The present study investigated the reliability and sensitivity of a wearable near-infrared spectroscopy (wNIRS) device in moderate and heavy exercise intensity domains. On three separate days, eleven males performed an incremental test to exhaustion, and in the following visits, four submaximal constant-load bouts (i.e., test and retest) were performed in the moderate-intensity domain (100 and 130 W) and heavy-intensity domain (160 and 190 W). The local tissue oxygen saturation index (SmO2) and pulmonary oxygen uptake (V̇O2) were measured continuously. The absolute SmO2 and V̇O2 values and the change (Δ) from the 3rd to 6th min of exercise were calculated. There was good reliability for SmO2 measurements, as indicated by the high intraclass correlation coefficient analysis (ICC ≥0.84 for all) and low coefficient of variation between the two trials (CV ≤4.1% for all). Steady-state responses were observed for SmO2 and V̇O2 from the 3rd to the 6th min in the two moderate-intensity bouts (P>0.05), whereas SmO2 decreased and V̇O2 increased from the 3rd to the 6th min in the two heavy-intensity bouts (P<0.05). Together, these findings suggested that the SmO2 measured with a wNIRS device is reliable and sensitive to track local metabolic changes provoked by slight increments in exercise intensity. nearinfrared near infrared (wNIRS domains days exhaustion visits constantload constant load i.e., ie i e (i.e. retest moderateintensity 100 (10 13 W heavyintensity 160 (16 19 W. . SmO (SmO2 VO2 VO V O2 O (V̇O2 continuously V̇O Δ (Δ rd th calculated measurements ICC 084 0 84 ≥0.8 all CV 41 4 1 ≤4.1 all. Steadystate Steady state P>0.05, P005 P P>0.05 , 05 (P>0.05) P<0.05. P<0.05 (P<0.05) Together i.e. (i.e 10 (1 16 (SmO (V̇O 08 8 ≥0. ≤4. P00 P>0.0 (P>0.05 P<0.0 (P<0.05 i.e ( ≥0 ≤4 P0 P>0. (P>0.0 P<0. (P<0.0 ≥ ≤ P>0 (P>0. P<0 (P<0. P> (P>0 P< (P<0 (P> (P< (P

There's limited evidence of the potential benefits of cardiopulmonary and metabolic rehabilitation (CPMR) in patients with heart failure with preserved ejection fraction (HFpEF) or mildly reduced ejection fraction (HFmrEF) and coronary artery disease (CAD). The aim of this study was to investigate the impact of CPMR on the myocardial ischemia response (MIR), exercise-induced arrhythmias (EIA), New York Heart Association (NYHA) functional class, heart rate recovery (HRR), Borg CR10 perceived symptoms, and the SF-36 physical and mental health summary scores. A prospective cohort study was conducted with 106 patients undergoing 12 weeks of CPMR who completed two exercise tests pre- and post-CPMR: 1) maximum incremental test (CPX) and 2) submaximal constant load test (SUB). After CPMR, the effects on MIR, EIA, NYHA functional class, and HRR during both tests were analyzed. There was a significant change in NYHA functional classes after CPMR, with 96% of the patients in class I (vs 62% pre-CPMR, P<0.0001), 4% in class II (vs 32%), and none in class III (vs 6%). There was a significant reduction in the frequency of EIA (P<0.05) and MIR (P<0.001) and a significantly improved performance on both CPX and SUB tests (P<0.0001). Lastly, there was significant progress in the recovery metrics like HRR (P<0.0001), the Borg CR10 (P<0.0001), and the SF-36 summary scores (P<0.0001). The CPMR resulted in a significant decrease in EIA, delayed ischemia threshold in CPX and SUB tests, increased functional capacity, and improved quality of life. Theres s (CPMR HFpEF (HFpEF HFmrEF (HFmrEF CAD. CAD . (CAD) , (MIR) exerciseinduced induced (EIA) (NYHA HRR, (HRR) CR CR1 symptoms SF36 SF 36 SF-3 10 1 pre postCPMR post post-CPMR (CPX 2 SUB. (SUB) analyzed 96 vs 62 preCPMR, preCPMR pre-CPMR P<0.0001, P00001 P P<0.0001 0 0001 P<0.0001) 4 32%, 32 32% 32%) 6%. 6 6% 6%) P<0.05 P005 05 (P<0.05 P<0.001 P0001 001 (P<0.001 P<0.0001. (P<0.0001) Lastly capacity life (CAD (MIR (EIA (HRR SF3 3 SF- (SUB 9 P0000 P<0.000 000 P<0.0 P00 (P<0.0 P<0.00 P000 00 (P<0.00 (P<0.0001 P<0. P0 (P<0. (P<0.000 P<0 (P<0 P< (P< (P

