Health care in the Czech Republic. A system in transition.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A Albert.
Explore the source record for details and available documents.
A prognostic index for nonfatal recurrences of ventricular tachycardia (VT) was developed using a retrospective analysis of a group of 206 patients with sustained monomorphic VT or ventricular fibrillation (VF) after healing of acute myocardial infarction. 74 patients (36%) (64 with VT and 10 with VF) had recurrences of sustained monomorphic VT during 3.4 +/- 9 years of follow-up. Three clinical variables were selected and weighted by stepwise logistic discriminant analysis of the study group. They were coded as follows: interval of myocardial infarction to arrhythmia (less than 2 months = 1; 2 to 6 months = 2; greater than 6 months = 3), drug therapy with or without sotalol (with = 1, without = 2), and VT or VF as the presenting arrhythmia (VT = 1, VF = 2). The prognostic index was: 3.41 - (0.56 x interval) - (1.94 x therapy) + (0.86 x arrhythmia). This index was validated prospectively in a test group of 158 consecutive patients with VT or VF after healing of acute myocardial infarction. Patients were allocated into different classes with decreasing prognostic index values associated with increasing risk for recurrences of VT. In the test group, 27 of 158 (17%) patients (22 with VT and 5 with VF) had recurrences of VT (follow-up of 2 +/- 2 years). Two risk classes of patients were identified: high risk for recurrences of VT (61%) corresponding to patients with a negative index; and low risk (4%) consisting of those with a positive index. Thus, using O as the cutoff point, the sensitivity, specificity, and positive and negative predictive values were 81, 89, 62 and 96%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
To determine if the occurrence and the consequences of spontaneous predischarge postinfarction ischemia could be predicted early after hospital admission, a consecutive series of patients with acute myocardial infarction was studied and followed for 3 years. No patient was treated by thrombolysis. Spontaneous predischarge ischemia was defined as angina that occurred at rest before hospital discharge, at least 3 days after the acute event, and that was accompanied by electrocardiographic changes, but not by an increase in cardiac enzymes. Patients who died within the first 3 days were excluded from analysis. Among the 943 patients who survived at least 3 days, 165 (17.5%) had spontaneous ischemia before discharge. They had a higher 1-year post-hospital mortality (16 vs. 10%), but did not have significantly higher total 3-year mortality rates. Four independent, early available variables predictive of the occurrence of spontaneous ischemia were selected from a stepwise logistic discriminant analysis: history of angina before infarction, non-Q-wave infarct, absence of smoking, and higher age. Among the 165 patients with spontaneous ischemia, 3 independent variables predictive of 3-year mortality were selected stepwise: left ventricular function score, history of previous infarction, and absence of smoking.
Biochemical parameters reflecting bone resorption [urinary calcium/creatinine (Ca/Cr) and hydroxyproline/creatinine (OH/Cr)] were related to serum estrogens [estrone (E1) and estradiol (E2)] in 262 healthy women including 158 patients receiving estrogen replacement therapy (ERT) for at least 6 months, 49 eugonadal women, and 55 untreated postmenopausal women. A significant (P < 0.001) correlation exists between serum E2 and Ca/Cr: Ca/Cr (mg/dl) = -0.00044 E2 (pg/ml) + 0.129 (n = 262; r = -0.37), serum E2 and OH/Cr: (OH/Cr (mg/g) = -0.049 E2 (pg/ml) + 18.76 (n = 262; r = -0.36), serum E1 and Ca/Cr: Ca/Cr (mg/dl) = -0.0003 E1 (pg/ml) + 0.127 (n = 261; r = -0.28) but not between serum E1 and OH/Cr. Women with circulating levels of E2 between 60 and 90 pg/ml have a significant (P < 0.01) reduction of Ca/Cr and OH/Cr when compared with those with lower levels of E2. Higher values of E2 do not provide additional benefit. We conclude that in postmenopausal women receiving an estrogen replacement therapy (ERT), a significant reduction of bone resorption is achieved when circulating levels of estradiol reach a value (60 pg/ml) corresponding to the one measured, in eugonadal women, during the last days of the early follicular phase of the menstrual cycle. We suggest that oral or percutaneous ERT should induce a minimal value of 60 pg/ml to prevent postmenopausal bone loss.
