Implantable cardioverter defibrillators and fitness to drive.
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Aged↗
Biomedical subjects
M Anderson
Publications and source records attributed to M Anderson.
p53 mutation hotspot in radon-associated lung cancer.
Mutations in gene p53 are the most common defects in lung cancer and may be a pathway through which environmental carcinogens initiate cancer. We investigated p53 mutations in lung cancers from uranium miners with high radon exposure. 16 (31%) of 52 large-cell and squamous-cell cancers from miners contained the same AGG to ATG transversion at codon 249, including cancers from 3 or 5 miners who had never smoked. This specific mutation has been reported in only 1 of 241 published p53 mutations from lung cancers. The codon 249 mutation may be a marker for radon-induced lung cancer.
Case-Control Studies↗
Comparison of defolliculated oocytes and intact follicles of the cockroach using the vibrating probe to record steady currents.
Follicle cells were removed by dissection from early vitellogenic oocytes of the cockroach Blattella germanica. The vibrating probe was used to record steady currents from 19 defolliculated oocytes and 19 intact follicles of the same developmental stage. Defolliculated oocytes generated currents that were stable and distinguishable (by intensity or selective direction) from background reference values. Distributions of the intensities of reference values and experimental values were, in general, similar in both intact and defolliculated preparations. The patterns of currents generated by preparations recorded in the mid-sagittal plane were analyzed for both defolliculated oocytes (n = 8) and intact follicles (n = 10). The larger, generally more mature preparations in both groups generated patterns of current similar to the pattern seen in mid-vitellogenic follicles (focused inward near the germinal vesicle (GV), the presumptive ventral side, and broadly outward on the apo-GV side, the presumptive dorsal side). Smaller sized preparations in both groups showed inward or outward current on the apo-GV aspect and, typically, inward current at the GV. Only two defolliculated oocytes, and no intact follicles, appeared to generate outward current at the GV, and we believe this observation resulted from recording slightly outside the mid-sagittal plane. We conclude that preparations during early-vitellogenesis initially generate currents without an asymmetric pattern and that the inward flux at the GV is the first step in developing patterns of currents. The results suggest that the oocyte (and not the follicle cell epithelium) is responsible for generating the various patterns of currents observed in early-vitellogenic stages. At the end of early-vitellogenesis, the follicle cell epithelium begins to adhere tightly to the oocyte. The possibility is considered that the follicle cells may influence the currents generated during mid-vitellogenesis.
Animals↗
Near-microscopic magnetic resonance imaging of the brains of phenylalanine hydroxylase-deficient mice, normal littermates, and of normal BALB/c mice at 9.4 Tesla.
The near-microscopic resolution of the mouse brain, by magnetic resonance imaging (MRI) at 9.4 T, permits in situ examination of the entire brain and longitudinal studies of neural development. MRI can be utilized to reveal brain structure at a resolution of 100 microns in the X, Y, and Z planes of brain, to differentiate the gray from white (myelin-rich) matter, and to reveal the ventricular compartments. The present report describes the structure of normal BALB/c mouse brain as revealed by imaging at 9.4 T and by histological stains; the structure of normal brain is compared with that from a phenylalanine hydroxylase-deficient mouse mutant line (Pah(enu2)) and those from normal littermates. The brains of patients with phenylketonuria (PKU) were reported to have demyelination and other structural abnormalities revealed by magnetic resonance imaging (MRI). Therefore, high-resolution MRI was used to examine the brain of this mutant, an animal model for the study of human phenylketonuria. Our study revealed no evidence of demyelination or other abnormalities in the brains of Pah(enu2) mice. Histologically, the mutant and normal mouse brains appear similar. This is consistent with a recent study from our laboratory which demonstrated that the histology of the brain of an untreated male patient, who died with PKU at the age of 29, was similar to control brain with the exception of changes directly related to visual blindness and seizures experienced by the patient.
Adult↗
Myopathy with ragged red fibres following renal transplantation: possible role of cyclosporin-induced hypomagnesaemia.