Immature hematopoietic progenitors are a constant source for renewal of hemocyte populations and the basic component of the tissue and cell repair apparatus. A unique property of these cells of internalizing extracellular double-stranded DNA has been previously shown. The leukostimulatory effect demonstrated in our pioneering studies was considered to be due to the feature of this cell. In the present research, we have analyzed the effects of DNA genome reconstructor preparation (DNAgr), DNAmix, and human recombinant angiogenin on both hematopoietic stem cells and multipotent progenitors. Treatment with bone marrow cells of experimental mice with these preparations stimulates colony formation by hematopoietic stem cells and proliferation of multipotent descendants. The main lineage responsible for this is the granulocyte-macrophage hematopoietic lineage. Using fluorescent microscopy as well as FACS assay, co-localization of primitive c-Kit- and Sca-1-positive progenitors and the TAMRA-labeled double-stranded DNA has been shown. Human recombinant angiogenin was used as a reference agent. Cells with specific markers were quantified in intact bone marrow and colonies grown in the presence of inducers. Quantitative analysis revealed that a total of 14,000 fragment copies of 500 bp, which is 0.2% of the haploid genome, can be delivered into early progenitors. Extracellular double-stranded DNA fragments stimulated the colony formation in early hematopoietic progenitors from the bone marrow, which assumed their effect on cells in G0. The observed number of Sca1+/c-Kit+ cells in colonies testifies to the possibility of both symmetrical and asymmetrical division of the initial hematopoietic stem cell and its progeny. apparatus doublestranded double stranded shown research DNAgr, DNAgr , (DNAgr) DNAmix descendants granulocytemacrophage granulocyte macrophage assay colocalization co localization cKit c Kit c-Kit Sca1positive Scapositive Sca 1 positive TAMRAlabeled TAMRA labeled agent inducers 14000 14 000 14,00 50 bp 02 0 2 0.2 G0 G Sca1+/cKit+ Sca1cKit ScacKit Sca1+/c Kit+ Sca1 Sca1+/c-Kit progeny (DNAgr 1400 00 14,0 5 0. Sca1+/cKit Sca1c Scac 140 14,

High-altitude hypoxia exposure can lead to phospholipase D-mediated lipid metabolism disorder in spleen tissues and induce ferroptosis. Nonetheless, the key genes underlying hypoxia-induced splenic phospholipase D and the ferroptosis pathway remain unclear. This study aimed to establish a hypoxia animal model. Combined transcriptomic and proteomic analyses showed that 95 predicted target genes (proteins) were significantly differentially expressed under hypoxic conditions. Key genes in phospholipase D and ferroptosis pathways under hypoxic exposure were identified by combining Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis techniques. Gene set enrichment analysis (GSEA) showed that the differential gene sets of the phospholipase D and ferroptosis signaling pathways were upregulated in the high-altitude hypoxia group. The genes in the phospholipase D signalling pathway were verified, and the expression levels of KIT and DGKG were upregulated in spleen tissues under hypoxic exposure. Subsequently, the mRNA and protein expression levels of genes from the exogenous pathway such as TFRC, SLC40A1, SLC7A11, TRP53, and FTH1 and those from the endogenous pathway such