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Biomedical subjects

R E Madrid

Publications and source records attributed to R E Madrid.

At least 19 recordsLinked to original sources
PubMed2000

Alpha2 macroglobulin elevation without an acute phase response in depressed adults with Down's syndrome: implications.

Studies of immune function during depression in persons without intellectual disability (ID) have revealed elevated levels of alpha2 macroglobulin (alpha2M) and an acute phase protein (APP) response. Clinical observation suggests that people with Down's syndrome (DS) may have associated genetic abnormalities in their immune systems. The APP response and alpha2M changes in depressed versus non-depressed adults with DS was the subject of the present study. The serum pan-proteinase inhibitor alpha2M, and the AP proteins c-reactive protein (CRP), alpha1 antitrypsin (alpha1AT), ceruloplasmin (Cp), beta2 Macroglobulin (beta2M), transthyretin (Trans), serum amyloid protein (SAP), and albumin (Alb) were measured in 38 adults with DS, 19 of whom were diagnosed with and 19 without depression using a sandwich enzyme-linked immunosorbent assay (ELISA). The DSM-IV criteria were used for diagnoses. Medical and neurological examinations excluded medical disorders associated with APP response. Only alpha2M and CRP were significantly different in the depressed versus non-depressed groups. The alpha2M was higher, a response similar to one observed in depressed people without ID, but the CRP was lower in the depressed group, especially in those subjects not on psychotropic medications, contrary to the expected APP response to depression. The results suggest that alpha2M elevation in depressed adults with DS is independent of the APP response. An alternative explanation for its elevation is proposed linking the core symptom of depression with the mammalian dormancy/hibernation process. Further studies are needed to confirm that alpha2M elevation is specific to depression and that it might provide a helpful marker for the diagnosis of depression in people with ID.

Acute-Phase Proteins↗
PubMed1999

Automatic on-line analyser of microbial growth using simultaneous measurements of impedance and turbidity.

An apparatus for the measurement of bacterial growth is described. The instrument applies alternate adequate sequential currents of two different frequencies through a pair of electrodes immersed in a cultured medium. It monitors, detects and quantifies the growth of micro-organisms based on the measurement of the impedance across the two electrodes and, simultaneously, it measures the variation in the medium turbidity. The medium conductivity and the interface electrode impedance changes can be extracted from the measured impedance. The variations in turbidity can be calibrated in absorbance or optical density units. Moreover, all these parameters are also proportional to bacterial proliferation. The computer-controlled apparatus processes and displays the parameters on a monitor showing bulk resistance, electrode impedance and turbidity changes as time course events. The equipment can detect aerobic or anaerobic micro-organisms and permits the operator simultaneously to assess impedance and turbidity, or it can produce each parameter as a separate event. Time growth curves of different micro-organisms are presented in the results.

Bacteria↗
PubMed1999

Impedance microbiology: quantification of bacterial content in milk by means of capacitance growth curves.

The impedancimetric method is a technique for the rapid evaluation of milk bacterial content and also of its subproducts. Several authors have made use of culture conductance changes during bacterial growth for quantitative and qualitative assessments of microbial growth. However, interface capacitance curves, Ci, have not been used. In this paper, we quantify bacteria in cow raw milk by following their growth as the above-mentioned capacitance change time course event. With it, bigger growth variations, shorter detection times and a better coefficient of correlation with the plate count method were obtained than those yielded by conductance curves. Calibration was performed by plotting initial known concentrations, IC (CFU/ml), as a function of the time detection theshold (TDT).

Animals↗
PubMed1996

Maternally inherited cardiomyopathy and hearing loss associated with a novel mutation in the mitochondrial tRNA(Lys) gene (G8363A).

A novel G8363A mutation in the mtDNA tRNA(Lys) gene was associated, in two unrelated families, with a syndrome consisting of encephalomyopathy, sensorineural hearing loss, and hypertrophic cardiomyopathy. Muscle biopsies from the probands showed mitochondrial proliferation and partial defects of complexes I, III, and IV of the electron-transport chain. The G8363A mutation was very abundant (>95%) in muscle samples from the probands and was less copious in blood from 18 maternal relatives (mean 81.3% +/- 8.5%). Single-muscle-fiber analysis showed significantly higher levels of mutant genomes in cytochrome (c) oxidase-negative fibers than in cytochrome (c) oxidase-positive fibers. The mutation was not found in >200 individuals, including normal controls and patients with other mitochondrial encephalomyopathies, thus fulfilling accepted criteria for pathogenicity.

Adolescent↗
PubMed1992

Imaging of human T-lymphotropic virus type I-associated chronic progressive myeloneuropathies.

