American Heart Association Council on cardiovascular nursing.

Biosensing is of vital importance for advancing public health through monitoring abnormalities in biological systems, which may be potentially associated with certain body dysfunctions. A wide range of luminescent materials have been actively pursued in the fabrication of biosensing platforms, particularly ones that can function in complex biological fluids with high selectivity and sensitivity. Recently, metal-organic frameworks (MOFs) have experienced rapid growth due to their tunable structures, large surface area, and being prone to surface engineering, etc. These virtues endow MOF materials with immense feasibility in the target-oriented construction of sensing platforms for specific applications. In this review, we extrapolated six sensing mechanisms for MOF-based photoluminescent biosensing platforms, including photoelectron transfer (PET), resonance energy transfer (RET), competition absorption (CA), structural transformation (ST), chemical conversion (CC), and quencher detachment (QD). Accordingly, recent progress of MOF-based materials in photoluminescence sensing of biomolecules, biomarkers, drugs, and toxins was highlighted. The objective of this review is to provide readers with an extensive overview of the design and synthesis of MOF materials for photoluminescence biosensing. The challenges and outlook are briefly discussed at the end.

Metal-organic frameworks as photoluminescent biosensing platforms: mechanisms and applications.

Galectin-3 (Gal-3) regulates basic cellular functions such as cell–cell and cell–matrix interactions, growth, proliferation, differentiation, and inflammation. It is not surprising, therefore, that this protein is involved in the pathogenesis of many relevant human diseases, including cancer, fibrosis, chronic inflammation and scarring affecting many different tissues. The papers published in the literature have progressively increased in number during the last decades, testifying the great interest given to this protein by numerous researchers involved in many different clinical contexts. Considering the crucial role exerted by Gal-3 in many different clinical conditions, Gal-3 is emerging as a new diagnostic, prognostic biomarker and as a new promising therapeutic target. The current review aims to extensively examine the studies published so far on the role of Gal-3 in all the clinical conditions and diseases, listed in alphabetical order, where it was analyzed.

https://www.mdpi.com/1422-0067/19/2/379/pdf

Galectin-3: One Molecule for an Alphabet of Diseases, from A to Z.

Osteocytes, the most abundant cells in bone, have been long postulated to detect and respond to mechanical and hormonal stimuli and to coordinate the function of osteoblasts and osteoclasts. The discovery that the inhibitor of bone formation sclerostin is primarily expressed in osteocytes in bone and downregulated by anabolic stimuli provided a mechanism by which osteocytes influence the activity of osteoblasts. Advances of the last few years provided experimental evidence demonstrating that osteocytes also participate in the recruitment of osteoclasts and the initiation of bone remodeling. Apoptotic osteocytes trigger yet-to-be-identified signals that attract osteoclast precursors to specific areas of bone, which in turn differentiate to mature, bone-resorbing osteoclasts. Osteocytes are also the source of molecules that regulate the generation and activity of osteoclasts, such as OPG and RANKL; and genetic manipulations of the mouse genome leading to loss or gain of function or to altered expression of either molecule in osteocytes markedly affect bone resorption. This review highlights these investigations and discusses how the novel concept of osteocyte-driven bone resorption and formation impacts our understanding of the mechanisms by which current therapies control bone remodeling.

Osteocyte-Driven Bone Remodeling

The identification of new bioactive compounds derived from medicinal plants with significant therapeutic properties has attracted considerable interest in recent years. Such is the case of the Tripterygium wilfordii, an herb used in Chinese medicine. Clinical trials performed so far using its root extracts have shown impressive therapeutic properties, but also revealed substantial gastrointestinal side-effects. The most promising bioactive compound obtained from Tripterygium wilfordii is celastrol. During the last decade, an increasing number of studies were published highlighting the medicinal usefulness of celastrol in diverse clinical areas. Here we systematically review the mechanism of action and the therapeutic properties of celastrol in inflammatory diseases, namely rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel diseases, osteoarthritis and allergy, as well as in cancer, neurodegenerative disorders and other diseases, such as diabetes, obesity, atherosclerosis and hearing loss. We will also focus in the toxicological profile and limitations of celastrol formulation, namely solubility, bioavailability and dosage issues that still limit its further clinical application and usefulness.

/pdf/celastrol-a-spectrum-of-treatment-opportunities-in-chronic-290j4ljnki.pdf

Celastrol: A Spectrum of Treatment Opportunities in Chronic Diseases.

Anti-atherosclerotic potential of baicalin mediated by promoting cholesterol efflux from macrophages via the PPARγ-LXRα-ABCA1/ABCG1 pathway.

