Obesity and the risk of heart failure

Aluminum is an abundant and high-quality material for plasmonics with potential for large-area, low-cost photonic technologies. Here we examine aluminum nanoclusters with plasmonic Fano resonances that can be tuned from the near-UV into the visible region of the spectrum. These nanoclusters can be designed with specific chromaticities in the blue-green region of the spectrum and exhibit a remarkable spectral sensitivity to changes in the local dielectric environment. We show that such structures can be used quite generally for colorimetric localized surface plasmon resonance (LSPR) sensing, where the presence of analytes is detected by directly observable color changes rather than through photodetectors and spectral analyzers. To quantify our results and provide a metric for optimization of such structures for colorimetric LSPR sensing, we introduce a figure of merit based on the color perception ability of the human eye.

Fano Resonant Aluminum Nanoclusters for Plasmonic Colorimetric Sensing.

Psoriasis is caused by a complex interplay among the immune system, genetic background, autoantigens, and environmental factors. Recent studies have demonstrated that patients with psoriasis have a significantly higher serum homocysteine (Hcy) level and a higher prevalence of hyperhomocysteinaemia (HHcy). Insufficiency of folic acid and vitamin B12 can be a cause of HHcy in psoriasis. Hcy may promote the immuno-inflammatory process in the pathogenesis of psoriasis by activating Th1 and Th17 cells and neutrophils, while suppressing regulatory T cells. Moreover, Hcy can drive the immuno-inflammatory process by enhancing the production of the pro-inflammatory cytokines in related to psoriasis. Hcy can induce nuclear factor kappa B activation, which is critical in the immunopathogenesis of psoriasis. There may be a link between the oxidative stress state in psoriasis and the effect of HHcy. Hydrogen sulfide (H2S) may play a protective role in the pathogenesis of psoriasis and the deficiency of H2S in psoriasis may be caused by HHcy. As the role of Hcy in the pathogenesis of psoriasis is most likely established, Hcy can be a potential therapeutic target for the treatment of psoriasis. Systemic folinate calcium, a folic acid derivative, and topical vitamin B12 have found to be effective in treating psoriasis.

/pdf/homocysteine-and-psoriasis-1eyadfzepx.pdf

Homocysteine and psoriasis

Myeloproliferative neoplasms are associated with increased risk for thrombotic complications. These conditions most commonly involve somatic mutations in genes that lead to constitutive activation of the Janus-associated kinase signaling pathway (eg, Janus kinase 2, calreticulin, myeloproliferative leukemia protein). Acquired gain-of-function mutations in these genes, particularly Janus kinase 2, can cause a spectrum of disorders, ranging from clonal hematopoiesis of indeterminate potential, a recently recognized age-related promoter of cardiovascular disease, to frank hematologic malignancy. Beyond thrombosis, patients with myeloproliferative neoplasms can develop other cardiovascular conditions, including heart failure and pulmonary hypertension. The authors review the pathophysiologic mechanisms of cardiovascular complications of myeloproliferative neoplasms, which involve inflammation, prothrombotic and profibrotic factors (including transforming growth factor-beta and lysyl oxidase), and abnormal function of circulating clones of mutated leukocytes and platelets from affected individuals. Anti-inflammatory therapies may provide cardiovascular benefit in patients with myeloproliferative neoplasms, a hypothesis that requires rigorous evaluation in clinical trials. 

https://doi.org/10.1016/j.jaccao.2022.04.002

Cardiovascular Disease in Myeloproliferative Neoplasms

Intracranial aneurysms (IAs) represent the most complex and relevant problem of modern neurology and neurosurgery They serve as one of the main causes of non-traumatic subarachnoid hemorrhage (SAH), causing up to 85% of all cases of intracranial hemorrhage, which is associated with frequent disability and high mortality among patients Unfortunately, the molecular mechanisms of the development and rupture of IAs are still under study Long non-coding RNAs (lncRNAs) are non-coding RNAs that typically have a length of more than 200 nucleotides It is known that lncRNAs regulate many processes, such as transcription, translation, cell differentiation, regulation of gene expression, and regulation of the cell cycle In recent years, a lot of evidence has established their role in human diseases from oncology to cardiovascular disease Recent studies have shown that lncRNAs may be involved in the pathogenesis of IAs The study of lncRNAs and its targets in various pathological conditions of a person is a rapidly developing field, and it is likely that the knowledge obtained from these studies regarding the pathogenesis of intracranial aneurysms will have the potential to use lncRNAs in therapy, as well as in the diagnosis and prediction of high aneurysms risk of rupture

https://www.mdpi.com/2075-1729/10/9/155/pdf

The Role of Long Non-Coding RNAs in Intracranial Aneurysms and Subarachnoid Hemorrhage.

