Microencapsulation of parathyroid cells via electric field and non-surgical transplantation approach.

PURPOSE: Hypoparathyroidism is a rare disease with low PTH, mostly seen as a consequence of neck surgery. Current management is the prescription of calcium and vitamin D, but the definitive treatment is parathyroid allotransplantation, which frequently triggers an immune response, thus cannot achieve the expected success. To overcome this problem, encapsulation of allogeneic cells is the most promising method. By optimizing the standard alginate cell encapsulation technique with parathyroid cells under high-voltage application, the authors reduced the size of parathyroid-encapsulated beads and evaluated these samples in vitro and in vivo. METHODS: Parathyroid cells were isolated, and standard-sized alginate macrobeads were prepared without any electrical field application, while microbeads in smaller sizes (< 500 µm), by the application of 13 kV. Bead morphologies, cell viability, and PTH secretion were evaluated in vitro for four weeks. For the in vivo part, beads were transplanted into Sprague-Dawley rats, and after retrieval, immunohistochemistry and PTH release were evaluated in addition to the assessment of cytokine/chemokine levels. RESULTS: The viability of parathyroid cells in micro- and macrobeads did not differ significantly. However, the amount of in vitro PTH secretion from microencapsulated cells was significantly lower than that from macroencapsulated cells, although it increased throughout the incubation period. Immunohistochemistry of PTH staining in both of the encapsulated cells identified as positive after retrieval. CONCLUSION: Contrary to the literature, a minimal in vivo immune response was developed for alginate-encapsulated parathyroid cells, regardless of bead size. Our findings suggest that injectable, micro-sized beads obtained using high-voltage may be a promising method for a non-surgical transplantation approach.

Cuprizone-induced demyelination in Wistar rats; electrophysiological and histological assessment.

OBJECTIVES: Multiple Sclerosis (MS) is a disease that affects the Central Nervous System by destructing myelin shield and also can affects the peripheral nervous system. Demyelination is acquired characteristics disease and appears with the degeneration of myelin which protects the axons. Cuprizone (CPZ) model is a toxic demyelination model. The purpose of this study was to develop an MS model by cuprizone exposure to Wistar rats. MATERIALS AND METHODS: Rats were separated into control and experimental groups and daily cuprizone was administered to experimental groups for 4, 5, 6 and 7 weeks. At the end of the experiments, spinal nerve conduction velocity was measured by EMG detected from the gastrocnemius muscle. After scarification, cerebrum and cerebellum of the animals were taken for histopathological investigation. RESULTS: Spinal cord nerve conduction velocity (SNCV) of control animals was 76.54 m/s. Whereas SNCV of the rats that were feed with CPZ for 6 weeks was significantly reduced to 46.35 m/s in comparison with the control group. Demyelinated areas and vacuolization were seen on the brain sections of CPZ exposed rats. CONCLUSIONS: SNCV of the rats were feed with cuprizone began tendency of decrease after 4th weeks. These reductions were observed as maximum at 6th weeks. At 7th week increments were observed at SNCV. These results indicated that 6 weeks of cuprizone feedings could be suitable to bring into existence of MS model in Wistar rats.

Assessment of in vivo spinal cord conduction velocity in rats in an experimental model of ischemic spinal cord injury.

STUDY DESIGN: Experimental laboratory investigation of spinal cord conductivity alterations in a rat model of ischemic spinal cord injury (SCI). OBJECTIVE: To observe the epidural spinal cord stimulation-induced electromyography responses, and to investigate the possible alterations of spinal cord conduction velocity (SCCV) and compound muscle action potentials (CMAPs) after ischemic SCI in rats. SETTINGS: Adnan Menderes University, Institute of Health Science, Aydin, Turkey. METHODS: SCI was induced by transient occlusion of the abdominal aorta in male Sprague-Dawley rats. Spinal cord histopathology was examined to determine neuronal damage and Tarlov scale was used to grade locomotor functions. Epidural electrical stimulation of spinal cord was performed by monopolar needle electrodes sequentially at L1-L2 and L5-L6 levels, and CMAPs were recorded from the left gastrocnemius muscle by surface electrodes. Amplitudes and durations of CMAPs were evaluated and SCCVs were calculated by analyzing the latency difference of CMAPs. RESULTS: Ischemia-induced SCI resulted in significant reduction of Tarlov scores and a significant decline in number of viable neurons. Similarly, a significant decrement was observed in SCCV following spinal cord ischemia. CONCLUSION: This study demonstrated that measurement of SCCV via epidural electrical stimulation is possible and displays a significant decline after spinal cord ischemia in rats. We suggest that this method can be beneficial to quantify neuronal damage after experimental ischemic SCI.