A 65-year-old man developed a painless proximal myopathy 7 years after commencing cyclosporin therapy following a successful cadaveric renal transplant. Muscle histology showed ragged red fibres and biochemical studies suggested mitochondrial dysfunction. The possible pathogenesis of this mitochondrial myopathy, particularly its relationship to cyclosporin-induced hypomagnesaemia, is discussed.
Aged↗
Preexercise meal affects ride time to fatigue in trained cyclists.
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Bicycling↗
Type-specific human papillomavirus DNA in abnormal smears as a predictor of high-grade cervical intraepithelial neoplasia.
Human papillomavirus (HPV) typing and quantitation by polymerase chain reaction was performed on exfoliated cells from 133 women referred for colposcopy because of an abnormal smear. High levels of HPV 16 correctly predicted cervical intraepithelial neoplasia (CIN) grade II-III in 93% of its occurrences, but only 59% of cases of CIN III were associated with high levels of this type. Eighty-four per cent of CIN III lesions contained high levels of at least one of HPV types 16, 18, 31, 33 and 35, but the other types were less specific for CIN III than HPV 16. Overall HPV testing compared favourably with cytology for predicting high-grade CIN lesions, but it would appear that some combination of the two modalities will produce better performance than either alone. In particular, HPV testing appears to be helpful in determining which women with mildly abnormal smears have high-grade underlying lesions in need of immediate referral for colposcopy.
Base Sequence↗
Autosomal recessive hereditary sensory neuropathy with spastic paraplegia.
Five patients are described with a progressive sensory neuropathy in association with a spastic paraplegia and a mutilating lower limb acropathy. Disease onset was in childhood. Two pairs of siblings were both the offspring of normal consanguinous parents, suggesting autosomal recessive inheritance. The fifth case was sporadic; her parents were normal and non-consanguinous. Nerve biopsy in three patients showed an axonopathy with a loss of myelinated nerve fibres of all diameters and also of unmyelinated axons. In combination with the previous report by Cavanagh et al. (Brain 1979; 102: 79-94), the present patients establish the existence of an autosomal recessive form of hereditary sensory neuropathy with spastic paraplegia. There have been previous descriptions of a dominantly inherited form.
Adolescent↗
Complete genomic sequence and patterns of transcription of a member of an unusual family of closely related, chromosomally dispersed Ig gene clusters in Raja.
Ig genes in cartilaginous fish are organized in clusters. This unique form of organization suggests major differences in the regulation of the segmental rearrangement mechanism from that found in mammals and other higher vertebrates. The complete DNA sequence of an IgX-type cluster in the species Raja eglanteria is defined, and shown to consist of four rearranging segmental elements and three constant region exons. Using fluorescence in situ hybridization it is shown that Raja clusters are present at multiple sites within the genome, and that there is no apparent relationship between the chromosomally dispersed IgX clusters and a second isotype (IgM type) in this species. Comprehensive examination of sequence motifs associated with transcription regulation reveals an abundance of short sequences closely resembling those found in higher vertebrate Ig and other genes. However, the linear relationship of these motifs differs markedly from that associated with regulation of expression of the mammalian Ig gene locus. Additional studies of the transcription products of the IgX gene loci emphasize the diversity of transcription and processing of these genes. Considerable variation was noted in the processing of putative IgX transcripts, including the detection of a heretofore unrecognized form containing at least four additional Ig-like domains. These results have profound significance in terms of understanding the selective expression and the evolutionary diversification of Ig genes.
Animals↗
A patient with de Quervain's tenosynovitis: a case report using an Australian approach to manual therapy.
This case report describes a 41-year-old female patient who had chronic de Quervain's tenosynovitis, which had progressed to include involvement of the cervical spine, shoulder girdle, and upper extremity. The patient complained of aching over the left scapula, a band of pain around the upper arm, and sharp shooting pain in the forearm, with numbness and tingling in the fingers. On examination, she had abnormal palpatory findings in the cervical spine, the shoulder quadrant maneuver was limited, and the upper-limb tension tests (neural structures) were positive. The case report demonstrates the use of an Australian approach to manual therapy as described by Maitland. This approach includes (1) development, refinement, and rejection of working hypotheses as to the possible cause(s) of a patient's symptoms; (2) development of a long-range treatment plan; and (3) use of data from treatment responses to guide further treatment selection.
