#Vascular Endothelial Growth Factor A

[myrawjcsmicasereports]

 Inhibition of EIF4E Downregulates VEGFA and CCND1 Expression to Suppress Ovarian Cancer Tumor Progression by Jing Wang in Journal of Clinical Case Reports Medical Images and Health Sciences

Abstract

This study investigates the role of EIF4E in ovarian cancer and its influence on the expression of VEGFA and CCND1. Differential expression analysis of VEGFA, CCND1, and EIF4E was conducted using SKOV3 cells in ovarian cancer patients and controls. Correlations between EIF4E and VEGFA/CCND1 were assessed, and three-dimensional cell culture experiments were performed. Comparisons of EIF4E, VEGFA, and CCND1 mRNA and protein expression between the EIF4E inhibitor 4EGI-1-treated group and controls were carried out through RT-PCR and Western blot. Our findings demonstrate elevated expression of EIF4E, VEGFA, and CCND1 in ovarian cancer patients, with positive correlations. The inhibition of EIF4E by 4EGI-1 led to decreased SKOV3 cell clustering and reduced mRNA and protein levels of VEGFA and CCND1. These results suggest that EIF4E plays a crucial role in ovarian cancer and its inhibition may modulate VEGFA and CCND1 expression, underscoring EIF4E as a potential therapeutic target for ovarian cancer treatment.

Keywords: Ovarian cancer; Eukaryotic translation initiation factor 4E; Vascular endothelial growth factor A; Cyclin D1

Introduction

Ovarian cancer ranks high among gynecological malignancies in terms of mortality, necessitating innovative therapeutic strategies [1]. Vascular endothelial growth factor (VEGF) plays a pivotal role in angiogenesis, influencing endothelial cell proliferation, migration, vascular permeability, and apoptosis regulation [2, 3]. While anti-VEGF therapies are prominent in malignancy treatment [4], the significance of cyclin D1 (CCND1) amplification in cancers, including ovarian, cannot be overlooked, as it disrupts the cell cycle, fostering tumorigenesis [5, 6]. Eukaryotic translation initiation factor 4E (EIF4E), central to translation initiation, correlates with poor prognoses in various cancers due to its dysregulated expression and activation, particularly in driving translation of growth-promoting genes like VEGF [7, 8]. Remarkably, elevated EIF4E protein levels have been observed in ovarian cancer tissue, suggesting a potential role in enhancing CCND1 translation, thereby facilitating cell cycle progression and proliferation [9]. Hence, a novel conjecture emerges: by modulating EIF4E expression, a dual impact on VEGF and CCND1 expression might be achieved. This approach introduces an innovative perspective to impede the onset and progression of ovarian cancer, distinct from existing literature, and potentially offering a unique therapeutic avenue.

Materials and Methods

Cell Culture

Human ovarian serous carcinoma cell line SKOV3 (obtained from the Cell Resource Center, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences) was cultured in DMEM medium containing 10% fetal bovine serum. Cells were maintained at 37°C with 5% CO2 in a cell culture incubator and subcultured every 2-3 days.

Three-Dimensional Spheroid Culture

SKOV3 cells were prepared as single-cell suspensions and adjusted to a concentration of 5×10^5 cells/mL. A volume of 0.5 mL of single-cell suspension was added to Corning Ultra-Low Attachment 24-well microplates and cultured at 37°C with 5% CO2 for 24 hours. Subsequently, 0.5 mL of culture medium or 0.5 mL of EIF4E inhibitor 4EGI-1 (Selleck, 40 μM) was added. After 48 hours, images were captured randomly from five different fields—upper, lower, left, right, and center—using an inverted phase-contrast microscope. The experiment was repeated three times.

GEPIA Online Analysis

The GEPIA online analysis tool (http://gepia.cancer-pku.cn/index.html) was utilized to assess the expression of VEGFA, CCND1, and EIF4E in ovarian cancer tumor samples from TCGA and normal samples from GTEx. Additionally, Pearson correlation coefficient analysis was employed to determine the correlation between VEGF and CCND1 with EIF4E.

RT-PCR

RT-PCR was employed to assess the mRNA expression levels of EIF4E, VEGF, and CCND1 in treatment and control group samples. Total RNA was extracted using the RNA extraction kit from Vazyme, followed by reverse transcription to obtain cDNA using their reverse transcription kit. Amplification was carried out using SYBR qPCR Master Mix as per the recommended conditions from Vazyme. GAPDH was used as an internal reference, and the primer sequences for PCR are shown in Table 1.

Amplification was carried out under the following conditions: an initial denaturation step at 95°C for 60 seconds, followed by cycling conditions of denaturation at 95°C for 10 seconds, annealing at 60°C for 30 seconds, repeated for a total of 40 cycles. Melting curves were determined under the corresponding conditions. Each sample was subjected to triplicate experiments. The reference gene GAPDH was used for normalization. The relative expression levels of the target genes were calculated using the 2-ΔΔCt method.

Western Blot

Western Blot technique was employed to assess the protein expression levels of EIF4E, VEGF, and CCND1 in the treatment and control groups. Initially, cell samples collected using RIPA lysis buffer were lysed, and the total protein concentration was determined using the BCA assay kit (Shanghai Biyuntian Biotechnology, Product No.: P0012S). Based on the detected concentration, 20 μg of total protein was loaded per well. Electrophoresis was carried out using 5% stacking gel and 10% separating gel. Subsequently, the following primary antibodies were used for immune reactions: rabbit anti-human polyclonal antibody against phospho-EIF4E (Beijing Boao Sen Biotechnology, Product No.: bs-2446R, dilution 1:1000), mouse anti-human monoclonal antibody against EIF4E (Wuhan Sanying Biotechnology, Product No.: 66655-1-Ig, dilution 1:5000), mouse anti-human monoclonal antibody against VEGFA (Wuhan Sanying Biotechnology, Product No.: 66828-1-Ig, dilution 1:1000), mouse anti-human monoclonal antibody against CCND1 (Wuhan Sanying Biotechnology, Product No.: 60186-1-Ig, dilution 1:5000), and mouse anti-human monoclonal antibody against GAPDH (Shanghai Biyuntian Biotechnology, Product No.: AF0006, dilution 1:1000). Subsequently, secondary antibodies conjugated with horseradish peroxidase (Shanghai Biyuntian Biotechnology, Product No.: A0216, dilution 1:1000) were used for immune reactions. Finally, super-sensitive ECL chemiluminescence reagent (Shanghai Biyuntian Biotechnology, Product No.: P0018S) was employed for visualization, and the ChemiDocTM Imaging System (Bio-Rad Laboratories, USA) was used for image analysis.

Statistical Analysis

GraphPad software was used for statistical analysis. Data were presented as (x ± s) and analyzed using the t-test for quantitative data. Pearson correlation analysis was performed for assessing correlations. A significance level of P < 0.05 was considered statistically significant.

Results

3D Cell Culture of SKOV3 Cells and Inhibitory Effect of 4EGI-1 on Aggregation

In this experiment, SKOV3 cells were subjected to 3D cell culture, and the impact of the EIF4E inhibitor 4EGI-1 on ovarian cancer cell aggregation was investigated. As depicted in Figure 1, compared to the control group (Figure 1A), the diameter of the SKOV3 cell spheres significantly decreased in the treatment group (Figure 1B) when exposed to 4EGI-1 under identical culture conditions. This observation indicates that inhibiting EIF4E expression effectively suppresses tumor aggregation.

