Degenerative Process Research Articles

Inner Choroidal Fibrosis: An Optical Coherence Tomography Biomarker of Severity in Chronic Central Serous Chorioretinopathy

To describe a potential biomarker termed as inner choroidal fibrosis in cases of chronic central serous chorioretinopathy (CSCR) presenting to a tertiary referral center. Observational case series. Five eyes of 4 patients with CSCR were noted to have a gray-white subretinal lesion in the macula, which was analyzed with multimodal imaging. The lesions were hypofluorescent on autofluorescence, fundus fluorescein angiography, and indocyanine angiography. In all cases, a characteristic heterogeneous, hyperreflective lesion in the inner choroid was seen on optical coherence tomography (OCT), corresponding to the white subretinal lesions. The lesion was distinct from the adjacent choroid, with greater reflectivity and greater thickness than the adjacent compressed choroidal vasculature. The dilated outer pachyvessels were pushed outward or sideways in all cases. On OCT-angiography, the corresponding lesion showed flow void areas. We have termed this zone of inner choroidal hyperreflectivity "inner choroidal fibrosis." Upon analyzing the clinical course, 3 of the patients had a history of choroidal neovascularization. The contralateral eye in 2 of these 3 patients also developed choroidal neovascularization. Three of the eyes had an overlying focal choroidal excavation. We report a potential biomarker of CSCR termed "inner choroidal fibrosis" in 4 cases of chronic CSCR. It can best be identified on enhanced depth or swept source OCT as a region of heterogeneous hyperreflectivity in the inner choroid. This fibrosis could be regarded as a degenerative process secondary to more severe disease in the past.

Exploring the Impact of TLR-2 Signaling on miRNA Dysregulation in Intervertebral Disc Degeneration.

Toll-like receptors (TLRs) are key mediators of inflammation in intervertebral disc (IVD) degeneration. TLR-2 activation contributes to the degenerative process by increasing the expression of extracellular matrix-degrading enzymes, pro-inflammatory cytokines, and neurotrophins. As potent post-transcriptional regulators, microRNAs can modulate intracellular mechanisms, and their dysregulation is known to contribute to numerous pathologies. This study aims to investigate the impact of TLR-2 signaling on miRNA dysregulation in the context of IVD degeneration. Small-RNA sequencing of degenerated IVD cells shows the dysregulation of ten miRNAs following TLR-2 activation by PAM2CSK4. The miR-155-5p is most significantly upregulated in degenerated and non-degenerated annulus fibrosus and nucleus pulposus cells. Sequence-based target and pathway prediction shows the involvement of miR-155-5p in inflammation- and cell fate-related pathways and TLR-2-induced miR-155-5p expression leads to the downregulation of its target c-FOS. Furthermore, changes specific to the activation of TLR-2 through fragmented fibronectin are seen in miR-484 and miR-487. Lastly, miR-100-3p, miR-320b, and miR-181a-3p expression exhibit degeneration-dependent changes. These results show that TLR-2 signaling leads to the dysregulation of miRNAs in IVD cells as well as their possible downstream effects on inflammation and degeneration. The identified miRNAs provide important opportunities as potential therapeutic targets for IVD degeneration and low back pain.

AMP-activated protein kinase as a mediator of mitochondrial dysfunction of multiple sclerosis in animal models: A systematic review.

Multiple sclerosis (MS) is a chronic central nervous system (CNS) disorder characterized by demyelination, neuronal damage, and oligodendrocyte depletion. Reliable biomarkers are essential for early diagnosis and disease management. Emerging research highlights the role of mitochondrial dysfunction and oxidative stress in CNS disorders, including MS, in which mitochondria are central to the degenerative process. Adenosine monophosphate-activated protein kinase (AMPK) regulates the mitochondrial energy balance and initiates responses in neurodegenerative conditions. This systematic review, following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, aimed to comprehensively assess the literature on AMPK pathways, mitochondrial dysfunction, and in vivo studies using MS animal models. The search strategy involved the use of AMPK syntaxes, MS syntaxes, and animal model syntaxes. The PubMed, Scopus, Web of Science, and Google Scholar databases were systematically searched onAugust 26, 2023 without publication year restrictions. The review identified and analyzed relevant papers to provide a comprehensive overview of the current state of related research. Eight studies utilizing various interventions and methodological approaches were included. Risk of bias assessment revealed some areas of low risk but lacked explicit reporting in others. These studies collectively revealed a complex relationship between AMPK, mitochondrial dysfunction, and MS pathogenesis, with both cuprizone and experimental autoimmune encephalomyelitis models demonstrating associations between AMPK and mitochondrial disorders, including oxidative stress and impaired expression of mitochondrial genes. These studies illuminate the multifaceted role of AMPK in MS animal models, involving energy metabolism, inflammatory processes, oxidative stress, and gene regulation leading to mitochondrial dysfunction. However, unanswered questions about its mechanisms and clinical applications underscore the need for further research to fully harness its potential in addressing MS-related mitochondrial dysfunction.

