calcium polycarbophil (Polyful / Colonel)

The rheological behavior, particle properties and supramolecular structure of low acyl gellan gum fluid gels: impact of the calcium concentration before fluid gel formation.

D'Oria Gabriele G, Zhu Yanshen Y, Limbach Hans Joerg HJ, Hartmann Christoph C et al.

Fluid gels are jammed microgel suspensions obtained by shearing a gelling hydrocolloid during its sol-gel transition. This study focused on calcium-induced low acyl gellan gum (LAGG) fluid gels and investigated the impact of calcium concentration before fluid gel formation on the resulting rheological behavior, fluid gel particle properties, and supramolecular structure. The elasticity and yield stress of fluid gels and quiescently cooled gels reached a maximum when the calcium concentration was increased from 0.78 to (approx.) 30 mmol/kg. Small angle X-ray scattering (SAXS) of fluid gels revealed a progressive increase in gel network connectivity up to the calcium concentration where the peak in rheological properties was observed followed by a less interconnected network at calcium concentrations above the peak. Furthermore, rheological measurements supplemented with free calcium and zeta-potential measurements, support that the decrease after the peak in rheological response is due to the combination of fluid gel particle softening with a decrease in surface charge. The results of this study enable to establish clearer links between rheological behavior, particle properties and supramolecular structure of calcium-induced LAGG fluid gels. This work enables a more effective design of fluid gel properties for different applications from food to pharma and biomaterials.

Reinventing the coronary calcium scan.

Arbab-Zadeh Armin A

Pinoresinol diglucoside from Eucommia ulmoides attenuates diabetic cardiomyopathy through suppressing the store-operated calcium entry and downregulating the STIM1/Orai1/NFAT3 signaling pathway.

Feng Yujie Y, Mao Yanan Y, Li Junshuai J, Sun Zhipeng Z et al.

Pinoresinol diglucoside (PDG), an active component derived from Eucommia ulmoides, exhibits therapeutic effects against apoptosis, inflammation, and hypertrophy, etc. However, whether PDG plays a protective role in diabetic cardiomyopathy (DCM) is not fully elucidated. This study aimed to investigate the role and potential mechanism of PDG in DCM. The possible mechanism of PDG targeting DCM was identified by network pharmacology, bioinformatics, machine learning and molecular docking methods. The heart function of mice was evaluated using echocardiography. The pathological changes in the heart of mice were detected using H&E staining. Changes of Ca2+ fluorescence intensity values in H9c2 cells were assessed by confocal microscopy. Apoptosis was evaluated by TUNEL staining and flow cytometry. The expression of DCM-related genes and proteins, both in vivo and in vitro, was examined by qRT-PCR and Western blot. The results showed that PDG effectively improved the cardiac function and suppressed cardiac hypertrophy, inflammation, and cardiomyocyte apoptosis caused by DCM. Intriguingly, molecular docking results revealed that the therapeutic effect of PDG on DCM was associated with stromal interaction molecule 1 (STIM1), calcium release-activated calcium channel protein 1 (Orai1), and nuclear factor of activated T-cells 3 (NFAT3) signaling. Consistently, animal experiments results indicated that PDG significantly downregulated the expression of STIM1, Orai1, NFAT3 at the protein level, as well as the associated store-operated calcium entry (SOCE). Therefore, our findings revealed that PDG can alleviate cardiac hypertrophy, inflammation and apoptosis in DCM by downregulating the STIM1, Orai1, and NFAT3 signaling molecules. Thus, PDG may be a promising therapeutic candidate for treating DCM.

The OMERACT core domain sets for calcium pyrophosphate deposition disease.

Dalbeth Nicola N, Zhang Yiling Y, Hensey Owen O, Grossberg David D et al.

To develop OMERACT core domain sets for chronic and recurrent calcium pyrophosphate deposition (CPPD) disease and acute calcium pyrophosphate (CPP) crystal arthritis. Following OMERACT methodology, the CPPD Working Group (comprising of patient research partners, fellows, clinicians, and methodologists) defined the core domain sets. The development of the core sets occurred through a scoping review, qualitative study, Delphi surveys, and ranking exercises to identify the most relevant domains. A virtual e-module was developed to enable members of the OMERACT community to discuss and vote for endorsement of the OMERACT CPPD core domain sets. The core domains for chronic and recurrent CPPD are pain intensity, joint tenderness, joint swelling, acute CPP crystal arthritis flares, overall function, patient global assessment of disease activity, physician global assessment of disease activity, and adverse events including death. In voting, this core domain set was endorsed by 14/14 (100%) patient research partners and 85/87 (98%) other participants. The core domains for acute CPP crystal arthritis are pain intensity, joint tenderness, joint swelling, duration of acute CPP crystal arthritis flare, overall function, patient global assessment of disease activity, and adverse events including death. In voting, this core domain set was endorsed by 14/14 (100%) patient research partners and 83/86 (97%) other participants. Definitions for all core domains have been developed. These core domains provide a foundation for future clinical trials and longitudinal studies in CPPD by defining the minimum outcomes that should be assessed and reported to ensure relevance and comparability across studies.