We studied magnetic resonance imaging (MRI) of the head and cervical spine and CT of the head in 46 patients (14 men, 32 women) with chronic progressive myeloneuropathy. The findings were correlated with human T-lymphotropic virus type I (HTLV-I) serology, race, country of origin, and age. We found a female predominance of 2:1. Most patients were aged between 30 and 50 years, and most were Caribbean immigrants and black. There were 9 men and 17 women with blood antibody titers to HTLV-I and 7 men and 15 women with cerebrospinal fluid (CSF) titers. All patients with virus or antibodies in blood or CSF were Caribbean immigrants or black. T2-weighted cranial MRI showed scattered areas of high signal intensity in the cerebral white matter, usually in the periventricular and subcortical areas, but not in the posterior cranial fossa. Cranial CT revealed periventricular low density areas, ventricular enlargement, and atrophy MRI of the cervical spine showed atrophy of the cord. Myelography was normal in all 15 patients examined. No imaging differences were observed between the HTLV-I-positive and -negative patients. These findings, although consistent with demyelination, are not specific.

Adolescent↗
PubMed1992

Impedance bacteriometry: medium and interface contributions during bacterial growth.

We measured impedance in a cell containing culture broth inoculated with E. coli, before and during bacterial growth. The electrode interface impedance components (Ri, Xi) and the culture medium component Rm were separated by making use of the Warburg's model frequency dependent properties. Measurements were carried out at different frequencies (from 18 Hz to 18 kHz) with a constant current impedance bridge as growth proceeded. It was found that: Growth curves for Ri and Xi showed a similar temporal pattern within the frequency range of 18-100 Hz. Dispersion was not observed in Rm, meaning that the same growth response was obtained within the 18-18,000 Hz range. At low frequency, the resistive and capacitive reactive components, or Rb and Xb, respectively, were directly measured, where Rb = (2.Ri + Rm) and Xb = 2.Xi and, at high frequency (above 5 kHz), Rm was obtained (for Zi is negligible). Thus, Ri was easily discriminated from Rm by simple arithmetic: Ri = [Rb (low f) - Rb (high f)]/2. In four experiments, the maximum spread of Xi, Ri, and Rm was smaller than 5%, indicating good repeatability. There is potential new information in dissecting out the growth curve in three separate component curves.

Bacteria↗
PubMed1988

Spino-cerebellar degeneration with polyneuropathy associated with ceroid lipofuscinosis in one family.

There are several clinically distinct forms of neuronal ceroid lipofuscinosis whose presentation and pathology are usually homogeneous within families. Several atypical variants have also been reported. We have studied an inbred sibship in which neuronal ceroid lipofuscinosis appeared to present in two completely different ways. In the proband, the course was compatible with a somewhat atypical juvenile variant. Ataxia and spasticity started at 4.5 years, followed by blindness with optic atrophy, intractable seizures, dementia, and death at 14 years. Atypical features included areflexia, hypotonia, and ataxia. Electron microscopic studies of her skin and her rectal ganglion cells showed lucent, dense, and fingerprint inclusions that were also found in the central nervous system at autopsy. Her brother and sister developed difficulty walking at ages 8.5 and 10.5 years and are alive at 24 and 18 years. They presented with slowly progressive spinocerebellar degeneration with sensorimotor neuropathy without dementia, seizures, or visual impairment. Lysosomal enzymes and lipoprotein analysis were normal in all three siblings and their parents. Elevated dolichol in the urine and lucent, dense, and fingerprint inclusions in skin, cutaneous nerve, buffy coat lymphocytes in both siblings and in the sural nerve of the brother suggest that their disease may represent a novel phenotype of neuronal ceroid lipofuscinosis. While it is possible that two different recessive genes may be segregating in this consanguineous family, we cannot dismiss the possibility that variability of gene expression may account for the divergent phenotypes.

Adolescent↗
PubMed1983

Chronic progressive experimental allergic encephalomyelitis (EAE) in adult guinea pigs.

Adult Hartley guinea pigs were inoculated with an increased dose of whole central nervous system tissue in complete Freund's adjuvant in order to determine the effects of high dose of neuroantigens on the clinical and pathological course of experimental allergic encephalomyelitis (EAE). An increased survival rate during the first attack and a change in the course of the disease from an acute fatal one to chronic progressive EAE were observed. The main clinicopathological features of the disease included a delayed onset of mild neurological signs and the presence of large demyelinated plaques in the brain and spinal cord. The relationship of the chronic progressive course of the disease and the induction of high-zone tolerance is discussed.

Animals↗
PubMed1982

Lipophilin-induced experimental allergic encephalomyelitis in guinea pigs.