The Effect of Slow Deep Breathing Exercises on Elderly Women With Hypertension

Background: The elderly or the elderly are the last stage of the human life cycle and experience degenerative processes in various aspects, especially in older women, which results in a higher risk of exposure to disease and ends in death, one of which is hypertension. Older women are closely related to the occurrence of hypertension when a woman experiences menopause. Treatment of hypertension can be done using non-pharmacological methods using slow deep breathing exercises. Purpose: To determine the effect of slow deep breathing exercises on older women with hypertension. Method: This study used the time series quasi-experimental method with one pre-test and post-test group. Results: The analysis of the Paired Sample T Test yielded p-values of 0.049 and 0.009 (p < 0.05), indicating that the alternative hypothesis (Ha) is supported. This implies that there is a significant impact of slow deep breathing exercises on blood pressure in older women when comparing the measurements before and after the intervention. Conclusion: Slow deep breathing exercises have an impact on the blood pressure of older women with hypertension.

Regulation of Oxygen Tension as a Strategy to Control Chondrocytic Phenotype for Cartilage Tissue Engineering and Regeneration.

Cartilage defects and osteoarthritis are health problems which are major burdens on health care systems globally, especially in aging populations. Cartilage is a vulnerable tissue, which generally faces a progressive degenerative process when injured. This makes it the 11th most common cause of global disability. Conservative methods are used to treat the initial phases of the illness, while orthopedic management is the method used for more progressed phases. These include, for instance, arthroscopic shaving, microfracturing and mosaicplasty, and joint replacement as the final treatment. Cell-based implantation methods have also been developed. Despite reports of successful treatments, they often suffer from the non-optimal nature of chondrocyte phenotype in the repair tissue. Thus, improved strategies to control the phenotype of the regenerating cells are needed. Avascular tissue cartilage relies on diffusion for nutrients acquisition and the removal of metabolic waste products. A low oxygen content is also present in cartilage, and the chondrocytes are, in fact, well adapted to it. Therefore, this raises an idea that the regulation of oxygen tension could be a strategy to control the chondrocyte phenotype expression, important in cartilage tissue for regenerative purposes. This narrative review discusses the aspects related to oxygen tension in the metabolism and regulation of articular and growth plate chondrocytes and progenitor cell phenotypes, and the role of some microenvironmental factors as regulators of chondrocytes.

Synovia tissue-specific exosomes participate in the dual variation of the osteoarthritis microenvironment via miR-182

Osteoarthritis (OA) is the most common type of joint disease and the leading cause of chronic disability among older adults. As an important component of the joint, synovium influences the inflammatory and degenerative process of OA. This study found that miRNA 182 (miR-182) in synovium-specific exosomes can modulate inflammation and apoptotic signaling. It also regulated different biological functions to promote the progression of OA. Experiments based on rat OA model and synovium samples from OA patients, we found that synovium-derived miR-182 regulates inflammatory response in the early stage of OA by regulating the expression level of forkhead box O-3 (FOXO3). However, the expression of miR-182 was significantly increased in synovial tissue of advanced OA, which was involved in the apoptotic signal of severe OA. These findings suggest that miR-182 may directly regulate OA progression by modulating FOXO3 production inflammation, and apoptosis.

Association Between Anterior Hip Capsule Thickening and Sagittal Pelvic Alignment Among Patients With Developmental Dysplasia of the Hip.