as GPX4, HMOX1, and ALOX15 differentials in the ferroptosis signalling pathway were verified, and the results indicated significant differential expression. In summary, exposure to high-altitude hypoxia mediated phospholipid metabolism disturbance through the phospholipase D signalling pathway and further induced ferroptosis, leading to splenic injury. Highaltitude High altitude Dmediated Nonetheless hypoxiainduced unclear model 9 proteins (proteins conditions GO (GO KEGG (KEGG techniques GSEA (GSEA highaltitude high group verified Subsequently TFRC SLC40A1 SLCA SLC A SLC7A11 TRP53 TRP FTH GPX4 GPX HMOX1 HMOX ALOX ALOX1 summary injury SLC40A SLC7A1 TRP5 SLC7A

Patients undergoing chemotherapy with cisplatin commonly present gastrointestinal effects such as constipation and gastric emptying (GE) delay. Both the purinergic system and physical exercise modulate the gastrointestinal (GI) tract. In the current study, we investigated the role of ATP, physical exercise, and P2X7 receptor blocking on GE delay induced by cisplatin in rats. Male rats were divided into the following groups: control (C), cisplatin (Cis), exercise (Ex), Brilliant Blue G (BBG), ATP, Cis+Ex, Cis+ATP, Cis+BBG, Cis+Ex+BBG, Cis+Ex+BBG+ATP, and Cis+ATP+BBG. GE delay was induced by treatment with 1 mg/kg cisplatin (1 time/week for 5 weeks, ip). The moderate physical exercise was swimming (1 h/day, 5 days/week for 5 weeks). At the end of the treatment or exercise and 30 min before the GE assessment, some groups received BBG (50 mg/kg, sc) or ATP (2 mg/kg, sc). Then, GE was assessed after a 10-min postprandial period. Chronic use of Cis decreased GE delay (P<0.05) compared to the control group. Both exercise and ATP prevented (P<0.05) GE delay compared to Cis. The pretreatment with BBG significantly inhibited (P<0.05) the effect of exercise and ATP. On the other hand, the association between exercise and ATP reversed (P<0.05) the effect of the BBG and prevented GE delay. Therefore, we suggest that both exercise and treatment with ATP activate P2X7 receptors and prevent GE delay induced by cisplatin in rats. (GE GI (GI tract study PX P X P2X C, C , (C) Cis, (Cis) Ex, Ex (Ex) BBG, (BBG) CisEx Cis+Ex CisATP Cis+ATP CisBBG Cis+BBG CisExBBG Cis+Ex+BBG CisExBBGATP Cis+Ex+BBG+ATP CisATPBBG Cis+ATP+BBG mgkg mg kg ( timeweek time week weeks ip. ip . ip) hday h day h/day daysweek days weeks. weeks) 3 assessment 50 (5 sc 2 sc. Then 10min 10 period P<0.05 P005 0 05 (P<0.05 group hand Therefore (C (Cis (Ex (BBG P<0.0 P00 (P<0.0 P<0. P0 (P<0. P<0 (P<0 P< (P< (P

Anti-glomerular basement membrane (GBM) disease is a rare and severe vasculitis that affects the glomerular and pulmonary capillaries and has an incidence of less than 2 cases per million individuals per year. Anti-GBM disease is mediated by autoantibodies against the α3 chain of type IV collagen. In the majority of cases, the autoantibodies are of the immunoglobulin G (IgG) class, with rare cases being mediated by immunoglobulin M (IgM) or immunoglobulin A (IgA); there are less than 15 IgA-mediated cases reported in the literature worldwide. The classic form of this disease manifests with rapidly progressive glomerulonephritis (RPGN), with or without pulmonary hemorrhage, and the diagnosis consists of identifying high titers of autoantibodies in the serum and/or deposited in the tissues. IgA antibodies are not identified in routine immunoassay tests, and renal biopsy with immunofluorescence is essential for diagnosis. We present a case of RPGN due to anti-GBM disease with linear IgA deposition, whose diagnosis was made exclusively by renal biopsy and with an unfavorable prognosis. Antiglomerular Anti GBM (GBM year AntiGBM α collagen IgG (IgG class IgM (IgM (IgA) 1 IgAmediated worldwide RPGN, , (RPGN) hemorrhage andor tissues tests antiGBM anti deposition prognosis (IgA (RPGN