Adult↗
Neuro-ophthalmic manifestations of the syndrome of ophthalmoplegia, ataxia and areflexia. Observations on 20 patients.
The neuro-ophthalmological manifestations of 20 patients with the syndrome of ophthalmoplegia, ataxia and areflexia are described. The symmetrical nature of the ophthalmoplegia and the associated cerebellar ataxia point to centrally placed lesions. Several supranuclear, nuclear and internuclear ophthalmological signs are identified. Some of these, like partial sparing of the levator palpebrae and normal downgaze in the presence of severe ophthalmoplegia are noted too frequently to be just unusual signs of peripheral oculomotor dysfunction. Other identified features included upper lid retraction on attempted upgaze and preserved Bell's phenomenon in the presence of paralysis of the latter, as well as several other central ophthalmological signs. These findings contrast with those seen in the Guillain-Barré syndrome and, thus, the syndrome of ophthalmoplegia, ataxia and areflexia is not a mere variant of it.
Adolescent↗
Neuro-ophthalmic manifestations of the syndrome of ophthalmoplegia, ataxia and areflexia: a review.
Controversy regarding the nosological position of the syndrome of ophthalmoplegia, ataxia and areflexia (Miller Fisher syndrome) exists. The oculomotor dysfunction was presumed to represent an unusually symmetrical peripheral cranial nerve dysfunction. To investigate the neuro-ophthalmic manifestations in this rare syndrome we reviewed 109 reports describing 243 cases. The ophthalmoplegia was remarkable in its constant association with a cerebellar type ataxia. It was described to be remarkably symmetrical at all stages of development and recovery. From the early description of the syndrome by Fisher the ophthalmoplegia was observed to evolve as a symmetrical failure of upgaze followed by loss of lateral gaze and last by downgaze, recovery develops in the opposite pattern. Despite the severe nature of the ophthalmoplegia, 58 patients were reported to have sparing of downgaze and 192 (79%) had relative sparing of the eye lids. Active lid retraction and preserved Bell's phenomenon, despite upgaze paralysis, were described in 22 and 15 patients respectively. Upper lid jerks were described in 2, Parinaud's syndrome in 2, convergence spasm in 6, internuclear ophthalmoplegia in 15 and horizontal dissociated nystagmus in 11. Interestingly 23 were reported to present with paralysis of abduction progressing to lateral gaze paralysis and 5 had paralysis of abduction and contralateral gaze paralysis. Four had defective vestibulo-ocular reflex despite recovery of upgaze, 10 had central type nystagmus including rotatory, retractory and rebound nystagmus. Relative preservation of optokinetic nystagmus and preservation of vestibulo-ocular reflex despite an otherwise complete ophthalmoplegia were reported in 6 and 2 patients respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Blepharoptosis↗
Causes of death in racehorses over a 2 year period.
Necropsies were performed on 496 horses that had a fatal injury or illness at a California racetrack during the period February 20th 1990 to March 1st 1992. The primary cause of death was categorised by breed, activity at time of injury or illness and organ system affected. Most of the submissions were Thoroughbred horses (432) and Quarter Horses (46). Most of the injuries occurred while racing (42%) and in training sessions (39%); with fewer non-exercise (12%) and accident (7%) related injuries or illnesses. Musculoskeletal injuries accounted for 83% of the Thoroughbred and 80% of the Quarter Horse submissions. The Thoroughbred horses incurred 306 fractures with 263 in the limbs and 90% of those in the forelimbs. The proximal sesamoid bone(s), third metacarpal bone and humerus were the most common bones fractured in Thoroughbred horses and Quarter Horses. Other major causes of death included respiratory, digestive and multi-organ system disorders.
Age Factors↗
Mesalazine induced interstitial nephritis.
5-Aminosalicylic acid (5-ASA) has structural similarities to both phenacetin and aspirin, which are known to cause 'analgesic nephropathy'. Because of the increasing use of 5-ASA, this paper draws attention to two cases of severe interstitial nephritis resulting from 5-ASA and emphasises the importance of monitoring renal functions of patients with inflammatory bowel diseases who are receiving 5-ASA preparations.
Adult↗
Congenital insensitivity to pain: a 20 year follow up.
