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F Alameda

Publications and source records attributed to F Alameda.

At least 19 recordsLinked to original sources
PubMed1999

Gene therapy for gliomas: p53 and E2F-1 proteins and the target of apoptosis.

Current therapy for glioma is suboptimal. The transfer of apoptosis genes to tumors constitutes one of the most promising strategies for cancer gene therapy. We have previously shown that massive apoptosis occurs when wild-type p53 or E2F-1 expression is induced in glioma. However, the mechanism of action and the efficiency in inducing apoptosis of these two proteins are not similar. Adenovirus-mediated p53 gene transfer is ineffective in causing apoptosis in glioma cells that retain wild-type p53 genotype or overexpress the p21 protein. The p16/Rb/E2F pathway is the most frequent target of genetic alterations in gliomas, and therefore constitutes a suitable target for gene therapy strategies. However, the transfer of either the p16 or Rb gene to glioma cells results in cytostatic effect. The E2F-1 protein is able to induce generalized apoptosis in gliomas independently of the p53, p16 or Rb status. In addition, p21- or p16-mediated growth arrest did not protect glioma cells from E2F-1-mediated apoptosis. The apoptotic molecule bax is induced in p53-mediated apoptosis, but bax is not induced in E2F-1-mediated apoptosis in glioma cells. Careful selection of patients may be necessary before designing therapeutic strategies using either p53 or E2F-1 as a therapeutic tools for glioma patients.

Apoptosis↗
PubMed1998

Protein kinase C-alpha activity inversely modulates invasion and growth of intestinal cells.

The phorbol ester phorbol 12-myristate 13-acetate induces remarkable phenotypic changes in intestinal HT-29 M6 cells; these changes consist of loss of homotypic adhesion and inactivation of E-cadherin. In parallel, cell growth is retarded. We have transfected HT-29 M6 cells with an activated form of the conventional protein kinase Calpha (cPK-Calpha). Expression of this isoform induced the acquisition of a scattered phenotype, similar to that adopted by cells after addition of phorbol 12-myristate 13-acetate, with very low cell-to-cell aggregation and undetectable levels of functional E-cadherin. These cell clones were highly motile and rapidly invaded embryonic chick heart fragments. Furthermore, cells expressing activated-cPK-Calpha showed decreased proliferation in comparison to control clones. We have also studied how these two apparently antagonistic changes affect the tumorigenic ability of HT-29 M6 cells. When the different cell clones were xenografted into athymic mice, the effect on cell growth seemed to predominate. Expression of activated-cPK-Calpha significantly reduced the size of the tumors; the cells with the highest level of expression did not even form subcutaneous tumors. Besides their smaller size, the morphology of these tumors was clearly different from those originated by HT-29 M6 cells, and they could be defined as infiltrative on anatomo-pathological basis. These results indicate that cPK-Calpha controls both cell-to-cell adhesion and proliferation of intestinal cells.

Animals↗
PubMed1998

[Hydatid cyst in the hepatic hilum causing a cavernous transformation in the portal vein].

Portal cavernomatosis consists in the substitution of the portal vein by many fine, twisting venules leading to the liver. This phenomenon is produced as a consequence of anterior thrombosis of the portal vein and is associated with chronic pancreatitis, cancer of the pancreas, intraabdominal sepsis and cholelithiasis. The symptomatology may be nul or present as obstructive jaundice or portal hypertension. Diagnosis is made by Doppler echography. The treatment is portal shunt when symptomatology is produced. In patients with cholelithiasis requiring surgery, the shunt is advised prior to biliary surgery since perioperative hemorrhage, if present, may be incoercible as in the case herein described. We present a 84-year-old woman with portal cavernomatosis the etiology of which was a hydatidic cyst located in the hepatic bifurcation and treated with mebendazol 10 years previously. This etiology has not been previously reported.

Aged↗
PubMed1995

[Isolated angiitis of the central nervous system. Clinical and neuropathological study of 2 cases].