Expression and Correlation Analysis of VEGFA, CCND1, and EIF4E in Ovarian Cancer Samples

To investigate the expression of VEGFA, CCND1, and EIF4E in ovarian cancer, we utilized the GEPIA online analysis tool and employed the Pearson correlation analysis method to compare expression differences between tumor and normal groups. As depicted in Figures 2A-C, the results indicate significantly elevated expression levels of VEGFA, CCND1, and EIF4E in the tumor group compared to the normal control group. Notably, the expression differences of VEGFA and CCND1 were statistically significant (p < 0.05). Furthermore, the correlation analysis revealed a positive correlation between VEGFA and CCND1 with EIF4E (Figures 2D-E), and this correlation exhibited significant statistical differences (p < 0.001). These findings suggest a potential pivotal role of VEGFA, CCND1, and EIF4E in the initiation and progression of ovarian cancer, indicating the presence of intricate interrelationships among them.

EIF4E, VEGFA, and CCND1 mRNA Expression in SKOV3 Cells

To investigate the function of EIF4E in SKOV3 cells, we conducted RT-PCR experiments comparing EIF4E inhibition group with the control group. As illustrated in Figure 3, treatment with 4EGI-1 significantly reduced EIF4E expression (0.58±0.09 vs. control, p < 0.01). Concurrently, mRNA expression of VEGFA (0.76±0.15 vs. control, p < 0.05) and CCND1 (0.81±0.11 vs. control, p < 0.05) also displayed a substantial decrease. These findings underscore the significant impact of EIF4E inhibition on the expression of VEGFA and CCND1, indicating statistically significant differences.

Protein Expression Profiles in SKOV3 Cells with EIF4E Inhibition and Control Group

Protein expression of EIF4E, VEGFA, and CCND1 was assessed using Western Blot in the 4EGI-1 treatment group and the control group. As presented in Figure 4, the expression of p-EIF4E was significantly lower in the 4EGI-1 treatment group compared to the control group (0.33±0.14 vs. control, p < 0.001). Simultaneously, the expression of VEGFA (0.53±0.18 vs. control, p < 0.01) and CCND1 (0.44±0.16 vs. control, p < 0.001) in the 4EGI-1 treatment group exhibited a marked reduction compared to the control group.

Discussion

EIF4E is a post-transcriptional modification factor that plays a pivotal role in protein synthesis. Recent studies have underscored its critical involvement in various cancers [10]. In the context of ovarian cancer research, elevated EIF4E expression has been observed in late-stage ovarian cancer tissues, with low EIF4E expression correlating to higher survival rates [9]. Suppression of EIF4E expression or function has been shown to inhibit ovarian cancer cell proliferation, invasion, and promote apoptosis. Various compounds and drugs that inhibit EIF4E have been identified, rendering them potential candidates for ovarian cancer treatment [11]. Based on the progressing understanding of EIF4E's role in ovarian cancer, inhibiting EIF4E has emerged as a novel therapeutic avenue for the disease. 4EGI-1, a cap-dependent translation small molecule inhibitor, has been suggested to disrupt the formation of the eIF4E complex [12]. In this study, our analysis of public databases revealed elevated EIF4E expression in ovarian cancer patients compared to normal controls. Furthermore, through treatment with 4EGI-1 in the SKOV3 ovarian cancer cell line, we observed a capacity for 4EGI-1 to inhibit SKOV3 cell spheroid formation. Concurrently, results from PCR and Western Blot analyses demonstrated effective EIF4E inhibition by 4EGI-1. Collectively, 4EGI-1 effectively suppresses EIF4E expression and may exert its effects on ovarian cancer therapy by modulating EIF4E.

Vascular Endothelial Growth Factor (VEGF) is a protein that stimulates angiogenesis and increases vascular permeability, playing a crucial role in tumor growth and metastasis [13]. In ovarian cancer, excessive release of VEGF by tumor cells leads to increased angiogenesis, forming a new vascular network to provide nutrients and oxygen to tumor cells. The formation of new blood vessels enables tumor growth, proliferation, and facilitates tumor cell dissemination into the bloodstream, contributing to distant metastasis [14]. As a significant member of the VEGF family, VEGFA has been extensively studied, and it has been reported that VEGFA expression is notably higher in ovarian cancer tumors [15], consistent with our public database analysis. Furthermore, elevated EIF4E levels have been associated with increased malignant tumor VEGF mRNA translation [16]. Through the use of the EIF4E inhibitor 4EGI-1 in ovarian cancer cell lines, we observed a downregulation in both mRNA and protein expression levels of VEGFA. This suggests that EIF4E inhibition might affect ovarian cancer cell angiogenesis capability through downregulation of VEGF expression.

Cyclin D1 (CCND1) is a cell cycle regulatory protein that participates in controlling cell entry into the S phase and the cell division process. In ovarian cancer, overexpression of CCND1 is associated with increased tumor proliferation activity and poor prognosis [17]. Elevated CCND1 levels promote cell cycle progression, leading to uncontrolled cell proliferation [18]. Additionally, CCND1 can activate cell cycle-related signaling pathways, promoting cancer cell growth and invasion capabilities [19]. Studies have shown that CCND1 gene expression is significantly higher in ovarian cancer tissues compared to normal ovarian tissues [20], potentially promoting proliferation and cell cycle progression through enhanced cyclin D1 translation [9]. Our public database analysis results confirm these observations. Furthermore, treatment with the EIF4E inhibitor 4EGI-1 in ovarian cancer cell lines resulted in varying degrees of downregulation in CCND1 mRNA and protein levels. This indicates that EIF4E inhibition might affect ovarian cancer cell proliferation and cell cycle progression through regulation of CCND1 expression.

In conclusion, overexpression of EIF4E appears to be closely associated with the clinical and pathological characteristics of ovarian cancer patients. In various tumors, EIF4E is significantly correlated with VEGF and cyclin D1, suggesting its role in the regulation of protein translation related to angiogenesis and growth [9, 21]. The correlation analysis results in our study further confirmed the positive correlation among EIF4E, VEGFA, and CCND1 in ovarian cancer. Simultaneous inhibition of EIF4E also led to downregulation of VEGFA and CCND1 expression, validating their interconnectedness. Thus, targeted therapy against EIF4E may prove to be an effective strategy for treating ovarian cancer. However, further research and clinical trials are necessary to assess the safety and efficacy of targeted EIF4E therapy, offering more effective treatment options for ovarian cancer patients.

Acknowledgments:

Funding: This study was supported by the Joint Project of Southwest Medical University and the Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University (Grant No. 2020XYLH-043).

Conflict of Interest: The authors declare no conflicts of interest.

[darkmaga-returns]

By Nicolas Hulscher, MPH

The study titled, Impact of mRNA and Inactivated COVID-19 Vaccines on Ovarian Reserve, was recently published in the journal Vaccines:

Objectives: This study aimed to elucidate the effects of messenger RNA (mRNA) and inactivated coronavirus disease 2019 (COVID-19) vaccines on ovarian histology and reserve in rats. Methods: Thirty female Wistar albino rats, aged 16–24 weeks, were randomly divided into three groups (n = 10): control, mRNA vaccine, and inactivated vaccine groups. Each vaccine group received two doses (on day 0 and day 28) at human-equivalent doses. Four weeks post-second vaccination, ovarian tissues were harvested for analysis. Results: Immunohistochemical analysis was performed to evaluate the expression of transforming growth factor beta-1 (TGF-β1), vascular endothelial growth factor (VEGF), caspase-3, and anti-Müllerian hormone (AMH) in ovarian follicles. Both vaccines induced significant increases in TGF-β1, VEGF, and caspase-3 expression, with more pronounced effects in the mRNA vaccine group. Conversely, AMH expression in the granulosa cells of primary, secondary, and antral follicles showed marked reductions (p < 0.001). The counts of primordial, primary, and secondary follicles decreased significantly in the inactivated vaccine group relative to controls and further in the mRNA vaccine group compared to the inactivated group (p < 0.001). Additionally, the mRNA vaccine group exhibited a decrease in antral and preovulatory follicles and an increase in atretic follicles compared to the other groups (p < 0.05). The serum AMH level was diminished with the mRNA vaccination in comparison with the control and inactivated groups.

