Biomedical subjects

P Kucera

Publications and source records attributed to P Kucera.

At least 19 recordsLinked to original sources

PubMed2006

Impaired cognitive functions in mild traumatic brain injury patients with normal and pathologic magnetic resonance imaging.

INTRODUCTION: Mild traumatic brain injury (MTBI) is a common neurological (neurotraumatological) diagnosis. As well as different subjective symptoms, many patients develop neuropsychological dysfunction with objective impairment of attention, memory and certain executive functions. Magnetic resonance imaging (MRI) is not routinely used in MTBI patients despite its proven greater sensitivity and specificity in comparison with computed tomography (CT). METHODS: The patient group consisted of 30 persons with MTBI and the control group consisted of 30 sex- and age-matched healthy volunteers. Both groups underwent neurological examination, neuropsychological testing (including the Postconcussion Symptoms Scale questionnaire, PCSS) and brain MRI (the patient group within 96 h after injury). RESULTS: The analyzed groups did not differ significantly in terms of sex, age, or level or duration of education. MRI pathological findings (traumatic and nonspecific) were present in nine patients. Traumatic lesions were found in seven patients. Nonspecific white matter lesions were found in five healthy controls. There were significant differences between MTBI patients and controls in terms of subjective symptoms (PCSS) and selected neuropsychological tests. Statistically significant neuropsychological differences were found between MTBI patients with true traumatic lesions and MTBI patients with nonspecific lesions. CONCLUSION: There is evidence that MTBI patients with true traumatic MRI lesions are neuropsychologically different from MTBI patients with nonspecific MRI lesions or normal brain MRI. These results support the hypothesis that some acute MTBI signs and symptoms have a real organic basis which can be detected by selected new MRI modalities.

Adult↗

PubMed2006

Magnet Tracking: a new tool for in vivo studies of the rat gastrointestinal motility.

Digestive motility was studied in the rat using a miniaturized version of the Magnet Tracking system which monitored the progression of a small magnetic pill through the entire digestive tract. The dynamics of movement was followed and three-dimensional (3-D) images of digestive tract were generated. After a retention period in the stomach and rapid passage through duodenum, the magnet progressed along the small intestine with gradually decreasing speed and longer stationary periods. It remained in the caecum for variable intervals. In the colon, periods of progress alternated with long quiescent periods. Gastric activity oscillated at 5-6 min(-1). In the small intestine, two frequency domains coexisted, showing independent modulations and proximo-distal gradients (40 to >32 and 28 to >20 min(-1)). Caecal oscillations were of 1.5 min(-1). The data allowed the magnet location and calculation of gastric and small intestinal transit times (58 +/- 36 and 83 +/- 14 min respectively), both significantly prolonged by oleate administration (243 +/- 130 and 170 +/- 45 min respectively). Magnet Tracking is a non-invasive tool to study the in vivo spatial and temporal organization of gastrointestinal motility in the rat.

Animals↗

PubMed2005

Magnetic pill tracking: a novel non-invasive tool for investigation of human digestive motility.

A new minimally invasive technique allowing for anatomical mapping and motility studies along the entire human digestive system is presented. The technique is based on continuous tracking of a small magnet progressing through the digestive tract. The coordinates of the magnet are calculated from signals recorded by 16 magnetic field sensors located over the abdomen. The magnet position, orientation and trajectory are displayed in real time. Ten young healthy volunteers were followed during 34 h. The technique was well tolerated and no complication was encountered. The information obtained was 3-D configuration of the digestive tract and dynamics of the magnet displacement (velocity, transit time, length estimation, rhythms). In the same individual, repeated examination gave very reproducible results. The anatomical and physiological information obtained corresponded well to data from current methods and imaging. This simple, minimally invasive technique permits examination of the entire digestive tract and is suitable for both research and clinical studies. In combination with other methods, it may represent a useful tool for studies of GI motility with respect to normal and pathological conditions.

Adult↗

PubMed2005

[Contemporary view on mild brain injuries in adult population].

