[Hip hemiplegia and parasagittal mass: different etiologies].
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Aged↗
Biomedical subjects
A Alvarez
Publications and source records attributed to A Alvarez.
Expression in Escherichia coli of the lpdA gene, protein sequence analysis and immunological characterization of the P64k protein from Neisseria meningitidis.
By making use of recombinant DNA technology it is possible to characterize meningococcal outer membrane proteins (OMPs) capable of stimulating a host immune response. The lpdA gene, which codes for an OMP (P64k) from Neisseria meningitidis, was cloned in Escherichia coli. The recombinant protein was recognized by sera from patients convalescing from meningococcal disease. The monoclonal antibodies obtained against the recombinant protein recognized the natural protein on a Western blot, and monoclonal antibody 114 was assayed in ELISA with a panel of 85 N. meningitidis strains. The protein was recognized in 81 strains (95.3%); the strains that were not recognized were neither epidemic nor isolated from systemic disease. The complete amino acid sequence of P64k was obtained by automatic sequencing and MS.
Amino Acid Sequence↗
Involvement of interleukin-6 in the biology and metastatic activity of B16F10 melanoma cells.
In previous studies, we demonstrated the presence of the interleukin-2 (IL-2) signalling system in B16F10 murine melanoma and observed that in vitro treatment of B16F10 cells with IL-2, enhanced metastasis. To further understand the role played by interleukins in melanoma, we examined the effect of IL-6 on the metastatic activity and properties of B16 melanoma cells. We observed that B16F10 cells, cultured in the presence of IL-6, showed a clear increase in their metastatic ability, both in the liver and in the lungs. Neither cell proliferation nor in vitro colony formation were affected by IL-6; however, the expression of CD44 and VLA-4 increased. The IL-6 gene was expressed in B16F10 cells as shown by RT-PCR. A slight induction of IL-6 mRNA expression by IL-2 was observed, but not after treatment with IL-1beta or IL-6. Nevertheless, no soluble IL-6 could be detected in cell supernatants even after treatment with IL-2. Finally, we tested the effect of IL-1beta, IL-6 and IL-2 on the expression of the IL-2 receptor (IL-2R). IL-1beta turned out to be the strongest inducer of IL-2R expression in B16F10 cells. Altogether, these data confirm the involvement of interleukins in the biology and metastatic activity of melanoma.
Animals↗
Retinal vulnerability to glutamate excitotoxicity in canine glaucoma: induction of neuronal nitric oxide synthase in retinal ganglion cells.
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Animals↗
[The evaluation of a self-measurement arterial pressure monitor: the OMRON-HM 722C].
OBJECTIVE: To evaluate a self-measuring blood pressure (BP) monitor, the OMRON-HM 722C. DESIGN: Based on the protocol of the British Hypertension Society (BHS). SETTING: Urban health centre. PARTICIPANTS: A sample of 120 people (69 women) excluded those with a brachial perimeter under 24 centimetres or over 32. MEASUREMENTS AND MAIN RESULTS: Each subject had four BP measurements in succession, separated by a minute: a) Manually, with a mercury sphygmomanometer (MSM); b) with self-measurement monitor; c) with self-measurement monitor; d) with MSM. Means and SD of systolic and diastolic pressures, means and SD of the differences and a graphic representation of these by the Bland and Altman method, were calculated. The cumulative percentages of differences the same as or below 5, 10 and 15 mm Hg were calculated. 89.1% of systolic BPs, and 92.5% of diastolic BPs, showed mean differences between monitor and observer equal to or below 5 mm Hg. The size of the differences was grade A in both cases, according to the BHS criteria. CONCLUSION: The OMRON-HM 722C self-measuring monitor could be useful for self-measurement of BP at home by primary care patients.
Aged↗
Acetylcholinesterase promotes the aggregation of amyloid-beta-peptide fragments by forming a complex with the growing fibrils.
