Search PubMed⌕ Search

Biomedical subjects

J R Taylor

Publications and source records attributed to J R Taylor.

At least 127 records · Page 7Linked to original sources
PubMed1993

Ultrastructural studies bearing on the mechanism of UVB-impaired induction of contact hypersensitivity to DNCB in man.

In both murine and human experimental systems, acute, low dose exposure of skin to ultraviolet B light (UVB) impairs the induction of allergic contact dermatitis (ACD) by haptens such as dinitrochlorobenzene (DNCB) in a significant proportion of individuals. By light microscopy, epidermal Langerhans cells (LC) have been reported to be depleted by UVB exposure as well as by epicutaneous hapten application, implying that LC may be the locus of action of the effects of both UVB and DNCB. However, light microscopy can not readily distinguish cell density changes secondary to LC necrosis from changes resulting from down-modulation of expression of LC surface molecules. Using a highly sensitive immunogold electron microscopic approach, we have evaluated the differential effects of UVB and/or DNCB on human epidermal LC. The results reveal that DNCB alone caused significant up-regulation of cell surface HLA class II expression on a very small number of LC, the major fraction of LC expressing normal levels of HLA class II. Furthermore, DNCB alone caused a modest reduction in the density of LC at the treated sites without evidence of cell necrosis. Treatment with UVB alone or UVB exposure followed by DNCB resulted in a reduction in the density of LC, with widespread evidence of LC necrosis. However, the few remaining intact LC were all intensely HLA class II-positive after UVB exposure followed by DNCB, whereas treatment with UVB alone did not result in changes in LC HLA class II expression. The findings that after DNCB painting only a small proportion of the LC were strongly HLA class II-positive, but after UVB exposure followed by DNCB all intact LC displayed significant up-regulation of cell surface HLA class II expression, imply that UVB exposure inhibits the migration of epidermal LC. This is consistent with the view that DNCB fails to induce ACD when hapten is painted on UVB-exposed skin because insufficient LC are available to initiate T cell activation in the draining lymph node.

Cell Count↗
PubMed1993

Neck sprain.

Neck sprain is characterised by 'soft tissue' lesions in the cervical discs, synovial joints, muscles and sometimes the nerve roots. Peripheral nociception in the outer annulus, joint capsules, muscles, meninges, arteries and nerves can cause neck pain, with headache, or upper torso and upper limb pain. Careful physical examination, or accurately placed local anaesthetic injections, may localise the sources of pain.

Cervical Vertebrae↗
PubMed1993

How to design a mental health system.

1. In 1989, mental illness costs increased an estimated 57% compared with a 17% increase in overall medical costs. Almost one half of U.S. workers felt stressed in 1991, and one fourth believed they suffered from work related illnesses. 2. The goal of health care cost management is to eliminate unnecessary and ineffective care. 3. Mental health/chemical dependency strategies should be integrated into an organization's other prevention programs. 4. A mental health plan must be designed in keeping with the individual nature of mental illness.

Humans↗
PubMed1993

Acute injury of the neck: anatomical and pathological basis of pain.

Headache, upper torso and upper limb pain can all originate in lesions of the cervical spine. The pain distribution is similar whether the cause is traumatic or degenerative. Nociceptive fibres are present in many cervical spine structures including the disc annulus, facet joint capsules, muscles, meninges, arteries, nerve roots and dorsal root ganglia. Such nerves are not present in the disc nucleus, facet articular cartilages and the ligamentum flavum. Central nervous connections between the trigeminal nucleus and upper cervical sensory input provide an explanation for some forms of headache and facial pain. This paper focuses on neck sprain from road traffic accidents as a cause of pain. Similar lesions are seen in the cervical spines of those who die immediately and survivors who die some years after a neck injury, from unrelated causes. Both discs and facet joints are injured. The common disc injury is a "rim lesion" or transverse tear near the anterior vertebral rim. It is caused by distraction and shearing in sudden extension. Both the posterior disc and the facets are compressed, causing disc contusion or herniation, facet haemarthroses, bruising around the C2 nerve, or fractures of articular processes. Suboccipital vascular congestion and annulus calcification are also seen in the "survivors". Chronic pain develops in 20-40% of the "survivors". The reasons include altered spinal mechanics, neural damage and vascular changes. Management must always start with an accurate diagnosis based on a history and physical examination. Simple investigations such as extension X-rays may reveal vacuum clefts in the same anatomical position as rim lesions. Nuclear scans detect increased uptake at damaged end plates or facet fractures.(ABSTRACT TRUNCATED AT 250 WORDS)

Accidents, Traffic↗
PubMed1992

Analysis of effects of ultraviolet B radiation on induction of primary allergic reactions.

