Energy translation and Proper-Time Eigenstates

The usual quantum mechanics describes the mass eigenstates. To describe the proper-time eigenstates, a duality theory of the usual quantum mechanics was developed. The time interval is treated as an operator on an equal footing with the space interval, and the quantization of the space-time intervals between events is obtained. As a result, one can show that there exists a zero-point time interval.Comment: 15 pages, No figur

Diffuse emission of TeV Neutrinos and Gamma-rays from young pulsars by Photo-meson interaction in the galaxy

It's generally believed that young and rapidly rotating pulsars are important sites of particle's acceleration, in which protons can be accelerated to relativistic energy above the polar cap region if the magnetic moment is antiparallel to the spin axis($\vec{\mu}\cdot\vec{\Omega}<0$). To obtain the galactic diffusive neutrinos and gamma-rays for TeV, firstly,we use Monte Carlo(MC) method to generate a sample of young pulsars with ages less than $10^6$ yrs in our galaxy ; secondly, the neutrinos and high-energy gamma-rays can be produced through photomeson process with the interaction of energetic protons and soft X-ray photons ($p+\gamma\rightarrow \Delta^+\rightarrow n+\pi^+/p+\pi^0$) for single pulsar, and these X-ray photons come from the neutron star surface. The results suggest that the diffusive TeV flux of neutrinos are lower than background flux, which indicated it is difficult to be detected by the current neutrino telescopes.Comment: 11pages,6figures. arXiv admin note: text overlap with arXiv:0812.1845 by other author

Perivascular adipose tissue (PVAT) in atherosclerosis: a double-edged sword

Abstract Perivascular adipose tissue (PVAT), the adipose tissue that surrounds most of the vasculature, has emerged as an active component of the blood vessel wall regulating vascular homeostasis and affecting the pathogenesis of atherosclerosis. Although PVAT characteristics resemble both brown and white adipose tissues, recent evidence suggests that PVAT develops from its own distinct precursors implying a closer link between PVAT and vascular system. Under physiological conditions, PVAT has potent anti-atherogenic properties mediated by its ability to secrete various biologically active factors that induce non-shivering thermogenesis and metabolize fatty acids. In contrast, under pathological conditions (mainly obesity), PVAT becomes dysfunctional, loses its thermogenic capacity and secretes pro-inflammatory adipokines that induce endothelial dysfunction and infiltration of inflammatory cells, promoting atherosclerosis development. Since PVAT plays crucial roles in regulating key steps of atherosclerosis development, it may constitute a novel therapeutic target for the prevention and treatment of atherosclerosis. Here, we review the current literature regarding the roles of PVAT in the pathogenesis of atherosclerosis.https://deepblue.lib.umich.edu/bitstream/2027.42/145729/1/12933_2018_Article_777.pd

Tetra-μ-benzoato-κ8 O:O′-bis­[(benzoic acid-κO)nickel(II)]

The title compound, [Ni2(C7H5O2)4(C7H6O2)2], is composed of two NiII ions, four bridging benzoate anions and two η1-benzoic acid mol­ecules. The [Ni2(PhCOO)4] unit adopts a typical paddle-wheel conformation. The center between the two NiII atoms represents a crystallographic center of inversion. In addition, each NiII ion also coordinates to one O atom from a benzoic acid mol­ecule. The crystal packing is realised by inter­molecular hydrogen-bonding inter­actions and π–π stacking inter­actions, with a centroid–centroid distance of 3.921 (1) Å

3-[(R)-3,3-Dichloro-2-hydroxy­prop­yl]-8-hydr­oxy-6-meth­oxy-1H-isochromen-1-one

The title compound, C13H12Cl2O5, is an isocoumarin compound which has been isolated from the ethyl acetate extract of the fermentation broth of actinomycete Streptomyces sp. (V4) from the South China Sea. There are intra- and inter­molecular hydrogen bonds and halogen bonds [Cl⋯Cl = 3.434 (2) Å; C—Cl⋯Cl = 121.6°]. The intermolecular O—H⋯O hydrogen bonds link mol­ecules into chains along the b axis

Network meta-analysis of the efficacy and safety of monoclonal antibodies and traditional conventional dichotomous agents for chronic obstructive pulmonary disease

IntroductionMonoclonal antibodies (mAbs) against cytokines and chemokines or their receptors promise to be a potential therapeutic option to address chronic obstructive pulmonary disease (COPD). We aim to provide a comprehensive literature review of the improvement in FEV1 and safety when comparing mAbs with conventional dichotomous agents.MethodsWe systematically searched 3 electronic databases (PubMed, EMBASE, and CENTRAL) up to August 1, 2023 to collect eligible randomized controlled trials (RCTs). A frequentist network meta-analysis using a random-effects model was deployed to calculate mean differences (MD) for FEV1, relative risk (RR) of treatment-emergent adverse events (TEAEs), and estimate the surface under cumulative rankings (SUCRA). A higher SUCRA indicates a better outcome.ResultsThis study included 23 RCTs involving a total of 20,853 patients. Overall, except for Dupilumab, mAbs did not significantly improve FEV1 compared to traditional conventional dichotomous agents. Among all the interventions included, Aclidinium bromide/Formoterol (AB/FF) (SUCRA 97.7%) ranked highest, followed by Umeclidinium/vilanterol (UMEC/VI) (SUCRA 93.5%), and Glycopyrrolate Formoterol Fumarate (GFF) (SUCRA 84.7%). Dupilumab (SUCRA 66.9%) ranked the fourth among all interventions but ranked the first among all the mAbs. Importantly, all mAbs demonstrated a good safety profile compared with placebo.ConclusionConsidering the improvement in FEV1 and its safety, the development of mAbs for COPD still holds significant clinical potential.Systematic review registrationPROSPERO, CRD42023452714