Acetylcholinesterase (AChE), an enzyme involved in the hydrolysis of the neurotransmitter acetylcholine, consistently colocalizes with the amyloid deposits characteristic of Alzheimer's disease and may contribute to the generation of amyloid proteins and/or physically affect fibril assembly. In order to identify the structural domains of the amyloid-beta-peptide (Abeta) involved in the aggregation induced by AChE, we have studied the effect of this cholinergic enzyme on Abeta peptide fragments of different sizes. AChE enhanced the aggregation of the Abeta(12-28) and Abeta(25-35) peptides but not of the Abeta(1-16) fragment. The inductive effect of AChE on the aggregation of Abeta(12-28) was abolished by the presence of either Abeta(1-16) or Abeta(9-21). The effect of the enzyme was also analysed using two different mutant fragments, possessing a low and the other a high capacity for fibrillogenesis. The fragments used were Abeta(12-28)Val18-->Ala and Abeta(12-28)Glu22-->Gln, respectively. AChE was able to promote the aggregation of these fragments in a very specific way and both mutant peptides were able to form amyloid fibrils, as revealed by negative staining under the electron microscope. Binding assays indicated that AChE was bound to Abeta(12-28), as well as to the Abeta(1-16) peptide. AChE was seen to form strong complexes with the Abeta(12-28) fibrils as such complexes stained positively for both thioflavine-T and AChE activity, were resistant to high ionic strength treatment, and were partially sensitive to detergents, suggesting that hydrophobic interactions may play a role in the stabilization of the AChE-Abeta complex. Our results suggest that such amyloid-AChE complexes are formed when AChE interacts with the growing amyloid fibrils and accelerates the assembly of Abeta peptides. This is consistent with the fact that AChE is known to be present within Abeta deposits including the pre-amyloid diffuse and mature senile plaques found in Alzheimer's brain.
Acetylcholinesterase↗
Rapid Up-regulation of IkappaBbeta and abrogation of NF-kappaB activity in peritoneal macrophages stimulated with lipopolysaccharide.
Lipopolysaccharide (LPS) administration to mice elicited the activation of nuclear factor kappaB (NF-kappaB) in several tissues including liver and macrophages. Maximal activation was observed 1 h after treatment but declined at 3 and 6 h. The levels of IkappaBalpha and IkappaBbeta were analyzed during this period in an attempt to correlate NF-kappaB activity with IkappaB resynthesis. Degradation of IkappaBalpha was very rapid and was followed by recovery 1 h after LPS administration. IkappaBbeta degradation, which has been associated with persistent NF-kappaB activation, was complete at 1 h. However, a rapid recovery of IkappaBbeta in these tissues was observed at 3 h in parallel with the abrogation of NF-kappaB activity. Immunolocalization of newly synthesized IkappaBbeta by confocal microscopy revealed its preferential accumulation in the cytosol. Analysis of IkappaBbeta by Western blot using high resolution polyacrylamide gel electrophoresis showed the presence of two bands in cytosolic extracts of LPS-treated macrophages at 3 h, but only one band with the same mobility as the control was detected at 6 h. Moreover, treatment of extracts of resynthesized IkappaBbeta with alkaline phosphatase resulted in the accumulation of the protein of slightly higher electrophoretic mobility, indicating the prevalence of a rapid phosphorylation of the newly synthesized IkappaBbeta. At the mRNA level, up-regulation of IkappaBbeta was observed in macrophages stimulated for 1 h with LPS. When the effect of pro-inflammatory cytokines was investigated, tumor necrosis factor alpha, but not interleukin-1 or interferon-gamma, promoted an important degradation of IkappaBbeta followed by an increase in the mRNA at 1 h. These results suggest the existence of LPS- and tumor necrosis factor alpha- specific pathways involved in a rapid IkappaBbeta degradation and resynthesis and might explain the transient period of activation of NF-kappaB in these tissues upon stimulation with these factors. This rapid control of NF-kappaB function may contribute to the attenuation of the inflammatory response of these cells.
Acute-Phase Reaction↗
[PCR study of bcl-2 rearrangement in autologous transplantation of peripheral stem cells in follicular non-Hodgkin's lymphoma].