The pathogenesis and pathology of secondary osteoarthritis (OA) of the hip, which is mainly due to developmental dysplasia of the hip (DDH), in Japan are obscure. There are some reports on the thickening of the hip capsule, but the relationship between the thickness of the hip capsule and the pelvic alignment due to hip deformity is not well known. This research investigated whether the capsular thickness of female DDH patients was related to pelvic alignment. This single-center cross-sectional study included female patients aged 50-79 years (n=13) who had undergone primary total hip arthroplasty (THA) due to secondary hip OA with a background of DDH. The part of the hip capsule including the iliofemoral ligament was resected and measured directly with a digital caliper. The Sharp angle, center-edge (CE) angle, sacral slope (SS), pelvic tilt (PT), pelvic incidence (PI), and lumbar lordosis angle (LLA) were measured with an X-ray image to investigate the relationship between the capsular thickness and the pelvic posture. Pearson's correlation coefficient showed a negative correlation between hip capsular thickness and Sharp angle (r=-0.57, p>0.05). No significant correlation was found between the thickness of the hip capsule and the sagittal X-ray parameters including SS, PT, PI, LLA, and CE angle in the coronal plane. The thickness of the hip capsule is moderately associated with the Sharp angle on the coronal plane. The results of this study suggest that the thickness of the joint capsule does not necessarily relate to the degenerative process among patients with DDH and the process can be complex to apply two-dimensional postural indices for the explanation.

Materials and methods used in microencapsulation of probiotic microorganisms

Objective: Probiotic microorganisms which constitute an important part of functional foods are living creatures that have been proven to benefit human health. However, most of the time they lose their vitality entirely or partly before reaching the human gastrointestinal system due to the various degenerative processes that they are exposed to during food production stages. Those who have been able to maintain their vitality are exposed to destructive bioprocesses in the digestive system. Conclusion: It is possible to provide the probiotic microorganisms to reach the target point by maintaining their vitality at an optimum level utilizing the microencapsulation method which we could consider as a technological packaging process. In this study, information is given about microencapsulation methods applied to probiotic microorganisms and the coating materials used.

The contribution of preclinical magnetic resonance imaging and spectroscopy to Huntington's disease.

Huntington's disease is an inherited disorder characterized by psychiatric, cognitive, and motor symptoms due to degeneration of medium spiny neurons in the striatum. A prodromal phase precedes the onset, lasting decades. Current biomarkers include clinical score and striatal atrophy using Magnetic Resonance Imaging (MRI). These markers lack sensitivity for subtle cellular changes during the prodromal phase. MRI and MR spectroscopy offer different contrasts for assessing metabolic, microstructural, functional, or vascular alterations in the disease. They have been used in patients and mouse models. Mouse models can be of great interest to study a specific mechanism of the degenerative process, allow better understanding of the pathogenesis from the prodromal to the symptomatic phase, and to evaluate therapeutic efficacy. Mouse models can be divided into three different constructions: transgenic mice expressing exon-1 of human huntingtin (HTT), mice with an artificial chromosome expressing full-length human HTT, and knock-in mouse models with CAG expansion inserted in the murine htt gene. Several studies have used MRI/S to characterized these models. However, the multiplicity of modalities and mouse models available complicates the understanding of this rich corpus. The present review aims at giving an overview of results obtained using MRI/S for each mouse model of HD, to provide a useful resource for the conception of neuroimaging studies using mouse models of HD. Finally, despite difficulties in translating preclinical protocols to clinical applications, many biomarkers identified in preclinical models have already been evaluated in patients. This review also aims to cover this aspect to demonstrate the importance of MRI/S for studying HD.

Renal aging and mitochondrial quality control.

Mitochondria are dynamic organelles that participate in different cellular process that control metabolism, cell division, and survival, and the kidney is one of the most metabolically active organs that contains abundant mitochondria. Perturbations in mitochondrial homeostasis in the kidney can accelerate kidney aging, and maintaining mitochondrial homeostasis can effectively delay aging in the kidney. Kidney aging is a degenerative process linked to detrimental processes. The significance of aberrant mitochondrial homeostasis in renal aging has received increasing attention. However, the contribution of mitochondrial quality control (MQC) to renal aging has not been reviewed in detail. Here, we generalize the current factors contributing to renal aging, review the alterations in MQC during renal injury and aging, and analyze the relationship between mitochondria and intrinsic renal cells. We also introduce MQC in the context of renal aging, and discuss the study of mitochondria in the intrinsic cells of the kidney, which is the innovation of our paper. In addition, during kidney injury and repair, the specific functions and regulatory mechanisms of MQC systems in resident and circulating cell types remain unclear. Currently, most of the studies we reviewed are based on animal and cellular models, the relationship between renal tissue aging and mitochondria has not been adequately investigated in clinical studies, and there is still a long way to go.

