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"Cheng, Han"
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Osteoporosis Due to Hormone Imbalance: An Overview of the Effects of Estrogen Deficiency and Glucocorticoid Overuse on Bone Turnover
Osteoporosis is a serious health issue among aging postmenopausal women. The majority of postmenopausal women with osteoporosis have bone loss related to estrogen deficiency. The rapid bone loss results from an increase in bone turnover with an imbalance between bone resorption and bone formation. Osteoporosis can also result from excessive glucocorticoid usage, which induces bone demineralization with significant changes of spatial heterogeneities of bone at microscale, indicating potential risk of fracture. This review is a summary of current literature about the molecular mechanisms of actions, the risk factors, and treatment of estrogen deficiency related osteoporosis (EDOP) and glucocorticoid induced osteoporosis (GIOP). Estrogen binds with estrogen receptor to promote the expression of osteoprotegerin (OPG), and to suppress the action of nuclear factor-κβ ligand (RANKL), thus inhibiting osteoclast formation and bone resorptive activity. It can also activate Wnt/β-catenin signaling to increase osteogenesis, and upregulate BMP signaling to promote mesenchymal stem cell differentiation from pre-osteoblasts to osteoblasts, rather than adipocytes. The lack of estrogen will alter the expression of estrogen target genes, increasing the secretion of IL-1, IL-6, and tumor necrosis factor (TNF). On the other hand, excessive glucocorticoids interfere the canonical BMP pathway and inhibit Wnt protein production, causing mesenchymal progenitor cells to differentiate toward adipocytes rather than osteoblasts. It can also increase RANKL/OPG ratio to promote bone resorption by enhancing the maturation and activation of osteoclast. Moreover, excess glucocorticoids are associated with osteoblast and osteocyte apoptosis, resulting in declined bone formation. The main focuses of treatment for EDOP and GIOP are somewhat different. Avoiding excessive glucocorticoid use is mandatory in patients with GIOP. In contrast, appropriate estrogen supplement is deemed the primary treatment for females with EDOP of various causes. Other pharmacological treatments include bisphosphonate, teriparatide, and RANKL inhibitors. Nevertheless, more detailed actions of EDOP and GIOP along with the safety and effectiveness of medications for treating osteoporosis warrant further investigation.
Journal Article
Fibronectin in Cancer: Friend or Foe
The role of fibronectin (FN) in tumorigenesis and malignant progression has been highly controversial. Cancerous FN plays a tumor-suppressive role, whereas it is pro-metastatic and associated with poor prognosis. Interestingly, FN matrix deposited in the tumor microenvironments (TMEs) promotes tumor progression but is paradoxically related to a better prognosis. Here, we justify how FN impacts tumor transformation and subsequently metastatic progression. Next, we try to reconcile and rationalize the seemingly conflicting roles of FN in cancer and TMEs. Finally, we propose future perspectives for potential FN-based therapeutic strategies.
Journal Article
A novel long non-coding RNA linc-ZNF469-3 promotes lung metastasis through miR-574-5p-ZEB1 axis in triple negative breast cancer
Triple-negative breast cancer (TNBC) patients usually lead to poor prognosis and survival because of metastasis. The major sites for TNBC metastasis include the lungs, brain, liver, and bone. Long non-coding RNAs (lncRNAs) are non-protein-coding transcripts longer than 200 nucleotides and have been reported as important regulators in BC metastasis. However, the underlying mechanisms for lncRNAs regulating TNBC metastasis are not fully understood. Here we found that
linc-ZNF469-3
was highly expressed in lung-metastatic LM2-4175 TNBC cells and overexpression of
linc-ZNF469-3
enhanced invasion ability and stemness properties in vitro and lung metastasis in vivo. Furthermore, we found
linc-ZNF469-3
physically interacted with
miR-574-5p
and overexpression of
miR-574-5p
attenuated
ZEB1
expression. Importantly, endogenous high expressions of
linc-ZNF469-3
and
ZEB1
were correlated with tumor recurrence in TNBC patients with lung metastasis. Taken together, our findings suggested that
linc-ZNF469-3
promotes lung metastasis of TNBC through
miR-574-5p
-
ZEB1
signaling axis and may be used as potential prognostic marker for TNBC patients.
