Abstract Sarcopenia is a pathology resulting from a progressive and severe loss of muscle mass, strength, and function in the course of aging, which has deleterious consequences on quality of life. Among the most widespread studies on the issue are those focused on the effect of different types of physical exercise on patients with sarcopenia. This randomized controlled study aimed to compare the effects of a whole-body vibration exercise (WBV) session on the inflammatory parameters of non-sarcopenic (NSG, n=22) and sarcopenic elderly (SG, n=22). NSG and SG participants were randomly divided into two protocols: intervention (squat with WBV) and control (squat without WBV). After a one-week washout period, participants switched protocols, so that everyone performed both protocols. Body composition was assessed by dual-energy radiological absorptiometry (DXA) and function through the six-minute walk test (6MWD) and Short Physical Performance Battery (SPPB). Plasma soluble tumor necrosis factor receptors (sTNFR) were determined by enzyme-linked immunosorbent assay (ELISA) and measured before and immediately after each protocol. After exercise with WBV, there was an increase in sTNFR2 levels in the NSG (P<0.01; d=-0.69 (-1.30; -0.08) and SG (P<0.01, d=-0.95 (-1.57; -0.32) groups. In conclusion, an acute session of WBV influenced sTNFr2 levels, with sarcopenic individuals showing a greater effect. This suggested that WBV had a more pronounced impact on sTNFr2 in those with loss of muscle strength and/or physical performance. Additionally, WBV is gaining recognition as an efficient strategy for those with persistent health issues. mass aging life sarcopenia wholebody whole body (WBV nonsarcopenic non NSG, (NSG n=22 n22 n 22 SG, (SG n=22. . protocols squat WBV. oneweek one week period dualenergy dual energy DXA (DXA sixminute six minute 6MWD MWD (6MWD SPPB. SPPB (SPPB) sTNFR (sTNFR enzymelinked enzyme linked ELISA (ELISA protocol P<0.01 P001 P 0 01 (P<0.01 d=0.69 d069 d d= 0.69 69 d=-0.6 1.30 130 1 30 (-1.30 0.08 008 08 -0.08 P<0.01, d=0.95 d095 0.95 95 d=-0.9 1.57 157 57 (-1.57 0.32 032 32 -0.32 groups conclusion sTNFr andor or performance Additionally issues n=2 n2 2 (SPPB P<0.0 P00 (P<0.0 d=0.6 d06 069 0.6 6 d=-0. 1.3 13 3 (-1.3 0.0 00 -0.0 d=0.9 d09 095 0.9 9 1.5 15 5 (-1.5 0.3 03 -0.3 n= P<0. P0 (P<0. d=0. d0 06 0. d=-0 1. (-1. -0. 09 P<0 (P<0 d=0 d=- (-1 -0 P< (P< (- - (P (

