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R M Garruto

Publications and source records attributed to R M Garruto.

At least 73 records · Page 4Linked to original sources
PubMed1989

Isolation of fetal mouse motor neurons on discontinuous Percoll density gradients.

The spinal cords of fetal NIH:CR mice, gestational age Day 12 to 14, were dissected free of meninges and dorsal root ganglia, chemically dissociated, and layered onto discontinuous Percoll gradients at densities 1.040, 1.050, and 1.060 g/ml. After centrifugation (800 Xg for 15 min at 4 degrees C), three morphologically, biochemically, and immunohistologically distinct cell populations were collected from the gradient interfaces. The first interface, located at a density of 1.040 g/ml, was choline acetyltransferase enriched (0.86 +/- 0.08) compared to the second and third fractions (0.42 +/- 0.01 and 0 pmol acetylcholine synthesized/microgram protein, respectively). When simultaneously cultured with fetal mouse cardiac muscle on a gelatin-polylysine-laminin substrate in serum-free medium, these cells developed the characteristics of motor neurons.

Animals↗
PubMed1988

The role of HTLV-I in tropical spastic paraparesis in Jamaica.

We report clinical and laboratory investigations of 47 native-born Jamaican patients with endemic tropical spastic paraparesis and of 1 patient with tropical ataxic neuropathy. Mean age at onset was 40 years, with a female-male preponderance (2.7:1). Neurological features of endemic tropical spastic paraparesis are predominantly those of a spastic paraparesis with variable degrees of proprioceptive and/or superficial sensory impairment. Using enzyme-linked immunoabsorbent assay (ELISA), IgG antibodies to human T-lymphotropic virus type I (HTLV-I) were present in 82% of sera and 77% of cerebrospinal fluids. On Western blot analysis, IgG antibodies detected the p19 and p24 gag-encoded core proteins in both serum and cerebrospinal fluid. Titers were tenfold higher by ELISA in serum than in cerebrospinal fluid, and some oligoclonal bands present in fluid were not seen in serum. Serum-cerebrospinal fluid albumin ratios were normal, and IgG indexes indicated intrathecal IgG synthesis. Histopathological changes showed a chronic inflammatory reaction with mononuclear cell infiltration, perivascular cuffing, and demyelination that was predominant in the lateral columns. In 1 patient, a retrovirus morphologically similar to HTLV-I on electron microscopy was isolated from spinal fluid. Our investigations show that endemic tropical spastic paraparesis in Jamaica is a retrovirus-associated myelopathy and that HTLV-I or an antigenically similar retrovirus is the causal agent.

Adolescent↗
PubMed1988

Tropical spastic paraparesis in Colombia.

A high-incidence focus of tropical spastic paraparesis (TSP) occurs on the South Pacific coast of Colombia. Of 55 patients studied, 52 (94.5%) had IgG antibodies to the human T-cell lymphotropic virus type I (HTLV-I) in serum and/or cerebrospinal fluid. Control groups did not show similar high positivity. Our results suggest that HTLV-I or other antigenically related retroviruses may be the cause of TSP in Colombia. Similar clinical, laboratory, and epidemiological findings have been reported in widely remote geographical regions of the world, with very similar clinical pictures of TSP in all high-incidence regions. The demonstration of IgG antibodies in serum and cerebrospinal fluid of patients with TSP in the Caribbean and Seychelles Islands, southern Japan, and the Ivory Coast indicate that the HTLV-I retrovirus could be the cause of this "tropical" myeloneuropathy.

Adolescent↗
PubMed1988

Epidemiology of tropical spastic paraparesis in Columbia and associated HTLV-I infection.

The clinical syndrome earlier designated as paraparesia espástica del Pacífico is an isolated form of tropical spastic paraparesis (TSP) that was reported in 1981 in the southern Pacific lowlands of Columbia in and near Tumaco. The clinical features are similar to those of TSP reported in Jamaica, Martinique, the Seychelles, and the Ivory Coast of Africa and resemble also those clinical features of the human T-lymphotropic virus type I (HTLV-I)-associated myelopathy described in southern Japan. Since HTLV-I infection is closely associated with TSP, we conducted a case-control study to evaluate the role of HTLV-I-associated risk factors among patients from the endemic focus in Tumaco, Colombia, and the seroprevalence rates of this virus in other geographical areas of the Pacific Colombian lowlands with and without TSP. From our seroprevalence study of antibodies to HTLV-I among TSP index patients, matched controls, household contacts (first- and second-degree relatives), and healthy controls from these areas, we found a strong association between HTLV-I and TSP. Also, there is a high seroprevalence of HTLV-I among sexual partners of patients and to a lesser extent among their offspring and other relatives some of whom had an early mean acquisition of antibodies to HTLV-I. Heterosexual promiscuity and other close interpersonal contact may play an important role in the transmission of TSP in the Pacific lowlands of Colombia.

