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Yang, Kan, Yuqing Yan, Anni Yu, Ru Zhang, Yuefang Zhang, Zilong Qiu, Zhengyi Li, Qianlong Zhang, Shihao Wu, and Fei Li. "Mitophagy in neurodegenerative disease pathogenesis." Neural Regeneration Research 19, no. 5 (September 22, 2023): 998–1005. http://dx.doi.org/10.4103/1673-5374.385281.
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Abstract Mitochondria are critical cellular energy resources and are central to the life of the neuron. Mitophagy selectively clears damaged or dysfunctional mitochondria through autophagic machinery to maintain mitochondrial quality control and homeostasis. Mature neurons are postmitotic and consume substantial energy, thus require highly efficient mitophagy pathways to turn over damaged or dysfunctional mitochondria. Recent evidence indicates that mitophagy is pivotal to the pathogenesis of neurological diseases. However, more work is needed to study mitophagy pathway components as potential therapeutic targets. In this review, we briefly discuss the characteristics of nonselective autophagy and selective autophagy, including ERphagy, aggrephagy, and mitophagy. We then introduce the mechanisms of Parkin-dependent and Parkin-independent mitophagy pathways under physiological conditions. Next, we summarize the diverse repertoire of mitochondrial membrane receptors and phospholipids that mediate mitophagy. Importantly, we review the critical role of mitophagy in the pathogenesis of neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Last, we discuss recent studies considering mitophagy as a potential therapeutic target for treating neurodegenerative diseases. Together, our review may provide novel views to better understand the roles of mitophagy in neurodegenerative disease pathogenesis.
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Ashu and Rakesh Sharma. "Nidanapanchakatmak study of Aamvata." Journal of Ayurveda and Integrated Medical Sciences 8, no. 4 (May 25, 2023): 46–48. http://dx.doi.org/10.21760/jaims.8.4.7.
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In Ayurveda there are various approaches to diagnose a disease; the concept of Nidan Panchak is one such modality of Ayurveda. Nidan Panchak helps to diagnose diseases at various stages. Knowing the definite Nidana (etiological factors), Dosha vitiation, Samprapti (pathogenesis or progress of disease) and to check it at early stage is given prime importance. Nidan Panchaka plays vital role to identify types of disease. It consists of five subtypes which are Nidan (causes), Purvarupa (Prodromal Features), Rupa (Clinical features), Upashaya (Therapeutic methods), and Samprapti (Pathogenesis). These five elements collectively or selectively help in making an accurate diagnosis. Aamvata is a diseased caused by Dushti of Rasavaha Strotas in which there is formation of Ama due to Jatharagni Mandya. The Aamvata condition closely resembles with Rheumatoid arthritis, an autoimmune inflammatory condition characterised by symmetrical polyarthritis. Aamvata disease was first described in Laghutrayee by Acharya Madhava. Before the Acharya Madhava the concept of Aamvata was vague. Aamvata develops due to Dushti or Prakopa of Ama as well as Vata Dosha. As the disease Aamvata is very prevalent in society, it’s important to know the exact diagnosis along with treatment. In our current review we had tried to elaborate about the Nidanapanchaka of Aamvata.
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ARAI, Satoshi. "Study on Pathogenesis of Periodontal Disease in Gnotobiotic Mice." Nihon Shishubyo Gakkai Kaishi (Journal of the Japanese Society of Periodontology) 36, no. 4 (1994): 776–93. http://dx.doi.org/10.2329/perio.36.776.
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Tsyganova, Tatiana Vasilyevna, and Anna Nikolaevna Melisheva. "ALZHEIMER’S DISEASE: MODERN VIEWS ON THE PATHOGENESIS OF THE DISEASE." Chronos 7, no. 11(73) (December 13, 2022): 39–41. http://dx.doi.org/10.52013/2658-7556-73-11-11.
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Alzheimer’s disease (AD) in the modern definition of the disease is a progressive neurodegenerative disease. Extracellular aggregates of amyloid plaques β (Aß) and intracellular neurofibrillary tangles, which consist of hyperphosphorylated tau protein, play a major role in the pathogenesis of this disease. BA is manifested by progressive dementia, which affects elderly people. Initially, clinical symptoms are manifested by memory loss, and in the later stages by neuropsychiatric disorders and, subsequently, by a change in a person’s personality. Based on new statistics, the prevalence of the disease is growing worldwide. There are about 50 million patients with AD, and the incidence tends to double every 5 years after the age of 65. As BA was studied, many pathogenetic mechanisms of the disease were formulated. Currently, the theory of the amyloid cascade and hyperphosphorylation of tau has received the main recognition, but all the processes of disease development are still unclear. Many other theories of the occurrence of the disease are also considered, therefore, the study of the pathogenesis of AD is quite an urgent problem.
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Santos-Ocaña, Carlos, María V. Cascajo, María Alcázar-Fabra, Carmine Staiano, Guillermo López-Lluch, Gloria Brea-Calvo, and Plácido Navas. "Cellular Models for Primary CoQ Deficiency Pathogenesis Study." International Journal of Molecular Sciences 22, no. 19 (September 22, 2021): 10211. http://dx.doi.org/10.3390/ijms221910211.
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Primary coenzyme Q10 (CoQ) deficiency includes a heterogeneous group of mitochondrial diseases characterized by low mitochondrial levels of CoQ due to decreased endogenous biosynthesis rate. These diseases respond to CoQ treatment mainly at the early stages of the disease. The advances in the next generation sequencing (NGS) as whole-exome sequencing (WES) and whole-genome sequencing (WGS) have increased the discoveries of mutations in either gene already described to participate in CoQ biosynthesis or new genes also involved in this pathway. However, these technologies usually provide many mutations in genes whose pathogenic effect must be validated. To functionally validate the impact of gene variations in the disease’s onset and progression, different cell models are commonly used. We review here the use of yeast strains for functional complementation of human genes, dermal skin fibroblasts from patients as an excellent tool to demonstrate the biochemical and genetic mechanisms of these diseases and the development of human-induced pluripotent stem cells (hiPSCs) and iPSC-derived organoids for the study of the pathogenesis and treatment approaches.
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Parfenova, M. A., I. E. Belousova, and A. V. Samtsov. "Ulceronecrotic Mucha Habermann’s disease: case study." Vestnik dermatologii i venerologii 89, no. 4 (August 15, 2013): 73–78. http://dx.doi.org/10.25208/vdv619.
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The rare dermatosis febrile ulceronecrotic Mucha Gabermann’s disease is described. Etiology, pathogenesis, clinical and pathomorphological criteria of diagnosis, treatment of the disease are discussed. Based on the literature review describes the historical and current data classification of the disease and patient management tactics.
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Tsimmerman, Y. S. "Wilson’s disease — hepatocerebral dystrophy." Bulletin of the Club of Pancreatologists 40, no. 2 (June 6, 2018): 54–60. http://dx.doi.org/10.33149/vkp.2018.02.08.
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The article presents a detailed review of modern ideas on Wilson’s disease – hepatocerebral dystrophy. The definition, terminology, history of the study of the disease are stated. Special attention is paid to the analysis of the pathogenesis of hepatocerebral dystrophy, including the genetic basis of its development, the disturbance of copper metabolism. The clinical picture is thoroughly described, taking into account the characteristics of liver lesion and extrahepatic manifestations, diagnostics, classification. Particular attention is paid to the means of pathogenetic and symptomatic treatment.
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Virata, M. J., and R. W. Zeller. "Ascidians: an invertebrate chordate model to study Alzheimer's disease pathogenesis." Disease Models & Mechanisms 3, no. 5-6 (March 2, 2010): 377–85. http://dx.doi.org/10.1242/dmm.003434.
