Добірка наукової літератури з теми "Pathegenesis"

Background: Systemic lupus erythematosus (SLE) is an autoimmune disease in which patients are often infected by viruses due to deficient immunity or immunosuppressant use. BK virus (BKV)mainly affects the kidney and can also cause multiple organ involvement throughout the body, which is similar to SLE. BKV is mostly a latent infection in vivo. The incidence of virus reactivation is higher in SLE patients. Reactivation of BKV can induce the production of autoantibodies, thereby promoting the occurrence and development of SLE. Purpose: Aim of this article is to review the prevalence and pathegenesis of BKV infection in SLE patients. Method: The literature search was conducted using four different databases including PubMed, Cochrane Library, Scopus and Web of Science. Results: BK virus is higher infection and reactivation in SLE patients. The "hapten carrier" mechanism may lead to the production of autoantibodies. Some immunosuppressive drugs, like leflumide and hydroxychloroquine, may show a protective effect. Conclusions: BKV infection plays a role in the occurrence and development of SLE, and its significance deserves further exploration.

ABSTRACT:Cerebrovascular accidents due to Moyamoya disease, a disorder characterized by arterial stenosis at the base of the brain accompanied by typical net-like collateral vessels, occurred in two young Japanese women with Graves' disease when they were in thyrotoxicosis. In one patient, a second attack of cerebral infarction occurred with the recurrence of thyrotoxicosis. Association of Moyamoya disease and Graves' thyrotoxicosis is rare and the pathegenetic relationship is discussed.

Fever is the most common symptom of most infectious diseases and, to a moderate extent, has a protective-compensatory effect with increased blood bactericidality and activation of immune mechanisms. A pathological variant of fever, in which there is a rapid and inadequate increase in body temperature, accompanied by microcirculation disorder, metabolic disorders, increasing dysfunction of vital organs and systems, in particular, the damage to the central nervous system is hyperthermic syndrome, which requires active antipyretic and symptomatic therapy. Polysystemic dysfunctions associated with hyperthermia and the course of the infectious process can change the metabolic status of antipyretic drugs and sensitivity to their action, which can increase the frequency and severity of side effects, including the development of hypothermia and/or a sharp decrease in body temperature. This will be prevented by a pathegenetic approach to the correction of hyperthermia using antipyretic drugs, the action of which is based on the stimulation of natural, endogenous anti-inflammatory and antipyretic mechanisms.

Background: Osteoarthritis (OA) is the predominant threaten to the health of the elderly, and it is crucial to understand the molecular pathegenetic mechanisms involved in it. This study aims to investigate the role of a well-studied cancer-related long noncoding RNA (lncRNA)-POU3F3 in OA and its implicated molecular mechanisms. Method: The expression of POU3F3 and miR-29a-3p was examined in osteoarthritis patients, destabilization of the medial meniscus (DMM) mouse OA model, and IL- 1β induced chondrocytes cell OA model by quantitative real-time PCR. The interaction between POU3F3, miR-29a-3p and transcription factor forkhead box O3 (FOXO3) was verified by via dual-luciferase reporter analysis and RNA immunoprecipitation analyses. Cell proliferation and apoptosis were evaluated by cell viability assay and flow cytometry, respectively. Cartilage extracellular matrix (ECM) degradation were investigated with ELISA and western blotting. In addition, the in vivo regulation of POU3F3 in OA was verified by intra-articular injection of lentivirus overexpression POU3F31 in mice models. Results: The expression level of POU3F3 was decreased in OA patients/animal cartilage tissues and IL-1β-stimulated in vitro chondrocyte model. POU3F3 overexpression inhibited IL-1β-induced injury of chondrocytes, enhancing cell viability, suppressing apoptosis and inflammatory cytokine secretion, rescuing metabolic dysfunction, and restrained autophagy in vitro. Mechanistically, Luciferase reporter and RNA immunoprecipitation (RIP) assays indicated that miR-29a-3p could directly bind to POU3F3 and FOXO3 was a target gene of miR-29a-3p. Functional rescue assays confirmed this POU3F3/miR-29a-3p/FOXO3 axis in chondrocytes during OA occurrence. Furthermore, intra-articularly delivery of lentivirus containing POU3F3 alleviates the damage in mouse OA model in vivo. Conclusion: this work highlights the function of POU3F3/miR-29a-3p/FOXO3 axis in OA pathogenesis, suggesting this axis as a potential progression of OA [12-15]. These studies indicate the potential contribution of lncRNAs in the development of OA and a promising target for disease diagnosis and treatment.

Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are major human pathogens. HSV establishes latency in the nervous system and reactivates to cause recurrent disease, resulting in transmission of progeny virions to naïve individuals. Though HSV-1 and HSV-2 share similar structure and genes, they have distinctive recurrence profiles. Generally, HSV-1 reactivation is associated with disease 'above the waist' and HSV-2 reactivation is associated with disease 'below the waist'. This phenomenon was described decades ago but still remains unexplained. The mechanism of HSV latent infection in the peripheral nervous system (PNS) has been extensively investigated, especially with in sensory neurons. Another component of the peripheral nervous system (PNS), autonomic neurons, were also known to be infected with HSV productively and latently, but largely ignored because of the assumption that there is no difference in the pathogenesis of HSV in the neurons and that both HSV-1 and HSV-2 behave in the same way in different types of neurons. However, autonomic neurons differ in physiological function compared to sensory neurons. Activation factors of autonomic neurons, such as emotional stress, trauma and hormonal fluctuation, are also known HSV reactivation triggering factors. Therefore, I hypothesized that autonomic neurons innervating the site of HSV infection are responsible the different reactivation frequencies of HSV-1 and HSV-2 after peripheral invasion. In this report, the role of autonomic neurons in HSV pathogenesis were examined using the female guinea pig reactivation model. Major findings of this report are that 1) parasympathetic ganglia innervating the ocular region support latent infection of HSV-1 selectively, thus contributing the more frequent HSV-1 reactivation, 2) mixed autonomic ganglia in the genital area support HSV-2 latent infection selectively, and 3) sympathetic neurons in the genital region supported productive and latent infection of HSV-1 and HSV-2 differently. All of the results in this report indicate that autonomic neurons play a distinctive role in HSV pathogenesis compared to the sensory neurons and are responsible for the different reactivation frequencies of HSV-1 and HSV-2. This report raises the importance of autonomic neurons in HSV pathogenesis and challenges the paradigm of HSV pathogenesis.
Ph. D.