OBJECTIVE: To value the usefulness of the bcl-2 rearrangement analysis by PCR in the study of the minimal residual disease in patients with follicular non-Hodgkin's B cell lymphoma (NHL) submitted to peripheral blood stem-cell transplantation (PSCT). PATIENTS AND METHOD: The study was done on 12 patients diagnosed with low grade B-cell NHL, who were entered in a program of myeloablative chemotherapy followed by rescue with progenitor cells obtained from peripheral blood. At the time of peripheral stem-cells (PSC) harvesting, 8 patients did not present medullar infiltration and four of them presented medullar infiltration according to conventional histological criteria. The study was done on DNA from samples taken from bone marrow and cells taken in the apheresis. The DNA samples were studied by PCR to determine the existence of the bcl-2 rearrangement. RESULTS: At the time of apheresis, 8 patients did not present medullar infiltration according to conventional histological criteria but 7 of them presented bcl-2/JH rearrangement. Most patients studied (10 out of 12) showed bcl-2/JH rearrangement (minimal residual disease) in apheresis products. However, in 2 of these 10 patients, such rearrangement was negative in the bone marrow samples obtained 3-6 and 12 months after transplantation. CONCLUSION: In some patients with follicular NHL submitted to PSCT, the bcl-2/JH rearrangement had negativized after transplantation, this implies that the tumoral cells present in apheresis products lost their clonogenic capacity and were not able to subsist in vivo and that the myeloablative polychemotherapy schedules are able to eradicate the t(14; 18) translocation bearing cells or, at least, to decrease their number in bone marrow to levels below those of PCR detection.
Adult↗
A monoclonal antibody against acetylcholinesterase inhibits the formation of amyloid fibrils induced by the enzyme.
A monoclonal antibody (mAb) 25B1 directed against fetal bovine-serum acetylcholinesterase (FBS AChE) was used to examine the ability of the cholinergic enzyme to promote the assembly of amyloid-beta peptides (A beta) into Alzheimerś fibrils. This mAb binds to the peripheral anionic site of the enzyme and allosterically inhibits catalytic activity of FBS AChE. Several techniques, including thioflavine-T fluorescence, turbidity, and negative-staining at the electron microscopy level, were used to assess amyloid formation. Inhibition of amyloid formation was dependent on the molar ratio AChE:mAb 25B1, and at least 50% of the inhibition of the AChE promoting effect occurs at a molar ratio similar to that required for inhibition of the esterase activity. Our results suggest that mAb 25B1 inhibits the promotion of the amyloid fibril formation triggered by AChE by affecting the lag period of the A beta aggregation process.
Acetylcholinesterase↗
Use of cardiac troponin T rapid assay in the diagnosis of a myocardial injury secondary to electrical cardioversion.
BACKGROUND AND HYPOTHESIS: This study was carried out to determine whether cardiac troponin T test in rapid assay gives positive results in patients previously submitted to cardioversion or electrical defibrillation. METHODS: Forty patients with supraventricular tachyarrhythmias lasting no more than 2 days were treated with electrical cardioversion. The total creatine phosphokinase (CPK)-MB isoenzyme and troponin T in rapid assay were measured at baseline and at 6, 12, and 24 h thereafter. RESULTS: Total CPK baseline levels were normal in all cases; within 4 h, the serum CPK levels increased by 98%, at 6 h by 111.5%, at 12 h by 168%, and at 24 h by 225% (p > 0.01). The CPK-MB isoenzyme showed no percentage increase of total CPK higher than 5%, measured at 6, 12, and 24 h after the shock, independent of the number of attempts of cardioversion. The troponin T test was also negative in all cases at baseline and at 6, 12, and 24 h after cardioversion. CONCLUSION: We conclude that the absence of elevations in CPK-MB levels and cardiac troponin T levels matched clinical and electrocardiographic results showing absence of myocardial damage after electrical cardioversion.
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Sinusoidal endothelium release of hydrogen peroxide enhances very late antigen-4-mediated melanoma cell adherence and tumor cytotoxicity during interleukin-1 promotion of hepatic melanoma metastasis in mice.
