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Biomedical subjects

D Aframian

Publications and source records attributed to D Aframian.

12 recordsLinked to original sources

Histopathologic changes in dental and oral soft tissues in 2-butoxyethanol-induced hemolysis and thrombosis in rats*.

BACKGROUND: 2-Butoxyethanol (2-BE; ethylene glycol monobutyl ether) is extensively used as a solvent in surface coatings, such as lacquers, enamels, and varnishes in industrial and household cleaning products. Its major toxicity is manifested in the circulation, as it induces hemolytic anemia and thrombosis in various organs. While 2-BE has been implicated in the induction of anemia in different species, the rat has proven most sensitive, especially the female of this species. The purpose of this study was to document the effects of 2-BE on dentition, the periodontal ligament, the tongue, the salivary glands, and the oral mucosa in male and female Fischer 344 rats. METHODS: The experiment included 40 rats divided into five groups. Four groups were exposed to 2, 3, or 4 daily doses of 2-BE, and a fifth group served as control. The rats were killed on days 2, 3, 4, and 29. The teeth and soft oral tissues were prepared for histopathologic observation. RESULTS: The histopathologic analysis showed that the major effect of 2-BE was exerted on the odontoblasts of the incisors and on molars, with greater effect on the incisors. Foci of damaged muscle cells in the tongue were also observed. The blood vessels were dilated and congested, and a primary thrombosis was seen in the dental pulp. CONCLUSIONS: The results of this study revealed a resemblance between the dental injuries in this rat model and those seen in sickle cell anemia in humans. This 2-BE animal model holds potential to assist in the discovery of preventive measures and/or treatment for dental injuries that occur in human diseases with hemolytic anemia.

Anemia, Hemolytic↗

Oral manifestations of primary immunological diseases.

BACKGROUND: Primary immunodeficiencies have many oral manifestations. The clinical presentation of these diseases demonstrates the roles of different immune cells for the maintenance of oral health. METHODS: The authors reviewed selected literature describing systemic and oral manifestations of the primary immunodeficiencies published between 1966 and 1999. RESULTS: The authors found that oral candidiasis and herpetic infections are seen frequently in patients with T-cell deficiencies, while patients with B-cell deficiencies are most susceptible to bacterial infections. Periodontitis and oral candidiasis are found in some, but not all, phagocyte deficiencies. CONCLUSIONS: These findings demonstrate that T cells, B cells and phagocytes all have roles in oral immunity. CLINICAL IMPLICATIONS: Acquired conditions that affect the immune system such as diabetes, alcoholism and acquired immunodeficiency syndrome, as well as certain medications, will affect oral defense mechanisms. The effects that acquired immunodeficiencies will have on oral health can be predicted from the oral manifestations of primary immunodeficiencies.

B-Lymphocytes↗

[Oral manifestations of bulimia nervosa].

Bulimia nervosa (BN) is an eating disorder frquently accompanied by changes of the hard and soft tissues of the oral cavity and of the salivary glands. Routine dental examination in a 25-year-old woman disclosed oral signs and symptoms characteristic of BN and she was referred for psychiatric evaluation. Oral evaluation of patients suspected of BN is recommended to prevent irreversible damage to the oral and perioral structures.

Adult↗

[Ramsay Hunt syndrome--differential diagnosis, pathogenesis and therapy].

Ramsay Hunt syndrome is caused by infection of the geniculate ganglion of the seventh cranial nerve by varicella-zoster virus. A case in an 82-year-old woman is described. She presented with oral lesions, right facial palsy and an eruption and pain in her right ear. Oral examination revealed small circumscribed erosions on the right anterior two-thirds of the tongue, with loss of taste. There were also lesions on her right palate. Early diagnosis and treatment are important as immediate treatment is more likely to prevent irreversible complications affecting the facial and other cranial nerves involved.

Acyclovir↗

Retinoid regulation of interleukin-2 receptors on human T-cells.

The ability of retinoids to regulate interleukin-2 receptor (IL-2R) levels on human T-cells may play a fundamental role in the immunomodulating effects of these compounds. As a cell line model for studying this phenomenon, we tested the effects of retinoic acid (RA) on the expression of IL-2Ralpha and IL-2Rbeta in Hut78 cells, a mature T-cell line derived from a Sezary T-cell leukemia. Our results demonstrated 4- to 20-fold increases in the surface expression and mRNA levels of both of these receptor components at RA concentrations starting at 10(-10) M with maximal induction at 1 microM RA. RA-induced upregulation of IL-2Rbeta was found to be transcriptionally mediated in a protein-synthesis-independent fashion; however, activation of the IL-2Rbeta promoter could not be demonstrated in transient transfection experiments utilizing reporter gene constructs containing all currently known regulatory elements of the IL-2Rbeta promoter. Enhancement of IL-2Ralpha/beta by RA was accompanied by upregulation of the expression of CD38, CD69, CD45RO, and HLA-DR, surface molecules known to be associated with T-cell activation. Parallel effects were induced by RA on T-blasts generated from primary human lymphocytes suggesting the physiologic relevance of the Hut78 cell line model. Taken together, our findings demonstrate the ability of RA to upregulate IL-2R expression and enhance the activation state of Hut78 cells. The dramatic enhancing ability of RA on IL-2Rbeta expression does not appear to be mediated through interaction with currently defined regions of the IL-2Rbeta promoter.

