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Biomedical subjects

L Rocha

Publications and source records attributed to L Rocha.

47 records · Page 3Linked to original sources
PubMed1982

The efficacy of radionuclide liver and bone scans in the evaluation of gynecologic cancers.

Between 1978 and 1980, 33 patients with cervical cancer, 40 patients with ovarian cancer, and 28 patients with uterine cancer underwent clinical diagnostic staging. Fifty-four patients had bone scans, and 101 patients received liver scans as a part of their staging work-up. No positive bone scan results were found. Eight of 33 patients with Stage IV disease had positive liver scan results consistent with hepatic metastases. Only 1 of 69 patients with Stage I-III disease had a positive test for metastases. While these numbers are small, the authors conclude that bone and liver scanning in asymptomatic patients with early stage gynecologic cancers may not be warranted as staging procedures.

Bone Neoplasms↗
PubMedDate not supplied

Massed amygdaloid kindling in encéphale isolé cats: its facilitation by naloxone.

The effect of repetitive administration of naloxone on the development of massed amygdaloid kindling in 'encéphale isolé' cats was studied. Electrical amygdaloid kindling was carried out with a 15 min inter-stimulus interval (ISI) in a control situation with intravenous (i.v.) naloxone administration (2, 4, and 8 mg/kg), 5 min prior to amygdaloid stimulation. It was found that it was possible to complete the amygdaloid kindling process in the encéphale isolé preparation reaching generalized electrographic tonic-clonic self-sustained seizures. The enhancement of the duration, frequency, and propagation of the after-discharge (AD) was accentuated by naloxone which also induced a progressive amplitude increment of the first potential evoked by the onset of the tetanus. The number of trials needed to achieve seizure generalization was reduced in dose-dependent manner by naloxone. The ability of naloxone to accelerate the development of amygdaloid kindling may be related to an inhibitory role of opioid peptides in this process.

Amygdala↗
PubMedDate not supplied

Effects of chronic naloxone pretreatment on amygdaloid kindling in rats.

Effects of chronic naloxone pretreatment (75 or 270 micrograms/h for 14 days) on the development of amygdaloid kindling in rats were evaluated. The acquisition of seizure activity was modified in the naloxone pretreated animals, depending on the nucleus stimulated: facilitation of stages IV and V occurred in 37%, variability of electrographic and behavioral responses to electrical stimulation during the kindling development in 33%, and facilitation of stages IV and V followed by long periods of seizure suppression in 29%. Enhancement of postictal seizure suppression during a recycling paradigm was observed in all the naloxone pretreated rats. It was concluded that the chronic administration of naloxone (known to induce opioid binding upregulation and supersensitivity), in association with the enduring changes in opioid mechanisms provoked by kindled seizures, were responsible for the facilitation and suppression of epileptic activity. These findings support bidirectional modulatory effects of opioid peptides on epileptic seizures as well as the view that epileptic seizures can induce enduring alterations in opioid mechanisms.

Amygdala↗
PubMedDate not supplied

Low frequency stimulation modifies receptor binding in rat brain.

Experiments were designed to reproduce the antiepileptic effects of low frequency stimulation (LFS) during the amygdala kindling process and to examine LFS-induced changes in receptor binding levels of different neurotransmitters in normal brain. Male Wistar rats were stereotactically implanted in the right amygdala with a bipolar electrode. Rats (n = 14) received twice daily LFS (15 min train of 1Hz, 0.1 ms at an intensity of 100 to 400 microA) immediately after amygdala kindling stimulation (1s train of 60 Hz biphasic square waves, each 1 ms at amplitude of 200-500 microA) during 20 days. The LFS suppressed epileptogenesis (full attainment of stage V kindling) but not the presence of partial seizures (lower stages of kindling) in 85.7% of the rats. Thereafter, normal rats (n = 7) received amygdala LFS twice daily for 40 trials. Animals were sacrificed 24 h after last stimulation and their brain used for labeling mu opioid, benzodiazepine (BZD), alpha(1)-adrenergic, and adenylyl cyclase binding. Autoradiography experiments revealed increased BZD receptor binding in basolateral amygdala (20.5%) and thalamus (29.3%) ipsilateral to the place of stimulation and in contralateral temporal cortex (18%) as well as decreased values in ipsilateral frontal cortex (24.2%). Concerning mu receptors, LFS decreased binding values in ipsilateral sensorimotor (7.2%) and temporal (5.6%) cortices, dentate gyrus (5.8% ipsi and 6.8% contralateral, respectively), and contralateral CA1 area of dorsal hippocampus (5.5%). LFS did not modify alpha(1) receptor and adenylyl cyclase binding values. These findings suggest that the antiepileptic effects of LFS may involve activation of GABA-BZD and endogenous opioid systems.

