The umbilical or L3 vertebral body level is often used for body fat quantification using computed tomography. To explore the feasibility of using clinically acquired pelvic magnetic resonance imaging (MRI) for visceral fat measurement, we examined the correlation of visceral fat parameters at the umbilical and L5 vertebral body levels. We retrospectively analyzed T2-weighted half-Fourier acquisition single-shot turbo spin echo (HASTE) MR axial images from Crohn\'s disease patients who underwent MRI enterography of the abdomen and pelvis over a three-year period. We determined the area/volume of subcutaneous and visceral fat from the umbilical and L5 levels and calculated the visceral fat ratio (VFR = visceral fat/subcutaneous fat) and visceral fat index (VFI = visceral fat/total fat). Statistical analyses involved correlation analysis between both levels, inter-rater analysis between two investigators, and inter-platform analysis between two image-analysis platforms. Correlational analysis of 32 patients yielded significant associations for VFI (r = 0.85; p < 0.0001) and VFR (r = 0.74; p < 0.0001). Intraclass coefficients for VFI and VFR were 0.846 and 0.875 (good agreement) between investigators and 0.831 and 0.728 (good and moderate agreement) between platforms. Our study suggests that the L5 level on clinically acquired pelvic MRIs may serve as a reference point for visceral fat quantification.

OBJECTIVE: Low-density lipoprotein (LDL) poses a risk for atherosclerotic cardiovascular disease (ASCVD). As LDL comprises various subtypes differing in charge, density, and size, understanding their specific impact on ASCVD is crucial. Two highly atherogenic LDL subtypes-electronegative LDL (L5) and Lp(a)-induce vascular cell apoptosis and atherosclerotic changes independent of plasma cholesterol levels, and their mechanisms warrant further investigation. Here, we have compared the roles of L5 and Lp(a) in the development of ASCVD.
RESULTS: Lp(a) tends to accumulate in artery walls, promoting plaque formation and potentially triggering atherosclerosis progression through prothrombotic or antifibrinolytic effects. High Lp(a) levels correlate with calcific aortic stenosis and atherothrombosis risk. L5 can induce endothelial cell apoptosis and increase vascular permeability, inflammation, and atherogenesis, playing a key role in initiating atherosclerosis. Elevated L5 levels in certain high-risk populations may serve as a distinctive predictor of ASCVD. L5 and Lp(a) are both atherogenic lipoproteins contributing to ASCVD through distinct mechanisms. Lp(a) has garnered attention, but equal consideration should be given to L5.

BACKGROUND: Lumbar spondylolysis, a common identifiable cause of low back pain in young athletes, reportedly has a higher incidence rate in males. However, the reason for its higher incidence in males is not clear. This study aimed to investigate the epidemiological differences between the sexes in adolescent patients with lumbar spondylolysis.
METHODS: A retrospective study was conducted in 197 males and 64 females diagnosed with lumbar spondylolysis. These patients visited our institution from April 2014 to March 2020 with their main complaint being low back pain, and they were followed-up until the end of their treatment. We investigated associations between lumbar spondylosis, their background factors, and characteristics of the lesions and analyzed their treatment results.
RESULTS: Males had a higher prevalence of spina bifida occulta (SBO) (p = 0.0026), more lesions with bone marrow edema (p = 0.0097), and more lesions in the L5 vertebrae (p = 0.021) than females. The popular sports disciplines were baseball, soccer, and track and field in males, and volleyball, basketball, softball in females. The dropout rate, age at diagnosis, bone union rate, and treatment period did not differ between the sexes.
CONCLUSIONS: Lumbar spondylolysis was more common in males than in females. SBO, bone marrow edema, and L5 lesions were more frequent in males, and sports discipline varied between the sexes.

L5, the most electronegative subfraction of low-density lipoprotein cholesterol (LDL-C), may play a role in the pathogenesis of cerebrovascular dysfunction and neurodegeneration. We hypothesized that serum L5 is associated with cognitive impairment and investigated the association between serum L5 levels and cognitive performance in patients with mild cognitive impairment (MCI). This cross-sectional study conducted in Taiwan included 22 patients with MCI and 40 older people with normal cognition (healthy controls). All participants were assessed with the Cognitive Abilities Screening Instrument (CASI) and a CASI-estimated Mini-Mental State Examination (MMSE-CE). We compared the serum total cholesterol (TC), LDL-C, and L5 levels between the MCI and control groups and examined the association between lipid profiles and cognitive performance in these groups. The serum L5 concentration and total CASI scores were significantly negatively correlated in the MCI group. Serum L5% was negatively correlated with MMSE-CE and total CASI scores, particularly in the orientation and language subdomains. No significant correlation between the serum L5 level and cognitive performance was noted in the control group. Conclusions: Serum L5, instead of TC or total LDL-C, could be associated with cognitive impairment through a disease stage-dependent mode that occurs during neurodegeneration.

