pathological condition
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2022 ◽  
Vol 23 (2) ◽  
pp. 735
Author(s):  
Elena V. Mitroshina ◽  
Maria M. Loginova ◽  
Roman S. Yarkov ◽  
Mark D. Urazov ◽  
Maria O. Novozhilova ◽  
...  

Ischemic brain injury is a widespread pathological condition, the main components of which are a deficiency of oxygen and energy substrates. In recent years, a number of new forms of cell death, including necroptosis, have been described. In necroptosis, a cascade of interactions between the kinases RIPK1 and RIPK3 and the MLKL protein leads to the formation of a specialized death complex called the necrosome, which triggers MLKL-mediated destruction of the cell membrane and necroptotic cell death. Necroptosis probably plays an important role in the development of ischemia/reperfusion injury and can be considered as a potential target for finding methods to correct the disruption of neural networks in ischemic damage. In the present study, we demonstrated that blockade of RIPK1 kinase by Necrostatin-1 preserved the viability of cells in primary hippocampal cultures in an in vitro model of glucose deprivation. The effect of RIPK1 blockade on the bioelectrical and metabolic calcium activity of neuron-glial networks in vitro using calcium imaging and multi-electrode arrays was assessed for the first time. RIPK1 blockade was shown to partially preserve both calcium and bioelectric activity of neuron-glial networks under ischemic factors. However, it should be noted that RIPK1 blockade does not preserve the network parameters of the collective calcium dynamics of neuron-glial networks, despite the maintenance of network bioelectrical activity (the number of bursts and the number of spikes in the bursts). To confirm the data obtained in vitro, we studied the effect of RIPK1 blockade on the resistance of small laboratory animals to in vivo modeling of hypoxia and cerebral ischemia. The use of Necrostatin-1 increases the survival rate of C57BL mice in modeling both acute hypobaric hypoxia and ischemic brain damage.


Polymers ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 230
Author(s):  
Salwa Omar Bajunaid ◽  
Bashayer H. Baras ◽  
Michael D. Weir ◽  
Hockin H. K. Xu

Denture stomatitis is a multifactorial pathological condition of the oral mucosa that affects up to 72% of denture wearers. It is commonly seen on the palatal mucosa and characterized by erythema on the oral mucosa that are in contact with the denture surface. The aim of this study was to incorporate 2-methacryloyloxyethyl phosphorylcholine (MPC) and dimethylaminohexadecyl methacrylate (DMAHDM) into a high impact polymethylmethacrylate heat-cured denture base acrylic resin as a potential treatment for denture stomatitis. We used a comparative study design to examine the effect of incorporating MPC as a protein repellent agent and DMAHDM as an antifungal agent to prevent the adherence of Candida albicans to the denture base material. The dual incorporation of MPC and DMAHDM reduced C. albicans biofilm colony-forming unit by two orders of magnitude when compared to the control group devoid of the bioactive agents. Although the addition of MPC and DMAHDM alone or in combination significantly reduced the flexural strength of the material, they showed reduced roughness values when compared to control groups. This new denture acrylic resin provides the benefit of enhancing C. albicans biofilm elimination through dual mechanisms of action, which could potentially reduce the prevalence of denture stomatitis.


2022 ◽  
Vol 12 ◽  
Author(s):  
Ivan Fumagalli ◽  
Piermario Vitullo ◽  
Christian Vergara ◽  
Marco Fedele ◽  
Antonio F. Corno ◽  
...  

Hypertrophic Cardiomyopathy (HCM) is a pathological condition characterized by an abnormal thickening of the myocardium. When affecting the medio-basal portion of the septum, it is named Hypertrophic Obstructive Cardiomyopathy (HOCM) because it induces a flow obstruction in the left ventricular outflow tract. In any type of HCM, the myocardial function can become compromised, possibly resulting in cardiac death. In this study, we investigated with computational analysis the hemodynamics of patients with different types of HCM. The aim was quantifying the effects of this pathology on the intraventricular blood flow and pressure gradients, and providing information potentially useful to guide the indication and the modality of the surgical treatment (septal myectomy). We employed an image-based computational approach, integrating fluid dynamics simulations with geometric and functional data, reconstructed from standard cardiac cine-MRI acquisitions. We showed that with our approach we can better understand the patho-physiological behavior of intraventricular blood flow dynamics due to the abnormal morphological and functional aspect of the left ventricle. The main results of our investigation are: (a) a detailed patient-specific analysis of the blood velocity, pressure and stress distribution associated to HCM; (b) a computation-based classification of patients affected by HCM that can complement the current clinical guidelines for the diagnosis and treatment of HOCM.


