Development and validation of a risk score model for predicting autism based on pre- and perinatal factors.

Background: The use of pre- and perinatal risk factors as predictive factors may lower the age limit for reliable autism prediction. The objective of this study was to develop a clinical model based on these risk factors to predict autism. Methods: A stepwise logistic regression analysis was conducted to explore the relationships between 28 candidate risk factors and autism risk among 615 Han Chinese children with autism and 615 unrelated typically developing children. The significant factors were subsequently used to create a clinical risk score model. A chi-square automatic interaction detector (CHAID) decision tree was used to validate the selected predictors included in the model. The predictive performance of the model was evaluated by an independent cohort. Results: Five factors (pregnancy influenza-like illness, pregnancy stressors, maternal allergic/autoimmune disease, cesarean section, and hypoxia) were found to be significantly associated with autism risk. A receiver operating characteristic (ROC) curve indicated that the risk score model had good discrimination ability for autism, with an area under the curve (AUC) of 0.711 (95% CI=0.679-0.744); in the external validation cohort, the model showed slightly worse but overall similar predictive performance. Further subgroup analysis indicated that a higher risk score was associated with more behavioral problems. The risk score also exhibited robustness in a subgroup analysis of patients with mild autism. Conclusion: This risk score model could lower the age limit for autism prediction with good discrimination performance, and it has unique advantages in clinical application.

miR-548ag promotes DPP4 expression in hepatocytes through activation of TLR(7/8)/NF-κB pathway.

OBJECTIVE: In our previous study, we identified a notable increase in miR-548ag content after obesity, which contributes to the progression of Type 2 diabetes Mellitus(T2DM) through the up-regulation of Dipeptidyl Peptidase-4(DPP4) expression within the liver. However, the precise molecular mechanisms underlying the upregulation of DPP4 by miR-548ag remain elusive. Mature miRNAs rich in GU sequences can activate the TLR(7/8)/NF-κB signalling pathway, which transcriptionally activates DPP4 expression. Notably, the proportion of GU sequences in hsa-miR-548ag was found to be 47.6%. The study proposes a hypothesis suggesting that miR-548ag could potentially increase DPP4 expression in hepatocytes by activating the TLR(7/8)/NF-κB signalling pathway. METHODS: Male C57BL/6J mice were fed normal chow diet (NCD, n = 16) or high-fat diet (HFD, n = 16) for 12 weeks. For a duration of 6 weeks, NCD mice received intraperitoneal injections of a miR-548ag mimic, while HFD mice and db/db mice (n = 16) were administered intraperitoneal injections of a miR-548ag inhibitor. qRT-PCR and Western Blot were used to detect the expression level of miR-548ag, DPP4 and the activation of TLR(7/8)/NF-κB signalling pathway. HepG2 and L02 cells were transfected with miR-548ag mimic, miR-548ag inhibitor, TLR7/8 interfering fragment, and overexpression of miR-548ag while inhibiting TLR7/8, respectively. RESULTS: (1) We observed elevated levels of miR-548ag in the serum, adipose tissue, and liver of obese mice, accompanied by an upregulation of TLR7/8, pivotal protein in the NF-κB pathway, and DPP4 expression in the liver. (2) miR-548ag promotes DPP4 expression in hepatocytes via the TLR(7/8)/NF-κB signalling pathway, resulting in a reduction in the glucose consumption capacity of hepatocytes. (3) The administration of a miR-548ag inhibitor enhanced glucose tolerance and insulin sensitivity in db/db mice. CONCLUSIONS: MiR-548ag promotes the expression of DPP4 in hepatocytes by activating the TLR(7/8)/NF-κB signalling pathway. MiR-548ag may be a potential target for the treatment of T2DM.

Association of saturated fatty acids with cancer risk: a systematic review and meta-analysis.

