Biomedical subjects

Miklós Tóth

Publications and source records attributed to Miklós Tóth.

At least 19 recordsLinked to original sources

PubMed2006

Diabetes mellitus attenuates the repolarization reserve in mammalian heart.

OBJECTIVE: In diabetes mellitus several cardiac electrophysiological parameters are known to be affected. In rodent experimental diabetes models changes in these parameters were reported, but no such data are available in other mammalian species including the dog. The present study was designed to analyse the effects of experimental type 1 diabetes on ventricular repolarization and its underlying transmembrane ionic currents and channel proteins in canine hearts. METHODS AND RESULTS: Diabetes was induced by a single injection of alloxan, a subgroup of dogs received insulin substitution. After the development of diabetes (8 weeks) electrophysiological studies were performed using conventional microelectrodes, whole cell voltage clamp, and ECG. Expression of ion channel proteins was evaluated by Western blotting. The QTc interval and the ventricular action potential duration in diabetic dogs were moderately prolonged. This was accompanied by significant reduction in the density of the transient outward K+ current (I(to)) and the slow delayed rectifier K+ current (I(Ks)), to 54.6% and 69.3% of control, respectively. No differences were observed in the density of the inward rectifier K+ current (I(K1)), rapid delayed rectifier K+ current (I(Kr)), and L-type Ca2+ current (I(Ca)). Western blot analysis revealed a reduced expression of Kv4.3 and MinK (to 25+/-21% and 48+/-15% of control, respectively) in diabetic dogs, while other channel proteins were unchanged (HERG, MiRP1, alpha(1c)) or increased (Kv1.4, KChIP2, KvLQT1). Insulin substitution fully prevented the diabetes-induced changes in I(Ks), KvLQT1 and MinK, however, the changes in I(to), Kv4.3, and Kv1.4 were only partially diminished by insulin. CONCLUSION: It is concluded that type 1 diabetes mellitus, although only moderately, lengthens ventricular repolarization, attenuates the repolarization reserve by decreasing I(to) and I(Ks) currents, and thereby may markedly enhance the risk of sudden cardiac death.

Action Potentials↗

PubMed2006

[Nucleotide sequence variants of the glucocorticoid receptor gene and their significance in determining glucocorticoid sensitivity].

Nucleotide sequence variants of the glucocorticoid receptor gene and their significance in determining glucocorticoid sensitivity. The physiologic response and sensitivity to glucocorticoids may significantly differ among species, individuals, tissues and cell types. The variability of the effect of endogenous and exogenous glucocorticoids is largely determined by genetic components, of which the authors review the knowledge on the glucocorticoid receptor gene. The authors describe the genomic and non-genomic pathways of receptor function, the significance of isoforms produced during receptor protein formation, the pathomechanism of glucocorticoid resistance syndrome and the results of clinical investigations related to receptor gene polymorphisms. Through subtle alteration of receptor function, the gene polymorphisms may increase or diminish sensitivity to glucocorticoids and may play a role in the pathogenesis of metabolic disorders. In their own studies the authors found, that the N363S polymorphism, which increases glucocorticoid sensitivity, may play a role in the pathogenesis of bilateral adrenal adenomas, it may modify the clinical phenotype of patients with congenital adrenal hyperplasia, and may have an impact on steroid-induced ocular hypertension. It is presumed that further research in other diseases will continue to complete our knowledge on the pathophysiology of glucocorticoid receptor gene polymorphisms.

Adenoma↗

PubMed2006

Activation energy determinations suggest that thiols reverse autooxidation of tetrahydrobiopterin by a different mechanism than ascorbate.