Ozone Exposure Controls Oxidative Stress and the Inflammatory Process of Hepatocytes in Murine Models.

(1) Background: Ozone exposure is a promising tool for treating liver damage since it is known to control the release of free radicals and increase the expression of antioxidant enzymes. The objective is to investigate the main intracellular pathways activated after exposure to ozone, considering the dosage of antioxidant enzymes and markers of oxidative stress. (2) Methods: This systematic review was performed based on the PRISMA guidelines and using a structured search in MEDLINE (PubMed), Scopus, and Web of Science. Bias analysis and methodological quality assessments were examined using the SYRCLE Risk of Bias tool. (3) Results: Nineteen studies were selected. The results showed that the exposure to ozone has a protective effect on liver tissue, promoting a decrease in inflammatory markers and a reduction in oxidative stress in liver tissue. In addition, ozone exposure also promoted an increase in antioxidant enzymes. The morphological consequences of controlling these intracellular pathways were reducing the tissue inflammatory process and reducing areas of degeneration and necrosis. (4) Conclusions: Ozone exposure has a beneficial effect on models of liver injury through the decrease in oxidative stress in tissue and inflammatory markers. In addition, it regulates the Nrf2/ARE antioxidant pathway and blocks the NF-κB inflammatory pathway.

Degeneration of the intervertebral disc as an interdisciplinary clinical problem in the context of neurosurgery - a summary of the state of knowledge - part I

Background: Degeneration of the intervertebral disc (IVD), resulting from various factors including both genetic and environmental, is a significant musculoskeletal disorder. It is characterized by a gradual deterioration of the structure and weakening the function of IVD, leading to a decline in the quality of life (QOL) or disability.Aim of the study: The aim of the study was to perform the review of scientific reports and summary of current knowledge regarding IVD degeneration in terms of etiopathogenesis, clinical symptoms, and various diagnostic methods.Materials and Methods: The literature review was based on searching key medical databases such as PubMed, MEDLINE, Scopus. A search strategy was defined, encompassing keywords, synonyms, and controlled keywords (MeSH terms). The search covered the last 20 years and focused on aspects of etiopathogenesis, clinical symptoms, and diagnostic methods. Papers meeting the inclusion criteria underwent a full-text analysis. Data and information gathered from the literature analysis were synthesized to provide a comprehensive overview of the current state of knowledge on the researched subject. Results: The process of IVD degeneration is extremely complex, involving biochemical, metabolic, and morphological changes that impact its structure and function. It entails a gradual loss of water in the nucleus pulposus (dehydration), resulting in impaired shock-absorbing function and leading to the formation of breaks in the annulus fibrosus, where the nucleus pulposus herniates. For years, mechanical injuries, especially work-related, were considered the primary factors causing IVD degeneration. Recent findings emphasize the significant role of genetic factors, with several genes encoding structural proteins of the IVD identified. Mutations in these genes may accelerate degeneration. Current clinical research results indicate a correlation between aortic calcifications and episodes of low back pain (LBP) and between lumbar artery stenosis, IVD degeneration, and subsequent LBP.Conclusions: Understanding the complexity of IVD degeneration and their neurological consequences is a crucial in planning effective treatment. It is essential to monitor the results of the latest research for the systematic updating of knowledge and practical guidelines in the discussed area. Collaboration between an experienced neurosurgeon and an interdisciplinary team of medical specialists can lead to achieving the best therapeutic outcomes.

Patellar tendon complaints and shear wave velocity patterns in maturing alpine skiers

