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Biomedical subjects

D Pupek-Musialik

Publications and source records attributed to D Pupek-Musialik.

At least 19 recordsLinked to original sources
PubMed2007

Circulating serum adiponectin concentrations do not differ between obese and non-obese caucasians and are unrelated to insulin sensitivity.

Reduced serum levels of adiponectin in obesity and insulin resistance seem paradoxical, since adipose tissue is the only source of adiponectin, and reports on that subject are contradictory. The aim of this study was to investigate the concentrations of adiponectin in non-obese and obese normoglycemic humans, and to determine the correlation between adiponectin and HOMA index of insulin sensitivity. Based on the WHO definition of obesity, 145 obese subjects and 49 non-obese controls (aged 20-55 years) were studied. The serum adiponectin concentrations did not differ between subjects and controls (p=0.6398) and were not correlated with HOMA index (r=-0.0211; p=0.8048, and r=-0.0523; p=0.4757, for subjects and controls, respectively). Adiponectin was not correlated with HOMA index in females (r=-0.0521; p=0.6546, and r=-0.0825; p=0.3981, for female subjects and controls, respectively) as well as in males (r=0.0033; p=0.9791, and r=0.0123; p=0.9131, for male subjects and controls, respectively). These results lead to the conclusion that neither the concentrations of adiponectin differ between obese and non-obese humans, nor does any relationship between adiponectin concentration and insulin sensitivity exist.

Adiponectin↗
PubMed2000

[Leptin and obesity].

Obesity is associated with increased incidence of cardiovascular diseases, insulin resistance, dyslipoproteinemia and cancer. The discovery of leptin in 1994 has provided a lot of new information about obesity. Leptin is a 167-amino acid peptide synthetized almost exclusively in adipose tissue. This hormone circulates in blood serum in both free and bound forms. The long isoform of leptin receptor is widely distributed in brain, whereas numerous short forms are also being present in peripheral tissues. Leptin acts by binding to the receptors in hypothalamus and altering a release of several neuropeptides, especially neuropeptide Y, regulating energy intake and expenditure. Apart from signaling energy reserves to the brain, leptin promotes hematopoiesis, influences pubertal development and contributes to the increase in arterial blood pressure. Leptin production regulation in humans is poorly understood, but appears to depend on the total body fat, changes in energy intake and serum level of several hormones. Despite the recent advances in the knowledge of both physiology and pathophysiology of leptin, several many important questions require further studies.

Animals↗
PubMed2000

[The role of rheological factors in the pathogenesis of diabetic nephropathy].

In this paper the stages and pathogenesis of diabetic nephropathy have been presented. Factors which influence blood rheology and hemorheologic abnormalities founded in diabetic patients have been reviewed. Attention was paid to the role of rheological parameters in initiating and progression of diabetic nephropathy. The possibilities of prevention of diabetic microvascular complications by influencing blood rheology have been presented.

Blood Viscosity↗
PubMed2000

[Digoxin as a cause of chromatopsia and depression in a patient with heart failure and hyperthyroidism].

67 year old patient with chronic heart failure and persistent atrial fibrillation had overdosed glycosides for several months. The symptoms of gastrointestinal system and nervous system appeared after long term therapy with toxic doses of glycosides. Originally depression was diagnosed based on the central nervous system disturbances. Even though overdose of glycosides was diagnosed the blood serum glycoside level was within the therapeutic limits. Based on the precise analysis of the data, it was concluded that the reason for normal blood serum glycoside level in this case was coexisting hyperthyreosis.

Aged↗
PubMed1998

Effects of extracorporeal shock wave lithotripsy on renal function in patients with kidney stone disease.