Adolescent↗
PubMed1988

Seroprevalence of antibodies to HTLV-I in patients with chronic neurological disorders other than tropical spastic paraparesis.

Human T-lymphotropic virus type I (HTLV-I), the etiological agent of adult T-cell leukemia/lymphoma, also appears to be the cause of tropical spastic paraparesis, a chronic myelopathy reported in several different regions of the world. The prevalence of antibodies to HTLV-I in patients with chronic neurodegenerative disorders other than tropical spastic paraparesis and in patients with some muscle inflammatory disorders has been investigated. IgG antibodies to HTLV-I were measured in the sera and/or cerebrospinal fluid from 82 Guamanian patients with amyotrophic lateral sclerosis and parkinsonism-dementia, 164 Guamanian normal controls, 10 patients with kuru from the Eastern Highlands of Papua New Guinea, 4 patients with Viliuisk encephalomyelitis from the Iakut region of eastern Siberia, 45 Italian patients with multiple sclerosis, and 56 patients with polymyositis (49 from the United States and 7 from Jamaica). As determined by enzyme-linked immunosorbent assay, Western immunoblot, and gelatin particle agglutination techniques, serological evidence of HTLV-I infection was found in 1 patient with amyotrophic lateral sclerosis and 1 control subject from Guam, and in 1 patient from the United States and all 7 Jamaican patients with polymyositis. Except for the high seropositivity rate among the group of Jamaican patients with polymyositis, our data indicate that HTLV-I is an unlikely causative agent in the spectrum of the neurological diseases examined. The seropositivity of the 7 Jamaican patients with polymyositis requires further study.

Adult↗
PubMed1988

Antibodies to HTLV-I in populations of the southwestern Pacific.

Sera collected from 1,102 individuals in 14 populations of the southwestern Pacific between 1956 and 1979 were tested by ELISA for antibodies to human T-cell leukemia virus type I (HTLV-I). Selected sera were also tested by particle agglutination and immunoblotting. Six of the populations had prevalences of antibodies greater than 4%, two populations had prevalences greater than 15%. Six populations had antibody prevalences of 2% or less. Three populations from the coast and northern islands of New Guinea had high prevalences of antibodies, while three New Guinea highland groups had virtually none. One population from the Solomon Islands had a high prevalence, while two others had very low prevalences. Two populations from small remote islands in Vanuatu both had high prevalences. Pacific sera did not neutralize a standard strain of virus readily neutralized by Japanese, European, and American sera. We conclude that infections with HTLV-I, some acquired more than 20 years ago, are widespread throughout the southwestern Pacific, even in several very isolated populations, although others have been spared. Some strains of HTLV-I in populations of the Pacific may have substantially different envelope proteins from prototype strains of America, Europe, and Japan.

Adolescent↗
PubMed1988

Histochemical and X-ray microanalytical localization of aluminum in amyotrophic lateral sclerosis and parkinsonism-dementia of Guam.

Histochemical staining for aluminum, using Solochrome azurine or Morin, provided a rapid, simple and reliable means of identifying areas and structures of the brain of interest for closer scrutiny by X-ray microanalysis in patients with amyotrophic lateral sclerosis and parkinsonism-dementia of Guam. Neuronal perikarya, dendritic processes, and the walls of some cerebral vessels were aluminum positive by Solochrome azurine staining. In some cases, the deposition of aluminum was rather diffuse, particularly in the white matter. Fluorescent localization of aluminum using Morin was equally sensitive and specific, but provided less morphological detail than Solochrome azurine. Confirmation of histochemical detection of aluminum was achieved by examining adjacent tissue sections using wavelength-dispersive spectrometry coupled to a computer-controlled electron beam X-ray microprobe. Although the minimum detectable limits for aluminum by these histochemical procedures are unknown, the lower detection limit of our X-ray microanalytical technique is 10-100 ppm dry weight. Solochrome and Morin staining, as verified by X-ray microanalysis, afford a useful and reliable means of surveying multiple anatomical regions for aluminum deposition in naturally occurring and experimentally induced neurodegenerative disorders.

Adolescent↗
PubMed1987

Amyloid of neurofibrillary tangles of Guamanian parkinsonism-dementia and Alzheimer disease share identical amino acid sequence.