Clinical signs of EAE were infrequently observed (1/20) in adult Hartley guinea pigs challenged with isolated human myelin lipophilin in complete Freund's adjuvant. However, CNS vasculitis and parenchymal infiltration by inflammatory cells were found in 10 of 20 inoculated animals. Localized, nonconfluent, small demyelinated lesions were detected in the brain and spinal cord of 5/20 Hartley guinea pigs during an observation period of 120 days. The frequency of both inflammatory and demyelinated lesions in Hartley animals appeared to be dose-dependent, but extensive demyelinated lesions were not induced. Persistent residual inoculation mixture at the site of injection was found in animals showing CNS inflammatory and/or demyelinated lesions. In contrast to the Hartley strain, young strain 13 guinea pigs were clinically and pathologically unresponsive to challenge with lipophilin and mycobacteria in water-in-oil emulsion.

Animals↗
PubMed1981

Relapsing experimental allergic encephalomyelitis induced with isolated myelin and with myelin basic protein plus myelin lipids.

To test the ability of different spinal cord fractions to reproduce the clinicopathological features of relapsing experimental allergic encephalomyelitis (R-EAE), groups of young guinea pigs were inoculated with: (1) spinal cord myelin; (2) delipidated myelin; (3) reconstituted myelin and (4) MBP plus myelin lipids. The four sets of antigens induced acute EAE in most of the animals tested. During an observation period of 18 months, only one clinical relapse was observed in animals sensitized with myelin and with MBP plus myelin lipids. Extensive CNS demyelination was found in relapsing animals injected with myelin. No demyelinated lesions were observed in non-relapsing animals. By contrast, half of the surviving guinea pigs injected with MBP plus myelin lipids had demyelinated lesions, irrespective of whether they relapsed or not. The inability of the spinal cord myelin fractions to fully reproduce the R-EAE model suggest that other non-myelin antigens may be involved in the pathogenesis of multiple relapses.

Animals↗
PubMed1979

Neuritogenic and chemical properties of guinea pig anterior and posterior root myelin.

In relapsing experimental allergic encephalomyelitis, recurrent demyelination was found in the anterior roots and dorsal root ganglia with minimal involvement of the posterior roots. To determine whether this is an antigen-related phenomenon, the distribution, type and intensity of the lesions in the proximal PNS of guinea pigs immunized with anterior roots or myelin were compared to those of animals immunized with posterior roots or myelin. Homologous anterior roots were less neuritogenic than posterior roots or posterior root myelin. Thin layer chromatography of myelin samples from anterior and posterior roots, dorsal root ganglia and sciatic nerve revealed the presence of a sulfogalactoglycerolipid, tentatively identified as sulfated galactosylglyceride (SGG) in all but the posterior root myelin samples. Although the PNS lesions of relapsing experimental allergic encephalomyelitis appear to recapitulate the regional distribution of SGG, the reason why its presence in anterior roots myelin renders them less neuritogenic is at present not clear.

Animals↗
PubMed1978

Peripheral nervous system pathology in relapsing experimental allergic encephalomyelitis.

A recurrent type of primary demyelination was found in the anterior roots and dorsal root ganglia of strain 13 guinea-pigs with relapsing experimental allergic encephalomyelitis. Single nerve fibre studies revealed a predominant nodal--paranodal distribution of the destruction of myelin in these nerves. Damage of the Schwann cell--axolemmal junction was found in the majority of the abnormal nodes of Ranvier. This was accompanied by the formation of supernumerary adaxonal Schwann cell processes which further altered the normal myelinating cell--axon relationship. It is concluded that variations in antigenic composition may play a role in the selective involvement of the anterior roots. The pathogenesis of the observed nodal changes is discussed.

Animals↗
PubMed1977

Axonal degeneration in demyelinating disorders.

Changes in the L7 and S1 segments of the spinal cord and the corresponding dorsal root ganglia (DRG), spinal roots and sciatic nerves of guinea pigs immunized with whole rabbit sciatic nerve in complete Freund's adjuvant have been studied and compared with the changes found in guinea pigs immunized with purified P.N.S. myelin. In both groups of animals, pathological changes were found in the posterior roots, DRG and root entry zones. In the posterior roots, axonal degeneration and segmental demyelination evolved in parallel, affected different populations of myelinated axons and showed no indication of interdependence. The aetiology of axonal degeneration in this and other demyelinating disorders is discussed. It is concluded that axons can be damaged by being in the vicinity of areas where cell-mediated immune reactions are taking place, i.e. as a consequence of the so-called 'bystander' effect.

Animals↗