[spacetimewithstuartgary]

Leads on cancer drugs, satellite sustainability, glass from magnesium silicates

Space-grown crystals could lead to targeted cancer drugs

Researchers used space-grown protein crystals to determine the structure of a helix-loop-helix (HLH) peptide (one with a double helix and connecting loop) in a complex with vascular endothelial growth factor-A (VEGF). VEGF prompts the formation of new blood vessels and inhibiting it can stop tumor growth. This finding suggests that HLH peptides could be used to create drugs to target disease-related proteins like VEGF.

JAXA PCG, an investigation from JAXA (Japan Aerospace Exploration Agency), grew protein crystals in microgravity and returned them to Earth for detailed analysis of their structures. Microgravity enables production of high-quality crystals, and examining their structures supports the design of new drugs and other types of research.

Wood could make satellites more sustainable

Wood exposed to space for approximately 10 months showed no change in weight and no erosion due to atomic oxygen. This finding could inform selection of the appropriate species and thickness of wood for use in building satellites.

Metal satellites reentering Earth's atmosphere can generate particles and aerosols that may harm the ozone layer. Wood becomes water and carbon dioxide on reentry, does not contribute to atmospheric pollution, and could provide a more sustainable option for future space exploration. JAXA's Exposure of Wood to Outer Space evaluated how atomic oxygen, galactic cosmic rays, and solar energetic particles in space affect the mechanical properties of wood.

Analyzing glass-forming ability of magnesium silicates

Researchers report detailed structural and atomic information for glassy and liquid magnesium silicates, which are important in glass science and geoscience. The results suggest that electronic structure does not play an important role in determining glass-forming ability, but atomic structure does.

JAXA's Fragility measured thermophysical properties such as density and viscosity of oxidized molten metals using the International Space Station's Electrostatic Levitation Furnace (ELF) to gain insight into glass formation and the design of novel materials. The ELF makes it possible to observe the behavior of materials without the use of a container, providing information crucial for examining glass formation.

TOP IMAGE: Japan Aerospace Exploration Agency astronaut Soichi Noguchi works on the PCG experiment aboard the International Space Station. Credit: NASA

CENTRE IMAGE: Different types of wood to be tested in space as a building material for satellites. Credit: Kyoto University

LOWER IMAGE: NASA astronaut Scott Kelly works on the Electrostatic Levitation Furnace aboard the International Space Station. Credit: NASA

[s-adenosylmethionin]

Sensorik im Alter und epigenetischer Einfluss: Mechanismen, Veränderungen und Regulation

Mit zunehmendem Alter kommt es zu einer Abnahme der sensorischen Fähigkeiten in verschiedenen Bereichen wie Sehen, Hören, Tastsinn, Geruch und Geschmack. Neben genetischen Faktoren spielen auch epigenetische Mechanismen eine wesentliche Rolle bei der altersbedingten sensorischen Degeneration. Diese Mechanismen können durch Umweltfaktoren, Lebensstil und Stress beeinflusst werden.

1. Sensorische Veränderungen im Alter

a) Sehen (Visuelle Wahrnehmung) Makula-Degeneration (AMD): Epigenetische Dysregulationen in VEGF-Genen (vascular endothelial growth factor) können zur degenerativen Veränderung der Netzhaut beitragen. ALTERSBEDINGTE MAKULADEGENERATION (AMD) An der Pathogenese der altersbedingten Makuladegeneration ist die DNA-Hypomethylierung beteiligt. Die altersbedingte Makuladegeneration (AMD) ist die häufigste Ursache für eine irreversible Blindheit bei Menschen ab 50 Jahren und kann nicht wirksam geheilt werden. Die Krankheit ist gekennzeichnet durch die fokale Ablagerung von azellulären und polymorphen Trümmern, Drusen genannt, zwischen retinalem Pigmentepithel (RPE) und Bruch-Membran. Eines der in Drusen akkumulierten Hauptproteine ist Clusterin, dessen Expression durch Promotor-Methylierung reguliert wird. Auch gibt es zahlreiche Hinweise, dass die durch oxidativen Stress aus der Atmungskette der Mitochondrien verursachten Störungen eine weitaus größere Bedeutung bei der Entstehung der AMD haben als bislang angenommen. Gerade der oxidative Stress (ROS) führt bei AMD-Patienten zu gravierenden DNA-Schäden der mitochondrialen DNA. Sowohl Alter als auch Rauchen sind bestätigte Risikofaktoren für AMD. Katarakt (Grauer Star): Oxidativer Stress und Histon-Modifikationen beeinflussen die Transparenz der Augenlinse. Reduzierte Kontrastwahrnehmung: Altersbedingte DNA-Methylierung im OPN1LW-Gen (Farbrezeptor) kann die Farbwahrnehmung reduzieren. b) Hören (Auditive Wahrnehmung) Presbyakusis (Altersschwerhörigkeit): Epigenetische Veränderungen in SOD2-Genen (Superoxiddismutase) führen zu einer erhöhten Anfälligkeit für oxidativen Stress in den Haarzellen der Cochlea. Methylierung des KCNQ4-Gens (Kaliumkanal) kann zur Degeneration der Hörzellen beitragen. c) Tastsinn und Schmerzempfindlichkeit Reduktion mechanosensitiver Rezeptoren (Meissner-Körperchen, Merkel-Zellen) durch Histon-Methylierung an NGF-assoziierten Genen (Nerve Growth Factor). Veränderte Schmerzempfindung: Hyper- oder Hypoalgesie (erhöhte oder verminderte Schmerzempfindlichkeit) durch epigenetische Modifikationen in TRPV1 (Schmerzrezeptor). In der Hypophyse wird ein Makromolekül aufgeteilt, wodurch im Anschluss Adrenocorticotrophes Hormon ACTH und Betaendorphin zur Verfügung stehen. Immer dann, wenn ein Molekül ACTH entsteht, entsteht chemisch zwingend auch ein Molekül Betaendorphin. Endorphine beruhigen das PANIC/Grief- System (Schmerz und Depression) d) Geruch und Geschmack Geruchsverlust (Hyposmie/Anosmie): Methylierung des OR2A1-Gens kann die Reduktion der Riechrezeptoren im Alter beeinflussen. Veränderter Geschmackssinn: Histon-Acetylierung in gustatorischen Signalwegen kann die Wahrnehmung von Süßem oder Salzigem reduzieren.

