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Biomedical subjects

R Gold

Publications and source records attributed to R Gold.

At least 163 records · Page 9Linked to original sources
PubMed1994

A trial of eye movement desensitization compared to image habituation training and applied muscle relaxation in post-traumatic stress disorder.

Thirty-six patients with PTSD were randomly allocated to individual treatment with imaginal exposure (image habituation training -- IHT), or applied muscle relaxation (AMR) or eye movement desensitization (EMD). Assessment by a blind independent rater and self-report instruments applied pre and posttreatment and at 3-month follow-up indicated that all groups improved significantly compared with a waiting list and that treatment benefits were maintained at follow-up. Despite a failure to demonstrate differences among groups, there was some suggestion that immediately after treatment EMD was superior for intrusive memories.

Adult↗
PubMed1994

Safety and immunogenicity of Haemophilus influenzae vaccine (tetanus toxoid conjugate) administered concurrently or combined with diphtheria and tetanus toxoids, pertussis vaccine and inactivated poliomyelitis vaccine to healthy infants at two, four and six months of age.

The safety and immunogenicity of Haemophilus influenzae vaccine (tetanus toxoid conjugate (PRP-T) administered concurrently in separate sites or mixed in the same syringe with diphtheria and tetanus toxoids, pertussis vaccine and inactivated poliomyelitis vaccine were assessed in 439 infants at 2, 4 and 6 months of age. The proportions with local redness, tenderness and swelling in the separate and combined groups were 18% vs. 11% (P < 0.001), 27% vs. 24% and 15% vs. 13%, respectively. Systemic reactions occurred at similar rates in both groups. The combined vaccine induced tetanus and diphtheria antitoxin titers > or = 0.01 IU/ml in 99.5 and 99.1% of infants, pertussis agglutinin titers > or = 64 in 92.4%, anti-polyribosylribitol phosphate titers > or = 0.15 microgram/ml in 93.8% and > or = 1.0 microgram/ml in 75% and polio-neutralizing titers > or = 8 in > 98% of infants. However, antibody concentrations to PRP-T, some pertussis antigens and tetanus toxoid were significantly lower after combined than after separate injections of DPT/diphtheria and tetanus toxoids, pertussis vaccine and inactivated poliomyelitis vaccine and PRP-T. The clinical significance of these differences is not known, but the interactions observed among the components of the pentavalent vaccine may be of concern because they might influence antibody persistence until the fourth dose is administered.

Diphtheria-Tetanus-Pertussis Vaccine↗
PubMed1994

Clinical and microbiologic features of children presenting with pertussis to a Canadian pediatric hospital during an eleven-year period.

To characterize the morbidity of pertussis in Canada, we did a retrospective review of all children with laboratory-confirmed pertussis seen at the Hospital for Sick Children, Toronto, between 1980 and 1990. A total of 975 patients were identified, of which 223 (23%) were admitted to hospital. The peak incidence of disease was observed in the fall. The incidence of disease did not vary with gender. Only 41% of children admitted had the classical symptoms of pertussis (paroxysmal cough and whoop). Compared with children older than 6 months of age, children younger than 6 months of age were more likely to be hospitalized, tended to be hospitalized longer, were less likely to be age-appropriately vaccinated and were more likely to require intensive care unit monitoring. Seventeen (8%) of 223 children required intensive care unit monitoring, and 12 of these children required mechanical ventilation therapy, for a duration of 3.5 +/- 0.6 days (mean +/- SD). One (0.1%) patient with secondary bacterial pneumonia died. This hospital-based study indicates that pertussis continues to be a cause of serious illness in children, particularly those younger than 6 months of age.

Age Distribution↗
PubMed1994

Eye-movement desensitisation. Symptom change in post-traumatic stress disorder.

