Abstract Soil salinity is one of the most devastating problems which reduces crop production and increases desertification. New approaches to overcome the negative effect of salinity on plants include the use of plant biostimulants, such as Xyloglucan oligosaccharides (XGOs) derived from the breakdown of xyloglucans from plant cell walls. The present study aimed at verifying the influence of exogenous XGOs derived from Tamarindus indica L. cell walls, on Arabidopsis thaliana’s tolerance to salt stress by understanding the gene expression, enzymatic and metabolic changes resulting from its application. A. thaliana plants were grown in liquid media and after 15 days they were treated by a salt shock with 100 mM of sodium chloride, with or without XGOs at 0.1 mg L-1. Gene expression of four oxidative stress markers as well as catalase and peroxidase activities and content of glutathione, total carbonyl, polyphenolics and chlorophyll were quantified. Bioinformatic models were used to obtain the co-expression network of the four oxidative stress response gene markers from microarray data of Arabidopsis under salt stress. Results showed that in saline conditions, XGOs dramatically increased catalase gene expression and enzymatic activity, peroxidase activity, and chlorophyll a/b ratio, while reducing protein oxidation and total polyphenols. Thus, XGOs may act to counteract negative effects of oxidative stress under saline conditions.

Polyglutamine diseases are inherited neurodegenerative conditions arising from expanded trinucleotide CAG repeats in the diseasecausing gene, which are translated into polyglutamine tracts in the resultant protein. Although these diseases share a common type of mutation, emerging evidence suggests that pathogenesis is complex, involving disruption of key cellular pathways, and varying with the disease context. An understanding of polyglutamine disease mechanisms is critical for development of novel therapeutics. Here we summarise theories of molecular pathogenesis, and examine ways in which this knowledge is being harnessed for therapy, with reference to work under way at the University of Cape Town. Despite a plethora of preclinical data, clinical trials of therapies for polyglutamine diseases have had only limited success. However, recently initiated trials, including those using gene silencing approaches, should provide valuable insights into the safety and efficacy of therapiesdirectly targeting polyglutamine pathogenesis. This is particularly relevant in the South African context, where the frequencies of 2 polyglutamine diseases, spinocerebellar ataxia types 1 and 7, are among the highest globally.

The goal of the present research was to elucidate the roles and mechanisms by which the sensory nervous system, through the actions of potent vasodilator neuropeptides, regulates cardiovascular function in both the normal state and in the pathophysiology of hypertension. The animal models of acquired hypertension studied were deoxycorticosterone-salt (DOC-salt), subtotal nephrectomy-salt (SN-salt), and Nomega-nitro-L-arginine methyl ester (L-NAME)-induced hypertension during pregnancy in rats. The genetic model was the spontaneously hypertensive rat (SHR). Calcitonin gene-related peptide (CGRP) and substance P (SP) are potent vasodilating neuropeptides. In the acquired models of hypertension, CGRP and SP play compensatory roles to buffer the blood pressure (BP) increase. Their synthesis and release are increased in the DOC-salt model but not in the SN-salt model. This suggests that the mechanism by which both models lower BP in SN-salt rats is by increased vascular sensitivity. CGRP functions in a similar manner in the L-NAME model. In the SHR, synthesis of CGRP and SP is decreased. This could contribute to the BP elevation in this model. The CGRP gene knockout mouse has increased baseline mean arterial pressure. The long-term synthesis and release of CGRP is increased by nerve growth factor, bradykinin, and prostaglandins and is decreased by alpha2-adrenoreceptor agonists and glucocorticoids. In several animal models, sensory nervous system vasoactive peptides play a role in chronic BP elevation. In the acquired models, they play a compensatory role. In the genetic model, their decreased levels may contribute to the elevated BP. The roles of CGRP and SP in human hypertension are yet to be clarified.