During the COVID-19 outbreak, there was a sharp increase in generalized anxiety disorder (GAD). Acupuncture therapy has the advantages of accurate clinical efficacy, safety and reliability, few adverse reactions, and no dependence, and is gradually becoming one of the emerging therapies for treating GAD. We present a study protocol for a randomized clinical trial with the aim of exploring the mechanism of brain plasticity in patients with GAD and evaluate the effectiveness and reliability of acupuncture treatment. Transcranial magnetic stimulation (TMS) will be used to assess cortical excitability in GAD patients and healthy people. Sixty-six GAD patients meeting the inclusion criteria will be randomly divided into two groups: TA group, (treatment with acupuncture and basic western medicine treatment) and SA group (sham acupuncture and basic western medicine treatment). Twenty healthy people will be recruited as the control group (HC). The parameters that will be evaluated are amplitude of motor evoked potentials (MEPs), cortical resting period (CSP), resting motor threshold (RMT), and Hamilton Anxiety Scale (HAMA) score. Secondary results will include blood analysis of γ-aminobutyric acid (GABA), glutamate (Glu), glutamine (Gln), serotonin (5-HT), and brain-derived nerve growth factor (BDNF). Outcomes will be assessed at baseline and after the intervention (week 8). This study protocol is the first clinical trial designed to detect differences in cerebral cortical excitability between healthy subjects and patients with GAD, and the comparison of clinical efficacy and reliability before and after acupuncture intervention is also one of the main contents of the protocol. We hope to find a suitable non-pharmacological alternative treatment for patients with GAD. COVID19 COVID 19 COVID-1 outbreak . (GAD) reactions dependence TMS (TMS Sixtysix Sixty six groups sham HC. HC (HC) MEPs, MEPs , (MEPs) CSP, CSP (CSP) RMT, RMT (RMT) HAMA (HAMA score γaminobutyric γ aminobutyric GABA, GABA (GABA) Glu, Glu (Glu) Gln, Gln (Gln) 5HT, 5HT HT 5 (5-HT) brainderived derived BDNF. BDNF (BDNF) week 8. 8 8) nonpharmacological non pharmacological COVID1 1 COVID- (GAD (HC (MEPs (CSP (RMT (GABA (Glu (Gln (5-HT (BDNF

Forkhead Box O1 (FOXO1) has been reported to play important roles in many tumors. However, FOXO1 has not been studied in pan-cancer. The purpose of this study was to reveal the roles of FOXO1 in pan-cancer (33 cancers in this study). Through multiple public platforms, a pan-cancer analysis of FOXO1 was conducted to obtained FOXO1 expression profiles in various tumors to explore the relationship between FOXO1 expression and prognosis of these tumors and to disclose the potential mechanism of FOXO1 in these tumors. FOXO1 was associated with the prognosis of multiple tumors, especially LGG (low grade glioma), OV (ovarian carcinoma), and KIRC (kidney renal clear cell carcinoma). FOXO1 might play the role of an oncogenic gene in LGG and OV, while playing the role of a cancer suppressor gene in KIRC. FOXO1 expression had a significant correlation with the infiltration of some immune cells in LGG, OV, and KIRC. By combining FOXO1 expression and immune cell infiltration, we found that FOXO1 might influence the overall survival of LGG through the infiltration of myeloid dendritic cells or CD4+ T cells. Functional enrichment analysis and gene set enrichment analysis showed that FOXO1 might play roles in tumors through immunoregulatory interactions between a lymphoid and a non-lymphoid cell, TGF-beta signaling pathway, and transcriptional misregulation in cancer. FOXO1 was associated with the prognosis of multiple tumors, especially LGG, OV, and KIRC. In these tumors, FOXO1 might play its role via the regulation of the immune microenvironment. O FOXO (FOXO1 However pancancer. pancancer pan 33 (3 study. . study) platforms low glioma, glioma , glioma) ovarian carcinoma, carcinoma carcinoma) kidney carcinoma. CD4 CD nonlymphoid non TGFbeta TGF beta pathway microenvironment (FOXO 3 (

