biochemical mechanism of covid 19

Multisystem inflammatory syndrome in children during the Coronavirus 2019 pandemic: a case series. In addition to understanding relevant risk factors, there is increasing suspicion of delayed but severe COVID-19 presentation, particularly in children, even after viral clearance (113). Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, Zhang L, Fan G, Xu J, Gu X, Cheng Z, Yu T, Xia J, Wei Y, Wu W, Xie X, Yin W, Li H, Liu M, Xiao Y, Gao H, Guo L, Xie J, Wang G, Jiang R, Gao Z, Jin Q, Wang J, Cao B. Premkumar L, Segovia-Chumbez B, Jadi R, Martinez DR, Raut R, Markmann A, Cornaby C, Bartelt L, Weiss S, Park Y, Edwards CE, Weimer E, Scherer EM, Rouphael N, Edupuganti S, Weiskopf D, Tse LV, Hou YJ, Margolis D, Sette A, Collins MH, Schmitz J, Baric RS, de Silva AM. Recent studies indicate that like other coronaviruses, SARS-CoV-2 also hijacks or Careers, Unable to load your collection due to an error. Given the correlation of IL-6 levels with increased fibrinogen and D-dimer in severe COVID-19 patients, it is likely that cytokine-mediated procoagulant changes are partially responsible for the specific thrombosis profile observed in critically ill patients (41, 110). The emerging impasse of angiotensin blockade, Coronaviruses post-SARS: update on replication and pathogenesis. The pleiotropic hepatic effects of IL-6 could play a particularly important role, inducing expression of serum amyloid A, fibrinogen, and CRP (121). Currently, there is insufficient evidence to support direct viral infection of cardiomyocytes, although SARS-CoV-2 genomes have been effectively detected in endomyocardial biopsies, mostly involving immune cell infiltrates (40, 149). A recent, large, multi-center U.S. study of 186 patients who met the broad CDC criteria for MIS-C reported 92% of patients had at least four laboratory results indicating inflammation, including but not limited to elevated CRP and ferritin, lymphocytopenia, neutrophilia, hypoalbuminemia, thrombocytopenia, anemia, as well as elevated D-dimer and fibrinogen (44). More comprehensive studies based on larger sample sizes are needed to better characterize the laboratory and clinical profile of mild versus severe pediatric COVID-19 and to help develop our understanding of immune pathogenesis. COVID and Coagulation: Bleeding and Thrombotic Manifestations of SARS-CoV2 Infection. Immunol. Soy M, Keser G, Atagndz P, Tabak F, Atagndz I, Kayhan S. Cytokine storm in COVID-19: pathogenesis and overview of anti-inflammatory agents used in treatment. TWC India. Scientists have been trying to understand the origin of COVID-19 and the virus that causes it: SARS-CoV-2. This work was supported by a Foundation Grant from the Canadian Institutes of Health Research (CIHR) (grant no. Single-cell RNA sequencing suggests that ACE2 is expressed in both the exocrine and islet cells of the pancreas (81). M.K.B. McNabb-Baltar J, Jin DX, Grover AS, Redd WD, Zhou JC, Hathorn KE, McCarty TR, Bazarbashi AN, Shen L, Chan WW. Vaira LA, Salzano G, Fois AG, Piombino P, De Riu G. Potential pathogenesis of ageusia and anosmia in COVID-19 patients. Procoagulant response is also associated with the inflammatory effects of cytokines in the vascular endothelium, including increased vascular permeability and damage as a result of immune-cell infiltration (62). Chiotos K, Bassiri H, Behrens EM, Blatz AM, Chang J, Diorio C, Fitzgerald JC, Topjian A, John ARO. Circulating levels of IL-1 in COVID-19 patients suggests local inflammasome activation with no systemic manifestations (61). To conclude, current evidence highlights that appropriate immune response is fundamental to COVID-19 pathogenesis, but much remains unknown regarding the key drivers of progression. Hyperglycemia, hypertriglyceridemia, and acute pancreatitis in COVID-19 infection: clinical implications. Current literature suggests seroconversion in COVID-19 patients occurs ~714 days post symptom onset (12). Characterization of spike glycoprotein of SARS-CoV-2 on virus entry and its immune cross-reactivity with SARS-CoV. In addition, direct viral infection of immune cells such as monocytes