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Biomedical subjects

M W Finkelstein

Publications and source records attributed to M W Finkelstein.

At least 19 recordsLinked to original sources
PubMed2000

Acquired tufted angioma: a unique vascular lesion not previously reported in the oral mucosa.

We describe two patients with acquired tufted angioma, a unique vascular lesion not previously reported in the oral mucosa. In one patient, the lesion manifested as a purple-red papule and, in the other, as a blue submucosal swelling. Both lesions were non-painful and neither was associated with a history of trauma. The histopathological features consisted of scattered, irregularly shaped tufts, primarily composed of poorly formed capillary spaces and slit-like vascular channels. Capillary spaces were often closely packed, producing solid areas which stained for smooth muscle actin. Staining for factor VIII-related antigen was positive only within endothelial cells lining well-formed vascular channels. Both lesions were treated by excision; short-term follow-up of one patient revealed no evidence of recurrence. Similarities between this and other vascular processes may have resulted in misdiagnosis of this lesion in the past. The clinical significance of acquired tufted angioma in the oral mucosa is not known.

Adult↗
PubMed2000

Oral mucosal hyperpigmentation secondary to antimalarial drug therapy.

A case of oral mucosal hyperpigmentation resulting from antimalarial drug therapy is presented. The patient reported a history of long-term quinacrine therapy and exhibited diffuse blue-gray pigmentation of the nail beds and the skin of the nasal ala. Microscopic examination of the involved mucosa showed macrophages, containing both melanin and ferric iron, scattered within the connective tissue adjacent to the epithelium. The clinical, historical, and microscopic features of antimalarial-induced pigmentation are discussed. Other causes of diffuse or multifocal oral pigmentation are also addressed.

Adult↗
PubMed1997

Geriatric patient simulations for dental hygiene.

The rapidly increasing number of this country's elderly requires that dental hygiene students practice the clinical problem-solving skills of information gathering, assessment, and treatment applied to geriatric patients. Computer-based simulations are purported to provide this experience, but little research has been completed with simulations in the education of dental hygienists. This paper summarizes the process used to design, develop, and evaluate a series of eighteen computer-based geriatric simulated patients. It contains a brief description of the simulations and a description of the design, validation, authoring, and formative evaluation phases. The paper also describes the summative evaluation, provides implementation suggestions, and summarizes future directions. The summative evaluation, conducted at four institutions, suggests that computer-based simulations are an effective instructional method as measured by pre/post-tests. The results suggest that simulations can provide a standardized set of geriatric patient experiences. These simulations may prove especially valuable at institutions that are unable to provide clinical geriatric experiences or lack the expertise to conduct a didactic course in geriatrics.

Aged↗
PubMed1994

Clinical and therapeutic features of polymorphous low-grade adenocarcinoma.

Polymorphous low-grade adenocarcinoma, also known as terminal duct or lobular carcinoma, was first described in two clinical case series in 1983. Before that time most of these neoplasms were diagnosed as benign salivary gland neoplasms including pleomorphic adenomas, variants of monomorphic adenomas, or salivary malignant conditions including malignant pleomorphic adenomas, adenoid cystic carcinomas, and adenocarcinoma not otherwise stated. This neoplasm with few exceptions originates in minor salivary gland tissue of the posterior hard and soft palates or buccal mucosa. It is characteristically slow to enlarge; clinical reports show the neoplasm present for many years before diagnosis. We have evaluated the clinical and microscopic features of 15 cases from the archives of The University of Iowa Surgical Oral Pathology Laboratory and added these to published case reports. A total of 204 cases were evaluated with a female/male ratio of almost 2/1. Forty-nine percent originated in palatal mucosa. Polymorphous low-grade adenocarcinomas arising from pleomorphic adenomas or de novo have been reported within major salivary glands and outside the oral cavity. A 17% recurrence rate was found with a regional metastasis rate of 9%. Five cases had multiple recurrences, and 13 recurrences were at or beyond 5 years after the initial diagnosis. Regional node metastases were identified at the time of initial treatment or at the time of recurrence in 9% of cases in which follow-up data were specified.

Adenocarcinoma↗
PubMed1993

Computer applications in oral diagnosis.

Eventually, computer technology may be used in the home or practice to satisfy continuing education requirements. Additionally, this technology may be used by state licensing agencies as a component of their testing procedure. At the present time, a Patient Simulation Consortium and Electronic Curriculum Consortium have been established within the American Association of Dental Schools.7, 15 These groups, and others, will continue to develop and test new technologies for use in dentistry.