The hepatic sinusoidal endothelium (HSE) releases large amounts of reactive oxygen species (ROS) in response to endotoxins and interleukin-1 (IL-1). Such pro-inflammatory mediators have been shown to promote hepatic metastasis. We have investigated the involvement of ROS released by IL-1-stimulated HSE in this promoting effect. Recombinant human interleukin-1 beta (rHuIL-1 beta) (5 micrograms/kg) was intravenously injected into C57BL/6J mice, and the hepatic metastasizing ability of B16 melanoma cells following intrasplenic injection was studied in the presence of ROS scavengers. rHuIL-1 beta-promoted hepatic metastases were significantly (P < .01) reduced by catalase (1 mg/kg) and enhanced by recombinant human superoxide dismutase (rHuSOD) (5 mg/kg). rHuIL-1 beta-stimulated HSE-conditioned medium (HSE-CM) significantly (P < .01) enhanced B16 melanoma cell adhesion to HSE compared with unstimulated HSE-CM, which in turn also significantly (P < .01) increased with melanoma cell adherence compared with basal medium. The addition of catalase completely abrogated proadhesive effects induced by rHuIL-1 beta-stimulated HSE-CM with respect to unstimulated HSE-CM, but did not affect the proadhesive effects induced by unstimulated HSE-CM over basal medium. The rat monoclonal antibody to mouse vascular cell adhesion molecule-1 (VCAM-1) significantly (P < .01) inhibited the enhanced melanoma cell adherence effects of both unstimulated and rHuIL-1 beta-stimulated HSE-CM, indicating that adherence was very late antigen-4 (VLA-4)-mediated. Not surprisingly, the percentage of VLA-4 expressing B16 melanoma cells significantly (P < .05) increased in response to unstimulated (21% of controls) and rHuIL-1 beta-stimulated (32% of controls) HSE-CM. Catalase addition abrogated these effects of rHuIL-1 beta-stimulated-HSE-CM. Melanoma cell damage was observed from the second hour of adhesion to HSE and significantly (P < .01) increased when the cells adhered to rHuIL-1 beta-stimulated HSE. This increase was abrogated by catalase. Cytolysis of the HSE was not observed during melanoma cell adhesion. Neither was the enhancement of B16 melanoma hydrogen peroxide production observed in response to rHuIL-1 beta. Thus, the effects of IL-1 in the liver may consist of a balance between the prometastatic effect of enhanced adherence to the HSE and the antimetastatic effect of H2O2-mediated cytotoxicity. Our results suggest that the enhancement of H2O2 production by the rHuIL-1 beta-stimulated HSE may contribute to the hepatic metastasis progression of ROS-resistant melanoma cells. Results in vitro indicate that this progression is associated with a H2O2-mediated increase in melanoma cell adhesion to HSE.
Animals↗
Large B-cell lymphoma of the uterine corpus: case report with immunohistochemical and molecular study.
Primary lymphoma of the uterine corpus (PLUC) is an extremely rare neoplasm. We report a case of PLUC in a 78-year-old woman with vaginal bleeding without hepatosplenomegaly, adenopathies, or bone marrow infiltration, classified as stage I. A diagnosis of diffuse large B-cell lymphoma was made in endometrial curettage tissue. Immunohistochemical study showed tumoral cells of B-cell nature. Two different polymerase chain reaction (PCR) techniques showed immunoglobulin heavy chain gene rearrangement and we could not demonstrate, with PCR technique, either Epstein-Barr virus or papilloma virus infection. Total hysterectomy with bilateral salpingo-oophorectomy was carried out and adjuvant chemotherapy was given. She was alive and free of disease after a follow-up period of 7 years, and the patient has been in perfect health.
Aged↗
The clinical, neuroradiographic, and endocrinologic profile of patients with bilateral optic nerve hypoplasia.
PURPOSE: The purpose of the study was to expand on ophthalmologic and endocrinologic data and report the neuroimaging findings of 35 patients with bilateral optic nerve hypoplasia (BONH). METHODS: A retrospective chart review of 35 children with BONH was conducted. Data on visual acuity, refractive error, and presence of nystagmus and strabismus were collected. Twenty-six children underwent full-endocrinologic evaluation and magnetic resonance imaging or computed tomography scanning. RESULTS: The male:female ratio was 2:1. Ten percent of eyes had visual acuity of 20/60 or better, whereas 34% had no light perception. Eighty-six percent of eyes had acuity less than 20/200, and 80% of patients were legally blind. Most patients (86%) had nystagmus or strabismus or both. Forty-six percent had absence of the septum pellucidum and corpus callosum on neuroimaging. Twenty-seven percent of patients had endocrinologic abnormalities, with growth hormone deficiency being the most common. Panhypopituitarism occurred in 11.5% of children. CONCLUSIONS: Although the visual prognosis of children with BONH generally is poor, 10% of such patients have excellent acuity. In contrast to previous reports, endocrine abnormalities were seen in only one quarter of patients, and the full-blown deMorsier syndrome (septo-optic dysplasia with panhypopituitarism) was seen in only 11.5% of patients with BONH.