In neutral aqueous solutions tetrahydrobiopterin is oxidized by dioxygen in a reaction that is succinctly described as autooxidation. Ascorbate and thiols moderate this reaction by reversing the oxidative process. In the present study the effect of various thiols on the apparent Arrhenius activation energy of tetrahydrobiopterin autooxidation was characterized and compared to that of ascorbate determined previously. We observed that - in sharp contrast to ascorbate - the efficiency of thiols to protect tetrahydrobiopterin decreased with the elevation of temperature from 22 to 37 degrees C. Accordingly, the apparent Arrhenius activation energies (in kJ/mol) measured in the presence of thiols were consistently greater than the value determined with tetrahydrobiopterin alone (59.6 +/- 1.4) or in the presence of ascorbate (59.9 +/- 2.8). Thus, the energy values were 88.8+/-1.1 with glutathione, 87.6 +/- 2.1 with N-acetylcysteine, 79.2 +/- 1.6 with cysteine, 75.1 +/- 2.4 with dithiotreitol and 70.3 +/- 0.9 with homocysteine. Since thiols are as potent reducing agents as ascorbate, these findings suggest that thiols and ascorbate protect tetrahydrobiopterin from oxidation acting at different steps of the oxidation process. It is likely that thiols reduce quinoidal dihydrobiopterin, whereas ascorbate scavenges the trihydrobiopterin radical to tetrahydrobiopterin. Furthermore, the results indicate that thiols are excellent tools to protect tetrahydrobiopterin from autooxidative decomposition in laboratory experiments conducted at relatively low temperatures, whereas the protective effect diminishes at 37 degrees C, i.e. under physiological conditions.

Ascorbic Acid↗

PubMed2006

Distinct modulation of angiotensin II-induced early left ventricular hypertrophic gene programming by dietary fat type.

Long-term dietary fatty acid intake alters the development of left ventricular hypertrophy, but the linking signaling pathways are unclear. We studied the role and underlying signaling mechanisms of dietary fat intake in the early phase of the hypertrophic process. Rats assigned for 4 weeks of high-oil, high-fat, or standard diet were subjected to angiotensin II (Ang II; 33 microg/kg/h, subcutaneous) or vehicle infusion for 24 h. The Ang II-induced increase in left ventricular mRNA levels of hypertrophy-associated genes was higher in rats fed the high-oil diet compared with the standard diet. Western blotting revealed that, in parallel with changes in gene expression, the high-oil diet increased c-Jun N-terminal kinase phosphorylation (P < 0.001). Ang II increased p38 mitogen-activated protein kinase (MAPK) phosphorylation in rats fed the high-fat diet (3-fold; P < 0.01). The increase in transcription factor activator protein-1 (AP-1) DNA binding activity in response to Ang II was higher in rats fed the high-oil diet compared with those fed the standard diet (P < 0.001). Ang II downregulated inducible nitric oxide synthase mRNA levels in fatty acid-supplemented groups compared with the standard diet group. These results show that dietary fat type modulates the early activation of hypertrophic genes in pressure-overloaded myocardium involving the distinct activation of AP-1 and MAPK signal transduction pathways.

Angiotensin II↗

PubMed2006

Soluble semicarbazide-sensitive amine oxidase (SSAO) activity is related to oxidative stress and subchronic inflammation in streptozotocin-induced diabetic rats.

Diabetes is known to increase the risk of Alzheimer's disease (AD) and vascular dementia via oxidative stress and inflammation. There are speculations that SSAO activity might be related to the development of AD. Our aim was to investigate whether changes of soluble SSAO activity, oxidative stress and inflammation markers are related to each other in diabetes. Soluble and tissue-bound SSAO activities (from serum and aorta, respectively) were determined in streptozotocin (STZ)-induced diabetic rats without insulin treatment, receiving insulin once, or twice daily compared to control animals. After three weeks of treatment soluble and tissue-bound SSAO activities (seSSAO and aoSSAO, respectively), serum total antioxidant status (TAS), high sensitivity C-reactive protein (hsCRP), fructose amine levels and routine laboratory parameters were determined. SeSSAO activity significantly increased in the diabetic groups without treatment and receiving insulin once daily, and a marked decrease in aoSSAO activity was seen in all diabetic groups. Increased oxidative stress was correlated with hsCRP elevation, while hsCRP and seSSAO activity were also significantly correlated. In all groups seSSAO and aoSSAO activities were in negative correlation with each other. Our results support the view that poor metabolic control leads to increased oxidative stress, which in turn may cause the elevation of hsCRP levels. Soluble SSAO on the one hand acts as an adhesion molecule--thus possibly being a factor responsible for the late complications of diabetes--and on the other hand, it may contribute to oxidative stress. Our parsimonious conclusion is that there is a relation between the risk factors of AD and vascular dementia (diabetes, oxidative stress and chronic inflammation) and SSAO activity, which may originate from the vessel wall.

