Magnesium is one of the commonly overlooked electrolytes, yet it plays a vital role in many of the processes in the human body. The balance of magnesium can translate into subtle changes in a person’s daily life, causing fatigue and confusion, to extreme cases that can end up causing central nervous system depression, respiratory failure, or cardiac arrhythmias. It is vital to be familiar with the physiology of magnesium regulation and knowledgeable regarding the causes that can lead to its toxicity to ensure the prevention of the possibly fatal condition. Magnesium balance can be summarised as the difference between magnesium intake and its excretion. Any factor overwhelming either of the two factors can cause pathological levels of the electrolyte. In addition to learning preventive measures to help patients against effects of magnesium toxicity, it is also important that the medical community trains to be able to treat cases of hypermagnesaemia. This review assesses the latest advancements in knowledge of magnesium metabolism, examines the case reports of hypermagnesaemia in an attempt to list the causes of magnesium toxicity, and enumerates management advances for the condition.
The European grapevine (Vitis vinifera L.) has been cultivated in North America for about 500 years. One of the major limitations to its culture is the powdery mildew (PM) fungus, Erysiphe necator Schw. This study reports on the most extensive screening of Vitis species from the southwestern United States and northern Mexico for resistance to PM, testing 147 accessions of 13 Vitis species. In addition, Vitis vinifera cv. Carignane, a highly susceptible wine grape cultivar, was used as a reference to evaluate the effect of the inoculum 14 days postinoculation. Inoculation was done with a vacuum-operated settling tower using a broadly virulent isolate of E. necator, the C-strain. Resistant accessions (nine), moderately susceptible accessions (39), and highly susceptible accessions (99) were detected. The resistant accessions were then inoculated with an additional fungal isolate, e1-101, and they retained their resistance. Vitis species susceptibility was not associated with a North-South gradation, but Western species were more susceptible than Midwestern and Eastern species. All five of the V. monticola accessions were susceptible, as were the accessions of V. treleasei. The species V. acerifolia, V. candicans, V. cinerea, and V. × doaniana had significantly more resistant to moderately susceptible accessions compared with V. arizonica, V. berlandieri, V. californica, V. × champinii, V. girdiana, V. riparia, and V. rupestris, which had relatively more susceptible accessions than the other species. This research identified new sources of PM resistance in Vitis from the southwestern United States that could be incorporated into PM resistance breeding programs throughout the world.
Diabetic kidney disease (DKD) has been an immense burden on the healthcare system, and is the leading cause of end stage kidney disease worldwide. DKD involves various intersecting pathways that lead to progressive kidney damage. Due to its versatile pathogenesis, DKD has been a formidable adversary. For many decades, there has not been much development in the arsenal in the fight against DKD, but recently, multiple new prospects have emerged due to the breakthrough in understanding of DKD pathology. Tireless research of the changes occurring in the kidney as a result of diabetes, and the factors driving these changes, has led to the invention of medications that hopefully will be highly impactful in preventing end stage kidney disease in patients with diabetes. In this review, the authors summarise the timeline of the pathological changes that occur in DKD, the mechanism driving these pathological changes, and the recent discoveries in the pathways leading to DKD. These span over changes in metabolic pathways, inflammatory cascades, epigenetic alterations, and the description of their effects at cellular to structural levels in the kidney as a byproduct of uncontrolled hyperglycaemia. The authors also correlate these mechanisms with a few of the medications that are being utilised to slow down DKD, and some in the pipeline, with some references to the trials that support their use.
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