The effects of extracorporeal shock wave lithotripsy on glomerular and tubular renal functions were determined by serum beta2-microglobulin (Sbeta2m) and urinary beta2-microglobulin (Ubeta2m) estimations in patients with nephrolithiasis. Unilateral treatment was performed in all patients. Urinary and serum creatinine levels were determined according to the method of Yatzidis. Sbeta2m and Ubeta2m were measured by radioimmunoassay the day before ESWL, on the day of ESWL, and then 1, 2, 5, 7, 8, 9, 14, and 28 days after treatment. Creatinine clearance, hourly urinary beta2m excretion (Ubeta2m/h), and tubular reabsorption of beta2m (TRbeta2m) were calculated. After lithotripsy, significant increases in Ubeta2m, Ubeta2m/h, and TRbeta2m were found (p < 0.001), whereas Sbeta2m, serum creatinine, and creatinine clearance values remained unchanged. Ubeta2m, Ubeta2m/h, and TRbeta2m reached their pretreatment values within 7-9 days after ESWL. We concluded that ESWL does not affect the glomerular filtration rate; however, it leads to a transient proximal tubular dysfunction.

Adult↗
PubMed1998

[Endothelin and arterial hypertension].

Endothelins (ETs) are peptides of 21 amino acids synthesized and released by variety of cells. Endothelin (now this peptide is called endothelin-1 (ET-1)) was isolated and identified in 1988 by Yanagisawa et al. Following studies revealed two other isoforms of endothelin': Endothelin-2 (ET-2) and endothelin-3 (ET-3). All of them bind to two types of receptors (A and B (ET-A r, ET-Br). ET-A r are responsible for concentration mediating. Two subtypes of ET-B r are known. ET-B1 r mediates vasorelaxation; ET-B2 vasoconstriction. ETs (especially ET-1) have variety of biological actions but the most important are vasoconstrictor and mitogenic action. Through these two mechanism ETs may participate in the pathogenesis and/or in the maintenance of hypertension in both experimental animal models and human essential hypertension. The intravenous infusion of synthetic ET induces a long-lasting elevation of blood pressure in experimental animals and in healthy humans. Number of studies have shown enhanced responses to ET in hypertensive subjects but decreased responses have also been reported. Similarly, plasma levels of ET-1 are either normal or elevated in experimental and human essential hypertension. Numerous investigators have suggested an interaction between ET and angiotensin-converting enzyme inhibitors through the renin-angiotensin system or through the accumulation of endogenous bradykinin. Also calcium antagonists of different classes prevent endothelin-induced contractions. Endothelin- converting enzyme inhibitor (phosphoramidon) and ET-A/B r antagonists (bosentan, BQ-123, FR139317) may have potential role as vasodilators in the treatment of hypertension.

Animals↗
PubMed1997

Acetylsalicylic acid (aspirin) test for the diagnosis of renovascular hypertension.

OBJECTIVE: To determine whether the administration of acetylsalicylic acid (ASA, also known as Aspirin) differentiates patients with renovascular hypertension from those with essential hypertension, in order to provide a simple alternative to more expensive forms of diagnosis for this condition. DESIGN: Trial of ASA test in patients with previously diagnosed essential and renovascular hypertension. SETTING: Inpatient department of an academic health sciences centre in Poznan, Poland. PATIENTS: Forty patients with essential hypertension and 21 patients with renovascular hypertension. INTERVENTIONS: Patients were given an intravenous injection of ASA (10 mg/kg body weight), blood pressure was measured and blood was sampled and assayed for plasma renin activity (PRA) before and 30 minutes after the injection. RESULTS: ASA infusion in patients with renovascular hypertension resulted in a decrease in PRA from 15.2 (standard deviation [SD] 12.4) ng/mL per hour to 7.2 (SD 9.8) ng/mL per hour, whereas in patients with essential hypertension the initial PRA was significantly lower before ASA administration and did not change afterward. In patients with renovascular hypertension, the mean systolic, diastolic and arterial pressure decreased significantly (p < 0.001) after ASA infusion, but these did not change in patients with essential hypertension. Based on the criterion of 4 mm Hg as a detectable decrease in mean blood pressure, the sensitivity of the ASA test was 95.0% and the specificity 82.5%; its positive predictive value was 74% and its negative predictive value 97%. CONCLUSION: The precise measurement of blood pressure during the ASA test may provide a useful method of differentiating between patients with renovascular and essential hypertension.