Acute, low-dose exposure to UVB light reveals a genetic polymorphism in humans with respect to the ability of irradiated skin to support the induction of contact hypersensitivity (CH) to dinitrochlorobenzene (DNCB). In healthy adult caucasians, as well as in humans with deeply pigmented skin, approximately 45% fail to develop CH when DNCB is painted on UVB-irradiated skin; these individuals are termed "UVB susceptible" (UVB-S), whereas those who develop CH at the challenge site are termed "UVB resistant" (UVB-R). The UVB-S trait is characteristic of virtually all patients with biopsy-proved basal/squamous cell cancer, and may therefore be a risk factor for this disease. We have investigated the effects of UVB on expression of primary allergic reactions (PAR) in healthy caucasian and black-skinned adults, as well as patients with skin cancer. Among UVB-R caucasians, very few (less than 25%) developed PAR at site exposed to UVB, whereas among black-skinned UVB-R subjects, all displayed a PAR at the UVB irradiated site. To determine whether the lack of PAR in UVB-R caucasian subjects was systemic or local in origin, DNCB was applied to UVB-exposed buttock skin, and each individual was then challenged with dilute DNCB on forearm skin twice: 11 and 30 d thereafter. When inflammatory responses were evaluated at the original hapten application site, as well as both challenge sites, complete concordance was observed between positive challenge reactions at 30 d (UVB-R) and positive challenge reactions at 11 d, whereas only one caucasian subject displayed a PAR at 12 d. Thus, UVB-R caucasians can display CH as early as 11 d following hapten application to UVB-treated skin, indicating that their failure to display PAR is a local, rather than a systemic, effect of UVB. Because UVB-induced phototoxicity was significantly greater in caucasian than in deeply pigmented skin, it is anticipated that phototoxicity leads to rapid hapten "washout" from UVB-exposed caucasian skin. We propose that PAR usually do not occur in UVB-treated caucasian skin because insufficient hapten remains at the site to trigger a spontaneous inflammation when systemic hapten-specific immunity emerges.

Adult↗
PubMed1992

Transforming growth factor-beta differentially regulates the adhesiveness of normal and psoriatic dermal microvascular endothelial cells for peripheral blood mononuclear cells.

Lymphocytes adhere to dermal microvascular endothelial cells (DMEC) as the first step in their migration from the bloodstream into diseased skin. Psoriasis is characterized by an intense T-lymphocytic infiltrate in the dermis, which may be a consequence of the abnormal regulation of endothelial adhesiveness by cytokines released locally. In the present study, we investigated the effects of tumor necrosis factor-alpha (TNF), interleukin-1 (IL-1), IL-4, and transforming growth factor-beta 1 (TGF-beta) on the adhesiveness of DMEC isolated from psoriatic plaques or normal skin for human peripheral blood mononuclear cells (PBMC). The results showed that DMEC from both normal and psoriatic skin retain the capacity to adhere to 51Cr-labeled PBMC. Pretreatment of DMEC from normal skin with human recombinant IL-1 or TNF alone or in combination for 8 h significantly (p less than 0.01) enhanced their capacity to adhere to human PBMC. Similarly, treatment of normal DMEC with IL-4 also increased endothelial adhesiveness, although this cytokine required an incubation period of 24 h. In parallel studies, DMEC from psoriatic plaques were found to respond to the stimulatory effects of TNF, IL-1, and IL-4 in similar dose- and time-dependent manner. In contrast, although pretreatment of normal DMEC with TGF-beta (0.1 to 0.25 ng/ml) for 6 to 12 h significantly reduced (p less than 0.01) both the unstimulated and IL-1- and TNF-stimulated endothelial adhesiveness for normal PBMC, TGF-beta had no effect on the binding of unstimulated or cytokine-stimulated psoriatic DMEC to PBMC, even at concentrations as high as 2 ng/ml and incubation period of 36 h. These results suggest that cytokines stimulate the adhesiveness of DMEC through distinct pathways and provide evidence that TGF-beta may play an important regulatory role in the control of lymphocyte extravasation into normal skin. The altered responsiveness of psoriatic DMEC to TGF-beta may contribute to the intense dermal lymphocytic infiltrates in psoriasis.