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Yao, Q., J. Myles, B. Shen, and C. McDonald. "NOD2-associated autoinflammatory disease: an exploratory study of its pathogenesis." Rheumatology 53, no. 5 (November 19, 2013): 958–60. http://dx.doi.org/10.1093/rheumatology/ket384.
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Shafik, Ahmed, Ismail Ahmed, Ali A. Shafik, and Olfat El Sibai. "Diverticular Disease: Electrophysiologic Study and a New Concept of Pathogenesis." World Journal of Surgery 28, no. 4 (March 4, 2004): 411–15. http://dx.doi.org/10.1007/s00268-003-7268-1.
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Masemann, Dörthe, Stephan Ludwig, and Yvonne Boergeling. "Advances in Transgenic Mouse Models to Study Infections by Human Pathogenic Viruses." International Journal of Molecular Sciences 21, no. 23 (December 5, 2020): 9289. http://dx.doi.org/10.3390/ijms21239289.
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Medical research is changing into direction of precision therapy, thus, sophisticated preclinical models are urgently needed. In human pathogenic virus research, the major technical hurdle is not only to translate discoveries from animals to treatments of humans, but also to overcome the problem of interspecies differences with regard to productive infections and comparable disease development. Transgenic mice provide a basis for research of disease pathogenesis after infection with human-specific viruses. Today, humanized mice can be found at the very heart of this forefront of medical research allowing for recapitulation of disease pathogenesis and drug mechanisms in humans. This review discusses progress in the development and use of transgenic mice for the study of virus-induced human diseases towards identification of new drug innovations to treat and control human pathogenic infectious diseases.
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Schapira, Anthony H. V., and Matthew Gegg. "Mitochondrial Contribution to Parkinson's Disease Pathogenesis." Parkinson's Disease 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/159160.
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The identification of the etiologies and pathogenesis of Parkinson's disease (PD) should play an important role in enabling the development of novel treatment strategies to prevent or slow the progression of the disease. The last few years have seen enormous progress in this respect. Abnormalities of mitochondrial function and increased free radical mediated damage were described in post mortem PD brain before the first gene mutations causing familial PD were published. Several genetic causes are now known to induce loss of dopaminergic cells and parkinsonism, and study of the mechanisms by which these mutations produce this effect has provided important insights into the pathogenesis of PD and confirmed mitochondrial dysfunction and oxidative stress pathways as central to PD pathogenesis. Abnormalities of protein metabolism including protein mis-folding and aggregation are also crucial to the pathology of PD. Genetic causes of PD have specifically highlighted the importance of mitochondrial dysfunction to PD: PINK1, parkin, DJ-1 and most recently alpha-synuclein proteins have been shown to localise to mitochondria and influence function. The turnover of mitochondria by autophagy (mitophagy) has also become a focus of attention. This review summarises recent discoveries in the contribution of mitochondrial abnormalities to PD etiology and pathogenesis.
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Singh, Devendra, Sisir Kumar Mandal, Rupashri Nath, and Renu . "Role of Raktapradoshaja Nidana in the manifestation of Kushtharoga in Ayurveda: a cross sectional survey study." International Journal of Advances in Medicine 7, no. 1 (December 23, 2019): 117. http://dx.doi.org/10.18203/2349-3933.ijam20195657.
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Background: In Ayurveda all the skin diseases are described under the term Kushtha which is mentioned as a Raktapradoshaja vikara. Due to Rakta dusti several disease pathogenesis accurse in population which leads to Raktapradoshaja vikara.Methods: Present study aimed to conduct a cross-sectional survey based study for investigating the role of Raktapradoshaja nidana in the pathogenesis Kushtha (skin diseases). A duly prepared proforma was prepared based on various etiology of Raktapradoshaja vikara mentioned in classical texts of Ayurveda. Total 500 patients diagnosed as skin disease were screened on the basis of prepared questionnaires prior obtaining the ethical clearance form IEC, NIA, Jaipur (IEC/ACA/2017/60 dated 26/04/2017).Results: Based on over all observation the present survey study explains an easy diagnostic criterion for the different types of Raktapradoshaja vikara mentioned in Ayurveda. Here a unique attempt was taken for quantitative analysis of various classical nidana in relation to the pathogenesis of the disease Raktapradoshaja vikara.Conclusions: Analyzed data of all these extreme exposure of nidana may provide a significant role for diagnosis, prognosis, as well as prevention of the disease of Raktapradoshaja vikara.
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Sonino, Nicoletta, Maria E. Girelli, Marco Boscaro, Francesco Fallo, Benedetto Busnardo, and Giovanni A. Fava. "Life events in the pathogenesis of Graves' disease. A controlled study." Acta Endocrinologica 128, no. 4 (April 1993): 293–96. http://dx.doi.org/10.1530/acta.0.1280293.
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Contradictory findings have been reported about a possible causal relationship of life stress to Graves' disease. We evaluated this issue by investigating the occurrence of stressful life events in the year before the first signs of disease onset, using methods that have been found to be valid and reliable in psychosomatic research. Seventy consecutive patients with Graves' disease and a control group of 70 healthy subjects, matched for sociodemographic variables, were studied. Paykel's Interview for Recent Life Events (a semistructured research interview covering 64 life events) was administered to patients, not during the acute phase of illness but while on remission, by antithyroid drug treatment. Patients with Graves' disease reported significantly more life events compared to controls (p<0.001). They also had more independent events (p<0.001) and events that had an objective negative impact (p <0.001) according to an independent rater, unaware whether the events had occurred in patients or controls. All categories of events were found to be significantly more frequent in patients suffering from Graves' disease than in controls. By rigorous methods (inclusion of patients with Graves' disease only, careful dating of the onset of symptoms, accurate event definition, delay of the interview upon disease remission, use of a blind rater for judging independence and objective negative impact), our results support the concept of an excess of life events in Graves' disease. Stressful life events may affect the regulatory mechanisms of immune function in a number of ways. Within the extreme complexity of the phenomena implicated in the pathogenesis of autoimmune thyroid hyperfunction, our findings emphasize the role of emotional stress.
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Kisli, Erol, Ahu Kemik, Aziz Sümer, and özgür Kemik. "Matrix Metalloproteinases in Pathogenesis of Hemorrhoidal Disease." American Surgeon 79, no. 11 (November 2013): 1181–84. http://dx.doi.org/10.1177/000313481307901122.
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The aim of this study is to investigate the accuracy of serum matrix metalloproteinase (MMP) levels in an effort to find a reliable factor that may play an important role in pathogenesis of hemorrhoidal disease. Twenty control subjects and 21 Grade I, 19 Grade II, 20 Grade III, and 21 Grade IV patients with internal hemorrhoid were included in this prospective study. The mean ages of control subjects were 47.65 ± 6.71 standard deviation (SD) years (range, 37 to 60 years). The mean age of internal Grade I, Grade II, Grade III, and Grade IV patients with internal hemorrhoid were 48.85 ± 6.44, 47.20 ± 6.75, 44.90 ± 6.13, and 42.95 ± 3.49 SD years (ranges, 38 to 58, 38 to 60, 34 to 55, and 38 to 50 years), respectively. Ten milliliters of blood was taken from all subjects. Enzymelinked immunosorbent assay (ELISA) for MMP-1, -2, -7, and -9 levels were performed using an ELISA kit (R&D Systems) following the manufacturer's instructions. There was an important difference between Grade I and Grade II groups in the serum levels of MMP-9 ( P < 0.01). Patients with Grade III hemorrhoidal disease had significantly higher serum levels of all MMP than patients with Grade I and Grade II hemorrhoidal disease ( P < 0.001). Also, patients with Grade 4 hemorrhoidal disease had higher serum levels of MMP-7 and -9 according to Grade I, II, and III groups ( P < 0.01, 0.001). High serum levels of MMP are present in patients with hemorrhoids, suggesting the possible mechanism in the pathogenesis of hemorrhoids.
