Differences of Anteroposterior Pelvic Radiographs Between Supine Position and Standing Position in Patients with Developmental Dysplasia of the Hip.

OBJECTIVE: To explore the difference in pelvic tilt and hip joint parameters with developmental dysplasia of the hip (DDH) comparing the anteroposterior (AP) pelvic radiographs taken in supine and standing positions. METHODS: A prospective study of DDH patients undergoing Bernese periacetabular osteotomy (PAO) was conducted. AP pelvic radiographs were taken in supine and standing positions before surgery The pelvic tilt and hip joint parameters from the two radiographs were compared. Contrast parameters included the distance between the pubic symphysis to sacrococcygeal distance (PSSC), lateral center-edge angle (LCEA), Tönnis angle (TA), and angle of sharp (SA). RESULTS: A total of 110 young DDH patients were enrolled, including 32 men and 78 women, aged 18-49 years. The male PSSC was 45.63 ± 13.69 mm in supine position and 36.91 ± 12.33 mm in standing position (P < 0.05). The female PSSC was 56.76 ± 13.54 mm in supine position and 48.62 ± 15.44 mm in standing position (P < 0.05). In this study, LCEA <20° in AP pelvic radiographs in the supine position was found in 52 men and 135 women. For male patients, in supine position and standing position, LCEA were 5.51° ± 11.88° and 4.45° ± 12.22°, respectively (P < 0.05); TA were 20.20° ± 9.63° and 21.30° ± 9.97°, respectively (P < 0.05), and SA comparison showed no significant differences. For female patients, in supine position and standing position, LCEA were 3.07° ± 12.07° and 1.69° ± 12.11°, respectively (P < 0.05), TA were 22.62° ± 9.31° and 23.82° ± 9.45°, respectively (P < 0.05), and SA were 48.01° ± 4.68° and 48.49° ± 4.74°, respectively (P < 0.05). CONCLUSION: Compared with the supine position, the young DDH patients have pelvic tilt backward and a decrease in hip coverage in the standing position.

The Influence of Pelvic Tilt on the Anteversion Angle of the Acetabular Prosthesis.

The concept of the "safe area" of the acetabular prosthesis has a long history and has been recognized by many scholars. It is generally believed that postoperative hip dislocation rate is low, when the acetabular anteversion angle is placed in the range of 15° ± 10°. Despite this, hip dislocation is a common complication after total hip arthroplasty. In recent years, more and more scholars have paid attention to the influence of pelvic tilt on the acetabular anteversion angle. The concept of acetabular anteversion changes as the pelvic tilt changes, and is challenging the traditional acetabular prosthesis "safe area." This study summarized the potential influencing factors of pelvic tilt and discussed the influence of the phenomenon on the anteversion angle of total hip arthroplasty (THA) acetabular prosthesis based on the literature review. We conclude that from the supine position to standing, followed by sitting, the pelvis tends to move backward. Pelvic sagittal activity, lumbar disease (ankylosing spondylitis), lumbar fusion (lumbar fusion, spine-pelvic fusion), and other factors related to the tilt are THA risk factors for postoperative dislocation and revision. With the change of body position, the degree of acetabular anteversion is directly related to the degree of pelvic tilt. The acetabular anteversion varies greatly, which leads to increased hip prosthesis wear and even hip dislocation. The lateral X-ray of the spine and pelvis is recommended in supine, standing, and sitting positions before THA. In addition, the pelvic tilt should be regarded as a reference of the acetabular prosthesis in the preoperative planning of THA.

Tanshinone IIA reduces SW837 colorectal cancer cell viability via the promotion of mitochondrial fission by activating JNK-Mff signaling pathways.

BACKGROUND: Mitochondrial homeostasis has been increasingly viewed as a potential target of cancer therapy, and mitochondrial fission is a novel regulator of mitochondrial function and apoptosis. The aim of our study was to determine the detailed role of mitochondrial fission in SW837 colorectal cancer cell viability, mobility and proliferation. In addition, the current study also investigated the therapeutic impact of Tanshinone IIA (Tan IIA), a type of anticancer adjuvant drug, on cancer mitochondrial homeostasis. RESULTS: The results of our data illustrated that Tan IIA promoted SW837 cell death, impaired cell migration and mediated cancer proliferation arrest in a dose-dependent manner. Functional investigation exhibited that Tan IIA treatment evoked mitochondrial injury, as witnessed by mitochondrial ROS overproduction, mitochondrial potential collapse, antioxidant factor downregulation, mitochondrial pro-apoptotic protein upregulation, and caspase-9-dependent apoptotic pathway activation. Furthermore, we confirmed that Tan IIA mediated mitochondrial damage by activating mitochondrial fission, and the inhibition of mitochondrial fission abrogated the proapoptotic effects of Tan IIA on SW837 cells. To this end, our results demonstrated that Tan IIA modulated mitochondrial fission via the JNK-Mff pathways. The blockade of the JNK-Mff axis inhibited Tan IIA-mediated mitochondrial fission and promoted the survival of SW837 cells. CONCLUSIONS: Altogether, our results identified mitochondrial fission as a new potential target to control cancer viability, mobility and proliferation. Furthermore, our findings demonstrate that Tan IIA is an effective drug to treat colorectal cancer by activating JNK-Mff-mitochondrial fission pathways.

