sgp 120, C3c and C1INH increased gradually up to the 5th day but only sgp 120 was significantly raised in relation to the initial value (P < 0.05).ConclusionIn our patients, we registered four diverse profiles of the acute‐phase proteins (Kruskal–Wallis test, P < 0.05) probably due to the diverse nature of the pre‐existing inflammatory stimuli. According to these results, the unexpected appearance of angioedema implies the contribution of sgp 120 as the main source of fragments with kinin‐like properties.
α‐tocopherol improves impaired physiology of rat type II pneumocytes isolated from experimentally injured lungs
Authors: Müller B. , Hochscheid R. , Seifart C. , Barth P. J. 
Published: March 2003

BackgroundOxidant stress delivered by nitrogen dioxide (NO2) inhalation impairs the function of extracellular surfactant as well as surfactant phospholipid metabolism in type II pneumocytes. Because protection against oxidant stress is important to normal lung function, the lung contains a variety of antioxidants, including vitamin E. Whether administration of this antioxidant during NO2 inhalation attenuates NO2‐induced alterations in phospholipid metabolism in type II pneumocytes has not been studied.MethodsWe exposed rats to identical NO2 body doses (720 p.p.m. x h) using continuous, intermittent, or repetitive protocols. During exposure periods, the animals received daily intramuscular injections of vitamin E (25 mg kg−1). We isolated type II pneumocytes from NO2‐exposed rats and evaluated them for cell yield and viability, as well as for synthesis and secretion of phosphatidylcholine (PC) as measures of surfactant metabolism.ResultsThe yield of type II pneumocytes was significantly elevated from animals that had been exposed continuously to NO2 whereas in intermittently and repeatedly exposed rats, cell yield was similar to yield from control animals. Viability of the isolated cells was similar in controls and all NO2 exposure protocols. Vitamin E treatment of the NO2‐exposed rats neither changed cell yield nor cell viability. Phospholipid de novo synthesis, as estimated by choline incorporation into PC, was increased most after continuous NO2 inhalation whereas in the other conditions there was only a slight increase. Vitamin E administration further increased phospholipid synthesis; this difference reached statistical significance only in the case of intermittent NO2 exposure. Secretion of phosphatidylcholine from type II cells was only reduced after continuous NO2 inhalation and administration of the antioxidant reduced the impairment.ConclusionBecause vitamin E appears to preserve the ability of type II pneumocytes isolated from NO2‐exposed rats to synthesize and secrete surfactant lipid, we conclude that administration of vitamin E may mitigate NO2‐induced lung injury.
Role of homocysteine, cystathionine and methylmalonic acid measurement for diagnosis of vitamin deficiency in high‐aged subjects
Authors: Herrmann W. , Schorr H. , Bodis M. , Knapp J. P. , Müller A. , Stein G. , Geisel J. 
Published: March 2003

Intracellular B‐vitamin and folate deficiency indicated by hyperhomocysteinemia is very frequent in the elderly population. Hyperhomocysteinemia increases the risk of atherothrombotic diseases and neuropsychiatric complications. Our aim was to evaluate the prevalence of increased serum metabolite concentrations in subjects of a higher age, and whether the measurement of metabolite concentrations is more effective in diagnosing B‐vitamin deficiency than mere homocysteine.Homocysteine (HCY), cystathionine (CYS) and methylmalonic acid (MMA) were investigated in serum together with vitamin B‐12, B‐6 and folate in 90 high‐aged subjects (85–102 years), 92 seniors (65–75 years), and in 50 younger subjects (19–50 years).Elderly subjects (high‐aged and senior) had elevated serum concentrations of metabolites. High‐aged subjects had a higher frequency of pathological increases than seniors: HCY 62% vs. 24%; MMA 62% vs. 23%; CYS 81% vs. 36%. Folate and vitamin B‐6 concentrations were significantly decreased in both elderly groups; vitamin B‐12 was only decreased in high‐aged subjects. Utilising vitamin B‐6, B‐12 and folate for diagnosis of intracellular vitamin deficiency, the rate was 30% in seniors and 55% in high aged subjects. However, utilising the metabolites (HCY, MMA and CYS) for the diagnosis of intracellular vitamin deficiency, there was a distinctly increased rate of 55% in seniors respective to 90% in high‐aged subjects. Backward multiple regression analysis revealed that only folate, MMA, creatinine and age were independent variables influencing the HCY concentration. Furthermore, the MMA concentration was significantly and independently influenced by folate, vitamin B‐12, HCY and creatinine, and the serum concentration of CYS by vitamin B‐12, creatinine and age.The metabolites HCY, MMA and CYS are sensitive indicators diagnosing impaired remethylation of homocysteine to methionine with parallel activation of catabolic pathway. Compared to mere HCY or B‐vitamins in serum, the efficiency of diagnosing a disturbed HCY metabolism increases very much in utilising the metabolites HCY, MMA and CYS. For differential diagnosis, parallel measurement of folate and creatinine is recommended. The early and correct diagnosis of B‐vitamin deficiency in elderly subjects is of high clinical relevance.
Nitric oxide inhibition intensifies the depressant effect of cocaine on the left ventricular function in anaesthetized pigs
Authors: Roig E. , Melis G. , Heras M. , Rigol M. , Epelde F. , DeCandia G. , Sanz G. 
Published: March 2003

