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The Role of the Gut Microbiome in Cardiovascular Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
To Reduce High Levels of Beta-Glucuronidase: Decrease meat intake and increase insoluble fiber.Take probiotics.Consider Silybum marianum for liver support.Take calcium-D-glucarate.
Tumors of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Tumor markers in the CSF: Carcinoembryonic antigen (CEA) is often elevated in adenocarcinoma.Beta-glucuronidase is frequently elevated in patients with leptomeningeal metastases from epithelial-derived tumors.Beta2–microglobulin is useful in hematopoietic malignancies involving the leptomeninges.AFP and β-HCG may be noted in metastatic germ cell tumors with leptomeningeal involvement.
Managing Pain in the Presence of Autoimmune Disease
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Beta glucuronidase: This tends to self-correct as the good bacteria should make an enzyme to break it down. If they don’t start doing this work by the first retest, consider calcium D-glucarate supplementation. Or possibly add a combination insoluble/soluble fiber supplement to bind up the toxins until they can be cleared from the gut and help to feed the good bacteria as a “prebiotic,” food for the good bacteria.
A New Approach to Polycystic Ovary Syndrome: The Gut Microbiota
Published in Journal of the American College of Nutrition, 2020
Gamze Yurtdaş, Yasemin Akdevelioğlu
In addition to the above-mentioned mechanisms, in recent studies, it has been suggested that androgens may lead to the development of PCOS by shaping the gut microbiota composition (10, 40, 41). Recent studies have shown that changes in gut microbiota are associated with hyperandrogenism in women with PCOS (40, 41). However, there is a limited number of studies to explain how sex steroids affect gut microbiota. It is thought that sex steroids may directly influence the composition of gut microbiota by changing beta-glucuronidase activity and energy production (10, 77). It has also been reported that sex steroids may indirectly regulate gut microbiota by the activation of steroid receptors in the host (10). Another potential effect is that changes in sex steroids are likely to alter the immune response by regulating the integrity of the intestinal barrier. Reduction of the integrity of the intestinal barrier results in the infiltration of gram-negative bacteria into the circulation and activation of the peripheral inflammatory response generated by LPS (10). It should be noted that gut microbiota may also play a role in PCOS by regulating sex steroids (40). However, the role of gut microbiota on steroid regulation is not fully understood (78). Future studies need to investigate mechanisms behind the relationship between hyperandrogenism and the gut microbiome.
Prodrugs for targeted cancer therapy
Published in Expert Review of Anticancer Therapy, 2019
Carla Souza, Diogo Silva Pellosi, Antonio Claudio Tedesco
One of the initial problems of ADEPT was the persistence of enzyme activity in the blood, which could result in a widespread activation of the prodrug. An anti-PEG antibody has also been utilized to clear an antibody-beta-glucuronidase conjugate that had been PEGylated. This method may result in efficient clearance [136]; however, an immune response to PEG must be taken into consideration for human applications [137]. Furthermore, the low number of tumor-selective antigens also limit the applicability of the ADEPT strategy, leading to the transformation of prodrugs in non-cancerous tissues [14,99]. Other drawbacks include the limited delivery of conjugates in poorly vascular tumors, the cost, and the difficulty involved in the development and cleaning of antibodies [3,14].
Neutrophil mediated inflammatory lung damage following single Sub lethal inhalation exposure to plant protein toxin abrin in mice
Published in Experimental Lung Research, 2019
Bhavana Sant, Pravin Kumar, A. K. Soni, G. M. Kannan, D. P. Nagar, G. B. K. S. Prasad, A. S. B. Bhaskar
During lung toxicity, ensuing death of the cells triggers an inflammatory response characterized by the recruitment of inflammatory mediators, neutrophils at the site of injury and release of cytoplasmic enzymes from the lysed cells. It is observed that phagocyte activity increase during lysis of cells. Increased phagocytic activity has been detected by measurement of lysosomal enzyme, beta-glucuronidase. Levels of beta-glucuronidase in BALF appear to be a good indicator of increased phagocytic activity in response to inhaled particles. Large increase in activity of beta-glucuronidase also correlates to the degree of inflammation in rats exposed to nickel by inhalation route.25 Inflammation is the most prominent clinical manifestation of mice following inhalation exposure. A massive recruitment of neutrophils and the stimulation of a turbulent pro-inflammatory cytokine storm within the lungs are the observed symptoms after intranasal exposure of abrin. Time dependent extensive infiltration of neutrophils was found in lungs after intranasal post exposure of abrin.5 In the case of intranasal ricin exposure, neutrophil infiltration resulted in severe pulmonary edematous inflammation which in turn led to respiratory failure and death.6 In this study we exposed mice to a real scenario of toxic protein aerosol. In complement with the reported findings, our results also reflect that abrin after inhalation exposure leads to increased phagocytic activity, inflammation and compromised permeability of alveolar epithelial cells confirmed by dose and time dependent increased activity of beta-glucuronidase and protein levels in BALF.