Isolated angiitis of the central nervous system (IAC) is an idiopatic, recurrent vasculitis confined to the CNS involving small blood vessels. We describe the clinical, angiographic, and neuropathological data in two patients with IAC and delineate the main clinical and neuropathological features in both cases as well as the importance of a complete autopsy for discovering subclinical vasculitic lesions outside the CNS. Patient 1 concerned a 40 year-old-man that evolved for the last three years, initially with focal seizures, headache, and neurological focal deficits, later on the left sided hemihyposthesia and preferentially left parieto-occipital dysfunctions. He presented an oligoclonal band in CSF with slight hyperproteinorraquia and 25 lymphocytes. A cerebral angiography was compatible with angiitis and a leptomeningeal/cerebral biopsy showed lymphocytic vasculitis in the leptomeningeal and intraparenchymatous cerebral small vessels. These results lead to start a treatment with Cyclophosphamide associated to high dose of steroids. The patient clearly improved and now is almost asymptomatic. Patient 2 concerned a 67 year-old-man that evolved for 4 years with encephalic ischemic lesions distributed and confined throughout the brain stem and cerebellum, temporary remissions occurred and the patient required high-dose steroids and Cyclophosphamide to improve. Conventional and MRI angiographies only suggested the diagnosis that was confirmed at autopsy. The patient died after a massive pulmonary thromboembolism and a complete necropsic study showed abundant lymphocytic infiltrates, without granulomatous lesions, in the intraparenchymatous and leptomeningeal cerebral small vessels specially at the brain stem and cerebellar level where many demyelinated greyish areas and few infarctions were to be seen. The inflammatory cells were, in both cases, predominantly CD4+ T lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

[Deletion of 17p11.2 chromosome in Spanish families with hereditary neuropathy and abnormal sensitivity to pressure].

Hereditary neuropathy with abnormal liability to pressure palsies (HNPP) is a dominant autosomally transmitted disease that gives rise to foci of peripheral nerve myelination, reducing conduction and leading to episodes of palsy and sensory changes that are all linked to sensitivity to pressure and traction on the affected nerve roots. The molecular basis of HNPP has been identified as a submicroscopic deletion of the 17p11.2 chromosome in exactly the same region that it is duplicated in Charcot-Marie-Tooth disease, type 1A (CMT1A). We report genetic analyses of 13 patients (belonging to 3 families) diagnosed of HNPP by means of physical examination and electrophysiologic and morphologic tests (the last in 3 cases only). Inter- and intrafamilial variation in symptomatology was studied. Some patients presented the usual clinical signs, such as recidivating brachial plexus palsy, permanent sensory polyneuropathy, foot deformities and others that might also be found in patients with CMT1A. All the patients showed electrophysiologic signs of underlying demyelinating polyneuropathy. Genetic study centered on detecting the deletion of 17p11.2 by segregation analysis with the polymorphic markers VAW409R3a (D17S122) and EW401HE (D17S61). Our results confirmed deletion at the CTM1A location of chromosome 17p11.2 in all 13 patients examined. These data suggest that the deletion of 17p11.2 plays a causal role in HNPP and that it is the most prevalent mutation in this disease; our findings constitute new evidence of the importance of the CMT1A/HNPP locus in the formation and control of peripheral myelin and in the ultimate functioning of peripheral nerves.

Adult↗
PubMed1995

[Spontaneous remission of cervical epidural hematoma with pathological confirmation].

Spontaneous cervical epidural hematoma (CEH) is a rare entity but one that can cause permanent neurologic deficit unless, it is widely believed, surgical evacuation is prompt. A diagnosis of CEH is confirmed by computed tomography and/or magnetic resonance imaging. Spontaneous remission is unusual, with only 7 such cases reported in the literature as of 1993. We present a case of CEH with clinical remission and confirmation by neuroimaging in a patient who died of an unrelated cause. We conclude that when neurologic deficit is incomplete and there are no signs of clinical progression after 48 h, surgical treatment should not be applied routinely.

Aged↗
PubMed1992

[Familial recurrent paralysis of the brachial plexus. Tomaculous neuropathy].

Familial recurrent plexopathy related to tomacular neuropathy is only the localized expression, with a familial predisposition, of a more diffuse disease. Such are the conclusions we drew from a study of 3 cases, in 2 families, of recurrent tomacular brachial plexopathy. In all 3 cases the condition was transmitted by the mother as an autosomal dominant trait. Biopsy of a sensory nerve was performed in 2 cases and showed, in one, typical images of myelinic degeneration at various stages, corresponding to the formation of tomacular tickenings. Tomacular brachial plexopathy must be distinguished from hereditary amyotrophic neuralgia.

