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Soft micro‐ and nanostructures have been extensively developed for biomedical applications. The main focus has been on multifunctional composite materials that combine the advantages of hydrogels and colloidal particles. Magnetic microgels and nanogels can be realized by hybridizing stimuli‐sensitive gels and magnetic nanoparticles. They are of particular interest since they can be controlled in a wide range of biological environments by using magnetic fields. In this review, we elucidate physical principles underlying the design of magnetic microgels and nanogels for biomedical applications. Particularly, this article provides a comprehensive and conceptual overview on the correlative structural design and physical functionality of the magnetic gel systems under the concept of colloidal biodevices. To this end, we begin with an overview of physicochemical mechanisms related to stimuli‐responsive hydrogels and transport phenomena and summarize the magnetic properties of inorganic nanoparticles. On the basis of the engineering principles, we categorize and summarize recent advances in magnetic hybrid microgels and nanogels, with emphasis on the biomedical applications of these materials. Potential applications of these hybrid microgels and nanogels in anticancer treatment, protein therapeutics, gene therapy, bioseparation, biocatalysis, and regenerative medicine are highlighted. Finally, current challenges and future opportunities in the design of smart colloidal biodevices are discussed.

Appropriate dietary adjustment in patients with chronic kidney disease (CKD) is important, and nutritional guidelines recommend different dietary management depending on the CKD stage. However, there is no study, to our knowledge, of the characteristics of dietary intake according to CKD stages. We tried to assess the comparison of nutritional intake according to CKD stages. A cross-sectional study was conducted to reveal the characteristics of dietary intake among patients with CKD based on the Korean National Health and Nutritional Examination Survey between 2011 and 2014. Of 16,878 participants, we classified non-CKD (n = 14,952) and CKD (n = 1,926), which was stratified into five groups (I, II, IIIa, IIIb, and IV–V). We investigated the characteristics of dietary intake, such as energy, water, protein, fat, carbohydrate, sodium, potassium, calcium, and phosphorus, according to stage of CKD. We also explored nutritional intake according to CKD stage among patients with early CKD (stage I and II) and advanced CKD (stage IIIa, IIIb, and IV–V). Intake of majority of nutrients and energy tended to be decreased as CKD progressed. In early CKD stage, intake of energy, water, protein, fat, carbohydrate, potassium, calcium and phosphorus seemed to be statistically significant decreased as CKD progressed. In advanced CKD stage, intake of potassium and calcium seemed to be decreased as CKD progressed, but the intake of energy was about to be lower limit. Appropriate dietary education and CKD recognition are needed to improve nutritional intake depending on the CKD stage.

Osteoporosis and other manifestations of bone disease are frequent in patients with systemic mastocytosis (SM) in association with the presence of mast cell infiltrates in bone marrow, although the mechanisms behind bone disease remain poorly understood. We find that extracellular vesicles (EVs) released by neoplastic mast cells and present in the serum of patients with SM (SM-EVs) block osteoblast differentiation and mineralization in culture, and when injected into mice diminish the expression of osteoblast markers, and trabecular bone volume and microarchitecture. We demonstrate that miRNA-30a and miRNA-23a, increased in SM-EVs and neoplastic mast cell-derived EVs, attenuate osteoblast maturation by suppressing expression of RUNX2 and SMAD1/5, essential drivers of osteogenesis. Thus, SM-EVs carry and deliver miRNAs that epigenetically interfere with bone formation and can contribute to bone mass reduction in SM. These findings also suggest possibilities for novel approaches to the management of bone disease in mast cell proliferative disorders. Osteoporosis and bone disease are common in patients with systemic mastocytosis. Here, the authors show that extracellular vesicles released by neoplastic mast cells of the patients block osteoblast differentiation and bone mineralization when injected into mice, via a mechanism involving suppression of osteogenic factors via miRNA-30a and miRNA-23a.

