16S rRNA gene sequencing reveals the correlation between the gut microbiota and the susceptibility to pathological scars

The gut microbiome profile in patients with pathological scars remains rarely known, especially those patients who are susceptible to pathological scars. Previous studies demonstrated that gut microbial dysbiosis can promote the development of a series of diseases via the interaction between gut microbiota and host. The current study aimed to explore the gut microbiota of patients who are prone to suffer from pathological scars. 35 patients with pathological scars (PS group) and 40 patients with normal scars (NS group) were recruited for collection of fecal samples to sequence the 16S ribosomal RNA (16S rRNA) V3-V4 region of gut microbiota. Alpha diversity of gut microbiota showed a significant difference between NS group and PS group, and beta diversity indicated that the composition of gut microbiota in NS and PS participants was different, which implied that dysbiosis exhibits in patients who are susceptible to pathological scars. Based on phylum, genus, species levels, we demonstrated that the changing in some gut microbiota (Firmicutes; Bacteroides; Escherichia coli, etc.) may contribute to the occurrence or development of pathological scars. Moreover, the interaction network of gut microbiota in NS and PS group clearly revealed the different interaction model of each group. Our study has preliminary confirmed that dysbiosis exhibits in patients who are susceptible to pathological scars, and provide a new insight regarding the role of the gut microbiome in PS development and progression

Fabrication of a Heterobinuclear Redox Cycle to Enhance the Photocatalytic Activity of BiOCl

La3+ and Ni2+-doped BiOCl were prepared by sol–gel method and characterized by physicochemical and spectroscopic techniques. Their photocatalytic performances were investigated by the degradation of gentian violet under visible light. The results indicated that the co-doping of Ni and La significantly enhanced the photocatalytic performance of BiOCl. The photodegradation efficiency of LaNiBiOCl reached 95.5% in 105 min, which was 1.5 times that of BiOCl. This significant enhancement in photocatalytic activity was mainly attributed to the effective capture and transfer of photogenerated electrons between heterobinuclear La and Ni redox cycle, which benefited the photodegradation of active h+ and the formation of active •O2−. Furthermore, the photodegradation activity did not show an obvious drop after five recycles, indicating that LaNiBiOCl was a promising semiconductor photocatalyst for the degradation of gentian violet

Phosphopeptides P140 cause oxidative burst responses of pulmonary macrophages in an imiquimod-induced lupus model

Abstract Recent studies challenge the dogma that a 21-mer phosphopeptide P140 protects against direct cell damage in the phase-III clinical trial (NCT02504645) for lupus, involving reactive oxygen species (ROS)-dependent release of citrullinated histone H3 (H3cit)-linked neutrophil extracellular traps. An open question is the cellular location of ROS production and H3cit formation in lupus. In this study, we examined the effects of P140 peptides on ROS production and H3cit location in lupus with in vivo and situ fluorescence imaging with subcellular resolution. We developed a mouse model of the B6 strain harbouring a bioluminescent reporter under the control of the Lysozyme M promoter. Based on the imiquimod-induced disease model of B6 mice, we used bioluminescent imaging, flow cytometry analysis, and immunohistology staining to study the effects of P140 peptides in lupus. We found a profound accumulation of CX3CR1-positive macrophages in the lungs of lupus mice after the application of P140, accompanied by lung fibrosis formation. The defined P140-mediated macrophage responses were associated with an increase of H3cit in the cytosol, interleukin-1 receptor type 1 on the extracellular membrane, and intracellular production of ROS. Of interest, the disease of imiquimod-induced lupus was prevented with an antioxidant drug apocynin. This study shows that P140 peptides play a role in aggravated murine lupus in a manner dependent on ROS production and H3cit upregulation through pulmonary macrophages

Neuron-specific enolase in hypertension patients with acute ischemic stroke and its value forecasting long-term functional outcomes

Abstract Background Neuron Specific Enolase (NSE), a neuro-biochemical protein marker, may correlate with the prognosis of stroke patients. Moreover, hypertension is the most common comorbidities in patients with acute ischemic stroke (AIS), and the relationship between NSE levels and long-term functional outcomes in such an increasingly large population is unclear. The aim of the study was to investigate the relationships mentioned above and optimize the prediction models. Methods From 2018 to 2020, 1086 admissions for AIS were grouped as hypertension and non-hypertension, while hypertension group was randomly divided into development and validation cohorts for internal validation. The severity of the stroke was staged by National Institutes of Health Stroke Scale (NIHSS) score. Stroke prognosis after 1 year of follow up was documented by modified Rankin Scale (mRS) score. Results Analysis revealed the following findings:(i) Serum NSE levels increased greatly in hypertension subjects with poor functional outcomes(p = 0.046). However, there was no association in non-hypertension individuals(p = 0.386). (ii) In addition to the conventional factors (age and NIHSS score), NSE (OR:1.241, 95% CI: 1.025–1.502) and prothrombin time were significantly related to the incidence of unfavorable outcomes. (iii)Based on the above four indicators, a novel nomogram was established to predict the prognosis of stoke in hypertension patients with the c-index values of 0.8851. Conclusions Overall, high baseline NSE is associated with poor 1-year AIS outcomes in hypertension patients, suggesting NSE may be a potential prognostic and therapeutic target for stroke in hypertension patients

Single‐Cell and Spatial Transcriptomics Decodes Wharton's Jelly‐Derived Mesenchymal Stem Cells Heterogeneity and a Subpopulation with Wound Repair Signatures

Abstract The highly heterogeneous characteristics of Wharton's jelly mesenchymal stem cells (WJ‐MSCs) may be responsible for the poor clinical outcomes and poor reproducibility of treatments based on WJ‐MSCs. Exploration of WJ‐MSC heterogeneity with multimodal single‐cell technologies will aid in establishing accurate MSC subtyping and developing screening protocols for dominant functional subpopulations. Here, the characteristics of WJ‐MSCs are systematically analyzed by single cell and spatial transcriptome sequencing. Single‐cell transcriptomics analysis identifies four WJ‐MSC subpopulations, namely proliferative_MSCs, niche‐supporting_MSCs, metabolism‐related_MSCs and biofunctional‐type_MSCs. Furthermore, the transcriptome, cellular heterogeneity, and cell‐state trajectories of these subpopulations are characterized. Intriguingly, the biofunctional‐type MSCs (marked by S100A9, CD29, and CD142) selected in this study exhibit promising wound repair properties in vitro and in vivo. Finally, by integrating omics data, it has been found that the S100A9+CD29+CD142+ subpopulation is more enriched in the fetal segment of the umbilical cord, suggesting that this subpopulation deriving from the fetal segment may have potential for developing into an ideal therapeutic agent for wound healing. Overall, the presented study comprehensively maps the heterogeneity of WJ‐MSCs and provides an essential resource for future development of WJ‐MSC‐based drugs