Cell Adhesion↗
PubMed1992

Effects of chloroquine on antigen-presenting functions of epidermal cells from normal and psoriatic skin.

The lysosomotropic drug chloroquine has been added to cultures containing peripheral blood mononuclear cells (PBMC) and allogeneic antigen-presenting cells obtained from the epidermis of normal human skin or from skin of patients with psoriasis. We found that in the presence of chloroquine, the allostimulatory properties of freshly obtained, normal epidermal antigen-presenting cells (EAPC) were profoundly impaired. By contrast, normal EAPC (cultured for 72 h prior to exposure to alloreactive T cells), as well as fresh EAPC from psoriatic skin were not impaired by chloroquine. In fact, in some experiments, cultured EAPC and psoriatic EAPC in the presence of chloroquine displayed significantly enhanced abilities to activate allogeneic T cells. Moreover, chloroquine partially reversed the inhibitory effect of transforming growth factor-beta (TGF beta) on T-cell activation induced by cultured normal EAPC. Fresh normal EAPC, which are normally impervious to the effects of TGF beta, were not protected by TGF beta from chloroquine inhibition. We conclude that the addition of chloroquine to tissue culture medium unmasks important differences in antigen processing and presenting properties of fresh, normal EAPC, on the one hand, and cultured normal EAPC and psoriatic EAPC on the other. The ability of chloroquine to exaggerate the accessory cell function of the latter cells may relate to the capacity of this drug to cause the secretion of acid hydrolases into their immediate microenvironment. Moreover, the capacity of chloroquine to enhance the accessory cell functions of freshly obtained psoriatic EAPC emphasizes an abnormality that psoriatic cells in the epidermis constitutively express. We postulate that this abnormality may be related to the clinical observations that psoriatic skin lesions may be induced or aggravated by chloroquine therapy.

Antigen-Presenting Cells↗
PubMed1992

Cumulative sunlight exposure and the risk of developing skin cancer in Florida.

Epidemiologic evidence suggests that the risk of developing skin cancer is higher in certain geographic regions where sunlight is excessive. Even in such high risk regions, two distinct populations of long-term residents exist: people with, and people without skin cancer. We have compared the quantitative lifetime sunlight exposure between 11 nonmelanoma skin cancer patients who have lived in South Florida for 23.7 +/- 5.1 years and 9 age-matched normal, healthy individuals who have lived in South Florida for 23.4 +/- 4.1 years. An estimation of personal cumulative sunlight exposure was determined for each subject from data collected through detailed interviews. We found that there was no detectable, significant quantitative difference in cumulative sunlight exposure during life between these two groups. Because these individuals had previously been phenotyped for the effects of ultraviolet-B (UVB) radiation on induction of contact hypersensitivity, our results suggest that UVB-susceptibility may be a better indicator of skin cancer risk than cumulative lifetime sunlight exposure. Thus, although there is little doubt that sunlight exposure is an important factor in the development of skin cancer, our results emphasize the importance of host genetic factors in the pathogenesis of this disease.

Aged↗
PubMed1992

Human intervertebral disc acid glycosaminoglycans.

Alcian blue critical electrolyte concentration (CEC) staining of intervertebral discs (annulus and nucleus of cervical, thoracic and lumbar discs) distinguished 3 groups where CEC staining correlated with age (less than 3 months; from 3 months to 5 years; over 10 years). The CEC increased markedly (implying increased sulphation of the glycosaminoglycans) in the period of maturation (fetal life to 10 years) and then remained constant throughout adult life. This is at variance with accepted views which attribute such changes to degenerative changes in old age. The major part of the CEC increase occurred after the disappearance of blood vessels from the disc, which is almost complete by 4 years. Our results are compatible with the hypothesis that keratan sulphate replaces chondroitin sulphate, functionally, in conditions of oxygen lack.