Introduction
 Patellar tendinopathy is frequent in adolescent athletes and particularly accentuated in competitive alpine skiers (Fröhlich et al., 2020). Tendinopathies are characterized by long disease histories, and whether they can be healed completely is an open question (Kettunen et al., 2002). Three-dimensional (3D) shear wave elastography (SWE) has proven valuable in the early detection of tendinopathies (Götschi et al., 2023). The aims of this study were to (1) describe the longitudinal progression of patellar tendon complaint prevalence in competitive alpine skiers during adolescence, (2) compare the SWV patterns of skiers that were symptomatic four years ago with those with no history of patellar tendon complaints and (3) analyse whether shear wave velocity (SWV) average values correlate with SWV coefficient of variation (CV).
 Methods
 Forty-seven subjects were analysed in this 4-year follow-up study regarding their patellar tendon complaints and SWV patterns. Symptomatic and asymptomatic skiers were identified by clinical examinations including the criteria of pain sensation under loading and palpation-induced pain. SWV was determined by ultrasound-based 3D SWE. Prevalence differences were assessed using Pearson’s χ2 tests. Group differences in the SWV patterns were analysed using unpaired sample t tests. Correlations between SWV average and CV values were analysed by means of Pearson’s correlation coefficient.
 Results
 With proceeding adolescence, the prevalence of patellar tendon complaints significantly decreased from 29.8% at baseline assessment (13-16 years) to 12.7% at follow-up assessment (Pearson’s χ2 = 9.429; p = 0.002). Those skiers who were symptomatic at baseline but asymptomatic at the follow-up still had lower average SWV values and higher CVs than asymptomatic skiers with no history of patellar tendon complaints (p = 0.054 and p = 0.011, respectively). Furthermore, there was a significant negative correlation between the tendon SWV average values and their CVs (R = -0.55; p < 0.001).
 Discussion/Conclusion
 Despite the decreasing prevalence of patellar tendon complaints in youth competitive alpine skiers after their growth spurt, structural abnormalities appear to remain in asymptomatic subjects with a previous history of patellar tendinopathy, indicating potential long-term implications for mechanical tendon proprieties. The SWV average and CV values were negatively correlated, which underlines our hypothesis that a low SWV is associated with a high CV. This altogether may reflect the degenerative processes in patellar tendons affected by complaints in the early stages of a sports career.
 References
 Fröhlich, S., Peterhans, L., Stern, C., Frey, W. O., Sutter, R., & Spörri, J. (2020). Remarkably high prevalence of overuse-related knee complaints and MRI abnormalities in youth competitive alpine skiers: A descriptive investigation in 108 athletes aged 13-15 years. BMJ Open Sport & Exercice Medicine, 6(1), Aticle e000738. https://doi.org/10.1136/bmjsem-2020-000738
 Götschi, T., Franchi, M. V., Schulz, N., Fröhlich, S., Frey, W. O., Snedeker, J. G., & Spörri, J. (2023). Altered regional 3D shear wave velocity patterns in youth competitive alpine skiers suffering from patellar tendon complaints – A prospective case–control study. European Journal of Sport Science, 23(6), 1068-1076. https://doi.org/10.1080/17461391.2022.2088404
 Kettunen, J. A., Kvist, M., Alanen, E., & Kujala, U. M. (2002). Long-term prognosis for jumper’s knee in male athletes. A prospective follow-up study. The American Journal of Sports Medicine, 30(5), 689-692. https://doi.org/10.1177/03635465020300051001

The excitation of high-order localized waves in (3+1)-dimensional Kudryashov-Sinelshchikov equation

The aim of this work is to explore the excitation of high-order localized waves in the (3+1)-dimensional Kudryashov-Sinelshchikov equation, which is used to describe the dynamic of liquid with gas bubble. First of all, classical N-soliton solutions are constructed by means of Hirota bilinear form and symbolic calculation. What’s more, the high-order breather waves are derived through the degeneration process of the N-soliton solutions with conjugate parameter. Then, high-order lump waves are constructed by taking long wave limit technique on N-soliton solutions. Finally, the high-order mixed localized waves involving resonant Y-type solitons, high-order breather waves and high-order lump waves are obtained by utilizing some comprehensive methods. Abundant dynamical and evolutionary behaviors of these results are investigated specifically, some figures are presented to shed light on the nonlinear phenomena hidden in the high-order localized waves vividly.

Beneficial Impact of Eicosapentaenoic Acid on the Adverse Effects Induced by Palmitate and Hyperglycemia on Healthy Rat Chondrocyte.