Alzheimer Disease↗

PubMed2006

Expression of human cationic trypsinogen with an authentic N terminus using intein-mediated splicing in aminopeptidase P deficient Escherichia coli.

High-level expression of human trypsinogens as inclusion bodies in Escherichia coli requires deletion of the secretory signal sequence and placement of an initiator methionine at the N terminus. Trypsinogen preparations obtained this way contain a mixture of abnormal N termini, as a result of processing by cytoplasmic aminopeptidases. Here, we describe an expression system that produces recombinant human cationic trypsinogen with a native, intact N terminus, using intein-mediated protein splicing and an aminopeptidase P (pepP) deficient E. coli strain. As a first application of this system, the effect of the pancreatitis-associated mutation A16V on the autoactivation of human cationic trypsinogen was characterized. The use of the novel pepP knock-out E. coli strain should be generally applicable to the expression of recombinant proteins, which undergo unwanted N-terminal trimming by aminopeptidase P.

Aminopeptidases↗

PubMed2006

[Diagnosis and treatment outcome in primary aldosteronism based on a retrospective analysis of 187 cases].

INTRODUCTION: Primary aldosteronism is the most common form of mineralocorticoid hypertension. The disease has been described by Jerome W. Conn in 1955; since that time there has been a great progress in the knowledge concerning the prevalence, diagnostics and treatment of the disease. AIMS: The authors retrospectively analyzed the efficacy of diagnostic procedures and the outcome of treatment by the analysis of data of 187 patients with primary aldosteronism examined between 1958 and 2004 at the 2nd Department of Medicine of Semmelweis University. METHODS: The efficacy of different methods used for the diagnosis, the frequency of the different subtypes of primary aldosteronism, as well as the surgical outcomes in patients with surgically treated subtypes of primary aldosteronism were studied. RESULTS: Aldosterone-producing adenoma was detected in more than two thirds of patients (n = 135), whereas idiopathic hyperaldosteronism was found in 46 patients. Other subtypes of primary hyperaldosteronism occurred less frequently (unilateral primary adrenocortical hyperplasia in 5 patients and adrenocortical carcinoma in one patient). For the diagnosis of familial hyperaldosteronism type I, molecular biological studies of the aldosterone-synthase/11beta-hydroxylase gene chimera were carried out in 30 patients but none of them showed the presence of the chimeric gene. When comparing the clinical parameters of patients with aldosterone-producing adenoma and idiopathic hyperaldosteronism, no significant differences were found in the time period between the diagnosis of hypertension and the diagnosis of primary aldosteronism, or in the systolic and diastolic blood pressure values. The mean of the lowest documented serum potassium concentration was slightly lower in patients with aldosterone-producing adenoma (2.8 +/- 0.1 mmol/l) compared to those with idiopathic hyperaldosteronism (3.1 +/- 0.2 mmol/l), but the difference was not significant. Normokalemic primary hyperaldosteronism was found in 7 cases. The ratio of plasma aldosterone concentration (ng/dl) to plasma renin activity (ng/ml/h) was above 20 in all patients with aldosterone-producing adenoma and in all but 5 cases with idiopathic hyperaldosteronism. To confirm the diagnosis and to differentiate the subtypes of primary aldosteronism, the postural test combined with furosemide administration was performed in the majority of patients. When cases showing an elevation of plasma cortisol level during the test were excluded, this test differentiated patients with aldosterone-producing adenoma from those with idiopathic hyperaldosteronism with a sensitivity of 69% and a specificity of 92%. In cases of adrenocortical adenomas not or not clearly detectable by radiological imaging techniques, as well as in cases with bilateral adrenocortical adenomas, selective adrenal vein sampling was performed (n = 55). All but 4 patients with aldosterone-producing adenoma underwent adrenalectomy. Histology and postoperative hormone results confirmed the preoperative diagnosis in all operated patients. After surgery serum potassium concentration returned to normal in all patients showing low serum potassium levels before surgery. Also, the moderate to severe preoperative hypertension disappeared or improved after surgery. CONCLUSIONS: These observations are in contrast with the results of international studies which showed a high frequency of normokalemic primary aldosteronism and a more frequent occurrence of idiopathic hyperaldosteronism well treatable with aldosterone-antagonists. Therefore, it can be presumed that a significant number of primary aldosteronism cases that are not accompanied with severe hypokalemia remain undetected in Hungary.

