Biomedical subjects

David K C Tay

Publications and source records attributed to David K C Tay.

6 recordsLinked to original sources

PubMed2006

Graded ephrin-A2 expression in the developing hamster superior colliculus.

During development, ephrin gradients guide retinal ganglion cell axons to their appropriate topographic locations in the superior colliculus (SC). Expression of ephrin-A2, assessed immunohistochemically in the developing hamster SC, revealed a rostral(low) to caudal (high) gradient that is most prominent at postnatal days P4 and P7 when topography is established. Double-labelling immunohistochemistry for ephrin-A2 and cell specific markers revealed that ephrin-A2 is expressed exclusively by a subset of neurons. The expression pattern has implications for mechanisms underlying establishment of topography during development and following injury.

Animals↗

PubMed2006

Expression of nicotinamide adenine dinucleotide phosphate-diaphorase in the retina of postnatal golden hamsters deprived of light stimulation.

Nicotinamide Adenine Dinucleotide Phosphate-Diaphorase (NADPH-d) expressing neurons in the retina of golden hamsters have been identified to be a subset of amacrine cells that provide a major source of Nitric Oxide (NO) in retina. This subset of amacrine cells in mouse retina was recently proved to contain the circadian clock gene Per1 (D.Q. Zhang, T. Zhou, G.X. Ruan, D.G. McMahon, Circadian rhythm of Period 1 clock gene expression in NOS amacrine cells of the mouse retina, Brain Res., 1050 (2005) 101-109). However, it remains unknown whether these clock-related NADPH-d amacrine cells can be regulated by light stimulation and thus synchronized to ambient day/night cycle. A previous study has reported that NADPH-d expressing amacrine cells in postnatal hamsters exhibited a surge after eye-opening (D. Tay, Y.C. Diao, Y.M. Xiao, K.F. So, Postnatal development of nicotinamide adenine dinucleotide phosphate-diaphorase-positive neurons in the retina of the golden hamster, J. Comp. Neurol., 446 (2002) 342-348) suggesting a possible effect of light on the NADPH-d amacrine cells. In order to further reveal the relationship between NADPH-d amacrine cells and light stimulation, the present study focuses on the changes of the expression of NADPH-d in the retina of postnatal hamsters reared in completely deprived light conditions. Prior to eye opening, P12 hamster pups were subjected to either bilateral eyelid suturing or dark rearing. On P28 a subgroup of light deprived hamsters was returned to lighting conditions and the expression of NADPH-d activities in the retina was assessed. In hamsters reared in the 12:12 light-dark cycle, the number of NADPH-d amacrine cells in the ganglion cell layer (GCL) increased right after eye-opening and reached the adult level gradually. However, hamsters subjected to both bilateral eyelid suturing and dark rearing, the number of NADPH-d amacrine cells in GCL was maintained at a low level but increased again upon returning to the 12:12 light-dark condition. In contrast, the number of NADPH-d expressing amacrine cells in the inner nuclear layer (INL) remained low and unaltered regardless of the lighting environment. This study demonstrates that there are two subpopulations of NADPH-d expressing amacrine cells with respect to different locations in the retina of hamsters. Different from those in INL, the NADPH-d amacrine cells in GCL of postnatal hamsters are dependent on the lighting environment implicating that these clock-related amacrine cells and the production of NO might be under a modulation of light stimulation.

Animals↗

PubMed2006

Nano neuro knitting: peptide nanofiber scaffold for brain repair and axon regeneration with functional return of vision.

Nanotechnology is often associated with materials fabrication, microelectronics, and microfluidics. Until now, the use of nanotechnology and molecular self assembly in biomedicine to repair injured brain structures has not been explored. To achieve axonal regeneration after injury in the CNS, several formidable barriers must be overcome, such as scar tissue formation after tissue injury, gaps in nervous tissue formed during phagocytosis of dying cells after injury, and the failure of many adult neurons to initiate axonal extension. Using the mammalian visual system as a model, we report that a designed self-assembling peptide nanofiber scaffold creates a permissive environment for axons not only to regenerate through the site of an acute injury but also to knit the brain tissue together. In experiments using a severed optic tract in the hamster, we show that regenerated axons reconnect to target tissues with sufficient density to promote functional return of vision, as evidenced by visually elicited orienting behavior. The peptide nanofiber scaffold not only represents a previously undiscovered nanobiomedical technology for tissue repair and restoration but also raises the possibility of effective treatment of CNS and other tissue or organ trauma.