In order to evaluate the potential inhibition of the acute anti-osteoclastic activity of salmon calcitonin (SCT) by specific antibodies (Ab), we compared the SCT-induced hypocalcemic effect in young male rabbits with significant titers of high affinity Ab and in matched animals without Ab. Immunization of rabbits was performed by repetitive s.c. injections of SCT and Freund adjuvant. Ab were present in four-fifths of SCT-treated rabbits (Ab+). Their titer varied from 0.8 x 10(-9) to 30 x 10(-9) M/liter and their constant of affinity from 0.97 x 10(9) to 4.2 x 10(9) L/M. Intravenous injection of 1 IU/kg SCT to Ab+ rabbits induced a significant decrease (P less than 0.01) of ionized serum calcium (Ca2+) after 30 minutes (mean +/- SD: -9 +/- 0.6%) and until the 240th minute of the test (-16.7 +/- 4.7%), with a maximum after 120 minutes (-22.6 +/- 2%). This was not significantly different from the hypocalcemic effect measured after the same procedure performed in matched animals without Ab (Ab-): significant decrease in Ca2+ (P less than 0.01) after 30 minutes (-8.2 +/- 2.2%), maximal after 150 minutes (-23.2 +/- 4.9%), and lasting until 210 minutes (-14.5 +/- 3.7%). We conclude that, in the particular model of the male young rabbit, specific anti-SCT Ab do not block or reduce the acute anti-osteoclastic activity of SCT.
Explore the source record for details and available documents.
Partial trisomy 8qter-->q23 or q24.1 has been reported in 15 literature cases. We add two further case reports here. Patient 1 inherited the derivative (2) of a balanced maternal reciprocal translocation t(2;8)(qter;q2300) after 2:2 disjunction and adjacent-1 segregation, and is trisomic for the segment 8qter-->q2300. Patient 2 inherited a recombinant (8) of a balanced maternal inverted insertion inv ins(8)(q1300;q2300q24.2) and is trisomic for the segment 8q24.2-->q2300. The phenotype of both patients is described and compared to the spectrum of symptoms established from the 15 literature cases. This spectrum contains all features observed with a frequency of > = 50%. Patient 1 had 35% of the features of this spectrum; Patient 2 had 47%. The intrauterine survival probability of unbalanced offspring is assumed to be the same in both cases, as nearly the same segments are trisomic. The pedigrees indicate that the inversion carrier may have a reduced production probability of unbalanced gametes and therefore a reduced risk compared to the translocation carrier.
Angiogenesis, a fundamental process in various physiological and pathological events, is generally studied using in vivo models, such as the chick chorioallantoic membrane or the rabbit cornea, which are difficult to quantitate. We developed the quantitation of angiogenesis in an in vivo model previously described by Dvorak et al [6]. Perforated plexiglass chambers filled with human or rat fibrin were implanted into the dorsal subcutaneous space of a Wistar rat. After four days of implantation, a sequentially organized invasion of the fibrin gel by various blood cell types occurred through the holes and neovascularized granulation tissue buds appeared. These buds presented mature neovessels and a new collagen matrix. Three dimensional computer image analysis of the chambers was performed using macroscopic and microscopic parameters: total vascularized area, bud height and equivalent diameter, number of vessels per bud and percentage of central vessels. The time course of the angiogenic response to rat or human fibrin gel was studied and 14 days was found to be the optimum period of implantation. The bud height and number of neovessels were not found to be significantly different when rat or human fibrin gels were used. This quantitative study was a prerequisite for further investigations of the effects of biological and pharmacological agents on angiogenesis.
The clinical and laboratory features of 47 cases of macrophage activation syndrome (MAS) were reviewed in a workshop within the Groupe Français d'Hématologie cellulaire. There was no predilection for a particular age group, while common symptoms at presentation included fever, hepatic and splenic enlargement and profound depression of blood count. Examination of bone marrow aspirates allowed diagnosis to be established in almost all cases. The most characteristic sign of MAS was the presence of well differentiated macrophages without notable cytologic abnormalities but shown to be actively ingesting haematopoietic elements. Haemophagocytic syndromes generally occur in patients who develop infections in the context of preexisting immunologic abnormalities or neoplasms. In the majority of patients evolution of the disease was regressive, once spontaneously but often after antibiotic, antiparasitic and/or antiviral treatment accompanied or not by corticotherapy and/or chemotherapy. Some regressive phases were followed by more or less long term relapse, especially in the case of associated systemic lupus erythematosus. There exists at present no explanation for the occurrence of MAS, although one may remark its association with other pathologies, in particular congenital or acquired immune deficiencies and haemopathies. Several hypotheses have been proposed to explain the appearance and evolution of the disease and at present two pathways of investigation of MAS seen to merit attention: exploration of macrophages themselves and their secretion products and exploration of lymphocytes and NK cells. The current possibilities for these investigations should lead to a greater understanding of the physiopathology of MAS and it is to be hoped that a better application of appropriate therapy will enable control of its evolution.