Mild brain injury is one of the most common neurological a neurotraumatological diagnoses. The pathophysiological basis of mild brain injury is frequently a diffuse axonal damage of variable degree. In the acute phase of mild brain injury we have to identify 1% of patients who will undergo neurosurgery because of vital need. The analysis of patient's personal history, screening of risk factors, neuropsychological testing and imaging methods (CT, MRI) are irreplaceable in the diagnostic process of mild brain injury. Though the mild brain injury is currently considered as an irrelevant traumatic event, approximately 10% of patients develop the so-called post-concussion syndrome.

Brain Concussion↗

PubMed2005

Chronic toxic neuropathy after organophosphorus poisoning in quails (Coturnix coturnix japponica).

Peripheral neuropathy was induced by the long-term administration of organo-phosphorus compounds (phtalimid/phosmet) in quails (Coturnix coturnix japponica). After 4 weeks, the first symptoms of organophosphorus (OPC) poisoning (apathy, diarrhea) were present. During the second month of a daily administration of the toxic substance using the probe, an apparent clinical autonomic and peripheral neuropathy with ataxia had developed. Toxic disturbance of the nervous system was confirmed by the examination of spinal and cortical somatosensory evoked potentials (SEP) after tibial nerve stimulation. The prolongation of the peripheral conduction time (wave P6 and N9 represent the response from the ischiadic nerve and the entry of the stimulus to spinal cord, respectively) confirmed a peripheral nerve lesion. We suggest that these clinical and electrophysiological changes, displayed by the disturbed nervous system, are caused by either slowing or stoppage of the axonal flow, transport of proteins and other substances, as well as by axon demyelination (Tab. 1, Fig. 1, Ref. 22).

Animals↗

PubMed2004

Effect of high glucose concentrations on expression of ELAM-1, VCAM-1 and ICAM-1 in HUVEC with and without cytokine activation.

Diabetes mellitus is associated with an increased prevalence of endothelial dysfunction and development of atherosclerotic vascular diseases. We demonstrate here that hyperglycemia results in the expression of adhesion molecules on endothelial cells in vitro. Incubation of human umbilical vein endothelial cells (HUVEC) in a culture medium with 11.0 mM, 16.5 mM and 22.0 mM glucose concentrations induced the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and endothelial-leukocyte adhesion molecule-1 (ELAM-1). This effect was detectable after 24 h incubation of HUVEC with a high glucose concentration. The effect of high glucose concentration on TNF-alpha induced expression of ELAM-1, VCAM-1 and ICAM-1 was negligible, if at all. These results show that even a short-term exposure of endothelial cells (ECs) to high glucose concentration leads to their activation associated with increased expression of adhesion molecules such as ELAM-1, VCAM-1 and ICAM-1.

Antineoplastic Agents↗

PubMed2004

Polymorphism of INS VNTR is associated with glutamic acid decarboxylase antibodies and postprandial C-peptide in patients with onset of diabetes after 35 years of age.

Variability in the number of tandem repeats of the insulin gene (INS VNTR) is probably involved in the genetic regulation of insulin secretion. The aim of this study was to investigate the association of INS VNTR polymorphism with the presence of glutamic acid decarboxylase antibodies (GADA) and C-peptide levels in patients with the onset of diabetes after 35 years of age. We investigated 117 patients, median of age 63 (range 40-83) years, median of diabetes duration 8 (range 1-30) years; 31 GADA-positive and 86 GADA-negative subjects. INS VNTR polymorphism was typed indirectly using - 23HphI (T/A) polymorphism, which is in complete linkage disequilibrium with INS VNTR. The I/I, I/III and III/III genotypes were found in 22 (71 %), 8 (26 %), 1 (3 %) GADA-positive individuals and in 39 (45 %), 35 (41 %), 12 (14 %) GADA-negative individuals, respectively. The Class I allele and the genotype I/I were significantly associated with the presence of GADA (OR=2.72, CI 95 %=1.29-5.73 and OR=2.95, CI 95 %=1.22-7.13). The presence of Class III allele was significantly associated with a higher level of postprandial C-peptide in GADA-positive subjects, even when regarding the duration of diabetes. Our results of INS VNTR polymorphism in patients with the onset of diabetes after 35 years of age confirm the association of Class I INS VNTR with autoimmune diabetes and the protective effect of Class III INS VNTR on the insulin secretion in GADA-positive subjects.

