[Vomiting as a clinical indicator of diarrhea caused by rotaviruses].
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Biomedical subjects
Publications and source records attributed to F Velasco.
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A female child was found to have a partial duplication of the long arm of chromosome 14 (14q24----qter). This duplication was due to paternal balanced translocation 46,XY,t(6;14) (q27;q24). Patient had craniofacial dysmorphism with microphtalmia, flat nasal bridge, lowest malformed ears, short neck, dolicocolon and mental retardation. A comparison is made between other reported cases in the literature and this observation. Most of the anomalies described in these published reports are not shared by the present patient. This can be explained by the simultaneous presence or not of a partial deletion and the size of the duplicated segment.
We have studied the main protease inhibitors of leukocytes, alpha-1-protease (alpha 1-PI), alpha-1-antichymotrypsin (alpha 1-Achy) and alpha-2-macroglobulin (alpha 2-M), as well as different parameters of coagulation and fibrinolysis in 21 cases of acute nonlymphoblastic leukemia (ANLL) before, during and after therapy. Nine of the patients presented signs of DIC, 8 of whom belonged to subtype M3 and to subtype 1 M1. The initial alpha 1-PI and alpha 1-Achy levels, which were elevated, increased during the treatment period. There was no significant difference between patients with and without DIC. However, those leukemic patients with DIC showed a significant decrease in plasminogen (p less than 0.005) and fast antiplasmin (p less than 0.01) only during the treatment compared with DIC free patients. All DIC cases demonstrated circulating plasmin-antiplasmin complex (P-AP) both before and during treatment. Independent of a possible proteolytic action of leukocyte enzymes on clotting factors in the clinical course of ANLL (mainly M3 subtype), our results suggest an activation of plasmin-mediated fibrinolysis related to the activation of plasminogen by leukocytes, reactive DIC or both.
The effect of unilateral mesencephalic (MRF) and pontine (PRF) lesions on EEG-EMG patterns of type B and C alumina cream induced focal motor seizures was studied on cats with chronically implanted electrode and cannula lesion systems. EEG patterns included number, amplitude and contralateral propagation of type B spikes and occurrence and duration of type C tonic-clonic discharges. EMG patterns included changes in muscular multiple unit activity (EMG-MUA) time locked to the onset of type B spikes and to the onset (tonic OTCD) and the end (clonic ETCD) of type C tonic-clonic EEG paroxysmal discharges. (1) MRF lesions ipsilateral to the cortical epileptogenic focus significantly increased number, amplitude and propagation of type B EEG spikes and the occurrence, but not the duration, of type C EEG tonic-clonic discharges. They also reduced amplitude of type B muscular jerks and blocked type C tonic contradversion with a significant decrease in EMG-MUA time locked to the onset of type B spikes and type C paroxysmal EEG discharges. (2) PRF lesions contralateral to the cortical epileptogenic focus produced an effect on muscular contractions of type B and C seizures similar to that produced by ipsilateral MRF lesions. PRF lesions, however, did not significantly change the EEG patterns of type B and C seizures. (3) Neither MRF lesions contralateral nor PRF lesions ipsilateral to the cortical epileptogenic focus produced significant changes on EEG and EMG patterns of types B and C epileptic seizures.
The effect of fentanyl (opioid agonist) and naloxone (morphine antagonist) on the amplitude, area and latency of the P300 auditory potential was studied in patients undergoing minor surgical procedures. Fentanyl (5.0 micrograms/kg), naloxone (3.0 micrograms/kg) and isotonic saline (for control) were injected intravenously through a catheter just before surgery, and following a single-blind procedure and three different pharmacological paradigms with three consecutive conditions each: (1) initial baseline (C), saline (S) and late baseline (C'); (2) C, fentanyl (F) and C'; (3) C, naloxone (N) and C'. Fentanyl significantly reduced the amplitude and area with no changes in the latency of small (S) and large (L) P300 potentials. Concomitantly, fentanyl increased the number of omitted counts of the target tones of the "odd ball" P300 test and the spatial threshold of the two point discrimination test in patients with small and large P300 potentials. Naloxone significantly increased the amplitude and area and decreased the latency of the small P300 potential and decreased the amplitude and area with no changes in latency of the large P300 potentials. Concomitantly, naloxone decreased the number of omitted counts of the patients with small but not large P300 potentials and decreased the spatial threshold in patients with both small and large P300 potentials. Neither fentanyl nor naloxone produced systematic changes in the evaluation of pain and hearing of patients with small and large P300 potentials. Although dramatic changes in pulse, blood pressure, respiration and EEG were found in some cases immediately after the administration of fentanyl and naloxone, these changes were not consistent and were not present at the time other tests were performed.
