Rod-shaped gold nanomaterials, known as gold nanorods (GNRs), may undergo specific surface modification, because of their straightforward surface chemistry. This feature makes them appropriate for use as functional and biocompatible nano-formulations. By optimizing the absorption of longitudinally localized surface plasmon resonance in the near-infrared region, which corresponds to the near-infrared bio-tissue window, GNRs with appropriate modifications may improve the results of photothermal treatment (PTT). In dermatology, potential noninvasive uses of GNRs to enhance wound healing, manage infections, combat cutaneous malignancies, and remodel skin tissues via PTT have attracted research attention in recent years. The review discussed the basic properties of GNRs, such as their shape, size, optical performance, photothermal efficiency, and metabolism. Then, the disadvantages of using these particles in photodynamic therapy are highlighted. Next, biological applications of GNRs-based PTT are explored in detail. Finally, the limitations and future perspectives of this research are addressed, providing a comprehensive perspective on the potential GNRs with PTT.

The macrophage-mediated inflammatory response is crucial for the recovery of skeletal muscle following ischemia. Therefore, macrophage-based therapeutic targets need to be explored for ischemic disease. In the current study, we found that the mRNA levels of scavenger receptor A1 (Sr-a1) were elevated in patients with critical limb ischemia, based on an analysis of the Gene Expression Omnibus data. We then investigated the role and underlying mechanisms of macrophage SR-A1 in a mouse hindlimb ischemia (HLI) model. Compared with the Sr-a1^fl/fl mice, the Lyz^Cre/+/Sr-a1^flox/flox (Sr-a1^ΔMΦ) mice showed significantly reduced laser Doppler blood flow in the ischemic limb on day seven after HLI. Consistently, histological analysis revealed that the ischemic limb of the Sr-a1^ΔMΦ mice exhibited more severe and prolonged necrotic morphology, inflammation, fibrosis, decreased vessel density, and delayed regeneration than that of the control Sr-a1^fl/fl mice. Furthermore, restoring wild-type myeloid cells to the Sr-a1 knockout mice effectively improved the Doppler perfusion in the ischemic limb and mitigated skeletal muscle damage seven days after HLI. Consistent with these in vivo findings, co-cultivating macrophages with the mouse myoblast cell line C2C12 revealed that the Sr-a1^−/− bone marrow macrophages significantly inhibited myoblast differentiation in vitro. Mechanistically, SR-A1 enhanced the skeletal muscle regeneration in response to HLI by inhibiting oncostatin M production via suppression of the NF-κB signaling activation. These findings indicate that SR-A1 may be a promising candidate protein to improve tissue repair and regeneration in peripheral ischemic arterial disease.

Premature ovarian insufficiency (POI) caused by chemotherapy is a common complication in female cancer survivors of childbearing age. Traditional methods, including mesenchymal stem cell (MSC) transplant and hormone replacement therapy, have limited clinical application because of their drawbacks, and more methods need to be developed. In the current study, the potential effects and underlying mechanisms of human umbilical cord MSC-derived extracellular vesicles (hUCMSC-EVs) were investigated in a cisplatin (CDDP)-induced POI mouse model and a human granulosa cell (GC) line. The results showed that hUCMSC-EVs significantly attenuated body weight loss, ovarian weight loss, ovary atrophy, and follicle loss in moderate-dose (1.5 mg/kg) CDDP-induced POI mice, similar to the effects observed with hUCMSCs. We further found that the hUCMSC-EVs inhibited CDDP-induced ovarian GC apoptosis by upregulating anti-apoptotic miRNA levels in GCs, thereby downregulating the mRNA levels of multiple pro-apoptotic genes. In general, our findings indicate that the moderate-dose chemotherapy may be a better choice for clinical oncotherapy, considering effective rescue of the oncotherapy-induced ovarian damage with hUCMSC-EVs. Additionally, multiple miRNAs in hUCMSC-EVs may potentially be used to inhibit the chemotherapy-induced ovarian GC apoptosis, thereby restoring ovarian function and improving the life quality of female cancer patients.

The extensive spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) throughout China in late 2022 has underscored the correlation between this virus and severe psychiatric disorders. However, there remains a lack of reported clinical and pathological features. Accordingly, we retrospectively reviewed the electronic medical records of psychiatric inpatients for seven days from early January 2023. Twenty-one inpatients who developed first-episode psychiatric disorders within two weeks after SARS-CoV-2 infection were recruited, while 24 uninfected first-episode psychiatric inpatients were selected as controls. Comparative analyses of clinical manifestations, routine laboratory tests, and imaging examinations were performed. Our investigation demonstrated a 330% increase in the incidence of first-episode psychiatric inpatients after SARS-CoV-2 infection in 2023, compared with the preceding year without SARS-CoV-2 infections. Most cases exhibited psychiatric symptoms within one week of SARS-CoV-2 infection, which resolved after approximately two weeks, with no residual symptoms after three months. One-way ANOVA demonstrated a significant difference in the highest fever temperature between inpatients with and without psychotic symptoms. Infected inpatients displayed elevated levels of interleukin-4, interleukin-8, and interferon-α, but decreased levels of eosinophils and basophils. These findings suggest that SARS-CoV-2 may contribute to the development of psychiatric disorders, likely mediated by the virus-induced inflammatory response and neuronal dysfunction in the context of psychological distress.

