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Biomedical subjects

R A Behmand

Publications and source records attributed to R A Behmand.

10 recordsLinked to original sources
PubMed1999

Shortening of the long forehead.

A long forehead disrupts the harmony among the facial components and may contribute to the semblance of facial aging. Slight forehead length disharmony on a senescent face can be corrected by placing the incision at the hairline, elevating the eyebrows through subcutaneous or subgaleal dissection, and removing excess skin without posterior scalp immobilization. For moderate to major reduction of the forehead length, the scalp is elevated back to the occipital region through a pretrichial incision, and relaxation incisions are made at a right angle to the vector of advancement. The entire scalp is then repositioned anteriorly, advancing the hairline caudally and shortening the forehead. Retraction of the scalp or excessive elevation of the eyebrows is prevented by anchoring the galeal fascia to the cranial bone using a bone-tunneling technique in one to three rows. The number of fixation rows is commensurate to the amount of advancement and rigidity of the scalp. The more immobile the scalp preoperatively, the more relaxation incisions and fixation tunnels are necessary. Following caudal repositioning of the scalp, the non-hair-bearing skin is excised, and a meticulous repair is done. These procedures have been performed in 180 patients with a high degree of satisfaction. Temporary hair loss was experienced in one smoker who underwent the most advancement through posterior scalp elevation and continued to smoke postoperatively. Also, on three patients in the subcutaneous forehead rhytidectomy group, two of whom were smokers, delayed healing was observed in the temple area because of compromised circulation requiring secondary revision.

Forehead↗
PubMed1996

Resection of bilateral orbital and cranial base basal cell carcinoma with preservation of vision.

The surgical resection of skull base tumors often presents technically challenging problems and can result in major deformities. In planning the operation, each individual patient must be evaluated not only with respect to the extent of the disease, but also with respect to the functional losses, which may severely affect the patient's quality of life. The patient presented is an elderly woman with a malignant anterior skull base basal cell carcinoma and multiple recurrences. The tumor extended to the orbits bilaterally, resulting in blindness in the right eye. The objective was to resect the tumor from the skull base and the orbits, while preserving vision in the left eye. Utilizing intraoperative frozen sections, extensive tumor resection in the left orbit was accomplished without compromising vision. This was followed by the reconstruction of the eyelids and periorbital tissues. Exenteration of the right orbit, anterior craniectomy, and partial dural resection were also performed. Ten years later, the patient remains free of tumor recurrence and has good vision in her left eye.

Aged↗
PubMed1996

Alar base abnormalities. Classification and correction.

Abnormalities of the alar base may be a consequence of base deformities, a secondary result of reduction of nasal base projection, or a consequence of maxillary abnormalities. A thorough clinical observation coupled with information procured from the analyzed lifesized photographs provides a consistent method for the evaluation of the alar base and the structures that affect its position. A critical step in choosing the surgical technique for correction is the classification of abnormalities. A systemic approach to such a classification is presented in this article and is accompanied by a description of the dynamic changes and optimal surgical procedures that would best benefit patients within each category.

Congenital Abnormalities↗
PubMed1995

Blepharolabioanal syndrome.

A previously unreported syndrome of congenital craniofacial and anorectal anomalies affecting a woman and her two daughters is described. Features include bilateral cleft lip, cleft palate, bilateral upper and lower lid lag, and imperforate anus. The findings are consistent with an autosomal dominant pattern of inheritance. There were no identifiable intrauterine fetal insults. A detailed description of these anomalies, the subsequent surgical corrections, and a discussion of previously unreported syndromes with isolated features are the subject of this report.

Abnormalities, Multiple↗
PubMed1994

Hypoxia increases glucose transport at blood-brain barrier in rats.

Prolonged hypoxia causes several adaptive changes in systemic physiology and tissue metabolism. We studied the effects of hypobaric hypoxia on glucose transport at the blood-brain barrier (BBB) in the rat. We found that hypoxia increased the density of brain microvessels seen on immunocytochemical stains using an antibody to the glucose transporting protein GLUT. In addition, we found that hypoxia increased the density of GLUT in isolated cerebral microvessels as determined by specific cytochalasin B binding. The higher GLUT density in isolated cerebral microvessels was evident after 1 wk of hypoxia and was associated with decreased activity of gamma-glutamyltranspeptidase. Consistent with these findings, we also demonstrated that 3 wk of hypobaric hypoxia caused increased unidirectional transport of glucose at the BBB in several brain regions in vivo, as determined by the doubly labeled single-pass indicator-fractionation atrial bolus injection method in anesthetized rats. We conclude that chronic hypobaric hypoxia is associated with increased glucose transport at the BBB.

Animals↗
PubMed1992

Nicotine enhances 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity.

Epidemiologic evidence of an inverse relationship between cigarette smoking and Parkinson's disease suggests that a component of cigarette smoke protects against nigrostriatal degeneration. Nicotine, a major component of cigarette smoke, is similar in chemical structure to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and is metabolized in part by the same enzymes that detoxify MPTP. We investigated the effect of chronic nicotine on MPTP neurotoxicity in two strains of mice and found that nicotine increases rather than decreases MPTP toxicity. These results are not compatible with the hypothesis that nicotine is that component of cigarette smoke that protects against nigrostriatal degeneration, at least in the MPTP experimental model of Parkinson's disease.

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

Correlation of MPTP neurotoxicity in vivo with oxidation of MPTP by the brain and blood-brain barrier in vitro in five rat strains.

We studied 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in 5 strains of rats by assessing mortality and brain monoamine changes after MPTP injections into the internal carotid artery. We then attempted to correlate the differences among rat strains in their susceptibility to MPTP neurotoxicity in vivo with MPTP oxidation by monoamine oxidase (MAO) of the cerebral cortex, striatum, and brain microvessels in vitro. Despite the fact that the carotid route delivers much higher amounts of MPTP to the ipsilateral cerebrum than can be achieved by systemic injections, no significant dopamine depletion occurred in ipsilateral striata of Sprague-Dawley rats (the most resistant strain), but significant reductions of about 40% in striatal dopamine were evident in the more sensitive strains. Decreased striatal dopamine levels in these latter rat strains were associated with increased dopamine turnover. Higher doses of MPTP resulted in acute death. MPTP-induced mortality was not affected, but striatal dopamine depletion was prevented, by MAO inhibition. Differences among rat strains in their susceptibility to MPTP neurotoxicity correlated best with MAO activity in their isolated brain microvessels, but not with MAO activity in their striata or cerebral cortices. These results are consistent with the hypothesis that the rats' resistance to MPTP neurotoxicity is to some extent a property of their unique brain endothelium which has high MAO activity.

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

Chronic hyperglycemia increases the density of glucose transporters in human erythrocyte membranes.

We investigated the effect of chronic hyperglycemia on glucose transporters in erythrocytes of subjects with and without diabetes mellitus. We found a 22% increase in D-glucose-displaceable cytochalasin-B binding in erythrocyte membranes of diabetic subjects over those of controls (311 +/- 13 vs. 254 +/- 8 pmol/mg protein; P less than 0.001). This increased binding was due to a higher density of binding sites without a significant change in binding affinity. Cytochalasin-B binding to erythrocyte membrane correlated positively with both erythrocyte glycohemoglobin and serum glucose levels, but not with plasma C-peptide levels. The data are compatible with up-regulation of glucose transporters in the erythrocytes of subjects with chronic hyperglycemia. We suspect that this is brought about by increased synthesis and membrane incorporation of the glucose transporter during erythropoiesis.

Adult↗