The presence of abundant intraneuronal amyloid in the form of neurofibrillary tangles (NFT) in the brains of Guamanian parkinsonism-dementia patients and the absence of extraneuronal amyloid in the form of vascular amyloid deposits or senile plaques permit the purification of NFT without contamination with extraneuronal amyloid. Thus, we have isolated and determined the amino acid sequence of the polypeptide subunit of the amyloid fibrils of these NFT and describe their ultrastructure. The NFT, which consist of single and paired helical filaments, similar to those of Alzheimer disease, and occasionally triple helical filaments, are composed of multimeric aggregates of a polypeptide of 42 amino acids (A4 protein). The relative molecular mass of the subunit protein, 4.0-4.5 kDa, is the same as the molecular mass of the amyloid of NFT, of the amyloid plaque cores, and of vascular amyloid deposits in Alzheimer disease and Down syndrome; the sequence of 15 amino acid residues at the N-terminus of the amyloid fibrils in the NFT of Guamanian parkinsonism-dementia is identical to that of the amyloid of NFT, amyloid plaque cores, and cerebrovascular deposits in Alzheimer disease and Down syndrome. Furthermore, the heterogeneity, or variation in polypeptide length, of the N-terminus of the amyloid of Guamanian parkinsonism-dementia is the same as in Alzheimer disease and Down syndrome. Our observations indicate that the brain amyloids of these diseases have a common subunit protein, which would also indicate a common pathogenesis.

Aged↗
PubMed1986

Amyotrophic lateral sclerosis and parkinsonism-dementia on Guam: a 25-year prospective case-control study.

Familial and genetic studies of high-incidence amyotrophic lateral sclerosis and parkinsonism-dementia among the Chamorro people of Guam were initiated in 1958 with the establishment of a prospective case-control registry. The major objective of this registry was to determine if first-degree relatives and spouses of patients with amyotrophic lateral sclerosis or parkinsonism-dementia had an increased risk of developing disease compared with relatives of nonaffected controls individually matched for age, sex, and village. At the time of its closing in 1963, the registry included 126 patients (77 with amyotrophic lateral sclerosis, 42 with parkinsonism-dementia, and seven with both amyotrophic lateral sclerosis and parkinsonism-dementia) and an equal number of controls; 994 living first-degree relatives (parents, siblings, and offspring) of patients and 1,218 of controls; and 88 living spouses of patients and 101 of controls. The present analysis of the 25-year follow-up study (1958-1983) demonstrated a significantly increased risk of developing amyotrophic lateral sclerosis or parkinsonism-dementia among parents, siblings, and spouses of patients, but not among relatives of controls. Offspring of both patients and controls showed no significantly increased risk of developing disease. The increased risk among spouses of patients and the lack of increase among their offspring, together with recent histochemical findings, support the contention that exogenous factors are strong contributors to the etiology of amyotrophic lateral sclerosis and parkinsonism-dementia. The present results also demonstrate a declining incidence of both diseases.

Aged↗
PubMed1986

Amyotrophic lateral sclerosis and parkinsonism-dementia on Guam: a 30-year evaluation of clinical and neuropathologic trends.

We reviewed the records of 279 Guamanian Chamorro patients with amyotrophic lateral sclerosis (ALS) and 293 patients with parkinsonism-dementia (PD), who had onset of symptoms between 1950 and 1979, to determine if there were changes in the clinical and neuropathologic features that might clarify the declining incidence rates in the past decade. There were no major temporal changes in the frequencies of physical findings or histopathologic features, but in the past three decades, an increase in age at onset was observed for both ALS and PD. There was also a shorter duration of illness in ALS and a longer duration in PD. Good correlation was found between the clinical and pathologic findings for both ALS and PD throughout this period.

Amyotrophic Lateral Sclerosis↗
PubMed1986

Observations on the clinical presentations and the neuropathological findings of amyotrophic lateral sclerosis in Australia and Guam.

Among 20 consecutive autopsies of amyotrophic lateral sclerosis (ALS) occurring in Caucasians in Western Australia (WA), 85% were males. The median age of onset was 58.9 years and the average duration of illness was 2.4 years. Twenty-two randomly selected ALS occurring among natives in Guam also showed a male predominance of 75%, younger age of onset (median 48.5 years) and longer survival period (median 3.4 years). 45% of the WA patients presented with bulbar involvement at the time of first examination. These patients had the lowest median survival period of 1.5 years when compared with the other forms of ALS, the classic upper and lower motor system involvement and progressive muscular atrophy. Theneuropathologic lesions of ALS in WA and Guam were similar with the exception that neurofibrillary tangles were frequently present in the Guamanian brains. In 14%, neuronal loss, gliosis and frequency of tangles in the cerebral cortex especially in Ammon's horn, substantia nigra, and locus ceruleus, were sufficiently severe to indicate the coexistence of another disorder, Parkinsonism-Dementia Complex. This condition was not clinically recognized. In the WA cases only one patient had tangles in the brain and he had concurrent Alzheimers disease. While senile plaques were present in this patient they were usually absent in the Guamanian brains.

Adolescent↗