Biomedical subjects

J Dadan

Publications and source records attributed to J Dadan.

15 recordsLinked to original sources

PubMed2000

[Primary hyperparathyroidism treated surgically].

Primary hyperparathyroidism is a systemic disease, more and more frequently recognized-concerning 1 to 3% of the population. Statistically appears in 1 of 1000 adults, with significant advantage of women. In Poland every year about 30 new cases are noticed and incidence increases with an age. In spite of significant advance of the knowledge, it still makes a lot of diagnostic troubles. It appears to be non-specific illness, characterised by just one symptom, mainly urolithiasis, sometimes chronic ulcer disease, chronic pancreatitis, arterial hypertension, disorders of the movement or psychic disorders. Parathyroid adenoma which is the main reason of the disease is usually single and small, multiple and bigger ones are found exceptionally. In about 2% of cases they are localized in mediastinum. In the article the basic symptoms, diagnostic and therapeutic problems were shown, especially concerning surgical treatment which is safe, radical and efficacious method when performed by experienced surgical team and the conduct from choice on primary and secondary hyperparathyroidism.

Adult↗

PubMed1999

[Surgical treatment of thyroid disease in adolescents].

Surgical treatment of goitre in children and teenagers under 18 is relatively rare and undertaken for strict therapeutic indications. It still arouses much controversy among surgeons, being loaded with a high percentage of complications, usually distant ones. The aim of the study was to analyse the surgical treatment of various goitre types under the age of 18 basing on 65 operations performed in the years 1994-1998. Operations for non-toxic and hyperactive nodular goitre, including Graves-Basedow disease, were predominant. Five cases of thyroid carcinoma were found. No serious complications were observed during and after the surgery. Our own material and the 5-year observation reveal that surgical treatment of thyroid diseases in children and adolescents carried out for definite indications by an experienced operating team is successful and causes only few complications.

Adolescent↗

PubMed1999

[Secondary cell transmitters in the human thyroid].

The process of signal transmission to the cell interior is very complex. The cell reads external stimuli through the system of specific receptors, activating suitable pathways of secondary cell transmitters. Recent studies have yielded a number of essential data concerned with the complex functioning of the system of secondary cell transmitter pathways in the thyreocyte and their role in the molecular base of thyroid diseases. The causes of many endocrine diseases are now known to be associated with mutations of membrane and nuclear receptors and proteins of signal transmission systems in the cell. Moreover, species specific differences and thyroid pathology-dependent changes have been revealed in the regulation of main pathways of secondary cell transmitters and interaction between them. The present paper intends to characterize the main systems of secondary signal transmitters in the thyroid cell and their role in the pathogenesis of thyroid diseases.

Cell Communication↗

PubMed1999

[Surgical management in the non-neoplastic and neoplastic thyroid goiter with Hürthla cells].

The routine preoperative cytological evaluation of pathological changes of the thyroid more and more frequently reveals single or multiple Hürthl cells in the material obtained by the method of fine-needle aspiration biopsy (FNA). Hürthl cells are a degenerative form of epithelial follicular cells of the thyroid and cytological examination is insufficient for unequivocal differentiation between adenoma and carcinoma. Management of patients with FNA-diagnosed Hürthl cells arouses a number of controversies. Therefore, the authors of the present study subjected the thyroids of patients with cytologically diagnosed Hürthl cells to postoperative histopathological analysis. Appropriate surgical management was indicated.

Adenoma, Oxyphilic↗

PubMed1997

[The effect of some drugs on the levels of selected cytokines in experimental septic shock].

The production of tumor necrosis factor (TNF-alpha), and interleukin 1 beta (IL-1 beta), IL-6, sTNFR-p55, sTNFR-p75 and their pharmacomodulation were evaluated in a model of septic shock induced in CD-1 mice by cecal ligation and puncture (CLP). This model of sepsis, which resembles the clinical situation of bowel perforation and peritonitis with subsequent septic shock was compared with that induced by administration of pure endotoxin (LPS). TNF-alpha was detectable in serum, liver, spleen and lungs during the first 4 h, with a peak 2 h after CLP. IL-1 beta was measurable in serum after 24 h, and levels increased significantly in spleen and liver 4 and 8 h after CLP. IL-6 levels increased significantly in serum throughout the first 16 h after CLP. sTNFR-p55 and p75 increased in both models of shock but with different kinetics. Cytokines were also detectable after LPS injection, with kinetics similar to those after CLP but a significantly higher level. Pretreatment with dexamethasone (DEX) and ibuprofen (IBU), significantly reduced survival, while TNF did not affect it. Only pentoxifylline (PTX) significantly increased survival in mice with CLP. However DEX protected the mice from LPS mortality. In conclusion, by inhibiting TNF-alpha with DEX and PTX survival was reduced or unchanged respectively, suggesting that the modulation of this cytokine does not play significant role in sepsis and septic shock induced by CLP, unlike treatment with LPS. The negative effects of IBU suggests a protective role by prostaglandins in sepsis induced by LPS.