OBJECTIVE: Extensive research has explored the link between saturated fatty acids (SFAs) and cardiovascular diseases, alongside other biological dysfunctions. Yet, their association with cancer risk remains a topic of debate among scholars. The present study aimed to elucidate this association through a robust meta-analysis. METHODS: PubMed, Embase, Cochrane Library, and Web of Science databases were searched systematically to identify relevant studies published until December 2023. The Newcastle-Ottawa Scale was used as the primary metric for evaluating the quality of the included studies. Further, fixed- or random-effects models were adopted to determine the ORs and the associated confidence intervals using the Stata15.1 software. The subsequent subgroup analysis revealed the source of detection and the cancer types, accompanied by sensitivity analyses and publication bias evaluations. RESULTS: The meta-analysis incorporated 55 studies, comprising 38 case-control studies and 17 cohort studies. It revealed a significant positive correlation between elevated levels of total SFAs and the cancer risk (OR of 1.294; 95% CI: 1.182-1.416; P-value less than 0.001). Moreover, elevated levels of C14:0, C16:0, and C18:0 were implicated in the augmentation of the risk of cancer. However, no statistically significant correlation of the risk of cancer was observed with the elevated levels of C4:0, C6:0, C8:0, C10:0, C12:0, C15:0, C17:0, C20:0, C22:0, and C24:0. Subgroup analysis showed a significant relationship between excessive dietary SFA intake, elevated blood SFA levels, and heightened cancer risk. Increased total SFA levels correlated with higher risks of breast, prostate, and colorectal cancers, but not with lung, pancreatic, ovarian, or stomach cancers. CONCLUSION: High total SFA levels were correlated with an increased cancer risk, particularly affecting breast, prostate, and colorectal cancers. Higher levels of specific SFA subtypes (C14:0, C16:0, and C18:0) are also linked to an increased cancer risk. The findings of the present study would assist in providing dietary recommendations for cancer prevention, thereby contributing to the development of potential strategies for clinical trials in which diet-related interventions would be used in combination with immunotherapy to alter the levels of SFAs in patients and thereby improve the outcomes in cancer patients. Nonetheless, further high-quality studies are warranted to confirm these associations.

KLF7 promotes adipocyte inflammation and glucose metabolism disorder by activating the PKCζ/NF-κB pathway.

In the obesity context, inflammatory cytokines secreted by adipocytes lead to insulin resistance and are key to metabolic syndrome development. In our previous study, we found that the transcription factor KLF7 promoted the expression of p-p65 and IL-6 in adipocytes. However, the specific molecular mechanism remained unclear. In the present study, we found that the expression of KLF7, PKCζ, p-IκB, p-p65, and IL-6 in epididymal white adipose tissue (Epi WAT) in mice fed a high-fat diet (HFD) was significantly increased. In contrast, the expression of PKCζ, p-IκB, p-p65, and IL-6 was significantly decreased in Epi WAT of KLF7 fat conditional knockout mice. In 3T3-L1 adipocytes, KLF7 promoted the expression of IL-6 via the PKCζ/NF-κB pathway. In addition, we performed luciferase reporter and chromatin immunoprecipitation assays, which confirmed that KLF7 upregulated the expression of PKCζ transcripts in HEK-293T cells. Collectively, our results show that KLF7 promotes the expression of IL-6 by upregulating PKCζ expression and activating the NF-κB signaling pathway in adipocytes.

Stress-inducible IL-6 is regulated by KLF7 in brown adipocytes.

Stress-inducible interleukin 6 (IL-6) is generated in brown adipocytes via beta-3 adrenergic receptor (ADRB3) signaling, which is necessary in stress hyperglycemia, the kind of metabolic adaptation enabling "fight or flight" response by means of liver gluconeogenesis. Nevertheless, the mechanism of ADRB3 signaling mediates IL-6 in brown adipocytes remains unclear. As a result, it is critical to understand how brown adipocytes produce IL-6 via ADRB3 signaling. We found that the ADRB3 agonist and cold stimulation promoted the expression of KLF7 and IL-6 in brown adipocytes of mice. In parallel to these results in vivo, treatment with ADRB3 agonist promoted the expression of KLF7 and the release of IL-6 in primary brown adipocytes of mice. Notably, we discovered that KLF7 positively controls the expression of IL-6 and downregulated KLF7 largely blunted ADRB3 agonist induced IL-6 expressions in brown adipocytes. Our findings suggest that KLF7 is required for the generation of IL-6 when ADRB3 signaling is activated in brown adipocytes.

Hepatic Glucose Metabolism Disorder Induced by Adipose Tissue-Derived miR-548ag via DPP4 Upregulation.

