Prevalence and practice characteristics of urban and rural or remote Australian chiropractors: Analysis of a nationally representative sample of 1830 chiropractors

Objective: To determine the prevalence and clinical management characteristics of chiropractors practising in urban and rural or remote Australia. Design: A cross-sectional analysis of the Australian Chiropractic Research Network project data. Setting: Nationally representative sample of registered chiropractors practising in Australia. Participants: Chiropractors who participated in the Australian Chiropractic Research Network project and answered a question about practising in urban or rural or remote areas in the practitioner questionnaire. Main outcome measure: The demographics, practice characteristics and clinical management of chiropractors. Results: The majority of chiropractors indicated that they practise in urban areas only, while 22.8% (n = 435) practice in rural or remote areas only and 4.0% (n = 77) practice in both urban and rural or remote areas. Statistically significant predictors of chiropractors who practice in rural or remote areas, as compared to urban areas, included more patient visits per week, practising in more than one location, no imaging facilities on site, often treating degenerative spinal conditions or migraine, often treating people aged over 65 years, frequently treating Aboriginal and Torres Strait Islander people and frequently using biomechanical pelvic blocking or the sacro-occipital technique. Conclusion: A substantial number of chiropractors practice in rural or remote Australia and these rural or remote-based chiropractors are more likely to treat a wide range of musculoskeletal cases and include an Indigenously diverse group of patients than their urban-located colleagues. Unique practice challenges for rural or remote chiropractors include a higher workload and a lack of diagnostic tools. Chiropractors should be acknowledged and considered within rural or remote health care policy and service provision

SATB1 down-regulation induced by oxidative stress participates in trophoblast invasion by regulating β-catenin.

Preeclampsia (PE) is characterized by abnormal placentation in the early stages of pregnancy. Adequate migration and invasion of trophoblasts into the uterine wall and spiral arteries to form a functional maternal-fetal interface are pivotal for normal placentation, but the exact mechanism remains unclear. Growing evidence has revealed that special AT-rich sequence-binding protein 1 (SATB1) is a tumor promoter that participates in cancer cell migration and invasion. However, the expression and function of SATB1 in trophoblasts is unknown. Here, we characterize the stimulatory effect of SATB1 on the migration and invasion of trophoblasts and identify the regulatory events and downstream signaling components. Down-regulated SATB1 was detected in PE placentae and villous explants cultured under hypoxia/re-oxygenation (H/R) conditions. H/R-treated trophoblasts with lower SATB1 levels exhibited weaker invasive and growth capacities, whereas up-regulation of the SATB1 level with recombinant SATB1 restored these impairments. This restoration was especially apparent with the sumoylation-deficientSATB1 variant, which contained a mutated site that blocked sumoylation. Moreover, the elevated concentration of SATB1 also increased the expression of β-catenin, which is involved in human placental trophoblast invasion and differentiation and is down-regulated in PE. However, a specific activator, namely, lithium chloride (LiCl), increased β-catenin expression but had no evident influence on SATB1expression. Furthermore, up-regulated SATB1 failed to restore trophoblast function when Wnt/β-catenin was suppressed by Dickkopf1(DKK1).Together, these data show thatSATB1expression in the human placenta is affected by oxidative stress and might regulate the migration and invasion of trophoblasts via β-catenin signaling

Trophoblastic proliferation and invasion regulated by ACTN4 is impaired in early onset preeclampsia.

Successful pregnancy requires normal placentation, which largely depends on the tight regulation of proliferation, invasion, and migration of trophoblast cells. Abnormal functioning of trophoblast cells may cause failure of uterine spiral artery remodeling, which may be related to pregnancy-related disorders, such as preeclampsia. Here, we reported that an actin-binding protein, α-actinin (ACTN)4, was dysregulated in placentas from early onset preeclampsia. Moreover, knockdown of ACTN4 markedly inhibited trophoblast cell proliferation by reducing AKT membrane translocation. Furthermore, E-cadherin regulated ACTN4 and β-catenin colocalization on trophoblast cell podosomes, and ACTN4 down-regulation suppressed the E-cadherin-induced cell invasion increase via depolymerizing actin filaments. Moreover, loss of ACTN4 recapitulated a number of the features of human preeclampsia. Therefore, our data indicate that ACNT4 plays a role in trophoblast function and is required for normal placental development.-Peng, W., Tong, C., Li, L., Huang, C., Ran, Y., Chen, X., Bai, Y., Liu, Y., Zhao, J., Tan, B., Luo, X., Wang, H., Wen, L., Zhang, C., Zhang, H., Ding, Y., Qi, H., Baker, P. N. Trophoblastic proliferation and invasion regulated by ACTN4 is impaired in early onset preeclampsia