PubMed Health⌕ Search

Biomedical subjects

A Ariza

Publications and source records attributed to A Ariza.

At least 37 records · Page 2Linked to original sources
PubMed2000

Evolution of granulomas in lungs of mice infected aerogenically with Mycobacterium tuberculosis.

Aerogenous infection of C57Bl/6 mice with a virulent strain of Mycobacterium tuberculosis (CL 511) leads to the formation of primary granulomas in the lung where neutrophils, macrophages and subsequently, lymphocytes accumulate progressively around an initial cluster of infected macrophages. The spread of infection through the lung parenchyma gives rise to secondary granulomas featuring numerous lymphocytes that surround a small number of infected macrophages. Afterwards, foamy macrophages add an outer layer to the granulomas, which characteristically respect the pulmonary interstitium and remain confined within the alveolar spaces. This feature, in conjunction with the constant presence of M. tuberculosis in the products of broncho-alveolar lavage, suggests that the upward bronchial migration of infected macrophages may contribute significantly to pulmonary dissemination of mycobacterial infection. The latter would be in agreement with the persistence of chronic pulmonary infection in spite of a concomitant strong T helper 1 cell response.

Animals↗
PubMed1999

The intravenous model of murine tuberculosis is less pathogenic than the aerogenic model owing to a more rapid induction of systemic immunity.

The detection of mRNA in the murine model of tuberculosis for key cytokines involved in protective immunity in the lung tissues revealed a much faster emergence of the interferon (IFN)-gamma response in the intravenous route than in the aerosol route of inoculation. This slower response in the lungs was associated with a stronger inflammatory response, resulting in large granulomatous structures and eventual tissue damage.

Administration, Inhalation↗
PubMed1999

Differential expression of c-Met in Kaposi's sarcoma according to progression stage and HIV infection status.

Several cytokines, growth factors and the HIV transactivator Tat have been shown to be involved in the pathogenesis of Kaposi's sarcoma (KS). Hepatocyte growth factor/scatter factor (HGF) is an angiogenic cytokine that stimulates proliferation of spindle cells cultured from human KS lesions. The receptor for HGF, the c-Met protein, is expressed by endothelial cells, dermal dendrocytes and KS tumor cells both in vitro and in vivo. KS cells synthesize and secrete HGF and express the hepatocyte growth factor receptor (c-Met), thus providing an autocrine loop for tumor proliferation and neovascularization which can be enhanced by proinflammatory cytokines. We studied the immunohistochemical expression of c-Met in 40 cases of classical Kaposi's sarcoma (C-KS) and AIDS-associated cutaneous Kaposi's sarcoma (AIDS-KS), including 22 plaque stage lesions (12 AIDS-KS cases) and 18 tumor stage lesions (7 AIDS-KS cases). Statistically significant differences in the average intensity of immunohistochemical staining according to the type of lesions progression stages) and the serologic status of the patients were identified. The staining intensity of c-Met was stronger in tumors than in plaques. When only plaques were taken into consideration, the mean staining score was nearly twice as high in C-KS as in AIDS-KS.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Absence of Fas (CD95) and FasL (CD95L) immunohistochemical expression suggests Fas/FasL-mediated apoptotic signal is not relevant in cutaneous Kaposi's sarcoma lesions.

It has been suggested that Fas ligand (FasL), expressed by several neoplastic cell lines and some tumors in vivo, is able to trigger the apoptotic process in activated T-lymphocytes and may constitute a key element of the immunological escape mechanisms used by many types of neoplasia. In order to evaluate the possible role of Fas-mediated apoptosis in Kaposi's sarcoma (KS), we have studied the immunocytochemical expression of Fas and FasL in biopsy specimens showing different histopathological stages of classic KS (C-KS) and AIDS-associated KS (AIDS-KS), as well as in cultured cells derived from C-KS lesions. KS biopsy tissue failed to show Fas expression in all epidemiologic forms and histopathologic stages studied, while FasL positivity was present in a small number of cells in just a few cases. Double immunostaining ruled out the lymphocytic nature of these cells, whose morphology in adjacent sections stained with hematoxylin and eosin was consistent with KS cells. In contrast, cultured KS cells exhibited strong immunocytochemical cytoplasmic expression of both Fas and FasL. These findings indicate that the Fas-FasL system does not play a major role as a trigger of apoptosis in KS cells in vivo and that the upregulation of these molecules observed in KS cells in vitro probably is the result of cell stress induced by growth in culture.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Dentatorubropallidoluysian atrophy in a spanish family: a clinical, radiological, pathological, and genetic study.