The present study aimed to explore the molecular mechanism underlying the regulation of glucose metabolism by miR-548ag. For the first time, we found that miR-548ag expression was elevated in the abdominal adipose tissue and serum of subjects with obesity and type 2 diabetes mellitus (T2DM). The conditional knockout of adipose tissue Dicer notably reduced the expression and content of miR-548ag in mouse adipose tissue, serum, and liver tissue. The combined use of RNAseq, an miRNA target gene prediction software, and the dual luciferase reporter assay confirmed that miR-548ag exerts a targeted regulatory effect on DNMT3B and DPP4. miR-548ag and DPP4 expression was increased in the adipose tissue, serum, and liver tissue of diet-induced obese mice, while DNMT3B expression was decreased. It was subsequently confirmed both in vitro and in vivo that adipose tissue-derived miR-548ag impaired glucose tolerance and insulin sensitivity by inhibiting DNMT3B and upregulating DPP4. Moreover, miR-548ag inhibitors significantly improved the adverse metabolic phenotype in both obese mice and db/db mice. These results revealed that the expression of the adipose tissue-derived miR-548ag increased in obese subjects, and that this could upregulate the expression of DPP4 by targeting DNMT3B, ultimately leading to glucose metabolism disorder. Therefore, miR-548ag could be utilized as a potential target in the treatment of T2DM.

Solid-in-oil nanodispersion as a novel topical transdermal delivery to enhance stability and skin permeation and retention of hydrophilic drugs l-ascorbic acid.

l-ascorbic acid （Vitamin C, VC） is the most abundant antioxidant in human skin. But its poor penetration into the skin and unstability limit the application. The aim of the study was to promote the topical skin permeation and retention of VC, increase the stability as well as effectiveness by a novel solid in oil nanodispersion. In the nanodispersions system, nano-sized particles of hydrophilic molecules are dispersed in an oil vehicle with the assistance of hydrophobic surfactants. The optimized formula composed of O170 and S1570 (12.5:1, w/w) showed high EE% of 98% and good stability. FTIR analysis confirmed that there may be hydrogen bond between VC and surfactants. The results of DSC, and XRD revealed that the drug was successfully encapsulated in the surfactants, which maintained the stability of drug. By analyzing and fitting the release data in vitro, the drug release mechanism of SONDs was predicted as a multi-dynamic model. Skin permeation of VC was improved 3.43-fold for SONDs compared with VC aqueous solution, highlighting that the lipophilicity and nano size of the carrier more easily penetrated into the skin. Finally, the photoaging study revealed that topical application of VC-SONDs provided the highest skin protection compared UV and VC aqueous solution treated group which was evident by the normal thick epidermal morphology, no obvious melanocytes and the densely arranged dermal elastic fibers. These results demonstrated that the solid-in-oil nanodispersions may be a potential transdermal delivery system for hydrophilic bioactive ingredients.

Purine signaling pathway dysfunction in autism spectrum disorders: Evidence from multiple omics data.

Introduction: Previous studies have suggested that the dysregulation of purine metabolism may be associated with autism spectrum disorder (ASD). Here, we adopted metabolomics and transcriptomics to verify and explore the underlying molecular mechanism of purine metabolism dysfunction in ASD and identify potential biomarkers within the purine metabolism pathway. Methods: Ultra-high-performance liquid chromatography-mass spectrometry was used to obtain the plasma metabolic profiles of 12 patients with ASD and 12 typically developing (TD) children. RNA sequencing was used to screen differentially expressed genes related to the purine metabolic pathway and purine receptor-coding genes in 24 children with ASD and 21 healthy controls. Finally, serum uric acid levels were compared in 80 patients with ASD and 174 TD children to validate the omics results. Results: A total of 66 identified metabolites showed significant between-group differences. Network analysis showed that purine metabolism was the most strongly enriched. Uric acid was one of the most highlighted nodes within the network. The transcriptomic study revealed significant differential expression of three purine metabolism-related genes (adenosine deaminase, adenylosuccinate lyase, and bifunctional enzyme neoformans 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) transformylase/inosine monophosphate (IMP) cyclohydrolase) (p < 0.01) and five purinergic receptor genes (P2X7, P2Y2, P2Y6, P2Y8, and P2Y10) (p < 0.05). In the validation sample, there was a significant difference in serum uric acid levels between the two groups (p < 0.001), and the area under the curve for uric acid was 0.812 (sensitivity, 82.5%; specificity, 63.8%). Discussion: Patients with ASD had dysfunctional purine metabolic pathways, and blood uric acid may be a potential biomarker for ASD.