Recent clinical experience on open prenatal surgery in human beings, although scarce, suggests that skin wound healing in the fetus differs from that in adult life. This fact is supported by several experimental studies. Three types of skin wounds have been practiced in a group of thirty 23rd-gestational-day rabbit fetuses: sutured incision, non-sutured incision, and electrocautery burn. Seven days later, the resulting scars were assessed by mechanical and hystological studies. The results obtained were compared with those seen in 30 newborn rabbits and 30 adult rabbits in which the same wounds were carried out. In the fetuses, rupture tension of the sutured wound was 20% of that of the normal skin. A similar relationship was found in the group of adult rabbits. The sutured wounds in the fetuses showed a better macroscopic repair than in older rabbits. However, the non-sutured wounds and burns did not heal in the fetuses, on the contrary, their opening increased from the time of the lesion. These results seem to suggest that wound repair in the fetus is more like a remodeling process than in older ages.
Fifty patients, twenty-five suffering from severe knee osteoarthritis and twenty-five from acute hip osteoarthritis, received pentazocine or a new preparation of tilidine-naloxone for a period of 2 weeks, in a double-blind study. The two drugs were found to have the same efficacy and tolerance in both diseases with a minor but not statistically significant superiority for tilidine-naloxone. Similar quantities of drugs were taken over the study period, while patients were allowed to take as many as 8 capsules per day to relieve pain. There were quite equivalent side-effects and no marked changes in laboratory tests.
The short and thick bowel found in gastroschisis has been attributed to contact with amniotic fluid, among other factors. We designed an original animal model in order to isolate the effect of amniotic fluid on the fetal bowel. We created experimental gastroschisis in fetal rabbits. Extruded bowel was kept out of the amniotic sac in half of the operated fetuses. At term, seven days after surgery, 21 surviving fetuses--12 intra-amniotic (GIA) and nine extra-amniotic (GEA)--and 16 control littermates were harvested for study. Five parameters were measured in each animal: body weight, intestinal weight, intestinal length, bowel diameter and bowel wall thickness. We found no statistically significant difference in body weight, intestinal weight or bowel wall thickness. An enormous difference was found in intestinal length among the three groups. Bowel diameter was significantly different in the extreme groups (GIA and controls), with the intestine being more dilated in GIA than in GEA and controls. Gastroschisis in the absence of amniotic fluid has not been as damaging to the fetal intestine as "natural" intraamniotic gastroschisis.
Expansion rate and incidence of rupture of abdominal aortic aneurysms in relation to their size is a source of debate. We studied 114 patients (out of a cohort of 752 consecutive patients admitted with abdominal aortic aneurysms) who were denied any immediate operation because of patient's refusal, high surgical risk, or small transverse diameter as assessed by CT scanning and ultrasonography. All patients not operated on underwent from two to six repeated examinations during an average follow-up period of 26.8 months (range, 3 to 132). Forty-seven patients (41.2%) were subsequently operated on electively because of marked increase of transverse diameter of the aneurysm (n = 44) or for other reasons (n = 3), with a death rate of 0%. Eighteen other patients underwent emergency operation for leaking or ruptured aneurysms, and there were five deaths. The incidence of rupture was clearly related to the final diameter value, rising from 0% in aneurysms less than 40 mm to 22% in large size aneurysms (greater than or equal to 50 mm). Among the 49 patients not operated on, one died of rupture before operation and five of causes unrelated to the disease. Using individual serial measurements, we determined the linear expansion rate of the aneurysm, which proved to be related to initial diameter values: 5.3 mm/year for diameters less than 40 mm (n = 49), 6.9 mm/year in the 40 to 49 mm group (n = 41), and 7.4 mm/year for diameters of 50 mm or more (n = 24).(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of this study was to see if the greater effect of insulin on hepatic glucose output when insulin is given using 13-min pulses in man remains when the same amount of insulin is delivered using 26-min pulses. The study was performed on nine male healthy volunteers submitted to a 325 min glucose-controlled glucose iv infusion using the Biostator. The endogenous secretion of pancreatic hormones was inhibited by somatostatin. Three experiments were performed in each subject on different days and in random order. In all cases glucagon was replaced (58 ng min-1). The amounts of insulin infused were identical in all instances and were 0.2 mU kg-1 min-1 (continuous), 1.3 mU kg-1 min-1, 2 min on and 11 min off (13-min pulses) or 2.6 mU kg-1 min-1, 2 min on and 24 min off (26-min pulses). Blood glucose levels and glucose infusion rate were monitored continuously by the Biostator, and classic methodology using D-[3-3H] glucose infusion allowed to study glucose turnover. When compared with continuous insulin, 13-min insulin pulses induced a significantly greater inhibition of endogenous glucose production. This effect disappeared when insulin was delivered in 26-min pulses. We conclude that, in man, an adequate pulse frequency is required to allow the appearance of the greater inhibition of pulsatile insulin on endogenous glucose production.