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Ross, Christopher A., Jonathan D. Wood, Gabriele Schilling, Matthew F. Peters, Frederick C. Nucifora, Jillian K. Cooper, Alan H. Sharp, Russell L. Margolis, and David R. Borchelt. "Polyglutamine pathogenesis." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1386 (June 29, 1999): 1005–11. http://dx.doi.org/10.1098/rstb.1999.0452.
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An increasing number of neurodegenerative disorders have been found to be caused by expanding CAG triplet repeats that code for polyglutamine. Huntington's disease (HD) is the most common of these disorders and dentato-rubral-pallidoluysian atrophy (DRPLA) is very similar to HD, but is caused by mutation in a different gene, making them good models to study. In this review, we will concentrate on the roles of protein aggregation, nuclear localization and proteolytic processing in disease pathogenesis. In cell model studies of HD, we have found that truncated N-terminal portions of huntingtin (the HD gene product) with expanded repeats form more aggregates than longer or full length huntingtin polypeptides. These shorter fragments are also more prone to aggregate in the nucleus and cause more cell toxicity. Further experiments with huntingtin constructs harbouring exogenous nuclear import and nuclear export signals have implicated the nucleus in direct cell toxicity. We have made mouse models of HD and DRPLA using an N-terminal truncation of huntingtin (N171) and full-length atrophin-1 (the DRPLA gene product), respectively. In both models, diffuse neuronal nuclear staining and nuclear inclusion bodies are observed in animals expressing the expanded glutamine repeat protein, further implicating the nucleus as a primary site of neuronal dysfunction. Neuritic pathology is also observed in the HD mice. In the DRPLA mouse model, we have found that truncated fragments of atrophin-1 containing the glutamine repeat accumulate in the nucleus, suggesting that proteolysis may be critical for disease progression. Taken together, these data lead towards a model whereby proteolytic processing, nuclear localization and protein aggregation all contribute to pathogenesis.
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Fiocchi, C. "Overview of Inflammatory Bowel Disease Pathogenesis." Canadian Journal of Gastroenterology 4, no. 7 (1990): 309–16. http://dx.doi.org/10.1155/1990/512038.
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Inflammatory bowel disease (IBD) represents a difficult and challenging condition for patients, clinicians and basic investigators alike. Its etiology and pathogenesis are still unclear in spite of extensive investigations that have yielded a wealth of clinical. epidemiological, biochemical, bacteriological and immunological data on Crohn 's disease and ulcerative colitis. Although the precise mechanism(s) responsible for the intestinal inflammatory process remain to be defined, enough information has been assembled to hypothesize which components are likely to be important for this probably multifactorial disease. A consistent association between class I or II histocompatibility antigens and either Crohn's disease or ulcerative colitis has yet to be found. Nevertheless, ample epidemiological studies leave no doubt about the high frequency of familial clustering, and it must be determined whether this phenomenon translates a true genetic predisposition or a common environmental exposure, or both. Immune events occurring in the gastrointestinal tract are unquestionably linked to the pathogenesis of IBD, but it is unknown which are primary or secondary in nature. While most immune abnormalities detected in patients with established disease are likely to represent secondary events, these are no less important, as they probably contribute to the perpetuation of gut inflammation and tissue damage. This does not exclude that IBD is due to a primary defect of intestinal immunity, but this may no longer be detectable at the time of clinical manifestations. The answer to the question of wh1ch of the various intestinal immune abnormalities is central to pathogenesis must wait for additional research. Whether immune responses to the luminal flora, antigen processing mechanisms, antibody production, immunoregulation, cytotoxic activity, cytokine and mediator release are defective or disregulated is under intense investigation. It is likely that several of these events are involved, but they may interact in a complex and unpredictable fashion. lt is almost certain that there are various initiating and secondary events, and different immune mechanisms share relatively few common pathways for damaging the intestine, eg, cytokines, arachidonic acid metabolites, and oxidants. Perseverance in the study of these substances is finally yielding promising new approaches to the manipulation of immune and inflammatory responses chat cause bowel destruction. Future drugs may consist of combinations of highly specific inhibitors, antagonists or receptor blockers, that may selectively block one or several steps of the inflammatory cascade which is chronically active in the intestine of affected individuals. Therefore, we may soon face a situation not too dissimilar from what we have recently witnessed for peptic ulcer disease. The specific cause of IBD may still be beyond our comprehension, but a better understanding of its pathogenesis al lows us to put highly effective therapies within reach.
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Martynova, L., A. Chaulin, V. Vankov, and Yu Grigoryeva. "Modern Ideas on the Role of Macrophages and Neutrophils in the Development of Endometriosis." Bulletin of Science and Practice, no. 9 (September 15, 2023): 159–74. http://dx.doi.org/10.33619/2414-2948/94/19.
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Endometriosis is one of the most common gynecological diseases. Methods of diagnosis and treatment of endometriosis are imperfect, which is probably due to insufficient knowledge of the pathogenesis of this disease. Recently, research efforts have focused on the study of immunoinflammatory mechanisms in the development and progression of endometriosis. Understanding the pathogenetic mechanisms of endometriosis is important for the discovery of new laboratory biomarkers for early diagnosis and new targets for therapeutic effects. This article summarizes information on the role of some of the main cells of the immune system (macrophages and neutrophils) in the pathogenesis of endometriosis.
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Ramis, Antonio, Jordi Tarrés, Dolors Fondevila, and Luis Ferrer. "Immunocytochemical study of the pathogenesis of Pacheco's parrot disease in budgerigars." Veterinary Microbiology 52, no. 1-2 (September 1996): 49–61. http://dx.doi.org/10.1016/0378-1135(96)00062-4.
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Kazymova, Olga E., Maria I. Yarmolinskaya, and Alevtina M. Savicheva. "Features of the reproductive tract microbiota in patients with genital endometriosis. A literature review." Journal of obstetrics and women's diseases 71, no. 1 (January 15, 2022): 129–39. http://dx.doi.org/10.17816/jowd88921.
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BACKGROUND: Due to the widespread prevalence, steady growth and insufficient effectiveness of existing treatment regimens for external genital endometriosis, further study of the etiology and pathogenesis of the disease remains relevant. Inflammation is known to be one of the links in the pathogenesis of endometriosis; therefore, there is reason to believe that microorganisms are involved in the pathogenesis of this disease.
AIM: The aim of this study was to analyze the role of the reproductive tract microbiota in patients with endometriosis.
MATERIALS AND METHODS: This literature review was performed using systematic reviews, meta-analyses and experimental studies from such electronic databases as PubMed, CyberLeninka, and ScienceDirect published in the period from 1992 to 2021.
RESULTS AND CONCLUSIONS: In the review, we present the pathogenetic relationship between pelvic inflammatory diseases and endometriosis. The quantitatively and qualitatively altered microbiota composition of the reproductive tract, the genetic-epigenetic theory on the pathogenesis of endometriosis, which is based on mutations that accumulate directly under the influence of infectious agents, as well as the mechanisms of an abnormal immune response modeled by microorganisms, reflect the interconnection between the microbiota and the pathogenesis of endometriosis. Based on a number of studies, the relationship between the intestinal microbiota and the abdominal microbiome has been confirmed. Since endometriosis is the estrogen-dependent disease, of importance is the ability of the intestinal microbiota to produce -glucuronidase, which is enhanced by gut microbial dysbiosis, thus possibly contributing to the progression of endometriosis. One of the important practical directions is the drug correction of dysbiotic conditions. The effectiveness of antibiotic therapy has been demonstrated by experimentally induced endometriosis model. Currently, there are very few highly specific methods for non-invasive diagnosis of the disease, therefore, the study of the reproductive tract and intestinal microflora of women with endometriosis is promising for the introduction of new laboratory diagnostic methods.
