Improved Screw Placement for Slipped Capital Femoral Epiphysis (SCFE) Using Robotically-Assisted Drill Guidance

Koutenaei, Bamshad Azizi; Güler, Özgür; Wilson, Emmanuel; Thoranaghatte, Ramesh U.; Oetgen, Matthew E.; Navab, Nassir; Cleary, Kevin

doi:10.1007/978-3-319-10404-1_61

Cited by 7 publications

(3 citation statements)

References 9 publications

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“…Furthermore, ZBTB16 involves in insulin signaling pathway regulation by reduction of phosphorylation levels of IRS1, Ake, and FoxO1 in the mouse model [46]. In our study, we described ZBTB16 negatively correlated to pancreatic beta cell apoptosis and contributed to beta cell viability.…”

Section: Discussionsupporting

confidence: 53%

E3 ubiquitin ligase FBW7-mediated ubiquitination of EZH2 prevents type I diabetes in NOD mice

Tian

Zhang

2020

Preprint

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Background Type I diabetes (T1D) is a heritable autoimmune disease targeting pancreatic beta cells. This study explores the molecular mechanism of E3 ubiquitin ligase FBW7 in reducing the occurrence of T1D. Methods The protein expression of FBW7, EZH2, and ZBTB16 was quantified in non-obese diabetic (NOD) mouse model of streptozotocin-induced T1D. Next, splenocytes and pancreatic beta cells were isolated to measure production of pro-inflammatory cytokines in splenocytes, as well as islet beta-cell apoptosis. Besides, the stability of EZH2 induced by FBW7 was analyzed by cycloheximide chase assay. The binding affinity of FBW7 and EZH2 and the consequence of ubiquitination were monitored by immunoprecipitation (IP) assay. Last, chromatin immunoprecipitation (ChIP) assay was employed to determine the accumulation of EZH2 and H3K27me3 at the ZBTB16 promoter region. Results We found downregulated FBW7 and ZBTB16, and upregulated EZH2 in diabetic NOD mice. Overexpression of FBW7 in the NOD mice inhibited the production of pro-inflammatory cytokines in the splenocytes and the apoptosis of islets beta cells. FBW7 destabilized EZH2 and accelerated ubiquitin-dependent degradation. EZH2 and H3K27me3 downregulated the ZBTB16 expression by accumulating in the ZBTB16 promoter and methylation. Conclusion FBW7 upregulates the expression of ZBTB16 by targeting histone methyltransferase EZH2 thus reducing the occurrence of T1D.

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Section: Discussionsupporting

confidence: 53%

E3 ubiquitin ligase FBW7-mediated ubiquitination of EZH2 prevents type I diabetes in NOD mice

Tian

Zhang

2020

Preprint

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“…Activation of ZBTB16 reduces serum advanced glycation end (AGE) products in STZ-induced diabetic mice and further inhibits AGE-induced apoptosis [39]. Furthermore, ZBTB16 involves in insulin signaling pathway regulation by reduction of phosphorylation levels of IRS1, Ake, and FoxO1 in the mouse model [40]. In our study, we described ZBTB16 negatively correlated to pancreatic beta cell apoptosis and contributed to beta cell viability.…”

Section: Discussionmentioning

confidence: 55%

Suppressive role of E3 ubiquitin ligase FBW7 in type I diabetes in non-obese diabetic mice through mediation of ubiquitination of EZH2

Guo

Fan

et al. 2021

Cell Death Discov.

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The current study tried to uncover the molecular mechanism of E3 ubiquitin ligase F-box and WD repeat domain-containing 7 (FBW7) in a heritable autoimmune disease, type I diabetes (T1D). After streptozotocin-induced T1D model establishment in non-obese diabetic (NOD) mouse, the protein expression of FBW7, enhancer of zeste homolog 2 (EZH2), and Zinc finger and BTB domain containing 16 (ZBTB16) was quantified. Next, splenocytes and pancreatic beta cells were isolated to measure the production of pro-inflammatory cytokines in splenocytes, as well as islet beta-cell apoptosis. Additionally, the stability of EZH2 induced by FBW7 was analyzed by cycloheximide chase assay. The binding affinity of FBW7 and EZH2 and the consequence of ubiquitination were monitored by co-immunoprecipitation assay. Last, a chromatin immunoprecipitation assay was employed to analyze the accumulation of EZH2 and H3K27me3 at the ZBTB16 promoter region. Our study demonstrated downregulated FBW7 and ZBTB16 and upregulated EZH2 in diabetic NOD mice. Overexpression of FBW7 in the NOD mice inhibited pro-inflammatory cytokine release in the splenocytes and the apoptosis of islets beta cells. FBW7 destabilized EZH2 and accelerated ubiquitin-dependent degradation. EZH2 and H3K27me3 downregulated the ZBTB16 expression by accumulating in the ZBTB16 promoter and methylation. FBW7 upregulates the expression of ZBTB16 by targeting histone methyltransferase EZH2 thus reducing the occurrence of T1D.

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“…The screw needs to be precisely positioned perpendicular on the physis and deep and central in the femoral head. Inappropriate screw placement can result in significant complications such as penetration of the hip joint, chondrolysis, vascular injury of the femoral head, avascular necrosis, and poor patient results [29].…”

Section: Discussionmentioning

confidence: 99%

Static Plantar Pressure under Different Conditions in Children with Surgically Treated Unilateral Slipped Capital Femoral Epiphysis

Negru,

Bolovan,

Amaricai

et al. 2024

Children

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Background: Slipped capital femoral epiphysis (SCFE) is the most common hip disease during infancy and adolescence. Our study aimed to analyze static plantar pressure in children with surgically treated unilateral SCFE. Methods: Twenty-two children with right SCFE with in situ fixation with one percutaneous screw were assessed by PoData plantar pressure analysis under three different conditions (open eyes, eyes closed, and head retroflexed). Results: The total foot loading was significantly higher on the unaffected limb compared with the affected one for all the three testing conditions (p < 0.05). When assessing the differences between testing conditions, there were no significant differences for the right and left foot loadings, or for the three sites of weight distribution, except for the right fifth metatarsal head (lower loading in eyes-closed condition in comparison to eyes open, p = 0.0068), left fifth metatarsal head (increased loading in head-retroflexed condition in comparison to eyes open, p = 0.0209), and left heel (lower loading in head-retroflexed condition in comparison to eyes open, p = 0.0293). Conclusion: Even after a successful surgical procedure, differences in foot loading can impact the postural static activities in different conditions (natural eyes-open, eyes-closed, or head-retroflexed posture).

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Improved Screw Placement for Slipped Capital Femoral Epiphysis (SCFE) Using Robotically-Assisted Drill Guidance

Cited by 7 publications

References 9 publications

E3 ubiquitin ligase FBW7-mediated ubiquitination of EZH2 prevents type I diabetes in NOD mice

E3 ubiquitin ligase FBW7-mediated ubiquitination of EZH2 prevents type I diabetes in NOD mice

Suppressive role of E3 ubiquitin ligase FBW7 in type I diabetes in non-obese diabetic mice through mediation of ubiquitination of EZH2

Static Plantar Pressure under Different Conditions in Children with Surgically Treated Unilateral Slipped Capital Femoral Epiphysis

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