Hydatid cyst in the interventricular septum: a rare cause of dizziness?
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Adult↗
Biomedical subjects
A Rubio
Publications and source records attributed to A Rubio.
Primary association of a TNF gene polymorphism with susceptibility to multiple sclerosis.
The associations of three promoter polymorphisms in the tumor necrosis factor (TNFA) gene have been studied in 238 patients and 324 control subjects. A significant correlation was found between MS susceptibility and the TNFA-376 polymorphism. This association was independent of the human leukocyte antigen (HLA) class II association and the combined inheritance of HLA-DRB1*1501 and the TNFA-376A allele more than additively increased susceptibility to MS.
Alleles↗
In vitro activation of macrophages by a novel proteoglycan isolated from corms of Crocus sativus L.
Saffron corms contain a proteoglycan that is highly cytotoxic on human tumor cells. The present work was undertaken to study the possible immunomodulatory and anti-invasive properties of this compound. Non-cytotoxic concentrations of this glycoconjugate promoted significant macrophage activation, detected by the release of nitric oxide. A rapid activation of protein kinase C and NF-kappaB was obtained after proteoglycan treatment, which could explain the induction of nitric oxide synthase. Proteoglycan concentrations ranging from 10-1000 ng/ml specifically promoted apoptosis of macrophages, probably triggered by their activation. This molecule did not inhibit in vitro migration or invasion of human tumor cells. Altogether these results support a plausible immuno-modulating activity for this saffron Crocus compound.
Adjuvants, Immunologic↗
Production of a cytotoxic proteoglycan using callus culture of saffron corms (Crocus sativus L.).
Saffron corms have been demonstrated to contain a proteoglycan that inhibits growth of human tumor cells. In this study, we show strong evidence indicating that callus cultures of saffron corm also synthesize such glycoconjugate. This compound is cytotoxic against human cervical epithelioid carcinoma cells (IC50 = 7 mg ml-1), and consists of approximately 90% carbohydrate and 10% protein. In order to optimize the glycoconjugate purification to complete functional and therapeutic studies, we have designed an improved method consisting of anion-exchange chromatography and reversed-phase HPLC, which can be easily scaled-up.
Antineoplastic Agents, Phytogenic↗
A 4-year-old girl with a ventriculoperitoneal shunt metastasis of a central nervous system atypical teratoid/rhabdoid tumor.
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Central Nervous System Neoplasms↗
Reduction of immune system activation in HIV-1-infected patients undergoing highly active antiretroviral therapy.
The aim of this work was to analyze the effects of highly active antiretroviral therapy on the chronically activated immune system of 26 antiretroviral-naive HIV-1-infected patients. Samples from baseline to week 24 or 36 of treatment were tested for serum levels of beta2-microglobulin, tumor necrosis factor alpha and soluble tumor necrosis factor alpha receptor type II, as well as for human leukocyte antigen-DR expression on T cells. After starting therapy, the mean HIV-1 RNA serum levels decreased and the mean CD4 + cell counts increased from baseline to week 36 (P< 0.001). Mean levels of tumor necrosis factor alpha receptor type II, tumor necrosis factor alpha and beta2-microglobulin as well as expression of human leukocyte antigen-DR were significantly reduced at the end of follow-up (P<0.01). Deactivation kinetics of these parameters was similar in patients with CD4+ counts>200 cells/microl at baseline versus those with CD4 + counts < 200 cells/microl at baseline, despite higher activation at baseline in the group with <200 cells/microl. In summary, this study shows that highly active antiretroviral therapy is able to induce a strong deactivation of the immune system of HIV-1-infected patients.
Acquired Immunodeficiency Syndrome↗
Evolution of blood coagulation factors and hemotherapeutic support in three pig-to-baboon orthotopic liver xenotransplants.
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Animals↗
Kaposi's sarcoma-associated herpesvirus-positive primary effusion lymphoma arising in the subarachnoid space.
Primary effusion lymphoma (PEL) is a rare and distinctive type of B-cell non-Hodgkin's lymphoma (NHL) that occurs primarily, although not exclusively, in patients with AIDS. It usually develops as a lymphomatous effusion in the absence of a tumor mass, characteristically contains the Kaposi's sarcoma-associated herpesvirus/human herpesvirus 8 (KSHV/HHV-8), usually also contains the Epstein-Barr virus (EBV), displays a characteristic cytomorphology bridging immunoblastic and anaplastic large cell lymphoma, often expresses an indeterminate immunophenotype, and a B-cell genotype. Thus far, PEL has been limited almost entirely to the pleural, peritoneal, and pericardial cavities. We describe a NHL occurring in a gay man with AIDS that is typical of PEL in that it arose in a body cavity or space without an associated tumor mass, displays the cytomorphology typical of PEL, is a clonal B-cell neoplasm, and contains KSHV as well as EBV. This case is singularly distinctive in that it is the first case of PEL reported to arise in the subarachnoid space. This unique case further supports the strong association between KSHV and malignant lymphoma arising in body cavities and growing as an effusion.