The effect of fentanyl (a morphine agonist) and naloxone (a morphine antagonist) on early and late components of somatic (SEP)- and auditory (AEP)-evoked potentials was studied in patients undergoing minor surgical procedures, in which these compounds were used in producing and regulating a state of neuroleptanalgesia. Fentanyl (2.5, 5.0 and 10.0 micrograms/kg), naloxone (1.5 and 3.0 micrograms/kg) and isotonic saline (for comparative purposes) were injected just before surgery, intravenously through a catheter and following a single blind procedure and three different pharmacological paradigms with four consecutive conditions each: (1) Initial baseline (C), first saline (S), second saline (S') and late baseline (C'). (2) C, First fentanyl (F), second naloxone (N') and C. (3) C, First naloxone (N), second fentanyl (F') and C'. Special care was taken in controlling the constancy of the muscular and cochlear receptor activation concomitant to somatic-evoked potentials and auditory-evoked potentials, determined by the amplitude of the muscular response at the tenar muscles (MP) and component I of the brain stem potentials ( ABSP ). Evaluation by the patients pain, topognoses and hearing and other somatic and autonomic indicators of the level of the analgesic response were also controlled. Fentanyl significantly reduced, while naloxone increased, the amplitude of late components P150 of somatic-evoked potentials and auditory-evoked potentials. Concomitantly, fentanyl increased, while naloxone decreased, the spatial threshold (two point discrimination test) at finger tip and arm. These effects were observed in patients taking various doses, although they were more consistent with larger doses of these compounds.(ABSTRACT TRUNCATED AT 250 WORDS)
The role of alumina cream (AC) epileptic granulomas in producing clinical convulsions and EEG spikes was evaluated by excising and transplanting such granulomas from donors to recipient cats. In donors, granulomas were produced by single microinjections of AC into the right motor cortex and were subsequently excised during latent premature (P), mature (M), convulsive, and remission stages. The excised granulomas from donors were homogenized and injected into the homologous cortices of the recipient cats. The epileptogenic effect of the AC granuloma transplant in the recipients and the antiepileptogenic effect of the AC granuloma excision in the donors were evaluated by the presence or absence of clinical convulsions and the maximal EEG spike density at the right motor cortex (MSD) after lesion excision and transplant. In addition, a correlation between MSD (spikes/10 min) of donors and recipients and the aluminum content (microgram/ml) in granuloma and perilesional cortex of control epileptic cats (neither excised nor transplanted) was established during latent P, M, convulsive, and remission stages. The epileptogenic effect of AC granulomas transplanted into recipients was significantly larger when they were excised from donors in latent P and M than in convulsive, and in convulsive than in remission. The antiepileptogenic effect of AC granuloma excision in donors was significantly larger in latent P than in latent M and convulsive, and in convulsive than in remission. The aluminum content of AC granuloma and perilesional and contralateral cortices in controls was significantly larger in latent P and M than in convulsive and in convulsive than in remission.(ABSTRACT TRUNCATED AT 250 WORDS)
Bipolar EEG and multiple unit activity (MUA) responses correlated to the vertex auditory brain stem potentials (ABSP) were recorded in different brain stem and diencephalic primary auditory pathways and other anatomically related structures of large monkeys under barbiturate anesthesia. Bipolar EEG responses were recorded bilaterally to monaural stimulation and were formed by 3 or more of 6 consecutive components labeled A, B, C, D, E and F (peak latencies of 3.8, 4.2, 4.6, 5.0, 7.8 and 11.8 msec) correlated in latency with waves III, IV, V, VI, VII and SP3 of the ABSP, respectively. Component B was prominent and showed clearcut reverse polarity at the trapezoid body (TB) and superior olivary complex (SOC), while components C and F inverted and everted polarity at the mesencephalic reticular formation (MRF) and medial geniculate nucleus thalami (MG). Subcortical MUA peaks A, B, C, D and E time locked to the stimulus presentation correlated in latency to those of the bipolar EEG responses. In addition, a significant correlation was found between percentage amplitude of the subcortical EEG response components and MUA peaks in different structures contra- (r = 0.847) and ipsilateral (r = 0.973) to the stimulated ear. Although a single wave of the vertex ABSP correlated in latency with more than one response component in different subcortical loci, amplitude of component A was significantly larger (P less than or equal to 0.02) at TB ipsilateral, B at TB and SOC bilateral, and C and F at MRF, and D and E at MG contralateral to the stimulated ear.
