[Generalized epileptic seizures in treatment with clozapine. Incidence, types, prognosis and recommendations with reference to therapeutic strategies].
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Biomedical subjects
Publications and source records attributed to J Kasper.
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In the period of two years the authors treated at the coronary care unit 146 patients inflicted by the acute myocardial infarction (AMI). In 15 of them (13 men, 2 women, 13 times Q and twice non-Q, 5 times anterior, 10 times inferior) they performed intravenous thrombolytic treatment by use of streptokinase. The success rate of the thrombolytic therapy was evaluated by noninvasive markers: 1.) rapid withdrawal of chest pain, 2.) rapid (in 6 hours) and essential improvement of ST segment elevation and 3.) presence of reperfusion arrhythmias (in 6 hours). The authors detected insufficient medicinal conciousness among their health district population as regard to their response after the AMI origin (absolute majority of patients delayed their arrival). Minor complications due to therapy (allergy and minor local hemorrhage) occurred in 4 patients. Nobody died. Only those cases were considered as being successful, in which all three success rate markers were present. This condition was fulfilled in 8 patients (i.e. in 53% of cases) and with minor insufficiencies in further two patients (which would increase the percentage of the success rate to 67%). This success rate of the thrombolytic therapy ranges within the limits given by literature. In five patients the authors evaluated the behaviour of the left ventricular asynergy (its range and index) prior to and following the thrombolytic therapy and this examination they consider to be appropriate for observance of the thrombolytic therapy success rate in patients with AMI. (Tab. 3, Ref. 20.).
The authors of the submitted paper describe the diagnosis, course and treatment of hypereosinophilic syndrome in a 36-year-old female patient with marked affection of the right ventricle: endomyocardial fibrosis with parietal thrombi obliterating the cavity of the right ventricle. The clinical picture was dominated by rapid progression of severe cardiac decompensation with a fatal outcome.
The authors present their experience concerning the time-delay in 357 patients with acute myocardial infarction admitted to the coronary unit over the years 1988-1991. This time indicator was evaluated by using two approaches, i.e. the global time-delay (the time between the onset of the patient's complaints and his/her admission to the coronary unit) and patient's time-delay (the time between the onset of the patient's complaints and his/her decision to notify the health care service). Arbitrary criteria were set up: 10 hours for the former and 5 hours for the latter parameter. The established criteria were met by 40% of the patients. Only 24% of the patients presented at the coronary unit within 6 hours, and these could receive thrombolytic treatment. The decision time (patient's time-delay) amounted that the education level of our population has to be enhanced so as to increase the number of patients with acute myocardial infarction presenting at the coronary unit at an early stage. (Tab. 1, Ref. 9.)
The relationship between changes in blood coagulation, the occurrence and severity of risk factors of ischemic heart disease and the clinical condition of the patient was investigated. The at risk group of patients 42.2% had more than 3 pathological parameters. Intravascular blood coagulation was not activated in any of the patients. In patients with acute myocardial infarction (MI), 62.2% had more than 3 pathological parameters on the first day of MI development. Demonstrable activation of intravascular blood coagulation was found in 28.2% of these patients. On day 5 of MI, activation of intravascular blood coagulation was recorded in 57.7% of the patients treated by classical approach and in 15.4-30.8% of the patients on thrombolytic treatment. In the at risk group, primary hemostasis and the fibrinolytic system were more affected, in patients with MI the whole hemostatic mechanism was involved. On day 5 of MI, in patients with classical therapy pathological laboratory findings still persisted or were even more deteriorated, particularly increases in fibrinogen level. At that time, in patients on thrombolytic therapy no substantial changes of initial values were recorded. No correlation was found to exist between changes in hemostasis and the risk profile or between changes in hemostasis and the clinical severity of MI. The obtained results justify the administration of antithrombotic substances, especially in patients with unstable angina pectoris. On observing time constraints, administration of thrombolytics is justified in MI. (Fig. 9, Ref. 25.)
The authors present a review of optimal treatment and prevention of dysrhythmias in the acute stage of myocardial infarction (AIM). They emphasize the necessity to shorten the pre-hospitalization stage of the disease (the prevalence of malignant dysrhythmias culminates) and elaborate in every hospital region an optimal plan of emergency care (ensure CPR, electrical defibrillation, pharmacological prevention of VT and VF). They draw attention to the fundamental importance of the therapeutic limitation ensuing from the size of the focus which implies at the same time prevention and treatment of an impaired cardiac rhythm. The authors recommend early recanalization treatment with subsequent anti-thrombocytic treatment, and if contraindications are absent, standard administration of beta blockers in the early stage of AIM. They draw attention to the asset of anti-arrhythmic treatment as well as to its undesirable effects. They discuss also indications and complications of temporary transvenous cardiac pacing.