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Hoshimaru, Minoru, Jun A. Takahashi, Haruhiko Kikuchi, Izumi Nagata, and Masakazu Hatanaka. "Possible roles of basic fibroblast growth factor in the pathogenesis of moyamoya disease: an immunohistochemical study." Journal of Neurosurgery 75, no. 2 (August 1991): 267–70. http://dx.doi.org/10.3171/jns.1991.75.2.0267.
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✓ Prominent features of moyamoya disease are fibrocellular thickening of the intima and enhanced angiogenesis. The pathogenesis of moyamoya disease is, however, unknown. Basic fibroblast growth factor (FGF) is an angiogenic factor as well as a potent mitogen for a number of cell types including vascular endothelial and smooth-muscle cells. In order to test the possibility that basic FGF takes part in the pathogenesis of moyamoya disease, the authors tested for the presence of this factor using a mouse monoclonal antibody against human recombinant basic FGF. The surgical specimens studied included two sections of the superficial temporal artery (STA) and four samples of dura mater from four patients with moyamoya disease. Surgical specimens were obtained from three patients with other diseases as control tissue. Sections of the STA obtained from the patients with moyamoya disease showed strong basic FGF immunoreactivity in endothelial and smooth-muscle cells, while control sections had only faint and scattered immunoreactivity. All sections of the dura mater obtained from the patients with moyamoya disease also revealed more intense immunohistochemical staining of basic FGF in meningeal and vascular cells than did control sections. These observations indicate that the amount of basic FGF is increased in the tissues of patients with moyamoya disease; thus, basic FGF may play an important role in the pathogenesis of moyamoya disease.
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Shcheglova, E. V., M. Kh Baykulova, and O. I. Boeva. "Cellular and molecular mechanisms of calcific aortic valve disease." Russian Journal of Cardiology, no. 9 (September 8, 2019): 86–91. http://dx.doi.org/10.15829/1560-4071-2019-9-86-91.
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The review provides current data on the pathogenesis of calcific aortic valve disease (CAVD) — a widespread disease with unfavorable prognosis. Currently, there are no effective therapeutic methods for the prevention and treatment of this pathology with the exception of valve replacement surgery. The role of genetic and hereditary factors in the occurrence of CAVD is considered, the leading pathogenetic mechanisms are described taking into account the stage of the disease. In particular, in the initiation phase of calcification, deposition of oxidized lipoproteins in the cusps and local inflammation plays the leading role. In the progression phase, active ectopic calcification dominates, similar to the process of bone formation. The study of the pathogenesis of CAVD seems appropriate taking into account the prospect of developing new effective therapeutic and prophylactic approaches.
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Wang, Xixin, Daniëlle Copmans, and Peter A. M. de Witte. "Using Zebrafish as a Disease Model to Study Fibrotic Disease." International Journal of Molecular Sciences 22, no. 12 (June 15, 2021): 6404. http://dx.doi.org/10.3390/ijms22126404.
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In drug discovery, often animal models are used that mimic human diseases as closely as possible. These animal models can be used to address various scientific questions, such as testing and evaluation of new drugs, as well as understanding the pathogenesis of diseases. Currently, the most commonly used animal models in the field of fibrosis are rodents. Unfortunately, rodent models of fibrotic disease are costly and time-consuming to generate. In addition, present models are not very suitable for screening large compounds libraries. To overcome these limitations, there is a need for new in vivo models. Zebrafish has become an attractive animal model for preclinical studies. An expanding number of zebrafish models of human disease have been documented, for both acute and chronic diseases. A deeper understanding of the occurrence of fibrosis in zebrafish will contribute to the development of new and potentially improved animal models for drug discovery. These zebrafish models of fibrotic disease include, among others, cardiovascular disease models, liver disease models (categorized into Alcoholic Liver Diseases (ALD) and Non-Alcoholic Liver Disease (NALD)), and chronic pancreatitis models. In this review, we give a comprehensive overview of the usage of zebrafish models in fibrotic disease studies, highlighting their potential for high-throughput drug discovery and current technical challenges.
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Kasimova, N. S., and E. N. Madjidova. "Immunologic investigations in diagnostics of acute cerebrovascular disease." NATIONAL JOURNAL OF NEUROLOGY, no. 5 (December 4, 2018): 41–44. http://dx.doi.org/10.28942/nnj.v1i5.108.
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Based on the literature data it can be argued that lateralization lesion determines the clinical and immunological parameters in patients with acute cerebral accidence. While there is a close relationship with the immune mechanisms of factors that play a role in the pathogenesis of cerebral circulation. It should be noted that further detailed study of immunopathological phenomena in early age children help outline new diagnostic and pathogenetic based pharmacotherapy of acute cerebrovascular events.
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Li, Wenli, Qian Wang, Fangfang Wei, Eying Lu, Yunzhi Ling, and Maosheng Wu. "Study on the Pathogenesis of Dengue Hepatitis." Nanoscience and Nanotechnology Letters 12, no. 4 (April 1, 2020): 476–83. http://dx.doi.org/10.1166/nnl.2020.3131.
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Dengue virus (DENV) is a single-stranded RNA virus that is transmitted by Aedes aegypti and Aedes albopictus. As a global health problem, early diagnosis and timely treatment of DENV are imperative. Therefore, it is important to explore the association between dengue fever and hepatitis and its pathogenesis and development mechanism of action. This may lead to the identification of biological markers for the prevention and treatment of dengue fever-induced hepatitis. In this study, we identified differentially expressed genes associated with interferon signaling to further understand the relationship between dengue fever and hepatitis. It has been speculated that during dengue-induced hepatitis, DEXD/H-box helicase 58 (DDX58) and interferon-induced protein with tetratricopeptide repeats 1 (IFIT1) are primarily responsible for pathogen identification. The joint action of HECT and RLD domain containing E3 ubiquitin protein ligase 5 (HERC5) and ubiquitinspecific peptidase 18 (USP18) regulate the biological effects of interferon and participate in the occurrence and development of this disease.
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Ristovska, Elena Curakova, Magdalena Genadieva-Dimitrova, Beti Todorovska, Vladimir Milivojevic, Ivan Rankovic, Igor Samardziski, and Maja Bojadzioska. "The Role of Endothelial Dysfunction in the Pathogenesis of Pregnancy-Related Pathological Conditions: A Review." PRILOZI 44, no. 2 (July 1, 2023): 113–37. http://dx.doi.org/10.2478/prilozi-2023-0032.
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Abstract In the recent decades, endothelial dysfunction (ED) has been recognized as a significant contributing factor in the pathogenesis of many pathological conditions. In interaction with atherosclerosis, hypercholesterolemia, and hypertension, ED plays a crucial role in the pathogenesis of coronary artery disease, chronic renal disease, and microvascular complications in diabetes mellitus. Although ED plays a significant role in the pathogenesis of several pregnancy-related disorders such as preeclampsia, HELLP syndrome, fetal growth restriction, and gestational diabetes mellitus, the exact pathogenetic mechanisms are still a matter of debate. The increased prevalence of these entities in patients with preexisting vascular diseases highlights the essential pathological role of the preexisting ED in these patients. The abnormal uteroplacental circulation and the release of soluble factors from the ischemic placenta into the maternal bloodstream are the main causes of the maternal ED underlying the characteristic preeclamptic phenotype. Besides the increased risk for maternal and fetal poor outcomes, the preexisting ED also increases the risk of development of future cardiovascular diseases in these patients. This study aimed to look deeper into the role of ED in the pathogenesis of several pregnancy-related hypertensive and liver diseases. Hopefully, it could contribute to improvement of the awareness, knowledge, and management of these conditions and also to the reduction of the adverse outcomes and additional long-term cardiovascular complications.
