Biomedical subjects

S C Fernandez

Publications and source records attributed to S C Fernandez.

5 recordsLinked to original sources

PubMed1998

BCL-2 overexpression attenuates cortical cell loss after traumatic brain injury in transgenic mice.

The proto-oncogene, BCL-2, has been suggested to participate in cell survival during development of, and after injury to, the CNS. Transgenic (TG) mice overexpressing human Bcl-2 (n = 21) and their wild-type (WT) littermates (n = 18) were subjected to lateral controlled cortical impact brain injury. Lateral controlled cortical impact brain injury resulted in the formation of a contusion in the injured cortex at 2 days, which developed into a well-defined cavity by 7 days in both WT and TG mice. At 7 days after injury, brain-injured TG mice had a significantly reduced cortical lesion (volume = 1.99 mm3) compared with that of the injured WT mice (volume = 5.1 mm3, P < 0.01). In contrast, overexpression of BCL-2 did not affect the extent of hippocampal cell death after lateral controlled cortical impact brain injury. Analysis of motor function revealed that both brain-injured WT and TG mice exhibited significant right-sided deficits at 2 and 7 days after injury (P < 0.05 compared with the uninjured controls). Although composite neuroscores (sum of scores from forelimb and hind limb flexion, lateral pulsion, and inclined plane tests) were not different between WT and TG brain-injured mice, TG mice had a slightly but significantly reduced deficit in the inclined plane test (P < 0.05 compared to the WT mice). These data suggest that the cell death regulatory gene, BCL-2, may play a protective role in the pathophysiology of traumatic brain injury.

Animals↗

PubMed1997

Insulin-like growth factor-1 (IGF-1) improves both neurological motor and cognitive outcome following experimental brain injury.

We evaluated the efficacy of insulin-like growth factor-1 (IGF-1) in attenuating neurobehavioral deficits following lateral fluid percussion (FP) brain injury. Male Sprague-Dawley rats (345-425 g, n = 88) were anesthetized and subjected to FP brain injury of moderate severity (2.4-2.9 atm). In Study 1, IGF-1 (1.0 mg/kg, n = 9) or vehicle (n = 14) was administered by subcutaneous injection at 15 min postinjury and similarly at 12-h intervals for 14 days. In animals evaluated daily for 14 days, IGF-1 treatment attenuated motor dysfunction over the 2-week period (P < 0.02). In Study 2, IGF-1 (4 mg/kg/day, n = 8 uninjured, n = 13 injured) or vehicle (n = 8 uninjured, n = 13 injured) was administered for 2 weeks via a subcutaneous pump implanted 15 min postinjury. IGF-1 administration was associated with increased body weight and mild, transient hypoglycemia which was more pronounced in brain-injured animals. At 2 weeks postinjury (P < 0.05), but not at 48 h or 1 week, brain-injured animals receiving IGF-1 showed improved neuromotor function compared with those receiving vehicle. IGF-1 administration also enhanced learning ability (P < 0.03) and memory retention (P < 0.01) in brain-injured animals at 2 weeks postinjury. Taken together, these data suggest that chronic, posttraumatic administration of the trophic factor IGF-1 may be efficacious in ameliorating neurobehavioral dysfunction associated with traumatic brain injury.

Animals↗

PubMed1997

Delayed administration of basic fibroblast growth factor (bFGF) attenuates cognitive dysfunction following parasagittal fluid percussion brain injury in the rat.

The present study evaluates the therapeutic effects of delayed administration of bFGF on cognitive dysfunction and histopathological damage following lateral fluid-percussion (FP) brain injury. Male Sprague-Dawley rats were trained to learn a visuospatial task in a Morris Water Maze (MWM) paradigm and then were anesthetized and subjected to either FP brain injury of moderate severity (2.5-2.8 atm, n = 32) or surgery without brain injury (n = 10). Twenty-four hours postinjury, an infusion cannula connected to a mini-osmotic pump was implanted into the area of maximal cortical injury to continuously infuse either bFGF (2.0 g) or vehicle for 7 days. Treatment with bFGF significantly attenuated posttraumatic memory dysfunction in the MWM at 8 days postinjury when compared to vehicle treatment (p < 0.05). The cortical lesion and significant cell loss in the ipsilateral CA3 region of the hippocampus, produced by FP injury, was not affected by bFGF treatment. However, immunohistochemical evaluation of glial fibrillary acidic protein revealed a trend toward increased astrocytosis in the injured cortex of bFGF-treated animals compared to vehicle-treated animals (p < 0.1). These results indicate that bFGF may be efficacious in attenuating cognitive dysfunction associated with traumatic brain injury.

Analysis of Variance↗

PubMed1976

Pre-intestinal stability of beta-carotene in ruminants.

The stability of beta-carotene in the rumen contents of cows, calves and sheep was investigated in vitro and in vivo. Incubation tests with rumen liquor consistently showed that carotene was relatively stable, less than 10% losses being found under a wide variety of incubation conditions and with different sources of carotene. There was no relation between the small carotene losses and the extent of fatty acid hydrogenation. Rumen liquor samples taken from a fistulated cow over a 24 h period after the feeding of alfalfa meal had a nearly constant ratio of carotene to unsaponifiable matter. Carotene was injected into the rumen of a ram after surgical ligation of the pylorus. The recovery of carotene from the combined contents of the reticulo-rumen, omassum and abomasum 24 h later amounted to 89% whereas vitamin A palmitate, under the same conditions, yielded a recovery of 70%. It is concluded that little carotene is lost normally during its passage through the pre-intestinal part of the alimentary canal of ruminants.

Animal Nutritional Physiological Phenomena↗

PubMed1976

Low utilization of carotene by sheep.

The apparent digestibility of beta-carotene was determined in Awassi rams by means of balance trials. In a first series carotene was supplied per os in constant daily amounts ranging from 2.88 to 8.52 mg in the form of pelleted alfalfa meal or as a water-dispersible synthetic preparation. The supplements were given with a basal low-carotene ration composed of barley, soybean meal and straw and supplying 82 mug carotene daily. Fecal recoveries for the carotene supplements ranged from 92 to 98%, whereas the unsupplemented basal diet yielded a recovery of 28%. In a second series single doses of carotene in various carriers were introduced into the abomasum of fistulated rams. With an aqueous carotene dispersion fecal recoveries were close to 90%. When dissolved in triglycerides, carotene yielded less than 50% recovery in the feces, and free fatty acids and monoglycerides gave intermediate values. Additional tests with 3H-labelled carotene revealed that the low fecal recovery of carotene given in oil was not due to improved absorption but to degradation of carotene in the lower intestinal tract. This was confirmed by measurement of blood radioactivity. The results show that carotene from different sources and with intakes bordering on minimum requirements is poorly absorbed by sheep. It is suggested that the peculair physiology of digestion in the ruminant creates unfavorable conditions for the efficient micellar solubilization of nonpolar lipids in the upper small intestine.

Abomasum↗