Overexpression of microRNA let-7 correlates with disease progression and poor prognosis in hepatocellular carcinoma.

The aim of the study was to explore the clinical significance of let-7 expression in hepatocellular carcinoma (HCC).A PCR array was conducted to screen for let-7 expression in early-stage HCC. Next, the deregulation of let-7 was confirmed by quantitative real-time RT-PCR (qRT-PCR) in another set of liver tissues, including normal control (NC), chronic hepatitis (CH), liver cirrhosis (LC), HCC, and adjacent nontumor (NT) tissues. In addition, as the potential target mRNA of let-7, alpha 2(I) collagen (COL1A2) mRNA was also quantified in the above liver tissues. Finally, an association study comparing let-7 and COL1A2 and their clinical significance in HCC was conducted.PCR array analysis revealed that the expression levels of let-7a/7b/7c were significantly downregulated in early-stage HCC compared to those in NT tissues. As compared to NC samples, qRT-PCR further confirmed that let-7a/7b/7c/7e were significantly upregulated in CH, LC, and NT tissues, while there were no significant differences in expression between the HCC and NC groups. Although COL1A2 may be the target mRNA of let-7, only let-7c expression was inversely correlated with COL1A2 mRNA expression in CH tissues. In HCC tissues, levels of let-7a/7b/7c/7e were positively correlated with that of COL1A2 mRNA. The clinical significance study revealed that elevated let-7a expression was significantly correlated with serosal and vein invasion, while elevated let-7c expression was significantly correlated with vein invasion and advanced TNM stage. Elevated let-7e expression was significantly correlated with vein invasion in HCC. Significantly shorter postoperative overall survival was observed in HCC patients with high let-7c expression.The results suggest that aberrant expression of let-7a/7b/7c/7e occurs in benign liver diseases and HCC. The upregulation of let-7 expression is associated with the progression and poor prognosis of HCC, and further mechanistic studies are warranted.

The MTHFR C677T mutation is not a risk factor recognized for HBV-related HCC in a population with a high prevalence of this genetic marker.

BACKGROUND: Polymorphism of the methylenetetrahydrofolate reductase (MTHFR) gene can affect disease progression in HBV infection. However, the results from different reports are inconsistent. The aim of this study was to investigate the association between the MTHFR C677T polymorphism and the outcome of HBV infection in a Tianjin Han population. METHODS: TaqMan SNP genotyping was employed to determine the alleles and genotypes of MTHFR C677T in 2511 subjects from various stages of HBV infection and 549 healthy controls. RESULTS: Of the 3060 subjects, the genotypic frequencies were CT 48.9%, TT 29.3% and CC 21.8%; the allelic frequencies were T 53.8% and C 46.2%. There was no significant difference in genotypic or allelic distribution among the different disease groups. When either healthy subjects or self-limited subjects were used as controls, the TT genotype and the T allele conferred protective effects against hepatocellular carcinoma (HCC) (HCC vs healthy subjects: OR=0.588, 95% CI=0.413-0.836, P=0.003; OR=0.768, 95% CI=0.645-0.915, P=0.003, respectively. HCC vs self-limited subjects: OR=0.598, 95% CI=0.404-0.886, P=0.010; OR=0.772, 95% CI=0.635-0.940, P=0.010, respectively). After sub-stratification by gender, the prevalence of the TT genotype or T allele was the lowest in the male HCC group (TT 23.5%, T 49.8%). The protective effects of the TT genotype and the T allele were observed in male HCC and cirrhotic subjects (HCC vs self-limited subjects: OR=0.470, 95% CI=0.288-0.766, P=0.002; OR=0.681, 95% CI=0.535-0.866, P=0.002, respectively. Liver cirrhosis vs self-limited subjects: OR=0.624, 95% CI=0.392-0.992, P=0.046; OR=0.791, 95% CI=0.627-0.998, P=0.048, respectively), but not in female. When the subjects were stratified according to the clinical features, no statistically significant difference in the genotypic distribution was observed (P>0.05). CONCLUSIONS: The TT genotype and T allele of MTHFR C677T may confer a protective effect on disease progression to HCC in HBV-infected individuals, especially among male patients, in a population with a high prevalence of this genetic marker.