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Simonetti, Giorgia, Maria Teresa Sabrina Bertilaccio, Paolo Ghia, and Ulf Klein. "Mouse models in the study of chronic lymphocytic leukemia pathogenesis and therapy." Blood 124, no. 7 (August 14, 2014): 1010–19. http://dx.doi.org/10.1182/blood-2014-05-577122.
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Abstract Mouse models that recapitulate human malignancy are valuable tools for the elucidation of the underlying pathogenetic mechanisms and for preclinical studies. Several genetically engineered mouse models have been generated, either mimicking genetic aberrations or deregulated gene expression in chronic lymphocytic leukemia (CLL). The usefulness of such models in the study of the human disease may potentially be hampered by species-specific biological differences in the target cell of the oncogenic transformation. Specifically, do the genetic lesions or the deregulated expression of leukemia-associated genes faithfully recapitulate the spectrum of lymphoproliferations in humans? Do the CLL-like lymphoproliferations in the mouse have the phenotypic, histological, genetic, and clinical features of the human disease? Here we compare the various CLL mouse models with regard to disease phenotype, penetrance, and severity. We discuss similarities and differences of the murine lymphoproliferations compared with human CLL. We propose that the Eμ-TCL1 transgenic and 13q14-deletion models that have been comprehensively studied at the levels of leukemia phenotype, antigen-receptor repertoire, and disease course show close resemblance to the human disease. We conclude that modeling CLL-associated genetic dysregulations in mice can provide important insights into the molecular mechanisms of disease pathogenesis and generate valuable tools for the development of novel therapies.
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Davydova, G. A., T. A. Lisitsyna, L. A. Kovaleva, E. S. Sorozhkina, A. A. Zaitseva, and A. A. Baisangurova. "Clinical Variations of Uveitis in Immuno-Inflammatory Diseases. Review of the Literature. Part 1." Ophthalmology in Russia 19, no. 3 (October 3, 2022): 465–74. http://dx.doi.org/10.18008/1816-5095-2022-3-465-474.
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Non-infectious uveitis is one of the main and insufficiently studied causes of disability and blindness in patients with immuno-inflammatory diseases. Uveitis associated with spondyloarthritis, Behcet’s disease, juvenile idiopathic arthritis, systemic sarcoidosis and Vogt-Koyanagi-Harada syndrome are described more often and better than others, but the pathogenesis of different variants of their course is not well understood. Also, there remains a need to study the clinical and pathogenetic features of uveitis in rare autoimmune inflammatory diseases. Despite the currently existing diagnostic and therapeutic schemes, further study of the pathogenesis of uveitis associated with immune-inflammatory diseases is required, the research of a personalized approach and an algorithm for joint multidisciplinary diagnosis by specialists in various fields. A deeper understanding of the specific pathogenetic mechanisms will reveal new possibilities in the treatment of patients with autoimmune uveitis. This article is devoted to the current clinical and differential diagnostic aspects, common features and distinctive features associated with various variants of the course of non-infectious uveitis in patients with immuno-inflammatory diseases.
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Oymans, Judith, Lucien van Keulen, Paul J. Wichgers Schreur, and Jeroen Kortekaas. "Early Pathogenesis of Wesselsbron Disease in Pregnant Ewes." Pathogens 9, no. 5 (May 13, 2020): 373. http://dx.doi.org/10.3390/pathogens9050373.
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Wesselsbron virus (WSLV) is a neglected, mosquito-borne flavivirus that is endemic to the African continent. The virus is teratogenic to ruminants and causes a self-limiting febrile illness in humans. Wesselsbron disease manifests with similar clinical signs and occurs in the same areas under the same climatic conditions as Rift Valley fever, which is therefore included in the differential diagnosis. Although the gross pathology of WSLV infection in pregnant ewes is reported in literature, the pathogenesis that leads to stillbirths, congenital malformations and abortion has remained undescribed. In the present study, pregnant ewes were inoculated with WSLV and subjected to detailed clinical- and histopathology 8 days later. The virus was mainly detected in foetal trophoblasts of the placenta and in neural progenitor cells, differentiated neurons, oligodendrocytes, microglia and astrocytes. Our study demonstrates that WSLV efficiently crosses the maternal–foetal interface and is highly neuroinvasive in the ovine foetus.
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Neely, Melody N., John D. Pfeifer, and Michael Caparon. "Streptococcus-Zebrafish Model of Bacterial Pathogenesis." Infection and Immunity 70, no. 7 (July 2002): 3904–14. http://dx.doi.org/10.1128/iai.70.7.3904-3914.2002.
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ABSTRACT Due to its small size, rapid generation time, powerful genetic systems, and genomic resources, the zebrafish has emerged as an important model of vertebrate development and human disease. Its well-developed adaptive and innate cellular immune systems make the zebrafish an ideal model for the study of infectious diseases. With a natural and important pathogen of fish, Streptococcus iniae, we have established a streptococcus- zebrafish model of bacterial pathogenesis. Following injection into the dorsal muscle, zebrafish developed a lethal infection, with a 50% lethal dose of 103 CFU, and died within 2 to 3 days. The pathogenesis of infection resembled that of S. iniae in farmed fish populations and that of several important human streptococcal diseases and was characterized by an initial focal necrotic lesion that rapidly progressed to invasion of the pathogen into all major organ systems, including the brain. Zebrafish were also susceptible to infection by the human pathogen Streptococcus pyogenes. However, disease was characterized by a marked absence of inflammation, large numbers of extracellular streptococci in the dorsal muscle, and extensive myonecrosis that occurred far in advance of any systemic invasion. The genetic systems available for streptococci, including a novel method of mutagenesis which targets genes whose products are exported, were used to identify several mutants attenuated for virulence in zebrafish. This combination of a genetically amenable pathogen with a well-defined vertebrate host makes the streptococcus-zebrafish model of bacterial pathogenesis a powerful model for analysis of infectious disease.
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Qin, Dan-Yi, and Ying-Ping Deng. "Transgenic dry eye mouse models: powerful tools to study dry eye disease." International Journal of Ophthalmology 15, no. 4 (April 18, 2022): 635–45. http://dx.doi.org/10.18240/ijo.2022.04.18.
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Dry eye disease (DED) is one of the most common chronic multifactorial ocular surface diseases with high prevalence and complex pathogenesis. DED results in several ocular discomforts, vision fluctuation, and even potential damage of the ocular surface, bringing heavy burdens both on individuals and the society. The pathology of DED consists of tear film hyperosmolarity and immune responses on the ocular surface. Mice are widely used for developing models that simulate human DED features for investigating its pathogenesis and treatment. DED can be classified into aqueous-deficiency dry eye (ADDE) and evaporative dry eye (EDE). ADDE can be further divided into Sjögren syndrome dry eye (SSDE) and non-Sjögren syndrome dry eye (NSSDE). SSDE mouse models include natural strains, typified by non-obese diabetic (NOD) mice, and genetically engineered ones, like Aire-/- and Id3 knockout mice. Intrinsic EDE mainly refers to meibomian gland dysfunction (MGD). Eda-/- Tabby, Sod1-/-, Elovl1-/- are the most common transgenic MGD mouse models. Transgenic mouse models provide useful tools for studying the pathogenesis of DED and evaluating its novel therapies. This review compares the major transgenic dry eye mouse models and discusses their applications in DED research.
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Zadionchenko, V. S., T. V. Adasheva, I. V. Fedorova, S. V. Pavlov, V. V. Li, and O. I. Nesterenko. "Arterial hypertension and chronic obstructive pulmonary disease: pathogenetic parallels and clinicofunctional features." CardioSomatics 1, no. 1 (March 15, 2010): 31–37. http://dx.doi.org/10.26442/cs44959.
