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OBJECTIVE: Cardiac magnetic resonance (CMR) is a diagnostic tool that provides precise and reproducible information about cardiac structure, function, and tissue characterization, aiding in the monitoring of chemotherapy response in patients with light-chain cardiac amyloidosis (AL-CA). This study aimed to evaluate the feasibility of CMR in monitoring responses to chemotherapy in patients with AL-CA. MATERIALS AND METHODS: In this prospective study, we enrolled 111 patients with AL-CA (50.5% male; median age, 54 [interquartile range, 49-63] years). Patients underwent longitudinal monitoring using biomarkers and CMR imaging. At follow-up after chemotherapy, patients were categorized into superior and inferior response groups based on their hematological and cardiac laboratory responses to chemotherapy. Changes in CMR findings across therapies and differences between response groups were analyzed. RESULTS: Following chemotherapy (before vs. after), there were significant increases in myocardial T2 (43.6 ± 3.5 ms vs. 44.6 ± 4.1 ms; P = 0.008), recovery in right ventricular (RV) longitudinal strain (median of -9.6% vs. -11.7%; P = 0.031), and decrease in RV extracellular volume fraction (ECV) (median of 53.9% vs. 51.6%; P = 0.048). These changes were more pronounced in the superior-response group. Patients with superior cardiac laboratory response showed significantly greater reductions in RV ECV (-2.9% [interquartile range, -8.7%-1.1%] vs. 1.7% [-5.5%-7.1%]; P = 0.017) and left ventricular ECV (-2.0% [-6.0%-1.3%] vs. 2.0% [-3.0%-5.0%]; P = 0.01) compared with those with inferior response. CONCLUSION: Cardiac amyloid deposition can regress following chemotherapy in patients with AL-CA, particularly showing more prominent regression, possibly earlier, in the RV. CMR emerges as an effective tool for monitoring associated tissue characteristics and ventricular functional recovery in patients with AL-CA undergoing chemotherapy, thereby supporting its utility in treatment response assessment.

Nitrogen removal from wastewater is one of the key steps in wastewater treatment. In order to remove high ammonia nitrogen content in water, Shigella boydii Y5, a strain with heterotrophic nitrification and aerobic denitrification performance, was screened from a chemical wastewater, and its optimal survival environment was investigated through single-factor experiments to examine its denitrification performance when applied to real wastewater. The results showed that the optimal environment was sucrose, C/N 10, pH 7, rotational speed 140 r/min, and the strain Y5 grown in this environment had high efficiency of denitrification in wastewater with initial mass concentration of 1 000 mg/L of ammonia nitrogen, and it was a salinophilic bacterium. When strain Y5 was applied to nucleic acid wastewater, the maximum degradation rates of ammonia nitrogen and total nitrogen reached 98.22% and 90.27%, respectively. High-throughput sequencing was used to analyze the stability and role of strain Y5 in the denitrification process of wastewater. The results demonstrated that there was a significant difference in the level of microbial diversity between the treatment group with the addition of carbon source and the treatment group with carbon source and strain Y5, suggesting that Shigella boydii Y5 had great application value for real wastewater treatment.

Objective Myocardial fibrosis is a potential mechanism of light-chain myocardial amyloidosis(AL-CA). This research aimed at exploring the correlation between multiparameter cardiac magnetic resonance (CMR) and myocardial fibrosis by relating the CMR myocardial tissue characteristics, the morphological and the functional parameters with gallium-68-labeledfibroblast activation protein inhibitor 04 positron emission tomography (68Ga-FAPI PET). Methods We gave the patients diagnosed with AL-CA in Peking Union Medical College Hospital from August to December 2021 the examinations of CMR and 68Ga-FAPI PET/CT. We recorded and analyzed the information on clinical manifestations and examinations of the patients. Results A total of 23 patients with AL-CA were included, 15 (65.2%)of which were male and the mean age was 58.3±6.5 years. Patients with high 68Ga-FAPI-04 uptake had shown growth in myocardial extracellular volume (ECV), significantly higher than those in the negative group (P=0.047). In addition, patients' myocardial ECV was positively correlated with myocardial FAPI uptake (r=0.628, P=0.001;r=0.727, P < 0.001;r=0.661, P=0.001). Patients in the positive group showd reduced left ventricular (LV) ejection fraction (EF)(P < 0.001).LVEF (r=-0.798, P < 0.001;r=-0.794, P < 0.001; r=-0.795, P < 0.001) and right ventricular (RV)EF (r=-0.735, P < 0.001;r=-0.739, P < 0.001;r=- 0.684, P < 0.001) showd negatively correlated with myocardial FAPI uptake, LV circumferential strain (r=0.668, P < 0.001;r=0.708, P < 0.001;r=0.705, P < 0.001), LV longitudinal strain (r=0.629, P=0.001;r=0.635, P=0.001; r=0.597, P=0.003), and RV longitudinal strain (r=0.575, P=0.004; r=0.792, P < 0.001;r=0.673, P < 0.001) were negatively correlated with myocardial FAPI uptake. Conclusions FAPI-related fibroblast activation is concurrent with CMR-related abnormal myocardial interstitial characteristics that leads to the decreased function of the myocardial movement. Patients with increased FAPI uptake present with increased ECV, decreased EF, and decreased strain with morphological abnormalities.