Adult↗

PubMed2004

An acute toxic neuropathy caused by organo-phosphate poisoning in hens.

OBJECTIVE: Organophosphorus compounds can induce an acute toxic peripheral neuropathy. In hens, the acute peripheral neuropathy was induced by poisoning with organo-phosphorus compound (OPC)--tri-ortho-cresyl phosphate (TOCP). METHODS: In the course of an acute TOCP-induced toxic neuropathy in hens the activity of following enzymes was analysed: asparaginase, glutaminase, glutamat-dehydrogenase, AMP and adenosine deaminases and 5'nucleotidase; ALT (SGPT), AST (SGOT) and proteins levels were estimated. RESULTS: A decrease in activity of all analysed enzymes was observed; the amount of proteins was increased. CONCLUSION: The biochemical changes display the slowing or stoppage in axonal transport of proteins. The disturbance of axoplasmic flow and the axonal demyelination may be considered as an attribute of peripheral neuropathy. (Tab. 1, Fig. 1, Ref. 32.).

Acute Disease↗

PubMed2004

Sympathetic skin response: review of the method and its clinical use.

Sympathetic skin response (SSR) represents a potential generated in skin sweat glands; it originates by activation of the reflex arch with different kinds of stimuli. The potential of rapid habituation after repeated stimuli is formed by biphasic or triphasic slow wave activity with relatively stable latency and variable amplitude. In healthy subjects younger than 60 years of age the response is always present in all extremities. SSR is most frequently used in diagnosing the functional impairment of non-myelinated postganglionic sudomotor sympathetic fibers in peripheral neuropathies. In this study a more complex and informative view on the anatomical and physiological substrates of SSR, its character, normal values and technique are presented, focusing on problems in evaluation of the response and factors that have influence on it. Based on personal experience normative latency and amplitude values of SSR in a group of 20 healthy individuals (x +/- SD), upper extremities: 1.48 +/- 0.80 sec., 444 +/- 167 microV, respectively; lower extremities: 2.06 +/- 0.93 sec., 203 +/- 87.4 microV, respectively) and recommendations for qualitative evaluation preference--the presence or absence of the response--over quantitative evaluation of latency and amplitude of the response in practical clinical use of the method are presented. (Tab. 1, Fig. 2, Ref. 148.).

Adolescent↗

PubMed2004

Clinically unapparent central motor pathways lesion in patients with type I diabetes mellitus. A transcranial magnetic stimulation study.

OBJECTIVE: There is an evidence of central nervous system (CNS) involvement in diabetic patients. The aim of the study was to determine a conduction slowing in CNS pathways using a transcranial magnetic stimulation (TMS) and F-wave latency measurement. METHODS: Diabetic patients and a control group, both without clinical symptoms and signs of CNS lesion were evaluated. Motor evoked potentials were recorded from upper and lower extremities and central conduction time (CCT) was calculated according to formula: CCT = MEP-[0.5x(F-M-1)+M]. Obtained results and data from literature were compared. RESULTS: There was a significant prolongation of CCT recorded from lower extremities. The prolongation of CCT recorded from upper extremities was not statistically significant. Our results correlate with previously published data. CONCLUSION: In spite of missing clinical signs of CNS lesion in diabetic patients, a significant prolongation of CCT compared to control group and literature data was recorded. We assume a presence of diffuse subclinical CNS lesion induced by metabolic changes in DM. Difference between CCT obtained from upper and lower extremities implicate, that changes are analogical to peripheral neuropathies ("central length-dependent injury?"). Measurement of CCT using TMS could become a complementary electrophysiological method for assessment of subclinical CNS involvement in diabetic patients. (Tab. 4, Ref. 17.)

Adolescent↗

PubMed2004

Autonomic nervous system dysfunction in multiple sclerosis patients.