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The great prevalence of comorbidities, such as arterial hypertension (AH) and chronic obstructive pulmonary disease (COPD), generates a need to study the impact of COPD on the pathogenesis, course, and clinical picture of associated cardiovascular diseases. The paper analyzes the data available in the literature on the pathogenesis and course of arterial hypertension in patients with COPD. The paper also gives the authors’ data on the clinicofunctional and pathophysiological features of AH in patients with COPD. The findings suggest that the study group has clinical vascular and organ dysfunction that may both play a role in the pathogenesis of AH in the presence of COPD and prevent a high cardiovascular risk. Key words: arterial hypertension, chronic obstructive pulmonary disease.
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Кuchinskaya, Е. М., M. M. Kostik, and N. А. Lyubimova. "Impaired immune function in the pathogenesis of systemic lupus erythematosus." Russian Journal for Personalized Medicine 2, no. 2 (June 2, 2022): 63–71. http://dx.doi.org/10.18705/2782-3806-2022-2-2-63-71.
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Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease characterized by variable clinical manifestations and a complex pathogenesis not fully understood at the moment. Various forms of cell death play an important role, eventually leading to the presentation of the autoantigen to immunocompetent cells, the production of pro-inflammatory cytokines, and an imbalance between the effectors and regulators of cellular immunity. The study of SLE pathogenesis pathways includes the search for potential objects for targeted therapy. This review briefly discusses the current knowledge about the pathogenetic mechanisms of this disease, including the researches latest to-date.
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Satoh, Jun-ichi. "Fundamental study on clarification of brain molecular pathology of Nasu-Hakola disease." Impact 2019, no. 8 (November 26, 2019): 24–26. http://dx.doi.org/10.21820/23987073.2019.8.24.
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Brain pathology expert Dr Jun-ichi Satoh, from the Department of Bioinformatics and Molecular Neuropathology of Meiji Pharmaceutical University in Tokyo, is drawing on his expertise on neurology and neuroimmunology to delve into some of the more complex diseases impacting the human brain. His knowledge and expertise have allowed him to direct his research interests to study neurodegenerative diseases, such as Alzheimer's disease (AD), and neuroinflammatory diseases, such as multiple sclerosis (MS), and the analysis of their molecular pathogenesis by using a bioinformatics approach. His current focus is on Nasu-Hakola disease (NHD), a disease whose rarity has posed significant barriers towards performing large-scale clinical research in order to understand what exactly causes this disease and develop effective novel therapies.
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Li, Yuhan. "A Study of HDAC6 for Ameliorating the Cognitive Function in Alzheimer's Disease." Theoretical and Natural Science 4, no. 1 (April 28, 2023): 498–503. http://dx.doi.org/10.54254/2753-8818/4/20220637.
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One of the most prevalent causes of dementia, Alzheimer's disease (AD) is characterized by gradual mental decline and memory loss over time. Several drugs are currently available for the treatment of AD, but they only address the disease's symptoms rather than its underlying pathogenesis. Researchers looked into epigenetic therapy and found that histone deacetylase 6 (HDAC6) could be an effective treatment for Alzheimer's disease. This paper uses a literature review approach to investigate the roles of HDAC6 inhibition in AD models and HDAC6 inhibitors, as well as the hypotheses surrounding the pathogenesis of AD. The amyloid cascade hypothesis, the tau hypothesis, and the role of oxygen species are identified as the most prominent pathogenesis hypotheses in this paper. A decrease in Hdac6 levels improves associative and spatial memory in an Alzheimer's disease mouse model and reverses the mitochondrial trafficking impairment in hippocampal neurons in vitro and in vivo. Therefore, inhibiting HDAC6 may represent a novel approach to treating AD-related cognitive decline. As a result of these issues, the FDA has yet to approve any HDAC6 inhibitor for use in the treatment of Alzheimer's disease (FDA)
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Medina, Reinhold J., Christina L. O'Neill, T. Michelle O'Doherty, Sarah E. J. Wilson, and Alan W. Stitt. "Endothelial Progenitors as Tools to Study Vascular Disease." Stem Cells International 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/346735.
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Endothelial progenitor cells (EPCs) have great clinical value because they can be used as diagnostic biomarkers and as a cellular therapy for promoting vascular repair of ischaemic tissues. However, EPCs also have an additional research value in vascular disease modelling to interrogate human disease mechanisms. The term EPC is used to describe a diverse variety of cells, and we have identified a specific EPC subtype called outgrowth endothelial cell (OEC) as the best candidate for vascular disease modelling because of its high-proliferative potential and unambiguous endothelial commitment. OECs are isolated from human blood and can be exposed to pathologic conditions (forward approach) or be isolated from patients (reverse approach) in order to study vascular human disease. The use of OECs for modelling vascular disease will contribute greatly to improving our understanding of endothelial pathogenesis, which will potentially lead to the discovery of novel therapeutic strategies for vascular diseases.
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Hoffman, Gary S., Joan M. G. Sechler, John I. Gallin, James H. Shelhamer, Anthony Suffredini, Frederick P. Ognibene, Richard J. Baltaro, et al. "Bronchoalveolar Lavage Analysis in Wegener's Granulomatosis: A Method to Study Disease Pathogenesis." American Review of Respiratory Disease 143, no. 2 (February 1991): 401–7. http://dx.doi.org/10.1164/ajrccm/143.2.401.
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Takebe, Noriyoshi, Masato Hojo, Shigeki Takada, Yoshito Sugita, Kenji Tanigaki, Masahiro Tanji, and Susumu Miyamoto. "Contribution of PROP1 in the pathogenesis of Cushing’s disease: A preliminary study." Interdisciplinary Neurosurgery 31 (March 2023): 101691. http://dx.doi.org/10.1016/j.inat.2022.101691.
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Vorberg, Ina, and Roberto Chiesa. "Experimental models to study prion disease pathogenesis and identify potential therapeutic compounds." Current Opinion in Pharmacology 44 (February 2019): 28–38. http://dx.doi.org/10.1016/j.coph.2019.02.002.
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Naif, Hassan M. "Pathogenesis of HIV infection." Infectious Disease Reports 5, no. 1S (June 6, 2013): 6. http://dx.doi.org/10.4081/idr.2013.s1.e6.
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Over the past three decades of intense research on the contribution of viral and host factors determining the variability in HIV-1 infection outcome, HIV pathogenesis is still a fascinating topic that requires further study. An understanding of the exact mechanism of how these factors influencing HIV pathogenesis is critical to the development of effective strate- gies to prevent infection. Significant progress has been made in identifying the role of CCR5 (R5) and CXCR4 (X4) HIV strains in disease progression, particularly with the persistence of R5 HIV-1 strains at the AIDS stage. This indicates that R5 strains are as fit as X4 in causing CD4+ T cell depletion and in contribution to disease outcome, and so questions the prerequisite of the shift from R5 to X4 for disease progression. In contrast, the ability of certain HIV strains to readily use CXCR4 for infection or entry into macrophages, as the case with viruses are homozygous for tropism by CCR5delta32. This raises another major paradox in HIV pathogenesis about the source of X4 variants and how do they emerge from a relatively homogeneous R5 viral population after transmission. The interactions between viral phenotypes, tropism and co-receptor usage and how they influence HIV pathogenesis are the main themes addressed in this review. A better understanding of the viral and host genetic factors involved in the fitness of X4 and R5 strains of HIV-1 may facilitate development of specific inhibitors against these viral populations to at least reduce the risk of disease progression.