Animals↗

PubMed1997

[Polymorphism of collagen in duodenal mucosa of ulcers].

Determinations of collagen in specimens of duodenal mucosa taken from 15 patients operated on because of duodenal ulcer with pyloric stenosis were performed. In the ulcer and surrounding tissue, total collagen values were significantly increased when compared with the results in unchanged wall of the duodenum. Collagen polymorphism study showed considerably higher percentage of type I and decreased type III in the ulceration than in control duodenal mucosa. In conclusion, extracellular components of connective tissue may play a role in the formation and course of duodenal ulcer disease.

Adult↗

PubMed1997

Hyperthyroid goitre treated surgically.

The aim of the study was the comparative analysis of the degree of intensity of male and female hyperthyroidism treated surgically in the years 1990 to 1996. In this period 295 females and 42 males underwent operation for hyperthyroid goitre. Female predominance was noted in hyperthyroidism (ratio 7:1), in Graves' disease (7.4:1) and in toxic nodular goitre (6.3:1). The clinical findings in pre- and postoperative patients, including laboratory, visual diagnosis, and intra- and postoperative complications were evaluated. In the preoperative period, the incidence of the thyreocardiac syndrome was greater in the male. Male hyperthyroidic goitres were more frequently located retrosternally and caused trachea compression. No significant sexual differences were found in routine laboratory tests. Operations for hyperthyroidic male goitres usually caused more intraoperative problems and were connected with greater blood loss. Estimation of cardio-vascular parameters in the early postoperative period showed higher intensification of hyperkinetic circulation and higher mean body temperature in men. Signs of psychosis developed postoperatively in two men. The analysis of patients with hyperthyroidic goitre treated surgically revealed more severe course of male thyreotoxicosis in the perioperative period.

Adult↗

PubMed1991

Platelet-activating factor alters glomerular barrier size selectivity for macromolecules in rats.

The effect of platelet-activating factor (PAF) on glomerular permeability to macromolecules was investigated in the isolated kidneys from normal male Sprague-Dawley rats perfused at constant pressure. Compared with basal values, infusion of PAF (10 nM final concentration) into the isolated kidneys induced a progressive and significant increase in protein excretion (6.7 +/- 2.7 vs. 40.7 +/- 10.4 micrograms/min, P less than 0.01), completely reversible 20 min after PAF infusion was discontinued (8.5 +/- 1.3 micrograms/min). In additional experiments, during PAF infusion the fractional clearance of small neutral dextrans (radius 24-48 A), defined as the ratio of the clearance of neutral dextrans to the clearance of creatinine, was comparable to preinfusion values, whereas fractional clearance of large dextrans (greater than 50 A) was significantly elevated (P less than 0.005) above preinfusion values. The specific PAF receptor antagonist L 652731 completely prevented the increased fractional clearance of large dextrans induced by PAF. Finally, lowering Ca2+ concentration in the perfusion medium from 2.5 to less than 0.1 mM markedly reduced proteinuria in isolated kidneys exposed to PAF (80.0 +/- 10.3, 42.8 +/- 3.1, and 22.0 +/- 7.6 micrograms/min, respectively, for 2.5, 1.25, and less than 0.1 mM). These results indicate that in isolated perfused kidneys 1) PAF-induced proteinuria is a functional phenomenon reversible on discontinuing PAF infusion, 2) PAF modifies glomerular size-selective properties by increasing transmural passage of large dextran molecules, and 3) PAF-induced change in glomerular permselective properties is dependent on Ca2+ concentration in the extracellular medium.

Animals↗

PubMed1990

Renal metabolism and urinary excretion of platelet-activating factor in the rat.