This study investigated the effects of a foot core intervention on the coordination of foot joints in recreational runners. This was a secondary analysis from a randomized controlled trial conducted with 87 recreational runners allocated to the control group (CG), which followed a placebo lower limb stretching protocol, or the intervention group (IG), which underwent an 8-week (3 times/week) foot core training. The participants ran on a force-instrumented treadmill at a self-selected speed (9.5-10.5 km/h) while the foot segment motion was captured. The vector coding technique was used to assess inter-joint coordination for four selected coupled segment and joint angles. The coordination patterns of the calcaneus and midfoot (CalMid) and midfoot and metatarsus (MidMet) joint pairs were affected. In the frontal plane, IG showed an in-phase with proximal dominancy coordination at heel strike, with a decrease in its frequency after the training (P=0.018), suggesting a longer foot supination. Additionally, IG showed an anti-phase with distal dominancy pattern at early stance compared to CG due to a smaller but earlier inversion of the CalMid-MidMet pair (P=0.020). The intervention also had an effect on the transverse plane of the CalMid-MidMet pair, with IG showing a significantly greater frequency of anti-phase coordination with proximal dominancy during propulsion than CG (P=0.013), probably due to a reduction in the CalMid abduction. Overall, the results suggested that the foot core intervention reduces the occurrence of running-related injuries by increasing the resistance to calcaneus pronation and building a more rigid and efficient lever during push-off. 8 CG, , (CG) protocol IG, (IG) 8week week 3 ( times/week timesweek times forceinstrumented force instrumented selfselected self 9.510.5 95105 9.5 10.5 9 5 10 (9.5-10. km/h kmh km h captured interjoint inter angles (CalMid MidMet (MidMet affected inphase phase strike P=0.018, P0018 P P=0.018 0 018 (P=0.018) supination Additionally antiphase anti CalMidMidMet P=0.020. P0020 P=0.020 . 020 (P=0.020) P=0.013, P0013 P=0.013 013 (P=0.013) abduction Overall runningrelated running related pushoff. pushoff push off. off push-off (CG (IG 510 9.510. 9510 95 9. 105 10. 1 (9.5-10 P001 P=0.01 01 (P=0.018 P002 P=0.02 02 (P=0.020 (P=0.013 51 9.510 951 (9.5-1 P00 P=0.0 (P=0.01 (P=0.02 9.51 (9.5- P0 P=0. (P=0.0 (9.5 P=0 (P=0. (9. P= (P=0 (9 (P= (P

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 (

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

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

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

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

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

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,

The treatment of arterial hypertension (AH) contributes to the reduction of morbidity and mortality. Gender differences are likely to play a role, as non-treatment is associated with clinical and sociodemographic aspects. The aim of this study was to investigate the factors associated with non-treatment of AH and gender differences in hypertensive individuals from the ELSA-Brasil cohort. The study was conducted with 5,743 baseline hypertensive cohort participants. AH was considered if there was a previous diagnosis or if systolic blood pressure (SBP) was ≥140 and/or diastolic BP (DBP) was ≥90 mmHg. Sociodemographic and anthropometric data, lifestyle, comorbidities, and use of antihypertensive medications were evaluated through interviews and in-person measurements. Treatment with renin-angiotensin-aldosterone system inhibitors (RAASi) or other antihypertensive medications and non-treatment were evaluated with multivariate logistic regression. Non-treatment was observed in 32.8% of hypertensive individuals. Of the 67.7% treated individuals, 41.1% received RAASi. Non-treatment was associated with alcohol consumption in women (OR=1.41; 95%CI: 1.15-1.73; P=0.001), lowest schooling level in men (OR=1.70; 95%CI: 1.32-2.19; P<0.001), and younger age groups in men and women (strongest association in males aged 35-44 years: OR=4.58, 95%CI: 3.17-6.6, P<0.001). Among those using RAASi, a higher proportion of white, older individuals, and with more comorbidities was observed. The high percentage of non-treatment, even in this civil servant population, indicated the need to improve the treatment cascade for AH. Public health policies should consider giving special attention to gender roles in groups at higher risk of non-treatment to reduce inequities related to AH in Brazil. (AH mortality role nontreatment non aspects ELSABrasil ELSA Brasil 5743 5 743 5,74 participants SBP (SBP 140 ≥14 andor DBP (DBP 90 ≥9 mmHg data lifestyle inperson person measurements reninangiotensinaldosterone renin angiotensin aldosterone RAASi (RAASi regression Nontreatment Non 328 32 8 32.8 677 67 7 67.7 411 41 1 41.1 OR=1.41 OR141 OR (OR=1.41 95%CI 95CI CI 95 1.151.73 115173 1.15 1.73 15 73 1.15-1.73 P=0.001, P0001 P P=0.001 , 0 001 P=0.001) OR=1.70 OR170 70 (OR=1.70 1.322.19 132219 1.32 2.19 2 19 1.32-2.19 P<0.001, P<0.001 P<0.001) strongest 3544 35 44 35-4 years OR458 4 58 OR=4.58 3.176.6, 31766 3.17 6.6, 3 17 6 3.17-6.6 P<0.001. . white nontreatment, treatment, population Brazil 574 74 5,7 14 ≥1 9 ≥ 32. 67. 41. OR=1.4 OR14 (OR=1.4 151 1.151.7 11517 115 1.1 173 1.7 1.15-1.7 P000 P=0.00 00 OR=1.7 OR17 (OR=1.7 322 1.322.1 13221 132 1.3 219 2.1 1.32-2.1 P<0.00 354 35- OR45 OR=4.5 176 3.176.6 3176 317 3.1 66 6.6 3.17-6. 57 5, OR=1. OR1 (OR=1. 1.151. 1151 11 1. 1.15-1. P00 P=0.0 1.322. 1322 13 21 2. 1.32-2. P<0.0 OR4 OR=4. 3.176. 31 3. 6. 3.17-6 OR=1 (OR=1 1.151 1.15-1 P0 P=0. 1.322 1.32-2 P<0. OR=4 3.176 3.17- OR= (OR= 1.15- P=0 1.32- P<0 (OR P= P<

