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Biology of Acinetobacter spp.
Published in E. Bergogne-Bénézin, M.L. Joly-Guillou, K.J. Towner, Acinetobacter, 2020
A wide range of extracellular enzymes are produced by acinetobacters, including lipases, esterases, amylase, collagenase, endo- ß-1,ß-glucanase, and at least one ß-lactamase. There are several interesting periplasmic enzymes, including an insulin-cleaving metalloproteinase, and numerous interesting membrane-bound en-zymes, including an NAD-independent malate dehydrogenase, various proteases, leucine aminopeptidase, alanine aminopeptidase, and NAD-independent aldehyde, alcohol, lactate and mandelate dehydrogenases (Towner et al., 1991). So far as cofactors are concerned, elucidation of the biological role of pyrroloquinoline quinone (PQQ), particularly in respect of its function in glucose dehydrogenase activity, has resulted largely from studies with various strains of Acinetobacter (Duine, 1991).
Non-Invasive Early, Quick Diagnostic Methods of Various Cancers (Part I) and Safe, Effective, Individualized Treatment of Cancer (Part II)
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
Human Papilloma Virus Type 16 is often associated with the development of various cancers. Originally, it was thought to be associated with cervical, ovarian cancer, and breast cancer only, and thought to be sexually transmitted but we are finding out that it is much more than that. In families where one member has a strong HPV 16 infection, other family members seem to have the same degree of infection. Even cancer specialists are at risk as they come into frequent close contact with cancer patients carrying the virus on a daily basis. We found using BDORT that even if the patient does not develop a malignancy there is increased tendency to develop Alzheimer's and autism. Giving optimal doses of vitamin D3, Taurine, and pyrroloquinoline quinone (PQQ) was found to be extremely beneficial. They are even more beneficial when used in a compatible combination of all three.
Mitochondrial Dysfunction Linking Obesity and Asthma
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Naveen K. Bhatraju, Anurag Agrawal
Restoration of mitochondrial function and thus metabolic flexibility is pivotal to gaining optimal control over this growing epidemic. This could be achieved through the use of scavengers to neutralize harmful ROS, simple lifestyle modifications or by drugs/small molecules that mimic these modifications, through mitochondrial donation. These methods based on the fundamental principles of repair, reprogram or replace (referred to a “3R model”) could be tailored to be used individually or in combination to develop personalized treatment strategies. Saying this, weight loss through caloric restriction (CR) and exercise can be considered as first line of recommendations, in obese-asthmatics, for their established beneficial roles both in obesity and metabolic syndrome (improves insulin sensitization), and asthma control (Mendes et al. 2010; Sideleva et al. 2013). The contextual and general health benefits of exercise and CR are thought to be coordinated through their ability to reset mitochondrial function by epigenetic reprogramming (Cheng & Almeida 2014). However, the contextual utilization of this strategy is restricted in some patients due to impaired exercise capacity and/or lack of compliance to energy-restricted diets over long time. In such conditions, chemical molecules that could mimic CR could be of great application. Metformin falls into this category and has been shown to improve insulin sensitivity and induce weight loss possibly via effects on gut microbiome (Hur & Lee 2015; Park et al. 2012). Metformin has also been shown to attenuate asthma features in obese mice (Calixto et al. 2013). This pinpoints to an old evolutionary microbe-mitochondria link that could be harnessed for efficient mitochondrial reprogramming. It may be noted that gut microbiome has been associated with both asthma and obesity (Cho and Blaser 2012; Fujimura & Lynch 2015; Riiser 2015). In this context, microbiome-derived metabolites, such as pyrroloquinoline quinone (PQQ), which is mitochondria-targeted antioxidant and potent inducer of mitochondrial biogenesis warrants further investigation.