Horizontal vestibulo-ocular response (VOR) evoked by continuous sinusoidal rotation (0.1 Hz, +/- 90 degrees) was recorded in 20 young and healthy volunteers by DC oculography (EOG). Arousal was assessed by EEG and by reaction time measurement. While alert subject showed the characteristic VOR with vestibular nystagmus, the quick repositioning flicks disappeared during light sleep and changed to largely compensatory smooth eye deviations. This state of reduced arousal was also characterized by EEG attenuation and slow reaction times. Furthermore, we observed brief states with complete extinction of the vestibular response but without significant EEG change. The results demonstrate the high variability of VOR with shifting arousal. The polysynaptic system in the reticular formation which generates the fast phase of the nystagmus beat is far more modifiable than the three-neuronal reflex arc of the slow nystagmus component.
This study examined determinants of expenditures and use of services by a group of elderly HMO enrollees. Study subjects were 895 elderly members of the Fallon Community Health Plan who enrolled between January 1, 1980 and December 31, 1983. We explored whether the determinants of expenditures and utilization varied across different types of services, specifically inpatient hospital care and ambulatory care. Having a heart problem, a mobility/disability, and arthritis were consistent predictors of high resource use. Having a mental health problem and a history of past hospitalization were also significant predictors across most models. The health policy implications of these data and their implications for quality assurance within the HMO setting are discussed.
Transforming growth factor-beta 1 (TGF-beta 1) is a pleiotropic polypeptide hormone known to play an important role as a modulator of hematopoietic processes in human and murine cells. One of the characteristics of TGF-beta 1 is the ability to inhibit the growth of several cell types, including cells of the myeloid lineage. To study the mechanism by which TGF-beta 1 inhibits the growth of myeloid cells, we have used three murine myeloid cell lines, the parental interleukin-3-dependent 32D-123 cell line and two retrovirally infected interleukin-3-independent cell lines (32D-abl, 32D-src), all of which are growth inhibited by TGF-beta 1. Each of these oncogene-transfected cells expresses a greater number of TGF-beta 1 receptors than the parental cell line and responds to TGF-beta 1 with increased sensitivity; 32D and 32D-src cells are 2- and 58-fold more sensitive to TGF-beta 1 inhibition than the parental cell line (ED50 = 35 pM). Both 32D-abl- and 32D-src-transformed cell lines expressed higher levels of the 65- and 85-kDa TGF-beta 1 receptor species than did the parental cells. We observed a correlation between the greater sensitivity of 32D-src cells to TGF-beta 1 and the more rapid down-modulation and reappearance of cell surface TGF-beta 1 receptors on 32D-src cells. Thus, the level of TGF-beta 1 receptor expression and rate of reexpression both have a crucial regulatory effect on the functional activity of the TGF-beta 1 ligand.
Using a combination of v-myc and v-ras oncogenes, we have established a growth factor-independent monocyte cell line from murine fetal liver (FL-ras/myc). Biologic and molecular characterization demonstrated that the gene for the macrophage growth factor CSF-1 and the c-fms proto-oncogene (CSF-1 receptor) are expressed in this cell line, thus suggesting autocrine regulation as a possible mechanism for the unregulated growth of these cells. To study this possibility, we used 1) mAb, to neutralize the CSF-1 protein produced by the cell line, and 2) antisense oligomers, to inhibit CSF-1 gene products by specific base-pairing of complementary nucleic acids. We report here that both approaches inhibited in vitro cell growth by 60 to 70%, whereas the combination of oligomer and mAb inhibited proliferation by 95%. However, control antisense oligomers (50% bp mismatch with CSF-1 mRNA) did not inhibit FL-ras/myc cell growth. Furthermore, the inhibitory effects of mAb and oligomers were reversible when they were removed from the media. Detection of cell-associated CSF-1 protein by immunofluorescence showed that cells treated with the antisense oligomer expressed significantly less CSF-1 protein. These results indicate that the FL-ras/myc cell line requires CSF-1 for autonomous growth and that oligomers can efficiently block production of autocrine growth factors.
Growth factor-independent 32D-src and 32D-abl cell lines, established by infecting the interleukin-3-dependent myeloid precursor cell line (32D-123) with retroviruses containing the src or abl oncogene, were used to study transcriptional regulation of transforming growth factor beta 1 (TGF-beta 1) mRNA. Analysis of different TGF-beta 1 promoter constructs regulated by pp60v-src indicated that sequences responsive to high levels of src induction contain binding sites for AP-1. Both src and serum induced expression of the c-fos and c-jun genes in myeloid cells, resulting in transcriptional activation of the TGF-beta 1 gene. We found that serum treatment increased TGF-beta 1 mRNA levels in 32D-123 cells and that the v-Src protein could replace the serum requirement by stimulating binding to the AP-1 complex of the TGF-beta 1 promoter, thereby mediating the induction of TGF-beta 1 transcription.