Myocardial ischaemia and left ventricular dysfunction have been described in cocaine users. Whether nitric oxide (NO) inhibition may potentiate the effects of cocaine on coronary circulation and ventricular function is still unknown.In order to test this hypothesis, 38 pentobarbital‐anaesthetized pigs were instrumented for systolic blood pressure, coronary blood flow, left ventricular dp/dt, cardiac output, left ventricular end‐diastolic and end‐systolic lengths and shortening fraction. The pigs were randomized into three groups: control group: i.v. saline (n = 5); group 1: i.v. cocaine, 10 mg kg−1 over 20 min (n = 17); group 2: the same doses of cocaine 30 min after i.c. L‐NAME 20 µg/kg min−1 infusion (n = 16). In order to know whether the observed effects were specific of NO inhibition, in five pigs i.c.
l‐arginine was simultaneously infused with L‐NAME, in five pigs i.c. NTG, an endothelial‐independent vasodilator, was simultaneously infused with L‐NAME before cocaine was administered, and in nine additional pigs the proximal left anterior descending (LAD) flow was reduced to around 20% of the basal value by means of a mechanical occluder before cocaine was administered.Cocaine i.v did not change the coronary blood flow, while it induced a significant reduction in cardiac output, left ventricular dp/dt and shortening fraction (15 ± 4–8 ± 4%, P < 0.05). When cocaine was administered after L‐NAME infused i.c. during 30 min
, a significantly more severe reduction of the shortening fraction (12 ± 3–4 ± 2%, P < 0.0001) was induced; this effect was abolished by simultaneous perfusion of
l‐arginine i.c. NTG. The results when cocaine was administered after the 20% LAD flow reduction by mechanical occluder did not differ from those of cocaine alone.NO inhibition intensifies the cocaine‐induced left ventricular dysfunction.
Increased erythropoietin synthesis in patients with COLD or left heart failure is related to alterations in renal haemodynamics
Authors: Pham I. , Andrivet P. , Sediame S. , Defouilloy C. , Moutereau S. , Wirquin V. , Chouaïd C. , Housset B. , Adnot S. 
Published: March 2003