and macrophages have been proposed to contribute to dysregulated immune response, as has been observed in SARS (23, 52, 136). Autopsy findings in SARS-CoV infections have shown strong evidence of neuro-invasion, with demonstrated viral presence in the cerebrospinal fluid (6, 95). TWC India. Wong SF, Chow KM, Leung TN, Ng WF, Ng TK, Shek CC, Ng PC, Lam PWY, Ho LC, To WWK, Lai ST, Yan WW, Tan PYH. SARS-CoV-2 viral entry has been described in detail elsewhere (138). WC,, Benoit The trinity of COVID-19: immunity, inflammation and intervention. Some cases of cutaneous manifestations in adult COVID-19 patients have been reported, although varying incidence among patients has been noted (68, 111, 120). Bloom PP, Meyerowitz EA, Reinus Z, Daidone M, Gustafson J, Kim AY, Schaefer E, Chung RT. Chan JFW, Kok KH, Zhu Z, Chu H, To KKW, Yuan S, Yuen KY. Genomic characterization of the 2019 novel human-pathogenic coronavirus isolated from a patient with atypical pneumonia after visiting Wuhan. Given the homology between these viruses, such direct viral invasion should not be discounted (100, 106). WebTo further elucidate the mechanism of COVID-19 severity, we conducted differential expression analysis between moderate disease versus severe disease group in ncMono. The neurological manifestations of COVID-19 have not been of much focus in the literature, but a few published reports are concerning. 2023 Apr 22;260:124577. doi: 10.1016/j.talanta.2023.124577. In a more recent study, hyperlipasemia was reported in 12.1% of COVID-19 patients (n = 71) but was not associated with worse outcome (91). However, a recent report in Blood characterized bleeding as a significant cause of morbidity in COVID-19 patients, emphasizing the need for randomized trials on the benefit of escalated prophylaxis (1). Several studies have demonstrated significantly elevated levels of classical markers of cardiac injury and failure [i.e., cardiac troponin and brain natriuretic peptides (BNP)] in patients with greater disease severity (53a, 78). Richardson S, Hirsch JS, Narasimhan M, Crawford JM, McGinn T, Davidson KW, Barnaby DP, Becker LB, Chelico JD, Cohen SL, Cookingham J, Coppa K, Diefenbach MA, Dominello AJ, Duer-Hefele J, Falzon L, Gitlin J, Hajizadeh N, Harvin TG, Hirschwerk DA, Kim EJ, Kozel ZM, Marrast LM, Mogavero JN, Osorio GA, Qiu M, Zanos TP; the Northwell COVID-19 Research Consortium . However, the validity of these mechanisms have been debated, since abnormal liver enzymes have been reported at hospital admission before any drug treatment as well as in patients without the need for mechanical ventilation (7). (B) Macrophage activation. A pneumonia outbreak associated with a new coronavirus of probable bat origin. A recently concluded study has revealed that during the initial 18 months of the COVID-19 pandemic, a higher number of minors in Finland than usual were diagnosed 1Molecular Medicine, Research Institute, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada, 2Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada, 3Department of Physiology, University of Toronto, Toronto, Ontario, Canada. WebThe coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is a highly contagious enveloped positive-strand RNA virus that causes respiratory diseases, fever, and severe pneumonia in humans (13). SARS-CoV-2 is mostly transmissible through large respiratory droplets, directly infecting cells of the upper and lower respiratory tract, especially nasal ciliated and alveolar epithelial cells (161). The exact contribution of risk factors to disease progression is still partially undefined. Trippella G, Ciarci M, Ferrari M, Buzzatti C, Maccora I, Azzari C, Dani C, Galli L, Chiappini E. COVID-19 in pregnant women and neonates: a systematic review of the literature with quality assessment of the studies. Laboratory/clinical profile and key potential mechanisms underlying extrapulmonary manifestations observed in severe COVID-19 patients. The association of GI manifestations with disease severity is not well described, with many conflicting results reported (25, 139, 154). Hadi A, Werge M, Kristiansen KT, Pedersen