Spider silk protein, renowned for its excellent mechanical properties, biodegradability, chemical stability, and low immune and inflammatory response activation, consists of a core domain with a repeat sequence and non-repeating sequences at the N-terminal and C-terminal. In this review, we focus on the relationship between the silk structure and its mechanical properties, exploring the potential applications of spider silk materials in the detection of energetic materials.

Background: Blast traumatic brain injury (bTBI) can result in depression-like behaviors in the acute and chronic phases. SSRIs have been shown to significantly alleviate depression-like behaviors in animal models of traumatic brain injury (TBI) by increasing serotonin (5-HT) and brain-derived neurotrophic factor (BDNF) in the hippocampus. However, the therapeutic effects of SSRIs on depression caused by bTBI remain unclear. Objective: Therefore, this study was aimed at investigating the therapeutic effects of SSRIs on depression-like behaviors in bTBI models. Methods: We created a rat model to study mild TBI by subjecting rats to increased blast overpressures (BOP) and injecting fluoxetine and escitalopram SSRIs intraperitoneally for 28 days. Results: On day 14 post-BOP exposure, rats treated with SSRIs showed decreased depression-like behaviors. This finding was accompanied by higher 5-HT levels in the hippocampus and increased numbers of Nestin-positive cells in the dentate gyrus. Furthermore, rats treated with SSRIs exhibited increased pCREB and BDNF protein expression in the hippocampus on days 7, 14, and 28 after bTBI. Conclusions: Overall, our findings indicate that SSRI-induced recovery from depression-like behaviors after mild bTBI is associated with the upregulation of 5-HT levels, pCREB and BDNF expression, and neurogenesis in the hippocampus.

Cisplatin resistance coupled with adverse effects presents substantial hurdles in the treatment of ovarian cancer. Both cold atmospheric plasma and plasma-activated liquid (PAL) hold the ability to induce DNA damage, which is a primary target of cisplatin. In this study, we investigate the potential of PAL in augmenting cisplatin sensitivity or diminishing the necessary drug dosage by impairing the DNA of cisplatin-resistant cancer cells. We found that plasma irradiated medium exceeding 40 s could decrease the viability, induce DNA damage, trigger cell cycle arrest, and augment apoptosis and autophagy in two types of cisplatin-resistant ovarian cancer cells (A2780/DDP and SKOV3/DDP) after a 24 h incubation period. Notably, pre-treatment with 40 s plasma-activated medium (PAM) for 2 h significantly enhanced the anti-cancer effect of cisplatin administered at lower doses on these cell types. RNA-seq, quantitative real-time PCR and Western blotting analysis revealed that PAM treatment could downregulate the expression of several pivotal proteins involved in nucleotide excision repair (NER) and homologous recombination repair (HRR). The mouse xenograft tumor model demonstrated that plasma-activated saline and cisplatin synergistically inhibited tumor growth and significantly suppressed the expression of proteins related to HRR and NER pathways. We identified plasma-derived peroxide generation in PAM as crucial in these processes. These results pave the way for considering PAM as an adjuvant treatment for cisplatin-resistant ovarian cancer and other abdominal cancers. Additionally, the findings indicate the feasibility of reducing cisplatin dosage to alleviate side effects through sensitization.

To identify the potential target genes of blast lung injury (BLI) for the diagnosis and treatment. This is an experimental study. The BLI models in rats and goats were established by conducting a fuel-air explosive power test in an unobstructed environment, which was subsequently validated through hematoxylin-eosin staining. Transcriptome sequencing was performed on lung tissues from both goats and rats. Differentially expressed genes were identified using the criteria of q ≤ 0.05 and |log₂ fold change| ≥ 1. Following that, enrichment analyses were conducted for gene ontology and the Kyoto Encyclopedia of Genes and Genomes pathways. The potential target genes were further confirmed through quantitative real-time polymerase chain reaction and enzyme linked immunosorbent assay. Observations through microscopy unveiled the presence of reddish edema fluid, erythrocytes, and instances of focal or patchy bleeding within the alveolar cavity. Transcriptome sequencing analysis identified a total of 83 differentially expressed genes in both rats and goats. Notably, 49 genes exhibited a consistent expression pattern, with 38 genes displaying up-regulation and 11 genes demonstrating down-regulation. Enrichment analysis highlighted the potential involvement of the interleukin-17 signaling pathway and vascular smooth muscle contraction pathway in the underlying mechanism of BLI. Furthermore, the experimental findings in both goats and rats demonstrated a strong association between BLI and several key genes, including anterior gradient 2, ankyrin repeat domain 65, bactericidal/permeability-increasing fold containing family A member 1, bactericidal/permeability-increasing fold containing family B member 1, and keratin 4, which exhibited up-regulation. Anterior gradient 2, ankyrin repeat domain 65, bactericidal/permeability-increasing fold containing family A member 1, bactericidal/permeability-increasing fold containing family B member 1, and keratin 4 hold potential as target genes for the prognosis, diagnosis, and treatment of BLI.