Heart failure (HF) constitutes a major determinant of outcome in chronic kidney disease (CKD) patients. The main pattern of HF in CKD patients is preserved ejection fraction (HFpEF), and left ventricular diastolic dysfunction (LVDD) is a frequent pathophysiological mechanism and specific preclinical manifestation of HFpEF. Therefore, exploring and intervention of the factors associated with risk for LVDD is of great importance in reducing the morbidity and mortality of cardiovascular disease (CVD) complications in CKD patients. We designed this retrospective cross-sectional study to collect clinical and echocardiographic data from 339 nondialysis CKD patients without obvious symptoms of HF to analyze the proportion of asymptomatic left ventricular diastolic dysfunction (ALVDD) and its related factors associated with risk by multivariate logistic regression analysis. Among the 339 nondialysis CKD patients, 92.04% had ALVDD. With the progression of CKD stage, the proportion of ALVDD gradually increased. The multivariate logistic regression analysis revealed that increased age (OR 1.237; 95% confidence interval (CI) 1.108–1.381, per year), diabetic nephropathy (DN) and hypertensive nephropathy (HTN) (OR 25.000; 95% CI 1.355–48.645, DN and HTN vs chronic interstitial nephritis), progression of CKD stage (OR 2.785; 95% CI 1.228–6.315, per stage), increased mean arterial pressure (OR 1.154; 95% CI 1.051–1.268, per mmHg), increased urinary protein (OR 2.825; 95% CI 1.484–5.405, per g/24 h), and low blood calcium (OR 0.072; 95% CI 0.006–0.859, per mmol/L) were factors associated with risk for ALVDD in nondialysis CKD patients after adjusting for other confounding factors. Therefore, dynamic monitoring of these factors associated with risk, timely diagnosis and treatment of ALVDD can delay the progression to symptomatic HF, which is of great importance for reducing CVD mortality, and improving the prognosis and quality of life in CKD patients. [ABSTRACT FROM AUTHOR]

Recurrent spontaneous abortions (RSA) affect reproductive health and increase the risk of subsequent abortions. To investigate the role of KISS-1/GPR-54 signaling in RSA progression. Villus tissue was collected from RSA patients, and human trophoblastic HTR-8/SVneo cells were used. KISS-1 and GRP54 levels were detected using RT-qPCR and immunohistochemistry. Western blotting was performed to analyze ZO-1 and ZEB1 levels. Cell proliferation was determined via CCK-8 and cell clone formation assays. Transwell assays were performed to assess cell migration and invasion abilities. KISS-1 was down-regulated in the villus tissues of RSA patients. KISS-1 overexpression dramatically inhibited trophoblast proliferation, migration, and invasion. Mechanistically, ZEB1 expression was down-regulated, whereas ZO-1 expression was up-regulated, after KISS-1 overexpression. GPR54 silencing neutralized the effect of KISS-1 in HTR-8/SVneo cells. Additionally, KISS-1 overexpression inactivated the PI3K/AKT signaling pathway through GRP54. The KISS-1/GPR-54 signaling axis regulates RSA progression by regulating the PI3K/AKT signaling pathway. [ABSTRACT FROM AUTHOR]

Photothermal therapy (PTT) is considered a promising treatment strategy for solid tumors. However, local hyperthermia (over 45°C) during PTT can cause severe side effects in neighboring healthy tissues. PTT with accurate temperature feedback is a compelling strategy to ablate tumors and reduce side effects, but it still faces challenges. Here, a new kind of phototheranostic nanoparticle, namely 17‐RF@Ag2Se is developed, enabling in vivo NIR‐II fluorescence tracking, PTT and fluorescence nanothermometry as well as synergistic heat‐shock protein (HSP) inhibition. Precise PTT with high spatiotemporal resolution is achieved with the help of the designed NIR‐II fluorescence imaging‐photothermal therapy linkage apparatus. Upon intravenous injection, 17‐RF@Ag2Se is specifically accumulated in tumors targeted by the overexpressed integrin αvβ3, which is monitored by NIR‐II fluorescence imaging of Ag2Se QDs. Further, the release of HSP inhibitor, tanespimycin (17‐AAG), enhances the thermosensitivity of tumor cells. Subsequently, the internal temperature of the tumor is precisely monitored and adjusted during PTT via the temperature‐dependent NIR‐II fluorescence feedback of Ag2Se QDs and the linkage apparatus calibration, thereby achieving efficient and safe tumor PTT. Also, the results present a new method for accurate temperature monitoring and control in vivo, which can be applied to other biomedical studies. [ABSTRACT FROM AUTHOR]

Aims: To investigate the association of methylation risk score (MRS) and its interactions with environmental factors with type 2 diabetes mellitus (T2DM) risk. Methods: We conducted a nested case–control study with 241 onset cases and 241 matched controls. Conditional logistic regression models were employed to identify risk CpG sites. Simple and weighted MRSs were constructed based on the methylation levels of ATP‐binding cassette G1 gene, fat mass and obesity associated gene, potassium voltage‐gated channel member 1 gene, and thioredoxin‐interacting protein gene previously associated with T2DM to estimate the association of MRS with T2DM risk. Stratified analyses were used to investigate interactions between MRS and environmental factors. Results: A total of 10 CpG loci were identified from the aforementioned genes to calculate MRS. After controlling for potential confounding factors, taking tertile 1 as reference, the odds ratios (ORs) and 95% confidence intervals (CIs) for T2DM of tertile 3 was 2.39 (1.36–4.20) for simple MRS and 2.59 (1.45–4.63) for weighted MRS. With per SD score increment in MRS, the OR (95% CI) was 1.66 (1.29–2.14) and 1.60 (1.24–2.08) for simple and weighted MRSs, respectively. J‐curved associations were observed between both simple and weighted MRSs and T2DM risks. Additionally, multiplication interactions for smoking and hypertension with simple MRS on the risk of T2DM were found, similarly for smoking and obesity with weighted MRS on the risk of T2DM (all Pinteraction <.05). Conclusion: Elevated simple and weighted MRSs were associated with increased risk of T2DM. Environmental risk factors may influence the association between MRS and T2DM. [ABSTRACT FROM AUTHOR]