Multifunctional cellulose-based aerogel with ultra-stable superhydrophobicity and thermal responsiveness for oil-water separation.

Aerogels are widely used in environmental remediation, but their application is hindered by brittleness, limited oil absorption and poor separation of viscous crude oil. In this study, a multifunctional superhydrophobic aerogel with electrothermal and photothermal effects was prepared from bacterial cellulose (BC), methyltrimethoxysilane (MTMS), and hydroxylated carbon nanotubes (HCNT) by soft-hard synergistic and directed freezing. The prepared aerogel exhibited an oriented layered porous structure with excellent compressibility and oil retention capacity.

RAG suppresses group 2 innate lymphoid cells.

Antigen specificity is the central trait distinguishing adaptive from innate immune function. Assembly of antigen-specific T cell and B cell receptors occurs through V(D)J recombination mediated by the Recombinase Activating Gene endonucleases RAG1 and RAG2 (collectively called RAG). In the absence of RAG, mature T and B cells do not develop and thus RAG is critically associated with adaptive immune function.

RAG suppresses group 2 innate lymphoid cells.

Antigen specificity is the central trait distinguishing adaptive from innate immune function. Assembly of antigen-specific T cell and B cell receptors occurs through V(D)J recombination mediated by the Recombinase Activating Gene endonucleases RAG1 and RAG2 (collectively called RAG). In the absence of RAG, mature T and B cells do not develop and thus RAG is critically associated with adaptive immune function.

A novel bystander effect in tamoxifen treatment: PPIB derived from ER+ cells attenuates ER- cells via endoplasmic reticulum stress-induced apoptosis.

Tamoxifen (TAM) is the frontline therapy for estrogen receptor-positive (ER+) breast cancer in premenopausal women that interrupts ER signaling. As tumors with elevated heterogeneity, amounts of ER-negative (ER-) cells are present in ER+ breast cancer that cannot be directly killed by TAM. Despite complete remissions have been achieved in clinical practice, the mechanism underlying the elimination of ER- cells during TAM treatment remains an open issue.

Identification and Preliminary Clinical Validation of Key Extracellular Proteins as the Potential Biomarkers in Hashimoto's Thyroiditis by Comprehensive Analysis.

Hashimoto's thyroiditis (HT) is an autoimmune disruption manifested by immune cell infiltration in thyroid tissue and the production of antibodies against thyroid-specific antigens, such as the thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TGAb). TPOAb and TGAb are commonly used in clinical tests; however, handy indicators of the diagnosis and progression of HT are still scarce. Extracellular proteins are glycosylated and are likely to enter body fluids and become readily available and detectable biomarkers.

Genetic Testing Enhances the Precision Diagnosis and Treatment of Breast Cancer.

The contemporary comprehension of breast cancer has progressed to the molecular level. As a heterogeneous malignancy, conventional pathological diagnosis and histological classification could no longer meet the needs of precisely managing breast cancer. Genetic testing based on gene expression profiles and gene mutations has emerged and substantially contributed to the precise diagnosis and treatment of breast cancer.

Antibody-Drug Conjugates for Breast Cancer Treatment: Emerging Agents, Targets and Future Directions.

To achieve the scheme of "magic bullets" in antitumor therapy, antibody-drug conjugates (ADCs) were developed. ADCs consist of antibodies targeting tumor-specific antigens, chemical linkers, and cytotoxic payloads that powerfully kill cancer cells. With the approval of ado-trastuzumab emtansine (T-DM1) and fam-trastuzumab deruxtecan (T-DXd), the therapeutic potentials of ADCs in breast cancer have come into the spotlight.

Immunotherapy Targeting PD-1/PD-L1 in Early-Stage Triple-Negative Breast Cancer.

The advent of immunotherapy, especially immune checkpoint inhibitors (ICIs), has revolutionized antitumor therapy. Programmed cell death receptor 1 (PD-1) and programmed cell death ligand 1 (PD-L1) are among the most promising targets for encouraging the immune system to eliminate cancer cells. PD-1/PD-L1 have made clinical remission for numerous solid tumors, including metastatic triple-negative breast cancer (TNBC).

An Integrative Transcriptomic and Metabolomic Study Revealed That Melatonin Plays a Protective Role in Chronic Lung Inflammation by Reducing Necroptosis.

It has been reported that melatonin can relieve the symptoms of chronic obstructive pulmonary disease (COPD) by improving sleep quality, that is to say, the pineal secreted hormone melatonin has a protective effect in the pathogenesis of COPD, but its underlying mechanism remains unclear. In this study, we recruited 73 people into control (n = 22), stable COPD (n = 20), and acute exacerbation of COPD (n = 31) groups to detect the serum melatonin levels. Then, through the mouse model, we employed a systematic study based on the metabolomic and transcriptomic analyses to investigate the molecular mechanisms involved in the progression of the disease.

A basophil-neuronal axis promotes itch.

Itch is an evolutionarily conserved sensation that facilitates expulsion of pathogens and noxious stimuli from the skin. However, in organ failure, cancer, and chronic inflammatory disorders such as atopic dermatitis (AD), itch becomes chronic, intractable, and debilitating. In addition to chronic itch, patients often experience intense acute itch exacerbations.

Scratching Beyond the Surface of Itchy Wounds.