A novel approach is described for the treatment of post-traumatic stress disorder (PTSD). Eye-movement desensitisation (EMD) requires the patient to generate images of the trauma in the mind and define physiological and emotional arousal states. While concentrating on these states, lateral multisaccardic eye movements are induced. Ten consecutive cases are reported who presented with symptoms originating from a range of traumas. The effectiveness of EMD in reducing symptoms outlined by DSM-III-R is described. An independent rater indicated that eight of the ten cases showed considerable improvement in PTSD symptoms following EMD, which was maintained at follow-up. Particular reference is given to the 'specificity' of EMD in treating symptoms and the changing pattern of effect at follow-up.

Adolescent↗
PubMed1994

[Therapy of acute polyradiculoneuritis (Guillain-Barré syndrome)].

The Guillain-Barre syndrome (GBS) is the most common cause of acute paralysis. It requires early institution of therapy to avoid life-threatening complications, to speed up recovery and minimize residual handicap. Advances in supportive care (treatment of infections, anticoagulation) and the introduction of intensive care (assisted ventilation, treatment of autonomic disturbances) have greatly improved the management of this disease and consequently its prognosis. A better understanding of the underlying immune mechanisms prompted pathogenetically oriented therapy. Plasma exchange and high dose intravenous immunoglobulin have been demonstrated in large controlled trials to hasten recovery in GBS. Problems of these studies are discussed and the presumed mode of action of these therapies is reviewed. Corticosteroids have shown no benefit. Ongoing trials are listed and future strategies for immunointervention are outlined.

Adrenal Cortex Hormones↗
PubMed1994

Differentiation between cellular apoptosis and necrosis by the combined use of in situ tailing and nick translation techniques.

BACKGROUND: A number of enzymatic techniques have recently been developed to detect DNA fragmentation in apoptosis at the cellular level. However, since DNA fragmentation also occurs in cellular necrosis, we studied to which extent the use of DNA polymerase (nick translation) or terminal transferase (tailing) allows the differentiation between internucleosomal DNA degradation, typical for apoptosis, and the more random DNA destruction in necrosis. EXPERIMENTAL DESIGN: We compared these techniques on in vitro and in vivo models for apoptotic or necrotic cell death. Apoptosis of thymocytes in vitro was induced by gamma-irradiation, necrosis by the cytotoxic action of antibody and complement. Cell death in vivo was examined on paraffin-embedded tissue material from animals with autoimmune encephalomyelitis that served as a model for apoptosis, or in kainic acid-induced nerve cell degeneration as a model for necrosis. RESULTS: DNA fragmentation was visualized by the incorporation of labeled nucleotides into the nuclei of affected cells utilizing tailing or nick translation techniques. In the early stages of cell degeneration in vitro, cells undergoing apoptosis were preferentially labeled by tailing, whereas necrotic cells were identified by nick translation. Similarly, early stages of necrosis in vivo were preferentially detected by nick translation, whereas tailing was slightly more sensitive for the detection of apoptosis. Results obtained with these enzymatic techniques were in accord with the assessment of cell death by morphologic criteria. Both techniques could be applied in tissue samples even after prolonged fixation in paraformaldehyde if the sections were pretreated with proteinase K digestion. CONCLUSIONS: Our studies show that both in situ nick translation and in situ tailing are useful in detecting DNA fragmentation in cell suspensions and tissue sections. These techniques may help to define the molecular mechanisms leading to cell death in experimental conditions and eventually in human tissue.

Animals↗
PubMed1993

Transforming growth factor beta expression in reactive spinal cord microglia and meningeal inflammatory cells during experimental allergic neuritis.