Clinical outcomes of mild versus moderate hypothermic circulatory arrest with antegrade cerebral perfusion in adult aortic arch surgery: A systematic review and meta-analysis.

OBJECTIVES: In adult aortic arch surgery, moderate hypothermic circulatory arrest (HCA) with selective antegrade cerebral perfusion (SACP) (MoHACP) is widely used, but the application of mild HCA with SACP (MiHACP) is still controversial. This meta-analysis aimed to compare clinical outcomes using MiHACP or MoHACP. METHODS: Studies comparing outcomes of MiHACP or MoHACP in adult aortic arch surgery were searched from four databases from inception through April 2022. Primary outcomes were postoperative permanent neurological deficit (PND), temporary neurological deficit (TND), and mortality. Secondary outcomes included other common complications. Meta-analysis was conducted using a random-effects model in all cases. RESULTS: Eleven comparative studies were included, with 1555 patients in MiHACP group and 1499 patients in MoHACP group, and the mean HCA temperature were 29.4°C and 24.8°C, respectively. Postoperative PND, TND, mortality, paraplegia, dialysis, tracheotomy, reexploration for bleeding, and chest tube drainage volume were comparable in the two groups (p > 0.05). Ventilator time, intensive care unit and in-hospital length of stay were shorter in MiHACP group (p < 0.05). Outcomes were also comparable or had some benefits in MiHACP group when subgroup analyses were conducted according to hemiarch or total arch replacement, unilateral or bilateral SACP, HCA time, emergency aortic dissection surgery, and concomitant procedure. CONCLUSION: The present meta-analysis showed acceptability of MiHACP in adult aortic arch surgery. Results need to be taken with caution as moderate risk of bias and very low quality of evidence were observed in this meta-analysis. Randomized controlled trials are needed for further analysis.

Risk factors for acute kidney injury after Stanford type A aortic dissection repair surgery: a systematic review and meta-analysis.

Background: Risk factors for acute kidney injury (AKI) after Stanford type A aortic dissection (TAAD) repair are inconsistent in different studies. This meta-analysis systematically analyzed the risk factors so as to early identify the therapeutic targets for preventing AKI.Methods: Studies exploring risk factors for AKI after TAAD repair were searched from four databases from inception to June 2022. The synthesized incidence and risk factors of AKI and its impact on mortality were calculated.Results: Twenty studies comprising 8223 patients were included. The synthesized incidence of postoperative AKI was 50.7%. Risk factors for AKI included cardiopulmonary bypass (CPB) time >180 min [odds ratio (OR), 4.89, 95% confidence interval (CI), 2.06-11.61, I2 = 0%], prolonged operative time (>7 h) (OR, 2.73, 95% CI, 1.95-3.82, I2 = 0), advanced age (per 10 years) (OR, 1.34, 95% CI, 1.21-1.49, I2 = 0], increased packed red blood cells (pRBCs) transfusion perioperatively (OR, 1.09, 95% CI, 1.07-1.11, I2 = 42%), elevated body mass index (per 5 kg/m2) (OR, 1.23, 95% CI, 1.18-1.28, I2 = 42%) and preoperative kidney injury (OR, 3.61, 95% CI, 2.48-5.28, I2 = 45%). All results were meta-analyzed using fixed-effects model finally (p < 0.01). The in-hospital or 30-day mortality was higher in patients with postoperative AKI than in that without AKI [risk ratio (RR), 3.12, 95% CI, 2.54-3.85, p < 0.01].Conclusions: AKI after TAAD repair increased the in-hospital or 30-day mortality. Reducing CPB time and pRBCs transfusion, especially in elderly or heavier weight patients, or patients with preoperative kidney injury were important to prevent AKI after TAAD repair surgery.

Alkyl group-decorated g-C3N4 for enhanced gas-phase CO2 photoreduction.

With excellent physical/chemical stability and feasible synthesis, g-C3N4 has attracted much attention in the field of photocatalysis. However, its weak photoactivity limits its practical applications. Herein, by easily planting hydrophobic alkyl groups onto g-C3N4, the hydrophilicity of g-C3N4 can be well regulated and its specific surface area be enlarged simultaneously. Such a modification ensures enhanced CO2 capture and increased active sites. In addition, the introduction of alkyl groups endows g-C3N4 with abundant charge density and efficient separation of photoinduced excitons. All these advantages synergistically contribute to the enhanced photocatalytic CO2 reduction performance over the optimized catalyst (DCN90), and the total CO2 conversion is 7.4-fold that of pristine g-C3N4 (CN).