The mechanisms controlling erythropoietin (EPO) synthesis by the kidney in patients with chronic obstructive lung disease (COLD) or congestive left heart failure (CLHF) remain incompletely understood. Renal dysfunction occurs as a consequence of decreased renal blood flow (RBF) in these diseases. Because alterations in renal haemodynamics may affect EPO synthesis and red blood cell production, we investigated the potential relationships between renal function and plasma EPO synthesis in patients with COLD or CLHF.Thirty‐two patients with COLD and 13 with CLHF underwent determination of renal physiology parameters, plasma EPO levels and haemoglobin levels.Plasma EPO concentrations were increased in patients with COLD or CLHF as compared to normal subjects, and were inversely correlated to haemoglobin concentrations. In patients with COLD or CLHF, plasma EPO was negatively correlated with both RBF and renal oxygen delivery (ROD) and positively correlated with filtration fraction. Plasma EPO was not correlated with glomerular filtration rate, fractional excretion of sodium, Po2 or Pco2. Among the patients with COLD, those with polycythemia (haemoglobin > 150 g L−1) had lower plasma EPO and higher RBF and ROD values than those with normocythemia (haemoglobin ≤ 150 g L−1).Taken together, our data suggest that in patients with COLD or CLHF the critical determinant for EPO production is impairment of renal haemodynamics.
Haemostatic profile in hypothyroidism as potential risk factor for vascular or thrombotic disease
Authors: Müller B. , Tsakiris D. A. , Roth C. B. , Guglielmetti M. , Staub J.‐J. , Marbet G. A. 
Published: March 2003

The influence of thyroid failure on haemostasis is controversial, both hypocoagulable and hypercoagulable states have been reported. Since both subclinical and overt hypothyroidism have been associated with atherosclerosis, a hypercoagulable state in addition might represent a risk factor for thromboembolic disease.We investigated various haemostatic variables in 42 women with subclinical hypothyroidism and compared them to 66 euthyroid controls. Prothrombin time, activated partial thromboplastin time, fibrinogen, factor VII activity (FVII:C), factor VII antigen (FVII:Ag), factor VIII activity, von Willebrand factor (vWF), antithrombin III, heparin cofactor II, protein C, protein S, plasminogen, antiplasmin, plasminogen activator inhibitor and tissue plasminogen activator, as well as common lipid variables, were measured.Factor VII:C (P < 0·02) and the ratio FVII:C/FVII:Ag (P < 0·01) were significantly increased in subclinical hypothyroid patients compared to the control group. Both parameters remained higher in hypothyroid patients after exclusion of 18 women on oestrogen replacement therapy. No differences were found between the groups with respect to vWF or the other haemostatic and lipid variables tested.Patients with subclinical hypothyroidism had significantly higher levels of FVII:C. The greater increase in FVII:C compared to that of FVII:Ag, as shown by the increase in their ratio, might reflect the presence of activated FVIIa. This might mean a hypercoagulable state, which could contribute to the increased prevalence of coronary heart disease reported in such patients. A hypercoagulable state might be another argument in favour of thyroxine replacement treatment in subclinical hypothyroidism, especially in patients with additional risk factors for vascular disease.
Vasorelaxant effects of oestradiols on guinea pigs: a role for gender differences
Authors: Naderali E. K. , Smith S. L. , Doyle P. J. , Williams G. 
Published: March 2003

Various studies have shown vasorelaxation properties for 17α‐ and 17β‐oestradiol.Here, we studied the effects of gender difference as well as oestrous cycle on oestradiol‐induced vasorelaxation in mesenteric arteries from male and female guinea‐pigs and in main uterine arteries from female guinea‐pigs in vitro.Both 17α‐ and 17β‐oestradiol (0·5–20 µmol L−1) induced concentration‐dependent relaxation of both mesenteric and uterine arteries preconstricted with either noradrenaline (NA; 10 µmol L−1) or KCl (125 mmol L−1) from both day‐7 and day‐15 female guinea‐pigs. 17β‐oestradiol was more potent in relaxing arteries precontracted with NA than those pretreated with KCl, while 17α‐oestradiol was more effective in relaxing those arteries precontracted with KCl. In mesenteric arteries from male animals, 17α‐oestradiol was significantly (P < 0·001) more potent on arteries precontracted with NA than KCl, an effect opposite to that seen on arteries from female animals. However, both 17α‐ and 17β‐oestradiol were more potent in relaxing arteries from male animals compared with their female counterparts.These data indicate a possible role for gender differences in the vascular effects of oestradiols.
The hormone sensitive lipase gene in familial combined hyperlipidemia and insulin resistance
Authors: Pihlajamäki J. , Valve R. , Karjalainen L. , Karhapää P. , Vauhkonen I. , Laakso M. 
Published: March 2003