Osteoarthritis (OA) is the most prevalent form of arthritis and a major cause of pain and disability. The pathology of OA involves the whole joint in an inflammatory and degenerative process, especially in articular cartilage. OA may be divided into distinguishable phenotypes including one associated with the metabolic syndrome (MetS) of which dyslipidemia and hyperglycemia have been individually linked to OA. Since their combined role in OA pathogenesis remains to be elucidated, we investigated the chondrocyte response to these metabolic stresses, and determined whether a n-3 polyunsaturated fatty acid (PUFA), i.e., eicosapentaenoic acid (EPA), may preserve chondrocyte functions. Rat chondrocytes were cultured with palmitic acid (PA) and/or EPA in normal or high glucose conditions. The expression of genes encoding proteins found in cartilage matrix (type 2 collagen and aggrecan) or involved in degenerative (metalloproteinases, MMPs) or in inflammatory (cyclooxygenase-2, COX-2 and microsomal prostaglandin E synthase, mPGES) processes was analyzed by qPCR. Prostaglandin E2 (PGE2) release was also evaluated by an enzyme-linked immunosorbent assay. Our data indicated that PA dose-dependently up-regulated the mRNA expression of MMP-3 and -13. PA also induced the expression of COX-2 and mPGES and promoted the synthesis of PGE2. Glucose at high concentrations further increased the chondrocyte response to PA. Interestingly, EPA suppressed the inflammatory effects of PA and glucose, and strongly reduced MMP-13 expression. Among the free fatty acid receptors (FFARs), FFAR4 partly mediated the EPA effects and the activation of FFAR1 markedly reduced the inflammatory effects of PA in high glucose conditions. Our findings demonstrate that dyslipidemia associated with hyperglycemia may contribute to OA pathogenesis and explains why an excess of saturated fatty acids and a low level in n-3 PUFAs may disrupt cartilage homeostasis.

Aortic Valve Embryology, Mechanobiology, and Second Messenger Pathways: Implications for Clinical Practice.

During the Renaissance, Leonardo Da Vinci was the first person to successfully detail the anatomy of the aortic root and its adjacent structures. Ever since, novel insights into morphology, function, and their interplay have accumulated, resulting in advanced knowledge on the complex functional characteristics of the aortic valve (AV) and root. This has shifted our vision from the AV as being a static structure towards that of a dynamic interconnected apparatus within the aortic root as a functional unit, exhibiting a complex interplay with adjacent structures via both humoral and mechanical stimuli. This paradigm shift has stimulated surgical treatment strategies of valvular disease that seek to recapitulate healthy AV function, whereby AV disease can no longer be seen as an isolated morphological pathology which needs to be replaced. As prostheses still cannot reproduce the complexity of human nature, treatment of diseased AVs, whether stenotic or insufficient, has tremendously evolved, with a similar shift towards treatments options that are more hemodynamically centered, such as the Ross procedure and valve-conserving surgery. Native AV and root components allow for an efficient Venturi effect over the valve to allow for optimal opening during the cardiac cycle, while also alleviating the left ventricle. Next to that, several receptors are present on native AV leaflets, enabling messenger pathways based on their interaction with blood and other shear-stress-related stimuli. Many of these physiological and hemodynamical processes are under-acknowledged but may hold important clues for innovative treatment strategies, or as potential novel targets for therapeutic agents that halt or reverse the process of valve degeneration. A structured overview of these pathways and their implications for cardiothoracic surgeons and cardiologists is lacking. As such, we provide an overview on embryology, hemodynamics, and messenger pathways of the healthy and diseased AV and its implications for clinical practice, by relating this knowledge to current treatment alternatives and clinical decision making.

Asymptotic behaviour for a parabolic p-Laplacian equation with an advection force

The rescaling method is presented to allow us establishing the interface functions and the nonnegative local solutions to the evolution of nonlinear degenerate parabolic p-Laplacian process with conservation laws that are posed in one-dimensional space. This equation has a self-similar solution which represents the main feature of this work. The Cauchy problem (CP) for this equation with specific restrictions in the range of parameters and the negative advection coefficient is considered. In this work, there are several regions to discuss the qualitative analysis for the local weak solutions and the asymptotic interfaces in the irregular domains. The dominating of the advection force over the p-Laplacian type diffusion will appear clearly in these regions. Moreover, the solutions of the CP for the degenerate parabolic p-Laplacian advection equations are asymptotically equal to the solutions of advection equations under some restrictions.

Penggunaan Gigi Tiruan pada Lansia dengan Obstructive Sleep Apnea

A person who has reached the elderly stage will have an experienced degenerative process that causes several disorders. Changes in the masticatory function due to the loss of the remaining teeth can cause a transformation not only in the mastication system but also in the upper airway system of respiration. This is due to orofacial deformation, tongue retraction while in the resting position, occlusal vertical dimension changes, and a decrease in facial height. Obstructive Sleep Apnea (OSA) is a sleep breathing disorder with 17 % prevalence rate in adults and increases up to 49% in the elderly stage. A complete denture can be a rehabilitative treatment option for the elderly OSA patient. Wearing dentures during sleep is against the principles of dentistry because it can cause the tongue to be positioned posteriorly. However, people, mostly women, still wears denture while sleeping. This might further increase the obstruction of upper airway system.