Heart failure is one of the most serious diseases worldwide, and can be caused by many factors, among them hyperhomocysteinemia can increase the risk for development of heart failure. In this study, we treated rats with high methionine diet (HMD), which can be conversed to homocysteine in human body, to induce a novel model of heart failure. We proved the successful establishment of this model by echocardiography and pathological evaluation at the termination of treatment. Ejection fraction and fractional shortening were significantly deceased after HMD treatment, while left ventricular volume in systole was increased. HMD treatment caused hypertrophy of cardiomyocytes, disarrangement of myofibers, and infiltration of inflammatory cells, as well as abundant apoptotic cells appeared after HMD treatment. Plasmatic homocysteine level was elevated after HMD treatment. Furthermore, through electrophoretic mobility shift assay and chromatin immunoprecipitation, the activity of NF-κB in nuclear extract was also significantly elevated, showing evidence of positive relationship between hyperhomocysteinemia and activation of NF-κB in HMD-induced heart failure. The successful development and validation of this model have made it a new tool for translational medical research of metabolic disorders-related cardiovascular disease.

A novel rat model of heart failure induced by high methionine diet showing evidence of association between hyperhomocysteinemia and activation of NF-kappaB.

Transforming growth factor (TGF)‑β1 is reported to be associated with the occurrence of atherosclerosis, although the mechanism remains unclear. Therefore, the present study aimed to investigate the involvement of TGF‑β1 signaling in atherosclerosis. A total of 56 patients with atherosclerosis and 44 healthy volunteers were involved in this study. Serum expression of TGF‑β1 and long non‑coding RNA‑ATB was detected by ELISA and quantitative polymerase chain reaction (qPCR). Receiver operating characteristic curve analysis was performed to analyze the diagnostic value of serum TGF‑β1 and lncRNA‑ATB for atherosclerosis. A human umbilical vein endothelial cell (HUVEC) line overexpressing lncRNA‑ATB was constructed. The effects of TGF‑β1 treatment and lncRNA‑ATB overexpression on HUVEC cell proliferation and viability was detected with Cell Counting Kit‑8 and MTT assays, respectively. Expression of TGF‑β1 and pro‑apoptotic Caspase‑3 in lncRNA‑ATB‑overexpressing HUVECs was detected by western blotting. In addition, the expression of lncRNA‑ATB in TGF‑β1‑treated HUVECs was detected by qPCR. It was demonstrated that serum TGF‑β1 and lncRNA‑ATB expression was significantly higher in atherosclerosis patients, compared with controls, and could be used to effectively distinguish patients from healthy individuals. TGF‑β1 treatment and lncRNA‑ATB overexpression reduced HUVEC viability and proliferation. TGF‑β1 treatment increased the expression of lncRNA‑ATB in HUVECs, while lncRNA‑ATB overexpression had no significant effect on TGF‑β1 expression. LncRNA‑ATB silencing with small interfering RNA significantly reduced the effects of TGF‑β1 treatment on the proliferation and viability of HUVECs. Furthermore, LncRNA‑ATB overexpression upregulated the expression of caspase‑3 in HUVECs. Therefore, it was concluded that TGF‑β1 may have upregulated the expression of lncRNA‑ATB to promote atherosclerosis, and lncRNA‑ATB may serve as a potential therapeutic target for atherosclerosis. However, the mechanism remains to be further investigated.

/pdf/tgf-b1-upregulates-the-expression-of-lncrna-atb-to-promote-46islsb6a8.pdf

TGF‑β1 upregulates the expression of lncRNA‑ATB to promote atherosclerosis.

InGaN/GaN light-emitting diode structures with Al-coated GaN nanorods were fabricated by using soft ultraviolet nanoimprint lithography. The intensity of light emission was found to be greatly enhanced due to the strong near-fields confined at the interface of Al/GaN and extended to the multiple quantum wells (MQWs) active region. The dynamics of carrier recombination and plasmon-enhanced Raman scattering were also investigated, providing a progressive view on the effective energy transfer between MQWs and surface plasmons.

/pdf/bloch-surface-plasmon-enhanced-blue-emission-from-ingan-gan-b37lj918qf.pdf

Bloch surface plasmon enhanced blue emission from InGaN/GaN light-emitting diode structures with Al-coated GaN nanorods

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A novel rat model of heart failure induced by high methionine diet showing evidence of association between hyperhomocysteinemia and activation of NF-kappaB.

TGF‑β1 upregulates the expression of lncRNA‑ATB to promote atherosclerosis.

Bloch surface plasmon enhanced blue emission from InGaN/GaN light-emitting diode structures with Al-coated GaN nanorods