scholarly journals Polyphenols as Alternative Treatments of COVID-19

Author(s):  
Yifei Wu ◽  
Scott D. Pegan ◽  
David Crich ◽  
Ellison Desrochers ◽  
Edward B. Starling ◽  
...  
2000 ◽  
Vol 62 (1) ◽  
pp. 83-88 ◽  
Author(s):  
Michihiro HIDE ◽  
Yumi YAMAMURA ◽  
Eishin MORITA ◽  
Osamu KORO ◽  
Shoso YAMAMOTO

Author(s):  
Susanne Fischer ◽  
Tabea Schumacher ◽  
Christine Knaevelsrud ◽  
Ulrike Ehlert ◽  
Sarah Schumacher

Abstract Background Less than half of all individuals with post-traumatic stress disorder (PTSD) remit spontaneously and a large proportion of those seeking treatment do not respond sufficiently. This suggests that there may be subgroups of individuals who are in need of augmentative or alternative treatments. One of the most frequent pathophysiological findings in PTSD is alterations in the hypothalamic–pituitary–adrenal (HPA) axis, including enhanced negative feedback sensitivity and attenuated peripheral cortisol. Given the role of the HPA axis in cognition, this pattern may contribute to PTSD symptoms and interfere with key processes of standard first-line treatments, such as trauma-focused cognitive behavioural therapy (TF-CBT). Methods This review provides a comprehensive summary of the current state of research regarding the role of HPA axis functioning in PTSD symptoms and treatment. Results Overall, there is preliminary evidence that hypocortisolaemia contributes to symptom manifestation in PTSD; that it predicts non-responses to TF-CBT; and that it is subject to change in parallel with positive treatment trajectories. Moreover, there is evidence that genetic and epigenetic alterations within the genes NR3C1 and FKBP5 are associated with this hypocortisolaemic pattern and that some of these alterations change as symptoms improve over the course of treatment. Conclusions Future research priorities include investigations into the role of the HPA axis in day-to-day symptom variation, the time scale in which biological changes in response to treatment occur, and the effects of sex. Furthermore, before conceiving augmentative or alternative treatments that target the described mechanisms, multilevel studies are warranted.


Author(s):  
William Eduardo Furtado ◽  
Lucas Cardoso ◽  
Paula Brando de Medeiros ◽  
Nicollas Breda Lehmann ◽  
Elisabeth de Aguiar Bertaglia ◽  
...  

2017 ◽  
Vol 17 (4) ◽  
pp. 278-285 ◽  
Author(s):  
Gino A. Vena ◽  
Marcus Maurer ◽  
Nicoletta Cassano ◽  
Torsten Zuberbier

2011 ◽  
Vol 142 (7) ◽  
pp. 842-849 ◽  
Author(s):  
Valeria V. Gordan ◽  
Joseph L. Riley ◽  
Paul K. Blaser ◽  
Eduardo Mondragon ◽  
Cynthia W. Garvan ◽  
...  

2017 ◽  
Vol 4 (6) ◽  
pp. 193-193

Das B, Sarkar C, Das D et al. Telavancin: a novel semisynthetic lipoglycopeptide agent to counter the challenge of resistant Gram-positive pathogens. Ther Adv Infect Dis. 2017 Mar; 4(2): 49–73. DOI: 10.1177/2049936117690501 The authors wish to highlight the following corrections, which should have appeared in the original text: 1.  Page 49, Abstract, lines 4–5: Telavancin is approved for hospital-acquired and ventilator-associated bacterial pneumonia (HABP/VABP) in the United States when alternative treatments are not available. In Russia and Canada, telavancin is approved for both complicated skin and skin-structure infections (cSSSI) and HABP/VABP. 2.  Page 50, right panel, para 2, lines 15–18: Revised per telavancin label based on latest PI and EMA (also pasted below). In the United States, telavancin is approved in adults for the treatment of cSSSI due to susceptible Gram-positive pathogens. In addition, telavancin is approved for HABP/VABP when alternative treatments are not suitable. In Canada and Russia, telavancin is approved for Gram-positive pathogens for the treatment of patients with cSSSI and HABP/VABP. In the European Union, telavancin is approved for the treatment of nosocomial pneumonia, known or believed to be caused by methicillin-resistant Staphylococcus aureus (MRSA) when other alternative medicines are unsuitable. 3.  Page 51, right panel, para 1, lines 1–6: Per the latest (2016) telavancin PI, HABP/VABP indication for telavancin should be included. 4.  Page 51, Figure 1 caption: The hydrophilic nature of telavancin contributes to its half-life. 5.  Page 53, left panel, para “In vitro activity”, lines 5–8: As per the following (newer) article, which states that “Telavancin MIC is 16-32 fold lower than vancomycin against MRSA.” Mendes RE, Flamm RK, Farrell DJ, et al. Telavancin activity tested against Gram-positive clinical isolates from European, Russian and Israeli hospitals (2011–2013) using a revised broth microdilution testing method: redefining the baseline activity of telavancin. J Chemother 2015; 28: 83–88. DOI: 10.1179/1973947815Y.0000000050 6.  Page 53, right panel, para 1, lines 11–16: Per the Mendes et al. (2015) article listed above, telavancin minimum inhibitory concentration (MIC) is 16- to 32-fold lower than vancomycin against MRSA. 7.  Page 54, Table 1: These MIC values were estimated using old methods. Revise the MIC values based on the references for new MIC methods (see below). Farrell DJ, Mendes RE, Rhomberg PR, et al. Revised reference broth microdilution method for testing telavancin: effect on MIC results and correlation with other testing methodologies. Antimicrob Agents Chemother 2014; 58(9): 5547–5551. DOI: 10.1128/AAC.03172-14 8.  Page 61, right panel, para “ATTAIN trials (ATTAIN 1 and 2)”, lines 9–12: The ATTAIN trials did not include patients with “healthcare-associated pneumonia,” therefore, any mention of this is not correct.


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