In this issue of Immunity, Xu et al. reveal that dermal dendritic cells produce interleukin-31, which acts on neurons to promote wound itch. Their findings link itch associated with deeper wounds-wounds that extend beyond the epithelium-to the cells and cytokines that mediate wound healing.

The Return of the Mast Cell: New Roles in Neuroimmune Itch Biology.

The mast cell-nerve unit classically has represented a fundamental neuroimmune axis in the development of itch because of the traditional prominence of histamine as a pruritogen. However, it is appreciated increasingly that most chronic itch disorders are likely nonhistaminergic in nature, provoking the hypothesis that other novel effector itch mechanisms derived from mast cells are important. In this review, we present an overview of classical mast cell biology and put these concepts into the context of recent advances in our understanding of the regulation and function of the mast cell-nerve unit in itch biology.

Blood natural killer cell deficiency reveals an immunotherapy strategy for atopic dermatitis.

Atopic dermatitis (AD) is a widespread, chronic skin disease associated with aberrant allergic inflammation. Current treatments involve either broad or targeted immunosuppression strategies. However, enhancing the immune system to control disease remains untested.

Pruritus in allergy and immunology.

Although evolutionarily conserved to expel ectoparasites and aid in the clearance of toxins and noxious environmental stimuli from the host, the type 2 immune response can become pathologic in the setting of a variety of allergic disorders. Itch can be a behavioral extension of type 2 immunity by evoking scratching and, in the setting of disease, can become chronic and thus highly pathologic as well. Classically, our understanding of itch mechanisms has centered around the canonical IgE-mast cell-histamine axis.

Mutual reinforcement between telomere capping and canonical Wnt signalling in the intestinal stem cell niche.

Critical telomere shortening (for example, secondary to partial telomerase deficiency in the rare disease dyskeratosis congenita) causes tissue pathology, but underlying mechanisms are not fully understood. Mice lacking telomerase (for example, mTR telomerase RNA template mutants) provide a model for investigating pathogenesis. In such mice, after several generations of telomerase deficiency telomeres shorten to the point of uncapping, causing defects most pronounced in high-turnover tissues including intestinal epithelium.

HMGB2 orchestrates the chromatin landscape of senescence-associated secretory phenotype gene loci.

Cellular senescence is a stable cell growth arrest that is characterized by the silencing of proliferation-promoting genes through compaction of chromosomes into senescence-associated heterochromatin foci (SAHF). Paradoxically, senescence is also accompanied by increased transcription of certain genes encoding for secreted factors such as cytokines and chemokines, known as the senescence-associated secretory phenotype (SASP). How SASP genes are excluded from SAHF-mediated global gene silencing remains unclear.

Use of Propranolol for Treating Hemangiomas in Infants with Previously Diagnosed Hypoglycemic Conditions.

Infantile hemangiomas (IHs) are the most common pediatric vascular tumors. They require therapy when they cause severe complications such as ulceration, amblyopia, or airway constriction. Propranolol is the only treatment that the U.

Enhancing a Wnt-Telomere Feedback Loop Restores Intestinal Stem Cell Function in a Human Organotypic Model of Dyskeratosis Congenita.

Patients with dyskeratosis congenita (DC) suffer from stem cell failure in highly proliferative tissues, including the intestinal epithelium. Few therapeutic options exist for this disorder, and patients are treated primarily with bone marrow transplantation to restore hematopoietic function. Here, we generate isogenic DC patient and disease allele-corrected intestinal tissue using clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9-mediated gene correction in induced pluripotent stem cells and directed differentiation.

Effects of palmitate on ER and cytosolic Ca2+ homeostasis in beta-cells.

There are strong links between obesity, elevated free fatty acids, and type 2 diabetes. Specifically, the saturated fatty acid palmitate has pleiotropic effects on beta-cell function and survival. In the present study, we sought to determine the mechanism by which palmitate affects intracellular Ca2+, and in particular the role of the endoplasmic reticulum (ER).

Roles of IP3R and RyR Ca2+ channels in endoplasmic reticulum stress and beta-cell death.

Objective: Endoplasmic reticulum (ER) stress has been implicated in the pathogenesis of diabetes, but the roles of specific ER Ca(2+) release channels in the ER stress-associated apoptosis pathway remain unknown. Here, we examined the effects of stimulating or inhibiting the ER-resident inositol trisphosphate receptors (IP(3)Rs) and the ryanodine receptors (RyRs) on the induction of beta-cell ER stress and apoptosis.

Research Design And Methods: Kinetics of beta-cell death were tracked by imaging propidium iodide incorporation and caspase-3 activity in real time.

Accumulation and biodegradation of phenanthrene and fluoranthene by the algae enriched from a mangrove aquatic ecosystem.

This study focused on the accumulation and biodegradation of two typical polycyclic aromatic hydrocarbons (PAHs), phenanthrene (PHE) and fluoranthene (FLA), by the diatoms enriched from a mangrove aquatic ecosystem in the Jiulong River estuary, China. After separation, purification and culture, Skeletonema costatum (Greville) Cleve and Nitzschia sp. were exposed to different concentrations of PHE, FLA, and a mixture of the two.

Glycosylation and annexin II cell surface translocation mediate airway epithelial wound repair.

Glycosylation of cell surface proteins can regulate multiple cellular functions. We hypothesized that glycosylation and expression of glycoproteins after epithelial injury is important in mediating repair. We report the use of an in vitro culture model of human airway epithelial cells (1HAEo(-)) to identify mediators of epithelial repair.