Biomedical subjects

S Babovic

Publications and source records attributed to S Babovic.

8 recordsLinked to original sources

PubMed2001

Experimental model for the long-term effects of laser resurfacing.

BACKGROUND AND OBJECTIVE: [corrected] Evaluation of the long-term effects of the laser resurfacing on development of the skin cancer after chronic ultraviolet B light exposure calls for the development of the appropriate animal model. STUDY DESIGN/MATERIALS AND METHODS: The 27 C3H nu/nu nude mice were used in the experiment. Five experimental groups were designed to evaluate the effects of laser energy delivered. RESULTS: Tru-Pulse(trade mark) Laser System produced char-free crust immediately after application. There was no histologic difference in laser effects on the skin between groups. Complete re-epithelialization occurred within 7 days. CONCLUSIONS: An entire lifetime in this mammal model can be studied in under 2.5 years. The back skin of the mice can be resurfaced by using one pass 500 mJ/cm(2) and complete healing will occur within a 7-day period. We believe that establishment of this experimental model has set the stage for the further study of the effect of laser energy on sun-damaged skin. Carbon dioxide laser resurfacing has become an increasingly popular method of facial rejuvenation, allowing the plastic surgeon to repair sun-damaged skin and wrinkles. Results obtained by laser resurfacing seem to be long lasting. Carbon dioxide laser resurfacing brings about histologic changes in the skin. This finding raises a new question: Does carbon dioxide laser skin resurfacing modulate the effects of ultraviolet (UV) light exposure on the skin? The purpose of this study was to establish a new experimental model for studying the long-term effects of laser skin resurfacing.

Animals↗

PubMed2000

Free fibula donor-site morbidity: the Mayo experience with 100 consecutive harvests.

A retrospective analysis of 100 consecutive patients undergoing free fibula harvest at the Mayo Clinic is presented. Every patient was analyzed by reviewing postoperative physical examination data. All patients were evaluated and followed in the early postoperative course by the physical medicine and rehabilitation services. Patients were followed from 3 to 60 months, with an average follow up of 17.42 months. In the patient group, 72 flaps were osseous and 28 osteocutaneous. Thirty-six complications at the donor site were observed in 30 patients. An additional 19 patients required prolonged pharmacologic pain control beyond the first 6 postoperative weeks, with no donor-site complications clinically detectable. Hammertoe was observed in six patients and wound dehiscence in seven patients. Tendon exposure was observed in five patients; partial split-thickness skin graft loss was observed in eight. Numbness of the foot was reported in 10 patients. Fifteen patient had limited maximum ambulatory distance to less than 1000 m. An additional six patients reported difficulty walking stairs. Attention to details and meticulous wound care are required to further reduce wound-healing complications. Immediate postoperative involvement of the physical medicine and rehabilitation services was beneficial in early patient mobilization and achievement of preoperative ambulation levels. After a short rehabilitation period, the majority of patients were able to engage in all daily activities.

Adult↗

PubMed2000

Traumatic carotid artery dissection causing blindness.

A case of delayed postoperative visual loss due to bilateral traumatic carotid artery dissection is presented. In patients with a major craniofacial injury due to a high-speed motor vehicle accident, we suggest that carotid artery duplex ultrasonography be used in the initial evaluation for possible carotid artery dissection. Magnetic resonance imaging of the head and neck with magnetic resonance angiography should be performed subsequently if indicated. Early diagnosis and initiation of therapy can minimize complications.

Accidents, Traffic↗

PubMed1998

Nerve regeneration in diabetic rats.

This study evaluated the capacity of diabetic rats to recover the ability to walk after nerve repair or nerve graft of the posterior tibial nerve at thigh level. Functional recovery of the posterior tibial nerve was evaluated by walking track analysis during regeneration in streptozotocin-induced diabetic rats. Surgical procedures were performed 8 weeks after induction of diabetes. The nerve repair was epineurial. The nerve graft was a 1.5 cm segment orthotopically replaced. There was no significant difference in functional recovery between normal and diabetic rats for both the nerve repair and nerve graft groups at 6, 12, and 24 weeks after nerve reconstruction. It is concluded that the presence of diabetes is not a contraindication for nerve reconstruction.

Animals↗

PubMed1998

Role of reactive oxygen species in optic nerve compression injury: a preliminary study.