Management of recurrent lumbar disc herniation: a comparative analysis of posterior lumbar interbody fusion and repeat discectomy

Background: For recurrent lumbar disc herniation, many experts suggest a repeat discectomy without stabilization due to its minimal tissue manipulation, lower blood loss, shorter hospital stay, and lower cost, recent research on the role of instability in disc herniation has made fusion techniques popular among spinal surgeons. The authors compare the postoperative outcomes of posterior lumbar interbody fusion (PLIF) and repeat discectomy for same-level recurrent disc herniation. Methods: The patients included had previously undergone discectomy and presented with a same-level recurrent lumbar disc herniation. The patients were placed into two groups: 1) discectomy only, 2) PLIF based on the absence or presence of segmental instability. Preoperative and postoperative Oswestry disability index scores, duration of surgery, blood loss, duration of hospitalization, and complications were analyzed. Results: The repeat discectomy and fusion groups had 40 and 34 patients, respectively. The patients were followed up for 2.68 (1–4) years. There was no difference in the duration of hospitalization (3.73 vs. 3.29 days P=0.581) and operative time (101.25 vs. 108.82 mins, P=0.48). Repeat discectomy had lower intraoperative blood loss, 88.75 ml (50–150) versus 111.47 ml (30–250) in PLIF (P=0.289). PLIF had better ODI pain score 4.21 (0–10) versus 9.27 (0–20) (P-value of 0.018). Recurrence was 22.5% in repeat discectomy versus 0 in PLIF. Conclusion: PLIF and repeat discectomy for recurrent lumbar disc herniation have comparable intraoperative blood loss, duration of surgery, and hospital stay. PLIF is associated with lower durotomy rates and better long-term pain control than discectomy. This is due to recurrence and progression of degenerative process in discectomy patients, which are eliminated and slowed, respectively, by PLIF.

T-type voltage-gated channels, Na+/Ca2+-exchanger, and calpain-2 promote photoreceptor cell death in inherited retinal degeneration

Inherited retinal degenerations (IRDs) are a group of untreatable and commonly blinding diseases characterized by progressive photoreceptor loss. IRD pathology has been linked to an excessive activation of cyclic nucleotide-gated channels (CNGC) leading to Na+- and Ca2+-influx, subsequent activation of voltage-gated Ca2+-channels (VGCC), and further Ca2+ influx. However, a connection between excessive Ca2+ influx and photoreceptor loss has yet to be proven.Here, we used whole-retina and single-cell RNA-sequencing to compare gene expression between the rd1 mouse model for IRD and wild-type (wt) mice. Differentially expressed genes indicated links to several Ca2+-signalling related pathways. To explore these, rd1 and wt organotypic retinal explant cultures were treated with the intracellular Ca2+-chelator BAPTA-AM or inhibitors of different Ca2+-permeable channels, including CNGC, L-type VGCC, T-type VGCC, Ca2+-release-activated channel (CRAC), and Na+/Ca2+ exchanger (NCX). Moreover, we employed the novel compound NA-184 to selectively inhibit the Ca2+-dependent protease calpain-2. Effects on the retinal activity of poly(ADP-ribose) polymerase (PARP), sirtuin-type histone-deacetylase, calpains, as well as on activation of calpain-1, and − 2 were monitored, cell death was assessed via the TUNEL assay.While rd1 photoreceptor cell death was reduced by BAPTA-AM, Ca2+-channel blockers had divergent effects: While inhibition of T-type VGCC and NCX promoted survival, blocking CNGCs and CRACs did not. The treatment-related activity patterns of calpains and PARPs corresponded to the extent of cell death. Remarkably, sirtuin activity and calpain-1 activation were linked to photoreceptor protection, while calpain-2 activity was related to degeneration. In support of this finding, the calpain-2 inhibitor NA-184 protected rd1 photoreceptors.These results suggest that Ca2+ overload in rd1 photoreceptors may be triggered by T-type VGCCs and NCX. High Ca2+-levels likely suppress protective activity of calpain-1 and promote retinal degeneration via activation of calpain-2. Overall, our study details the complexity of Ca2+-signalling in photoreceptors and emphasizes the importance of targeting degenerative processes specifically to achieve a therapeutic benefit for IRDs.9rDzNFNpqNfiW7CgYpAk_tVideo