Inhibition of p38MAPK signalling pathway alleviates radiation-induced testicular damage through improving spermatogenesis.

BACKGROUND AND PURPOSE: Damage to the testis following exposure to ionizing radiation has become an urgent problem to be solved. Here we have investigated if inhibition of p38 mitogen-activated protein kinase (p38MAPK) signalling could alleviate radiation-induced testicular damage. EXPERIMENTAL APPROACH: In mice exposed to whole body radiation (2-6 Gy), morphological changes of the epididymis and testis was measured by histochemical staining. immunohistochemical and immunofluorescence procedures and western blotting were used to monitor expression and cellular location of proteins. Expression of genes was assessed by qPCR and RNA-Seq was used to profile gene expression. KEY RESULTS: Exposure to ionizing radiation induced dose-dependent damage to mouse testis. The sperm quality decreased at 6 and 8 weeks after 6 Gy X-ray radiation. Radiation decreased PLZF+ cells and increased SOX9+ cells, and affected the expression of 969 genes, compared with data from non-irradiated mice. Expression of genes related to p38MAPK were enriched by GO analysis and were increased in the irradiated testis, and confirmed by qPCR. Levels of phospho-p38MAPK protein increased at 28 days after irradiation. In irradiated mice, SB203580 treatment increased spermatozoa, SOX9+ cells, the area and diameter of seminiferous tubules, sperm movement rate and density. Furthermore, SB203580 treatment increased SCP3+ cells, accelerating the process of spermatogenesis. CONCLUSION AND IMPLICATIONS: Exposure to ionizing radiation clearly changed gene expression in mouse testis, involving activation of p38MAPK signalling pathways. Inhibition of p38MAPK by SB203580 partly alleviated the testicular damage caused by radiation and accelerated the recovery of sperms through promoting spermatogenesis.

A double methylene blue labeled single-stranded DNA and hairpin DNA coupling biosensor for the detection of Fusarium oxysporum f. sp. cubense race 4.

The DCL gene in Fusarium oxysporum f. sp. cubense Race 4 (Foc4) is a pivotal pathogenic factor causing banana fusarium wilt. Precise DCL detection is crucial for Foc4 containment. Here, we present a novel ssDNA-hDNA coupling electrochemical biosensor for highly specific DCL detection. The sensing interface was formed via electrodeposition of a composite containing reduced graphene oxide (rGO) and gold nanoparticles (AuNPs) onto a carbon screen-printed electrode (SPE), followed by thiol-modified ssDNA functionalization. Additionally, the incorporation of hDNA, with methylene blue (MB) at both ends, binds to ssDNA through base complementarity, forming an ssDNA-hDNA coupling probe with bismethylene blue. This sensing strategy relies on DCL recognition by the hDNA probe, leading to DNA hairpin unfolding and detachment of hDNA bearing two MBs from ssDNA, generating a robust "on-off" signal. Empirical results demonstrate the sensor's amplified electrical signals, reduced background currents, and an extended detection range (6.02 × 106-3.01 × 1010 copies/µL) with a limit of detection (3.01 × 106 copies/µL) for DCL identification. We applied this sensor to analyze soil, banana leaves, and fruit samples, confirming its high specificity and stability. Moreover, post-sample detection, the sensor exhibits reusability, offering a cost-effective and rapid approach for banana wilt detection.

Transcriptome Changes of Hematopoietic Stem and Progenitor Cells in the Peripheral Blood of COVID-19 Patients by scRNA-seq.

Coronavirus disease 2019 (COVID-19) threatens public health all over the world. It is well-accepted that the immune cells in peripheral blood are widely involved in the pathological process of COVID-19. However, hematopoietic stem and progenitor cells (HSPCs), as the main source of peripheral immune cells, have not been well studied during COVID-19 infection. We comprehensively revealed the transcriptome changes of peripheral blood HSPCs after COVID-19 infection and vaccination by single-cell RNA-seq. Compared with healthy individuals, the proportion of HSPCs in COVID-19 patients significantly increased. The increase in the proportion of HSPCs might be partly attributed to the enhancement of the HSPCs proliferation upon COVID-19 infection. However, the stemness damage of HSPCs is reflected by the decrease of differentiation signal, which can be used as a potential specific indicator of the severity and duration of COVID-19 infection. Type I interferon (IFN-I) and translation signals in HSPCs were mostly activated and inhibited after COVID-19 infection, respectively. In addition, the response of COVID-19 vaccination to the body is mild, while the secondary vaccination strengthens the immune response of primary vaccination. In conclusion, our study provides new insights into understanding the immune mechanism of COVID-19 infection.