METHODS: Basic science (finite element analysis).
OBJECTIVE: Pedicle subtraction osteotomy (PSO) at L5 is an effective treatment for sagittal imbalance, especially in select cases of patients showing kyphosis with the apex at L4-L5 but has been scarcely investigated. The aim of this study was to simulate various \"high-demand\" instrumentation approaches, including varying numbers of rods and sacropelvic implants, for the stabilization of a PSO at L5.
METHODS: A finite element model of T10-pelvis was modified to simulate posterior fixation with pedicle screws and rods from T10 to S1, alone or in combination with an L5 PSO. Five additional configurations were then created by employing rods and novel porous fusion/fixation implants across the sacroiliac joints, in varying numbers. All models were loaded using pure moments of 7.5 Nm in flexion-extension, lateral bending, and axial rotation.
RESULTS: The osteotomy resulted in a general increase in motion and stresses in posterior rods and S1 pedicle screws. When the number of rods was varied, three- and four-rod configurations were effective in limiting the maximal rod stresses; values approached those of posterior fixation with no osteotomy. Maximum stresses in the accessory rods were similar to or less than those observed in the primary rods. Multiple sacropelvic implants were effective in reducing range of motion, particularly of the SIJ.
CONCLUSIONS: Multi-rod constructs and sacropelvic fixation generally reduced maximal implant stresses and motion in comparison with standard posterior fixation, suggesting a reduced risk of rod breakage and increased joint stability, respectively, when a high-demand construct is utilized for the correction of sagittal imbalance.

Non-alcoholic fatty liver disease (NAFLD) is an umbrella term for a range of conditions caused by a build-up of fat in the liver. It is usually seen in people who are overweight or obese. Increasingly common around the world, this disease is the most common chronic liver disease in the United States, affecting about a quarter of the population. Recently, the designation of NAFLD as \'metabolic dysfunction-associated fatty liver disease\' (MAFLD) has been a subject of current debate. In this context, \'insulin resistance\' is the underlying common and basic pathophysiological mechanism of metabolic dysfunction due to its association with obesity, type 2 diabetes mellitus (T2DM), metabolic syndrome, dyslipidemia and NAFLD. All these pathological conditions are among the metabolic risk factors for cardiovascular diseases, too. Also, due to the bidirectional causality between NAFLD and cardiovascular diseases, a liver-heart axis is suggested. Therefore, various factors such as insulin resistance as well as systemic inflammation, cytokines, oxidative stress, adipokines, hepatokines, genes and intestinal microbiota have been identified as possible pathogenic factors that play a role in the explanation of the complex NAFLD and cardiovascular risk relationship. Recent data and cumulative evidence show that electronegative low-density lipoprotein [LDL (-)/L5] cholesterol is a promising biomarker for complex organ interactions and diseases associated with liver-heart axis. In this mini review, we focus not only on recent data on NAFLD mechanisms, but also on the potential of the lipid mediator LDL (-)/L5 as a diagnostic and therapeutic target for liver-heart line diseases.

Atherosclerosis has been linked with an increased risk of atherosclerotic cardiovascular disease (ASCVD). Autoimmune rheumatic diseases (AIRDs) are associated with accelerated atherosclerosis and ASCVD. However, the mechanisms underlying the high ASCVD burden in patients with AIRDs cannot be explained only by conventional risk factors despite disease-specific factors and chronic inflammation. Nevertheless, the normal levels of plasma low-density lipoprotein (LDL) cholesterol observed in most patients with AIRDs do not exclude the possibility of increased LDL atherogenicity. By using anion-exchange chromatography, human LDL can be divided into five increasingly electronegative subfractions, L1 to L5, or into electropositive and electronegative counterparts, LDL (+) and LDL (-). Electronegative L5 and LDL (-) have similar chemical compositions and can induce adverse inflammatory reactions in vascular cells. Notably, the percentage of L5 or LDL (-) in total LDL is increased in normolipidemic patients with AIRDs. Electronegative L5 and LDL (-) are not recognized by the normal LDL receptor but instead signal through the lectin-like oxidized LDL receptor 1 (LOX-1) to activate inflammasomes involving interleukin 1β (IL-1β). Here, we describe the detailed mechanisms of AIRD-related ASCVD mediated by L5 or LDL (-) and discuss the potential targeting of LOX-1 or IL-1β signaling as new therapeutic modalities for these diseases.