We present the results of our study dealing with autonomic nervous system (ANS) function in multiple sclerosis (MS) patients. We performed a cardiovascular reflex examination (heart rate variation in deep breathing and active standing) and spectral analysis of heart rate variability in 36 MS patients who fulfilled the criteria for this diagnosis. We evaluated several various indexes used for the assessment of ANS function: I/E, I-E in deep breathing test; RRmax/RRmin in active standing, spectral analysis of heart rate variability in VLF, LF and HF bands were performed. We found a significant difference in I-E index values during deep breathing test in MS patients when compared to the healthy control group; we did not find any difference in I/E index (deep breathing test) and RRmax/RRmin (active standing) values. The spectral analysis of heart rate variability in the rest-tilt-rest test showed a significant difference in spectral powers in MS patients when compared to the healthy control group in all frequency bands. (Tab. 2, Fig. 7, Ref 17.)

Adult↗

PubMed2003

Postanoxic functional recovery of the developing heart is slightly altered by endogenous or exogenous nitric oxide.

Nitric oxide synthase (NOS) is strongly and transiently expressed in the developing heart but its function is not well documented. This work examined the role, either protective or detrimental, that endogenous and exogenous NO could play in the functioning of the embryonic heart submitted to hypoxia and reoxygenation. Spontaneously beating hearts isolated from 4-day-old chick embryos were either homogenized to determine basal inducible NOS (iNOS) expression and activity or submitted to 30 min anoxia followed by 100 min reoxygenation. The chrono-, dromo- and inotropic responses to anoxia/reoxygenation were determined in the presence of NOS substrate (L-arginine 10 mM), NOS inhibitor L-NIO (1-5 mM), or NO donor (DETA NONOate 10-100 microM). Myocardial iNOS was detectable by immunoblotting and its activity was specifically decreased by 53% in the presence of 5 mM L-NIO. L-Arginine, L-NIO and DETA NONOate at 10 microM had no significant effect on the investigated functional parameters during anoxia/reoxygenation. However, irrespective of anoxia/reoxygenation, DETA NONOate at 100 microM decreased ventricular shortening velocity by about 70%, and reduced atrio-ventricular propagation by 23%. None of the used drugs affected atrial activity and hearts of all experimental groups fully recovered at the end of reoxygenation. These findings indicate that (1) by contrast with adult heart, endogenously released NO plays a minor role in the early response of the embryonic heart to reoxygenation, (2) exogenous NO has to be provided at high concentration to delay postanoxic functional recovery, and (3) sinoatrial pacemaker cells are the less responsive to NO.

Animals↗

PubMed2003

Gliadin, endomysial and thyroid antibodies in patients with latent autoimmune diabetes of adults (LADA).

Latent autoimmune diabetes of adults (LADA) manifested after the age of 35 is characterized by the presence of disease-specific autoantibodies (anti-glutamate decarboxylase GADAb, anti-IA2Ab). However, autoimmunity in Type 1 diabetes mellitus is not targeted only to pancreatic beta-cells. No data have so far been published concerning the antibodies associated with other autoimmune disease in LADA patients. The presence of anti-thyroglobulin (TGAb), anti-thyroid peroxidase (TPOAb), anti-gliadin IgA (AGAAb) and IgG (AGGAb) and endomysial antibodies (EMAb) in sera of 68 diabetics typed as LADA was compared with the antibody presence in sera of 85 patients with Type 2 diabetes. We found a significantly higher occurrence of gliadin antibodies in LADA patients: the rate of AGGAb was 19.1% in comparison with 3.5% in the T2DM group (P = 0.0026), the rate of AGAAb was 13.2% in comparison with 3.5% (P = 0.035). The prevalence of EMAb was very low in both groups (1.5% and 0). The two groups differed significantly in the TPOAb rate: 22.1% in LADA compared to 9.4% in T2DM (P = 0.04), whereas no significant difference was found in the presence of TGAb (8.8% and 3.5%, P = 0.187). In comparison with T2DM patients, LADA patients were found to express higher antibody activity against gluten-related antigens and against TPO.

Age of Onset↗

PubMed2003

Comparison of aminolevulinic acid and hexylester aminolevulinate induced protoporphyrin IX distribution in human bladder cancer.