Computer-Assisted Instruction↗
PubMed1990

Dental diagnosis and treatment (DDx & Tx): interactive videodisc patient simulations for dental education.

Judgement skills and critical thinking in dentistry are developed through: (1) a systematic approach to gathering and processing information, and (2) an essential amount of practical experience. A new system of interactive videodisc patient simulations titled 'Dental Diagnosis and Treatment' or 'DDx & Tx' has been developed to provide students or practicing dentists an opportunity to develop and practice their critical thinking skills. The DDx & Tx system consists of patient simulation software, a laser-reflective videodisc with its accompanying database, a patient simulation management system, and documentation. An authoring tool is under development. Faculty-authored simulations require students to gather information, formulate diagnoses, order appropriate treatments and properly sequence those treatments. The students' performance is automatically scored and a critique is provided as a review.

Computer Simulation↗
PubMed1988

Aspartate-induced neuronal necrosis in infant mice: protective effect of carbohydrate and insulin.

Infant mice given large doses of glutamate or aspartate develop hypothalamic neuronal necrosis. Studies by others demonstrated that simultaneous administration of carbohydrate or prior injection with insulin markedly decreased glutamate-induced neuronal damage. We investigated whether carbohydrate and insulin exert a similar protective effect against aspartate-induced neuronal necrosis. Eight-day-old mice administered aspartate at 750 and 1000 mg/kg body weight developed neuronal necrosis (45.9 +/- 7.2 and 80.8 +/- 17.3 necrotic neurons/section, respectively). When carbohydrate (1 g/kg body weight) was administered simultaneously no lesions were detected in mice administered 750 mg/kg body weight aspartate, while 30.1 +/- 14.2 necrotic neurons/section were noted at 1000 mg aspartate/kg body weight. Mice administered 1000 mg/kg body weight aspartate with prior injection of insulin had 28.4 +/- 12.6 necrotic neurons/section, while 4.2 +/- 1.4 necrotic neurons/section were noted in insulin treated mice given 750 mg aspartate/kg body weight. Carbohydrate and insulin treatments has only minimal effects on plasma aspartate concentrations.

Animals↗
PubMed1985

Delayed mandibular reconstruction following removal of a mesenchymal chondrosarcoma. Report of a case.

An unusual case of mesenchymal chondrosarcoma is presented. Initially seen when the patient was 8 years old, the lesion was repeatedly biopsied and curetted with a diagnosis of odontogenic fibroma. In 1971 a diagnosis of osteosarcoma of the chondroblastic type was made. At that time, the patient underwent a partial mandibulectomy with immediate graft. The patient did well until 1981, when a recurrence of the lesion was noted. The microscopic diagnosis at this time was mesenchymal chondrosarcoma. The treatment of this lesion as a staged procedure with initial resection of the mandible and placement of a silicone rubber mandibular prosthesis is discussed. The second stage of the procedure was definitive mandibular reconstruction, with an allogeneic mandible as a crib for autologous particulate cancellous bone from the iliac crest. Although the prognosis of mesenchymal chondrosarcoma is usually grave, this case is unusual because of its long history of multiple procedures performed prior to the definitive treatment of the lesion 14 years after its discovery. Two-year follow-up since the definitive mandibular reconstruction shows adequate range of motion, excellent healing, and no recurrence.

Bone Transplantation↗
PubMed1985

Correlation of glutamate plus aspartate dose, plasma amino acid concentration and neuronal necrosis in infant mice.

Eight-day-old mice were given by gavage glutamate and aspartate mixtures providing each amino acid at 125, 250 or 500 mg/kg body weight (250, 500 and 1000 mg total dicarboxylic amino acids/kg) and the degree and extent of neuronal necrosis were determined. Similar studies were carried out in mice given monosodium L-glutamate at 250 or 500 mg/kg body weight. Plasma aspartate and glutamate concentrations were determined at each dose level. No animal given either glutamate or the glutamate plus aspartate mixture at 250 mg/kg developed neuronal necrosis. However, neuronal necrosis developed in 30% of animals given glutamate at 500 mg/kg (12+/-2 necrotic neurons/section in the region of maximal damage) and in 17% of animals given 250 mg glutamate/kg plus 250 mg aspartate/kg (11-13 necrotic neurons/section in the region of maximal damage). The threshold mean peak plasma glutamate plus aspartate concentration associated with neuronal necrosis was 128+/-24 mumol/dl. Using these data, and previously published data for aspartate-induced neurotoxicity (Finkelstein et al. Toxicology 1983, 29, 109), the individual threshold plasma glutamate and aspartate concentrations associated with neuronal necrosis were calculated to be 110 mumol/dl for aspartate and 75 mumol/dl for glutamate.