Coenzyme Q10 (CoQ10) is a potent antioxidant that is implicated in the inhibition of osteoclastogenesis, but the underlying mechanism has not been determined. We explored the underlying molecular mechanisms involved in this process. RAW264.7 cells received receptor activator of NF-κB ligand (RANKL) and CoQ10, after which the differentiation and viability of osteoclasts were assessed. After the cells were treated with CoQ10 and/or H2O2 and RANKL, the levels of reactive oxygen species (ROS) and proteins involved in the PI3K/AKT/mTOR and MAPK pathways and autophagy were tested. Moreover, after the cells were pretreated with or without inhibitors of the two pathways or with the mitophagy agonist, the levels of autophagy-related proteins and osteoclast markers were measured. CoQ10 significantly decreased the number of TRAP-positive cells and the level of ROS but had no significant impact on cell viability. The relative phosphorylation levels of PI3K, AKT, mTOR, ERK, and p38 were significantly reduced, but the levels of FOXO3/LC3/Beclin1 were significantly augmented. Moreover, the levels of FOXO3/LC3/Beclin1 were significantly increased by the inhibitors and mitophagy agonist, while the levels of osteoclast markers showed the opposite results. Our data showed that CoQ10 prevented RANKL-induced osteoclastogenesis by promoting autophagy via inactivation of the PI3K/AKT/mTOR and MAPK pathways in RAW264.7 cells. Q Q1 CoQ (CoQ10 determined process RAW2647 RAW RAW264 7 RAW264. NFκB NF κB RANKL (RANKL assessed CoQ1 andor HO H O H2O (ROS PI3KAKTmTOR PIKAKTmTOR PI3K AKT mTOR PI K tested Moreover agonist autophagyrelated related measured TRAPpositive TRAP positive PIK ERK p p3 reduced FOXO3LC3Beclin1 FOXOLCBeclin FOXO3 LC3 Beclin1 FOXO LC Beclin FOXO3/LC3/Beclin augmented results RANKLinduced induced (CoQ1 RAW26 KAKTmTOR FOXO3LC3Beclin (CoQ RAW2

25-hydroxycholesterol (25-HC) plays a role in the regulation of cell survival and immunity. However, the effect of 25-HC on myocardial ischemia/reperfusion (MI/R) injury remains unknown. Our present study aimed to investigate whether 25-HC aggravated MI/R injury through NLRP3 inflammasome-mediated pyroptosis. The overlapping differentially expressed genes (DEGs) in MI/R were identified from the GSE775, GSE45818, GSE58486, and GSE46395 datasets in Gene Expression Omnibus (GEO) database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted using the database of Annotation, Visualization and Integration Discovery (DAVID). The protein-protein interaction (PPI) network of the overlapping DEGs was established using the Search Tool for the Retrieval of Interacting Genes (STRING) database. These bioinformatics analyses indicated that cholesterol 25-hydroxylase (CH25H) was one of the crucial genes in MI/R injury. The oxygen-glucose deprivation/reoxygenation (OGD/R) cell model was established to simulate MI/R injury. Western blot and RT-qPCR analysis demonstrated that CH25H was significantly upregulated in OGD/R-stimulated H9C2 cardiomyocytes. Moreover, knockdown of CH25H inhibited the OGD/R-induced pyroptosis and nod-like receptor protein 3 (NLRP3) inflammasome activation, as demonstrated by cell counting kit-8 (CCK8), lactate dehydrogenase (LDH), RT-qPCR, and western blotting assays. Conversely, 25-HC, which is synthesized by CH25H, promoted activation of NLRP3 inflammasome in OGD/R-stimulated H9C2 cardiomyocytes. In addition, the NLRP3 inhibitor BAY11-7082 attenuated 25-HC-induced H9C2 cell injury and pyroptosis under OGD/R condition. In conclusion, 25-HC could aggravate OGD/R-induced pyroptosis through promoting activation of NLRP3 inflammasome in H9C2 cells. 