Experimental allergic neuritis (EAN), an inflammatory demyelinating disorder of the peripheral nervous system, is preceded and accompanied by a massive microglial reaction in the spinal cord which occurs in the absence of inflammatory cells infiltrating the cord parenchyma. Since transforming growth factor beta (TGF-beta) has been shown to play a beneficial role in experimental autoimmune disease and might be involved in the regulation of glial activity, we have investigated the expression of TGF-beta in EAN spinal cord and nerve root tissue. Adoptive transfer EAN was induced by the injection of neurotogenic T-cells specific for the P2 myelin protein. In normal spinal cord tissue, both TGF-beta 1 and TGF-beta 3 mRNA were constitutively expressed at low levels. Already 3 days following injection of P2-specific T-cells, TGF-beta 1 mRNA levels began to increase, peaked at day 6 at levels about tenfold above normal, and thereafter declined. TGF-beta 3 was induced even earlier with a sharp rise at day 3 and a peak fourfold above normal at day 4. In situ hybridization for TGF-beta 1 performed on spinal cord sections 6 days after injection of cells localized TGF-beta 1 mRNA to many nonneuronal cells with the typical morphology of microglia. In addition, TGF-beta 1 mRNA was observed in the meninges, and massive accumulation of signal was seen over inflammatory cells infiltrating the nerve roots. Our data indicate that TGF-beta 1 and -beta 3 are involved in regulating the glial response in EAN and that activated microglial cells might control their own activity state by expressing TGF-beta 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Microglial involvement in experimental autoimmune inflammation of the central and peripheral nervous system.

Microglial cells form a network of potential antigen presenting cells throughout the nervous system. Much progress has recently been made towards a better understanding of their immunological properties. This study examines their activation in 2 models of T cell-mediated autoimmune inflammation of the nervous system, experimental autoimmune encephalomyelitis (EAE) and its peripheral counterpart, experimental autoimmune neuritis (EAN), induced by the transfer of antigen-specific T cell lines. In both models microglial activation occurs at early stages of the disease. Activated microglial cells show an increased expression of MHC class I and II antigens. In EAE ultrastructural analysis revealed that MHC antigen expression is pronounced on perivascular microglial cells, suggesting this cell population may be important for antigen presentation at a site close to the blood-brain barrier. In contrast to EAE, the microglial reaction in EAN occurs at sites remote from the inflammatory response in the peripheral nerve, not only in the spinal cord but also in the terminal projection fields of primary sensory neurons in the lower brainstem. This early microglial activation in EAN suggests that a rapid and remote signaling mechanism can operate following peripheral inflammation. Immuno-electron microscopy revealed that activated microglial cells are also involved in the synaptic deafferentation of spinal cord motoneurons during autoimmune reactions. The rapid involvement of microglial cells in experimental autoimmune inflammation of the nervous system further points to their role as the main intrinsic immuneffector cell population of the central nervous system.

Animals↗
PubMed1993

Progression of myopathology in Kearns-Sayre syndrome: a morphological follow-up study.

We report on the progression of myopathology by comparing two biopsies from a patient with a Kearns-Sayre-Syndrome. The first biopsy was taken in 1979 and showed 10% ragged-red fibers. Myopathic changes were slight including internal nuclei and fiber splitting in 10% of the fibers. Electron microscopy revealed typical mitochondrial abnormalities with regard to number and shape. In 1989 a second biopsy was performed for an extended analysis of mitochondrial DNA. This time less than 5% of all fibers were ragged-red. Severe myopathic changes could be detected which so far has rarely been reported in mitochondrial cytopathy.

Blotting, Southern↗
PubMed1993

The use of monoclonal antibodies in diagnostic tests for Becker and Duchenne muscular dystrophy.

Monoclonal antibodies recognizing different epitopes of dystrophin have now been widely applied in diagnostic tests for Duchenne and Becker muscular dystrophy (BMD). The preservation of the C-terminus in BMD patients necessitates the routine use of one antibody raised against this region. Additional antibodies against deletion-prone regions of dystrophin further increase the diagnostic power of the tests. We describe two cases which illustrate that the combined use of different antibodies is necessary to avoid misdiagnoses of BMD at the protein level.

Adult↗
PubMed1993

Detection of DNA fragmentation in apoptosis: application of in situ nick translation to cell culture systems and tissue sections.