Adult↗
PubMed1994

[Effect of nifedipine on proximal tubular function in patients with essential hypertension].

The effect of a single 20 mg sublingual dose of nifedipine on function of proximal tubule of nephron in patients with essential hypertension was studied by measuring changes in renal excretion of water, sodium, uric acid and beta-2-microglobulin (B2m) after nifedipine administration. Fifteen patients at the mean age of 40.1 +/- 7 years, with mild to moderate essential hypertension were studied. Systolic (SBP) and diastolic (DBP) blood pressure as well as heart rate (HR) were recorded every hour. Urine was sampled over 60-min, four times. The first two periods were regarded controls and the last two periods followed the administration of a 20 mg sublingual nifedipine dose. Blood samples were taken 1 h before and 1 h after that. Sodium, uric acid, B2m and creatinine in urine and plasma were determined. Nifedipine caused a significant fall in SBP and DBP (p < 0.001) and a marked increase in HR (p < 0.001). Diuresis, sodium (CNa) and uric acid (Cua) clearances were significantly increased (p < 0.001). Similarly, fractional excretion of sodium (FENa) was higher (p < 0.01). B2m excretion (UB2m) showed a two fold increase after nifedipine administration (p < 0.01). A positive correlations were found between the changes in CNa and Cua (r = 0.835, p < 0.001) and between the changes in UB2m and CNa (r = 0.747, p < 0.001). The results indicate that nifedipine induces an increase in diuresis, natriuresis and excretion of uric acid and B2m. These findings and the relationship between the changes in UB2m and Cua proves effect of nifedipine on proximal tubular function.

Adult↗
PubMed1993

[Evaluation of uric acid transport in nephrons of patients with calcium nephrolithiasis and hyperuricosuria].

Renal excretion of uric acid was studied in 48 patients with recurrent calcium nephrolithiasis. Hyperuricosuria was found in 16 patients (33%) and among them 10 patients had increased values of urate clearance and fractional excretion. The tubular transport of urate was evaluated by means of pharmacological tests with pyrazinamide (PZA) and benzbromarone (BB) in these 11 patients with hyperuricosuria of renal origin. PZA suppression test was normal in 10 patients while in one case uric acid excretion was not suppressed sufficiently by PZA. Maximal uricorusirc response to BB was increased in two patients, normal in one patient and impaired in eight patients. PZA and BB tests revealed isolated defect of uric acid postsecretory reabsorption in seven patients, impaired reabsorption at both pre- and postsecretory site in one case and enhanced tubular secretion of uric acid in two patients. This study indicates that different defects of uric acid transport in nephron are the frequent cause of hyperuricosuria in patients with recurrent calcium nephrolithiasis.

Absorption↗
PubMed1992

[Nephrotoxic effect of gentamicin on the function of the proximal tubules of the nephron and glomerular filtration].

The purpose of the study was assessment of gentamicin nephrotoxicity with reference to proximal tubule function and glomerular filtration. The study was carried out in 20 patients with nephrolithiasis and chronic pyelonephritis, and 33 patients with respiratory and bile tract infections treated with gentamicin in doses of 2-3 mg/kg/2 h. In 3 patients with nephrolithiasis and chronic pyelonephritis signs of increased nephrotoxicity of gentamicin (according to Schentag criteria) were found. Similar signs were demonstrated in 3 patients with non-urinary tract infections. The abnormalities included increased excretion of low-molecular protein and beta-2-microglobulin (B2m), reduction of B2m reabsorption and lower glomerular filtration. Beta-2-microglobulinuria increase precede by 4-5 days the fall of the glomerular filtration rate which suggests that beta-2-microglobulinuria assessment is an early sign of gentamicin neurotoxicity.

Adult↗
PubMed1990

[Nephrotoxicity of aminoglycosides].

The paper presents recent views on the aminoglycoside (AG) nephrotoxicity. The risk factors for nephrotoxicity in the patients treated with AG are discussed.

Aminoglycosides↗