To assess leukocyte activation during cardiopulmonary bypass, we measured white blood cell and neutrophil counts and lysosomal enzyme release, especially myeloperoxidase and elastase, throughout the operation and for 5 days postoperatively. A newly developed double antibody radioimmunoassay of myeloperoxidase and an enzyme-linked immunosorbent assay for detection of the polymorphonuclear elastase-alpha 1-proteinase inhibitor complex were used to determine their plasma levels in 15 patients undergoing elective aorta-coronary bypass grafting. Preoperatively white blood cell counts and plasmatic levels of myeloperoxidase and elastase-alpha 1-proteinase inhibitor were normal. Because no correlation has yet been established between levels of myeloperoxidase and elastase-alpha 1-proteinase inhibitor, the aim of this prospective study was to evaluate the use of these enzyme levels as markers for leukocyte activation in vivo. We addressed the clinical situation of cardiopulmonary bypass because it offered the possibility of monitoring the comparative evolution of blood levels of these enzymes in parallel to white blood cell counts through well-defined steps corresponding to known events. We document the advantages of myeloperoxidase blood levels over elastase measurement as reflecting more rapidly the in vivo activation of leukocytes. The time course kinetics of these three measurements were not parallel. White blood cell counts remained stable at the beginning of bypass, whereas myeloperoxidase levels increased sharply and continuously as soon as bypass was instituted until the end of bypass. Elastase levels also increased, but later than myeloperoxidase, beginning when the patients was rewarmed. High elastase plasma levels persisted later than myeloperoxidase after bypass, in parallel with white blood cell counts. It thus clearly appears that changes in myeloperoxidase levels more rapidly reflect the activation state of leukocytes induced by cardiopulmonary bypass and surgery, whereas peak levels of elastase were delayed and parallel to white blood cell counts. From this model, in which the evolution of leukocyte numbers could be followed in relation with known steps of stimulation, it appears that myeloperoxidase is a sensitive marker for monitoring in vivo activation of white blood cells.
Fetal life develops in a fluid environment. Amniotic fluid is not inert. It contains proteins, hormones, fetal urine and electrolytes, known to interact with a variety of fetal processes such as wound healing, intestinal growth, etc. Interest in its study has been increasing recently. In order to determine the effect of amniotic fluid, intra-amniotic and extra-amniotic fetuses should be compared. We describe a model that allows isolation of a fetal portion from amniotic fluid. Sixty 23-day pregnant rabbits were operated on. Surgery was performed in two fetuses of each mother. One fetus was replaced into the amniotic sac; the other was sutured along its waist to the histerotomy orifice, leaving the caudal half of the fetus in an extra-amniotic position. The mothers continued their pregnancy and were sacrificed on day 30. Maternal survivance rate was 82 per 100. Twelve intra-amniotic fetuses (FIA) and nine extra-amniotic fetuses (FEA) were obtained, as well as 16 nonoperated littermates that served as controls. The average weight of FIA fetuses was 31 g, FEA fetuses weighed 37 g and controls 36 g. The difference was not statistically significant between any of the groups. This model allows the study of a variety of fetal conditions in the absence of amniotic fluid. The survivance rate of this technique of extrauterine fixation has been 75 per 100.
Eighty-three patients suffering from upper abdominal pain were studied to evaluate the contribution of commonly used biochemical markers in the diagnosis of acute pancreatitis. On admission to hospital, serum amylase, lipase, total bilirubin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyl transferase activities were measured. By stepwise logistic discrimination, only two determinations appeared to be of clinical value: lipase and alkaline phosphatase activities. A classification rule was established including these two measurements and its diagnostic performance evaluated by a jackknifed method amounted .83%. ROC curves were used to assess sensitivity and specificity. Our study clearly shows that serum lipase measurements should be preferred to amylase measurements, and that our two-test classification rule provides an efficient aid in clinical decision-making.
Bone mineral content (BMC) and bone mineral density (BMD) of lumbar spine have been measured in 695 healthy postmenopausal and 64 type I osteoporotic Belgian, Caucasian females. Bone loss is strongly correlated to time elapse from menopause (Tm) with a maximum rate of bone loss during the first five years of menopause. BMC (gHA) = 461 + 0.662 ln Tm -0.481 (ln Tm)2 and BMD (gHA/cm2) = 0.91 + 0.00711 ln Tm - 0.00846 (ln Tm)2 (in both cases p less than 0.001 and Tm expressed in months of menopause). After 20 years of menopause, 50 to 60% of normal women have vertebral BMC and BMD values below the 90th percentile of women with vertebral fractures and, thus, might be considered to have asymptomatic osteoporosis. We conclude that prevention of postmenopausal osteoporosis should be initiated as soon as possible after the onset of menopause and that bone density screening should be extended in elderly in order to detect and allow treatment of asymptomatic "densitometric" osteoporosis.