2022 ◽  
Vol 19 (1) ◽  
Author(s):  
Alicia Bedolla ◽  
Aleksandr Taranov ◽  
Fucheng Luo ◽  
Jiapeng Wang ◽  
Flavia Turcato ◽  
...  

Abstract Background Two recently developed novel rodent models have been reported to ablate microglia, either by genetically targeting microglia (via Cx3cr1-creER: iDTR + Dtx) or through pharmacologically targeting the CSF1R receptor with its inhibitor (PLX5622). Both models have been widely used in recent years to define essential functions of microglia and have led to high impact studies that have moved the field forward. Methods Using either Cx3cr1-iDTR mice in combination with Dtx or via the PLX5622 diet to pharmacologically ablate microglia, we compared the two models via MRI and histology to study the general anatomy of the brain and the CSF/ventricular systems. Additionally, we analyzed the cytokine profile in both microglia ablation models. Results We discovered that the genetic ablation (Cx3cr1-iDTR + Dtx), but not the pharmacological microglia ablation (PLX5622), displays a surprisingly rapid pathological condition in the brain represented by loss of CSF/ventricles without brain parenchymal swelling. This phenotype was observed both in MRI and histological analysis. To our surprise, we discovered that the iDTR allele alone leads to the loss of CSF/ventricles phenotype following diphtheria toxin (Dtx) treatment independent of cre expression. To examine the underlying mechanism for the loss of CSF in the Cx3cr1-iDTR ablation and iDTR models, we additionally investigated the cytokine profile in the Cx3cr1-iDTR + Dtx, iDTR + Dtx and the PLX models. We found increases of multiple cytokines in the Cx3cr1-iDTR + Dtx but not in the pharmacological ablation model nor the iDTR + Dtx mouse brains at the time of CSF loss (3 days after the first Dtx injection). This result suggests that the upregulation of cytokines is not the cause of the loss of CSF, which is supported by our data indicating that brain parenchyma swelling, or edema are not observed in the Cx3cr1-iDTR + Dtx microglia ablation model. Additionally, pharmacological inhibition of the KC/CXCR2 pathway (the most upregulated cytokine in the Cx3cr1-iDTR + Dtx model) did not resolve the CSF/ventricular loss phenotype in the genetic microglia ablation model. Instead, both the Cx3cr1-iDTR + Dtx ablation and iDTR + Dtx models showed increased activated IBA1 + cells in the choroid plexus (CP), suggesting that CP-related pathology might be the contributing factor for the observed CSF/ventricular shrinkage phenotype. Conclusions Our data, for the first time, reveal a robust and global CSF/ventricular space shrinkage pathology in the Cx3cr1-iDTR genetic ablation model caused by iDTR allele, but not in the PLX5622 ablation model, and suggest that this pathology is not due to brain edema formation but to CP related pathology. Given the wide utilization of the iDTR allele and the Cx3cr1-iDTR model, it is crucial to fully characterize this pathology to understand the underlying causal mechanisms. Specifically, caution is needed when utilizing this model to interpret subtle neurologic functional changes that are thought to be mediated by microglia but could, instead, be due to CSF/ventricular loss in the genetic ablation model.


2021 ◽  
pp. 8-17
Author(s):  
A. F. Belyaev ◽  
T. S. Kharkovskaya ◽  
O. N. Fotina ◽  
A. A. Yurchenko