2. Epigenetische Mechanismen und Sensorik im Alter

a) DNA-Methylierung Altersabhängige Hypermethylierung in sensorischen Genen führt zur reduzierten Expression von Rezeptorproteinen. Beispiele: Hypermethylierung von BDNF (Brain-Derived Neurotrophic Factor) kann sensorische Plastizität im Gehirn einschränken. MAO A SIPS (STRESS-INDUCED PREMATURE SENESCENCE) - MONOAMINOOXIDASEN, OXIDATIVER STRESS UND VERÄNDERTE MITOCHONDRIALE DYNAMIK BEI DER HERZALTERUNG: Mitochondrien sind in dem Seneszenz-Prozess verwickelt, hauptsächlich, weil sie sowohl Quellen als auch Ziele von reaktiven Sauerstoffspezies (ROS) sind. Stressbedingte vorzeitige Seneszenz in Herzzellen durch erhöhte MAO A führt zu mitochondrialen Schäden, Kardiomyozytentod und Herzinsuffizienz und steuert in Herzzellen zur ROS-Produktion, mitochondrialer Dysfunktion und Mitophagie-Hemmung bei. Zusätzlich beeinträchtigt MAO A-erzeugter oxidativer Stress die Lysosomenfunktion, was zu einer Blockade des autophagischen Flusses führt.

Abb.: ROLLE VON MAO A BEI HERZINSUFFIZIENZ Quelle: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5435992/figure/fig2/ b) Histon-Modifikationen H3K27me3 (Trimethylierung an Histon H3, Lysin 27) ist mit neurodegenerativen Veränderungen und sensorischer Degeneration assoziiert. Reduzierte H3K9-Acetylierung führt zu einer schwächeren Synapsenfunktion in sensorischen Bahnen. c) microRNAs (miRNAs) miRNA-183 reduziert die Funktion sensorischer Neuronen bei Hörverlust. miRNA-29 ist in alternden Riechzellen überaktiv und hemmt die Regeneration von Geruchsrezeptoren.

3. Einfluss externer Faktoren auf Epigenetik und Sensorik

a) Oxidativer Stress und Ernährung Antioxidative Ernährung (Vitamin A, C, E, Polyphenole) kann epigenetische Schäden reduzieren und die Sensorik im Alter erhalten.   - Mangelernährung (Vitamin B12, Zink, Omega-3-Fettsäuren) fördert epigenetische Veränderungen, die Seh-, Hör- und Geschmacksverlust beschleunigen.   Die Biosynthese von S-Adenosylmethionin (SAM-e, Ademetionin) nimmt bereits im frühen Erwachsenen Alter ab. Eine S-Adenosylmethionin (SAM-e, Ademetionin) ist ratsam, insbesondere wenn es zu epigenetischen Dysregulationen, neurodegenerativen Erkrankungen oder erhöhtem oxidativen Stress kommt. 1. Warum nimmt die SAM-e-Biosynthese im Alter ab? SAM-e wird in der Zelle aus Methionin und ATP durch das Enzym Methionin-Adenosyltransferase (MAT) synthetisiert. Mehrere Faktoren beeinflussen die SAM-e-Bildung mit zunehmendem Alter: Erhöhte oxidative Belastung: Oxidativer Stress kann die Aktivität der Methionin-Zyklenzyme verringern. Niedrigere Verfügbarkeit von Vorläufermolekülen: Ein Mangel an Methionin, Vitamin B12, B6 oder Folat reduziert die SAM-e-Synthese. Epigenetische Veränderungen: Altersbedingte Veränderungen in der DNA-Methylierung können die Enzymaktivität für die SAM-e-Synthese beeinflussen. Dysfunktion des Methionin-Homocystein-Zyklus: Eine Akkumulation von Homocystein, die im Alter häufiger vorkommt, kann die Verfügbarkeit von Methionin für die SAM-e-Synthese senken. ➡ Bereits ab dem frühen Erwachsenenalter kann eine verringerte SAM-e-Produktion nachweisbar sein, was zu epigenetischen Fehlregulationen führt. 2. Ist eine SAM-e-Supplementation ratsam? Ja, eine Supplementation mit SAM-e kann in verschiedenen Situationen vorteilhaft sein, insbesondere bei: a) Epigenetische Regulation und Zellgesundheit SAM-e ist der wichtigste Methylgruppendonator in der DNA-Methylierung. Eine ausreichende Verfügbarkeit ist essenziell für die Regulation von Genexpression, Zellgesundheit und epigenetischer Plastizität. b) Neuroprotektion und Stimmungsregulation SAM-e fördert die Produktion von Neurotransmittern (Dopamin, Serotonin, Noradrenalin) und wird zur Behandlung von Depressionen eingesetzt. Studien zeigen, dass SAM-e neuroprotektiv wirken kann und bei Alzheimer, Parkinson und kognitiven Störungen nützlich sein könnte. c) Lebergesundheit SAM-e ist wichtig für Glutathion-Synthese (antioxidatives Schutzsystem der Leber). Studien deuten darauf hin, dass eine Supplementation bei Fettlebererkrankungen und Leberzirrhose vorteilhaft sein könnte. d) Unterstützung der Gelenkgesundheit SAM-e zeigt entzündungshemmende und knorpelschützende Eigenschaften und wird bei Arthrose und Gelenkbeschwerden als natürliche Alternative zu NSAIDs verwendet. 3. Wann ist eine SAM-e-Supplementation nicht ratsam? Bei bipolaren Störungen: SAM-e kann die Manie verstärken, da es die Neurotransmitterproduktion ankurbelt. Bei bestimmten Krebserkrankungen: Da SAM-e an der Zellproliferation beteiligt ist, gibt es Hypothesen, dass eine Überdosierung das Wachstum bestimmter Krebszellen begünstigen könnte. Bei Überempfindlichkeit gegen Methylierungsprozesse: Menschen mit MTHFR-Mutationen sollten eine Supplementation nur unter ärztlicher Aufsicht durchführen. 4. Kurz gefasst ✅ Die SAM-e-Biosynthese nimmt bereits im frühen Erwachsenenalter ab.✅ Eine Supplementation kann epigenetische Fehlregulationen, neurodegenerative Erkrankungen und oxidative Stressfaktoren ausgleichen.✅ Besonders sinnvoll bei Depressionen, Lebererkrankungen, Gelenkbeschwerden und altersbedingtem kognitiven Abbau (Neurodegeneration wie bei der Alzheimer Demenz-Erkrankung). Nicht für alle Personen geeignet – insbesondere bei bipolaren Störungen oder bestimmten Krebsarten mit Vorsicht anwenden. Falls eine Supplementation in Erwägung gezogen wird, sollte sie idealerweise mit B-Vitaminen (B6, B12, Folat) kombiniert werden, um den Methionin-Homocystein-Zyklus optimal zu unterstützen.   b) Chronischer Stress und Hormonveränderungen Erhöhte Cortisolspiegel im Alter führen zu einer Hypermethylierung von Stress-assoziierten Genen (NR3C1, FKBP5), was die sensorische Wahrnehmung beeinflusst. Beispiel: Dauerstress reduziert die Regeneration sensorischer Neuronen in der Retina und im Innenohr. c) Umweltgifte und Schadstoffe Schwermetalle (Blei, Quecksilber) beeinflussen epigenetische Regulationsmechanismen in sensorischen Neuronen und fördern altersbedingte Degeneration. Luftverschmutzung kann durch DNA-Methylierung die Riechzellen schädigen.