Adenoma↗

PubMed2006

Mutations of human cationic trypsinogen (PRSS1) and chronic pancreatitis.

Ten years ago, the groundwork for the discovery of the genetic basis of chronic pancreatitis was laid by linkage analyses of large kindreds with autosomal dominant hereditary chronic pancreatitis. Subsequent candidate gene sequencing of the 7q35 chromosome region revealed a strong association of the c.365G > A (p.R122 H) mutation of the PRSS1 gene encoding cationic trypsinogen with hereditary pancreatitis. In the following years, further mutations of this gene were discovered in patients with hereditary or idiopathic chronic pancreatitis. In vitro the mutations increase autocatalytic conversion of trypsinogen to active trypsin and thus probably cause premature, intrapancreatic trypsinogen activation in vivo. The clinical presentation is highly variable, but most affected mutation carriers have relatively mild disease. In this review, we summarize the current knowledge on trypsinogen mutations and their role in pancreatic diseases.

DNA Mutational Analysis↗

PubMed2006

Development of the anterior chordal canal.

Resent advances have led to the reexamination of the intraosseous pathway of the chorda tympani a few years ago and they stated that the nerve never enters the mandibular fossa and its exit the skull base in the sphenopetrosal fissure. In our report, 58 temporal bones were investigated after maceration and formalin fixation in order to understand the development of the anterior chordal canal. Our study revealed that the chorda tympani leaves the tympanic cavity through the tympanosquamosal fissure before formation of the anterior chordal canal of Huguier. This canal is situated parallel to and in front of the musculotubal canal and formed by the processus inferior tegminis tympani and the sphenoid bone between the second and fifth years of age. Prior to the age of 2, only the exit of the bony canal exists which is gradually followed by the appearance of a groove in the growing processus inferior tegminis tympani. The borders of the groove elevate and develop to upper and lower plates which lengthen with similar plates of the sphenoid bone, completing the anterior chordal canal by the fifth postnatal year. The entrance of the canal develops above the petrotympanic fissure and similar to the canal itself, it is also completely formed in the fifth year. In case of an incomplete development the anterior chordal canal remains partially opened laterally which might allow the head of the mandibula to effect the chorda tympani mechanically causing Costen's syndrome.

Adolescent↗

PubMed2006

Development and surgical anatomy of the round window niche.

The round window niche is a bony pouch of the tympanic cavity and clinically frequently explored, therefore its topography has fundamental impact on microsurgery. A total of 783 macerated and formalin-fixed temporal bones were used to study the normal anatomy of the round window and its development. The ossification of the niche starts in the 16th fetal week and is complete at birth. A process of the otic capsule, called the cartilage bar, forms the inferior wall of the round window niche. The anterior and superior walls of the niche form by intramembranous ossification, whereas the posterior and inferior walls predominantly form by enchondral ossification. The uneven growth of different walls of the round window niche can alter the shape of the entrance, which results in eight different types of niches: extremely narrow, descending tegmen, anterior septum, bony membrane, open fundus, exostosis, jugular dome and trabeculae.

