Sehirli, Ahmet OzerSayiner, Serkan
3页查看更多>>摘要：Declared as a pandemic by the World Health Organization， COVID-19 causes damage to tissues with the cytokine storm。 It even causes death in people who are fond of it。 In this case， the role of the immune system is vital。 In particular， the cycle of melatonin and 5-methoxytryptophol released from the pineal hormone ensures that immunity continues for 24 h。 While 5-MTX is active in sunlight， melatonin secretion increases in the dark at night。 5-MTX， like melatonin， has shown antioxidant and immunomodulatory properties in studies。 Therefore， people who are sick and those who are not must strictly comply with the 24-h circadian rhythm during this period。 We think that it is crucial in terms of being protected from the disease that we should carry out our activities according to the circadian rhythm。
原文链接:
NSTL
Elsevier
Liu, ZiyangJiang, WenboHai, YongLiu, Yufu...
2页原文链接:- NSTL
- Elsevier
Serra-Mestres, JordiIsetta, MarcoCastagna, AlbertoManzo, Ciro...
4页查看更多>>摘要：The association of the coronavirus disease 2019 (COVID-19) with significant neurological and neuropsychiatric complications has been increasingly reported， both during the acute illness and in its aftermath。 However， due to the short duration of patient follow up until now， it is not clear whether this infection will be associated with longer-term neurological and/or neuropsychiatric sequelae。 In particular， the question of whether COVID-19 will be associated with an increased risk and rate of future dementia remains open and subject to speculation。 During the course of the COVID-19 pandemic， an increasing number of patients have reported sudden anosmia or other olfactory dysfunction as concurrent symptoms。 The possibility that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may reach the brain via the olfactory nerve or an upper nasal trancribrial route is an interesting working hypothesis。 Among the identified genetic risk factors for Late-onset Alzheimer's disease (LOAD)， Apo E4 is one of the strongest and most frequent。 People carrying one or two copies of the e4 allele of Apo E4 have significant odor recognition deficits in comparison to those not carrying this haplotype。
原文链接:- NSTL
- Elsevier
da Costa, Luis Filipe Teixeira
5页查看更多>>摘要：The investigation of familial hypercholesterolemia (FH) and its relationship to atherosclerosis has led to enormous scientific and medical progress， including the identification of genetic defects underlying FH， the elucidation of molecular mechanisms crucial for cellular cholesterol homeostasis and the development of current pharmaceutical tools for FH treatment (which are directed at increasing LDL uptake)。 These successes also led to the establishment of a model centered on cellular rather than whole organism processes， and a view of FH as resulting from a deficiency in LDL uptake。 On the other hand， whole organism fluxes of cholesterol (like those of other nutrients) are centered on the liver， LDL (ultimately derived from the liver) is the main cholesterol transporter in plasma， and there is evidence of evolutionary pressure favoring mechanisms to maintain LDL plasma concentrations。 Furthermore， the alterations in cellular metabolism observed in FH are consistent with a coordinated response by the liver to increase the levels of plasma LDL， suggesting that a signaling defect (rather than an uptake deficiency) is the fundamental problem underlying hypercholestemlemia - an hypothesis that explains the occurrence of hypercholestemlemia in CESD， despite normal LDL binding and uptake。 I therefore propose that the liver contains a mechanism to assess and regulate plasma levels of LDL (an "LDL-ostat")， and that hypercholesterolemia is caused by defects in it。 This model has implications for future research directions， and suggests alternative therapeutic approaches， particularly centered on efforts to restore LDL measurement/ signaling (rather than its uptake)， some of which are in stark contrast to those currently in use。
原文链接:- NSTL
- Elsevier
Alicandri-Ciufelli, MatteoMolinari, Giulia
1页原文链接:- NSTL
- Elsevier
Manti, SaraParisi, Giuseppe FabioPapale, MariaMule, Enza...
