Integrated genetic and epigenetic analyses uncover MSI2 association with allergic inflammation

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Microbiome-induced antigen-presenting cell recruitment coordinates skin and lung allergic inflammation

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Targeted protein degraders march towards the clinic for neurodegenerative diseases

Protein degraders are emerging as potent therapeutic tools to address neurological disorders and many complex diseases. It offered several key advantages, including the doses, drug resistance, and side effects over traditional occupancy-based inhibitors. Translation of chemical degraders into a clinical therapy for neurodegenerative disorders has a well-documented knowledge and resource gap. Researchers strive to develop clinical candidates employing chemical degraders' technologies, including hydrophobic tagging, molecular glues, proteolysis targeting chimeras (PROTACs), specific and nongenetic Inhibitor of Apoptosis Protein (IAP)-dependent protein erasers (SNIPERs), autophagy targeted chimeras, and autophagosome-tethered compounds for targeted degradation of pathological markers in neurodegenerative disease. Herein, we examined the present state of chemical-mediated targeted protein degradation in the quest for medications to treat neurodegenerative diseases. We further identified targeted degraders under clinical development for neurodegenerative diseases summarizing pertinent discoveries guiding the future of degradation therapeutics. We also addressed the necessary pharmacological interventions needed to achieve unprecedented therapeutic efficacy and its associated challenges.     

Skin-resident natural killer T cells participate in cutaneous allergic inflammation in atopic dermatitis

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COPD-associated miR-145-5p is downregulated in early-decline FEV1 trajectories in childhood asthma

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Cardiovascular changes during peanut-induced allergic reactions in human subjects

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Ceramide in apoptosis and oxidative stress in allergic inflammation and asthma

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Protein arginine methyltransferase 1 contributes to the development of allergic rhinitis by promoting the production of epithelial-derived cytokines

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Increased nasal mucosal interferon and CCL13 response to a TLR7/8 agonist in asthma and allergic rhinitis

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Ssu72 regulates alveolar macrophage development and allergic airway inflammation by fine-tuning of GM-CSF receptor signaling

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Chromatin interactions in differentiating keratinocytes reveal novel atopic dermatitis– and psoriasis-associated genes

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Low incidence of hepatitis B virus reactivation in patients with hematological malignancies receiving novel anticancer drugs: A report from a high epidemic area and literature review

BackgroundMore and more novel anticancer drugs have been approved for patients with hematological malignancies in recent years, but HBV reactivation (HBV-R) data in this population is very scarce. This study aimed to evaluated HBV-R risk in patients with hematological malignancies receiving novel anticancer drugs.MethodsHBV markers and serum HBV DNA levels of patients with hematological malignancies receiving novel anticancer drugs in a tertiary cancer hospital were retrospectively collected. HBV-R risk in the whole cohort and subgroups was described. The relevant literature was reviewed to make a pooled analysis.ResultsOf 845 patients receiving novel anticancer drugs, 258 (30.5%) were considered at risk for HBV-R. The median duration of exposure to novel drugs was 5.6 (0.1–67.6) months. The incidence of HBV-R was 2.1% in patients with past HBV infection without prophylactic antiviral treatment (PAT) and 1.2% in all patients at risk of HBV-R. In a pooled analysis of 11 studies with 464 patients, the incidence of HBV-R was 2.4% (95% CI: 1.3–4.2) in all at-risk patients receiving novel anticancer drugs and 0.6% (95% CI: 0.03–3.5) in patients with anticancer drugs plus PAT. The incidence of death due to HBV-R was 0.4% (95% CI: 0.1–1.6) in all at-risk patients and 18.2% (95% CI: 3.2–47.7) in patients with HBV-R.ConclusionMost episodes of HBV-R are preventable, and most cases with HBV-R are manageable. We recommend that novel anticancer drugs should not be intentionally avoided when treating cancer patients with HBV infection.