Adolescent↗

PubMed2006

Development of the protympanum.

The protympanum, the only opening of the tympanic cavity, has enormous significance in the pathogenesis of middle ear inflammation. In our study, we analyzed 70 macerated temporal bones stereomicroscopically to understand the development of the protympanum. Details of this embryonic process were attained using histological sections made in frontal and horizontal planes. In contrast to recent descriptions, the present work reveals that almost the entire protympanum develops from different processes of the petrous bone. The tympanic bone takes part in forming only the posterior border of the lateral wall of the protympanum. Consequently the tympanic plate, which forms the inferior half of the mandibular fossa, is formed by two anlages. The anterosuperior quarter is formed by the petrous bone and the remainder by the tympanic bone. The main structures of the medial wall of the protympanum are the carotid canal with the internal carotid artery (ICA). The carotid canal starts to develop as two laminae of the petrous bone in the 18th fetal week. In cases of incomplete closure of these laminae the carotid canal occupies dehiscences increasing the danger of injury to the ICA. The presence of the ICA is necessary for the development of the carotid canal. If the artery takes an aberrant pathway in the tympanic cavity, or is absent, there is no sign of the carotid canal.

Adult↗

PubMed2006

Surgical anatomy of the cochlea for cochlear implantation.

The anatomy of the cochlea was investigated to obtain precise data for surgical cochlear implantation. The aim of this study has been to find the optimal site for cochleostomy, to determine the course of the basal turn and to define the relationship of the cochlea to the middle ear. Our study is the first to depict the cochlea in a classical coordinate system, to compare the anatomical situation to the surgical approaches, and, consequently, to offer firm anatomical basis for minimal invasive intervention. Thirty-five macerated temporal bones of otologically healthy individuals were used to study the surgical anatomy of the cochlea. The cochlea could be divided into three portions: promontorial, muscular and geniculo-tegmental, respectively. In the promontorial part, the basal turn has a characteristic turning around its own axis which is also indicated by the shifting with the bony spiral Lamina. In addition to the basal turn, a small part of the second and third turns of the cochlea can be also revealed behind the promontory. The most superficial part of the cochlea forming the promontory is positioned behind the Jacobson's canal providing an optimal approach for cochleostomy. The geniculo-tegmental portion of the cochlea is almost as large as the promontorial part tying immediately under the tegmen tympani. This area is accessible only from the top using a transtemporal supralabyrinthine approach. The promontorial and muscular portions can be investigated from two directions: through the facial recess and through the external acoustic meatus.

Adult↗

PubMed2005

Synthesis and dopamine receptor binding of sulfur-containing aporphines.

We investigated acid-catalyzed rearrangement of thebaine 14 and its N-propyl analog 15 with methanesulfonic acid in the presence of the nucleophiles methanethiol and hydrogen sulfide. R(-)-2-methylthioapocodeine 16, R(-)-2-methylthioapomorphine 18, and their N-n-propyl analogs 17, 19 were obtained by rearrangement in the presence of methanethiol. However, with hydrogen sulfide, rearrangement of thebaine 14 and its N-n-propyl analog 15 produced sulfide-linked bis-aporphines 21-24 instead of expected R(-)-2-mercaptoapocodeines 12, 13 and R(-)-2-mercaptoapomorphines 10, 11. R(-)-2-Methylthio-N-n-propylnorapomorphine 19 had higher affinity (Ki = 3.7 nM) at D2 receptors in rat forebrain tissue than other novel 2-substituted sulfur-containing aporphines (Ki > or = 50 nM). Behavioral testing of the novel agents in rat indicated moderate locomotor arousal after systemic injection, and none after intragastric administration, indicating poor oral bioavailability.

Animals↗

PubMed2005

Pheromonal activity of compounds identified from male Phyllotreta cruciferae: field tests of racemic mixtures, pure enantiomers, and combinations with allyl isothiocyanate.