The principle of magnetic hyperthermia is to generate localized heating on target proteins, cells and tissue that are targeted by magnetic nanoparticles (MNPs) upon stimulation by remotely applied high frequency alternating magnetic field (AMF). Beyond its traditional applications in hyperthermia therapy, recent studies demonstrated the feasibility of magnetic hyperthermia as a new strategy for neural stimulation. The objective of this study is to examine the feasibility of localized magnetic hyperthermia (i.e. MNP/AMF hyperthermia) as a new strategy for brain stimulation, especially in modulating microglia activity and behaviors in vivo. This was examined by correlating a varying degree of MNP/AMF-induced thermal dose with the extent of microglial activation in the mouse brain. The MNP/AMF hyperthermia stimulation applied at a mild thermal dose to the mouse hippocampus significantly increased the infiltration of microglia and altered their morphology towards reactive and ameboid-like phenotypes in a thermal dose-dependent manner. Importantly, these responses were associated with increased expression of heat shock protein 70 (HSP70), a molecular chaperon protein, and LC3II, a marker of autophagic activity. Our findings support the feasibility of developing mild magnetic hyperthermia as a new strategy for localized stimulation of brain tissue.

We had previously investigated the expression and functional role of C-X-C Motif Chemokine Ligand 12 (CXCL12) during the hair cycle progression. CXCL12 was highly expressed in stromal cells such as dermal fibroblasts (DFs) and inhibition of CXCL12 increased hair growth. Therefore, we further investigated whether a CXCL12 neutralizing antibody (αCXCL12) is effective for androgenic alopecia (AGA) and alopecia areata (AA) and studied the underlying molecular mechanism for treating these diseases. In the AGA model, CXCL12 is highly expressed in DFs. Subcutaneous (s.c.) injection of αCXCL12 significantly induced hair growth in AGA mice, and treatment with αCXCL12 attenuated the androgen-induced hair damage in hair organ culture. Androgens increased the secretion of CXCL12 from DFs through the androgen receptor (AR). Secreted CXCL12 from DFs increased the expression of the AR and C-X-C Motif Chemokine Receptor 4 (CXCR4) in dermal papilla cells (DPCs), which induced hair loss in AGA. Likewise, CXCL12 expression is increased in AA mice, while s.c. injection of αCXCL12 significantly inhibited hair loss in AA mice and reduced the number of CD8+, MHC-I+, and MHC-II+ cells in the skin. In addition, injection of αCXCL12 also prevented the onset of AA and reduced the number of CD8+ cells. Interferon-γ (IFNγ) treatment increased the secretion of CXCL12 from DFs through the signal transducer and activator of transcription 3 (STAT3) pathway, and αCXCL12 treatment protected the hair follicle from IFNγ in hair organ culture. Collectively, these results indicate that CXCL12 is involved in the progression of AGA and AA and antibody therapy for CXCL12 is promising for hair loss treatment.

The number of patients with diabetes and impaired fasting blood glucose in Korea is rapidly increasing compared to the past, and other metabolic indicators of population are also changed in recent years. To clarify the mechanism more clearly, we investigated the association between fasting blood glucose and incidence of pancreatic cancer in this retrospective cohort study. In Korea National Health Information Database, 19,050 participants without pancreatic cancer in 2009 were enrolled, and followed up until 2013. We assessed the risk of incident pancreatic cancer according to the quartile groups of fasting blood glucose level (quartile 1: <88 mg/dL, quartile 2: 88-97 mg/dL, quartile 3: 97-109 mg/dL and quartile 4: ≥109 mg/dL). Multivariate Cox-proportional hazard model was used in calculating hazard ratios (HRs) and 95% confidence interval (CI) for incident pancreatic cancer. Compared with quartile1 (reference), unadjusted HRs and 95% CI for incident pancreatic cancer significantly increased in order of quartile2 (1.39 [1.01-1.92]), quartile3 (1.50 [1.09-2.07]) and quartile4 (2.18 [1.62-2.95]), and fully adjusted HRs and 95% CI significantly increased from quartile2 (1.47 [1.05-2.04]), quartile3 (1.61 [1.05-2.04]) to quartile4 (2.31 [1.68-3.17]). Fasting blood glucose even with pre-diabetic range was significantly associated with the incident pancreatic cancer in Korean.