CCL21/CCR7 enhances the proliferation, migration, and invasion of human bladder cancer T24 cells

Objective To investigate the effects of CCL21/CCR7 on the proliferation, migration, and invasion of T24 cells and the possible associated mechanisms: expression of MMP-2 and MMP-9, and regulation of BCL-2 and BAX proteins. Methods T24 cells received corresponding treatments including vehicle control, antibody (20ng/mL CCR7 antibody and 50 ng/ml CCL21), and 50, 100. and 200 ng/ml CCL21. Proliferation was evaluated by MTT assay; cell migration and invasion were assayed using a transwell chamber. Cell apoptosis was induced by Adriamycin (ADM). The rate of cell apoptosis was examined by flow cytometry using annexin V-FITC/PI staining. Western-blot was used to analyze MMP-2 and MMP-9 and BCL-2 and BAX proteins. Results CCL21 promoted T24 cell proliferation in concentration-dependent manner with that 200 ng/mL induced the largest amount of proliferation. Significant differences of cell migration were found between CCL21treatment groups and the control group in both the migration and invasion studies (P \u3c 0.001 for all). The expressions of MMP-2 and MMP-9 proteins were significantly increased after CCL21 treatment (p \u3c 0.05 for all). Protein expression of Bcl-21 follows an ascending trend while the expression of Bax follows a descending trend as the concentration of CCL21 increases. No difference was found between the control group and antibody group for all assessments. Conclusion CCL21/CCR7 promoted T24 cell proliferation and enhanced its migration and invasion via the increased expression of MMP-2 and MMP-9. CCL21/CCR7 had antiapoptotic activities on T24 cells via regulation of Bcl-2 and Bax proteins. CCL21/CCR7 may promote bladder cancer development and metastasis

Electroacupuncture at ST25 corrected gut microbial dysbiosis and SNpc lipid peroxidation in Parkinson’s disease rats

IntroductionParkinson’s disease (PD) remains one kind of a complex, progressive neurodegenerative disease. Levodopa and dopamine agonists as widely utilized PD therapeutics have not shown significant positive long-term outcomes. Emerging evidences indicate that electroacupuncture (EA) have potential effects on the therapy of nervous system disorders, particularly PD, but its specific underlying mechanism(s) remains poorly understood, leading to the great challenge of clinical application and management. Previous study has shown that acupuncture ameliorates PD motor symptoms and dopaminergic neuron damage by modulating intestinal dysbiosis, but its intermediate pathway has not been sufficiently investigated.MethodsA rat model of PD was induced using rotenone. The therapeutic effect of EA on PD was assessed using the pole and rotarod tests and immunohistostaining for tyrosine hydroxylase (TH) in the substantia nigra (SN) of brain. The role of gut microbiota was explored using 16S rRNA gene sequencing and metabonomic analysis. PICRUSt2 analysis, lipidomic analysis, LPS and inflammatory factor assays were used for subsequent exploration and validation. Correlation analysis was used to identify the key bacteria that EA regulates lipid metabolism to improve PD.ResultsThe present study firstly reappeared the effects of EA on protecting motor function and dopaminergic neurons and modulation of gut microbial dysbiosis in rotenone-induced PD rat model. EA improved motor dysfunction (via the pole and rotarod tests) and protected TH+ neurons in PD rats. EA increased the abundance of beneficial bacteria such as Lactobacillus, Dubosiella and Bifidobacterium and decreased the abundance of Escherichia-Shigella and Morganella belonging to Pseudomonadota, suggesting that the modulation of gut microbiota by EA improving the symptoms of PD motility via alleviating LPS-induced inflammatory response and oxidative stress, which was also validated by various aspects such as microbial gene functional analysis, fecal metabolomics analysis, LPS and inflammatory factor assays and SNpc lipidomics analysis. Moreover, correlation analyses also verified strong correlations of Escherichia-Shigella and Morganella with motor symptoms and SNpc lipid peroxidation, explicating targets and intermediate pathways through which EA improve PD exercise symptom.ConclusionOur results indicate that the improvement of motor function in PD model by EA may be mediated in part by restoring the gut microbiota, which intermediate processes involve circulating endotoxins and inflammatory mediators, SNpc oxidative stress and lipid peroxidation. The gut-microbiome - brain axis may be a potential mechanism of EA treatment for the PD