UG, Karstensen JG, Novovic S, Gluud LL. COVID-19 in children and adolescents in Europe: a multinational, multicentre cohort study. In addition, unlike other coronaviruses, SARS-CoV-2 has been reported to possess a furin-like cleavage site in the S-protein domain, located between the S1 and S2 subunits (31, 138). Notably, in a case study series of 5,700 patients from New York City, the most commonly observed comorbidities were hypertension, obesity, and diabetes (112). Cheung CY, Poon LLM, Ng IHY, Luk W, Sia S-F, Wu MHS, Chan K-H, Yuen K-Y, Gordon S, Guan Y, Peiris JSM. sharing sensitive information, make sure youre on a federal Although these reports indicate a milder COVID-19 profile in pediatric patients compared with adults (159), reports from China and the CDC indicate that the documented hospitalization and mortality rates in pediatric cases are concerning and emphasize the importance of comprehensive studies to examine the clinical picture of pediatric disease (15a, 36). The pathophysiological mechanisms behind key events in the progression from mild to severe disease remain unclear, warranting further investigation to inform therapeutic decisions. 1) Potential mechanisms of COVID-pain (SARS-CoV-2/COVID-19-induced pain) (A) ACE2/RAS pathway and the direct virus-induced damage. government site. Few case reports have observed acute pancreatitis in COVID-19 patients (2, 45, 54), although it is expected to be quite uncommon. Coronavirus disease 2019 (COVID-19) is caused by a novel beta-coronavirus known as Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). The outbreak of COVID-19 has inspired multiple drug repurposing screens to find antiviral therapeutics that can be rapidly brought to the clinic ().To date, more than 1974 drugs and investigational drugs have been reported to have in vitro activity against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ().Because almost all of these However, as described above, there is potential for SARS-CoV-2 to significantly affect the placenta and thus negatively impact fetal development. COVID-19 and myocarditis: What do we know so far? Diabetic ulcers (DUs) are one of the most serious complications of diabetes mellitus. Further studies are needed to evaluate the contribution of antibodies to both physiological and pathogenic host response (39, 160). Clinical characteristics of 138 hospitalized patients with 2019 novel Coronavirus-infected pneumonia in Wuhan, China. The involvement of the gastrointestinal (GI) tract and hepatic system in COVID-19 disease progression is being increasingly reported. Pancreatic injury has also been reported in patients with COVID-19. why and to what extent? The global epidemiology of coronavirus disease 2019 (COVID-19) suggests a wide spectrum of clinical severity, ranging from asymptomatic to fatal. Based on the current evidence, it is clear that, although direct SARS-CoV-2 infection of multiple organs as well as hypoxia and stress-related injury may contribute to COVID-19 pathophysiological progression, systemic inflammation and aberrant cytokine regulation is a hallmark of disease severity. Cytokine-mediated inflammatory AKI has been described previously in the literature in other clinical contexts such as CAR-T-cell treatment in cancer patients (102, 104, 117). Preliminary reports from the Chinese Center for Disease Control and Prevention have estimated that the large majority of confirmed SARS-CoV-2 cases are mild (81%), with ~14% progressing to severe pneumonia and 5% developing acute respiratory distress syndrome (ARDS), sepsis, and/or multisystem organ failure (MOF) (144). Similar to SARS-CoV, several researchers have identified human angiotensin converting enzyme 2 (ACE2) as an entry receptor for SARS-CoV-2 (75, 99, 148, 156). Chen N, Zhou M, Dong X, Qu J, Gong F, Han Y, Qiu Y, Wang J, Liu Y, Wei Y, Xia J, Yu T, Zhang X, Zhang L. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study, Structure analysis of the receptor binding of 2019-nCoV. prepared figures; M.K.B., A.H., L.S., B.J., and K.A. Front. Open in a separate Received 2020 Jun 23; Revised 2020 Jul 7; Accepted 2020 Jul 7. coagulation, COVID-19, cytokine storm, multisystem organ failure, pathophysiolog. Zeng JH, Liu YX, Yuan J, Wang FX, Wu WB, Li JX, Wang LF, Gao H, Wang Y, Dong CF, Li YJ, Xie XJ, Feng C, Liu L. First case of COVID-19 complicated with fulminant myocarditis: a case report and insights. Zhang JJ, Dong X, Cao YY, Yuan YD, Yang YB, Yan YQ, Akdis CA, Gao YD. High expression of ACE2 receptor of 2019-nCoV on the epithelial cells of oral mucosa. Zuo Y, Yalavarthi S, Shi H, Gockman K, Zuo M, Madison JA, Blair C, Weber A, Barnes BJ, Egeblad M, Woods RJ, Kanthi Y, Knight JS. March 28, 2023 A team of scientists led by the Department of Energys Oak Ridge National Laboratory designed a molecule that disrupts the infection mechanism of the SARS-CoV-2 coronavirus and could be used to develop new treatments for COVID-19 and other viral diseases. Before Evaluating the risk of severe outcomes of SARS-CoV-2 infection in pregnant women is imperative for both mother and child. A more plausible mechanism behind liver dysfunction in COVID-19 is the observed systemic inflammatory response, as described previously, leading to cytotoxic T-cell-mediated necrosis and MOF. This paper proposes a model algorithm based on convolutional neural network combined with attention mechanism to realize fast and accurate identification of biological image. Finally, several comorbidities have been associated with poor outcomes, likely due to the fact that organ and immune function may already be compromised and in a state of subclinical inflammation (53, 158). Liver biochemistries in hospitalized patients with COVID-19. Altered sense of taste or smell can be present in up to 80% of patients with mild to moderate COVID-19 (73). RA,, Plebani Zhu L, She ZG, Cheng X, Qin JJ, Zhang XJ, Cai J, Lei F, Wang H, Xie J, Wang W, Li H, Zhang P, Song X, Chen X, Xiang M, Zhang C, Bai L, Xiang D, Chen MM, Liu Y, Yan Y, Liu M, Mao W, Zou J, Liu L, Chen G, Luo P, Xiao B, Zhang C, Zhang Z, Lu Z, Wang J, Lu H, Xia X, Wang D, Liao X, Peng G, Ye P, Yang J, Yuan Y, Huang X, Guo J, Zhang BH, Li H. Association of blood glucose control and outcomes in patients with COVID-19 and pre-existing Type 2 diabetes, Coronavirus infections in children including COVID-19: An overview of the epidemiology, clinical features, diagnosis, treatment and prevention options in children, Dissecting antibody-mediated protection against SARS-CoV-2. Furthermore, limited available data in the pediatric population suggests a distinct and diverse spectrum of disease completely different from adults, further reinforcing the importance of age-related immune responses (84, 145). Ranucci M, Ballotta A, Di Dedda U, Bayshnikova E, Dei Poli M, Resta M, Falco M, Albano G, Menicanti L. The procoagulant pattern of patients with COVID-19 acute respiratory distress syndrome, Cutaneous manifestations in COVID-19: a first perspective. The urgent need to appropriately identify these patients has led the World Health Organization (WHO) and other regulatory bodies to develop a preliminary case definition known as Multisystem Inflammatory Disorder in Children and adolescents (MIS-C) (142a). In a more in-depth study of 183 patients by Tang et al., 71.4% of non-survivors and 0.6% of recovered cases met the criteria for disseminated intravascular coagulation during hospitalization (128). Naunyn-Schmiedeberg's Arch Pharmacol 393, Recent autopsy data from Italy also observed fibrin thrombi in pulmonary small arterial vessels in 87% of fatal cases examined, suggesting the contribution of coagulation in diffuse alveolar and endothelial damage (15). Escher F, Pietsch H, Aleshcheva G, Bock T, Baumeier C, Elsaesser A, Wenzel P, Hamm C, Westenfeld R, Schultheiss M, Gross U, Morawietz L, Schultheiss H. Detection of viral SARSCoV2 genomes and histopathological changes in endomyocardial biopsies, Severe COVID-19 infection associated with endothelial activation. 2: pulmonary recruitment of macrophages and dendritic cells in response to chemokine and cytokine release (early phase). However, other contributing mechanisms have been proposed and are explored below (FIGURE 3). The cell uses the mRNA from the vaccine as the blueprint to build the SARS-CoV-2 spike protein. Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation, Characteristics of and important lessons from the Coronavirus Disease 2019 (COVID-19) outbreak in China: summary of a report of 72,314 cases From the Chinese Center for Disease Control and Prevention. ACE2 is expressed in the kidney, and although previous studies suggested absence of viral particles in postmortem renal specimens from SARS patients (27), electron microscopic examination of 26 postmortem COVID-19 patients demonstrated direct virulence in tubular epithelium and podocytes (126). was supported by a Restracomp Scholarship (Hospital for Sick Children) and an Ontario Graduate Scholarship (OGS). Jones VG, Mills M, Suarez D, Hogan CA, Yeh D, Segal JB, Nguyen EL, Barsh GR, Maskatia S, Mathew R. COVID-19 and Kawasaki Disease: novel virus and novel case, COVID-19 can present with a rash and be mistaken for dengue. In a case study series of 214 patients diagnosed with COVID-19, neurological symptoms were observed in 36.4% of patients, and this percentage increased to 45.5% when examining patients with severe infection (86). Gender differences in patients with COVID-19: focus on severity and mortality. Before this, TMPRSS2 has presented biological functions in cancer, but the roles remain controversial and the mechanism remains unelucidated. Bioinformatics analysis of potential common pathogenic mechanisms for COVID-19 infection and primary Sjogrens syndrome. In addition to the lungs, ACE2 is also expressed in various other human tissues, such as the small intestine, kidneys, heart, thyroid, testis, and adipose tissue, indicating the virus may directly infect cells of other organ systems when viremia is present (77). Furin-like proteases are ubiquitously expressed, albeit at low levels, indicating that S-protein priming at this cleavage site may contribute to the widened cell tropism and enhanced transmissibility of SARS-CoV-2 (123). No conflicts of interest, financial or otherwise, are declared by the author(s). Matsuyama S, Ujike M, Morikawa S, Tashiro M, Taguchi F. Protease-mediated enhancement of severe acute respiratory syndrome coronavirus infection. Although direct damage of pancreatic -cells has been proposed as a plausible mechanism behind this phenotype, immune destruction of -cells has also been suggested in addition to bystander death due to exocrine infection (101). Most of our knowledge on COVID-19 pathophysiological progression has been observed through a laboratory lens, inferring potential causative mechanisms from observed biomarker trends across patients. Collapsing glomerulopathy in a patient with Coronavirus Disease 2019 (COVID-19). Their study demonstrated frequent elevations in CRP, procalcitonin, and LDH in severe pediatric COVID-19, similar to adult findings (56). Due to the paucity of data in this area, further research is required to elucidate what mechanisms confer protection from COVID-19 in most pediatric patients as well as what factors predispose children to progress to MIS-C. M.K.B. Previous data from the SARS epidemic suggests 35% of heart specimens showed presence of viral RNA in the myocardium. Effect of gastrointestinal symptoms on patients infected with COVID-19. These data clearly suggest a state of hypercoagulability in severe COVID-19. The main drivers of this response have been postulated and thoroughly reviewed elsewhere (125, 130, 151). The immune system mobilizes and records the shape of the SARS-CoV-2 protein. Jin JM, Bai P, He W, Wu F, Liu XF, Han DM, Liu S, Yang JK. Amanat F, Stadlbauer D, Strohmeier S, Nguyen THO, Chromikova V, McMahon M, Jiang K, Arunkumar GA, Jurczyszak D, Polanco J, Bermudez-Gonzalez M, Kleiner G, Aydillo T, Miorin L, Fierer DS, Lugo LA, Kojic EM, Stoever J, Liu STH, Cunningham-Rundles C, Felgner PL, Moran T, Garca-Sastre A, Caplivski D, Cheng AC, Kedzierska K, Vapalahti O, Hepojoki JM, Simon V, Krammer F. A serological assay to detect SARS-CoV-2 seroconversion in humans. Some chemicals have been WebCoronavirus disease 2019 (COVID-19) vaccines can protect people from the infection; however, the action