PURPOSE: Successful photodynamic therapy of epithelial cancer requires a specific photosensitization of malignant tissue. We evaluate the intensity and localization of protoporphyrin IX (PpIX) in superficial transitional cell carcinoma and nonmalignant cells of the human bladder following topical administration of its precursor, either aminolevulinic acid (ALA) or hexylester aminolevulinate (HAL). MATERIALS AND METHODS: Solutions of ALA or HAL were instilled into the bladder of 18 patients presenting with recurrent transitional cell carcinoma. The distribution of PpIX through the bladder wall was studied on frozen biopsies using fluorescence microscopy and correlated with pathological findings. RESULTS: Topical bladder instillation with 180 mmol (3%) ALA administered for 6 hours or 8 mmol (0.2%) HAL administered for 4 hours gave similar results regarding intensity and tissue distribution of PpIX fluorescence, whereas 8 mmol HAL administered for 2 hours followed by 2 hours of resting time (2+2 hours concept) induced a PpIX fluorescence twice as high. The fluorescence remained limited to cancer cells. Only a trace of PpIX fluorescence was observed in suburothelial connective tissue, that is chorion, but none in the bladder smooth muscle regardless of experiment conditions. CONCLUSIONS: HAL is an excellent precursor for PpIX synthesis in bladder cancer. With the 2+2 hour topical administration condition it yielded the highest PpIX fluorescence intensity and fluorescence contrast between normal and malignant urothelial cells. This approach allows us to optimize PpIX tissue distribution for photodynamic therapy in superficial bladder cancer.

Administration, Intravesical↗

PubMed2003

HLA in Czech adult patients with autoimmune diabetes mellitus: comparison with Czech children with type 1 diabetes and patients with type 2 diabetes.

Type 1 diabetes results from an autoimmune insulitis, associated with HLA class II alleles. The evidence about HLA allele association is not clear in patients diagnosed after 35 years of age. In this study we have analyzed HLA alleles of DQB1 and DRB1 genes by sequence specific primer (SSP)-PCR technique in adult patients with disease onset after 35 years of age. Two hundred and eighty-one patients were divided into three groups according to the insulin therapy, the level of C peptide (CP), and GAD antibodies (anti-GAD). Group 1 (type 1 diabetes in adults) was characterized by CP less than 200 pmol/L and anti-GAD more or less than 50 ng/mL (n = 80). All of them had insulin therapy within 6 months after diagnosis. Group 2 latent autoimmune diabetes mellitus in adults (LADA) was defined by a minimum 6-month-long phase after diagnosis without insulin therapy, and was characterized by CP more than 200 pmol/L and anti-GAD more than 50 ng/mL (n = 70). Group 3 (type 2 diabetes) was characterized by CP more than 200 pmol/L and anti-GAD less than 50 ng/mL (n = 131). None ever had insulin therapy. In group 1, there was increased frequency of DRB1*04 (45.0% vs. controls 14.1%, OR = 5.0, P < 0.0005) and DQB1*0302 alleles (43.3% vs. controls 11.1%, OR = 6.1, P < 0.00005). There was increased frequency of DRB1*03 and DQB1*0201, and decreased frequency of DQB1*0602 (3.3% vs. controls 20.2%), but it was not significant. In group 2, there was a significantly increased frequency of DRB1*03 only (50.0% vs. controls 21.2%, OR = 3.7, P < 0.05). Compared with children with type 1 diabetes and adults with type 2 diabetes (group 3), we conclude that the presence of predisposing DQB1 alleles in adults with type 1 diabetes decreases with the age, probably due to environmental factors. Only the DRB1*03, but not the DQB1 gene, becomes the main predisposing allele in LADA patients. These findings suggest that the presence of HLA-DQB1*0302 identifies patients at high risk of requiring insulin treatment. Type 1 diabetes mellitus (DM) in children or adults may have partly different immunogenetic etiopathogenesis than LADA.

Adult↗

PubMed2003

Ectopic pacing at physiological rate improves postanoxic recovery of the developing heart.