25hydroxycholesterol hydroxycholesterol 25 25HC HC (25-HC immunity However ischemiareperfusion ischemia reperfusion MIR MI R (MI/R unknown NLRP inflammasomemediated mediated (DEGs GSE775 GSE GSE45818 GSE58486 GSE4639 GEO (GEO GO (GO KEGG (KEGG Annotation DAVID. DAVID . (DAVID) proteinprotein PPI (PPI STRING (STRING 25hydroxylase hydroxylase CHH CH H (CH25H oxygenglucose oxygen glucose deprivationreoxygenation deprivation reoxygenation OGDR OGD (OGD/R RTqPCR RT qPCR OGD/Rstimulated OGDRstimulated stimulated C H9C cardiomyocytes Moreover OGD/Rinduced OGDRinduced induced nodlike nod like (NLRP3 kit8 kit 8 kit- CCK8, CCK8 CCK , (CCK8) LDH, LDH (LDH) RTqPCR, qPCR, assays Conversely 25HC, HC, addition BAY117082 BAY BAY11 7082 BAY11-708 25HCinduced HCinduced condition conclusion cells 2 GSE77 GSE4581 GSE5848 GSE463 (DAVID Rstimulated Rinduced (NLRP (CCK8 (LDH BAY11708 BAY1 708 BAY11-70 GSE7 GSE458 GSE584 GSE46 (CCK BAY1170 70 BAY11-7 GSE45 GSE58 GSE4 BAY117 7 BAY11- GSE5

Expanding uterine masses can be the cause of pregnancy loss and add technical difficulties to uterus evacuation due to the intense anatomical distortion of the endocervical canal and uterine cavity. The literature is scarce in the peculiarities of the management of missed abortions in uterus with important distorted anatomies. We report a case of a primigravida patient who presented a rapid and expressive increase of abdominal volume due to a giant uterine mass, evolving to miscarriage. Ultrasound can be a useful tool, allowing visualization of the endocervical path and uterine cavity, helping to perform uterine evacuation in the presence of anatomical distortion without compromising the reproductive future. To the best of our knowledge, no such case has been previously reported. cavity anatomies mass miscarriage tool future knowledge reported

Variations in lipid profile have been observed in sickle cell disease (SCD) and understanding their relationship with disease severity is crucial. This study aimed to investigate the association of polymorphisms of the CETP gene and laboratory markers of disease severity with lipid profile in a pediatric population with SCD. Biochemical and anthropometric analyses and CETP and alpha-thalassemia genotyping were performed. The study included 133 children and adolescents with sickle cell anemia (SCA) or hemoglobin SC disease (SCC), in steady-state. The SCA and no hydroxyurea (no HU) groups had higher values of ApoB, total cholesterol, low-density lipoprotein cholesterol (LDL-C), and non-high-density lipoprotein cholesterol (non-HDL-C) compared to the SCC and HU groups. However, there were no significant differences in ApoA1 and HDL-C levels between the groups based on genotype. Furthermore, the groups with altered levels of ApoA1, HDL-C, and the triglyceride/HDL ratio exhibited lower hemoglobin (Hb) levels and higher white blood cell counts. Hb level was associated to HDL-C levels. Analysis of CETP gene variants showed that the minor alleles of rs3764261 (C>A), rs247616 (C>T), and rs183130 (C>T), as well as the TTA haplotype, are explanatory variables for HDL-C levels. These findings suggested that dyslipidemia