MicroRNA (miR)-143 and miR-145 have been identified as molecular regulators in cell proliferation, cell growth, clone formation, apoptosis, cell cycle, invasion, and migration. We previously found that rs353292 in the flanking region of miR-143/145 showed a high frequency in patients with colorectal cancer (CRC). To identify whether the rs353292 polymorphism is a risk factor for CRC, we conducted this study with larger samples. A total of 809 patients with CRC and 1005 gender matched controls were collected. The rs353292 polymorphism was genotyped by using TaqMan allelic discrimination. Dual luciferase reporter assay was carried out to measure the transcriptional activity. We found that the rs353292 polymorphism was associated with an increased risk for developing CRC in heterozygous comparison (adjusted OR = 1.70, 95% CI, 1.32–2.20, P < 0.001), dominant genetic model (adjusted OR = 1.62, 95% CI, 1.26–2.09, P < 0.001), and allele comparison (adjusted OR = 1.46, 95% CI, 1.16–1.84, P = 0.001). The rs353292 CT/TT carriers exhibited a lower expression of miR-143 compared to the CC carriers (P = 0.04). Moreover, the pGL3-rs353292T displayed a significantly lower luciferase activity than pGL3-rs353292C (P < 0.01). These findings indicate that the rs353292 polymorphism is functional and may be a risk factor for the development of CRC.

To observe the histological changes in human skin within 32 days after death to explore its potential significance in forensic practice. The intact full-thickness skin and subcutaneous tissue from the sternum of eight corpses were placed in an environment of 4–6 °C for 4 h, 6 h, 12 h, 18 h, 24 h, 36 h, 48 h, 60 h, 72 h, 84 h, 96 h, 6 d, 8 d, 10 d, 12 d, 16 d, 20 d, 24 d, 28 d, and 32 d. Then, the whole layer of the skin was stained with haematoxylin & eosin. The histological morphology of the epidermis, dermis and appendages (sweat glands, hair follicles, and sebaceous glands) was observed under an light microscope. The epithelial nucleus condensed at 24 h after death, and cell lysis was exhausted after 20 days. The post-mortem changes in the dermis occurred later than that of the epidermis (72 h), but after epidermal changes started, the change was more rapid. At 16 d, the layers had become homogenized. The epidermis and dermis had completely separated 24 d after death. The changes in the sweat glands appeared earlier (24 h) and disappeared later (32 days); the sebaceous glands and hair follicles began to undergo degenerative changes at 96 h after death, and at approximately 20 d, only their contour remained. There were individual and structural differences in the post-mortem histological changes in the skin. At 4–6 °C ambient temperature, some structures of the human skin still exist for a long time after death, and these structures can be used to identify the source of the tissue; post-mortem histological changes in the skin occur at specific times, which can be used to help infer the time of death. A comprehensive observation of changes in the skin composition/structure is required to comprehensively analyse possible death times.

Attrition of heterologous virus-specific CD8⁺ T cells has been demonstrated in murine viral infection; however, little is known regarding this phenomenon in human viral infections. In this study, we observed that CMV-specific CD8⁺ T cells displayed numerical decline and functional impairment in the early phase of acute infection, whereas programmed death-1 (PD-1) expression was significantly up-regulated by these CMV-specific CD8⁺ T cells. This early PD-1 up-regulation was found to be closely associated with the increased apoptotic sensitivity of CMV-specific CD8⁺ T cells. The in vitro addition of anti-PD-1 further enhanced the spontaneous apoptosis of CMV-specific CD8⁺ T cells; however, blockade of the PD-1-mediated pathway with anti-PD-L1 significantly restored the CMV-specific CD8⁺ T cell proliferation and IFN-γ production. Thus, PD-1 plays a crucial role in the attrition of CMV-specific CD8⁺ T cells in acute hepatitis B virus infection, which in turn, influences the preexisting homeostatic virus-specific CD8⁺ T cell pool.