Ocular surface changes in moderate-to-severe acne vulgaris.

AIM: To investigate ocular surface disorders and tear function changes in patients with acne vulgaris and explore the potential relationship between acne vulgaris and dry eye. METHODS: This cross-sectional study included right eyes of 53 patients with acne vulgaris and 54 healthy controls. The participants completed the Ocular Surface Disease Index (OSDI) questionnaire. The following ocular surface-related parameters were measured: tear meniscus height (TMH), noninvasive tear breakup time (NIBUT), Schirmer I test (SIT), lipid layer thickness (LLT) score of the tear film, meibum score, meibomian gland orifice obstruction score, the ratio of meibomian gland loss, conjunctival hyperemia score, and corneal fluorescein staining (CFS) score. RESULTS: The stability of the tear film decreased in acne vulgaris patients. In the acne group, the TMH and NIBUT were lower, whereas the OSDI, meibum score, meibomian gland orifice obstruction score, ratio of meibomian gland loss, and conjunctival hyperemia score were higher compared with controls (P<0.05). There were no significant differences in the CFS score, SIT, or LLT score between the groups (P>0.05). In two dry eye groups, the TMH, NIBUT, and LLT score were lower in the acne with dry eye (acne-DE) group, and the meibum score, meibomian gland orifice obstruction score, ratio of meibomian gland loss and conjunctival hyperemia score in the acne-DE group were higher (P<0.05). There were no significant differences between OSDI, SIT, and CFS score (P>0.05). CONCLUSION: Patients with moderate-to-severe acne vulgaris are more likely to experience dry eye than those without acne vulgaris. Reduced tear film stability and meibomian gland structure dysfunction are more pronounced in patients with moderate-to-severe acne and dry eye.

Topology optimization for near-junction thermal spreading of electronics in ballistic-diffusive regime.

Hotspots in electronic devices can cause overheating and reduce performance. Enhancing the thermal spreading ability is critical for reducing device temperature to improve the reliability. However, as devices shrink, phonon ballistic effects can increase thermal resistance, making conventional optimization methods less effective. This paper presents a topology optimization method that combines the phonon Boltzmann transport equation with solid isotropic material with penalization method to optimize high thermal conductivity (HTC) material distributions for thermal spreading problems. Results show that the contraction-expansion structure can effectively reduce thermal resistance. Optimal distributions differ from that based on Fourier's heat conduction law, and only the trunk structure appears in optimized layouts due to the size effect. Additionally, HTC material with longer mean free paths tends to be filled around the heat source with a gap in a ballistic-diffusive regime. This work deepens understanding of thermal spreading and aids in thermal optimization of microelectronic chips.

Androgen deprivation restores ARHGEF2 to promote neuroendocrine differentiation of prostate cancer.

Androgen receptor (AR) plays an important role in the progression of prostate cancer and has been targeted by castration or AR-antagonists. The emergence of castration-resistant prostate cancer (CRPC) after androgen deprivation therapy (ADT) is inevitable. However, it is not entirely clear how ADT fails or how it causes resistance. Through analysis of RNA-seq data, we nominate ARHGEF2 as a pivotal androgen-repressed gene. We show that ARHGEF2 is directly suppressed by androgen/AR. AR occupies the enhancer and communicates with the promoter region of ARHGEF2. Functionally, ARHGEF2 is important for the growth, lethal phenotype, and survival of CRPC cells and tumor xenografts. Correspondingly, AR inhibition or AR antagonist treatment can restore ARHGEF2 expression, thereby allowing prostate cancer cells to induce treatment resistance and tolerance. Overall, our findings provide an explanation for the contradictory clinical results that ADT resistance may be caused by the up-regulation of ARHGEF2 and provide a novel target.

Increased expression of CELSR3 indicates a poor prognostic factor for Prostate Cancer.

Background: Cadherin EGF LAG Seven-Pass G-Type Receptor 3 (CELSR3) gene was reported to be overexpressed in various human cancers and involved in the regulation of neurite-dependent neurite outgrowth and may play a role in tumor formation. However, the clinical significance of CELSR3 in prostate cancer (PCa) has not been fully studied. Methods: The expression of CELSR3 was detected by crossover analysis of the public datasets and cell lines. MTT assay and migration assay were performed to evaluate the cells' physiological functioning. Co-expressed genes and enrichment analysis was performed to investigate the biological significance of CELSR3 in PCa. Quantitative real-time polymerase chain reaction was used to detect the expression levels of hub genes (CENPE, CENPA, CDC20, NUF2, ESPL1, PLK1) related to CELSR3. Results: We found a significant increase in CELSR3 expression in PCa patients and cell lines. Furthermore, immunohistochemical analysis showed that CELSR3 protein expression was significantly more highly expressed in the PCa tissues compared to the non-cancerous PCa tissues. CELSR3 downregulation significantly suppressed cell proliferation and migration potential. CELSR3-related hub genes (CENPE, CENPA, CDC20, NUF2, ESPL1, PLK1) were selected and the functions of these hub genes showed that the function of CELSR3 was closely related to the cell cycle-related signaling pathways. The upregulation of CELSR3 mRNA expression in the PCa tissues significantly correlated with the presence of high serum PSA levels, high pathological stage, high Gleason score, short overall survival time and short disease-free survival time. Conclusion: Our data suggest that CELSR3 may play an important role in the progression of PCa. More importantly, an increase in CELSR3 expression may be indicative of poor disease-free survival and poor prognosis in PCa patients.