Abnormalities, Multiple↗
Age-dependent modifications in rat hepatocyte antioxidant defense systems.
BACKGROUND/AIMS: Age-dependent changes in the hepatic antioxidant systems were studied in hepatocytes from newly weaned (21 days) to 30-month-old rats. RESULTS: Biphasic changes were observed in superoxide dismutase (SOD), glucose-6-phosphate dehydrogenase (G6PDH) and malic enzyme (ME), in which noticeable decreases were detected in hepatocytes from newly weaned to 6-month-old rats: Cu-Zn SOD decreased to 46% (p < 0.001), Mn SOD to 41% (p < 0.001), G6PDH to 71% and ME to 19% (p < 0,001), and significant increases were observed from 6 to 30 months. In hepatocytes from 6- to 30- month-old rats the enzymes involved in antioxidant defense underwent increases in their activities as well in their mRNA: Cu-Zn SOD (142%, p < 0.001), catalase (182%, p < 0.001) and glutathione peroxidase (325%, p < 0.001). However, chronological decreases were observed in the levels of reduced glutathione (69%, p < 0.001), in the GSH/GSSG ratio (78%) and in protein thiol groups (55%, p < 0.001), with concomitant increases in peroxides (155%, p < 0.001) and malondialdehyde (142%, p < 0.001) levels. DNA ploidy was also assayed by flow cytometry; a sharp increase in tetraploid (2.5-40.1%, p < 0.001) and octoploid (0.1-16.1%; p < 0.001) populations, and a noticeable decrease in diploid hepatocytes (92.9-34.3%; p < 0.001), were observed. Populations involved in 2C-->4C DNA synthesis decreased from 3.6 to 0.9% (p < 0.001), while those involved in 4C-->8C increased from 0.9% to 5.2% (p < 0.001). A hypodiploid population (apoptotic cells) was detected from 12 months, increasing thereafter. CONCLUSIONS: These results show that the antioxidant cell defense system increases with age but the rate of reactive oxygen species generation exceeds the induced antioxidant ability, generating a situation that favors oxidative stress and peroxidation. The progressive polyploidization is accompanied by changes in the proliferative potential that decreases from 2C to 4C and increased from 4C to 8C. The relationship between the modifications of the oxidant/antioxidant system and increased polyploidy is not clear and may be interpreted as two independent manifestations of the aging process.
Aging↗
Interleukin-2 increases intracellular glutathione levels and reverses the growth inhibiting effects of cyclophosphamide on B16 melanoma cells.
Glutathione (GSH) plays an essential role in the metabolism of melanoma. As changes in intracellular GSH content can modify the processes of cell proliferation and detoxification, this could determine the therapeutic response to some cancer treatment strategies. The purpose of this study was to test the effects of treatment with interleukin-2 (IL-2), alone and in combination with cyclophosphamide (CY), on survival of mice bearing B16 melanoma liver metastases, and to determine the influence of these therapeutic agents on the GSH metabolism of B16 cells. In the in vivo test system, B16 melanoma liver metastases were induced in C57BL/6 mice which were subsequently treated with IL-2, CY and CY plus IL-2. Survival time was used to determine the response to treatment. In the in vitro system, we evaluated the effects of IL-2, acrolein (an active metabolite of CY responsible for GSH depletion) and acrolein plus IL-2 on GSH levels and proliferation of B16 melanoma cells. Results indicated that, in vivo, all treatments increased mouse survival times with respect to control mice. However, the addition of IL-2 to CY therapy decreased survival time compared with treatment with CY alone. In vitro, whereas acrolein produced a GSH depletion and inhibited B16 cell proliferation, IL-2 increased GSH content and cell proliferation rate compared with untreated cells. Moreover, addition of IL-2 to cells preincubated with acrolein increased GSH levels and proliferation with respect to acrolein alone. In summary, the data suggest that GSH plays a critical role in the growth-promoting effects of IL-2 on B16F10 melanoma cells and in the antagonistic effect of IL-2 on CY inhibitory activity on these tumor cells.