Adult↗
PubMed1991

Neck injuries.

Explore the source record for details and available documents.

Accidents, Traffic↗
PubMed1991

Altered membrane anisotropy gradients of plasma membranes of living peripheral blood leukocytes in aging and Alzheimer's disease.

Several reports have suggested that membrane rigidity, a term that refers to the relative motion of membrane constituents, is decreased in Alzheimer's Disease. Accordingly, a series of fluorescent membrane probes was used to evaluate the rigidity from the surface to the center of the outer hemi-leaflet of the plasma membrane of living neutrophils, monocytes and lymphocytes. Anisotropy, a parameter which increases with increasing membrane rigidity, was calculated from flow cytometric measurements of vertically and horizontally polarized components of the fluorescence emission of the probes. These preliminary experiments suggest that whereas membrane rigidity in certain regions of the plasma membrane of peripheral blood leukocytes is increased as expected in elderly controls, it is decreased in Alzheimer's disease.

Aging↗
PubMed1991

Efficacy of bladder training in older women with urinary incontinence.

The efficacy of bladder training was evaluated in a randomized clinical trial involving 123 noninstitutionalized women 55 years and older with urinary incontinence. Subjects were urodynamically categorized as those with urethral sphincteric incompetence (N = 88) and those with detrusor instability with or without concomitant sphincteric incompetence (N = 35). Bladder training reduced the number of incontinent episodes by 57%; the effect was similar for both urodynamic diagnostic groups. The quantity of fluid loss was reduced by 54%. This was greater for patients with detrusor instability than for those without it. Diurnal and nocturnal voluntary micturitions were also reduced. The effect on nocturnal micturition, however, was not observed in subjects with unstable detrusor function. It is recommended that bladder training be considered as an initial step in treatment of women with urinary incontinence. Provided prior comprehensive clinical evaluation is done, it can be prescribed without the need for urodynamic characterization.

Aged↗
PubMed1991

Grafting of fetal substantia nigra to striatum reverses behavioral deficits induced by MPTP in primates: a comparison with other types of grafts as controls.

Fetal substantia nigra (SN) cells were transplanted into the caudate nucleus (CN) of four vervet monkeys (Cercopithecus aethiops sabaeus) that had been treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). MPTP treatment appears to produce a syndrome similar to that observed in patients with idiopathic Parkinson's disease. Normal and parkinsonian behaviors were quantitated by trained observers 5 days/week. Twenty-eight behaviors based on previous factor analyses were individually scored and rated. Parkinsonian signs included freezing, head and limb tremor, difficulty in eating, delayed initiation of movement, poverty of movement, tremor that stopped with intention, decreased response to threats, and lying immobile in the cage. These signs were combined to give an overall rating of parkinsonism. A summary measure of 'normal' healthy behavior was also examined, including such behaviors as yawning, scratching, self-grooming, shifting, and eating. Overall ratings of parkinsonism increased and those of healthy behavior decreased after MPTP. In the 4 monkeys grafted with fetal SN cells into the CN, behavior returned to pre-treatment levels by the time of sacrifice (2, 5, or 7.5 months after grafting). Three control subjects were transplanted with either SN cells into an inappropriate brain site (cortex) or inappropriate, non-dopaminergic, cells (cerebellar) into the CN. Subjects were also compared with three control animals that did not receive MPTP but received cryopreserved or fresh SN and other cells into the CN. Only MPTP-treated subjects that received SN cells into the CN showed evidence of a reversal of the MPTP syndrome after transplantation. In addition, grafting in animals that were not MPTP-treated did not appear to affect behavior. This paper reports the specific behavioral effects of severe MPTP toxicity that were or were not reversed after transplantation and suggests that only fetal SN cells grafted into the CN may be able to reverse behavioral deficits in MPTP-treated monkeys.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1991

Lumbar facet joint fat pads: their normal anatomy and their appearance when enlarged.

