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Study Design: A retrospective cohort study using the Kaplan-Meier method with propensity-score matching. Purpose: To evaluate whether the presence of prevalent morphometric vertebral fractures (VFs) poses a risk for subsequent clinical VFs after short-fusion surgery in women aged ≥60 years with degenerative spondylolisthesis. Overview of Literature: VFs are common osteoporotic fractures and are associated with a low quality of life. Subsequent VFs are a complication of instrumented fusion in patients with degenerative lumbar disorders. Thus, risk factors for subsequent VFs after fusion surgery must be analyzed. Population-based studies have suggested that prevalent morphometric VFs led to a higher incidence of subsequent VFs in postmenopausal women; however, no studies have investigated whether prevalent morphometric VFs are a risk factor for subsequent VFs after fusion surgery in patients with degenerative spondylolisthesis. Methods: The study enrolled a total of 237 older female patients: 50 and 187 patients had prevalent morphometric VFs (VF [+] group) and nonprevalent morphometric VFs (VF [−] group), respectively. The time to subsequent clinical VFs after fusion surgery was compared between the two groups using the Kaplan-Meier method. Moreover, 40 and 80 patients in the VF (+) and VF (−) groups, respectively, were analyzed and matched by propensity scores for age, follow-up duration, surgical procedure, number of fused segments, body mass index, and number of patients treated for osteoporosis. Results: Kaplan-Meier analysis indicated that the VF (+) group had a higher incidence of subsequent clinical VFs than the VF (−) group, and Cox regression analysis showed that the presence of prevalent morphometric VFs was an independent risk factor for subsequent clinical VFs before matching. Kaplan-Meier analysis demonstrated comparable results after matching. Conclusions: The presence of prevalent morphometric VFs may be a risk factor for subsequent clinical VFs in older women with degenerative spondylolisthesis who underwent short-fusion surgery. [ABSTRACT FROM AUTHOR]

Study Design: A retrospective case-control propensity score-matching study. Purpose: This study aimed to longitudinally evaluate whether preoperative ligamentous stenosis at the spondylolisthetic segments could affect the incidence of symptomatic adjacent canal stenosis following one-segment fusion surgery. Overview of Literature: Several risk factors for symptomatic adjacent canal stenosis following fusion surgery have been assessed. Patients with lumbar canal stenosis mainly due to ligamentum flavum (LF) hypertrophy (ligamentous stenosis) also have LF hypertrophy in other segments. Methods: In total, 76 patients participated in this case-control study (neurologically symptomatic adjacent canal stenosis, n=33; neurologically asymptomatic cases at follow-up, n=43). Their risk factors during surgery and magnetic resonance (MR) images before the surgery and at follow-up were evaluated. Data from the two groups (n=25 each) were matched using propensity scores for age, sex, time to MR imaging at follow-up, surgical procedure, and LF hypertrophy in adjacent segments before the surgery and analyzed. Results: Compared with the asymptomatic group, the symptomatic adjacent canal stenosis group had a significantly larger LF area/spinal canal area in the spondylolisthetic segments before the surgery. During the follow-up periods (in months), they had a larger LF area/spinal canal area in the adjacent segments: the two values were significantly correlated. The sensitivity, specificity, and positive and negative predictive values for determining symptomatic adjacent canal stenosis were high compared with on the cutoff value for the LF area/spinal canal area at the spondylolisthetic segments before the surgery. These results were the same after matching. Conclusions: Symptomatic adjacent canal stenosis is mainly caused by LF hypertrophy. Ligamentous stenosis at the spondylolisthetic segments before fusion surgery might be strongly associated with symptomatic adjacent canal stenosis at follow-up. [ABSTRACT FROM AUTHOR]

The effects of transmural pressure alone on cell proliferation and DNA synthesis and the role of platelet-derived growth factor (PDGF) and basic fibroblast growth factor, candidates for mediation of glomerular diseases, in the pressure-induced events were investigated. Findings showed that the pressure by itself increases DNA synthesis and proliferation of cultured rat mesangial cells possibly through activation of protein kinase C and tyrosine kinases, and PDGF-B could be partially involved in these pathways.

Nakamura, Ei'ichiro, Yasuhito Uezono, Ken'ichiro Narusawa, Izumi Shibuya, Yosuke Oishi, Masahiro Tanaka, Nobuyuki Yanagihara, Toshitaka Nakamura, and Futoshi Izumi. ATP activates DNA synthesis by acting on P2X receptors in human osteoblast-like MG-63 cells. Am J Physiol Cell Physiol 279: C510-C519, 2000.--In human osteoblast-like MG-63 cells, extracellular ATP increased [[sup.3]H]thymidine incorporation and cell proliferation and synergistically enhanced platelet-derived growth factor- or insulin-like growth factor I-induced [[sup.3]H]thymidine incorporation. ATP-induced [[sup.3]H]thymidine incorporation was mimicked by the nonhydrolyzable ATP analogs adenosine 5'-O-(3-thiotriphosphate) and adenosine 5'-adenylylimidodiphosphate and was inhibited by the P2 purinoceptor antagonist suramin, suggesting involvement of P2 purinoceptors. The P2Y receptor agonist UTP and UDP and a P2Y receptor antagonist reactive blue 2 did not affect [[sup.3]H]thymidine incorporation, whereas the P2X receptor antagonist pyridoxal phosphate-6-azophenyl-2',4-disulfonic acid inhibited ATP-induced [[sup.3]H]thymidine incorporation, suggesting that ATP-induced DNA synthesis was mediated by P2X receptors. RT-PCR analysis revealed that MG-63 cells expressed [P2X.sub.4], [P2X.sub.5], [P2X.sub.6], and [P2X.sub.7], but not [P2X.sub.1], [P2X.sub.2], and [P2X.sub.3], receptors. In fura 2-loaded cells, not only ATP, but also UTP, increased intracellular [Ca.sup.2+] concentration, and inhibitors for several [Ca.sup.2+]-activated protein kinases had no effect on ATP-induced DNA synthesis, suggesting that an increase in intracellular [Ca.sup.2+] concentration is not indispensable for ATP-induced DNA synthesis. ATP increased mitogen-activated protein kinase activity in a [Ca.sup.2+]-independent manner and synergistically enhanced platelet-derived growth factor- or insulin-like growth factor I-induced kinase activity. Furthermore, the mitogen-activated protein kinase kinase inhibitor PD-98059 totally abolished ATP-induced DNA synthesis. We conclude that ATP increases DNA synthesis and enhances the proliferative effects of growth factors through P2X receptors by activating a mitogen-activated protein kinase pathway. calcium imaging; cell proliferation; extracellular nucleotide; mitogen-activated protein kinase; osteoblast

