Pathophysiology : the official journal of the International Society for Pathophysiology最新文献

{"title":"SARS-CoV-2-Induced Pathology-Relevance to COVID-19 Pathophysiology.","authors":"Vsevolod A Zinserling,&nbsp;Natalia Yu Semenova,&nbsp;Anastasia E Bikmurzina,&nbsp;Natalia M Kruglova,&nbsp;Oksana V Rybalchenko,&nbsp;Alexander G Markov","doi":"10.3390/pathophysiology29020021","DOIUrl":"https://doi.org/10.3390/pathophysiology29020021","url":null,"abstract":"<p><p>In spite of intensive studies of different aspects of a new coronavirus infection, many issues still remain unclear. In a screening analysis of histopathology in l200 lethal cases, authors succeeded in performing a wide spectrum of immune histochemical reactions (CD2, CD 3, CD 4, CD 5, CD 7, CD 8, CD14, CD 20, CD 31, CD 34, CD 56, CD 57, CD 68, CD 163, collagen 1,3, spike protein SARS-CoV-2, caspase-3, MLCM; ACE2 receptor, occludin, and claudin-1 and -3) and electron microscopy. The results of the histological and IHC studies of deceased people with varying degrees of severity of coronavirus infection confirmed the ability of these pathogens to cause cytoproliferative changes, primarily in epithelial and endothelial cells. Lesions of various organs are possible, while the reasons for significant differences in organotropy remain unclear. Severe respiratory failure in COVID-19 in humans is associated with a very peculiar viral pneumonia. In the pathogenesis of COVID-19, the most important role is played by lesions of the microcirculatory bed, the genesis of which requires further study, but direct viral damage is most likely. Endothelial damage can be associated with both thrombosis in vessels of various calibers, leading to characteristic complications, and the development of DIC syndrome with maximal kidney damage. Such lesions can be the basis of clinically diagnosed septic shock, while usually there are no morphological data in favor of classical sepsis caused by bacteria or fungi. A massive infiltration of the lung tissue and other organs, mainly by T lymphocytes, including those with suppressor properties, makes it necessary to conduct a differential diagnosis between the morphological manifestation of the protective cellular immune response and direct viral lesions but does not exclude the hypothesis of an immunopathological component of pathogenesis. In many of the deceased, even in the absence of clear clinical symptoms, a variety of extrapulmonary lesions were also detected. The mechanism of their development probably has a complex nature: direct lesions associated with the generalization of viral infection and vascular disorders associated with endothelial damage and having an autoimmune nature. Many aspects of the pathogenesis of coronavirus infection require further comprehensive study.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"281-297"},"PeriodicalIF":0.0,"publicationDate":"2022-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9229620/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40268466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Exposomes in the Pathophysiology of Autoimmune Diseases II: Pathogens.","authors":"Aristo Vojdani,&nbsp;Elroy Vojdani,&nbsp;Avi Z Rosenberg,&nbsp;Yehuda Shoenfeld","doi":"10.3390/pathophysiology29020020","DOIUrl":"https://doi.org/10.3390/pathophysiology29020020","url":null,"abstract":"<p><p>In our continuing examination of the role of exposomes in autoimmune disease, we use this review to focus on pathogens. Infections are major contributors to the pathophysiology of autoimmune diseases through various mechanisms, foremost being molecular mimicry, when the structural similarity between the pathogen and a human tissue antigen leads to autoimmune reactivity and even autoimmune disease. The three best examples of this are oral pathogens, SARS-CoV-2, and the herpesviruses. Oral pathogens reach the gut, disturb the microbiota, increase gut permeability, cause local inflammation, and generate autoantigens, leading to systemic inflammation, multiple autoimmune reactivities, and systemic autoimmunity. The COVID-19 pandemic put the spotlight on SARS-CoV-2, which has been called \"the autoimmune virus.\" We explore in detail the evidence supporting this. We also describe how viruses, in particular herpesviruses, have a role in the induction of many different autoimmune diseases, detailing the various mechanisms involved. Lastly, we discuss the microbiome and the beneficial microbiota that populate it. We look at the role of the gut microbiome in autoimmune disorders, because of its role in regulating the immune system. Dysbiosis of the microbiota in the gut microbiome can lead to multiple autoimmune disorders. We conclude that understanding the precise roles and relationships shared by all these factors that comprise the exposome and identifying early events and root causes of these disorders can help us to develop more targeted therapeutic protocols for the management of this worldwide epidemic of autoimmunity.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"243-280"},"PeriodicalIF":0.0,"publicationDate":"2022-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9231084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40268467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelet Distribution Width and Increased D-Dimer at Admission Predicts Subsequent Development of ARDS in COVID-19 Patients.","authors":"Iviana P Yovchevska,&nbsp;Alexandar B Trenovski,&nbsp;Maria H Atanasova,&nbsp;Martin N Georgiev,&nbsp;Radka K Tafradjiiska-Hadjiolova,&nbsp;Simeon D Lazarov,&nbsp;Plamen H Yovchevski","doi":"10.3390/pathophysiology29020019","DOIUrl":"https://doi.org/10.3390/pathophysiology29020019","url":null,"abstract":"<p><p>In the current pandemic of coronavirus disease (COVID-19), the identification of the patients admitted with severe infection-who are disposed to a high risk of acute respiratory distress syndrome (ARDS) development, is of a major significance for the determination of the appropriate therapeutic strategy. Laboratory records in admission were retrospectively reviewed from 493 cases of severe COVID-19 divided into two groups: Group 1 with ARDS and Group 2 without ARDS. The platelet distribution width (PDW) difference between Group 1 and Group 2 is significant-15.10 ± 2.08 fl for those who developed ARDS versus 12.94 ± 2.12 fl for those without ARDS. The sensitivity and the specificity of this parameter is lower than that of D-dimer. After grouping of the PDW values into intervals and combining them with the rate of increase in D-dimer (D-PDWf index) to form a forecasting index, a significant increase in the specificity and sensitivity of the two parameters is identified-area under the ROC curve (AUC) is 0.874 for D-PDWf index, with respective AUC for PDW 0.768 and AUC for D-dimer 0.777. Conclusion: PDW is a significant predictive parameter at admission for subsequent development of ARDS in patients, with increased significance in combination with the degree of increase in D-dimer.