Journal Article
Validation of Acute Myocardial Infarction Cases in the National Health Insurance Research Database in Taiwan
Background: The aim of this study was to determine the validity of acute myocardial infarction (AMI) diagnosis coding in the National Health Insurance Research Database (NHIRD) by cross-comparisons of discharge diagnoses listed in the NHIRD with those in the medical records obtained from a medical center in Taiwan. Methods: This was a cross-sectional study comparing records in the NHIRD and discharge notes in one medical center (DNMC) in the year 2008. Positive predictive values (PPVs) for AMI diagnoses were evaluated by reviewing the relevant clinical and laboratory data recorded in the discharge notes of the medical center. Agreement in comorbidities, cardiac procedures, and antiplatelet agent (aspirin or clopidogrel) prescriptions between the two databases was evaluated. Results: We matched 341 cases of AMI hospitalizations from the two databases, and 338 cases underwent complete chart review. Of these 338 AMI cases, 297 were confirmed with clinical and lab data, which yielded a PPV of 0.88. The consistency rate for coronary intervention, stenting, and antiplatelet prescription at admission was high, yielding a PPV over 0.90. The percentage of consistency in comorbidity diagnoses was 95.9% (324/338) among matched AMI cases. Conclusions: The NHIRD appears to be a valid resource for population research in cardiovascular diseases.
Journal Article
Transcriptional activation of Jun and Fos members of the AP‐1 complex is a conserved signature of immune aging that contributes to inflammaging
Diverse mouse strains have different health and life spans, mimicking the diversity among humans. To capture conserved aging signatures, we studied long‐lived C57BL/6J and short‐lived NZO/HILtJ mouse strains by profiling transcriptomes and epigenomes of immune cells from peripheral blood and the spleen from young and old mice. Transcriptional activation of the AP‐1 transcription factor complex, particularly Fos, Junb, and Jun genes, was the most significant and conserved aging signature across tissues and strains. ATAC‐seq data analyses showed that the chromatin around these genes was more accessible with age and there were significantly more binding sites for these TFs with age across all studied tissues, targeting pro‐inflammatory molecules including Il6. Age‐related increases in binding sites of JUN and FOS factors were also conserved in human peripheral blood ATAC‐seq data. Single‐cell RNA‐seq data from the mouse aging cell atlas Tabula Muris Senis showed that the expression of these genes increased with age in B, T, NK cells, and macrophages, with macrophages from old mice expressing these molecules more abundantly than other cells. Functional data showed that upon myeloid cell activation via poly(I:C), the levels of JUN protein and its binding activity increased more significantly in spleen cells from old compared to young mice. In addition, upon activation, old cells produced more IL6 compared to young cells. In sum, we showed that the aging‐related transcriptional activation of Jun and Fos family members in AP‐1 complex is conserved across immune tissues and long‐ and short‐living mouse strains, possibly contributing to increased inflammation with age. Here we show that transcriptional activation of the AP‐1 transcription factor (TF) complex members, particularly Fos, Junb, and Jun genes, is the most significant and conserved aging signature across immune cells and tissues in both short (NZO) and long‐living (B6) mice strains. Genomic and functional data showed that chromatin accessibility levels around these genes and the binding activity of their TFs increase with age. These TFs target pro‐inflammatory molecules (e.g., Il6); therefore contributing to increased inflammation with age.
Journal Article
Sexual-dimorphism in human immune system aging
Differences in immune function and responses contribute to health- and life-span disparities between sexes. However, the role of sex in immune system aging is not well understood. Here, we characterize peripheral blood mononuclear cells from 172 healthy adults 22–93 years of age using ATAC-seq, RNA-seq, and flow cytometry. These data reveal a shared epigenomic signature of aging including declining naïve T cell and increasing monocyte and cytotoxic cell functions. These changes are greater in magnitude in men and accompanied by a male-specific decline in B-cell specific loci. Age-related epigenomic changes first spike around late-thirties with similar timing and magnitude between sexes, whereas the second spike is earlier and stronger in men. Unexpectedly, genomic differences between sexes increase after age 65, with men having higher innate and pro-inflammatory activity and lower adaptive activity. Impact of age and sex on immune phenotypes can be visualized at
https://immune-aging.jax.org
to provide insights into future studies.
Whether the immune system aging differs between men and women is barely known. Here the authors characterize gene expression, chromatin state and immune subset composition in the blood of healthy humans 22 to 93 years of age, uncovering shared as well as sex-unique alterations, and create a web resource to interactively explore the data.
