Morphological measurements and classification of the navicular bone: a study based on computed tomography imaging.

OBJECTIVE: The purpose of this study was to present the classification of navicular bones and the anatomical basis for the diagnosis and treatment of navicular fractures of the foot. METHOD: 351 computed tomographic (CT) images of the navicular bone were analyzed and classified. The navicular bone's anatomical morphology was measured by three independent researchers in each type. Analysis and recording of the measurement results followed. RESULT: Navicular bones were assorted into three types: I shape(37.04%), II shape(54.41%), and III shape(8.55%). The left and right sides did not differ in any appreciable ways, except ab, bc, and ∠abc (P < 0.05); And all data were statistically different between men and women except for ∠abc (p > 0.05). CONCLUSION: The classification of the navicular bone in this study may be helpful in making the treatment decision for navicular fracture. LEVEL OF CLINICAL EVIDENCE: 4.

Skeletal Features of Talus in Hepple V Lesion.

The present study was to determine the characteristics of the ankle skeletal structure in patients with talus Hepple V type. We conducted a retrospective study on the skeletal structure of the talus in 110 patients with Hepple V osteochondral lesions of the talus and in control participants. The radiographic measurements taken include the following: in the coronal plane - depth of talus frontal curvature, length of the lateral and medial malleolus; in the sagittal plane - radius and height of talus, angle of tibial lateral surface, tibiotalar sector, and vertical neck angle. The osteochondral lesion of the talus showed a significantly larger mean radius (mean ± SD, 21.4 ± 2.5 mm; p < .001) and height (mean ± SD, 26.0 ± 2.7 mm; p < .005). It also demonstrated a longer mean medial malleolus length (mean ± SD, 15.7 ± 2.4 mm; p < .005), a larger mean vertical neck angle (mean ± SD, 86.2 ± 5.4°; p < .050), and a greater mean tibial lateral surface angle (mean ± SD, 80.0 ± 4.5°; p < .001). And there was a greater mean frontal curvature depth (mean ± SD, 3.9 ± 0.6 mm; p < .005). Overall, this study found that patients with Hepple V osteochondral lesions of the talus had a larger vertical neck angle and tibial lateral surface angle, a longer talus radius and medial malleolus length, a higher talus height, and a deeper frontal curvature depth. STUDY DESIGNS: Retrospective Case-Control Study.

Association between the distal tibiofibular syndesmosis morphology classification and ankle osteoarthritis: a retrospective study.

BACKGROUND: Syndesmosis injury is proposed to contribute to ankle stability and osteoarthritis (OA). However, whether distal tibiofibular syndesmosis structure is closely related to ankle OA is unclear. We hypothesized that different DTS morphology classifications would affect the biomechanics properties in ankle OA. The study aimed to determine the association between the distal tibiofibular syndesmosis (DTS) morphological classification and ankle OA. METHODS: This is a retrospective study examining imaging data of 147 patients (87 males and 60 females) with ankle OA. Magnetic resonance imaging was used to access the DTS morphological classification, according to measuring various parameters. Joint space narrowing and osteophytes were measured using ankle weight-bearing radiography. The classification and parameters were analyzed to determine the relationship between the syndesmosis classification and the abnormality of ankle OA. RESULTS: Five morphological classifications of the DTS, including Chevron (19.6%), Widow's peak (16.2%), Flat (22.3%), Trapezoid (32.0%), and Crescent (19.6%), were shown. There were statistical differences between DTS classification and tibial angle surface angle (TAS) (P = .009) and talar tilt angle (TTA) (P = .014). The TAS (degree) of the Crescent (86.47 ± 3.21) was less than Chevron (88.75 ± 2.72) (P = .006), Widow's peak (89.26 ± 3.15) (P = .001), Flat (88.83 ± 3.62) (P = .003) and Trapezoid (88.11 ± 2.62) (P = .041), respectively. The TTA (degree) of Crescent (86.83 ± 5.30) was less than Chevron (89.28 ± 2.46) and Widow's peak (89.82 ± 3.41). The men were greater than women for TAS (P = .008) and angle (P = .003), which are consistent with osteophyte (P = .019) and the modified Kellgren-Lawrence grades (P = .041) between gender. CONCLUSIONS: DTS morphological classification might affect the biomechanics properties in TAS and TTA in ankle OA. In clinical practice, surgeons should pay attention to the effects of DTS on ankle OA. LEVEL OF EVIDENCE: Level III, retrospective study.

Cholecalciferol pretreatment ameliorates ischemia/reperfusion-induced acute kidney injury through inhibiting ROS production, NF-κB pathway and pyroptosis.