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Hasan Sulimani, Zainbganayah, Manal Abdulaziz Murad, Amal Mohammed Abushal, Mohsen Daghustani, Joud Nasir Bazaid, Malak Mohammed Al-Jraib, Shahad Abid Alsreihi, et al. "A CROSS-SECTIONAL STUDY OF THE IMPACT OF ENDODONTIC INFECTIONS ON THE PATHOGENESIS OF CARDIOVASCULAR DISEASE." International Journal of Advanced Research 8, no. 12 (December 31, 2020): 888–94. http://dx.doi.org/10.21474/ijar01/12229.
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Introduction: The apical periodontitis possesses an association with the increased inflammatory markers levels, which contribute to the systematic immune response, leading towards systematic inflammation. The endodontic infections were reported to contribute to the CVD via the metastatic pathways however, there is a requirement to analyse the impact of endodontic infections on the pathogenesis of the cardiovascular disease. Aim:This research aims to assess the impact of endodontic infections on the pathogenesis of the cardiovascular disease. Material andMethod:This research was conducted using a cross-sectional research design by recruiting N=120 inpatients and outpatients visiting the healthcare organisation located in Saudi Arabia. Results:The endodontic infections are likely to increase the overall inflammatory burden, which might increase the risk of CVD among the individuals. Due to the multifactorial aetiology of CVD, the oral diseases are perceived to possess associated with the CVD. Thestatistical analysis revealed that there is no association between the presence of the lesion of endodontic origin and cardiovascular diseases. Conclusion:There is no association between the presence of the lesion of endodontic origin and cardiovascular diseases.
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Loshkova, E. V., E. I. Kondratyeva, A. I. Khavkin, E. K. Zhekaite, Yu V. Kotova, Yu L. Melyanovskaya, M. I. Erokhina, E. A. Yablokova, and V. A. Zhelev. "Vitamin D: genetic regulation of inflammation in autoimmune, metabolic and microbial models." Experimental and Clinical Gastroenterology, no. 8 (October 9, 2023): 151–66. http://dx.doi.org/10.31146/1682-8658-ecg-216-8-151-166.
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The study of cytokine production and its genetic regulation in diseases of various pathogenesis in childhood, which include several mechanisms of inflammation - this is autoimmune against the background of celiac disease, type 1 diabetes and CAI, lymphoproliferative against the background of oncohematological diseases, microbial-inflammatory against the background of chronic pyelonephritis and cystic fibrosis and metabolic against the background of obesity and a decrease in bone mineral density is necessary to expand understanding of pathogenesis, predict variants of the clinical course of diseases (clinical phenotypes) and complications, as well as response to therapy. The literature review is devoted to the analysis and interpretation of data on the effect of vitamin D supply and its genetic regulation on the course of diseases, combined according to the leading pathogenetic mechanism of inflammation into autoimmune, microbial, and lymphoproliferative models.
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Yao, Xiao-Hong, Tao Luo, Yu Shi, Zhi-Cheng He, Rui Tang, Pei-Pei Zhang, Jun Cai, et al. "A cohort autopsy study defines COVID-19 systemic pathogenesis." Cell Research 31, no. 8 (June 16, 2021): 836–46. http://dx.doi.org/10.1038/s41422-021-00523-8.
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AbstractSevere COVID-19 disease caused by SARS-CoV-2 is frequently accompanied by dysfunction of the lungs and extrapulmonary organs. However, the organotropism of SARS-CoV-2 and the port of virus entry for systemic dissemination remain largely unknown. We profiled 26 COVID-19 autopsy cases from four cohorts in Wuhan, China, and determined the systemic distribution of SARS-CoV-2. SARS-CoV-2 was detected in the lungs and multiple extrapulmonary organs of critically ill COVID-19 patients up to 67 days after symptom onset. Based on organotropism and pathological features of the patients, COVID-19 was divided into viral intrapulmonary and systemic subtypes. In patients with systemic viral distribution, SARS-CoV-2 was detected in monocytes, macrophages, and vascular endothelia at blood–air barrier, blood–testis barrier, and filtration barrier. Critically ill patients with long disease duration showed decreased pulmonary cell proliferation, reduced viral RNA, and marked fibrosis in the lungs. Permanent SARS-CoV-2 presence and tissue injuries in the lungs and extrapulmonary organs suggest direct viral invasion as a mechanism of pathogenicity in critically ill patients. SARS-CoV-2 may hijack monocytes, macrophages, and vascular endothelia at physiological barriers as the ports of entry for systemic dissemination. Our study thus delineates systemic pathological features of SARS-CoV-2 infection, which sheds light on the development of novel COVID-19 treatment.
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O’Keefe, Louise, and Donna Denton. "Using Drosophila Models of Amyloid Toxicity to Study Autophagy in the Pathogenesis of Alzheimer’s Disease." BioMed Research International 2018 (2018): 1–14. http://dx.doi.org/10.1155/2018/5195416.
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Autophagy is a conserved catabolic pathway that involves the engulfment of cytoplasmic components such as large protein aggregates and organelles that are delivered to the lysosome for degradation. This process is important in maintaining neuronal function and raises the possibility of a role for autophagy in neurodegenerative diseases. Alzheimer’s disease (AD) is the most prevalent form of these diseases and is characterized by the accumulation of amyloid plaques in the brain which arise due to the misfolding and aggregation of toxic peptides, including amyloid beta (Aβ). There is substantial evidence from both AD patients and animal models that autophagy is dysregulated in this disease. However, it remains to be determined whether this is protective or pathogenic as there is evidence that autophagy can act to promote the degradation as well as function in the generation of toxic Aβ peptides. Understanding the molecular details of the extensive crosstalk that occurs between the autophagic and endolysosomal cellular pathways is essential for identifying the molecular details of amyloid toxicity. Drosophila models that express the toxic proteins that aggregate in AD have been generated and have been shown to recapitulate hallmarks of the disease. Here we focus on what is known about the role of autophagy in amyloid toxicity in AD from mammalian models and how Drosophila models can be used to further investigate AD pathogenesis.
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Zaidman, Alla Mikhailovna, Anastasia Viktorovna Korel, Andrey Valentinovich Sakharov, Tatyana Vasilyevna Rusova, and Valentina Ivanovna Rykova. "SCHEUERMANN’S DISEASE MORPHOGENESIS." Hirurgiâ pozvonočnika, no. 2 (May 26, 2005): 073–83. http://dx.doi.org/10.14531/ss2005.2.73-83.
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Objective. To specify a morphogenetic pathogenesis of the Scheuermann’s disease. Material and Methods. Growth plates, intervertebral discs, vertebral body tissue (surgical material) from 25 patients of 12–14 years old with Scheuermann’s disease of Grade II–III were examined. In-depth morphohystochemical, biochemical, and ultrastructural analyses were used to study glycosaminoglycans, oxidation-reduction enzymes, alkaline and acid phosphatase, RNA, DNA, and qualitative and quantitative composition of glycosaminoglycans. Results. Pathogenetic mechanisms of Scheuermann’s disease development are presented basing of previously obtained data on genetic dependence of this pathology. The starter of the spine kyphotic deformity is a disturbance of proteoglycan molecule synthesis and conformation in ventral growth plates of vertebral bodies. The structural change in proteoglycans, which perform barrier-trophic, informational, and antiinvasive functions results in a decreased mitotic and proliferative activity of chondroblasts. The spine kyphotic deformity develops in association with an active osteogenesis.
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Roldan, Carlos A., Oleksandr Schevchuck, Kirsten Tolstrup, Paola C. Roldan, Leonardo Macias, Clifford R. Qualls, Ernest R. Greene, Reyaad Hayek, Gerald A. Charlton, and Wilmer L. Sibbitt, Jr. "Lambl's Excrescences: Association with Cerebrovascular Disease and Pathogenesis." Cerebrovascular Diseases 40, no. 1-2 (2015): 18–27. http://dx.doi.org/10.1159/000381906.