4. Möglichkeiten zur epigenetischen Prävention und Therapie

Ernährungsstrategien zur Förderung epigenetischer Balance ( S-Adenosylmethionin (SAM-e, Ademetionin), Folat, Polyphenole, Omega-3-Fettsäuren). Gezieltes Hör-, Seh- und Taktiltraining zur Modulation epigenetischer Programme (neuronale Plastizität erhöhen). Epigenetische Medikamente in der Forschung (HDAC-Inhibitoren zur Förderung der Sinnesfunktion). Histon-Deacetylase-Inhibitoren (HDAC-Inhibitoren) sind eine Klasse von Verbindungen, die die Aktivität von Histon-Deacetylasen hemmen und dadurch die Genexpression beeinflussen. Kritische Aspekte von HDAC-Inhibitoren: Unspezifische Wirkungen: HDAC-Inhibitoren können eine breite Palette von Genen beeinflussen, was zu unerwünschten Nebenwirkungen führen kann. Die Herausforderung besteht darin, spezifische HDAC-Isoformen gezielt zu hemmen, um die therapeutische Wirkung zu maximieren und Nebenwirkungen zu minimieren. mcgill.ca Langzeitwirkungen und Sicherheit: Die langfristigen Auswirkungen der HDAC-Hemmung sind noch nicht vollständig verstanden. Es besteht die Möglichkeit, dass dauerhafte Veränderungen in der Genexpression zu unvorhergesehenen gesundheitlichen Problemen führen könnten. Epigenetische Plastizität: Epigenetische Modifikationen sind dynamisch und können durch Umweltfaktoren beeinflusst werden. Die Manipulation dieser Mechanismen durch HDAC-Inhibitoren könnte daher komplexe und nicht immer vorhersehbare Effekte haben. Fazit - Die altersbedingte Einschränkung der Sensorik ist nicht nur genetisch bedingt, sondern auch stark durch epigenetische Mechanismen reguliert. - Umweltfaktoren, Stress, Ernährung und Lebensstil beeinflussen die epigenetische Regulation sensorischer Gene. - Gezielte Prävention z.B. 100% bioaktives SAM-e - S -Adenosylmethionin - Supplementation kann helfen, epigenetische Alterungsprozesse der Sinneswahrnehmung zu verlangsamen.

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Ihr Eduard Rappold Read the full article

[worldnewsbd]

Can COPD be treated with stem cell therapy?

Introduction

Chronic obstructive pulmonary disease, or COPD, refers to a group of progressive lung diseases characterized by long-term breathing problems and poor airflow. The two main conditions that fall under the COPD umbrella are chronic bronchitis and emphysema. As the lungs and airways become damaged from environmental pollutants like cigarette smoke, it becomes progressively harder for the lungs to function normally. This often leads to symptoms like shortness of breath, coughing, wheezing, fatigue, and other issues that significantly impact quality of life.

Currently, medication is relied on to treat and manage COPD symptoms, though it does not reverse underlying damage or restore lung function. Other options like pulmonary rehabilitation, oxygen therapy, lung transplantation, and smoking cessation can also help in severe cases. However, there remains an unmet need for an intervention that can repair damaged tissue and regenerate lost lung cells. This has led researchers to explore whether stem cell therapy may hold promise as a treatment for COPD.

What are stem cells?

Stem cells are unique cells in our bodies that can both self-renew and differentiate into specialized cell types. There are different classes of stem cells:

Embryonic stem cells: Derived from embryos within a few days of fertilization, these cells are considered pluripotent, meaning they can become any cell type in the body. However, research on human embryos faces ethical issues.

Induced pluripotent stem cells (iPSCs): Adult cells that have been genetically reprogrammed to an embryonic stem cell-like state with pluripotency. iPSCs avoid the use of embryos.

Adult (somatic) stem cells: Present in adult tissues like bone marrow, brain, blood, skin, and muscles. They are multipotent, with the ability to become a few specialized cell types.

In the context of COPD, mesenchymal stem cells (MSCs) hold particular promise. MSCs are multipotent adult stem cells that can differentiate into cells that make up muscles, bones, cartilage, fat, and other connective tissues. They are most commonly derived from bone marrow but can also be found in fat, dental pulp, and umbilical cord blood.

How could stem cells help treat COPD?

Research suggests MSCs may help treat COPD through these mechanisms:

Lung regeneration: MSCs have the potential to differentiate into lung cell types like epithelial cells, endothelial cells, and pneumocytes that form the gas exchange surface in the lungs. This raises hopes that MSCs could help regrow damaged or missing lung tissue.

Immunomodulation: MSCs secrete cytokines and growth factors that reduce inflammation and regulate the immune system. Persistent inflammation driven by the immune response is a major factor in COPD progression.

Angiogenesis: MSCs stimulate the growth of new blood vessels. In COPD, impaired vascularization and oxygen delivery to lung tissues are issues that may be addressed in this manner.

Antifibrotic effects: COPD lungs experience fibrosis or scarring of pulmonary tissue. Studies show MSCs help reduce fibrosis and promote wound healing through matrix remodeling enzymes.

Neurotrophic support: Dysregulation of the pulmonary neuroimmune axis occurs in COPD. MSCs secrete neurotrophins to stabilize the local neural microenvironment in the lungs.

Overall, through their multipotent and immunomodulatory properties, MSCs aim to suppress lung destruction, restore lung function, and mitigate symptoms in COPD through tissue repair and regeneration. Let's explore the evidence behind this stem cell approach.

Clinical trial evidence

A range of small, early-phase safety and proof-of-concept trials have investigated the potential of stem cell therapy in COPD patients so far:

Intravenous infusion: In a phase I trial, 20 COPD patients received two intravenous infusions of autologous bone marrow-derived MSCs a month apart. At six months, significant increases in exercise capacity and health-related quality of life were observed compared to baseline, along with decreased emphysema in high-resolution CT scans. Similar improvements were seen in other studies testing intravenous MSC administration.

Endobronchial transplantation: Another phase I study involving 14 patients delivered autologous bone marrow-derived MSCs via a bronchoscope into the lungs. At three months, lung function and walking distance increased while clinical symptoms decreased relative to before treatment. Endobronchial delivery likely enhances engraftment in the target tissues.

Intratracheal infusions: A trial in 16 COPD patients evaluated fat-derived MSCs administered by bronchoscope through the trachea. Post-treatment, they saw elevated levels of the lung surfactant-associated protein-A and reduced numbers of inflammatory cells in bronchoalveolar lavage fluid, implying a dampened inflammatory reaction alongside potential regeneration.

While the numbers are still low, no significant safety issues have been reported with MSC use in COPD trials thus far. Further evaluation in larger cohorts continues across the world. Platform trials like ONE-BRIDGE are also exploring more variables including factors like donor age, route of administration, and dosage levels.

Real-world examples

R3 Stem Cell is a stem cell bank based in India with facilities for treating patients using autologous adipose stem cell therapy for various conditions. On their site, they discuss indications for which they have seen benefits with COPD patients, including:

Improved breathing patterns and lung capacity parameters like FEV1 and FVC. Following treatment, patients demonstrate measurable gains in pulmonary function parameters.

Reduced exacerbations and fewer hospitalizations. Patients experience far fewer worsenings of respiratory symptoms requiring medication changes or hospital admissions post-treatment.

Enhanced quality of life. Patients note returned abilities to conduct daily chores, perform physical work and exercise, and an overall better feeling of well-being.

Improved breathing comfort and exercise tolerance. Shortness of breath is diminished. Patients find they no longer get breathless from routine movements and can walk longer distances without gasping for air.

Mitigation of chronic lung infections. With strengthened immunity and fewer exacerbation-prompted hospital visits where patients are exposed to illnesses, recurring lung infections tend to attenuate.