Backround Insulin resistance in the most common familial dyslipidemia, familial combined hyperlipidemia (FCHL), could be due to variations in the hormone sensitive lipase (HSL) gene.Materials and methods The coding region of the HSL gene was screened with the single strand conformation polymorphism analysis in probands of 27 FCHL families with 228 members. In addition, the C‐60G promoter substitution of the HSL gene was determined by the restriction fragment length polymorphism analysis in these subjects.Results No variants in the coding region of the HSL gene were found and the allele frequencies of the C‐60G promoter substitution and the silent variant (G3138A) in the 3′ untranslated region did not differ between 110 control subjects and 27 probands with FCHL. However, in control women the C‐60G substitution was associated with high body mass index [30·6 ± 0·9 kg m−2 (mean ± SD) in subjects with the C/G genotype and 24·8 ± 4·6 in subjects with the C/C genotype, P = 0·012], and in control men with high rates of insulin‐stimulated whole body glucose uptake (70·1 ± 14·7 vs. 56·7 ± 14·2 µmol kg−1 min−1, P = 0·014). In 228 FCHL family members this substitution was associated with high low‐density lipoprotein cholesterol levels in men (4·51 ± 1·12 vs. 5·17 ± 1·28 mmol L−1, P = 0·049), but not in women.Conclusions The HSL gene is not a major gene for FCHL. However, the − 60G allele of this gene may affect body weight, insulin sensitivity and serum cholesterol levels.
Effects of OPB‐9195, anti‐glycation agent, on experimental diabetic neuropathy
Authors: Wada R. , Nishizawa Y. , Yagihashi N. , Takeuchi M. , Ishikawa Y. , Yasumura K. , Nakano M. , Yagihashi S. 
Published: March 2003

Background Nonenzymatic glycation of neural proteins and their end‐products (advanced glycation end‐products, AGE) have been implicated in the pathogenesis of diabetic neuropathy. We need a development of effective ant‐glycation agents for future clinical use.Materials and methods We examined the effects of OPB‐9195 (OPB), a new inhibitor of glycation, on the peripheral nerve structure and function in diabetic rats. Eight‐week‐old Wistar rats were made diabetic by streptozotocin (40 mg kg−1, i.v.) and OPB (60 mg kg−1 day−1) was given by gavage for 24 weeks. Age‐ and sex‐matched normal Wistar rats were used for comparison.Results During the experimental period, OPB treatment did not affect the reduced body weight, elevated levels of blood glucose and glycated haemoglobin in diabetic rats. At the end of the experiment, delayed tibial motor nerve conduction velocity was significantly improved (by 60%) in treated diabetic rats, with reduction of serum AGE levels. Expression of immunoreactive AGE in the sciatic nerve was reduced in treated diabetic rats compared with those in untreated rats. Sciatic nerve (Na+,K+)‐ATPase activity was also restored in treated diabetic rats. On the cross‐sectioned sciatic nerves, positive cells with oxidative stress‐related DNA damage, as expressed by 8‐hydroxy‐2′‐deoxyguanosine, were less in the peripheral nerve of treated diabetic rats compared with those of untreated rats.Conclusion The current study suggested that OPB is beneficial for the reduction of serum AGE and the prevention of diabetic neuropathy.
Relationship between bone mass density and tensile strength of the skin in women
Authors: Piérard G. E. , Piérard‐Franchimont C. , Vanderplaetsen S. , Franchimont N. , Gaspard U. , Malaise M. 
Published: March 2003

Background Skin and bone may be affected similarly during the climacteric and during long‐term corticotherapy. Little is known about the correlation between the respective alterations in bone mass density (BMD) and tensile strength of the skin. Materials and methods A total of 100 women aged 19–88 years, receiving, or not, hormone replenishment therapy or systemic corticosteroids, were enrolled in the study. Tensile strength of the inner forearm skin was measured using the suction method operated in both the steep and progressive‐force application modes. BMD was measured by dual X‐ray absorptiometry at the hip, femoral neck and lumbar spine. Results Being heterogeneous, the population of volunteers yielded a wide range of BMD and cutaneous tensile strength values. However, significant correlations were found between BMD and tensile skin parameters. In particular, a positive correlation was yielded between the biological elasticity of skin and the BMD of the hip and femoral neck. Conclusion An overall correlation is shown between skin elasticity on a relatively sun‐protected area and cortico‐trabecular BMD.
Homocysteine in breast cyst fluid
Authors: Tallova J. , Tomandl J. , Bicikova M. , Simickova M. 
Published: March 2003