“Penumbra sign” is a characteristic finding in magnetic resonance imaging (MRI) of Brodie's abscess, a rare variant of subacute osteomyelitis. We aimed to discuss the imaging finding penumbra sign that will help in the diagnosis of osteomyelitis and may be useful to clinicians in differential diagnosis. A 26-year-old male patient presented to the emergency department with complaints of pain and limping in the right knee that did not go away. He had a history of arthroscopic debridement and percutaneous fixation surgery due to osteochondral fragment 3 years ago. There were no additional findings in the patient's vital parameters, physical examination, and medical history. X-ray imaging revealed two screws in the distal femur and a well-defined sclerotic rim surrounding a radiolucent lesion anterior to the screws. MRI revealed a lesion in the distal femoral metaphysis with low-density fluid and hyperintense granulation tissue surrounding it. After surgical abscess drainage and local debridement, bone cement was placed in the resulting cavity. Teicoplanin treatment was started. The patient was discharged and complete recovery was achieved in the second month. The diagnosis of osteomyelitis is often missed or confused with bone tumors in non-traumatic cases presenting with persistent bone pain. MRI imaging is frequently used in differential diagnosis, and detection of characteristic imaging signs such as the penumbra sign accelerates the diagnosis. In this context, emergency department clinicians, in particular, should be cautious and not forget that early treatment can be started by recognizing these signs. Penumbra (MRI Brodies Brodie s 26yearold yearold 26 year old away ago patients parameters examination Xray X ray welldefined well defined lowdensity low density it cavity month nontraumatic non traumatic context particular 2

This study aimed to analyze the safety and applicability of a 90-min duration of infusion (SDI) of obinutuzumab in patients with B-cell non-Hodgkin's lymphoma (NHL) in a tertiary hospital in China. This exploratory clinical trial was performed at Jiangsu Province Hospital. All patients were treated with the standard infusion regimen for the first infusion. If no grade ≥3 infusion-related reactions (IRRs) occurred, the subsequent infusions were given as SDI. The primary endpoint was the incidence of IRR during the standard infusion (3-4 h) and 90-min SDI regimens. This study enrolled 208 patients and all completed cycle 1. Forty-one patients (19.71%) had IRRs: five (2.40%) with grade 1, twenty-eight (13.46%) with grade 2, and eight (3.85%) with grade 3. The 41 patients had 71 IRRs, mainly fever (40.85%), chest pain/tightness (12.68%), and dyspnea (9.86%). The occurrence of IRRs in the first infusion was significantly lower in patients who received oral acetaminophen prophylaxis than those who did not (10.72% vs 30.21%, P<0.001). For the subsequent cycles with 90-min SDI, only two (0.25%) IRRs occurred among 814 infusions (one grade 1 hand numbness and one grade 2 chill/fever). The 90-min obinutuzumab SDI might be safe and feasible in patients with B-cell NHL in China. 90min min 90 (SDI Bcell B cell nonHodgkins non Hodgkin s (NHL China Hospital 3 ≥ infusionrelated related (IRRs 34 4 (3- h regimens 20 Fortyone Forty 19.71% 1971 19 (19.71% 2.40% 240 40 (2.40% twentyeight twenty 13.46% 1346 13 46 (13.46% 3.85% 385 85 (3.85% 7 40.85%, 4085 40.85% , (40.85%) paintightness pain tightness 12.68%, 1268 12.68% 12 68 (12.68%) 9.86%. 986 9.86% . 9 86 (9.86%) 10.72% 1072 10 72 (10.72 3021 30 21 30.21% P<0.001. P0001 P P<0.001 0 001 P<0.001) 0.25% 025 25 (0.25% 81 chill/fever. chillfever chill/fever chill chill/fever) (3 19.71 197 (19.71 2.40 24 (2.40 13.46 134 (13.46 3.85 38 8 (3.85 408 40.85 (40.85% 126 12.68 6 (12.68% 98 9.86 (9.86% 10.72 107 (10.7 302 30.21 P000 P<0.00 00 0.25 02 (0.25 ( 19.7 (19.7 2.4 (2.4 13.4 (13.4 3.8 (3.8 40.8 (40.85 12.6 (12.68 9.8 (9.86 10.7 (10. 30.2 P00 P<0.0 0.2 (0.2 19. (19. 2. (2. 13. (13. (3. 40. (40.8 12. (12.6 9. (9.8 10. (10 30. P0 P<0. 0. (0. (19 (2 (13 (40. (12. (9. (1 P<0 (0 (40 (12 (9 P< (4