Adult↗
Fibro-osseous lesions of the central nervous system: report of four cases and literature review.
Fibro-osseous lesions, also reported as calcifying pseudoneoplasms of the neural axis, are uncommon lesions of the CNS. We report four additional cases: two extraaxial and two intraaxial, in patients ages 33, 47, 49, and 59 years at presentation. Fibro-osseous lesions involving the CNS demonstrate variable proportions of fibrous stroma, bone, palisading spindle to epithelioid to multinucleated cells in association with a highly distinctive, perhaps pathognomonic, chondromyxoid-like matrix often distributed in a nodular pattern. This histopathologically distinctive lesion can be seen in many regions of the neuraxis, often with a dural association, and most commonly along the vertebral column. It appears to be a slow-growing lesion and, with wide excision, the prognosis is excellent. The etiology remains unclear, but the preponderance of data favors a reactive rather than neoplastic process. If this putative pseudotumor is not recognized histopathologically, a neoplastic or infectious differential might result in inappropriate investigations and potentially harmful therapies.
Adult↗
Presence of genotypic resistance in nucleoside analogue-treated HIV-1-infected patients with undetectable viral load.
Patients harbouring drug-resistance viruses usually suffer a rise in serum viraemia after a variable period of time. We have investigated the relationship between the appearance of resistant genotypes and the viral load of each patient after treatment. Our objective was to assess the association between human immunodeficiency virus (HIV) RNA plasma levels and the number of drug resistance-associated point mutations after treatment. A total of 150 patients from three reference centres in Spain (Madrid, Barcelona and Seville) from a previous study (Erase Study) were included. Patients had at that time undergone antiretroviral treatment with nucleoside analogues for at least 1 year (zidovudine/didanosine; zidovudine/zalcitabine; zidovudine/zalcitabine/lamivudine; zidovudine/didanosine/lamivudine). In this study, plasma viraemia in these patients was quantified and a line probe assay was used to determine the genotype of the virus. Viral load was significantly higher in patients harbouring virus with more than three mutations than in those individuals who harboured wild-type strains (P < 0.05). Surprisingly, when patients with viral load < 500 copies/ml (13/150) were analysed, only two carried wild-type strains, whereas three had virus with more than three point mutations. The viral load of six samples was assayed using an ultrasensitive test (detection limit < 20 copies/ml). Of the three samples where viral load was < 20 copies/ml, one patient harboured wild-type virus, whereas two carried mutant virus strains. These results suggest that even in patients with undetectable viral loads by conventional methods, viral replication may continue and mutations develop. Therefore, standard values of plasma viraemia for measuring the effectiveness of the treatment should be reconsidered when patients are on antiviral regimens of just two or three nucleoside analogues.
Acquired Immunodeficiency Syndrome↗
Efficiency of drug resistance genotypic tests in specimens with low HIV viral load.
The early recognition of resistance to antiretroviral agents could allow a rapid switch in therapy and therefore avoid the accumulation of mutations and reduce the risk of cross-resistance. However, the efficiency of genotypic tests in specimens with low viral load (VL) is severely compromised since human immunodeficiency virus (HIV) RNA in these samples often goes unrecognized. The frequency of results provided by a line probe assay (LiPA, Murex), a commercially available drug resistance test and a home-made point mutation assay (PMA) for recognizing the codon 151 multidrug-resistance mutation was examined in 664 plasma samples stratified with respect to VL values. Overall, 421 (63%) samples could be interpreted by both LiPA and PMA. The sensitivity decreased as plasma VL lowered: 89% for samples with VL > 10,000 HIV RNA copies/ml, 77% for those with VL between 500 and 10,000 HIV RNA copies/ml and 37% for specimens with VL < 500 HIV RNA copies/ml. A good agreement existed comparing the sensitivity of the home-made PMA and LiPA. Although the former tends to produce more results, the difference did not achieve statistical significance. Our results support that new, more sensitive, HIV RNA extraction methods need to be implemented for the rapid recognition of drug-resistant mutants in patients experiencing an early rebound in plasma viraemia.
Acquired Immunodeficiency Syndrome↗
Evolution of genotypic resistance to nucleoside analogues in patients receiving protease inhibitor-containing regimens.