Introduction. The 2019 coronavirus infection (COVID-19) pandemic caused by a novel coronavirus strain (SARS-CoV-2) posed a serious threat to public health around the world. Postcoid syndrome (post-COVID-19 condition, according to ICD-10 code U09 State after COVID-19 or Postcoid state, Postcoid syndrome) is a pathological condition after a coronavirus infection, accompanied by cardio-respiratory, neurological, musculoskeletal, metabolic disorders. According to a number of studies, osteopathic methods of correction increase the lymph flow, immunological protection of the body, help to reduce pain, reduce the restriction of mobility in the chest, and therefore improve the function of external respiration. There are practically no studies that allow assessing the effect of osteopathic correction methods on the function of external respiration at the modern evidence-based level in patients who have undergone COVID pneumonia.The aim was to study the effect of a single procedure of osteopathic correction on the function of external respiration in patients during the rehabilitation period after coronavirus pneumonia.Materials and methods. On the basis of the Primorsky Institute of Vertebroneurology and Manual Medicine (Vladivostok) the rehabilitation of patients after coronavirus pneumonia was carried out using osteopathic correction. The study included 73 patients over the age of 60 years with varying degrees of lung damage and impaired respiratory function. To assess the function of external respiration, spirometry was performed and the vital capacity of the lungs was assessed; pulse oximetry was performed to measure the saturation of arterial blood hemoglobin with oxygen (SpO2). Osteopathic testing and treatment were carried out according to clinical guidelines, and the biomechanics of the chest was additionally investigated. The Statistica-10 software package was used for the statistical analysis of the obtained data.Results. Osteopathic examination revealed the presence of local somatic dysfunctions in 98,8 % of patients (spinal dysfunction, rib dysfunction, diaphragm dysfunction). 87,6 % of patients were diagnosed with regional somatic dysfunctions of thoracic region. Global somatic dysfunctions were diagnosed in 78,4 % of patients. After a single procedure of osteopathic correction, patients had a statistically significant improvement of the external respiration function, manifested in an increase in vital capacity from 78,27±2,79 to 85,36±3,38 % (p=0,0006). Also, the effectiveness of osteopathic correction is confirmed by a significant increase in the average hemoglobin saturation of arterial blood with oxygen. Thus, in patients with low SpO2 levels, the index increased from 94,21±0,21 to 95,09±0,3 % (p=0,02). After a single osteopathic correction procedure, the number of patients with local somatic dysfunctions decreased from 98,8 to 17,7 %; global somatic dysfunctions were revealed only in 16,3 % of patients. All patients noted an improvement in their general condition, a decrease in symptoms of respiratory discomfort and shortness of breath, and an increase in chest excursion.Conclusion. A single procedure of somatic dysfunctions' osteopathic correction in patients after coronavirus pneumonia leads to a statistically significant improvement in respiratory function. The vital capacity and the oxygen saturation of the blood increase in patients. This is caused by the increase of the mobility of the chest (increase in its excursion), diaphragm, ribs, spine. The obtained results allow recommend the inclusion of osteopathic correction in the rehabilitation programs for patients who have undergone coronavirus infection.


2021 ◽  
Vol 7 (12) ◽  
pp. 115094-115110
Author(s):  
Higor Zuchetto Rosa ◽  
Andressa Karine Nodari ◽  
Gabriela Suthovski ◽  
Eslen Giovana da Silva Cordeiro ◽  
Marcia Regina Hossa ◽  
...  

Eurytrematosis is a helminthic disease caused by trematodes belonging to the genus Eurytrema spp. that parasitize the pancreas of many animals and humans. This parasitosis causes chronic fibrosing pancreatitis, fat infiltration in the pancreatic parenchyma, besides damaging the exocrine pancreas, which is similar to that found in patients with Diabetes Mellitus type 1 (DM1). The current work aimed to evaluate the use of bovine pancreas infected with E. coelomaticum as a model to study DM1 pathophysiology. It was carried out macroscopic analyses, parasite identification, total pancreatic lipid determination and oxidative damage biomarkers levels of pancreas naturally infected with E. coelomaticum. Macroscopically, we observed that the infected pancreas had duct obstruction, organ stiffness due to the visible presence of fibrosis, increased adipose tissue deposition, increased protein and lipid damage, as well as increased antioxidant biomarkers (GSH, CAT and VIT C). Thus, it is possible to show that DM1 may have pancreatic parasitism as a possible primary origin. However, more studies are needed to better investigate this possible primary origin; the results obtained here suggest that the use of pancreas parasitized by E. coelomaticum could be a model to investigate DM1 pathophysiology.


2021 ◽  
Author(s):  
Janaranjani Murugesan ◽  
Ajithkumar Balakrishnan ◽  
Premkumar Kumpati ◽  
Hemamalini Vedagiri

Proteinuria is one of the hallmarks of preeclampsia (PE) that differentiates other hypertensive disorders of pregnancy. Protein misfolding and aggregation is an emerging pathological condition underlying many chronic metabolic diseases and neurodegenerative diseases. Recent studies indicate protein aggregation as an emerging biomarker of preeclampsia, wherein several proteins are aggregated and dysregulated in the body fluids of preeclamptic women, provoking the multi-systemic clinical manifestations of the disease. At the cellular level, these misfolded and aggregated proteins are potentially toxic interfering with the normal physiological process, eliciting the unfolded protein response (UPR) pathway activators in the endoplasmic reticulum (ER) that subsequently augments the ER quality control systems to remove these aberrant proteins. ER resident chaperones, folding enzymes and other proteins serve as part of the ER quality control machinery in restoring nascent protein folding. These ER chaperones are crucial for ER function aiding in native protein folding, maintaining calcium homeostasis, as sensors of ER stress and also as immune modulators. Consequently, ER chaperones seems to be involved in many cellular processes, yet the association is expanding to be explored. Understanding the role and mechanism of ER chaperones in regulating protein misfolding and aggregation would provide new avenues for therapeutic intervention as well as for the development of new diagnostic approaches.