Plasma interleukin-6 is a potential predictive biomarker for postoperative delirium among acute type a aortic dissection patients treated with open surgical repair.

OBJECTIVES: The relationship between inflammatory cytokines and postoperative delirium (POD) remains to be further investigated, especially in patients undergoing acute type A aortic dissection (AAD). Interleukin-6 (IL-6) is involved in the inflammatory process and has recently been identified as a biomarker of cerebral dysfunction. We explored the hypothesis that IL-6 was one of the critical causes of POD after surgical repair of AAD. METHODS: Plasma IL-6 was measured using electrochemiluminescence technology in patients preoperatively and 24 h, 48 h, and 72 h after surgical repair of acute type A aortic dissection. After the first three postoperative days, delirium was evaluated twice daily using the Confusion Assessment Method. ROC curves were used to evaluate the ability of IL-6 measurements to distinguish POD. RESULTS: The incidence of POD was 14.03% (31 of 221 patients). The patients in the POD group were significantly older than the patients in the non-POD group (56.48 ± 11.68 years vs 52.22 ± 10.50 years, P = 0.040). Plasma IL-6 concentrations were significantly higher in the POD group than in the non-POD group at three time points: preoperatively, after 24 h, and after 48 h. The AUC values corresponding to IL-6 preoperatively and 24 h after surgery were 0.73 and 0.72, respectively. CONCLUSIONS: Cerebral dysfunction after the surgical repair of AAD shows elevated stress levels and inflammatory responses. Plasma IL-6 is a potential biomarker to predict the onset of POD in acute type A aortic dissection patients following surgical repair.

Establishment and effect evaluation of an aortic dissection model induced by different doses of ß-aminopropionitrile in rats.

INTRODUCTION: Given the controversy regarding the appropriate dose of ß-aminopropionitrile for induction of aortic dissection models in rats, the purpose of this study was to explore the most suitable concentration of ß-aminopropionitrile to establish a high-incidence and low-mortality aortic dissection model. METHODS: Eighty three-week-old male Sprague-Dawley rats were equally divided into four groups: a control group, a 0.06% ß-aminopropionitrile group, a 0.08% ß-aminopropionitrile group and a 0.1% ß-aminopropionitrile group. Initial experiments were performed on the control group, which was not treated with ß-aminopropionitrile (and drank water freely), and the other three groups, which were given different concentrations of ß-aminopropionitrile solution daily (0.06%, 0.08% and 0.1%). Subsequently, on the 40th day, osmotic minipumps administering 1 µg/kg per min angiotensin II (Ang II) were implanted subcutaneously into the ß-aminopropionitrile groups, while the control group was continuously pumped with normal saline. The rats were euthanized 48 h after implantation. All rats that died before the expected end time of the experiment were autopsied immediately, and the aortas were dissected. The rats surviving at the end of the experiment were sacrificed by an overdose of sodium pentobarbital, and tissue samples were harvested for further analyses. RESULTS: The mean survival days were significantly different among the groups, with 39.1 ± 6.04 days in the 0.08% ß-aminopropionitrile group and 32.7 ± 9.85 days in the 0.1% ß-aminopropionitrile group (P = 0.0178) at the end of the experiment. Compared with those in the 0.06% ß-aminopropionitrile group, the rates of aortic dissection were significantly higher in the 0.08% ß-aminopropionitrile group and the 0.1% ß-aminopropionitrile group (P = 0.0015 and P = 0.0005, respectively), while there was no significant difference between the 0.08% ß-aminopropionitrile group and the 0.1% ß-aminopropionitrile group (P = 0.723) at 70% and 75%, respectively. However, the rupture rates were significantly different between the 0.08% ß-aminopropionitrile group and the 0.1% ß-aminopropionitrile group (55% versus 20%, P = 0.022). Hematoxylin-eosin staining of the aortic tissue sections of the ß-aminopropionitrile group showed that red blood cells entered the pseudocavity in the vascular wall, while the vascular wall structure of the control group was intact. Compared with control rats, which were intact and free from fracture, ß-aminopropionitrile-treated rats had fewer collagen fibers and exhibited fracture. Magnetic resonance imaging showed that the aortic intimae of the aortic dissection rats showed double lumens and intimal tears. CONCLUSIONS: An aortic dissection model with a high incidence and low mortality was successfully and stably developed with 0.08% ß-aminopropionitrile. This model will enable further studies investigating aortic dissection pathogenesis and drug therapy. Magnetic resonance imaging may be a reliable technique for imaging the aorta in rats.