Four himachalene sesquiterpenes and (+)-gamma-cadinene, previously identified as possible pheromone components from males of a North American population of Phyllotreta cruciferae Goeze (Coleoptera, Chrysomelidae), were tested for attractiveness in field trapping experiments in Hungary. A mixture of the four synthetic racemic himachalene derivatives and (+)-gamma-cadinene from a botanical source was slightly attractive to beetles, but much more attractive when blended with the known host-plant-derived attractant allyl isothiocyanate. This result was consistent with a previous study in North America. In tests with optically pure synthetic compounds, a blend of the same himachalene enantiomers found from male beetles was equivalent to the corresponding blend of racemic compounds, whereas a blend of the opposite enantiomers was not active. Through subtraction tests, it was found that the single compound, (6R,7S)-2,2,6,10-tetramethylbicyclo[5.4.0.]undeca-9,11-diene [compound (+)-A in this study], was as active as the whole mixture, suggesting that this compound is the key pheromone component of the European population of P. cruciferae. During field trials, several congeneric species, including P. vittula, P. nemorum, P. nodicornis, and P. ochripes, also were caught, suggesting that the same compound(s) may be relatively widespread as pheromone components in this genus.

Animals↗

PubMed2005

[Clinical symptoms, diagnosis and treatment of multiple endocrine neoplasia type 1. Results of genetic screening in Hungarian patients].

Multiple endocrine neoplasia type 1 syndrome is an autosomal dominant disorder characterized by endocrinopathies involving the parathyroid glands, anterior pituitary gland, and pancreas. Also, it may be associated with foregut carcinoid, adrenocortical tumors and non-endocrine tumors. After reviewing the prevalence, genetic background, clinical symptoms, diagnosis and treatment of the disorder, the authors present their genetic screening method used for the detection of mutations of the MEN1 gene (prescreening of polymerase chain reaction amplified exons using temporal temperature gradient gel electrophoresis followed by direct DNA sequencing). Using this method, the authors identified disease-causing MEN1 gene mutations in 9 probands (small deletions in 2 cases, insertion in 2 cases, nonsense mutations in 2 cases and missense mutations in 3 cases). Of the 9 mutations, 4 proved to be novel mutation not reported in the literature. Family screening indicated de novo mutations in 2 probands. In addition to mutations, several sequence polymorphisms were also detected. The authors conclude that one of the major advantages of genetic screening in families with MEN1 syndrome was the identification of family members carrying the mutation who should be regularly screened for disease manifestations and those not carrying the mutation in whom clinical screening is unnecessary. Also, genetic screening may be useful in cases when MEN1 syndrome is suspected, but the clinical manifestations do not fully establish the diagnosis of MEN1 syndrome.

Adrenal Cortex Neoplasms↗

PubMed2005

[Improvement of bone metabolism after infliximab therapy in Crohn's disease].

BACKGROUND: Osteoporosis has received increasing attention as a potential complication of Crohn's disease. Among cytokines tumor necrosis factor-alpha plays a pivotal role in the pathogenesis of inflammatory bowel diseases by inducing a wide variety of inflammatory responses, including bone resorption. Only few data are present about the effect of infliximab on bone metabolism. AIMS: The authors evaluated the effect of infliximab on bone metabolism in patients with Crohn's disease. PATIENTS AND METHODS: Twenty seven patients (17 females, 10 males, mean age 32.58 yrs) with refractory fistulizing Crohn's disease were treated with a series of three infusions of 5 mg infliximab per kg at weeks 0, 2, and 6. Biochemical markers of bone formation (osteocalcin) and bone resorption (beta-CrossLaps) were measured before administration of each infliximab infusion. 54 patients were studied with inactive Crohn's disease (Crohn's disease activity index < 150) as a control. RESULTS: There were significant differences in beta-CrossLaps concentrations (ng/ml) between the day 0 and 14 (0.57 +/- 0.32 vs. 0.46 +/- 0.29, p < 0.01) and the day 0 and 42 (0.57 +/- 0.32 vs. 0.45 +/- 0.26, p < 0.05). The osteocalcin levels significantly increased from day 0 to day 42 (21.31 +/- 12.14 vs. 25.64 +/- 16.97, p < 0.05). The serum beta-CrossLaps and osteocalcin levels were 0.47 +/- 0.24, 27.2 +/- 8.44 in the control group respectively. These results differed from the serum levels of active patients before the treatment, but there were no notable differences at the day 42. CONCLUSION: Infliximab therapy in Crohn's disease patients displayed a rapid influence on bone metabolism by enhancing bone formation and decreasing bone resorption. In addition to its mucosal effect affecting the bone homeostasis, indicate a further rationale usage of tumor necrosis factor-alpha blockade in the therapy of inflammatory bowel diseases.