2021 ◽  
Author(s):  
Sameeha V Pathan ◽  
Anant Pande ◽  
J.A Johnson ◽  
Sivakumar Kuppusamy

A relict dugong population resides in the Gulf of Kachchh in Gujarat state of India. Very little is known on this population stemming from a lack of focused studies and inadequate examinations of previous strandings. In this study, crucial ecological information is gathered through a systematic necropsy on stranded dugongs in the gulf. As indicated through dorsal tusk-rake scars on both the carcasses, this study presents the first records of derivative physical evidence to the presence of a socially interacting population. Progressive healing and differences in the width of the scars indicated more than two individuals had participated in a sexual agnostic or courtship event. Conversely, our findings report that both the animals suffered relative effects of asphyxiation after fishing net entanglement. An implication of a prior pathological condition(s) in the form of dermal cysts, swollen mesenteric lymph nodes, and endoparasites are also reported. Stomach content was examined for a qualitative dietary characterization. Other potential threats along with fishing net microfilaments found in the stomach contents of both dugongs are discussed in brief.


2021 ◽  
Vol 12 ◽  
Author(s):  
Chao Zhong ◽  
Kisuk Min ◽  
Zhiqiang Zhao ◽  
Cheng Zhang ◽  
Erhe Gao ◽  
...  

Cardiac fibrosis, a pathological condition due to excessive extracellular matrix (ECM) deposition in the myocardium, is associated with nearly all forms of heart disease. The processes and mechanisms that regulate cardiac fibrosis are not fully understood. In response to cardiac injury, macrophages undergo marked phenotypic and functional changes and act as crucial regulators of myocardial fibrotic remodeling. Here we show that the mitogen-activated protein kinase (MAPK) phosphatase-5 (MKP-5) in macrophages is involved in pressure overload-induced cardiac fibrosis. Cardiac pressure overload resulting from transverse aortic constriction (TAC) leads to the upregulation of Mkp-5 gene expression in the heart. In mice lacking MKP-5, p38 MAPK and JNK were hyperactivated in the heart, and TAC-induced cardiac hypertrophy and myocardial fibrosis were attenuated. MKP-5 deficiency upregulated the expression of the ECM-degrading matrix metalloproteinase-9 (Mmp-9) in the Ly6Clow (M2-type) cardiac macrophage subset. Consistent with in vivo findings, MKP-5 deficiency promoted MMP-9 expression and activity of pro-fibrotic macrophages in response to IL-4 stimulation. Furthermore, using pharmacological inhibitors against p38 MAPK, JNK, and ERK, we demonstrated that MKP-5 suppresses MMP-9 expression through a combined effect of p38 MAPK/JNK/ERK, which subsequently contributes to the inhibition of ECM-degrading activity. Taken together, our study indicates that pressure overload induces MKP-5 expression and facilitates cardiac hypertrophy and fibrosis. MKP-5 deficiency attenuates cardiac fibrosis through MAPK-mediated regulation of MMP-9 expression in Ly6Clow cardiac macrophages.


2021 ◽  
Vol 22 (24) ◽  
pp. 13640
Author(s):  
Fabio Vescini ◽  
Iacopo Chiodini ◽  
Alberto Falchetti ◽  
Andrea Palermo ◽  
Antonio Stefano Salcuni ◽  
...  

Male osteoporosis is a still largely underdiagnosed pathological condition. As a consequence, bone fragility in men remains undertreated mainly due to the low screening frequency and to controversies in the bone mineral density (BMD) testing standards. Up to the 40% of overall osteoporotic fractures affect men, in spite of the fact that women have a significant higher prevalence of osteoporosis. In addition, in males, hip fractures are associated with increased morbidity and mortality as compared to women. Importantly, male fractures occur about 10 years later in life than women, and, therefore, due to the advanced age, men may have more comorbidities and, consequently, their mortality is about twice the rate in women. Gender differences, which begin during puberty, lead to wider bones in males as compared with females. In men, follicle-stimulating hormones, testosterone, estrogens, and sex hormone-binding levels, together with genetic factors, interact in determining the peak of bone mass, BMD maintenance, and lifetime decrease. As compared with women, men are more frequently affected by secondary osteoporosis. Therefore, in all osteoporotic men, a complete clinical history should be collected and a careful physical examination should be done, in order to find clues of a possible underlying diseases and, ultimately, to guide laboratory testing. Currently, the pharmacological therapy of male osteoporosis includes aminobisphosphonates, denosumab, and teriparatide. Hypogonadal patients may be treated with testosterone replacement therapy. Given that the fractures related to mortality are higher in men than in women, treating male subjects with osteoporosis is of the utmost importance in clinical practice, as it may impact on mortality even more than in women.


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