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Biomedical subjects

S Jankauskas

Publications and source records attributed to S Jankauskas.

5 recordsLinked to original sources
PubMed1991

Curette fat sculpture in rhytidectomy: improving the nasolabial and labiomandibular folds.

The nasolabial and labiomandibular folds develop with facial aging by an anterior caudal descent of the fat prominences of the same name. Young patients with minimal folding can be corrected by substances inserted in the fold; however, this and other techniques have failed satisfactorily to improve the folds naturally and permanently. Identification of the prominences and removal of the fat superficial to the skin by curettes have proven safe and effective and superior to fat suction. Complications include small hematomas and visible depressions in the sculpted areas. There was no nerve or skin injury. Follow-up of this technique (an improvement of a previous technique) is 3 1/2 years.

Adipose Tissue↗
PubMed1990

Achieving standardized photographs in aesthetic surgery.

The plastic surgeon who wishes to share clinical experience with colleagues is obligated to produce accurate data in the form of photographs. Moreover, accurate photographs are essential to enable an objective critical appraisal of one's own surgical skill and to display postoperative results to patients in an unbiased fashion. Change should not be a function of either the photograph or the photographer. The use of an acetate screen grid in conjunction with anatomic boundaries is described as a means to achieve accurate, reproducible standard photographs of the face and body in aesthetic surgical patients.

Acetates↗
PubMed1986

Mitochondrial death in sepsis: a failed concept.

The concept of early selective mitochondrial injury has been proposed to explain the global metabolic dysfunction observed in the septic state. A two phase study was undertaken to test the validity of this hypothesis. In the initial phase, an endotoxin shock model was employed in the rat to delineate the function of skeletal muscle mitochondria. Mitochondrial function was determined polarimetrically, comparing state three and state four rates, respiratory control index (RCI) and ADP:O ratios. No significant alteration in these parameters was observed in the endotoxic state. Phase II of the study was designed to investigate mitochondrial function in a bacterial peritonitis rat model. Both liver and skeletal muscle mitochondrial function were determined to control for possible alterations in liver metabolism. Neither muscle nor liver mitochondria exhibited functional impairment during sepsis. We conclude from this study that neither endotoxemia nor peritonitis selectively "kills" mitochondria as previously suggested.

Animals↗