Since DNA fragmentation is a key feature of programmed cell death (PCD) and also occurs in certain stages of necrosis, we have adapted the methodology of in situ nick-translation (ISNT) to detect DNA fragmentation on a single-cell level. We first established the technique for cell preparations. Apoptosis was induced by gamma-irradiation on freshly isolated rat thymocytes. After fixation procedures, ISNT was performed by overnight incubation either with fluorescein-12-dUTP or with digoxigenin-labeled 11-dUTP and DNA polymerase I. The enzymatic incorporation of labeled nucleotides at sites of DNA fragmentation was detected by flow cytometry either directly or indirectly with fluorescein-conjugated anti-digoxigenin. The quantitative results demonstrated close correlation with morphological essays for apoptosis, DNA gel electrophoresis, and ISNT. Proliferating cells determined by bromodeoxyuridine immunofluorescence were not labeled by ISNT. Immunocytochemistry for cell surface antigens in combination with ISNT allowed the identification of specific cell types undergoing PCD. Furthermore, the simultaneous application of photolabeling techniques with ethidium monoazide and ISNT led to the identification of DNA fragmentation in cells with still intact membranes. Extending ISNT to tissue sections of paraformaldehyde-fixed, paraffin-embedded material reliably revealed labeling of cells with typical morphological features of apoptosis. However, this technique was not useful in detecting early stages of necrotic cell death.

Animals↗
PubMed1993

Apoptosis of T lymphocytes in experimental autoimmune encephalomyelitis. Evidence for programmed cell death as a mechanism to control inflammation in the brain.

In experimental autoimmune encephalomyelitis (EAE) myelin-specific T lymphocytes attack the myelinated tissue of the central nervous system (CNS). In the Lewis rat, EAE as a rule has an acute, monophasic course. With spontaneous clinical recovery the inflammatory CNS infiltrates are cleared from the nervous tissue within a few days. This is well in line with the remarkably low incidence of myelin-specific T cells present in EAE infiltrate. Combining immunocytochemical techniques, ultrastructural criteria and in situ nick translation we found up to 49% of T lymphocytes in EAE lesions showing signs of apoptosis at the time of recovery from disease. Our results suggest that apoptosis of T lymphocytes may be one possible mechanism to eliminate T lymphocytes from inflammatory brain lesions.

Animals↗
PubMed1992

Becker muscular dystrophy: detection of unusual disease courses by combined approach to dystrophin analysis.

The rapid progress of research on the structure of the dystrophin gene has enormously increased our understanding of the molecular basis of Duchenne (DMD) and Becker (BMD) muscular dystrophy. Apart from "classical" clinical presentations, asymptomatic or only mildly affected individuals with deletions in the dystrophin gene have now been reported. We describe two families which were initially classified as metabolic myopathies, until the diagnosis of atypical BMD was established after dystrophin analysis at the protein and DNA level. A modern diagnostic approach to myopathies should, therefore, not only include morphological and biochemical investigations, but also be extended to the analysis of the dystrophin gene.

Adolescent↗
PubMed1992

Muscle pathology correlates with permanent weakness in hypokalemic periodic paralysis: a case report.

We present a morphological follow-up in a case of familial hypokalemic periodic paralysis with progressive weakness. At age 12 years muscle biopsy revealed mild vacuolar changes. Seventeen years later, after the patient had developed permanent weakness, light and electron microscopy disclosed tubular aggregates in about 15% of the fibers and medium-grade myopathic alterations. We describe correlation of muscle pathology with permanent weakness in hypokalemic periodic paralysis.

Child↗
PubMed1992

Mycobacterial brain abscess possibly due to bacille Calmette-Guérin in an immunocompromised child.

Disseminated infection with bacille Calmette-Guérin (BCG) is rare, even in immunocompromised patients who receive BCG injections as immunotherapy or immunization. When such infection occurs, it is usually in patients with decreased cellular immunity. A 6-year-old Caucasian girl who was receiving maintenance chemotherapy for acute lymphoblastic leukemia presented with symptoms of meningitis. A temporal-lobe biopsy revealed acid-fast bacilli that were identified as Mycobacterium bovis BCG. Neither the patient nor any family members had been immunized previously. Appropriate therapy resulted in a complete recovery.

Biopsy↗