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1.
J Infect Public Health ; 15(11): 1299-1314, 2022 Nov.
Article in English | MEDLINE | ID: mdl-36279686

ABSTRACT

As of 25th July, 2022, global Disease burden of 575,430,244 confirmed cases and over 6,403,511 deaths have been attributed to coronavirus disease 2019 (COVID-19). Co-infections/secondary infections continue to plague patients around the world as result of the co-morbidities like diabetes mellitus, biochemical changes caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) especially significant elevation in free iron levels, immune suppression caused by SARS-CoV-2, and indiscriminate use of systemic corticosteroids for the treatment of severe COVID-19 disease. In such circumstances, opportunistic fungal infections pose significant challenge for COVID-19 disease therapy in patients with other co-morbidities. Although COVID-19-associated Mucormycosis (CAM) has been widely recognized, currently extensive research is being conducted on mucormycosis. It has been widely agreed that patients undergoing corticosteroid therapy are highly susceptible for CAM, henceforth high index of screening and intensive care and management is need of an hour in order to have favorable outcomes in these patients. Diagnosis in such cases is often delayed and eventually the disease progresses quickly which poses added burden to clinician and increases patient load in critical care units of hospitals. A vast perusal of literature indicated that patients with diabetes mellitus and those with other co-morbidities might be highly vulnerable to develop mucormycosis. In the present work, the case series of three patients presented at Chest Disease Hospital Srinagar, Jammu and Kashmir infected with CAM has been described with their epidemiological data in supplementary section. All these cases were found to be affected with co-morbidity of Diabetes Mellitus (DM) and were under corticosteroid therapy. Furthermore, given the significant death rate linked with mucormycosis and the growing understanding of the diseases significance, systematic review of the literature on CAM has been discussed and we have attempted to discuss emerging CAM and related aspects of the disease.


Subject(s)
COVID-19 , Coinfection , Diabetes Mellitus , Mucormycosis , Humans , Mucormycosis/drug therapy , Mucormycosis/epidemiology , SARS-CoV-2 , Diabetes Mellitus/epidemiology , Adrenal Cortex Hormones/therapeutic use
2.
Plant Physiol Biochem ; 153: 20-29, 2020 Aug.
Article in English | MEDLINE | ID: mdl-32464490

ABSTRACT

Soil phosphorus (P) occurs in pools of lower availability due to soil P fixation and therefore, it is a key constrain to crop production. Long term molybdenum-induced effects in wheat and rhizosphere/non-rhizosphere soil P dynamics have not yet been investigated. Here, a long term field experiment was conducted to explore these effects in wheat consisting of two treatments i.e. with molybdenum (+Mo) and without molybdenum (-Mo). The results revealed that molybdenum (Mo) supply increased plant biomass, grain yield, P uptake, preserved the configuration of chloroplast, stomata, and mesophyll tissue cells, suggesting the complementary effects of Mo on wheat yield and P accumulation. During the periods of vegetative growth, soil organic carbon, organic matter, and microbial biomass P were higher and tended to decrease in rhizosphere soil at maturity stage. In +Mo treatment, the most available P fractions [H2O-Pi (16.2-22.9 mg/kg and 4.24-7.57 mg/kg) and NaHCO3-Pi (130-149 mg/kg and 77.2-88 mg/kg)] were significantly increased in rhizosphere and non-rhizosphere soils, respectively. In addition, the +Mo treatment significantly increased the acid phosphatase activity and the expression of phoN/phoC, aphA, olpA/lppC gene transcripts in rhizosphere soil compared to -Mo. Our research findings suggested that Mo application has increased P availability not only through biochemical and chemical changes in rhizosphere but also through P assimilation and induced effects in the leaf ultra-structures. So, it might be a strategy of long term Mo fertilizer supply to overcome the P scarcity in plants and rhizosphere soil.


Subject(s)
Molybdenum/pharmacology , Phosphorus/metabolism , Plant Leaves/ultrastructure , Rhizosphere , Triticum/drug effects , Carbon , Soil , Triticum/metabolism
3.
PLoS Genet ; 10(9): e1004499, 2014 Sep.
Article in English | MEDLINE | ID: mdl-25187989

ABSTRACT

In all animals managing the size of individual meals and frequency of feeding is crucial for metabolic homeostasis. In the current study we demonstrate that the noradrenalin analogue octopamine and the cholecystokinin (CCK) homologue Drosulfakinin (Dsk) function downstream of TfAP-2 and Tiwaz (Twz) to control the number of meals in adult flies. Loss of TfAP-2 or Twz in octopaminergic neurons increased the size of individual meals, while overexpression of TfAP-2 significantly decreased meal size and increased feeding frequency. Of note, our study reveals that TfAP-2 and Twz regulate octopamine signaling to initiate feeding; then octopamine, in a negative feedback loop, induces expression of Dsk to inhibit consummatory behavior. Intriguingly, we found that the mouse TfAP-2 and Twz homologues, AP-2ß and Kctd15, co-localize in areas of the brain known to regulate feeding behavior and reward, and a proximity ligation assay (PLA) demonstrated that AP-2ß and Kctd15 interact directly in a mouse hypothalamus-derived cell line. Finally, we show that in this mouse hypothalamic cell line AP-2ß and Kctd15 directly interact with Ube2i, a mouse sumoylation enzyme, and that AP-2ß may itself be sumoylated. Our study reveals how two obesity-linked homologues regulate metabolic homeostasis by modulating consummatory behavior.


Subject(s)
Drosophila Proteins/metabolism , Drosophila melanogaster/metabolism , Drosophila melanogaster/physiology , Feeding Behavior/physiology , Meals/physiology , Obesity/metabolism , Obesity/physiopathology , Animals , Cell Line , Feedback , Homeostasis/physiology , Hypothalamus/metabolism , Male , Mice , Mice, Inbred C57BL , Neurons/metabolism , Octopamine/metabolism , Potassium Channels/metabolism , Transcription Factor AP-2/metabolism
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