Disease stabilization halts further decline. For patients whose lung function was progressively deteriorating each year, treatment allows stabilization preventing additional loss.

These observations provide real-world insight into how adipose stem cell therapy may benefit COPD patients outside the constraints of clinical trials. Of course, larger studies are still vital to fully validate the approach.

Future considerations

While preliminary results are promising, stem cell therapy for COPD remains in the exploratory phase. Questions that still need answers include:

Determining the optimal cell dose and route of administration. More research aims to establish standardized protocols.

Longer-term follow-up data. Currently, most trials only follow patients up to 6-12 months. Longitudinal studies spanning years are essential.

Delineating which COPD subgroups benefit most. Further stratification is important based on disease severity, emphysema presence, exacerbation frequency, and other criteria.

Elucidating the precise mechanisms of action via lung tissue analysis. Further validation of stem cell effects on regeneration, remodeling, and inflammation modulation is underway.

Conducting comparative effectiveness studies. Head-to-head trials against conventionally available COPD treatments will help define the treatment landscape.

Ensuring consistent quality and safety across providers. Optimization of donor screening, cell manufacturing, and administration standards on large cohorts will strengthen the field.

As more long-term safety and efficacy results emerge, stem cell therapy could become an accepted component of COPD management. It holds great potential to improve care for a condition representing a major worldwide health burden. Further clinical advances and research remain on the horizon.

Conclusion

In summary, while definitive conclusions are still being drawn, initial experiments show stem cell therapy may effectively treat COPD symptoms through regenerative and immunomodulating actions. Mesenchymal stem cells administered through various routes seem to help minimize lung injury and enhance recovery by regenerating tissue and counteracting inflammation. Real-world cases also confirm gains in lung function and quality of life following treatment through adipose stem cell therapy. While larger controlled studies are still warranted, early evidence establishes stem cell therapy as a promising avenue worth further exploration for COPD, a progressive and irreversible disease currently lacking an intervention that can reverse the damage. Continued investigation will likely optimize this cell-based approach and bring it closer to becoming part of standardized COPD care pathways.

[stemcellcareindia]

Study Finds How to Upsurge the Survival Time of Stem Cells | Medical Updates |

The researcher's team found that by fastening a protein called vascular endothelial growth factor (VEGF) to microscopic particles can upsurge the survival time of stem cells, which could be used to help the healing of tissues, after the inoculation into the body. To comprehend how this protein can upsurge the survival of the cells, the researchers tested the molecules called “micro RNAs,” which are imperative for the function of the cells.

https://www.stemcellcareindia.com/news/study-finds-how-to-upsurge-the-survival-time-of-stem-cells/

Email id- info@stemcellcareindia.com Ph no- +91 8743024344

[kneexpertindore]

Knee Pain Treatment with Knee Xpert SVF Therapy

Chronic knee pain affects millions worldwide, often limiting mobility, reducing quality of life, and leading to invasive surgeries. Fortunately, regenerative medicine offers new hope-especially with innovative treatments like SVF therapy. If you're struggling with knee pain and looking for an advanced, non-surgical solution, Knee Xpert's SVF therapy could be the breakthrough you need.

What Is SVF Therapy?

SVF, or Stromal Vascular Fraction, is a regenerative cell therapy derived from a patient’s own adipose (fat) tissue. It contains a rich concentration of:

Mesenchymal cells (MSCs)

Endothelial progenitor cells

Growth factors and cytokines

These biologically active components help regenerate damaged tissues, reduce inflammation, and improve overall joint function.

Unlike traditional methods such as corticosteroid injections or knee replacement surgery, SVF therapy addresses the root cause of pain by aiding natural healing.

Why SVF Therapy Is Effective for Knee Pain

SVF therapy is showing impressive results for patients suffering from:

Knee osteoarthritis

Meniscal tears

Cartilage degeneration

Knee ligament injuries

Other chronic knee joint diseases

Benefits of SVF Therapy:

Minimally invasive (no need for open surgery)

Autologous (uses the patient’s own cells, reducing rejection risk)

Fast recovery with minimal downtime

Long-term pain relief and functional improvement

Knee Xpert: The Trusted Leader in SVF Therapy for Knee Pain

When choosing a provider for SVF therapy, expertise and precision matter. Knee Xpert is India’s first dedicated regenerative knee care clinic specializing in minimal invasive treatment of joint issues.

Here’s why Knee Xpert stands out:

Led by Dr. Reetadyuti Mukhopadhyay, a renowned knee surgeon and regenerative medicine specialist

Advanced diagnostic tools like MRI and gait analysis for precision therapy

Comprehensive care model-from assessment to post-therapy rehabilitation

Successful outcomes in thousands of patients with knee ligament injury treatment and chronic joint disorders

Who Can Benefit from SVF Therapy?

You might be an ideal candidate if you:

Have chronic knee pain that hasn’t responded to physiotherapy or medications

Are not ready or eligible for knee replacement surgery

Want to avoid long recovery periods or surgical risks

Suffer from knee joint diseases like osteoarthritis, ligament tears, or meniscal damage

FAQs About Knee Pain Treatment with SVF Therapy

1. Is SVF therapy safe?

Yes. SVF uses your own body’s cells, significantly reducing the risk of allergic reactions or infection.

2. How long does it take to see results?

Patients typically report reduced pain and improved function within 4 to 12 weeks, though results may vary.

3. Can SVF help with knee ligament treatment?

Absolutely. SVF therapy promotes regeneration of soft tissues, making it effective for knee ligament injury treatment and cartilage repair.

4. Is this therapy suitable for all knee joint diseases?

It is especially effective for degenerative conditions like osteoarthritis and meniscus tears. A thorough assessment at Knee Xpert determines suitability.

Take the Next Step Toward Pain-Free Mobility

If chronic knee pain is holding you back, consider a revolutionary approach with Knee Xpert’s SVF therapy. With cutting-edge technology, expert clinicians, and a patient-first approach, Knee Xpert is redefining how we treat knee joint diseases.

[graphicabhi]

8 Emerging Bispecific Antibodies Reshaping Non-Small Cell Lung Cancer (NSCLC) Treatment

Non-small cell lung cancer (NSCLC) therapy is undergoing a paradigm shift, fueled by the development of bispecific antibodies that target both immune checkpoints and tumor-promoting pathways. At the forefront of these innovations are bispecific programmed cell death protein 1 (PD-1)/vascular endothelial growth factor (VEGF) antibodies, aiming to tackle immune evasion and angiogenesis in tumors.

Explore ongoing PD-1/VEGF bispecific trials and their impact on lung cancer therapy today: https://www.delveinsight.com/blog/bispecific-antibodies-for-nsclc?utm_source=blog&utm_medium=promotion&utm_campaign=akpr 

A leading candidate in this space is ivonescimab (AK112), now in Phase I/II clinical development (NCT05499390, currently recruiting). While NCT05184712 involving ivonescimab (AK112) remains a significant trial, other bispecific programmed cell death protein 1 (PD-1)/vascular endothelial growth factor (VEGF) antibody clinical trials are gaining traction, offering alternatives beyond AK112. The pipeline of programmed cell death protein 1 (PD-1)/vascular endothelial growth factor (VEGF) bispecific monoclonal antibody clinical trials apart from AK112 is rapidly expanding, with multiple agents showing early signs of clinical benefit.