in SCD, specifically related to HDL-C levels, may be influenced by individual genetic background. Additionally, further investigation is needed to determine if clinical manifestations are impacted by CETP gene variants. SCD (SCD crucial alphathalassemia alpha thalassemia performed 13 (SCA SCC, , (SCC) steadystate. steadystate steady state. state steady-state ApoB lowdensity low density LDLC, LDLC LDL C (LDL-C) nonhighdensity non high nonHDLC HDL (non-HDL-C However ApoA HDLC genotype Furthermore HDLC, C, triglycerideHDL triglyceride (Hb counts rs rs376426 C>A, CA C>A A (C>A) rs24761 C>T, CT C>T T (C>T) rs18313 haplotype background Additionally 1 (SCC (LDL-C rs37642 (C>A rs2476 (C>T rs1831 rs3764 rs247 rs183 rs376 rs24 rs18 rs37 rs2 rs1 rs3

Health literacy (HL) is defined as a cognitive and social skill that determines the motivation and ability of individuals to understand and use information to promote and maintain proper health. Inadequate HL has been associated with worse outcomes in diabetes control, poor self-care, and higher hospitalization rates for some chronic diseases. We hypothesized that HL influences the prevalence of diabetic retinopathy (DR) among individuals with type 2 diabetes mellitus (T2DM) and that inadequate glycemic control would mediate this association. This was a cross-sectional study carried out with 288 participants of the “Brazilian Diabetes Study” cohort. Inclusion criteria were people diagnosed with T2DM aged between 40 and 70 years and ability to read and write. In the adequate HL group, DR was found in 16.5% of participants and in the inadequate HL group, it was found in 32.8% (P=0.0081). Individuals with inadequate HL had a higher risk of having DR, and this association was still statistically significant after adjusting for HbA1c, low-density lipoprotein cholesterol, systolic blood pressure, and diastolic blood pressure. In conclusion, HL is related to DR without the mediation of classical clinical variables. (HL health selfcare, selfcare self care, care self-care diseases (DR TDM T DM (T2DM crosssectional cross sectional 28 Brazilian Study cohort 4 7 write group 165 16 5 16.5 328 32 8 32.8 P=0.0081. P00081 P P=0.0081 . 0 0081 (P=0.0081) HbA1c HbAc HbA c lowdensity low density cholesterol pressure conclusion variables 1 16. 3 32. P0008 P=0.008 008 (P=0.0081 P000 P=0.00 00 (P=0.008 P00 P=0.0 (P=0.00 P0 P=0. (P=0.0 P=0 (P=0. P= (P=0 (P= (P

Polystyrene nanoplastics (PS-NPs) are ubiquitous environmental pollutants that can cause oxidative stress in various organs, including the liver. Didymin is a dietary flavanone that displays multiple pharmacological activities. Therefore, the present study evaluated the palliative role of didymin against PS-NPs-induced hepatic damage in rats. Albino rats (n=48) were randomly distributed into 4 groups: control, PS-NPs treated group, PS-NPs + didymin co-administered group, and didymin supplemented group. After 30 days, PS-NPs intoxication lowered the expression of Nrf-2 and anti-oxidant genes [catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GSR), glutathione-S-transferase (GST), and heme oxygenase-1 (HO-1)], whereas the expression of KEAP1 kelch like ECH associated protein 1 (Keap-1) was increased. PS-NPs exposure also reduced the activities of anti-oxidants enzymes (CAT, SOD, GPx, GSR, GST, GSH, and OH-1), while malondialdehyde (MDA) and reactive oxygen species (ROS) levels were increased. The levels of alanine transaminase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were increased in PS-NPs-exposed rats. Moreover, inflammatory indices [interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), nuclear factor-kappa B (NF-κB), and