This study was conducted to evaluate how sterubin affects rotenone-induced Parkinson's disease (PD) in rats. A total of 24 rats were distributed into 4 equal groups: normal saline control and rotenone control were administered saline or rotenone (ROT), respectively, orally; sterubin 10 received ROT + sterubin 10 mg/kg po; and sterubin alone was administered to the test group (10 mg/kg). Rats of the normal saline and sterubin alone groups received sunflower oil injection (sc) daily, 1 h after receiving the treatments cited above, while rats of the other groups received rotenone injection (0.5 mg/kg, sc). The treatment was continued over the course of 28 days daily. On the 29th day, catalepsy and akinesia were assessed. The rats were then euthanized, and the brain was extracted for estimation of endogenous antioxidants (MDA: malondialdehyde, GSH: reduced glutathione, CAT: catalase, SOD: superoxide dismutase), nitrative (nitrite) stress markers, neuroinflammatory cytokines, and neurotransmitter levels and their metabolites (3,4-dihydroxyphenylacetic acid (DOPAC), dopamine (DA), norepinephrine (NE), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid (HVA)). Akinesia and catatonia caused by ROT reduced the levels of endogenous antioxidants (GSH, CAT, and SOD), elevated the MDA level, and altered the levels of nitrites, neurotransmitters, and their metabolites. Sterubin restored the neurobehavioral deficits, oxidative stress, and metabolites of altered neurotransmitters caused by ROT. Results demonstrated the anti-Parkinson's activities of sterubin in ROT-treated rats. rotenoneinduced induced Parkinsons Parkinson s PD (PD 2 ROT, , (ROT) respectively orally mgkg mg kg po (1 mg/kg. . mg/kg) sc (sc daily above 0.5 05 0 5 (0. sc. sc) th day assessed euthanized (MDA malondialdehyde GSH glutathione CAT catalase SOD dismutase, dismutase dismutase) nitrite (nitrite markers cytokines 3,4dihydroxyphenylacetic 34dihydroxyphenylacetic dihydroxyphenylacetic 3,4 3 DOPAC, DOPAC (DOPAC) DA, DA (DA) NE, NE (NE) 5HT, 5HT HT (5-HT) 5hydroxyindoleacetic hydroxyindoleacetic 5HIAA, 5HIAA HIAA (5-HIAA) HVA. HVA (HVA)) GSH, (GSH SOD, SOD) level nitrites deficits antiParkinsons anti ROTtreated treated (ROT ( 0. (0 4dihydroxyphenylacetic 34 3, (DOPAC (DA (NE (5-HT (5-HIAA (HVA) (HVA