UNLABELLED: The object was to describe the clinical, radiological, pathological, and genetic findings in a Spanish family with dentatorubropallidoluysian atrophy (DRPLA). This is an inherited neurodegenerative disease, well recognised in Japan, but with few cases reported from Europe and America and no cases published from Spain. The clinical misdiagnosis of Huntington's disease is not infrequent. Pedigree analysis and clinical data of a family were collected. A genetic study was performed in two patients. Pathological information was obtained from the necropsy of one patient. RESULTS: Pedigree analysis showed an autosomal dominant pattern of inheritance. Age at onset varied from 5 to 55 years. Ataxia and chorea were present in most of the members. Some of these had a long course disease with late dementia. Four patients had seizures and early mental impairment. In one patient, cranial MRI showed cortical, brain stem and cerebellar atrophy, and white matter changes. In another patient, necropsy showed atrophy of the globus pallidus and lipofuscin deposits in dentate and pallidal neuronal cells. Genetic study showed an abnormal CAG triplet expansion in the B37 gene on chromosome 12. As in other cases previously reported, Spanish cases of DRPLA show intrafamilial phenotypic heterogeneity. Clinical and MRI data could differentiate DRPLA from Huntington's disease but definitive diagnosis requires molecular studies. Pathological studies are still necessary to correlate DRPLA brain involvement with the clinical and molecular findings.

Adolescent↗
PubMed1999

[Measure of the slow phase angular speed by the trigonometric method].

We compare trigonometric and traditional systems for nystagmus slow phase speed measures. Results are detailed in Table I. Mean difference between both procedures is 0.88 +/- 0.51 degree/sec. so we conclude that trigonometric system is a reliable method for these measures.

Electronystagmography↗
PubMed1999

[Head-thrust test: its validity as a diagnostic clinical test].

The head-thrust test is presented as an ideal test to investigate the horizontal vestibulo-ocular reflex. We review its theoretical basis, and assess it as a diagnostic test with a 22 patient series. Its specificity accounts for 100% and the sensibility for 54%. Would this test substitute in the future the caloric test?

Caloric Tests↗
PubMed1998

A dysfunctional desmin mutation in a patient with severe generalized myopathy.

Mice lacking desmin produce muscle fibers with Z disks and normal sarcomeric organization. However, the muscles are mechanically fragile and degenerate upon repeated contractions. We report here a human patient with severe generalized myopathy and aberrant intrasarcoplasmic accumulation of desmin intermediate filaments. Muscle tissue from this patient lacks the wild-type desmin allele and has a desmin gene mutation encoding a 7-aa deletion within the coiled-coil segment of the protein. We show that recombinant desmin harboring this deletion cannot form proper desmin intermediate filament networks in cultured cells, nor is it able to assemble into 10-nm filaments in vitro. These findings provide direct evidence that a mutation in desmin can cause human myopathies.

Amino Acid Sequence↗
PubMed1998

expression patterns of cyclins D1 and E in condyloma acuminatum in comparison with psoriatic proliferative lesions.

Human papillomavirus (HPV) is able to subvert the host cell replication machinery so as to foster viral reproduction. Specifically, HPV infection is known to induce expression of proliferation antigens such as Ki67 and proliferative cell nuclear antigen (PCNA) in differentiated keratinocytes which have ceased to replicate. In order to determine whether cyclin D1 or cyclin E deregulation is also a feature of HPV infection, an immunohistochemical investigation of cyclin D1, cyclin E, Ki67, and PCNA expression has been carried out in 38 cases of HPV 6/11-related condyloma acuminatum (CA). Results were compared with those obtained from 15 psoriatic proliferative lesions. Whereas 35 (92.1 per cent) CA samples exhibited positive nuclear immunostaining for cyclin E, no cyclin D1 immunoreaction was detected in any of the CA samples studied. All psoriatic lesions showed immunostaining for both cyclins. All CA cases revealed a positive immunoreaction for Ki67 and 33 for PCNA, both in the parabasal and in the differentiated upper epithelial layers. Parabasal keratinocytes of psoriatic lesions were always positive for both Ki67 and PCNA. These results indicate that in the onslaught of HPV 6/11 upon the keratinocyte replication machinery, cyclin E, PCNA, and Ki67 are amongst the targeted cell cycle modulators, whereas cyclin D1 is spared the main effects of virus-cell interplay. In contrast, both cyclins seem to be induced in psoriasis, a non-viral proliferative skin condition.

Cell Division↗
PubMed1998

Induction of proliferating cell nuclear antigen and Ki-67 expression by cytomegalovirus infection.

With the goal of facilitating viral reproduction, cytomegalovirus (CMV) induces changes in the host cell replication machinery. Very little information is available, however, on the effects brought about by CMV on proliferating cell nuclear antigen (PCNA) and Ki-67 expression in infected cells. Fifty-five paraffin-embedded tissue samples (43 gastrointestinal, 10 skin, and 2 kidney biopsies) with both histological and immunohistochemical evidence of CMV infection were investigated for PCNA and Ki-67 expression by the avidinbiotin-peroxidase method. Of the 55 cases studied, 47 were positive for PCNA and 46 for Ki-67. PCNA and Ki-67 immunostaining was more striking in CMV-immunoreactive, inclusion-free cell nuclei, whereas cell nuclei exhibiting well-developed CMV inclusions either showed a weak peripheral signal for both proliferation markers, or were completely negative. Enhanced PCNA and Ki-67 expression appears to be among the changes induced by CMV infection in host cells. Moreover, this induction seems to reach its peak during the earlier phases of CMV infection and abate as the infection proceeds to its inclusion-forming phases, when a sufficiently high viral load would have been attained.