The prevalence of genotypic resistance to nucleoside analogues (NA) was examined using a line probe assay (LiPA, Innogenetics, Spain) and a point mutation assay to test for codon 151 polymorphism in plasma from 34 individuals who had been exposed to NA for longer than 1 year. The testing was repeated in the same population after 6 months of being on a new potent protease inhibitor (PI)-containing antiretroviral combination. Only nine (47%) of the 19 patients initially carrying the codon 41 mutation restored zidovudine wild-type (WT) virus population. Similarly, eight (33%) out of 24 carrying the codon 215 mutation restored the wild-type variant. Two subjects carrying codon 74 didanosine mutation reverted to wild-type genotype, as well as two (18%) out of 11 harbouring the codon 184 lamivudine-resistant variant. To conclude, the extent to which drug recycling might be of benefit in subjects showing a restoration of genotypic sensitivity to former drugs needs to be explored.
Acquired Immunodeficiency Syndrome↗
Chromosome abnormalities in peripheral blood lymphocytes from Macaca fascicularis and Erythrocebus patas (Cercopithecidae, Catarrhini) after X-ray irradiation.
In this paper, we describe the results of a qualitative and quantitative study of chromosomal reorganizations in X-irradiated (1 Gy and 2 Gy) lymphocytes from Macaca fascicularis (MFA) and Erythrocebus patas (EPA). A total of 515 breakpoints in M. fascicularis and 271 breakpoints in E. patas have been detected, identified and localized in the ideogram of the species. The Chi square test indicates that the distribution of breakpoints along the chromosomes is not random in M. fascicularis, and is not random for the p and q arms and bands in both species. Chromosome 5 of M. fascicularis (MFA5), chromosome 1 of E. patas (EPA1), and chromosome arms MFA5q, and EPA 1p are significantly more affected than expected, while chromosome MFA9 is less affected. Terminal regions of chromosome arms accumulate a higher number of breakpoints than the rest of the chromosome (44.4% in M. fascicularis and 45.98% in E. patas); 92.06% and 91.97% of breakpoints are observed in G negative bands in M. fascicularis and E. patas, respectively.
Animals↗
Prevalence of genotypic resistance to nucleoside analogues in antiretroviral-naive and antiretroviral-experienced HIV-infected patients in Spain.
OBJECTIVE: To determine the prevalence of genotypic resistance to nucleoside analogues (NA) in a large group of HIV-infected individuals in Spain, some of whom had no previous treatment with antiretroviral drugs (antiretroviral-naive) and some of whom had such experience (antiretroviral-experienced). SETTING: Cross-sectional study in out-patient clinics in three reference hospitals for HIV/AIDS located in Barcelona, Madrid and Seville, Spain. PATIENTS AND METHODS: Primary mutant genotypes were examined in plasma HIV RNA collected from 150 antiretroviral-naive subjects, half in 1993 and the other half in 1997. Furthermore, drug resistance mutations were analysed in plasma collected from another 150 antiretroviral-experienced patients who had received 2 NA for longer than 1 year, either in sequence as monotherapy or as combination therapy. A line probe assay was used for recognizing mutations conferring resistance to zidovudine (ZDV), didanosine (ddI), zalcitabine (ddC), and lamivudine (3TC). A point-mutation nested-PCR assay was used for examining a codon 151 mutation associated with multiple drug resistance. RESULTS: One or more mutations associated with primary resistance to NA were seen in 10 antiretroviral-naive (13.3%) patients in 1993 and in nine (12%) in 1997. In all but two cases, they were associated with ZDV resistance. In contrast, all but six (96%) of the antiretroviral-experienced subjects harboured drug-resistant mutant viruses. The codon 184 mutation (associated with resistance to 3TC) was detected in 92% of patients treated with 3TC, but also in 18% of those treated with only ddI or ddC. The codon 215 mutation was found in 67.3% of patients who had been exposed to ZDV; the codon 69 mutation was found in 15% of patients treated with ddC; and the codon 74 mutation was found in only 7.2% of patients treated with ddI. Finally, the codon 151 multidrug resistant mutation was found in four (2.7%) of 150 patients with a long-term exposure to NA. CONCLUSIONS: Overall, the prevalence of drug-resistant HIV-1 genotypes was 12.7% in antiretroviral-naive patients, most of whom had ZDV-resistant mutants. There is no evidence of an increase during the last 5 years. However, multidrug-resistant HIV genotypes are currently circulating in Spain.
Adult↗
Chromosome abnormalities in peripheral blood lymphocytes from Cebus apella (Cebidae, Platyrrhini) after X-ray irradiation.
