Advanced Hybrid Strategies of GelMA Composite Hydrogels in Bone Defect Repair.

To date, severe bone defects remain a significant challenge to the quality of life. All clinically used bone grafts have their limitations. Bone tissue engineering offers the promise of novel bone graft substitutes.

Role of TOMM34 on NF-κB activation-related hyperinflammation in severely ill patients with COVID-19 and influenza.

Background: Highly pathogenic respiratory RNA viruses such as SARS-CoV-2 and its associated syndrome COVID-19 pose a tremendous threat to the global public health. Innate immune responses to SARS-CoV-2 depend mainly upon the NF-κB-mediated inflammation. Identifying unknown host factors driving the NF-κB activation and inflammation is crucial for the development of immune intervention strategies.

Abnormal dermal microvascular endothelial cells in psoriatic excessive angiogenesis.

Psoriasis is characterized by excessive angiogenesis, with increased distortion and dilation of the dermal blood vessels. These vascular alterations are ascribed, at least in part, to the changes in dermal microvascular endothelial cell functions. However, despite the recognition of vascular normalization as an emerging strategy for the treatment of psoriasis, in-depth studies of human dermal microvascular endothelial cells (HDMECs) have been missing.

Downregulation of lysine 2-hydroxyisobutyrylation of ErbB3 binding protein 1 at amino acid 210 promotes keratinocyte proliferation via induction of transcription initiation factor IA-mediated rRNA synthesis.

Background: Psoriasis is a prevalent chronic inflammatory dermatosis characterized by the excessive proliferation of keratinocytes (KCs). Lysine 2-hydroxyisobutyrylation (Khib) is a newly identified post-translational modification that regulates various biological processes. Abnormal Khib modification has been associated with the development of autoimmune diseases.

A germline exon12 mutation and a late somatic mutation in a patient with essential thrombocythemia.

Background: It has been discovered that Janus kinase 2 () exon12 mutations lead to the polycythemia vera (PV) phenotype, while somatic mutations of calreticulin () are associated with essential thrombocythemia (ET) or primary myelofibrosis. In this article, we report a case of ET with coexistence of exon12 and mutations. The objective of this study was to elucidate the pathogenicity mechanism of a exon12 mutation (N533S) and the role of the coexistence of mutations on the hematological phenotype.

IL-17A is involved in the hyperplasia of blood vessels in local lesions of psoriasis by inhibiting autophagy.

Objective: Increased angiogenesis is a pathological feature of psoriasis, but the pathomechanisms of angiogenesis in psoriasis are not clear. Interleukin-17A (IL-17A) is the major effect factor in the pathogenesis of psoriasis. Our results showed that IL-17A can promote angiogenesis and cause endothelial cell inflammation.

Nanostructured ionic hydrogel with integrated conductivity, stretchability and thermal responsiveness for a high-performance strain and temperature sensor.

Ionic conductive hydrogels are promising candidates for fabricating wearable sensors for human motion detection and disease diagnosis, and electronic skin. However, most of the existing ionic conductive hydrogel-based sensors primarily respond to a single-strain stimulus. Only a few ionic conductive hydrogels can respond to multiple physiological signals.

Autophagy Inhibits Inflammation via Down-Regulation of p38 MAPK/mTOR Signaling Cascade in Endothelial Cells.

Objective: Autophagy, an intracellular process of self-digestion, has been shown to modulate inflammatory responses. In the present study, we determined the effects of autophagy on inflammatory response induced by M5 cytokines.

Methods: Human umbilical vein endothelial cells (HUVECs) were treated with M5 cytokines to induce inflammation.

The mRNA Expression Profile of Psoriatic Lesion Distinct from Non-Lesion.

Purpose: Psoriasis is a chronic recurring autoimmune skin disease with a complex etiology and chronic progression; however, its molecular mechanisms remain unclear.

Patients And Methods: We performed transcriptomic analysis to profile the mRNA expression of psoriatic lesions (PL) and non-lesion (NL) tissues from psoriasis patients along with normal skin from healthy donors. RT-qPCR was used to validate the mRNA expression profiles.

Psoriatic Dermal-Derived Mesenchymal Stem Cells Induced C3 Expression in Keratinocytes.

Purpose: Our recent studies found a splice region mutation in C3 accompanied by a significantly increased C3 in psoriatic peripheral blood. Mesenchymal stem cells (MSCs) are a key immunological suppression cell. We further investigate the regulation of MSCs on C3 in psoriasis.

Variants in PRKCE and KLC1, Potential Regulators of Type I Psoriasis.

Purpose: Psoriasis is a multifactorial disease with a complex genetic predisposition. The pathophysiology of psoriasis is associated with genetic variants. To better characterize gene variants in psoriasis and identify the relationship between clinical characteristics and variant genes in its pathogenesis.

Normal mesenchymal stem cells can improve the abnormal function of T cells in psoriasis via upregulating transforming growth factor-β receptor.

Psoriasis, a chronic inflammatory skin disease, is a refractory disorder. Previous studies have shown that the imbalance of the T-helper (Th)17/regulatory T cells (Treg) results in the immune imbalance of T cells in psoriatic patients, and that mesenchymal stem cells display an immunosuppressive role by promoting the differentiation of T cells into Treg, leading to a reduction in the proportion of Th17/Treg. Utility of mesenchymal stem cells is becoming a new approach for the treatment of immune disorders.

Psoriatic Serum Induce an Abnormal Inflammatory Phenotype and a Decreased Immunosuppressive Function of Mesenchymal Stem Cells.

Background And Objectives: Mesenchymal stem cells (MSCs) have immunomodulatory function and participate in the pathogenesis of many immunoregulation-related diseases, including psoriasis. Previously, we found that MSCs from psoriatic lesions overexpress the proinflammatory microRNA, miR-155 and exhibit a decreased immunosuppressive capacity. But the origin of these aberrant characteristics is still not clear.

MicroRNA-31 Overexpression may Aggravate the Formation of Psoriasis-like Lesions by STAT3/p53 Pathway.

Background: Psoriasis is a chronic inflammatory skin disease with an unknown pathogenesis. Recently, miR-31 have been shown to play an important role in psoriasis. Moreover, STAT3/p53 pathway has been used in tumor studies, but rarely in psoriasis studies.

MiR-155 inhibits TP53INP1 expression leading to enhanced glycolysis of psoriatic mesenchymal stem cells.

Background: Psoriasis is a systemic disease with multiple associated comorbidities, including metabolic syndrome. Studies suggest that chronic inflammation is a central link between psoriasis and metabolic abnormalities. MiR-155 is a well-known microRNA that plays an important regulatory role in inflammation.