3页查看更多>>摘要：Coronavirus disease 2019 (COVID-19) caused more than 52。775。271 million confirmed cases， 1。293。106 deaths， globally， and afflicted 208 countries， areas， or territories; and almost three months have passed since the World Health Organisation (WHO) declared COVID-19 as a pandemic。 Despite the dramatic and global impact of the Coronavirus， the knowledge about the SARS-CoV-2 infection has been improved remarkably。 Herein， we provided the rationale for SARS-CoV-2 infection as endothelial dysfunction rather than respiratory disease。 Accordingly， we strongly invited the researchers to look beyond pulmonary injury and shift their attention from respiratory disease to endothelial disorder。 This strategy could be particularly relevant to identifying therapeutic weapons stabilizing the endothelium rather than the lungs。
原文链接:- NSTL
- Elsevier
Suzuki, Yuichiro J.Nikolaienko, Sofia, IShults, Nataliia, VGychka, Sergiy G....
3页查看更多>>摘要：Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing the current pandemic of coronavirus disease 2019 (COVID-19) that have killed over one million people worldwide so far。 To date， over forty million people have officially been identified to be infected with this virus with less than 3% death rate。 Since many more people are expected to have been infected with this virus without the official diagnosis， the number of people who have recovered from the SARS-CoV-2 infection should be substantial。 Given the large number of people recovered from either the mild SARS-CoV-2 infection or more severe COVID-19 conditions， it is critical to understand the long-term consequences of the infection by this virus。 Our histological evaluations revealed that patients died of COVID-19 exhibited thickened pulmonary vascular walls， one important hallmark of pulmonary arterial hypertension (PAH)。 By contrast， such pulmonary vascular remodeling lesions were not found in patients died of SARS-CoV-1 during the 2002-2004 SARS outbreak or due to the infection by H1N1 influenza。 The advancement in the treatment for the human immunodeficiency virus (HIV) infection has been remarkable that HIV-infected individuals now live for a long time， in turn revealing that these individuals become susceptible to developing PAH， a fatal condition。 We herein hypothesize that SARS-CoV-2 is another virus that is capable to triggering the increased susceptibility of infected individuals to developing PAH in the future。 Given the large number of people being infected with SARS-CoV-2 during this pandemic and that most people recover from severe， mild or asymptomatic conditions， it is imperative to generate scientific information on how the health of recovered individuals may be affected long-term。 PAH is one lethal consequence that should be considered and needs to be monitored。 This may also foster the research on developing therapeutic agents to prevent PAH， which has not so far been successful。
原文链接:- NSTL
- Elsevier
Nejadghaderi, Seyed AriaNazemalhosseini-Mojarad, EhsanAghdaei, Hamid Asadzadeh
4页查看更多>>摘要：At the end of 2019， an emerging outbreak caused by severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) that first reported from Wuhan， China。 The first manifestations of patients infected with SARS-CoV-2 was flu-like symptoms， while other type of manifestations， especially gastrointestinal manifestations were discovered recently。 As of June 2020， there is no specific drug or treatment strategy for COVID-19， a disease caused by SARSCoV-2， so different combination of antiviral drugs is currently being used。 Gut microbiota mostly consists of four phyla， including Firmicutes， Bacteroidetes， Proteobacteria， and Actinobacteria。 The interaction between gut microbiota and immune system through releasing some cytokines such as IL-1 beta， IL-2， IL-10， TNF-alpha， and IFN-gamma that play roles in the severity of COVID-19。 In this article， a new potential treatment for COVID-19 by fecal microbiota transplantation (FMT) is described。 FMT revealed promising results in different diseases， especially recurrent clostridium difficile infection， and it might reduce length of hospital admission and severity of the disease by modification of gut microbiota composition。
原文链接:- NSTL
- Elsevier
O'Kennedy, NiamhDuttaroy, Asim K.
4页查看更多>>摘要：The ongoing coronavims disease 2019 (COVID-19) pandemic caused by the SARS-CoV-2 virus is now considered a global public health threat。 The primary focus has been on reducing the viral spread and treating respiratory symptoms; as time goes on， the impact of COVID-19 on neurological and haemostatic systems becomes more evident。 The clinical data suggest that platelet hyperactivity plays a role in the pathology of COVID-19 from its onset and that platelets may serve critical functions during COVID-19 progression。 Hyperactivation of blood platelets and the coagulation system are emerging as important drivers of inflammation and may be linked to the severity of the 'cytokine storm' induced in severe cases of COVID-19， in which disseminated intravascular coagulation， and platelet hyperactivity are associated with poor prognosis and increased risk of mortality。
原文链接:- NSTL
- Elsevier
