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G Cano

Publications and source records attributed to G Cano.

27 records · Page 2Linked to original sources
PubMed1990

[Fatal hyperinfectious strongyloidiasis: report of 3 cases].

The present paper reports three fatal cases of massive strongyloidiasis. Case 1. A 37-year-old woman with a record of arthropathy and corticosteroids treatment, died in shock. The postmortem examination showed massive intestinal strongyloidiasis with larvae dissemination to lungs, liver, spleen and the adipose tissue located around adrenal glands. Case 2. A 12-year-old, malnourished girl died of peritonitis. The autopsy findings were lithiasis and perforation of jejunum, hyperinfectious strongyloidiasis of intestines and lungs, acute and chronic peritonitis. Case 3. A 7-year-old, cachectic girl with corticosteroid therapy, died in cardiorespiratory arrest. The autopsy revealed hyperinfection by S. stercoralis affecting stomach, intestines, lungs, liver and brain. In Venezuela, literature on massive strongyloidiasis is scarce. The present report stresses the importance of considering this syndrome in patients at risk, in endemic areas, like Venezuela, to prevent unnecessary deaths.

Adult↗
PubMedDate not supplied

Alterations of excitatory amino acid receptors in the brain of manganese-treated mice.

An excessive activation of excitatory amino acid (EAA) receptors has been associated with oxidative stress, which is considered the primary cause of manganese (Mn) poisoning neurotoxicity. Therefore, the EAA receptor distribution was analyzed by autoradiographic methods in several brain regions during Mn intoxication. We found that chronic treatment of mice with MnCl2 during 8 wk significantly alters the L-[3H]glutamate (L-[3H]Glu) binding to total glutamate (Glu) receptors, as well as to N-methyl-D-aspartate (NMDA) and quisqualate (QA) receptor subtypes. A generalized decrease of 16-24% of the L-[3H]Glu binding to total Glu receptors was found in all cortex, hippocampus, basal ganglia (except globus pallidus), and cerebellum. Saturation studies showed a significant reduction of the maximal number of receptors (Bmax) in Mn-treated mice, whereas the affinity (Kd) was not altered. L-[3H]Glu binding to NMDA sites was mainly decreased (10-21%) in a few cortical regions, basal ganglia (except globus pallidus), and hippocampus, whereas binding to QA receptor subtype was diminished (16-30%) in cortex, hippocampus, and cerebellum. The decrease of Glu receptor binding sites during Mn poisoning could reflect a receptor downregulation more than neuronal loss, since these reductions are moderate and diffuse. Thus, this down-regulation might mean a protection mechanism against an excitotoxic process associated with Mn toxicity.

Animals↗
PubMedDate not supplied

Neuroanatomical specificity of the circuits controlling sympathetic outflow to different targets.

1. Despite the emerging framework that central neural pathways controlling the activity of the sympathetic nervous system are capable of producing highly selective responses, the specific neural pathways governing different sympathetic outflows are poorly understood. 2. Anatomical studies suggest that five brain areas, namely the rostral ventrolateral medulla, the rostral ventromedial medulla, the caudal raphe nuclei, the region containing the A5 noradrenergic neurons and the paraventricular hypothalamic nucleus, provide dominant supraspinal innervation of sympathetic preganglionic neurons. 3. The anatomical parcellation of different functions within and among these cell groups is uncertain. However, recent studies using transynaptic retrograde labelling of neural pathways connected to various sympathetic targets suggest that the circuits controlling these different targets may be partially distinct. Similarly, anatomical studies relying on stimulus-evoked expression of immediate early genes, such as c-fos, suggest that different sympathetic responses may be controlled by distinct, neural circuits. 4. Thus, although many similarities exist in the anatomical circuits innervating different sympathetic targets, possibly supporting the orchestration of global sympathetic responses, differences are also discernible.

Adipose Tissue, Brown↗
PubMedDate not supplied

[Sphenoid metastasis mimicking a meningioma as the initial feature of adenocarcinoma of the prostate].

INTRODUCTION: Presentation of adenocarcinoma of the prostate as an intracranial metastasis is uncommon. This metastasis tends to be seen in the sphenoid bone, and in this case it is difficult to differentiate radiologically from a meningioma. Because this cancer is treatable, the differential diagnosis must be resolved as soon as possible. CLINICAL CASE: A 72 year old man presented with a rapidly progressive left parasellar syndrome. On neuroimaging there was a tumour at the level of the left lesser wing of the sphenoid, which was isodense and iso-intense and also showed homogeneous uptake of contrast material. On angiography the circulation was pathological with homogeneous delayed filling. The initial diagnosis was meningioma of the lesser wing of the sphenoid. Months later the patient complained of bone and respiratory problems. At this time plain chest X-ray was compatible with carcinomatous lymphangitis. Therefore, tumour markers were studied and for the first time the specific prostatic antigen was investigated and found to be raised. Although there were no symptoms of prostatism, per rectum there was a malignant prostatic mass. In spite of complete hormone block, his illness followed an unfavorable course. At necropsy there was adenocarcinoma of the papillary prostate and a metastasis in the left lesser wing of the sphenoid. CONCLUSIONS: In elderly men, detection of a sphenoid tumour, which radiologically may appear to be a meningioma and although prostatism has not been diagnosed, the possibility of prostatic metastasis should be considered. Per rectum examination and specific prostatic antigen determination should be done in these patients.

Adenocarcinoma↗