Optic nerve compression is one of the complications in craniofacial surgery and blepharoplasty. We have shown previously that acute and chronic nerve compression produce significant tissue injury in rat sciatic nerve. In the present study the optic nerve was evaluated for possible ischemia/reperfusion injury after acute compression in an animal model. Male New Zealand White rabbits were used in the experiment. The optic nerve was subjected to 2-hour compression followed by reperfusion for 1 hour. Nerve compression was established by banding the optic nerve with silastic tubing. The compressed optic nerve was assayed for malondialdehyde, an indicator of lipid peroxidation, measured as thiobarbituric acid reactive substances (TBARS). The TBARS levels increased significantly to 2.5 times normal, from 37+/-6 pmoles per milligram tissue (N=6) to 90+/-12 pmoles per milligram tissue dry weight (N=5) in the compressed/reperfused nerve (p < 0.05). Much of these increases were prevented by treatment with deferoxamine, an iron chelator and antioxidant. The results indicate that optic nerve is injured by acute compression followed by reperfusion. The nerve compression injury appears to be due to reactive oxygen species and can be ameliorated by treatment with free radical scavengers.

Animals↗

PubMed1995

Free radical damage in acute nerve compression.

Nerve compression causes injury by local ischemia and direct mechanical distortion. Peripheral nerves in diabetes mellitus are more prone to injury than those of nondiabetics. We sought to determine whether reperfusion-induced, oxygen-derived free radical injury occurs in peripheral nerves subjected to acute compression in normal and chronically diabetic rats. Female Sprague-Dawley rats weighing 250 to 275 g (N = 347) were divided into two groups: normal and streptozocin-induced diabetics. A total of 187 normal and 160 diabetic nerves were analyzed. After 8 weeks of untreated hyperglycemia, the sciatic nerves of normal and diabetes mellitus rats were subjected to one of three operations: a sham operation, 24-hour compression alone, and 24-hour compression followed by 1-hour reperfusion (CR). Nerve compression was established by banding the right sciatic nerve with a Silastic tubing, 1 cm long and 0.62 mm internal diameter, which was secured with 6-0 nylon suture. In the CR group, after 24 hours of compression, the tubings were released for 1 hour to permit reperfusion. Nerve tissue within the zone of compression underwent biopsy examination and was frozen for subsequent analysis. Blood flow to the nerve was quantified by injecting fluorescein (10 mg/kg intravenously) 10 minutes before harvest and measuring tissue levels fluorometrically. Compression with the Silastic tubing significantly reduced neural blood flow by 75%. Blood flow improved but failed to return to baseline levels after tubing release in diabetes mellitus nerves while perfusion returned to baseline in non-diabetes mellitus nerves. Nerve homogenate was assayed for malonyldialdehyde, an indicator of lipoperoxidation, as well as enzymes of cellular defense and glucose metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Effects of tissue expansion on secondary ischemic tolerance in experimental free flaps.

The effects of tissue expansion on free flap tolerance and metabolic response to secondary ischemia were evaluated. A total of 178 male syngeneic Lewis rats were used: 28 in perfusion study and 75 donor and 75 recipient animals in flap survival study. Animals were organized in three experimental groups: control, sham operation, and expansion group. Sham group animals had the expander implanted but not insufflated. After 4 weeks of tissue expansion, 3 x 5-cm epigastric free flaps were transplanted to recipient animals. Twenty-four hours later, secondary ischemia was produced by 3-hour venous occlusion. Flap survival, perfusion, and enzyme activities were determined. Pre-expanded skin flaps had an increase in perfusion of approximately 700% as measured by fluorescein levels compared with control flaps (p < 0.001) and demonstrated a better success rate (76%) compared with those of the control (40%) (p < 0.05) and sham (28%) groups (p < 0.05). Glutathione peroxidase, glutathione reductase, and glucose 6-phosphate dehydrogenase of the antioxidant defense systems significantly increased in skin in both the sham and the expansion groups. In response to secondary ischemia, the control and sham groups exhibited a decrease in enzyme activities of the glutathione redox cycle, whereas the expansion group showed no significant changes from the elevated baseline activities. Tissue expansion improved flap tolerance to secondary ischemia by increasing flap circulation and probably by augmenting tissue metabolic response to oxidative stress.

Animals↗

PubMed1994

Flap tolerance to ischaemia in streptozotocin-induced diabetes mellitus.

The effects of diabetes mellitus (DM) on skin flap tolerance to 3 h of secondary venous ischaemia were evaluated. Epigastric island flaps were elevated 3, 6 and 12 weeks after induction of DM in rats. In the non-diabetic control groups, the flap survival was 85% in the 3-week group, 72% in the 6-week, and 78% in the 12-week. In untreated DM groups, the flap survival significantly decreased to 40% in the 3-week group, 25% in the 6-week, and 17% in the 12-week (P < 0.05 in all groups). Flap survival in the DM/insulin group decreased to 31% in the 3-week group. Effects of insulin therapy, however, were observed in later stages of DM: 71% and 62% survival in the 6- and 12-week group, respectively. Significant linear correlations between enzymatic responses and the flap survival were found. The results suggest that DM is detrimental to flap tolerance and is associated with the lack of metabolic responses to secondary ischaemia.

Animals↗