Animals↗
PubMedDate not supplied

Subacute and chronic electrical stimulation of the hippocampus on intractable temporal lobe seizures: preliminary report.

Recent animal experiments show that the application of an electrical stimulus to the amygdala or hippocampus following the kindling stimulus produced a significant and long-lasting suppressive effect on this experimental model of epilepsy. This is a preliminary report on the development of a surgical neuromodulatory procedure by chronic electrical stimulation of the hippocampus (CHCS) for control of intractable temporal lobe seizures in patients in whom anterior temporal lobectomy is not advisable, i.e., patients with bilateral temporal foci or a unilateral focus spreading to surrounding cerebral regions of the dominant hemisphere. This work was divided in two main consecutive stages. In the first stage, we demonstrated that subacute hippocampal stimulation (SAHCS) blocks intractable temporal lobe epileptogenesis with no additional damage to the stimulated tissue, and in a second stage, we attempt to demonstrate that CHCS may produce a sustained, long-lasting antiepileptic condition without additional undesirable effects on language and memory. In addition, taking advantage of this unique and ethically permissible situation, we attempt to determine whether or not the antiepileptic effects of SAHCS and CHCS are due to inhibition of the stimulation of hippocampal tissue by means of a number of electrophysiological, single photon computed tomography (SPECT) perfusion, and autoradiographic techniques.SAHCS during 3-4 weeks prior to anterior temporal lobectomy applied to a critical area located either at the anterior Pes hippocampus close to the amygdala or at the parahippocampal gyrus close to the entorhinal cortex abolished clinical seizures and significantly decreased the number of interictal spikes at focus after 5-6 days. Microscopy analysis of the stimulated tissue showed no evident histopathological differences between stimulated vs. non-stimulated hippocampal tissues. Additionally, CHCS persistently blocked temporal lobe epileptogenesis for 3-4 months with no apparent additional undesirable effects on short memory. Also, inhibition of the stimulated hippocampus seems to be one of the possible mechanisms underlying the beneficial antiepileptic effects of SAHCS and CHCS. This was revealed by increased threshold and decreased duration of the afterdischarges induced by hippocampal stimulation, flattening of the hippocampal-evoked response recovery cycles, SPECT hypoperfusion of the hippocampal region, and increased hippocampal benzodiazepine receptor binding. Future studies increasing the number and time of follow-up of patients under hippocampal stimulation are necessary before considering CHCS a reliable procedure for controlling intractable temporal lobe seizures.

Amygdala↗
PubMedDate not supplied

Epileptogenesis and muscular hypertonic postictal phenomena induced by naloxone in intact cats.

Epileptogenesis produced by repeated i.p. administration of naloxone chloride and sensory stimulation (photoacoustic stimulation at 1, 3, 10, and 15 Hz) every 15 min was studied in freely moving cats. The repeated administration of naloxone provoked some behavioral manifestations that resemble those produced by electrical amygdaloid kindling. Photoacoustic stimulation accentuated the manifestations. All the animals presented generalized behavioral seizures when total naloxone administration reached 80 mg/kg. None of the animals demonstrated postictal depression. These results suggest an inhibitory role of endogenous opioids and/or GABA in epileptogenesis.

Acoustic Stimulation↗
PubMedDate not supplied

Generation of memory CD4+, CD8+, CD45RO+ and CD16- lymphocytes activated with IL-2, INF-gamma, and TNF-alpha with specific cytotoxicity against autologous cervical cancer cells in a mixed leukocyte-tumour cell culture.

Cytotoxic T lymphocytes (CTL) specific against autologous human cervical cancer cells were generated in vitro from peripheral blood leukocytes (PBL) from four patients with non-keratinized epidermoid carcinoma. For this purpose, these patients' PBL were co-cultured for 28 days either with IL-2 or a mixture of IL-2, IFN-gamma and TNF-alpha in the presence of autologous tumour cells (ATC). Our results showed that these CTL were highly cytotoxic for ATC, weakly cytotoxic for heterologous cervical cancer tumour cells, and not cytotoxic for carcinoma cell lines, normal cervix cells nor autologous PBL. Proliferation and cytotoxicity against ATC were greater when the PBL were activated with the three cytokines. These CTL had a CD4:CD8 ratio of 1:1, were CD16- and CD45RO+ and their killing activity was inhibited by antibodies against CD3, CD8 and MHC-class I but not by antibodies against CD4, CD16 or HLA-class II. The possibility of generating specific CTL in long term cultures for cervical cancer therapy is also discussed.

Antibodies, Monoclonal↗