Background Elevated plasma homocysteine concentrations have been reported in a variety of carcinoma, including those of the breast. The risk of breast cancer is higher in patients suffering from gross cystic disease. The breast cyst fluid contains unusual amounts of low‐ and high‐ molecular substances, including steroid hormones and their conjugates. The present study was undertaken to find out the presence of homocysteine in the fluid filling the cysts and have its concentration compared with other thiols, levels of Na+/K+ ratio and steroid hormones. Materials and methods Fourteen women suffering from gross cystic disease were enrolled in this study. Cystic concentrations of homocysteine (Hcy), cysteine (Cys), cysteinylglycine (Cys‐Gly) and glutathione (GSH) were determined by high performance liquid chromatography, with fluorescence detection; estradiol (E2), progesterone, allopregnanolone and pregnenolone sulfate (PregS) by RIA methods. Results Mean levels of Hcy, Cys, Cys‐Gly, Na+/K+, E2 and PregS in the fluid filling the breast cysts were significantly higher than the corresponding plasma concentrations. In addition, a negative correlation was found between cystic Hcy and the Na+/K+ ratio (Rs = −0·72, P = 0·003) and positive correlations between cyst Hcy and estradiol (Rs = 0·64, P = 0·018) and Hcy and PregS (Rs = 0·60, P = 0·025). Conclusion The study provides the first evidence of thiol concentrations in the breast cyst fluid. The finding of a negative correlation between homocysteine and the Na+/K+ ratio support the idea that the homocysteine concentration in breast cysts might be used clinically as a marker for the development of breast cancer disease.
Fibroblast studies documenting a case of peroxisomal 2‐methylacyl‐CoA racemase deficiency: possible link between racemase deficiency and malabsorption and vitamin K deficiency
Authors: Van Veldhoven P. P. , Meyhi E. , Squires R. H. , Fransen M. , Fournier B. , Brys V. , Bennett M. J. , Mannaerts G. P. 
Published: March 2003

Background 2‐Methylacyl‐CoA racemase interconverts the 2‐methyl group of pristanoyl‐CoA or the 25‐methyl group of hydroxylated cholestanoyl‐CoAs, allowing further peroxisomal desaturation of these compounds in man by the branched chain acyl‐CoA oxidase, which recognise only the S‐isomers. Hence, oxidation studies in fibroblasts, currently based on the use of racemic substrates such as [1–14C] pristanic acid, do not allow us to distinguish between a deficient racemase or an impaired oxidase.Design To evaluate the racemase activity directly, the 2R‐isomer of[1–14C] pristanic acid, as well as the 2R‐isomer of 2‐methyl‐[1–14C] hexadecanoic, a synthetic pristanic acid substitute, were prepared and their degradation by cultured human skin fibroblasts was compared to that of the racemic substrates.Results In fibroblasts in a young girl, presenting with elevated urinary levels of trihydroxycholestanoic acid metabolites but normal plasma levels of very long chain fatty acids, a partial deficient degradation of racemic [1–14C] pristanic acid was observed. Incorporation of 2R‐[1–14C] pristanic acid in glycerolipids of the patient's fibroblasts proceeded normally, but breakdown was impaired. Similar findings were seen with the 2R‐isomer of 2‐methyl‐[1–14C] hexadecanoic. These data, combined with the fact that the branched chain acyl‐CoA oxidase, catalyzing the first oxidation step of pristanic acid and bile acid intermediates in man, appeared normal, suggested a peroxisomal β‐oxidation defect in the patient at the level of 2‐methylacyl‐CoA racemase.Conclusion Carboxy‐labelled 2R‐methyl branched chain fatty acids might be useful tools to document cases of racemase deficiencies. Because a brother of the patient died with a diagnosis of vitamin K deficiency, an impaired racemase might be responsible for other cases of unexplicable malabsorption.