Recently, rapid and transient cardiac pacing was shown to induce preconditioning in animal models. Whether the electrical stimulation per se or the concomitant myocardial ischemia affords such a protection remains unknown. We tested the hypothesis that chronic pacing of a cardiac preparation maintained in a normoxic condition can induce protection. Hearts of 4-day-old chick embryos were electrically paced in ovo over a 12-h period using asynchronous and intermittent ventricular stimulation (5 min on-10 min off) at 110% of the intrinsic rate. Sham (n = 6) and paced hearts (n = 6) were then excised, mounted in vitro, and subjected successively to 30 min of normoxia (20% O(2)), 30 min of anoxia (0% O(2)), and 60 min of reoxygenation (20% O(2)). Electrocardiogram and atrial and ventricular contractions were simultaneously recorded throughout the experiment. Reoxygenation-induced chrono-, dromo-, and inotropic disturbances, incidence of arrhythmias, and changes in electromechanical delay (EMD) in atria and ventricle were systematically investigated in sham and paced hearts. Under normoxia, the isolated heart beat spontaneously and regularly, and all baseline functional parameters were similar in sham and paced groups (means +/- SD): heart rate (190 +/- 36 beats/min), P-R interval (104 +/- 25 ms), mechanical atrioventricular propagation (20 +/- 4 mm/s), ventricular shortening velocity (1.7 +/- 1 mm/s), atrial EMD (17 +/- 4 ms), and ventricular EMD (16 +/- 2 ms). Under anoxia, cardiac function progressively collapsed, and sinoatrial activity finally stopped after approximately 9 min in both groups. During reoxygenation, paced hearts showed 1) a lower incidence of arrhythmias than sham hearts, 2) an increased rate of recovery of ventricular contractility compared with sham hearts, and 3) a faster return of ventricular EMD to basal value than sham hearts. However, recovery of heart rate, atrioventricular conduction, and atrial EMD was not improved by pacing. Activity of all hearts was fully restored at the end of reoxygenation. These findings suggest that chronic electrical stimulation of the ventricle at a near-physiological rate selectively alters some cellular functions within the heart and constitutes a nonischemic means to increase myocardial tolerance to a subsequent hypoxia-reoxygenation.

Animals↗

PubMed2002

Autoimmune thyroiditis in non-obese subjects with initial diagnosis of Type 2 diabetes mellitus.

Autoimmune thyroiditis is often associated with Type 1 diabetes mellitus (T1DM). In non-obese adult-onset diabetes diagnosed initially as Type 2 diabetes mellitus (T2DM), there is a proportion of cases with so far undiagnosed T1DM. The objective of this study was to estimate the frequency of autoimmune thyroiditis (AT) among non-obese (BMI <30.0 kg/m2) patients with T2DM and to compare the frequency of AT in subgroups of patients according to the presence of glutamic acid decarboxylase antibodies (GADA), insulin requirement, and post-breakfast C-peptide levels. The study included 118 adult patients (55 men and 63 women) with the initial diagnosis of T2DM and age at the onset of diabetes > 35 yr. Median of age was 66 yr (range 39-82), and median duration of diabetes was 9 (range 1-27) yr. AT was diagnosed using thyroid peroxidase antibodies, TG-antibodies, US and TSH levels. Nineteen per cent of the subjects were found to have AT, and the frequency of AT did not significantly differ between the groups of GADA+ and GADA- subjects. There was no difference in the frequency of AT between the group treated with hypoglycemic agents and/or diet and the group requiring insulin. The frequency of AT was higher in the group with post-breakfast C-peptide levels < or = 0.8 nmol/l compared to the group with post-breakfast C-peptide levels > 0.8 nmol/l (37% vs 16%), however the group with post-breakfast C-peptide levels < or = 0.8 nmol/l had longer duration of diabetes.

Adult↗

PubMed2002

Pathogenesis of alcoholic neuropathy.

Chronic alcoholism is a medical, economical and social problem. Motility and mental function disorders are among the complications of chronic alcoholism and have been known for more than two centuries as "alcoholic paralysis", and are caused by alcoholic neuropathy. The pathogenesis of alcoholic neuropathy does not appear to be identical with central nervous system disorders which are caused by chronic alcoholism and it seems that it results from a failure of the protection barrier systems in the peripheral nervous system. To the pathogenesis of alcoholic neuropathy includes: 1. direct toxic effects of alcohol on the cellular population of the central nervous system and other tissues, especially of parenchymatous organs (in particular of the liver), 2. indirect metabolic and exotoxic changes mediated by malabsorption, maldigestion and secondary caloric and energy deprivation, 3. effects of genetic factors. (Fig. 2, Ref. 23.)

Alcoholic Neuropathy↗