Ischemia-reperfusion injury (IRI) remains an unavoidable challenge in liver surgery, with macrophages playing a critical role in its pathogenesis. However, the mechanisms by which macrophages regulate the pathogenesis of IRI are not well understood. Through a target-guided screening approach, we identified a small 3 kDa peptide (SjDX5-271) from various schistosome egg-derived peptides that induced M2 macrophage polarization. SjDX5-271 treatment protected mice against liver IRI by promoting M2 macrophage polarization, and this protective effect was abrogated when the macrophages were depleted. Transcriptomic sequencing showed that the TLR signaling pathway was significantly inhibited in macrophages from the SjDX5-271 treatment group. We further identified that SjDX5-271 promoted M2 macrophage polarization by inhibiting the TLR4/MyD88/NF-κB signaling pathway and alleviated hepatic inflammation in liver IRI. Collectively, SjDX5-271 exhibited some promising therapeutic effects in IRI and represented a novel therapeutic approach, potentially applicable to other immune-related diseases. The current study demonstrates the potential of new biologics from the parasite, enhances our understanding of host-parasite interplay, and provides a blueprint for future therapies for immune-related diseases.

The KCNQ family of genes (KCNQ1-KCNQ5), encoding voltage-gated K⁺ (Kv) channels, have been demonstrated to play potential pathophysiological roles in cancers. However, the associations between genetic variants located in KCNQ family genes and gastric cancer survival remain unclear. In this study, a large-scale cohort comprising 1135 Chinese gastric cancer patients was enrolled to identify genetic variants in KCNQ family genes associated with overall survival (OS). Based on the survival evaluation of all five KCNQ family genes, KCNQ1 was selected for subsequent genetic analysis. In both Cox regression model and stepwise Cox regression model used to evaluate survival-related genetic variants, we found that KCNQ1 rs10832417G>T was associated with an increased OS in gastric cancer patients (adjusted hazards ratio [HR] = 0.84, 95% confidence interval [CI]: 0.72-0.98, P = 0.023). Subsequently, a nomogram was constructed to enhance the prognostic capacity and clinical translation of rs10832417 variants. The rs10832417 T allele was predicted to increase the minimum free energy of the secondary structure. Furthermore, we observed that gastric cancer patients with downregulated KCNQ1 expression had a poorer survival across multiple public datasets. The findings of the present study indicate that KCNQ1 rs10832417 may serve as an independent prognostic predictor of gastric cancer, providing novel insights into the progression and survival of the disease.

Glioblastoma multiforme (GBM) is a highly aggressive and lethal brain tumor with limited treatment options. To improve therapeutic efficacy, we developed a novel multifunctional nanoplatform, GM@P(T/S), comprised of polymeric nanoparticles coated with GBM cell membranes as well as co-loaded with temozolomide (TMZ) and superparamagnetic iron oxide (SPIO) nanoparticles. The successful preparation was confirmed in terms of particle size, morphology, stability, the in vitro drug release, and cellular uptake assays. We demonstrated that GM@P(T/S) exhibited the enhanced homotypic targeting, the prolonged blood circulation, and efficient blood-brain barrier penetration in both in vitro and in vivo studies. The combination of TMZ and SPIO nanoparticles within GM@P(T/S) synergistically improved chemo-radiation therapy, leading to a reduced tumor growth, an increased survival, and minimal systemic toxicity in the orthotopic GBM mouse models. Our findings suggest that GM@P(T/S) holds a great promise as a targeted and efficient therapeutic strategy for GBM.

Hypertension (HT) is a major risk factor for cardiovascular diseases. Krüppel-like factors (KLFs) are important transcription factors in eukaryotes. Studies have reported that KLF4 and KLF5 are correlated with several cardiovascular diseases, but population-based studies on associations between HT and KLF4 or KLF5 have rarely been reported. Therefore, the current study investigated the associations of genetic variants and mRNA expression levels of KLF4 and KLF5 with HT, as well as the effects of antihypertensive drugs on the expression levels of these genes. The associations of one single-nucleotide polymorphism (SNP) in KLF4 and three SNPs in KLF5 with HT were analyzed using a combination of case-control and cohort studies. The study populations were selected from a community-based cohort in four regions of Jiangsu province. The risks of HT were estimated through logistic and Cox regression analyses. In addition, mRNA expression levels of KLF4 and KLF5 were detected in 246 controls and 385 HT cases selected from the aforementioned cohort. Among the HT cases, 263 were not taking antihypertensive drugs [AHD(−)] and 122 were taking antihypertensive drugs [AHD(+)]. In the case-control study, SNP rs9573096 (C>T) in KLF5 was significantly associated with an increased risk of HT in the additive model (adjusted odds ratio [OR], 1.106; 95% confidence interval [CI], 1.009 to 1.212). In the cohort study of the normotensive population, rs9573096 in KLF5 was also significantly associated with an increased risk of HT in the additive model (adjusted hazards ratio [HR], 1.199; 95% CI, 1.070 to 1.344). KLF4 and KLF5 mRNA expression levels were significantly higher in the AHD(−) group than in the control group (P < 0.05), but lower in the AHD(+) group than in the AHD(−) group (P < 0.05). The current study demonstrated the associations of KLF4 and KLF5 genetic variants with hypertension, as well as the association of the indicative variations in mRNA expression levels of KLF4 and KLF5 with the risk of hypertension and antihypertensive treatment.