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"233-242"},"PeriodicalIF":0.0,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9228300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40267577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic Cannabis Intoxication and Propofol-Induced Salivation: Causes and Considerations.","authors":"Allison Derise,&nbsp;Carey Ford,&nbsp;Nazar Hafiz,&nbsp;Sudha Pandit,&nbsp;Aditya Vyas,&nbsp;Samuel Igbinedion,&nbsp;James Morris,&nbsp;Paul Jordan,&nbsp;Qiang Cai,&nbsp;Jonathan Steven Alexander","doi":"10.3390/pathophysiology29020018","DOIUrl":"https://doi.org/10.3390/pathophysiology29020018","url":null,"abstract":"<p><p>Legalization/decriminalization of cannabis will increase the numbers of patients who have had recent exposure to recreational or medical cannabis. Currently, little has been reported about potential interactions between cannabis use and Propofol anesthesia e.g., for oropharyngeal procedures. We describe three cases of 'cannabis-induced hypersalivation after propofol' (CHAP) and present our institutions' experience with this unique pharmacological combination. Increased hypersalivation may complicate procedures and represent a procedural risk of suffocation. We evaluate possible pharmacological interactions that might underlie this phenomenon and consider management options going forward.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"223-232"},"PeriodicalIF":0.0,"publicationDate":"2022-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9229402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40267576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolomics and EMT Markers of Breast Cancer: A Crosstalk and Future Perspective.","authors":"Ajay Kumar Pal,&nbsp;Prateek Sharma,&nbsp;Alishan Zia,&nbsp;Deepali Siwan,&nbsp;Dipali Nandave,&nbsp;Mukesh Nandave,&nbsp;Rupesh K Gautam","doi":"10.3390/pathophysiology29020017","DOIUrl":"https://doi.org/10.3390/pathophysiology29020017","url":null,"abstract":"<p><p>Cancer cells undergo transient EMT and MET phenomena or vice versa, along with the parallel interplay of various markers, often correlated as the determining factor in decoding metabolic profiling of breast cancers. Moreover, various cancer signaling pathways and metabolic changes occurring in breast cancer cells modulate the expression of such markers to varying extents. The existing research completed so far considers the expression of such markers as determinants regulating the invasiveness and survival of breast cancer cells. Therefore, this manuscript is crosstalk among the expression levels of such markers and their correlation in regulating the aggressiveness and invasiveness of breast cancer. We also attempted to cover the possible EMT-based metabolic targets to retard migration and invasion of breast cancer.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"200-222"},"PeriodicalIF":0.0,"publicationDate":"2022-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9230911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40268465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic Fatigue Exhibits Heterogeneous Autoimmunity Characteristics Which Reflect Etiology.","authors":"Olga V Danilenko,&nbsp;Natalia Y Gavrilova,&nbsp;Leonid P Churilov","doi":"10.3390/pathophysiology29020016","DOIUrl":"https://doi.org/10.3390/pathophysiology29020016","url":null,"abstract":"<p><p>Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is considered to be associated with post-viral complications and mental stress, but the role of autoimmunity also remains promising. A comparison of autoimmune profiles in chronic fatigue of different origin may bring insights on the pathogenesis of this disease. Thirty-three patients with CFS/ME were divided into three subgroups. The first group included Herpesviridae carriers (group V), the second group included stress-related causes of chronic fatigue (distress, group D), and the third group included idiopathic CFS/ME (group I). Were evaluated thirty-six neural and visceral autoantigens with the ELISA ELI-test (Biomarker, Russia) and compared to 20 healthy donors, either without any fatigue (group H), or \"healthy but tired\" (group HTd) with episodes of fatigue related to job burnout not fitting the CFS/ME criteria. β2-glycoprotein-I autoantibodies were increased in CFS/ME patients, but not in healthy participants, that alludes the link between CFS/ME and antiphospholipid syndrome (APS) earlier suspected by Berg et al. (1999). In CFS/ME patients, an increase in levels of autoantibodies towards the non-specific components of tissue debris (double-stranded DNA, collagen) was shown. Both CFS and HTd subgroups had elevated level of autoantibodies against serotonin receptors, glial fibrillary acidic protein and protein S100. Only group V showed an elevation in the autoantibodies towards voltage-gated calcium channels, and only group D had elevated levels of dopamine-, glutamate- and GABA-receptor autoantibodies, as well as NF200-protein autoantibodies. Therefore, increased autoimmune reactions to the multiple neural antigens and to adrenal medullar antigen, but not to other tissue-specific somatic ones were revealed. An increase in autoantibody levels towards some neural and non-tissue-specific antigens strongly correlated with a CFS/ME diagnosis. Autoimmune reactions were described in all subtypes of the clinically significant chronic fatigue. Visceral complaints in CFS/ME patients may be secondary to the neuroendocrine involvement and autoimmune dysautonomia. CFS may be closely interrelated with antiphospholipid syndrome, that requires further study.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"187-199"},"PeriodicalIF":0.0,"publicationDate":"2022-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9231045/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40267575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}