cyclooxygenase-2 (COX-2)] were increased in PS-NPs-exposed rats. Furthermore, PS-NPs intoxication increased the expressions of apoptotic markers including Bax and Caspase-3, as well as reducing Bcl-2 expression. The histopathological analysis showed significant damage in PS-NPs-treated rats. However, didymin supplementation ameliorated all the PS-NPs-induced damage in the liver of rats. Therefore, it was concluded that didymin can act as a remedy against PS-NPs-induced liver toxicity due to its anti-apoptotic, anti-oxidant, and anti-inflammatory activities. PSNPs PS NPs (PS-NPs organs Therefore PSNPsinduced induced n=48 n48 n 48 (n=48 groups control group coadministered co administered 3 days Nrf2 Nrf 2 Nrf- antioxidant anti oxidant catalase CAT, CAT , (CAT) SOD (SOD) GPx (GPx) GSR (GSR) glutathioneStransferase S transferase GST (GST) oxygenase1 oxygenase oxygenase- HO1, HO1 HO (HO-1)] KEAP Keap1 Keap (Keap-1 antioxidants oxidants (CAT GSH OH1, OH1 OH OH-1) MDA (MDA ROS (ROS ALT, ALT (ALT) AST, AST (AST) ALP (ALP PSNPsexposed exposed Moreover interleukin1β interleukinβ interleukin 1β β IL1β, IL1β ILβ IL (IL-1β) TNFα, TNFα TNF α (TNF-α) interleukin6 6 interleukin- IL6, IL6 (IL-6) factorkappa kappa NFκB, NFκB NF κB (NF-κB) cyclooxygenase2 cyclooxygenase cyclooxygenase- COX2 COX (COX-2) Furthermore Caspase3, Caspase3 Caspase 3, Caspase-3 Bcl2 Bcl Bcl- PSNPstreated However antiapoptotic, antiapoptotic apoptotic, anti-apoptotic antioxidant, oxidant, antiinflammatory n=4 n4 (n=4 (SOD (GPx (GSR (GST (HO-1) (Keap- OH-1 (ALT (AST (IL-1β (TNF-α (IL-6 (NF-κB (COX-2 Caspase- n= (n= (HO-1 (Keap OH- (IL- (COX- (n (HO- (IL (COX (HO

Peri-implant disease (PID) is a general term for inflammatory diseases of soft and hard tissues that occur around implants, including peri-implant mucositis and peri-implantitis. Cytokines are a class of small molecule proteins, which have various functions such as regulating innate immunity, adaptive immunity, and repairing damaged tissues. In order to explore the characteristics and clinical significance of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-10, and tumor growth factor (TGF)-β1 expression levels in serum of patients with peri-implant disease, 31 patients with PID and 31 patients without PID were enrolled. The modified plaque index (mPLI), modified sulcus bleeding index (mSBI), and peri-implant probing depth (PD) were recorded. The levels of serum TNF-α, IL-6, IL-10, and TGF-β1 were detected by ELISA. TNF-α, mPLI, mSBI, and PD levels were significantly higher in the PID group. TGF-β1 levels were significantly higher in the control group. There was a significant positive correlation between TNF-α and mPLI, mSBI, and PD. TGF-β1 was negatively associated with TNF-α, mPLI, mSBI, and PD. Multiple logistic regression analysis showed that TNF-α and PD were risk factors for the severity of PID. The receiver operating curve analysis showed that high TNF-α levels (cut-off value of 140 pg/mL) and greater PD values (cut-off value of 4 mm) were good predictors of PID severity with an area under the curve of 0.922. These results indicated that TNF-α and PD can be used as a biological indicator for diagnosing the occurrence and progression of PID. Periimplant Peri implant (PID implants periimplant peri periimplantitis. periimplantitis implantitis. implantitis peri-implantitis proteins immunity TNFα, TNFα TNF α, α (TNF)-α IL6, IL6 IL 6, 6 (IL)-6 IL10, IL10 10, 10 IL-10 TGFβ1 TGFβ TGF β1 β (TGF)-β 3 enrolled mPLI , (mPLI) mSBI (mSBI) (PD recorded IL-6 TGF-β ELISA group cutoff cut off 14 pg/mL pgmL pg mL mm 0922 0 922 0.922 (IL)- IL1 1 IL-1 (mPLI (mSBI IL- 092 92 0.92 (IL) 09 9 0.9 (IL 0.