Cell Nucleus↗

Down-regulation of human tumor necrosis factor-beta gene expression by cells with suppressive activity.

Human TNF-beta (lymphotoxin) gene expression is down-regulated by immunosuppression. Induction of TNF-beta mRNA in lymphoid cells is greatly enhanced by gamma-irradiation, cyclophosphamide and cimetidine, agents that each inhibit activation of suppressive cells. The level of TNF-beta mRNA expressed in response to stimulation, whether by mitogen or antigen, is reduced strongly by concomitant activation of suppressive cell subsets. Removal of CD8 or CD11b cells leads to a pronounced superinduction of TNF-beta mRNA in the depleted cell population. Induction of TNF-beta mRNA precedes appearance of suppressive cell activity, allowing for temporary expression. The TNF-beta gene is as sensitive as IFN-gamma and IL-2 genes to suppression. Hence, three genes characteristically expressed in Th1 cells, encoding IL-2, IFN-gamma, and TNF-beta, are similarly regulated by cell-mediated suppression. Actual levels of TNF-beta during an immune response are determined by the balance between activities of expressing and suppressing cell subsets, both transiently manifested.

CD8 Antigens↗

Necrotizing Sialometaplasia after Silastic Ring Vertical Gastroplasty: Case Report and Review of Literature.

Necrotizing sialometaplasia (NS) is a self-limiting benign condition of unknown origin that affects mainly the minor salivary glands on the hard palate. In its clinical and histological appearance, it mimics malignancy. This report presents a patient with NS who suffered from frequent bouts of vomiting subsequent to silastic ring vertical gastroplasty which resulted in remarkably low pH of the oral cavity. The literature pertaining to NS appearing in conjunction with gastrointestinal disorders was reviewed, and the possible contribution of recurrent emesis to the pathogenesis of NS is discussed.

Journal Article↗

Role of autoimmunity in contralateral delayed endolymphatic hydrops.

Contralateral delayed endolymphatic hydrops is described as the development of fluctuating hearing loss and episodic vertigo in a normal ear years following sensorineural hearing loss in the opposite ear. This condition is a variant of delayed endolymphatic hydrops in which new symptoms of severe episodic vertigo develop years later in an ear that has lost most or all of its hearing. The possible etiologies of these two conditions are unknown and may be different. This report presents seven cases of the contralateral form of this disease and experimental evidence that suggests that these patients may be suffering from the initiation of an autoimmune event directed against the remaining inner ear. In Western blot analysis, their serum was reacted against cow cochlear inner ear antigen preparations, and six of the seven cases had serum antibodies directed against a 68 or a 35-36 kilodalton (kd) molecular weight antigen in contrast to three of 43 normal controls (p < .001 Fisher's exact test), the significance of which had previously been reported for autoimmune inner ear disease.

Adult↗

Orbital impalement by a gearshift knob: case report.

Penetrating trauma to the orbit may cause complex injuries involving the bone, globe, and brain. Successful treatment requires a strategic scheme for preoperative assessment and management and a multidisciplinary surgical approach. These principles are demonstrated by report of a motor vehicle accident in which the driver sustained orbital impalement by a gearshift knob.

Accidents, Traffic↗

Destabilization of junctional ACh receptors by a reinnervating frog motor nerve.

The distribution of ACh receptors (AChRs) in neuromuscular junctions of the frog cutaneous pectoris muscle has been investigated at various times after denervation, as the motor nerve regenerates to reinnervate the junctions. Original extent of synaptic gutter is judged by the distribution of ACh esterase, which is compared with the staining pattern of rhodamine-labelled alpha-bungarotoxin. It is found that within 8-10 days after the beginning of reinnervation, many junctions show loss of AChR from large stretches of original gutter, in contrast to other regions, which still have a high density of receptors. This loss of receptor does not happen if the muscle remains denervated. It is suggested that the innervated portions of the junctions retain AChR, while the receptors in uninnervated portions are destabilized and rapidly lost. These findings indicate a powerful role for the nerve in eliminating both extrajunctional receptors and junctional receptors that are not stabilized by the direct action of an overlying nerve. One can imagine that a similar removal of AChR or other important synaptic molecules from gutters that are innervated later or by a terminal of lower efficacy might account for the competitive elimination of certain inputs and retention of others during development of reinnervation.

Acetylcholinesterase↗