Solid-in-oil nanodispersions as a novel delivery system to improve the oral bioavailability of bisphosphate, risedronate sodium.

The aim of the current study was to modify the oral absorption of risedronate sodium (RS) using solid-in-oil nanodispersions (SONDs) technology. The oral therapeutic effect of RS is limited in vivo because of its low membrane permeability and the formation of insoluble precipitates with bivalent cations (such as Ca2+) in the gastrointestinal (GI) tract.We used SONDs to prepare medium-chain triglyceride (MCT)-based nanodispersions of the hydrophilic drug, which used the oral absorption mechanism of MCT digestion to improve bioavailability of RS in vivo. SONDs exhibited high encapsulation efficiency of RS and excellent enzymatic degradation-dependent release behavior. The result of an everted gut sac test showed that the Papp value of the SONDs was 6.29-fold (p<0.05) higher than that of RS aqueous solutions in simulated intestinal fluid containing 5 mM Ca2+, this was because MCT can be digested to form the fatty acids C8 and C10, which have an adsorption-promoting effect on RS. Further, solid-in-oil-in-water (S/O/W) emulsion droplets formedafter emulsification by bile salts and MCT digestionwere effective in disrupting epithelial tight junctions (TJs), facilitating the paracellular permeation of RS throughout the intestine. Moreover, in vivo absorption study in rats revealed that the AUC0-12h of RS in SONDs was approximately 4.56-fold (p<0.05) higher than with RS aqueous solutions at the same dose (15 mg/kg). This approach demonstrates a potential drug delivery system to improve the bioavailability of risedronate sodium.

Transcutaneous Delivery of Immunomodulating Pollen Extract-Galactomannan Conjugate by Solid-in-Oil Nanodispersions for Pollinosis Immunotherapy.

Japanese cedar pollinosis is a type I allergic disease and has already become a major public health problem in Japan. Conventional subcutaneous immunotherapy (SCIT) and sublingual immunotherapy (SLIT) cannot meet patients' needs owing to the side effects caused by both the use of conventional whole antigen molecules in the pollen extract and the administration routes. To address these issues, a surface-modified antigen and transcutaneous administration route are introduced in this research. First, the pollen extract (PE) was conjugated to galactomannan (PE-GM) to mask immunoglobulin E (IgE)-binding epitopes in the PE to avoid side effects. Second, as a safer alternative to SCIT and SLIT, transcutaneous immunotherapy (TCIT) with a solid-in-oil (S/O) nanodispersion system carrying PE-GM was proposed. Hydrophilic PE-GM was efficiently delivered through mouse skin using S/O nanodispersions, reducing the antibody secretion and modifying the type 1 T helper (Th1)/ type 2 T helper (Th2) balance in the mouse model, thereby demonstrating the potential to alleviate Japanese cedar pollinosis.

Whole Body Vibration Immediately Decreases Lower Extremity Loading During the Drop Jump.

Chen, Z-R, Peng, H-T, Siao, S-W, Hou, Y-T, and Wang, L-I. Whole body vibration immediately decreases lower extremity loading during the drop jump. J Strength Cond Res 30(9): 2476-2481, 2016-The purpose of this study was to evaluate the acute effect of whole body vibration (WBV) on lower extremity loading during the drop jump (DJ). Fifteen male collegiate physical education students randomly completed 3 experimental sessions on 3 separate days with 4 days interval between sessions (performing 3 trials of DJ from 30-, 40-, and 50-cm drop heights before WBV and 4 minutes after WBV). Eight cameras and 2 force platforms were used to record kinematic and kinetic data, respectively. Peak impact force and loading rate significantly decreased after WBV during DJ from 40 and 50 cm. Knee angular displacements significantly increased after WBV during DJ from 30, 40, and 50 cm. Whole body vibration may help immediately reduce lower extremity loading.