The origin of platelet-activating factor (PAF) in the urine remains ill defined. The present study documents that [3H]PAF (3.5 mu Ci) injected into the renal artery of isolated control rat kidney preparations perfused at constant pressure with a cell-free medium containing 1% bovine serum albumin (BSA) was excreted in negligible amounts (0.034%) in the urine, whereas 6% was retained by the kidney. When kidneys were perfused with a BSA-free medium, 0.029 and 71% of the total radioactivity added to the perfusate was recovered in the urine and in the renal tissue, respectively. [3H]PAF urine excretion in proteinuric kidneys from adriamycin-treated rats was still negligible (0.015%). Analysis of the renal tissue-retained radioactivity in control and proteinuric kidneys perfused with 1% BSA indicated metabolism into long chain acyl-sn-glycero-3-phosphorylcholine species, lyso-PAF, glycerols, and intact PAF. Thin layer chromatography analysis of [3H]glycerol fraction in these renal extracts showed two major components comigrating with 1-O-alkylglycerol and 1-O-alkyl-2-fatty acylglycerol. Isolated proximal tubules, but not glomeruli from nephrotic rats exposed to increasing concentrations of BSA (0-4%), had a higher PAF uptake than control tubules for BSA concentrations ranging from 0 to 0.1%. Our findings in the isolated perfused kidneys indicate that, in normal conditions, circulating PAF is excreted in the urine in negligible amounts and that the altered glomerular permeability to proteins does not affect this excretion rate. Moreover, analysis of renal tissue radioactivity documented that the renal metabolism of PAF is comparable in control and nephrotic kidneys.

Animals↗

PubMed1990

Ticlopidine prevents renal disease progression in rats with reduced renal mass.

Functional and morphological studies were done in three groups of male Sprague-Dawley rats after removal of the right kidney and infarction of approximately five-sixths of the left. Group 1 received no specific therapy. Group 2 was treated with ticlopidine, 150 mg/kg per os, for 50 days starting 10 days after surgical ablation. Group 3 was given the thromboxane antagonist, GR 32191, 3 mg/kg b.i.d. orally for 50 days, like ticlopidine. Untreated Group 1 rats developed renal insufficiency, systemic hypertension, progressive proteinuria and glomerulosclerosis. In Group 2 treatment with ticlopidine was associated with less severe impairment of renal function. Proteinuria was significantly lower and animals were partially protected from the development of glomerulosclerosis. These animals had significantly prolonged skin bleeding time. In vitro ADP and arachidonic acid (AA)-induced platelet aggregation was inhibited. Systemic blood pressure was significantly lower than in controls. In Group 3 rats GR 32191 failed to influence progressive proteinuria and severity of glomerulosclerosis which were comparable to those in Group 1. Bleeding time was not prolonged, and in vitro platelet aggregation was inhibited only when AA was used as aggregating agent. Systemic blood pressure was not influenced. These studies suggest that a drug like ticlopidine, which has a broad spectrum of pharmacological actions on platelets and platelet-cell interactions, does retard the development of progressive renal injury when nephron number is reduced. Specific blocking of thromboxane A2 (TxA2) biological activity does not influence progressive renal disease in rats with remnant kidney.

Animals↗

PubMed1990

Functional implications of decreased renal cortical atrial natriuretic peptide binding in experimental diabetes.

Glomerular hyperfiltration in streptozotocin-induced diabetes mellitus in rats may be mediated by atrial natriuretic peptide (ANP). We wanted to evaluate plasma levels of ANP and plasma volume in relation to renal ANP receptor density and affinity in rats 6 weeks after induction of diabetes. Plasma levels of immunoreactive ANP were significantly higher in hyperglycemic diabetic (75.2 +/- 8.3 pg/ml) than in control animals (34.7 +/- 8.1 pg/ml; p less than 0.01). Administration of insulin to keep diabetic rats normoglycemic normalized plasma levels of immunoreactive ANP (30.5 +/- 5.2 pg/ml). In contrast, plasma volume did not show significant differences among the groups (hyperglycemic diabetes, 46.6 +/- 3.8; normoglycemic diabetes, 42.4 +/- 3.2; controls, 43.2 +/- 2.0 ml/kg body wt). No correlation was found between plasma levels of immunoreactive ANP and plasma volume. By autoradiography a significant reduction in the number of renal cortical ANP receptors was observed in hyperglycemic diabetic rats as compared with controls. At variance, ANP receptor affinity did not change either in the cortex or in the medulla in hyperglycemic diabetics in comparison with control animals. The pathophysiological implication of cortical ANP receptor down-regulation was underscored by the blunted response of glomerular filtration rate to ANP infusion in diabetic animals as compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Endothelin mediates the renal vasoconstriction induced by cyclosporine in the rat.

