Auditory Cue Effects on Gait-Phase-Dependent Electroencephalogram (EEG) Modulations during Overground and Treadmill Walking.

Walking rehabilitation following injury or disease involves voluntary gait modification, yet the specific brain signals underlying this process remains unclear. This aim of this study was to investigate the impact of an auditory cue on changes in brain activity when walking overground (O) and on a treadmill (T) using an electroencephalogram (EEG) with a 32-electrode montage. Employing a between-group repeated-measures design, 24 participants (age: 25.7 ± 3.8 years) were randomly allocated to either an O (n = 12) or T (n = 12) group to complete two walking conditions (self-selected speed control (sSC) and speed control (SC)). The differences in brain activities during the gait cycle were investigated using statistical non-parametric mapping (SnPM). The addition of an auditory cue did not modify cortical activity in any brain area during the gait cycle when walking overground (all p > 0.05). However, significant differences in EEG activity were observed in the delta frequency band (0.5-4 Hz) within the sSC condition between the O and T groups. These differences occurred at the central frontal (loading phase) and frontocentral (mid stance phase) brain areas (p < 0.05). Our data suggest auditory cueing has little impact on modifying cortical activity during overground walking. This may have practical implications in neuroprosthesis development for walking rehabilitation, sports performance optimization, and overall human quality-of-life improvement.

Muscle Activation and Ground Reaction Force between Single-Leg Drop Landing and Jump Landing among Young Females during Weight-Acceptance Phase.

Single-leg drop landing (SLDL) and jump landing (SLJL) are frequently used as assessment tools for identifying potential high-risk movement patterns; thus, understanding differences in neuromuscular responses between these types of landings is essential. This study aimed to compare lower extremity neuromuscular responses between the SLDL and SLJL. Thirteen female participants performed an SLDL and SLJL from a 30-cm box height. Vertical ground reaction force (vGRF), time to peak vGRF, and surface electromyography (sEMG) data were collected. Continuous neuromuscular responses, peak vGRF, and time to peak vGRF were compared between the tasks. Statistical parametric mapping (SPM) analysis demonstrated that the SLJL had a significantly higher sEMG activity in the rectus femoris (RF), vastus lateralis (VL) and vastus medialis (VM) within the first 10% of the landing phase compared with SLDL. At 20-30% of the landing phase, sEMGs in the RF and VL during the SLDL were significantly higher compared with SLJL (p < 0.05). A higher peak vGRF and shorter time to peak vGRF was observed during SLJL (p < 0.05). In conclusion, our findings highlight that SLJL exhibited greater RF, VL, and VM activities than SLDL at initial impact (10% landing), coinciding with a higher peak vGRF and shorter time to attain peak vGRF. Our findings support the role of the quadriceps as the primary energy dissipator during the SLJL.

Progesterone stimulates the proliferation of female and male cholangiocytes via autocrine/paracrine mechanisms.

During cholestatic liver diseases, cholangiocytes express neuroendocrine phenotypes and respond to a number of hormones and neuropeptides by paracrine and autocrine mechanisms. We examined whether the neuroendocrine hormone progesterone is produced by and targeted to cholangiocytes, thereby regulating biliary proliferation during cholestasis. Nuclear (PR-A and PR-B) and membrane (PRGMC1, PRGMC2, and mPRalpha) progesterone receptor expression was evaluated in liver sections and cholangiocytes from normal and bile duct ligation (BDL) rats, and NRC cells (normal rat cholangiocyte line). In vivo, normal rats were chronically treated with progesterone for 1 wk, or immediately after BDL, rats were treated with a neutralizing progesterone antibody for 1 wk. Cholangiocyte growth was measured by evaluating the number of bile ducts in liver sections. The expression of the progesterone synthesis pathway was evaluated in liver sections, cholangiocytes and NRC. Progesterone secretion was evaluated in supernatants from normal and BDL cholangiocytes and NRC. In vitro, NRC were stimulated with progesterone and cholangiocyte supernatants in the presence or absence of antiprogesterone antibody. Aminoglutethimide was used to block progesterone synthesis. Cholangiocytes and NRC express the PR-B nuclear receptor and PRGMC1, PRGMC2, and mPRalpha. In vivo, progesterone increased the number of bile ducts of normal rats, whereas antiprogesterone antibody inhibited cholangiocyte growth stimulated by BDL. Normal and BDL cholangiocytes expressed the biosynthetic pathway for and secrete progesterone. In vitro, 1) progesterone increased NRC proliferation; 2) cholangiocyte supernatants increased NRC proliferation, which was partially inhibited by preincubation with antiprogesterone; and 3) inhibition of progesterone steroidogenesis prevented NRC proliferation. In conclusion, progesterone may be an important autocrine/paracrine regulator of cholangiocyte proliferation.

Mechanisms of biliary carcinogenesis and growth.

Cholangiocarcinoma is a rare cancer originating from the neoplastic transformation of the epithelial cells (i.e. cholangiocytes) that line the biliary tract. The prognosis for patients with cholangiocarcinoma is grim due to lack of viable treatment options. The increase in world-wide incidence and mortality from cholangiocarcinoma highlights the importance of understanding the intracellular mechanisms that trigger the neoplastic transformation of cholangiocytes and the growth of biliary cancers. The purpose of the following review is to address what has been learned over the past decade concerning the molecular basis of cholangiocarcinogenesis. The material presented is divided into two sections: (1) mechanisms regulating neoplastic transformation of cholangiocytes; and (2) factors regulating cholangiocarcinoma growth. An understanding of the growth regulatory mechanisms of cholangiocarcinoma will lead to the identification of therapeutic targets for this devastating cancer.