One such agent is PM8001, a bispecific targeting programmed death-ligand 1 (PD-L1) and vascular endothelial growth factor (VEGF), jointly developed by Bio-Thera and BeiGene. The PM8001 programmed death-ligand 1 (PD-L1)/vascular endothelial growth factor (VEGF) bispecific trial—including trials registered under PM8001 programmed death-ligand 1 (PD-L1)/vascular endothelial growth factor (VEGF) bispecific clinical trial NCT entries—is progressing through early-stage studies and represents a novel dual-targeting approach. These emerging bispecific monoclonal antibody programmed cell death protein 1 (PD-1)/vascular endothelial growth factor (VEGF) clinical trials, including those beyond AK112, are transforming the future of lung cancer immunotherapy.

Another noteworthy contender is GEN1046 from Genmab, which targets programmed death-ligand 1 (PD-L1) and 4-1BB, reflecting a new class of Genmab bispecific platforms. Alongside this, epidermal growth factor receptor (EGFR)/mesenchymal epithelial transition (MET) bispecifics—such as the FDA-approved amivantamab—continue to be pivotal for certain NSCLC subtypes.

Several trials are actively recruiting, including NCT04900363 and NCT05499390 (ivonescimab AK112 status), highlighting the momentum in this field. Additional trials like “programmed cell death protein 1 (PD-1)/vascular endothelial growth factor (VEGF) bispecific monoclonal antibody clinical trial active recruiting 2024” and “bispecific monoclonal antibody programmed cell death protein 1 (PD-1)/vascular endothelial growth factor (VEGF) clinical trial active recruiting October 2024,” as well as HB0025 programmed cell death protein 1 (PD-1)/vascular endothelial growth factor (VEGF) bispecific trial (NCT), are also being closely followed.

Discover how bispecific antibodies are changing NSCLC treatment—learn more in this clinical trial update: https://www.delveinsight.com/blog/bispecific-antibodies-for-nsclc?utm_source=blog&utm_medium=promotion&utm_campaign=akpr 

As the ongoing landscape of programmed cell death protein 1 (PD-1)/vascular endothelial growth factor (VEGF) bispecific antibody clinical trials evolves, the promise of bispecific antibody therapies for lung cancer is coming into sharper focus. By 2025, the bispecific programmed cell death protein 1 (PD-1)/vascular endothelial growth factor (VEGF) clinical trial and bispecific monoclonal domain are expected to unlock new standards of care in NSCLC treatment.

Latest Reports Offered By DelveInsight:

Human Papilomavirus Market | Hydrocephalus Treatment Market | Hyperammonemia Market | Hyperglycemia Market | Hyperlipidemia Market | Hypoplastic Left Heart Syndrome Hlhs Market | Hypothalamic Obesity Market | Hypoventilation Market | Hypovolemic Shock Market | Idiopathic Membranous Nephropathy Market | Membranous Nephropathy Market | Iga Nephropathy Market | Igg4 – Related Disease Market | Igg4 Related Diseases Market | Cardiac Implantable Electronic Devices Market | Intrathecal Pumps Market | Indolent Lymphoma Market | Inflammatory Bowel Disease Market | Infusion Pumps Market | Inguinal Hernia Market | Injectable Drug Delivery Devices | Insulin Glargine Biosimilar | Interbody Cages Market | Interspinous Spacers Market | Intestinal Fistula Market 

Other Reports Offered By DelveInsight:

https://www.delveinsight.com/sample-request/gaba-transaminase-inhibitor-pipeline-insighthttps://www.delveinsight.com/sample-request/galactosemia-market

[visionhealthandcare]

Can new treatments stop vision loss before it starts in millions of patients?

Vision loss is one of the most feared medical conditions globally, and for many aging adults, it’s not just about seeing less clearly — it’s about losing independence and quality of life. One of the silent culprits behind sudden vision deterioration is choroidal neovascularization, a serious condition linked with age-related macular degeneration and other retinal diseases. But breakthroughs in treatment are turning the tide.

So what’s driving growth in the Choroidal Neovascularization Market, and how are emerging therapies reshaping the future of eye care?

What exactly is choroidal neovascularization and why is it dangerous?

Choroidal neovascularization (CNV) occurs when abnormal blood vessels grow beneath the retina and leak fluid or blood, leading to blurred or distorted vision. If left untreated, CNV can cause irreversible damage to the central vision — the part that allows us to read, recognize faces, and drive.

CNV is often associated with diseases like age-related macular degeneration (AMD), pathologic myopia, and ocular histoplasmosis. As the global population ages, the number of individuals at risk is climbing rapidly, making early detection and treatment more critical than ever.

Why is the CNV treatment landscape evolving so quickly?

The market is undergoing a revolution due to the development of advanced biologics, anti-VEGF therapies, and sustained-release drug delivery systems. Current treatments like intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) agents have shown remarkable success in halting the progression of CNV and even improving vision in some patients.

According to recent research, the Choroidal Neovascularization Market is expanding rapidly due to ongoing innovation in drug formulations and delivery methods. Companies are now investing in longer-lasting treatments to reduce the frequency of eye injections, a major concern for patients.

How are AI and imaging tech improving CNV diagnosis and monitoring?

Advancements in optical coherence tomography (OCT), fundus imaging, and AI-assisted diagnostics are transforming how ophthalmologists detect and track CNV. These technologies provide high-resolution cross-sectional images of the retina, allowing for early and more accurate diagnosis.

AI tools are even being developed to flag potential CNV signs automatically during routine exams, helping doctors act sooner and improving outcomes. With earlier intervention, patients stand a much better chance of preserving their vision.

Is there a preventive approach for CNV on the horizon?

While current treatments focus on controlling existing CNV, researchers are exploring preventive strategies as well — including genetic testing, lifestyle interventions, and nutrient-based therapies. This aligns with the growing trend toward holistic eye health and preventive care.

The rising popularity of eye-focused wellness products in places like the South Korea Health Supplements Market shows consumers are becoming more proactive about vision. Supplements rich in lutein, zeaxanthin, and omega-3 fatty acids are gaining attention for their potential role in retinal protection and long-term eye health.

In parallel, the China Health Supplements Market is also seeing a boom in demand for eye-care formulations, reflecting broader public interest in preserving vision as part of overall well-being.

Can emerging markets catch up in CNV treatment access?

Access remains a critical issue, especially in developing regions where retinal specialists and advanced diagnostic tools are limited. However, increased investment from healthcare companies and public-private partnerships are helping to bridge the gap. Portable diagnostics and biosimilar drugs are making effective CNV care more accessible and affordable.

As awareness grows and technology becomes more affordable, these markets are expected to become key drivers in the global expansion of CNV treatment solutions.

Final focus

Vision loss doesn’t have to be an inevitable part of aging. The Choroidal Neovascularization Market is proof that science is catching up with one of the most threatening eye diseases of our time. With earlier detection, smarter diagnostics, and evolving therapies, millions could soon see a brighter future — literally.

