Assessment of corn starch as substitute for agarose in DNA gel electrophoresis.

OBJECTIVE: The use of agarose in nucleic acid electrophoresis is the gold standard. However, agarose is very expensive and not readily available in resource limited developing countries like Ghana. Hence, finding a more affordable and readily available alternative to agarose will be a major boost to molecular research in developing countries. This study was aimed at investigating the use of corn starch as a potential substitute for agarose in DNA gel electrophoresis. RESULTS: Genomic deoxyribonucleic acid (DNA) extracted from Plasmodium falciparum and primers were obtained from the West African Centre for Cell Biology of Infectious Pathogens and amplified using polymerase chain reaction. The amplicon was run on agarose gel to ascertain the molecular weight (as a positive control). When visualized under both blue light and ultraviolet light, the DNA and ladder showed clear and clean bands with the expected molecular weight. Corn starch was then modified with sodium borate buffer, casted into a gel and used to run the same DNA sample. Our findings indicated that similar to agarose, the DNA sample and ladder migrated successfully through the modified starch gel but no bands were visible when visualized under blue and ultra-violet light.

A Rare Case of Thyrotoxic Periodic Paralysis After Epidural Steroid Injection: A Case Report and Literature Review.

BACKGROUND Thyrotoxic periodic paralysis (TPP) is a rare cause of acute paralysis, which if not promptly recognized and treated, can lead to significant morbidity and mortality. TPP can be precipitated by several factors, including a high carbohydrate diet and exercise. This report is of a rare case of TPP after epidural steroid injection in a young man, with a review of the literature of previous cases. CASE REPORT A 36-year-old Asian man presented to the emergency department with sudden onset of paralysis of all his limbs following epidural steroid injection for traumatic low back pain. At presentation, he was found to have severe hypokalemia of 1.8 mEq/L. Further investigations led to the diagnosis of hyperthyroidism and Graves' disease. In the process of correcting his potassium, there was an unexpected rebound hyperkalemia that was successfully corrected. He had a rapid recovery and an early discharge from hospital. CONCLUSIONS Although several factors can lead to paralysis after an epidural steroid injection, TPP should be considered in the differential diagnosis, especially in individuals who have predisposing factors of ethnicity and gender. If patients have undiagnosed hyperthyroidism on presentation, the diagnosis of TPP can be delayed or missed. In the management of patients with TPP, care should be taken when correcting potassium levels.

Microglial Activation Results in Inhibition of TGF-ß-Regulated Gene Expression.

Chronic inflammation mediated by persistent microglial activation is associated with the pathogenesis of neurodegenerative diseases. The mechanisms underlying chronic microglial activation are poorly understood. We have previously shown that anti-inflammatory TGF-ß signaling is inhibited in LPS-treated microglia. In this study, we assessed whether different disease-related microglial activators could downregulate TGF-ß induction of gene expression. We examined the effects of amyloid ß (Aß) (1-42)- or heat-killed Listeria monocytogenes (HKLM) on the TGF-ß-regulated gene expression in primary rat microglia. We found that Aß (1-42) oligomers and HKLM, in addition to LPS, suppressed TGF-ß-mediated induction of gene expression in part through reducing expression of TßR1 mRNA encoding the TGF-ß receptor 1 in primary microglia. Aß (1-42) and LPS also prevented induction of TGF-ß-induced genes in primary microglia. Additionally, Aß (1-42) rescued primary microglia from TGF-ß-mediated cell death without increasing cell proliferation. Blockage of NFκB signaling, but not the ERK or IRF3 pathways, inhibited Aß (1-42)- and LPS-mediated reduction of TßR1 mRNA. Finally, LPS and Aß (1-42) induced transient upregulation of mRNAs encoding SnoN and Bambi, inhibitors of TGF-ß signaling. Our data indicate that one mechanism through which activators may prolong microglial stimulation is through direct inhibition of anti-inflammatory signaling. A more detailed understanding of the interaction between inflammatory and anti-inflammatory pathways may reveal potential targets for ameliorating chronic inflammation and hence speed the development of therapeutics to address neurodegenerative diseases.