Animals↗
PubMed1985

Effect of carbohydrate ingestion on plasma aspartate concentrations in infant mice administered sodium L-aspartate.

Previous studies of infant pigs have demonstrated that simultaneous ingestion of carbohydrate (1 g/kg body weight) and glutamate (300 mg/kg body weight) resulted in markedly lower mean peak plasma glutamate concentration and a smaller area under the plasma glutamate concentration-time curve (AUC) than ingestion of the equivalent amount of glutamate alone. This study was carried out to investigate whether a similar carbohydrate-induced effect occurred with the other dicarboxylic amino acid, aspartate. Eight-day-old mice were administered sodium L-aspartate at 250, 500 and 1000 mg/kg body weight with and without 1.0 g/kg body weight of partially hydrolyzed cornstarch. Mean peak plasma aspartate concentration and plasma aspartate AUC values increased in proportion to the aspartate dose. The addition of carbohydrate to the aspartate solution had no significant effect on either mean peak plasma aspartate concentrations or AUC values at aspartate doses of 250 and 500 mg/kg body weight. A modest, but significant effect of carbohydrate was noted on the mean peak plasma aspartate levels in animals administered 1000 mg/kg body weight aspartate (P less than 0.05, Student's t-test). However, analysis of variance showed no significant carbohydrate effect and plasma AUC values were not significantly affected. These data indicate that carbohydrate affects the metabolism of aspartate and glutamate differently.

Animals↗
PubMed1984

Midline "nonhealing" granuloma.

Destructive processes of the midface can occur in a wide variety of diseases. Intrinsic in consideration of these is a cluster of lesions, including Wegener's granulomatosis (WG), idiopathic midline granuloma (IMG), polymorphic reticulosis (PR), and lymphoma. Although there is still confusion as to whether the latter three represent a spectrum of the same malignant process, there is general agreement that WG is a separate entity on the basis of clinical presentation and therapeutic response. It is probable that PR is an emergent lymphoma, with the same prognostic and therapeutic features. Idiopathic midline granuloma is clinically similar to PR and lymphoma, but histologically it appears to be inflammatory in nature with no clearly definable malignant cell type present. At this point in time three diseases are best collectively referred to as midline "nonhealing" granuloma. The cases presented represent the spectrum of this enigmatic process.

Adult↗
PubMed1984

Recurrent "traumatic" bone cysts of the mandible.

An unusual case of several recurrences of multiple and bilateral "idiopathic, traumatic, hemorrhagic" bone cysts in the same patient, with long-term follow-up, is presented. The etiology and pathogenesis of idiopathic bone cysts are discussed. It is recommended that patients be followed for a longer period of time after treatment.

Adult↗
PubMed1983

Correlation of aspartate dose, plasma dicarboxylic amino acid concentration, and neuronal necrosis in infant mice.

Eight-day-old mice were administered aspartate at 0, 1.88, 3.76, 4.89, 5.64 and 7.52 mmol/kg body wt and the degree and extent of neuronal necrosis determined. In addition, plasma aspartate and glutamate concentrations were determined at each aspartate dose. Animals administered aspartate at 0, 1.88 and 3.76 mmol/kg body wt did not develop neuronal necrosis. Hypothalamic neuronal necrosis (7.33 +/- 1.52 necrotic neurons/section of maximal damage) was found in 3 of 10 animals administered aspartate at 4.89 mmol/kg body wt. The extent of neuronal necrosis was proportional to dose once a neurotoxic dose of aspartate was reached. All 12 animals administered aspartate at 5.64 mmol/kg body wt developed lesions (49.5 +/- 7.2 necrotic neurons/section of maximal damage). Similarly, all 18 mice administered aspartate at 7.52 mmol/kg developed hypothalamic lesions (80.8 +/- 17.8 necrotic neurons/section of maximal damage). Infant mice administered the highest dose of aspartate not producing neuronal necrosis (3.76 mmol/kg) had a mean (+/- S.D.) peak plasma aspartate concentration of 87 +/- 23 mumol/dl and a mean peak plasma glutamate concentration of 64 +/- 22 mumol/dl. Thus, the toxic threshold for these amino acids must be greater than those values.

Amino Acids, Dicarboxylic↗