In this paper, we describe the results of a qualitative and quantitative study of chromosomal reorganizations observed in X-irradiated (1Gy and 2Gy) and cultured lymphocytes from Cebus apella. A total of 646 breakpoints have been detected, identified and localized in the ideogram of the species. The breakpoint distribution along chromosomes, p and q arms, and bands is not random. Chromosomes #11, #12 and chromosome arms 1p, 12p, 13p, 15p, 11q, and 12q are significantly more affected than expected, while chromosome #19 and chromosome arm 19q are less affected. Terminal regions of chromosome arms accumulate a higher number of breakpoints than the rest of the chromosome (37.82%). A high percentage (93.66%) of breakpoints is found in G negative bands.
Animals↗
(2S,4S)-amino-4-(2,2-diphenylethyl)pentanedioic acid selective group 2 metabotropic glutamate receptor antagonist.
(2S,4S)-2-Amino-4-(4,4-diphenylbut-1-yl)-pentane-1,5-dioic acid 1m, is a novel metabotropic glutamate receptor (mGluR) antagonist with insignificant ionotropic affinity. It is selective antagonist of negatively-coupled cAMP-linked mGluRs with no effect on phosphoinositide coupled mGluRs. A series of 4-substituted glutamic acid analogues were prepared and it was found that compound 1k is tenfold more potent than 1m. Compound 1k has neither significant affinity for ionotropic glutamate receptors nor group 1 and 3 metabotropic receptors.
Animals↗
Short-term evolution of HIV-1 viraemia and CD4+ cell counts in patients who have a primary mutation to zidovudine.
OBJECTIVE: To investigate the different responses to antiretroviral treatment including zidovudine, of patients harbouring HIV with primary resistance to zidovudine, serum viral load, and CD4+ cell counts, for 24 weeks in a group of antiretroviral-naive patients with the codon 215 mutation of the HIV pol gene and in a control group at the start of treatment. DESIGN: A case-control retrospective study (1989-1996). METHOD: Nineteen out of 210 patients previously studied harboured the codon 215 mutation, had a self-reported compliance with treatment, a minimum follow-up of 24 weeks, and were treated with zidovudine alone or in combination with other nucleoside analogues. These patients were matched with 19 patients with wild-type strains at entry by initial CD4+ cell counts, clinical status, and antiretroviral treatment. RESULTS: During the first 12 weeks, CD4+ cell counts increased (76+/-26 and 64+/-26 x 10(6)/l in wild-type and mutant virus-infected groups, respectively), decreasing slightly until week 24, although no significant differences were found between the two groups studied. Serum viral load decreased in both groups (change in serum viral load of 0.80+/-0.11 log10 and 0.87+/-0.26 log10 copies/ml, wild-type and mutant virus-infected, respectively), although no significant differences were found between groups. CONCLUSION: No significant differences were found between patients with the primary mutation to zidovudine and control patients harbouring wild-type virus in terms of short-term response measured by serum viral load and CD4+ cell counts.
Adult↗
Malignant ependymomas in a patient with Turcot's syndrome: case report and management guidelines.
BACKGROUND: Turcot's Syndrome is the association of multiple adenomatous polyps of the colon with a primary tumor of the central nervous system. We present the first reported case of Turcot's Syndrome in a patient with malignant ependymomas. Recent advances in the elucidation of the genetic basis for the hereditary forms of colon cancer have provided a clearer understanding of the etiology of Turcot's Syndrome. This new information is relevant to the neurosurgical community and provides updated guidelines in the diagnosis and management of patients with this complex disease process. RESULTS: Turcot's Syndrome is related to two distinct genetic errors. The first involves a germ-line mutation in the adenomatous polyposis coli (APC) gene, which is postulated to act as a tumor suppressor gene. The second is a germ-line defect in one of a group of genes responsible for DNA nucleotide mismatch repair. CONCLUSION: The elucidation of the gene defects responsible for the hereditary forms of colon cancer has provided a clearer understanding of the molecular basis of Turcot's Syndrome. Patients with hereditary forms of colon cancer and neurologic symptoms require immediate and thorough investigation because of their significantly increased risk of developing CNS tumors. Previously healthy patients diagnosed with a CNS tumor with a family history of adenomatous polyposis coli should undergo screening and surveillance colonoscopy as the CNS lesion may precede colonic symptoms. CNS screening guidelines for asymptomatic patients with adenomatous polyposis coli requires further risk analysis studies. All patients diagnosed with Turcot's Syndrome should be tested for the gene defect, including the CNS tumor tissue to provide further data on the genetic relationship between Turcot's Syndrome and the hereditary forms of colon cancer.
Adenomatous Polyposis Coli↗