Background The risk of non-Hodgkin’s lymphoma in patients with primary Sjögren’s syndrome (pSS) is well established. However, the association between pSS and the risk of gastrointestinal cancers remains underexplored. This study aims to assess the risk of gastrointestinal cancers in pSS patients in Korea compared with the general population. Methods We included 320,082 participants from National Health Insurance Service-National Sample Cohort (NHIS-NSC) database. Of these, there were 850 patients with pSS and 319,232 in the non-pSS group. All participants were followed-up until 2019 or the development of gastrointestinal cancers, whichever occurred first. Hazard ratio (HR) and 95% confidence intervals (95% CI) for gastrointestinal cancers were calculated by multivariable Cox proportional hazards models. Results Compared with the non-pSS group, patients with pSS had a higher risk of developing all gastrointestinal cancers, but the association did not reach statistical significance (adjusted HR: 1.240, 95% CI: 0.990–1.543). Site-specific analyses showed that pSS patients had a higher risk of colorectal cancer (adjusted HR: 1.597, 95% CI: 1.122–2.273) and pancreatic cancer (adjusted HR: 2.294, 95% CI: 1.267–4.151). The association was found to be more prominent in females and elderly (aged ≥ 60) individuals according to subgroup analyses. Conclusions pSS was associated with increased risks of colorectal and pancreatic cancers, particularly among females and older adults. Further research should explore the underlying mechanisms and the impact of pSS duration and severity on cancer risk.

Optogenetic approaches for controlling Ca 2+ channels provide powerful means for modulating diverse Ca 2+ -specific biological events in space and time. However, blue light-responsive photoreceptors are, in principle, considered inadequate for deep tissue stimulation unless accompanied by optic fiber insertion. Here, we present an ultra-light-sensitive optogenetic Ca 2+ modulator, named monSTIM1 encompassing engineered cryptochrome2 for manipulating Ca 2+ signaling in the brain of awake mice through non-invasive light delivery. Activation of monSTIM1 in either excitatory neurons or astrocytes of mice brain is able to induce Ca 2+ -dependent gene expression without any mechanical damage in the brain. Furthermore, we demonstrate that non-invasive Ca 2+ modulation in neurons can be sufficiently and effectively translated into changes in behavioral phenotypes of awake mice. Optogenetic applications in the brain of live animals often require the use of optic fibers due to poor tissue-penetration of blue light. Here the authors present monSTIM1, an improved high sensitivity optogenetic tool able to modulate Ca 2+ signaling in the brain of awake mice using non-invasive light stimulation.

We investigated the relationship between the peripapillary retinal nerve fiber layer and peripapillary retinal thickness in patients with diabetic macular edema. Fifty eyes (group I) with non-proliferative diabetic retinopathy and diabetic macular edema receiving intravitreal anti-VEGF injection, and 90 eyes (group II) without diabetic macular edema were included in this case-control study. The peripapillary retinal nerve fiber layer thickness, peripapillary retinal thickness, and a new retinal nerve fiber layer index using a modeled relationship between the two parameters were evaluated with spectral-domain optical coherence tomography, at baseline and at the 6-month follow-up. In group I, the peripapillary retinal nerve fiber layer thickness decreased from 126.4 μm at baseline to 117.6 μm at 6 months (p < 0.001), while the peripapillary retinal thickness decreased from 376.0 μm at baseline to 359.6 μm at 6 months (p < 0.001) after intravitreal anti-VEGF injection. In group II, however, both the parameters remained stable at the 6-month follow-up (100.7 to 102.1 μm and 311.1 to 316.2 μm, respectively, and all p > 0.01). Analysis with the new index to adjust for retinal edema showed no significant change from baseline to 6 months in both groups (p = 0.593 and p = 0.101, respectively). The peripapillary retinal nerve fiber layer thickness is strongly affected by the peripapillary retinal thickness. Therefore, the measured changes in peripapillary retinal nerve fiber layer thickness may not represent the real gain or loss of the retinal nerve fiber layer. Therefore, the new retinal nerve fiber layer index, which corrects for the component of macula edema, could be a better means of assessing the changes of peripapillary retinal nerve fiber layer thickness in patients with diabetic macular edema.