Cell Division↗
PubMed1998

CD44 isoform expression follows two alternative splicing pathways in breast tissue.

The repertoire of distinct CD44 protein isoforms is generated by means of alternative pre-mRNA splicing of 10 variable exons located in the central region of the CD44 gene. We have used human breast ductal carcinoma as a model to identify two alternative splicing pathways of the CD44 pre-mRNA variable region that account for the generation of all of the CD44 isoforms described in breast tissue. An alternative splicing pathway that reflects inclusion of variable exons in a gradual 3'-to-5' fashion is evidenced in breast ductal carcinoma and its lymph node metastases. This pathway is compatible with a mechanism that generates the standard form of CD44 (devoid of variable exons) and is distinguishable from an alternative splicing pathway that involves exclusively variant exon 3 and is observable in both normal and carcinoma breast tissue. We show that both pathways are detectable in the same cell type in the breast and provide a speculative model by which these splicing routes could take place.

Alternative Splicing↗
PubMed1998

Seventy-two hour epirubicin infusion plus quinidine in unresectable and metastatic adenocarcinoma of the pancreas: a phase II trial.

Twenty-two previously untreated patients who had unresectable and metastatic pancreatic cancer were treated in a prospective phase II trial with high-dose continuous infusion epirubicin (45 mg/m2 once every 24 hours continuous infusion days 4 through 6) plus quinidine (495 mg once every 24 hours on days 1-6). There were no objective responses (0 of 18 evaluable patients). Subjective responses were achieved in 2 of 21 evaluable patients (9%), all of whom had good performance status (Eastern Cooperative Oncology Group: 0-1). Median survival was 5.7 months for the overall population. Two patients who exhibited symptomatic improvement achieved responses lasting 7 and 13 months, respectively. Toxicity was generally mild and tolerable. Little benefit regarding survival and quality of life was observed with the use of this regimen. The role in chemoresistance of mdrl, p53, and the mismatch repair system was examined.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1998

Overexpression of Ki-67 and cyclins A and B1 in JC virus-infected cells of progressive multifocal leukoencephalopathy.

Both SV40 and JC virus (JCV) appropriate the host cell replicative machinery to attend to their own reproductive needs. SV40 large T antigen is able to induce the expression of cyclins A, B1, and E (but not of cylin D1) in transfected diploid cells. Whether JCV infection influences cyclin expression in a similar fashion in the setting of progressive multifocal leukoencephalopathy (PML) remains unknown. Brain lesions from 7 PML cases (4 autopsies and 3 biopsies) were immunohistochemically investigated for the expression of Ki-67 and cyclins A, B1, and D1. All 7 cases showed strong positivity for Ki-67 and cyclins A and B1 in JCV-infected oligodendrocytes and astrocytes, the nuclear immunolocalization of cyclin A being in strong contrast to the cytoplasmic distribution of cyclin B1. No immunostaining for cyclin D1 was obtained in any of the 7 cases. These findings suggest that JCV infection is associated with overexpression of Ki-67 and cyclins A and B1 in PML host glial cells. Since cyclin changes in JCV-infected cells recapitulate SV40 T antigen-associated cyclin fluctuations, it appears reasonable to think that JCV T antigen shares some of the previously described capabilities of SV40 T antigen to alter cyclin expression for the sake of viral replication.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Differential expression of CD44v6 in metastases of intestinal and diffuse types of gastric carcinoma.

AIMS: To assess whether standard and variant isoforms of CD44 (CD44s, CD44v5, and CD44v6) have a differential expression profile in early versus advanced gastric adenocarcinoma of the diffuse and intestinal types and their metastases. METHODS: Immunohistochemical expression of CD44s, CD44v5, and CD44v6 was evaluated in 14 early gastric cancers (nine intestinal and five diffuse) and 37 advanced adenocarcinomas (21 intestinal and 16 diffuse) as well as in 18 cases of perigastric lymph node metastasis. Ten normal and five metaplastic gastric mucosa samples were also included in the study. RESULTS: Although no significant association was found between the degree of invasion and the CD44 expression profile, CD44v6 positivity was detected more frequently in metastases of intestinal-type carcinomas (66%) than in metastases of diffuse-type neoplasms (11%) (p < 0.05). Weak CD44s, CD44v5, and CD44v6 expression was observed focally in both normal and metaplastic gastric mucosa samples. CONCLUSIONS: These data suggest that CD44v6 expression may be involved in the production of lymph node metastases in intestinal-type gastric carcinoma but not in the diffuse-type disease, the metastatic potential of which is most likely unrelated to the CD44 family of adhesion molecules.

Adenocarcinoma↗