Background This study evaluated dynamic changes in eyebrow position related to aging. Methods Female participants were recruited and separated into two groups aged 20–30 years (the younger group, n=20; mean age, 24.8 years) and 50–70 years (the older group, n=20; mean age, 55.8 years). Photogrammetry was used to determine the eyebrow position at the medial canthus (MC), lateral limbus, lateral canthus, and lateral end point (EP) for 6 actions: smooth opening (the reference action) and closing of the eye, forward gaze, maximum opening and closing of the eye, and maximum frown. Videos were also recorded. Results No differences in eyebrow position were detected at the MC when opening or closing the eyes smoothly, gazing straight ahead, or closing the eyes maximally. For all 6 actions, the position of the lateral EP in the older group was significantly lower than in the younger group (P=0.003), and the smallest degree of vertical movement at this point was found in both age groups (P<0.001). Vertical movement at the 4 landmarks of the eyebrows decreased with aging. Conclusions Eyebrow position was unchanged at the MC with aging, except at maximal eye opening and maximal frown. No differences in eyebrow position were observed between the younger and older groups when eyes were maximally closed, except at the EP. It is important to focus on correction of the lateral EP for periorbital rejuvenation.

Epidemiologic studies have shown an association between tuberculosis and lung cancer. The altered tumor microenvironment after tuberculosis infection appears to contribute to cancer progression. Pleural effusions are enriched in exosomes, which act as mediators of intercellular communication. We hypothesized that tuberculous pleural effusion (TPE)-derived exosomes mediate intercellular communication. Then, we examined the interaction between TPE-derived exosomes and cancer cells. Exosomal miRNA profiling of TPE was performed using a microRNA array. An in vitro lung cancer cell experiment and an in vivo mouse xenograft tumor model were used to evaluate the effects of the selected exosomal microRNAs. TPE-derived exosome treatment enhanced the growth of A549 cells both in vitro and in a nude mouse xenograft model. Neighboring cancer cells were observed to take up TPE-derived exosomes, which promoted cancer cell invasion. Exosome-mediated transfer of the selected microRNAs, including miR-130b-3p and miR-423-5p, to A549 lung cancer cells activated cyclin D1 signaling and increased the expression of phosphorylated p65, a cyclin D1 transcription factor. Inhibitors of miR-130b and miR-423-5p suppressed the promotion of lung cancer by TPE-derived exosomes and reduced the expression of p65 and cyclin D1. These results suggest that TPE-derived exosomal miRNAs can serve as a novel therapeutic target in tuberculous fibrosis-induced lung cancer.

Ultrasound-indicated cerclage (UIC) is recommended to prevent spontaneous preterm birth (sPTB) in women with a short cervix at mid-trimester and a history of PTB. We assessed the factors related to sPTB after UIC and determined the corresponding risks. This retrospective cohort study was conducted at a university hospital. UIC was performed between 15 and 26 weeks of gestation in women with a cervical length of <2.5 cm. Univariate and multivariate analyses were used to examine factors associated with sPTB after UIC. An earlier gestational age and shorter cervical length at UIC were associated with sPTB after UIC. While PTB history was not associated with an increased risk of sPTB, it did increase the risk of repeat cerclage after UIC. Higher levels of preoperative serum inflammatory markers and obesity significantly increased the risk of sPTB after UIC. These findings provide helpful guidance for patient counseling and management in predicting the delivery timing after UIC in women with a short cervix in the mid-trimester.

Epidemiologic studies have shown an association between tuberculosis and lung cancer. The al-tered tumor microenvironment after tuberculosis infection appears to contribute to cancer pro-gression. Pleural effusions are enriched in exosomes, which act as mediators of intercellular communication. We hypothesized that tuberculous pleural effusion (TPE)-derived exosomes mediate intercellular communication. Then we examined the interaction between TPE-derived exosomes and cancer cells. Exosomal miRNA profiling of TPE was performed using a microRNA array. An in vitro lung cancer cell experiment and an in vivo mouse xenograft tumor model were used to evaluate the effects of select exosomal microRNAs. TPE-derived exosome treatment en-hanced the growth of A549 cells both in vitro and in a nude mouse xenograft model. Neighboring cancer cells were observed to take up TPE-derived exosomes, which promoted cancer cell inva-sion. Exosome-mediated transfer of select microRNAs, including miR-130b-3p and miR-423-5p, to A549 lung cancer cells activated cyclin D1 signaling and increased the expression of phos-phorylated p65, a cyclin D1 transcription factor. Inhibitors of miR-130b and miR-423-5p sup-pressed the promotion of lung cancer by TPE derived exosomes and reduced the expression of p65 and cyclin D1. These results suggest that TBE-derived exosomal miRNAs can serve as a novel therapeutic target in tuberculous fibrosis-induced lung cancer.

Antimicrobial peptides, such as beta-defensin 2 (BD2), are vital in controlling infections and immune responses. In this study, we investigated the expression and role of BD2 in the amniotic membrane and human amniotic epithelial cells (hAECs) from patients with preterm birth and chorioamnionitis, focusing on its regulation of inflammatory cytokines and its protective effect on the epithelial barrier. Our results show increased BD2 expression in chorioamnionitis, and Lipopolysaccharide (LPS)-induced inflammation increased BD2 release from hAECs in a dose- and time-dependent manner. BD2 treatment effectively modulated the inflammatory response by reducing pro-inflammatory cytokines (IL-6, IL-1β) and enhancing the release of the anti-inflammatory cytokine IL-10. Additionally, BD2 helps preserve epithelial barrier integrity by restoring E-cadherin expression and reducing Snail expression in inflamed hAECs. In an LPS-induced preterm birth mouse model, BD2 treatment delayed preterm delivery and reduced inflammatory cytokine levels. These results suggest that BD2 plays a protective role in preventing preterm birth by regulating inflammation and maintaining epithelial barrier function, highlighting its therapeutic potential for inflammation-related preterm birth.