Acute kidney injury (AKI) is a common complication in patients with potentially life-threatening diseases, and it is also usually associated with unacceptable morbidity and mortality rates. Therefore, new and efficient therapies are urgently required to relieve AKI. It is well known that, reactive oxygen species (ROS), the NF-κB signaling pathways and pyroptosis are involved in AKI induced by ischemia/reperfusion (I/R). The present study seeks to further confirm the internal relationship between vitamin D deficiency and I/R-induced AKI in patients, and to explore the underlying mechanisms of ROS, NF-κB signaling pathways and pyroptosis in the renal ischemia-reperfusion injury, as well as investigating the protective role of cholecalciferol. Patients with vitamin D deficiency show worse renal function reflected by postoperative glomerular filtration rate (GFR) and more release of proinflammatory cytokine IL-1ß and IL-18. Renal cell injury and renal dysfunction induced by I/R surgery were attenuated in the ICR mice administered with cholecalciferol. Cholecalciferol reduced ROS production, suppressed activated NF-κB signaling, and inhibited gasdermin D (GSDMD, a pyroptosis execution protein)-mediated pyroptosis. Cholecalciferol therefore has potential, as a clinical drug, to protect renal function in I/R-induced AKI through reducing ROS production, NF-κB activation and GSDMD-mediated pyroptosis.

Constitutive BAK/MCL1 complexes predict paclitaxel and S63845 sensitivity of ovarian cancer.

We previously found that preformed complexes of BAK with antiapoptotic BCL2 proteins predict BH3 mimetic sensitivities in lymphohematopoietic cells. These complexes have not previously been examined in solid tumors or in the context of conventional anticancer drugs. Here we show the relative amount of BAK found in preformed complexes with MCL1 or BCLXL varies across ovarian cancer cell lines and patient-derived xenografts (PDXs). Cells bearing BAK/MCL1 complexes were more sensitive to paclitaxel and the MCL1 antagonist S63845. Likewise, PDX models with BAK/MCL1 complexes were more likely to respond to paclitaxel. Mechanistically, BIM induced by low paclitaxel concentrations interacted preferentially with MCL1 and displaced MCL1-bound BAK. Further studies indicated that cells with preformed BAK/MCL1 complexes were sensitive to the paclitaxel/S63845 combination, while cells without BAK/MCL1 complexes were not. Our study suggested that the assessment of BAK/MCL1 complexes might be useful for predicting response to paclitaxel alone or in combination with BH3 mimetics.

Curcumin Negatively Regulates Cigarette Smoke-Induced Renal Cell Carcinoma Epithelial-Mesenchymal Transition Through the ERK5/AP-1 Pathway.

BACKGROUND: So far, little research has been conducted regarding the underlying mechanism of renal carcinogenesis at molecular level. Epithelial-mesenchymal transition (EMT) exerts an important part during tumor genesis as well as the development through mitogen-activated protein kinase (MAPK) pathways. Therefore, we hypothesized that EMT could promote renal cell carcinoma (RCC) progression via the ERK5/AP-1pathway. MATERIALS AND METHODS: The RCC cell lines were utilized to be the models with in vitro exposure to cigarette smoke extract (CSE). We used the curcumin for the EMT intervention study. In the present study, immunohistochemistry (IHC), Western blotting, and real-time quantitative reverse transcription PCR had been used to determine the experimental results. EMT phenotypic alterations were assessed by changes in cell morphology, invasion and transfer ability, as well as expression of epithelial and mesenchymal markers. RESULTS: In human renal cell carcinoma tissue, E-cadherin expression within the smoking renal cancer patients was down-regulated compared with that among the non-smokers. However, Vimentin, N-cadherin, and TWIST levels increased (P<0.05). Significantly, we clarified that ERK5/AP-1 exerted positive regulation on the renal cell carcinoma EMT mediated by CS, which was suggested based on the results of CS activating the ERK5/AP-1 pathway, as well as ERK5 inhibition via XMD8-92 reversed AP-1 protein levels and the EMT process. Furthermore, curcumin showed the same inhibitory effect as XMD8-92 and significantly reversed CS-induced EMT through inhibiting the ERK5/AP-1 signaling pathway. CONCLUSION: The above results indicated that ERK5/AP-1 signaling pathway exerts a vital part for CS-associated RCC development and cancer intervention.

Nanog mediates tobacco smoke-induced enhancement of renal cancer stem cell properties.

Nanog plays an important role in the regulation of cancer stem cells (CSCs) which participate in tumorgenesis and progression. In renal cancer, tobacco smoke (TS) is considered a major risk factor. However, the molecular mechanism by which TS induces the development of renal CSC properties remains largely unknown. In this study, we showed that the level of Nanog was elevated in renal cell carcinoma (RCC) patients with a smoking history, and that Nanog overexpression promoted the traits of CSCs in renal cancer. We further demonstrated that a 8-week exposure of TS enhanced the formation of renal tumorspheres, increased the population of CD133-positive cells, and stimulated the expression of Nanog and CSC markers. In addition, TS was found to play a role in accelerating the cell growth transition from G1 to S phase in renal CSCs. Finally, we demonstrated that the TS-induced effects in renal CSCs could be reversed through the downregulation of Nanog. Our results suggested that Nanog plays a role in mediating TS-induced renal CSC properties. This study may provide new insights into the molecular mechanism of TS-related renal tumorigenesis, which can contribute to the future development of therapeutics for renal cancer.