Aging↗

PubMed2005

Light delays synaptic deafferentation and potentiates the survival of axotomized retinal ganglion cells.

Knowledge of the cellular mechanism underlying the therapeutic effect of stimulation and the optimal doses of such stimulation to maximize neuronal recovery is essential to guide clinical practice in neural rehabilitation. Using hamsters, we transected the optic nerve to demonstrate how light stimulation affects neuronal recovery. The c-fos protein was used as a neuronal connectivity marker. Here we show that: (a) in addition to cell death, a population of cells undergoes synaptic deafferentation and (b) light stimulation delays cell death and deafferentation. Among the three rearing conditions studied (6:18LD, 12:12LD, and 18:6LD), the 12:12LD condition appears to be the one achieving the optimal therapeutic effect. This study provides a solid base in the understanding of the neuroanatomical changes after traumatic brain injury and the need to establish an optimal level and timing for the environmental stimulation.

Animals↗

PubMed2003

Effects of a therapeutic laser on the ultrastructural morphology of repairing medial collateral ligament in a rat model.

BACKGROUND AND OBJECTIVES: Low energy laser therapy has been shown to enhance mechanical strength of healing medial collateral ligament (MCL) in rats. The present study investigated its effects on the ultrastructural morphology and collagen fibril profile of healing MCL in rats. STUDY DESIGN/MATERIALS AND METHODS: Thirty-two mature male Sprague-Dawley (SD) rats were used. Twenty-four underwent surgical transection to their right MCLs and eight received only skin wound. Immediately after surgery, eight of the MCL transected rats were treated with a single dose of laser therapy at 63.2 J cm(-2), eight were treated with a single dose of laser therapy at 31.6 J cm(-2), the rest had no treatment and served as control. At 3 and 6 weeks after surgery, the MCLs were harvested and examined with electron microscopy for collagen fibril size, distribution, and alignment. RESULTS: Significant differences (P < 0.001) were found in fibril diameters from the same anatomical site and time period among different groups. The mass-averaged diameters of the laser-treated (64.99-186.29 nm) and sham (64.74-204.34 nm) groups were larger than the control group (58.66-85.89 nm). The collagen fibrils occupied 42.55-59.78, 42.63-53.94, and 36.92-71.64% of the total cross-sectional areas in the laser-treated, control and sham groups, respectively. Mode obliquity was 0.53-0.84 among the three groups. CONCLUSIONS: Single application of low energy laser therapy increases the collagen fibril size of healing MCLs in rats.

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PubMed2002

Therapeutic low energy laser improves the mechanical strength of repairing medial collateral ligament.

BACKGROUND AND OBJECTIVES: Low energy laser therapy has been shown to enhance collagen production but its effect on tissue strength is not well reported. We tested the effects of therapeutic laser on the strength of healing medial collateral ligaments (MCLs) in rats. STUDY DESIGN/MATERIALS AND METHODS: Twenty-four rats received surgical transection to their right MCL and eight received sham operation. After surgery, 16 received a single dose of gallium aluminum arsenide laser to their transected MCL for 7.5 minutes (n = 8) or 15 minutes (n = 8) and eight served as control with placebo laser, while the sham group didn't receive any treatment. The MCLs were biomechanically tested at either 3 or 6 weeks post-operation. RESULTS: The normalized ultimate tensile strength (UTS) and stiffness of laser and sham groups were larger than control (P < 0.001). The UTS of laser and sham groups were comparable. Laser and sham groups had improved in stiffness from 3 to 6 weeks (P < 0.001). CONCLUSIONS: A single dose of low energy laser therapy improves the UTS and stiffness of repairing MCL at 3 and 6 weeks after injury.

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