Animals↗
Detection of antibodies to Candida albicans germ tubes for diagnosis and therapeutic monitoring of invasive candidiasis in patients with hematologic malignancies.
We prospectively investigated the ability of detection of antibodies to Candida albicans germ tubes (CAGT) to diagnose invasive candidiasis in 95 consecutive admissions of 73 patients with hematologic disorders undergoing intensive chemotherapy. The episodes were divided into three groups according to clinical and microbiological diagnosis. Group 1 comprised eight admissions of eight patients with invasive candidiasis. Group 2 comprised 42 admissions of 34 patients without evidence of invasive candidiasis. Group 3 comprised the remaining 45 admissions of 37 patients with febrile episodes which were not diagnosed by microbiological culture. Antibodies to CAGT were detected in 87.5% of group 1 patients. Detection of antibodies to CAGT in patients with Candida fungemia was delayed somewhat relative to the time the blood culture was positive, but antibodies to CAGT were detected earlier than a diagnosis was made in patients with deep-tissue candidiasis. Sera from 2 admissions in group 2 and 12 admissions in group 3 revealed antibodies to CAGT. At a titer of > or = 1:20, detection of antibodies to CAGT had a sensitivity of 87.5%, specificity of 95.2%, positive predictive value of 77.8%, and negative predictive value of 97.6%. Antibodies to CAGT were usually detected before beginning of empiric antifungal therapy. Titers of antibodies to CAGT were maintained in most patients who died but declined and eventually disappeared in the patients who survived. Since antibodies to CAGT were detected in all patients with tissue-proven invasive candidiasis but negative by blood culture, detection of antibodies to CAGT complemented blood cultures for diagnosis and therapeutic monitoring of patients with hematologic malignancies and invasive candidiasis.
Adolescent↗
Hypopituitarism due to lymphocytic hypophysitis in a patient with retroperitoneal fibrosis.
We present a 78-year-old woman with clinical acute hypopituitarism in whom pathologic findings showed lymphocytic hypophysitis and retroperitoneal fibrosis. Lymphocytic hypophysitis should be included in the differential diagnosis of hypopituitarism at any age. The association with idiopathic retroperitoneal fibrosis suggest an autoimmune origin for this entity.
Aged↗
C1-esterase inhibitor prevents early pulmonary dysfunction after lung transplantation in the dog.
The success of lung transplantation to a large extent depends on effective protection of the graft from ischemic injury after reperfusion. Although mechanisms have not been clarified, the pathologic findings of ischemic injury after reperfusion are similar to adult respiratory distress syndrome, a condition in which the blood coagulation contact system is activated. This study evaluates the effect of C1-esterase inhibitor (C1-INH), the main inhibitor of the blood coagulation contact system, on short-term lung function in a dog model of orthotopic lung transplantation. Twelve lung transplantations were performed after 24 h of ischemic time. Dogs were randomly assigned to receive either vehicle (Control) or C1-INH. After the lung transplantation in the control group, Pao2 decreased by 84% and both the AaPO2 and the Qs/Qt% increased (340 and 530%, respectively, p < 0.01); these parameters remained unchanged in the C1-INH group. The hypoxemia observed in control animals was associated with decreased blood coagulation contact factors, complement consumption, increased expression of adhesion glycoproteins in leukocytes, and extensive intraalveolar and interstitial neutrophil infiltration. In contrast, C1-INH administration prevented hypoxemia, the decrease in blood coagulation contact factors, the activation of the complement system, the increase in expression of leukocyte adhesion molecules, and inflammatory cell infiltrate. This study has demonstrated that in a dog model of lung transplantation, the administration of C1-INH prevents early pulmonary dysfunction, and it suggests that activation of blood coagulation contact system and complement are important mechanisms causing ischemic injury after reperfusion.
Animals↗