[darkmaga-returns]

By Nicolas Hulscher, MPH

The study titled, Altered Circulating Cytokine Profile Among mRNA‐Vaccinated Young Adults: A Year‐Long Follow‐Up Study, was just published in the journal Immunity, Inflammation and Disease:

Objectives This longitudinal study aimed to assess the impact of COVID-19 vaccination on cytokine profile. Methods A total of 84 Saudi subjects (57.1% females) with mean age of 27.2 ± 12.3 participated in this longitudinal study. Anthropometric data and fasting blood samples were obtained at baseline and after final vaccination, with an average follow-up duration of 14.1 ± 3.6 months for adolescents and 13.3 ± 3.0 months for adults, calculated from the first dose of vaccination. Assessment of cytokine profiles was done using commercially available assays. Results After follow-up, a significant increase in weight and body mass index was observed overall (p = 0.003 and p = 0.002, respectively). Postvaccination, significant increases were observed in several cytokines, including basic fibroblast growth factor 2 (p < 0.001), interferon gamma (IFNγ) (p = 0.005), interleukin-1 beta (IL1β) (p < 0.001), IL4 (p < 0.001), IL6 (p = 0.003), IL7 (p = 0.001), IL17E (p < 0.001), monocyte chemoattractant protein-1 (MCP1) (p = 0.03), MCP3 (p = 0.001), tumor necrosis factor alpha (TNFα) (p < 0.001), and VEGFA (p < 0.001). A significant reduction was observed only in macrophage colony-stimulating factor (p < 0.001). When adjusted for age, epidermal growth factor (EGF), IL4, IL6, MCP3, TNFα, and vascular endothelial growth factor (VEGFA) remained statistically significant. Gender-based analysis revealed that men experienced greater increases in IL6 (p = 0.008), IL4 (p = 0.04), and TNFα (p = 0.015) compared to women. Age-based analysis showed that older participants had more pronounced increases in EGF (p = 0.011), IL6 (p = 0.029), MCP1 (p = 0.042), and TNFα (p = 0.017), while younger participants had a greater increase in VEGFA (p = 0.025). Conclusions The findings of this study indicated that COVID-19 vaccination resulted in an increase in cytokine levels, which signifies the persistence of the humoral immune response to messenger RNA (mRNA) vaccines. This effect may be attributed to the persistent production of spike protein and highly inflammatory nature of mRNA–lipid nanoparticle. Additionally, the results suggested differences in cytokine levels based on gender and age. Notably, the cytokine profile remains favorably altered in young adults who received mRNA vaccinations, even after 1 year.

[moleculardepot]

Anti-Phospho KDR/FLK-1/VEGFR2 (Tyr1059) Antibody

Anti-Phospho KDR/FLK-1/VEGFR2 (Tyr1059) Antibody Catalog number: B2024272 Lot number: Batch Dependent Expiration Date: Batch dependent Amount: 200 uL Molecular Weight or Concentration: ~230 kDa Supplied as: Solution Applications: a molecular tool for various biochemical applications Storage: 2-8°C Keywords: Vascular endothelial growth factor receptor 2, VEGFR-2, Fetal liver kinase 1, FLK-1,…

[worldnewsbd]

Stem Cell Therapy for Peripheral Artery Disease in India

Peripheral artery disease, also known as PAD, affects millions of people globally by restricting blood flow to their limbs. Conventionally, treatment options for PAD include medications, lifestyle changes, angioplasty, and bypass surgery.

However, a promising new treatment is emerging - stem cell therapy. In this article, we'll discuss how stem cell therapy works for PAD, research on its effectiveness, and options to access top-quality treatment at r3stemcell India in New Delhi, India.

What is Peripheral Artery Disease?

Peripheral artery disease, or PAD, occurs when fatty deposits called plaque build up in the arteries that supply blood to the head, organs, and limbs. This narrows the arteries and reduces blood flow.

PAD most commonly affects the arteries in the legs. However, it can impact any peripheral arteries outside of the heart. The classic symptom is calf pain or cramping in the legs and hips while walking, known as intermittent claudication. Other signs include sores on the feet/legs that won't heal or color changes in the skin.

PAD is caused by atherosclerosis, a disease where plaque builds up in the arteries. Risk factors for developing atherosclerosis and PAD include:

Smoking High blood pressure High cholesterol Diabetes Obesity Older age

Without treatment, PAD can progress to severe leg pain at rest or non-healing wounds. In rare cases, it may require amputation if blood flow is severely restricted.

How Does Stem Cell Therapy Work for PAD?

Stem cell therapy for PAD aims to regenerate new blood vessels and improve circulation in the affected limbs. It works through the following mechanisms:

Stem cells promote angiogenesis:

Stem cells secrete factors that stimulate the growth of new blood vessels, a process called angiogenesis. They recruit the body's own stem cells to develop new networks that bypass blockages.

Reduced inflammation:

Stem cells have anti-inflammatory properties. They help reduce inflammation in the arteries and vessel walls caused by PAD. This eases blood flow.

Generation of healthy cells:

Some stem cell types can differentiate into endothelial cells, which line the inside of blood vessels. They form new endothelial layers over damaged areas to improve vascular function.

Bypass artery obstructions:

The new blood vessels generated around narrowed or blocked areas provide pathways for blood to flow, bypassing restrictions in the primary arteries. This restores adequate blood flow.

In summary, stem cells repair and regenerate the blood vessel network from within via multiple regenerative mechanisms. When administered via injections, they home in on sites of injury in peripheral arteries and enact healing.

Research on Stem Cell Therapy for PAD

Research into stem cell therapy for PAD is still emerging but shows promise. Here are some key study findings:

A 2021 review found stem cell therapy significantly improved pain-free walking distance in PAD patients compared to conservative treatments alone.

Animal studies show stem cells increase capillary density and blood flow in ischemic limb muscle tissue with minimal side effects.

A 2017 study of 36 patients found adipose-derived stem cell therapy improved ankle-brachial pressure index (a measure of blood flow) and reduced amputation risk.

A Korean trial of 52 participants found bone marrow-derived mononuclear cell therapy increased pain-free walking time by 165% at 6 months follow-up.

No serious adverse events were reported across multiple clinical trials, indicating stem cell therapy for PAD appears safe when administered properly.

While more large-scale human trials are still needed, current research suggests stem cell therapy improves vascular function, reduces symptoms, and helps avoid amputation in PAD patients. Its safety profile also makes it a promising alternative or addition to standard PAD treatments.

Accessing Stem Cell Therapy for PAD in India

For individuals seeking stem cell therapy for peripheral artery disease, r3stemcell India is one of the top centers in the world. Here are some benefits it offers:

Experienced US-board-certified doctors with over 10,000 successful regenerative procedures completed.

State-of-the-art stem cell lab and facilities cleared by DCGI, India's FDA equivalent.

Full evaluation by a medical team prior to developing a customized treatment plan.

Use of autologous (patient's own) stem cells sourced from adipose tissue or bone marrow.

Minimally invasive stem cell injections or intravenous therapies depending on each case.

Affordable all-inclusive packages including accommodation, meals, transportation, and more.

Additional support services like physiotherapy, supplements, and oxygen therapies.

High success rates were reported across multiple conditions treated, including PAD.

For patients who want to access safe and effective stem cell therapy for peripheral artery disease, r3stemcell India is an excellent choice. Consultations can be arranged online or via phone prior to booking treatment.

Conclusion

In summary, peripheral artery disease affects millions worldwide by restricting blood flow to the limbs. While medications, angioplasty, and surgery are standard treatment protocols currently, stem cell therapy shows promise as an innovative option.

Research suggests it improves vascular function, reduces symptoms, increases walking distance and lowers amputation risks for PAD patients. When administered at reputed centers like r3stemcell India, stem cell therapy also appears to be a safe alternative for peripheral artery disease.

With successful clinical studies already conducted and more in progress, stem cell therapy could emerge as an important addition to the PAD treatment paradigm. It offers hope for regenerative healing with minimal long-term reliance on medications. For individuals seeking this promising treatment, r3stemcell India is a suitable choice.