Journal Article
The ALMA Legacy Survey of Class 0/I Disks in Corona australis, Aquila, chaMaeleon, oPhiuchus north, Ophiuchus, Serpens (CAMPOS). I. Evolution of Protostellar Disk Radii
We surveyed nearly all the embedded protostars in seven nearby clouds (Corona Australis, Aquila, Chamaeleon I and II, Ophiuchus North, Ophiuchus, Serpens) with the Atacama Large Millimeter/submillimeter Array at 1.3 mm observations with a resolution of 0.″1. This survey detected 184 protostellar disks, 90 of which were observed at a resolution of 14–18 au, making it one of the most comprehensive high-resolution disk samples across various protostellar evolutionary stages to date. Our key findings include the detection of new annular substructures in two Class I and two flat-spectrum sources, while 21 embedded protostars exhibit distinct asymmetries or substructures in their disks. We find that protostellar disks have a substantially large variability in their radii across all evolutionary classes. In particular, the fraction of large disks with sizes above 60 au decreases as the protostar evolves from Class 0 to Class I. Compiling the literature data, we discovered an increasing trend of the gas disk radii to dust disk radii ratio (R gas,Kep/R mm) with increasing bolometric temperature (T bol). Our results indicate that the dust and gas disk radii decouple during the early Class I stage. However, in the Class 0 stage, the dust and gas disk sizes are similar, which allows for a direct comparison between models and observational data at the earliest stages of protostellar evolution. We show that the distribution of radii in the 52 Class 0 disks in our sample is in high tension with various disk formation models, indicating that protostellar disk formation remains an unsolved question.
Journal Article
Surface charge transfer doping for two-dimensional semiconductor-based electronic and optoelectronic devices
Doping of semiconductors, i.e., accurately modulating the charge carrier type and concentration in a controllable manner, is a key technology foundation for modern electronics and optoelectronics. However, the conventional doping technologies widely utilized in silicon industry, such as ion implantation and thermal diffusion, always fail when applied to two-dimensional (2D) materials with atomically-thin nature. Surface charge transfer doping (SCTD) is emerging as an effective and non-destructive doping technique to provide reliable doping capability for 2D materials, in particular 2D semiconductors. Herein, we summarize the recent advances and developments on the SCTD of 2D semiconductors and its application in electronic and optoelectronic devices. The underlying mechanism of STCD processes on 2D semiconductors is briefly introduced. Its impact on tuning the fundamental properties of various 2D systems is highlighted. We particularly emphasize on the SCTD-enabled high-performance 2D functional devices. Finally, the challenges and opportunities for the future development of SCTD are discussed.
Journal Article
The Development of Maillard Reaction, and Advanced Glycation End Product (AGE)-Receptor for AGE (RAGE) Signaling Inhibitors as Novel Therapeutic Strategies for Patients with AGE-Related Diseases
Advanced glycation end products (AGEs) are generated by nonenzymatic modifications of macromolecules (proteins, lipids, and nucleic acids) by saccharides (glucose, fructose, and pentose) via Maillard reaction. The formed AGE molecules can be catabolized and cleared by glyoxalase I and II in renal proximal tubular cells. AGE-related diseases include physiological aging, neurodegenerative/neuroinflammatory diseases, diabetes mellitus (DM) and its complications, autoimmune/rheumatic inflammatory diseases, bone-degenerative diseases, and chronic renal diseases. AGEs, by binding to receptors for AGE (RAGEs), alter innate and adaptive immune responses to induce inflammation and immunosuppression via the generation of proinflammatory cytokines, reactive oxygen species (ROS), and reactive nitrogen intermediates (RNI). These pathological molecules cause vascular endothelial/smooth muscular/connective tissue-cell and renal mesangial/endothelial/podocytic-cell damage in AGE-related diseases. In the present review, we first focus on the cellular and molecular bases of AGE–RAGE axis signaling pathways in AGE-related diseases. Then, we discuss in detail the modes of action of newly discovered novel biomolecules and phytochemical compounds, such as Maillard reaction and AGE–RAGE signaling inhibitors. These molecules are expected to become the new therapeutic strategies for patients with AGE-related diseases in addition to the traditional hypoglycemic and anti-hypertensive agents. We particularly emphasize the importance of “metabolic memory”, the “French paradox”, and the pharmacokinetics and therapeutic dosing of the effective natural compounds associated with pharmacogenetics in the treatment of AGE-related diseases. Lastly, we propose prospective investigations for solving the enigmas in AGE-mediated pathological effects.
Journal Article