The aim of this study was to assess the expression patterns of serum galectin-1 (Gal-1), galectin-3 (Gal-3), galectin-9 (Gal-9), and galectin-3 binding protein (Gal-3BP) and their associations with stroke outcome in large artery atherosclerotic (LAA) stroke. The serum levels of Gal-1, Gal-3, Gal-9, and Gal-3BP were measured by ELISA in 130 patients with LAA stroke and 130 age- and sex-matched controls. Serum samples were collected from the patients on day 1, day 6, and in the 4th week after ischaemic stroke (IS). An unfavourable outcome was defined as a modified Rankin Scale score of >2 on day 90 after IS. Our results indicated that the Gal-3 and Gal-9 levels were higher in patients with LAA stroke than in controls. A higher Gal-3 level was independently associated with an unfavourable outcome both on day 1 and day 6 after IS. In addition, Gal-9 and Gal-1 levels were upregulated on day 6 and in the 4th week after IS, respectively. For Gal-3BP, no difference was detected between patients and controls and no predictive value was found in patients. In conclusion, these findings suggest that the serum levels of Gal-1, Gal-3, and Gal-9 may be associated with LAA stroke.

/pdf/serum-levels-of-galectin-1-galectin-3-and-galectin-9-are-nxmvnqqp0b.pdf

Serum levels of galectin-1, galectin-3, and galectin-9 are associated with large artery atherosclerotic stroke.

Background: Celastrol may have an anti-atherosclerosis effect. This study aimed to investigate if celastrol had an anti-AS effect using a rabbit experimental carotid atherosclerosis model. Methods: Forty male Japanese white rabbits were divided into the sham group (normal diet), the model group (high fat diet), the group treated with celastrol (high fat diet) and the group treated with atorvastatin (high fat diet) randomly. The rabbits fed a high fat diet underwent balloon injury of the right common carotid artery and were treated with dimethyl sulfoxide (DMSO) (the model group, 3.5 ml/kg/d), celastrol and its dissolvent DMSO (the celastrol group, 1 mg/kg/d and 3.5 ml/kg/d) and atorvastatin and its dissolvent DMSO (the atorvastatin group, 2.5 mg/kg/d and 3.5 ml/kg/d) for 12 weeks by gavage. Results: The ratio of the plaque area and the arterial wall cross-section area in the celastrol group was significantly less than the model group (P < 0.001), and there was no significant difference compared with the atorvastatin group. The serum level of LDL-C of the celastrol group was significantly lower than the model group (P = 0.014), and there was no significant difference compared with the atorvastatin group. The expression of VEGF in the celastrol group was significantly less compared with the model group (P = 0.014), whereas the expression of VEGF in the atorvastatin group and the model group showed no significant differences. Conclusion: Our findings suggest that celastrol effectively reduced the plaque ratio, decreased the serum levels of LDL and downregulated the expression of VEGF, suggesting an anti-AS effect of celastrol.

Celastrol may have an anti-atherosclerosis effect in a rabbit experimental carotid atherosclerosis model.

The aim of the current study was to explore the possible association of the polymorphism of C(-735)T in MMP-2 with the vulnerable plaque risk in ultrasound-confirmed carotid atherosclerosis cases. Serum MMP-2 levels were measured to investigate the relationship between the MMP-2 level and the genetic variability. The MMP-2 polymorphism was detected by PCR-RFLP in the 243 cases with stable plaque and 221 cases with vulnerable plaque. Serum MMP-2 levels were measured with ELISA. The results showed that MMP-2 was significantly higher in the cases with vulnerable plaque than in the cases with stable plaque. A statistical difference was found between the genotype distributions in the vulnerable plaque cases and that in the stable cases. T-allele frequency was also found to be over-represented in the stable plaque cases than in the vulnerable plaque cases, which might partially explain the observed difference in the serum MMP-2 levels in the different plaque cases. The current results also suggested that MMP-2 was a risk factor in the cases with vulnerable plaques, whereas TT genotype and T allele might be protective factors in the cases with vulnerable plaques.

https://journals.sagepub.com/doi/pdf/10.1177/1358863X10394237

Genotype association of C(-735)T polymorphism of the MMP-2 gene with the risk of carotid atherosclerosis-vulnerable plaque in the Han Chinese population:

Increasing evidence supports the involvement of periostin in the pathophysiological processes of stroke and atherosclerosis. The aim of this study was to assess circulating periostin levels at different times after large-artery atherosclerotic (LAA) stroke and their association with stroke. Serum periostin levels were measured using enzyme-linked immunosorbent assay on day 1 in 162 patients with LAA stroke and in 108 age- and sex-matched controls, on day 6 after stroke in 134 patients, and during the 4th week after stroke in 46 of the 162 patients. Stroke severity was determined using the National Institutes of Health Stroke Scale (NIHSS), and the stroke volume was measured. Outcome at 3 months was measured using the modified Rankin Scale (mRS). Our results indicated that periostin levels increased significantly on day 6 after stroke, and this increasing trend persisted for at least 4 weeks after the event. In addition, the increase in periostin levels was positively correlated with the NIHSS scores and stroke volume, but not with the mRS scores after adjusting for the NIHSS scores. In conclusion, these findings suggest that the increase in serum periostin levels observed after stroke may be associated with the stroke severity in patients with LAA stroke.

/pdf/longitudinal-evaluation-of-serum-periostin-levels-in-46khvnz76v.pdf

Longitudinal evaluation of serum periostin levels in patients after large-artery atherosclerotic stroke: A prospective observational study.

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