Point of care blood glucose devices in the hospital setting
Published in Critical Reviews in Clinical Laboratory Sciences, 2023
Nam K. Tran, Clayton LaValley, Berit Bagley, John Rodrigo
Amperometric electrochemical biosensors serve as the mainstay for glucose monitoring technology [23]. Figure 1 illustrates a typical amperometric glucose-oxidase (GO)-based biosensor. In brief, an electrical signal is produced during an enzymatically catalyzed reduction-oxidation reaction. Glucose oxidase is the most common enzyme used in BGMS biosensors. Early GO-amperometric biosensors relied on oxygen as an electron carrier as shown in Figure 1 [24]. Later GO-biosensors utilized artificial electron carriers that had the added benefit of reducing the applied electrical potential on the sensor. Utilizing GO offers the benefit of its high specificity for glucose, but this enzyme can be affected by oxygen tension, as discussed below [9,24]. As such, some manufacturers have developed amperometric sensors that use glucose dehydrogenase (GDH) coupled to electron carriers such as nicotinamide adenine dinucleotide, flavin adenine dinucleotide, or pyrroloquinoline quinone (PQQ). The drawback in using GDH is its reduced specificity for glucose [25]. Glucose sensors using coulometric, colorimetric, or spectrophotometric principles also exist but have become less common.
Effect of high-dose intravenous vitamin C on point-of-care blood glucose level in septic patients: a retrospective, single-center, observational case series
Published in Current Medical Research and Opinion, 2021
Juan He, Guanhao Zheng, Xian Qian, Huiqiu Sheng, Bing Chen, Bing Zhao, Erzhen Chen, Enqiang Mao, Xiaolan Bian
Interestingly, we observed that POCG testing results were lower than referential LG test results. This was different than other studies’ results that reported higher POCG testing results leading to false hyperglycemia status23,25,36. We found that other studies used the glucose dehydrogenase pyrroloquinoline quinone (GDH-PQQ) amperometric method as the POCG testing method. This method differs in terms of mechanism from the GOD-POD colorimetric method23,25,36. A representative study was conducted by Cho et al. comparing the accuracy of the GDH-PQQ and modified GOD methods compared with the hexokinase spectrophotometric method at different VC concentrations and blood glucose levels. They found that the GDH-PQQ method produced significantly higher results than those obtained with the LG test method regardless of blood glucose level, especially at high VC concentrations (15–30 mg/dL). Conversely, the modified GOD method must be discussed in two scenarios: at low (80 mg/dL) blood glucose levels, the method was highly accurate; whereas at moderate (126 mg/dL) and high (300 mg/dL) blood glucose levels, it produced moderately lower results compared with those obtained with the LG test method regardless of VC concentration48. The patients included in our study had moderate to high levels of blood glucose. Thus, our observation regarding artificially low POCG testing results during hdVC therapy using the GOD method is in accordance with the aforementioned study.
Effects of Pyrroloquinoline Quinone (PQQ) Supplementation on Aerobic Exercise Performance and Indices of Mitochondrial Biogenesis in Untrained Men
Published in Journal of the American College of Nutrition, 2020
Paul S. Hwang, Steven B. Machek, Thomas D. Cardaci, Dylan T. Wilburn, Caelin S. Kim, Emiliya S. Suezaki, Darryn S. Willoughby
Pyrroloquinoline quinone (PQQ) has been identified as a novel supplement that appears to promote benefits related to cognitive, immune, anti-diabetic, and anti-oxidative properties (12,13). Furthermore, there is data suggesting its role in continuous redox-cycling activity to oxidize nicotinamide adenine dinucleotide (NADH) to modulate lactate dehydrogenase (LDH) activity in an animal model (14). Moreover, there has been research examining the mechanisms of action behind PQQ supplementation on mitochondrial biogenesis (13,15–18). In fact, there are data in rodents to show that PQQ treatment enabled elevations in markers of mitochondrial biogenesis such as PGC-1α, NRF-1/2, cAMP response element-binding protein (CREB), as well as TFAM (15,16). Furthermore, the overexpression of PGC-1α activity in skeletal muscle has been attributed to the remodeling of muscle tissue to a fiber-type composition that is metabolically more oxidative and less glycolytic (6,9,19).