The exact nosological status of "congenital insensitivity to pain" remains in doubt. Possible pathological correlates of this clinical syndrome include sensory neuropathy, central lesions at the level of the reticular formation or dorsal horn of the spinal cord, or a central indifference to, or asymbolia for, pain. The reassessment of two members of a kindred previously reported more than 20 years ago as having congenital insensitivity to pain indicated that they in fact had an inherited sensory and autonomic neuropathy. Prolonged follow up and morphometric analysis of sequential nerve biopsies may be necessary to definitively establish this diagnosis.
Adult↗
Hypoxic induction of interleukin-8 gene expression in human endothelial cells.
Because leukocyte-mediated tissue damage is an important component of the pathologic picture in ischemia/reperfusion, we have sought mechanisms by which PMNs are directed into hypoxic tissue. Incubation of human endothelial cells (ECs) in hypoxia, PO2 approximately 14-18 Torr, led to time-dependent release of IL-8 antigen into the conditioned medium; this was accompanied by increased chemotactic activity for PMNs, blocked by antibody to IL-8. Production of IL-8 by hypoxic ECs occurred concomitantly with both increased levels of IL-8 mRNA, based on polymerase chain reaction analysis, and increased IL-8 transcription, based on nuclear run-on assays. Northern analysis of mRNA from hypoxic ECs also demonstrated increased levels of mRNA for macrophage chemotactic protein-1, another member of the chemokine superfamily of proinflammatory cytokines. IL-8 gene induction was associated with the presence of increased binding activity in nuclear extracts from hypoxic ECs for the NF-kB site. Studies with human umbilical vein segments exposed to hypoxia also demonstrated increased elaboration of IL-8 antigen compared with normoxic controls. In mice exposed to hypoxia (PO2 approximately 30-40 Torr), there was increased pulmonary leukostasis, as evidenced by increased myeloperoxidase activity in tissue homogenates. In parallel, increased levels of transcripts for IP-10, a murine homologue in the chemokine family related to IL-8, were observed in hypoxic lung tissue. Taken together, these data suggest that hypoxia constitutes a stimulus for leukocyte chemotaxis and tissue leukostasis.
Animals↗
Canine distemper epizootic in lions, tigers, and leopards in North America.
Canine distemper virus (CDV) infection occurred in captive leopards (Panthera pardus), tigers (Panthera tigris), lions (Panthera leo), and a jaguar (Panthera onca) in 1991 and 1992. An epizootic affected all 4 types of cats at the Wildlife Waystation, San Fernando, California, with 17 mortalities. CDV-infected raccoons were thought to be the source of infection in these cats. Two black leopards died at the Naibi Zoo, Coal Valley, Illinois, and 2 tigers died at the Shambala Preserve, Acton, California. Initial clinical signs were anorexia with gastrointestinal and/or respiratory disease followed by seizures. Canine distemper virus was isolated from 3 leopards, 3 tigers, and 3 lions that died or were euthanized when moribund. Monoclonal antibody testing identified the virus isolates as CDV. Gross and histopathologic findings were similar to those found in canids with distemper with a few exceptions. There were fewer lesions in the brain, and there was a pronounced type 2 cell proliferation in the lung, with inclusion bodies and CDV antigen demonstrated by immunohistology. Neutralizing antibody to CDV was found in high titers in serum from most animals but was absent or was found only in low titers in some cats that succumbed after CDV infection. There was a marked difference in neutralizing antibody titers when tests were done with different strains of CDV.
Animals↗
Ultrasonography: not useful in detecting susceptibility to malignant hyperthermia.
MH is a rare, potentially fatal complication of general anesthesia. Halothane-caffeine contracture testing of a muscle biopsy is the only accepted diagnostic test for MH. A previous report indicated that ultrasonography may aid in diagnosis of MH. Using sonographic examination of the thigh and calf, we evaluated eight patients with proved susceptibility to MH and eight control patients. Two radiologists independently evaluated the sonograms for echogenicity and definition of fascial planes. We detected no consistent and reliable differences between control and MH patients. We conclude that, in our hands, ultrasonography is not useful in differentiating patients with MH from normal persons.
Adipose Tissue↗