Plasma protein C exerts anticoagulatory effects by inactivating factors V and VIII. Hereditary protein C deficiency is transmitted as an autosomal dominant disorder. Homozygous individuals usually develop purpura fulminans as newborns; heterozygous protein C-deficient individuals are at increased risk for venous thrombosis and pulmonary embolism. However, arterial thrombosis has been only rarely observed. We describe a young patient with heterozygous protein C deficiency who experienced a severe stroke due to thrombotic occlusion of the left middle cerebral artery.
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The authors give an account of their experience with early echocardiography (two-dimensional examination, division of left ventricle into 20 segments) during stratification of patients with acute myocardial infarction (a group of patients with a first infarction). They evaluated the presence or absence of serious asynergy (akinesia or dyskinesia) of the left ventricle and its relationship to the incidence of complications (serious dysrhythmia, decompensation, cardiogenic shock and death). The relations between asynergy and different complications were tested by means of multidimensional contingency tables. A statistically significant partial correlation (p less than 0.01) was recorded between the most serious asynergy and the presence of decompensation and also cardiogenic shock. The detection of serious asynergy of the left ventricle is a useful stratification indicator of the risk of the acute infarction, as no patient without asynergy died or overcame cardiogenic shock.
The authors present a clinical and electrophysiological characteristic in two cases of symptomatic sustained ventricular tachycardia (VT) with a QRS morphology of left bundle branch block, refractory to common antiarrhythmic treatment. It was confirmed that the mechanism of this arrhythmia associated with a high risk of sudden death is the reentry phenomenon and the authors analyzed its relationship to arrhythmogenic dysplasia of the right ventricle. In a way uncommon in our literature the authors demonstrate the importance of comprehensive electrophysiological examination in these serious cases and its usefulness in confirming the origin of VT in the right ventricle, its importance for mapping the accurate localization of tachycardia and the investigation of effectiveness of drugs and the evaluation of aptness of non-pharmacological treatment.
We recorded extracellularly, in decerebrate, labyrinthectomized cats, from spontaneously active L4 neurons whose activity was modulated by head rotation, and studied the effects of stimulation of ipsilateral hindlimb nerves. Rotation of the head about the longitudinal (roll) axis was more effective than rotation about the transverse (pitch) axis or vertical (yaw) axis for this group of neurons. Most units received convergent excitatory or inhibitory inputs from several nerves, with excitation being more prominent. The most effective muscle nerves were quadriceps (37/43 neurons), sartorius (19/21) and tibialis anterior (17/35); stimulation of biceps posterior-semitendinosus, biceps anterior-semimembranosus, or gastrocnemius rarely influenced the firing of the neurons. Group I effects were present in only a small fraction of neurons; however, short latency (central latency less than or equal to 5 ms) group II effects were observed in almost one-third. Longer latency group II as well as group III inputs were also common. All neurons received inputs from mixed and cutaneous nerves which usually had low thresholds and central latencies greater than 5 ms. Most recording sites were in medial lamina VII or lamina VIII; some of the units were identified by antidromic stimulation as propriospinal neurons which projected to the lumbar enlargement.
Mortality of aged Medicare enrollees in three demonstration health maintenance organizations (HMOs) was compared with that of three cohorts of local fee-for-service (FFS) beneficiaries as a measure of group differences in health status. Mortality of the HMO and FFS cohorts was tracked via life-table analysis for 6 years after enrollment to measure the persistence of health status differences existing at enrollment. After adjustment for age, sex, Medicaid-eligibility, and institutional status, HMO enrollee mortality was lower than FFS at all three plans in the first year after enrollment. Enrollee mortality at two plans increased to near FFS levels in year 2 and remained relatively stable thereafter. Enrollee mortality at the third plan increased toward FFS levels more gradually and was significantly below FFS levels for the first 5 years of follow-up. Mortality of disenrollees in the 2 years after disenrollment was significantly higher than that of the continuously enrolled in one plan and marginally significantly higher in a second. These findings suggest a pattern of favorable selection at enrollment, followed by different rates of decay in the favorable health status of enrollees. Other health status measures may exhibit different patterns, however. Selection effects may cause payments based on Medicare's AAPCC to be too high or low, in some cases for several years after enrollment.