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The effect of peduncular and midline tegmental lesions on EEG-EMG patterns of type B and C alumina cream-induced focal motor seizures was studied on cats with chronically implanted electrodes and cannula lesion systems. EEG patterns included number, amplitude and contralateral propagation of type B spikes and occurrence and duration of type C tonic-clonic discharges. EMG patterns included phasic multiple unit activity (EMG MUA) time locked to the onset of type B EEG spikes and time locked to the onset (contradversive OTCD) and end (clonic ETCD) of type C tonic-clonic EEG paroxysmal discharges. (1) Lesions of the middle third of the cerebral peduncle, ipsilateral to the cortical epileptogenic focus, blocked type B muscular convulsions and significantly decreased phasic EMG MUA at contralateral face, neck and limbs. (2) Bilateral peduncular lesions blocked clonic type C muscular convulsions and significantly decreased phasic clonic ETCD EMG MUA at the same body regions. (3) Midline tegmental lesions blocked phasic type C muscular convulsions and significantly decreased phasic contradversive OTCD EMG MUA at neck muscles. (4) Bilateral peduncular lesions significantly increased and midline tegmental lesions significantly decreased (below the previous interictal) contradversive OTCD EMG MUA. (5) Neither peduncular nor midline tegmental lesions significantly changed EEG patterns of type B and C seizures.
Nine 'encéphale isolé' cats had 'push-pull' perfusions of pentylenetetrazol (PTZ) in various loci of the brain stem, while the EEG from the right and left motor cortices, EMG from neck muscles, ocular movements and clinical changes were recorded. Perfusions in the rostral MRF induced bilateral rhythmic paroxysmal EEG discharges and myoclonic twitching of neck and head, more prominent in the muscles contralateral to the perfused side. PTZ in the caudal MRF induced tonic-clonic paroxysmal EEG discharges and EMG seizures, similar to those seen when PTZ is injected systemically. Perfusion in the PRF induced EEG spindle bursts, muscular hypotonia and myosis. When perfusion in the MRF inducing rhythmic paroxysmal EEG discharges and myoclonic twitching was followed by perfusion in the PRF, the EEG discharges were not modified, but the myoclonic movements were abolished. Perfusions outside the MRF and PRF did not produce obvious changes other than tonic gaze deviation to the contralateral side or nystagmus. The results suggest that PTZ has a differential effect in various structures of the CNS, producing primary generalized convulsive seizures when acting directly on the MRF.
The effect of extensive and circumscribed sagittal transections of the brain stem tegmentum on types B (epilepsia partialis continua) and C (contradversive tonic-clonic seizures) alumina cream-induced focal motor seizures in cats was investigated. The neurological abnormalities of cats with transections and differences in the EEG-EMG patterns of types B and C seizures between operated and intact animals were statistically analyzed. Animals with either extensive or superior central nucleus transections showed bilateral neglect and internuclear palsy syndromes, no tonic type C seizures (contradversion), and a significant decrease in electromyogram multiple-unit activity (EMG MUA) from 0 to 10 s or more after the onset of EEG paroxysmal tonic-clonic discharges. Animals with rostral transections showed a unilateral neglect and internuclear palsy or ataxic syndromes with a concomitant partial reduction of contradversive seizures and a significant decrease in EMG MUA from 0 to 5 s or less after the onset of EEG tonic-clonic discharges; those with dorsal and caudal transections showed a transient neglect and insomniac syndromes with no differences in contradversion and EMG MUA at the onset of EEG tonic-clonic discharges in relation to intacts. Experimental and intact animals showed neither differences in types C and B EEG patterns nor in EMG MUA at the end of type C EEG tonic-clonic discharges and type B EEG spikes. These results support the idea that tonic and clonic muscular seizures are due to epileptic impulses originating in the cerebral cortex and mediated at the level of the brain stem by different pathways.
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