Adolescent↗
PubMed1992

[Paraneoplastic encephalomyelitis and Lambert-Eaton syndrome].

In two men presenting with muscle weakness and disturbances of equilibrium neurophysiological examination by repeated stimulations revealed responses suggestive of Lambert-Eaton syndrome. In the first month of the disease very high levels of anti-Hu antibody were found in the serum and CSF, betraying a malignant lesion. This was confirmed by autopsy 4 months later in one patient and by bronchial biopsy 16 months later in the other patient. Both had small-cell lung carcinoma associated with paraneoplastic encephalomyelitis.

Aged↗
PubMed1990

Primary cerebral abscess due to nocardia presenting as 'ghost tumor'. Clinical and pathological study.

We report a case of a primary cerebral abscess due to Nocardia asteroides in a nonimmunocompromised patient with a particular clinical course. The first symptom (right subacute brachial palsy) and the lesion in a computed tomographic (CT) scan (left parietofrontal edema suggestive of brain tumor) disappeared after corticosteroid treatment and the patient was discharged with total recovery. After 2 months she complained of headache and visual disturbance. A new CT scan showed an annular lesion in the left occipital lobe. A cerebral biopsy was diagnosed of nocardia infection. The patient died 2 weeks after this biopsy. A postmortem study showed an occipital brain abscess but not structural abnormalities were seen in the left parietofrontal area. We believe that the first episode could be a local inflammatory response to cerebral implantation of nocardia which disappeared clinically in the CT scan and in the postmortem study after corticosteroid treatment. Then the nocardia could have displaced by the hematological route to the second and definitive cerebral lesion.

Aged↗
PubMed1989

Carcinoid tumors with focal mucin production.

50 carcinoid tumors of different locations in the gastrointestinal and respiratory tracts were examined histochemically for mucin production. Isolated discrete aggregates of mucosubstances were identified in a large number of cases (46% of all carcinoid tumors, ranging from 53 to 36% in different organ locations). Acidity and composition of mucosubstances (sulfomucin vs. sialomucin contents) in carcinoids were not different from those described in their corresponding locations. These data support numerous other observations that point to a common stem cell precursor for both enterochromaffin and mucus-secreting epithelial cells in gastrointestinal and respiratory tract mucosal membranes. A shared endodermal derivation is favored over a separate neuroectodermal origin for the chromaffin cell system.

Adult↗
PubMed1987

[Systemic Candida infections].

Seven cases of neonatal systemic candidiasis are summarized. This means an incidence of 8.3% respect total amount of newborns admitted and 3.7% of babies admitted in the intensive care unit. Clinical presentation was not specific. Five blood cultures were positive and in two cases meningitis was recognized. Two cases died. Six cases were treated with amphotericin B and 5-fluorocytosine and in one case renal toxicity appear.

Amphotericin B↗
PubMedDate not supplied

Clear cell meningioma of the lumbo-sacral spine with chordoid features.

Clear cell meningioma (CCM) is a peculiar variant that differs from conventional meningioma in affecting younger patients, arising more often in spinal or cerebellopontine locations, and showing a higher recurrence rate. Classical meningothelial areas are scarce in these tumors and the differential diagnosis with other neoplasms, particularly metastatic carcinoma, is often difficult. We report a case of clear cell meningioma from the lumbosacral spine in which location, radiologic presentation, light microscopic appearance in initial sampling, and some of the ultrastructural findings were reminiscent of chordoma. The tumor cells were diffusely positive for vimentin and very focally positive for epithelial membrane antigen. Ultrastructural demonstration of interdigitating cell processes joined by numerous desmosomes confirmed the diagnosis of CCM.

Adult↗
PubMedDate not supplied

Meningeal melanocytoma: a case report and literature review.

The clinicopathologic, immunocytochemical, and electron microscopic features of a case of meningeal melanocytoma arising in the phylum terminale are reported. Meningeal melanocytoma is an uncommon tumor that must be distinguished from metastatic or primary malignant melanoma, meningeal melanocytic nevi, pigmented meningioma, pigmented schwannoma or neurofibroma, and pigmented primitive neuroectodermal tumor. This is a difficult differential diagnosis that can be best archived by complementing histological examination with a selected panel of antibodies and, most important, electron microscopic study. The distinctive ultrastructural appearance of most of these lesions point to this technique as the gold standard in pigmented proliferations of the nervous system.

Aged↗