mechanism of vaccine-mediated metabolism remains unclear. Toscano G, Palmerini F, Ravaglia S, Ruiz L, Invernizzi P, Cuzzoni MG, Franciotta D, Baldanti F, Daturi R, Postorino P, Cavallini A, Micieli G. Guillain-Barr Syndrome associated with SARS-CoV-2. Initial studies have reported varying incidences (315%) of AKI during illness (20, 22, 155). Characteristics of women of reproductive age with laboratory-confirmed SARS-CoV-2 infection by pregnancy statusUnited States, January 22-June 7, 2020. Genetic predispositions have also been proposed, including polymorphisms in ACE2 and genetic variability in histocompatibility complex (MHC) class I genes (96). Chai X, Hu L, Zhang Y, Han W, Lu Z, Ke A, Zhou J, Shi G, Fang N, Fan J, Cai J, Fan J, Lan F. Specific ACE2 expression in cholangiocytes may cause liver damage after 2019-nCoV infection. Electronic address: https://www.lancovid.org . Cheung EW, Zachariah P, Gorelik M, Boneparth A, Kernie SG, Orange JS, Milner JD. The covid-19 pandemic during the time of the diabetes pandemic: Likely fraternal twins? TWC India. Although the clinical picture of COVID-19 in pediatrics and pregnancy is less understood, their respective characteristics appear different when compared with nonpregnant adults. Severe Coronavirus infections in pregnancy: a systematic review. Further research is urgently needed to better characterize the clinical picture of COVID-19 at each trimester of pregnancy. 8600 Rockville Pike Bethesda, MD 20894, Web Policies Naunyn-Schmiedeberg's Arch Pharmacol 393, 11531156 (2020). Now considered a valuable prognostic indicator for COVID-19 survival, AKI is estimated to affect 2040% of critically ill patients in intensive care, necessitating renal replacement therapy and extracorporeal support therapies such as blood purification (112, 155). link.springer.com. Since its emergence in December 2019 in Wuhan, China, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) created a worldwide pandemic of coronavirus disease (COVID-19) with nearly 136 million cases and approximately 3 million deaths. The severity of COVID-19 is positively correlated to the level of inflammatory cytokines such as interleukins (IL-2, IL-6, IL-7, IL-10), granulocyte colony-stimulating factor (GCSF), interferon gamma-induced protein 10 (IP-10), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein 1 alpha (MIP-1A) and tumor necrosis factor In addition to direct infection, uncontrolled cytokine release, thrombosis, and ischemia can also result in further kidney dysfunction, characterized by intrarenal inflammation, increased vascular permeability, and volume depletion (88). Prospective validation of these proposed cut-offs across different assay methodologies and patient populations are urgently awaited to establish clinical utility. Kidney involvement in COVID-19 and rationale for extracorporeal therapies, Management of acute kidney injury in patients with COVID-19, Understanding SARS-CoV-2-related multisystem inflammatory syndrome in children. Bertram S, Glowacka I, Mller MA, Lavender H, Gnirss K, Nehlmeier I, Niemeyer D, He Y, Simmons G, Drosten C, Soilleux EJ, Jahn O, Steffen I, Phlmann S. Cleavage and activation of the severe acute respiratory syndrome coronavirus spike protein by human airway trypsin-like protease. This could in part be explained by the viruss Immune dysregulation, auto-immunity, endothelial dysfunction, occult viral persistence, as well as coagulation activation are the main underlying pathophysiological mechanisms so far. Notably, increased levels of IL-6, IL-2, IL-7, IL-10, granulocyte colony-stimulating factor (G-CSF), IP-10, MCP1, IFN, macrophage inflammatory protein 1 (MIP1), and tumor necrosis factor (TNF) have all been implicated in COVID-19 severity, suggesting a combined T-helper type 1 (Th1) and Th2 cell response (61, 130). Mao L, Jin H, Wang M, Hu Y, Chen S, He Q, Chang J, Hong C, Zhou Y, Wang D, Miao X, Li Y, Hu B. Neurologic manifestations of hospitalized patients with Coronavirus Disease 2019 in Wuhan, China, Possible link between anosmia and COVID-19: sniffing out the truth.

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