Adult↗

PubMed2005

[New intraoperative diagnostic methods parathyroid surgery. Adenoma localization by gamma probe].

INTRODUCTION: The key to heal primary hyperparathyroidism is to find the hyper functioning parathyroid gland(s). Promoting this the perioperative isotope guided localization technique is worldwide used in the last years. AIM: Authors use this method since February, 2000. They present their experiences. METHODS: At 122 patients undergoing parathyroidectomy in last 5 years with diagnosis of primary hyperparathyroidism perioperative sestamibi scanning by gamma probe was taken to localize the adenoma. Tc-99m-sestamibi was administered 90-150 minutes before starting anesthesia. The distribution of activity was measured before operation percutaneously on the neck and during operation directly at explored parathyroid regions. Finally the removed specimens were ex vivo scanned. RESULTS: Because of the thyroid lobes also accumulate sestamibi the localizability of adenomas depended on direction of scanning. Important factor is the correct timing of isotope administration in order to achieve domination of parathyroid activity in time of measurement. Localization of adenomas by percutaneous measurement was correct in 36.1% of cases and by perioperative direct scanning in 66.4%. Furthermore, ex vivo scan of removed adenomas showed impressively high activity in all cases. CONCLUSIONS: In their experience sestamibi scanning lightens the operation only in a part of cases but probably it will be the most important method of localization if isotope selectively accumulating in parathyroid gland could be found. For the moment the greatest profit of this method is that the ex vivo measurement indicates the success of operation with great probability.

Adenoma↗

PubMed2005

Insulin treatment decreases the antioxidant defense mechanism in experimental diabetes.

BACKGROUND: Hyperglycemia-induced oxidative stress and left ventricular hypertrophy is an independent risk factor for cardiovascular disease. Our aim was to determine the relationship between left ventricular hypertrophy and the total scavenger capacity (TSC) in diabetic rats. MATERIAL/METHODS: Control animals (n=30) were compared to streptozotocin-induced diabetic rats (n=38) and diabe-tic rats receiving insulin treatment (n=30) for 22 days. Half of the animals received angiotensin II on day 21. The left ventricular mass, TSC and carbohydrate parameters were determined. RESULTS: Diabetes did not alter left ventricular mass; however, diabetes with insulin treatment was associated with left ventricular hypertrophy. The extent of ventricular hypertrophy did not change significantly in this group after angiotensin II treatment. TSC increased very significantly in diabetic rats. These differences remained high when angiotensin II-treated control rats [CA] were compared with treated diabetic rats [DA] (p<0.005). TSC decreased significantly when diabetic rats were treated with insulin. CONCLUSIONS: Diabetes results in oxidative stress, which in turn enhances the activity of antioxidant enzymes. This increase in enzyme activity inhibits the subcellular remodeling processes, thus also inhibiting concomitant cardiac hypertrophy. Insulin treatment decreases the activity of the antioxidant system and can enhance the function of other localized tissue-specific growth factors. These changes may contribute to the early onset of cardiovascular damage detected in diabetic patients.

Angiotensin II↗