The effect of cyclosporine on renal function was first investigated in the isolated perfused rat kidney. Kidneys from normal male Sprague-Dawley rats were perfused at constant pressure. After control clearance periods, cyclosporine (0.6, 1.2, or 3 mg/min) or vehicle was infused over 5 min period in the renal artery and then four 10-min experimental periods followed. Cyclosporine, but not vehicle caused a dose dependent fall in renal perfusate flow associated with a concomitant increase in renal vascular resistance. Glomerular filtration rate was also decreased in parallel. We also examined whether endogenous endothelin mediates cyclosporine-induced acute renal vasoconstriction. In isolated kidneys pre-exposed to specific anti-endothelin antibody and then challenged with cyclosporine (1.2 mg/min) the renal perfusate flow, renal resistance, and glomerular filtration rate were 22.3 +/- 1.8 ml/min, 4.50 +/- 0.36 mmHg/ml.min-1, 1.06 +/- 0.05 ml/min, respectively, as compared with 12.9 +/- 1.2 ml/min, 7.8 +/- 1.2 mmHg/ml.min-1, 0.55 +/- 0.06 ml/min (P less than 0.01) measured in isolated kidneys pre-exposed to a non-immunized rabbit serum. The effectiveness and specificity of anti-endothelin antibody were confirmed by its capability of preventing the renal function deterioration caused by a single bolus dose (150 pmol) of synthetic endothelin, but not by infusion of angiotensin II, norepinephrine, or thromboxane A2 mimetic U-46619 in isolated kidneys. To test further the relationship between endogenous endothelin and cyclosporine-induced renal vasoconstriction, a second series of in vivo studies was performed in normal rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗

PubMed1990

Cyclooxygenase products and atrial natriuretic peptide modulate renal response to endothelin.

The effects of porcine endothelin on renal function were investigated in the isolated perfused rat kidney. After control clearance periods, endothelin (80, 120 or 320 pmol) or vehicle was added to the perfusate, and four 10-min experiments followed. Endothelin markedly reduced renal perfusate flow (RPF) as a result of its potent renal vasoconstrictor effect. At the highest but not low doses of endothelin, glomerular filtration rate (GFR) fell disproportionately to the reduction in RPF. Fractional Na excretion was also increased after kidney exposure to endothelin, suggesting an inhibition of tubular Na reabsorption by the peptide. Perfusion with low [Ca] severely blunted the hemodynamic effects of endothelin. Pharmacological blocking of renal cyclooxygenase by indomethacin or ibuprofen caused a further decline in RPF, GFR and absolute but not fractional Na excretion in kidneys challenged with endothelin. Atrial natriuretic peptide increased GFR and filtration fraction (FF), but not RPF, in kidneys previously exposed to 120 pmol endothelin. This was associated with a dramatic diuretic and natriuretic effect. The results demonstrate that 1) endothelin acts directly on the kidney, eliciting hemodynamic, diuretic and natriuretic responses that are dependent on the dose used and partially on the availability of extracellular Ca, 2) the renal effects of endothelin are exacerbated by cyclooxygenase blocking, suggesting that the vasoconstrictor effect of the peptide may be modulated by vasodilatory prostaglandins, and 3) atrial natriuretic peptide counteracts the renal function deterioration induced by endothelin, raising the possibility of an interplay between these vasoactive hormones in the control of renal function.

Animals↗

PubMed1989

[Bilateral parathyroid adenoma].

A patient with multiple parathyroid adenomas is reported. Their size was considerable, and the course of primary hyperparathyroidism was stormy. A rapid regression of symptoms followed surgical treatment. The rarity of multiple parathyroid adenomas of large size is stressed.

Adenoma↗

PubMedDate not supplied

AgNORs in duct epithelial lesions in chronic pancreatitis and in pancreas cancer cells.

BACKGROUND/AIMS: Argyrophilic nucleolar organizer regions (AgNORs) reflect the proliferative activity of cells. Since the majority of pancreatic cancers are ductal carcinomas, the aim of the study was to determine the AgNORs expression of potential pre-neoplastic ductal epithelial lesions in advanced chronic pancreatitis compared with pancreatic cancer cells. METHODOLOGY: Histological preparations obtained from 24 patients with chronic pancreatitis and 16 patients with pancreatic cancer were used to estimate the number of AgNORs per nucleus. Four types of AgNORs were distinguished and histograms with cell percentage of each type were performed for all forms of epithelial anomalies. RESULTS: In simple hyperplasia, squamous and mucous metaplasia the number of AgNORs ranged from 1.92 to 2.23; type I was predominant. In papillary hyperplasia, dysplasia and in situ carcinoma the number ranged from 2.98 to 3.34, with a predominance of type II-IV. In invasive carcinoma the number was 4.29 and 74% of cells were of type II-IV. CONCLUSIONS: Both counts of AgNORs and the percentage of type II-IV cells showed a gradual increase from simple hyperplasia through papillary hyperplasia and dysplasia to invasive carcinoma which in this respect differs significantly from all forms of the epithelial anomalies examined.

Carcinoma in Situ↗