Introduction: This study aimed to investigate the relationship between childbirth and lower back pain and determine the health-related quality of life of female patients with lower back pain., Methods: A total of 111 patients were divided into three groups: those who had given birth and developed lower back pain due to pregnancy, childbirth, or child-rearing movements (childbirth group, n=41), those who had given birth and developed lower back pain due to other causes (childbirth and other cause group, n=29), and those who were nulliparous (nulliparous group, n=41). A total of 22 physical therapists evaluated the patients during initial rehabilitation. Basic information and health-related quality of life were compared among the three groups using a one-way analysis of variance for the visual analog scale scores for lower back pain, summary scores (physical health [physical component summary] and mental health [mental component summary]), and subscales (physical functioning, role-physical, bodily pain, general health, vitality, social functioning, role-emotional, and mental health) of the Short Form-8 Health Survey. These values were also compared with the national standard values for health-related quality of life. The chi-square test of independence was used to compare distributions, and Fisher's exact probability test was used for cells with an expected value of <5., Results: Most participants had physical component summary scores below the national standard values. The visual analog scale scores for lower back pain were significantly higher in the birth group than in the nonbirth group. The physical component summary, physical functioning, and general health scores were significantly lower in the birth group than in the nonbirth group. Moreover, bodily pain scores were significantly lower in the birth group than in the other groups., Conclusions: For female patients with lower back pain due to pregnancy, childbirth, or childcare activities, physical conditions unique to postpartum women should be considered, and if necessary, instructions for activities of daily living should be provided., Competing Interests: Conflicts of Interest: The authors declare that there are no relevant conflicts of interest., (Copyright © 2024 The Japanese Society for Spine Surgery and Related Research.)

Aims: Eicosapentaenoic acid (EPA) has shown beneficial effects on coronary plaque stabilization. Based on our previous study, we speculated that EPA might be associated with the development of healed plaques and might limit thrombus size. This study aimed to elucidate the association between EPA and arachidonic acid (AA) ratios and various plaque characteristics in patients with plaque rupture., Methods: A total of 95 patients with acute coronary syndrome (ACS) caused by plaque rupture who did not take lipid-lowering drugs and underwent percutaneous coronary intervention using optical coherence tomography (OCT) were included. Clinical characteristics, lipid profiles, and OCT findings were compared between patients with lower and higher EPA/AA ratios (0.41) according to the levels in the Japanese general population., Results: In the high EPA/AA (n=29, 30.5%) and low EPA/AA (n=66, 69.5 %) groups, the high EPA/AA group was significantly older (76.1 vs. 66.1 years, P＜0.01) and had lower peak creatine kinase (556 vs. 1651 U/L, P=0.03) than those with low EPA/AA. Similarly, patients with high EPA/AA had higher prevalence of layered and calcified plaque (75.9 vs. 39.4 %, P＜0.01; 79.3 vs. 50.0 %, P＜0.01, respectively) than low EPA/AA group. Multivariate logistic regression analysis demonstrated that a high EPA/AA ratio was an independent factor in determining the development of layered and calcified plaques., Conclusion: A high EPA/AA ratio may be associated with the development of layered and calcified plaques in patients with plaque rupture.

Background: The mechanisms and clinical impact of acute kidney injury (AKI) after acute myocardial infarction (AMI) may differ depending on whether AKI develops during the early or late phase after AMI. The present study assessed the timing of AKI onset and the prognostic impact on long-term outcomes in patients hospitalized with AMI., Methods: The present study enrolled consecutive AMI survivors who had undergone successful percutaneous coronary interventions at admission. AKI was defined as an increase in the serum creatinine level of ≥0.3 mg/dL above the admission value within 7 days of hospitalization. AKI patients were further divided into two subgroups (early-phase AKI: within 3 days vs. late-phase AKI: 4 to 7 days after AMI onset). The primary endpoint was all-cause death., Results: In total, 506 patients were included in this study, with 385 men and a mean age of 69.5 ± 13.5 years old. The mean follow-up duration was 1289.5 ± 902.8 days. AKI developed in 127 patients (25.1%). Long-term mortality was significantly higher in the AKI group than in the non-AKI group (log-rank p < 0.001). Early-phase AKI developed in 98 patients (19.3%), and late-phase AKI developed in 28 patients (5.5%). In the multivariable analysis, early-phase AKI was significantly associated with all-cause mortality (HR 2.83, 95% CI [1.51-5.29], p = 0.0012), while late-phase AKI was not., Conclusion: Early-phase AKI but not late-phase AKI was associated with poor long-term mortality. Careful clinical attention and intensive care are needed when AKI is observed within 3 days of AMI onset., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2021 The Authors.)