The polar recesses, superior and inferior to lumbar facet joints, are filled by fat pads from which fat-filled synovial folds project between the articular surfaces for a distance of two to four millimetres. The intracapsular superior recess lies between the ligamentum flavum and the lamina above. The extracapsular inferior recess lies on the back of the lamina below and communicates with the joint through a hole in the inferior capsule. The intracapsular folds move freely in and out of the joint during movements. These features are demonstrated in anatomic studies using transverse sections and radiologic studies using computed tomography. In about 4% of lumbar spines examined, the intraarticular fat pads are enlarged and extend from the joint recess(es) into the middle third of one or more facet joints. The fat pads can be identified in CT scans by their radiolucency and distinguished from vacuum phenomenon by measuring their attenuation values. The cause of the intra-articular enlargement of the fat pads is unknown, but it is suggested that their extension into the middle third of the joint may be secondary to degenerative change in the motion segment with capsular laxity in the affected joint.

Adipose Tissue↗
PubMed1991

Yohimbine co-treatment during chronic morphine administration attenuates naloxone-precipitated withdrawal without diminishing tail-flick analgesia in rats.

Noradrenergic neuronal hyperactivity following chronic morphine administration has been postulated to cause withdrawal signs and symptoms. Suppression of this hyperactivity, for example, by clonidine attenuates withdrawal. It might follow, therefore, that the prevention of suppression of noradrenergic systems during chronic morphine administration might diminish hyperactivity and prevent withdrawal. If the normalization of noradrenergic activity during opioid administration did not also suppress analgesia, it might be of medical and theoretical interest. To test this hypothesis, we gave the alpha-2-antagonist yohimbine to rats in order to increase noradrenergic activity during morphine treatment and then subsequently precipitated morphine withdrawal with naloxone. Six groups were examined: saline controls (N = 11), morphine (N = 11), morphine + 2.0 mg/kg/day yohimbine (N = 15), morphine + 3.0 mg/kg/day yohimbine (N = 5), 2.0 mg/kg/day yohimbine (N = 11) and 3.0 mg/kg/day yohimbine (N = 5). Subjects received 75 mg morphine pellets implanted on day 1,4 and 6 of the treatment or sham implantation. Yohimbine was delivered throughout the morphine treatment by subcutaneously implanted osmotic pumps. On day 7, all subjects were given 1.0 mg/kg naloxone and rated for behavioral signs of withdrawal. Analgesia was measured by observing tail flick latencies (TFL) before and after chronic drug treatments. Naloxone-precipitated withdrawal was characterized by irritability, ptosis, penile erection, diarrhea, rhinorrhea, abnormal posture, wet-dog shakes, jumping, and teeth chattering, none of which were observed in groups receiving only saline or yohimbine. Withdrawal behavior was attenuated in a dose-dependent manner when yohimbine was administered during morphine treatment but analgesia was not attenuated.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗
PubMed1991

Potentiation of the effects of reward-related stimuli by dopaminergic-dependent mechanisms in the nucleus accumbens.

Three experiments examined the behavioural, pharmacological and neural specificity of the previously reported potentiation of responding with conditioned reinforcement following intra-accumbens d-amphetamine, by studying the effects of intra-accumbens dopamine (DA) and noradrenaline, using an acquisition of a new response procedure. In experiment 1, the effects of intra-cerebral DA infusions (5, 20, 50 micrograms/2 microliters) were compared in four conditions: (i) intra-accumbens DA following positive pairing of the conditioned stimulus (CS) and water during training; (ii) as (i) but also following a systemic dose of the DA receptor antagonist alpha-flupenthixol; (iii) intra-accumbens DA following random pairing of the CS and water during training; and (iv) as (i) but with intra-caudate rather than intra-accumbens DA. The results showed that only with intra-accumbens DA in the positive pairing condition was there a significant dose-dependent increase in responding. In experiment 2, the effects of a higher range of doses (20, 100, 200 micrograms) and smaller infusion volume (5, 25, 50 micrograms/l microliters) of intra-accumbens DA were studied, in comparison with a similar range of doses (5, 25, 50 micrograms/l microliters) of intra-accumbens noradrenaline (NA). Only DA produced a selective, dose-dependent increase in responding with conditioned reinforcement. In experiment 3 neurotoxic lesions of the dorsal noradrenergic bundle (DNAB) using 6-hydroxydopamine producing profound (about 90%) depletion of cortical and nucleus accumbens NA levels had no effect on the increased responding with conditioned reinforcement produced by intra-accumbens d-amphetamine (3, 10, 30 micrograms/l microliters).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