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Background: Lambl's excrescences (LEx) are detected by transesophageal echocardiography (TEE) and are characterized as thin, elongated, and hypermobile structures located at the leaflets' coaptation point of the heart valves. The association of LEx with cerebrovascular disease (CVD) is still undefined and yet patients with LEx and suspected CVD receive unproven effective antiplatelet or anticoagulant therapy or even undergo valve surgery. Also, the association of LEx with aging and atherogenic, inflammatory, or thrombogenic parameters has not been reported. Methods: Seventy-seven patients with systemic lupus erythematosus (SLE) (71 women, age 37 ± 12 years) and 26 age- and sex-matched healthy controls (22 women, age 34 ± 11 years) prospectively underwent routine history and physical exam, transcranial Doppler, brain MRI, TEE, carotid duplex, and clinical and laboratory evaluations of atherogenesis, inflammation, platelet activity, coagulation, and fibrinolysis. Subjects without stroke/TIA on enrollment (with and without LEx) had a median follow-up of 57 months. Results: On enrollment, 33 (43%) of 77 patients had CVD manifested as acute stroke/TIA (23 patients), cerebromicroembolism by transcranial Doppler (17 patients), or cerebral infarcts by MRI (14 patients). Mitral or aortic valve LEx were equally frequent in healthy controls (46%) as in patients with and without any CVD (39 and 43%), stroke/TIA (35 and 43%), cerebromicroembolism (41 and 42%), or cerebral infarcts (36 and 43%) (all p ≥ 0.72). Also, other mechanisms for CVD other than LEx such as Libman-Sacks vegetations, patent foramen ovale or interatrial septal aneurysm, aortic or carotid atherosclerosis, or thrombogenesis were found in ≥94% of patients with CVD. In addition, 36 subjects with and 44 without LEx had similar low incidence of stroke/TIA (1 (1.3%) and 2 (2.5%), respectively, p = 1.0) during follow-up. Finally, LEx were not associated with aging, atherogenic risk factors, atherosclerosis, inflammation, or thrombogenesis. Conclusions: In this study, LEx are similarly prevalent in healthy controls and SLE patients, are not associated with CVD, and are not associated with pathogenic risk factors. Therefore, the study findings suggest that LEx may not be cardioembolic substrates, may not represent pathologic valve structures, and may not require therapy.
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Xu, Xuan, Hui Wang, David A. Bennett, Qing-Ye Zhang, Gang Wang, and Hong-Yu Zhang. "Systems Genetic Identification of Mitochondrion-Associated Alzheimer’s Disease Genes and Implications for Disease Risk Prediction." Biomedicines 10, no. 8 (July 24, 2022): 1782. http://dx.doi.org/10.3390/biomedicines10081782.
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Cumulative evidence has revealed the association between mitochondrial dysfunction and Alzheimer’s disease (AD). Because the number of mitochondrial genes is very limited, the mitochondrial pathogenesis of AD must involve certain nuclear genes. In this study, we employed systems genetic methods to identify mitochondrion-associated nuclear genes that may participate in the pathogenesis of AD. First, we performed a mitochondrial genome-wide association study (MiWAS, n = 809) to identify mitochondrial single-nucleotide polymorphisms (MT-SNPs) associated with AD. Then, epistasis analysis was performed to examine interacting SNPs between the mitochondrial and nuclear genomes. Weighted co-expression network analysis (WGCNA) was applied to transcriptomic data from the same sample (n = 743) to identify AD-related gene modules, which were further enriched by mitochondrion-associated genes. Using hub genes derived from these modules, random forest models were constructed to predict AD risk in four independent datasets (n = 743, n = 542, n = 161, and n = 540). In total, 9 potentially significant MT-SNPs and 14,340 nominally significant MT-nuclear interactive SNPs were identified for AD, which were validated by functional analysis. A total of 6 mitochondrion-related modules involved in AD pathogenesis were found by WGCNA, from which 91 hub genes were screened and used to build AD risk prediction models. For the four independent datasets, these models perform better than those derived from AD genes identified by genome-wide association studies (GWASs) or differential expression analysis (DeLong’s test, p < 0.05). Overall, through systems genetics analyses, mitochondrion-associated SNPs/genes with potential roles in AD pathogenesis were identified and preliminarily validated, illustrating the power of mitochondrial genetics in AD pathogenesis elucidation and risk prediction.
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Ghoshal, Kakali, and Maitree Bhattacharyya. "Overview of Platelet Physiology: Its Hemostatic and Nonhemostatic Role in Disease Pathogenesis." Scientific World Journal 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/781857.
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Platelets are small anucleate cell fragments that circulate in blood playing crucial role in managing vascular integrity and regulating hemostasis. Platelets are also involved in the fundamental biological process of chronic inflammation associated with disease pathology. Platelet indices like mean platelets volume (MPV), platelets distributed width (PDW), and platelet crit (PCT) are useful as cheap noninvasive biomarkers for assessing the diseased states. Dynamic platelets bear distinct morphology, whereαand dense granule are actively involved in secretion of molecules like GPIIb , IIIa, fibrinogen, vWf, catecholamines, serotonin, calcium, ATP, ADP, and so forth, which are involved in aggregation. Differential expressions of surface receptors like CD36, CD41, CD61 and so forth have also been quantitated in several diseases. Platelet clinical research faces challenges due to the vulnerable nature of platelet structure functions and lack of accurate assay techniques. But recent advancement in flow cytometry inputs huge progress in the field of platelets study. Platelets activation and dysfunction have been implicated in diabetes, renal diseases, tumorigenesis, Alzheimer’s, and CVD. In conclusion, this paper elucidates that platelets are not that innocent as they keep showing and thus numerous novel platelet biomarkers are upcoming very soon in the field of clinical research which can be important for predicting and diagnosing disease state.
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Xintong, Xie. "Pathogenesis of anorexia nervosa." SHS Web of Conferences 171 (2023): 01005. http://dx.doi.org/10.1051/shsconf/202317101005.
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Anorexia nervosa is a potentially life-threatening psychiatric disorder that threatens the life and health of the patient. Patients are characterized by a very low body mass index, rapid weight loss, an irrational fear of weight gain, and a distorted view of their body image. The disease is closely related to genetic factors, neuroendocrine imbalances, and psychosocial and family factors. In recent years, its morbidity and mortality rates have gradually increased. The causes of death are not only organ failure due to extreme starvation, but also complications due to overmedication and depression and suicide. Currently, nutritional therapy and psychotherapy are the main treatments for the disease. It is mainly found in the adolescent and female population, and the mortality rate of patients is very high. The study of the pathogenesis of anorexia nervosa is of great importance to actively improve the prognosis and save the lives of patients.
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Mounsey, Ross B., and Peter Teismann. "Mitochondrial Dysfunction in Parkinson's Disease: Pathogenesis and Neuroprotection." Parkinson's Disease 2011 (2011): 1–18. http://dx.doi.org/10.4061/2011/617472.
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Mitochondria are vitally important organelles involved in an array of functions. The most notable is their prominent role in energy metabolism, where they generate over 90% of our cellular energy in the form of ATP through oxidative phosphorylation. Mitochondria are involved in various other processes including the regulation of calcium homeostasis and stress response. Mitochondrial complex I impairment and subsequent oxidative stress have been identified as modulators of cell death in experimental models of Parkinson's disease (PD). Identification of specific genes which are involved in the rare familial forms of PD has further augmented the understanding and elevated the role mitochondrial dysfunction is thought to have in disease pathogenesis. This paper provides a review of the role mitochondria may play in idiopathic PD through the study of experimental models and how genetic mutations influence mitochondrial activity. Recent attempts at providing neuroprotection by targeting mitochondria are described and their progress assessed.