L5, the most negatively charged subfraction of low-density lipoprotein (LDL), is implicated in atherogenesis, but the pathogenic association is relatively unexplored in patients with rheumatoid arthritis (RA). We examined the role of L5 LDL in macrophage foam cell formation and the association of L5 with CD11c expression in THP-1 cells and RA patients. Using quantitative real-time PCR, we determined mRNA expression levels of ITGAX, the gene for CD11c, a marker associated with vascular plaque formation and M1 macrophages in atherogenesis, in 93 RA patients. We also examined CD11c expression on THP-1 cells treated with L5 by flow cytometry analysis and the plasma levels of inflammatory mediators using a magnetic bead array. We found a dose-dependent upregulation of foam cell formation of macrophages after L5 treatment (mean ± SEM, 12.05 ± 2.35% in L5 (10 µg/mL); 50.13 ± 3.9% in L5 (25 µg/mL); 90.69 ± 1.82% in L5 (50 µg/mL), p < 0.01). Significantly higher levels of CD11c expression were observed in 30 patients with a high percentage of L5 in LDL (L5%) (0.0752 ± 0.0139-fold) compared to 63 patients with normal L5% (0.0446 ± 0.0054-fold, p < 0.05). CD11c expression levels were increased in the L5-treated group (30.00 ± 3.13% in L5 (10 µg/mL); 41.46 ± 2.77% in L5 (50 µg/mL), p < 0.05) and were positively correlated with plasma levels of interleukin (IL)-6 and IL-8. L5 augmented the expression of IL-6, IL-8, and tumor necrosis factor-α (TNF-α) on monocytes and macrophages. Our findings suggest that L5 may promote atherogenesis by augmenting macrophage foam cell formation, upregulating CD11c expression, and enhancing the expression levels of atherosclerosis-related mediators.

The most electronegative constituents of human plasma LDL (i.e., L5) and VLDL (i.e., V5) are highly atherogenic. We determined whether the combined electronegativity of L5 and V5 (i.e., L5 + V5) plays a role in coronary heart disease (CHD). In 33 asymptomatic individuals (ages 32-64), 10-year hard CHD risk correlated with age (r = 0.42, p = 0.01). However, in age-adjusted analyses, 10-year hard CHD risk correlated with L5 + V5 plasma concentration (r = 0.43, p = 0.01) but not age (p = 0.74). L5 + V5 plasma concentration was significantly greater in the group with high CHD risk (39.4 ± 22.0 mg/dL; n = 17) than in the group with low CHD risk (16.9 ± 14.8 mg/dL; n = 16; p = 0.01). In cultured human aortic endothelial cells, L5 + V5 treatment induced significantly more senescence-associated-β-Gal activity than did equal concentrations of L1 + V1 (n = 4, p < 0.001). To evaluate the in vivo relevance of these findings, we fed ApoE-/- and wild-type mice with a high-fat diet and found that plasma LDL, VLDL, and LDL + VLDL from ApoE-/- mice exhibited significantly greater electrophoretic mobility than did wild-type counterparts (n = 6, p < 0.01). The increased electronegativity of LDL and VLDL in ApoE-/- mice was accompanied by increased aortic lipid accumulation and cellular senescence (n = 6, p < 0.05). Clinical trials are warranted to test the predictive value of L5 + V5 concentration in patients with CHD.

Studies focusing on human rhythmicity show that human circadian rhythm suffers constant changes across lifespan. Changes in rest-activity patterns can be studied through nonparametric variables of actigraphy: L5 (an individual\'s least active 5 h), M10 (an individual\'s most active 10 h) and RA (relative amplitude of the rest-activity rhythm). The variable RA is the normalized difference between L5 and M10 - the higher the RA, the greater the difference between these two variables. This study used the data bank of the Human Chronobiology Laboratory of Federal University of Paraná (Brazil). It analyzed actimetric data of 93 children between 4 and 11 years of age in their naturalistic context in order to describe the development of nonparametric variables. Correlation between age and L5 was significantly negative (rho = - 0.29, p = 0.004), while correlation between age and RA was significantly positive (rho = 0.31, p = 0.003). The variables M10, sL5 (start of L5) and sM10 (start of M10) did not show significant correlation to age. Furthermore, there were no statistical differences between genders. The population of this study, healthy children, has been poorly assessed by similar literature. Through our results, we have demonstrated that, as children age, L5 significantly decreases, which reflects a smaller fragmentation of circadian rhythm. As an expected consequence, RA significantly increases. In other words, these nonparametric variables of actimetry successfully demonstrate that children tend to reduce nocturnal activity as they age, a phenomenon that reflects the ongoing consolidation of circadian rhythm.