Distinguishable short-term effects of tea and water drinking on human saliva redox.

Food consumption can alter the biochemistry and redox status of human saliva, and the serving temperature of food may also play a role. The study aimed to explore the immediate (3 min) and delayed (30 min) effects of hot tea (57 ± 0.5 °C) ingestion and cold tea (8 ± 0.5 °C) ingestion on the salivary flow rate and salivary redox-relevant attributes. The saliva was collected from 20 healthy adults before, 3-min after and 30-min after the tea ingestion. The hot or cold deionised water at the same temperatures were used as control. The salivary flow rate and redox markers in hot tea (HBT), cold tea (CBT), hot water (HW) and cold water (CW) group were analysed and compared. The results demonstrated that neither the black tea nor the water altered the salivary flow rate; the black tea immediately increased the salivary thiol (SH) and malondialdehyde (MDA) content while reduced salivary uric acid (UA) significantly. The tea ingestion showed a tendency to elevate the ferric reducing antioxidant power (FRAP) in saliva, although not significantly. The water ingestion decreased the MDA content immediately and increased the UA level significantly. Cold water was found to induce a greater delayed increase in total salivary total protein (TPC) than the hot water. In conclusion, the black tea ingestion affects the redox attributes of human saliva acutely and significantly, while the temperature of drink makes the secondary contribution.

Experience and Lessons Learned in the Treatment of Transforming Small Cell Neuroendocrine Carcinoma of the Prostate: A Case Report and Literature Review.

Introduction: Small cell neuroendocrine carcinoma of the prostate (SCNECP) is a rare and highly malignant tumor that commonly transforms into conventional prostate adenocarcinoma (CPAC). Most of SCNECP cases cannot be detected and diagnosed early, and SCNECP is often diagnosed when there is liver and lung metastasis. Therefore, the early detection of the process from CPAC to SCNECP is crucial. Case Report: We present a case of a 73-year-old man who was initially admitted to our hospital with metastatic CPAC. He was administered goserelin acetate 3.6 mg combined with bicalutamide tablets (50 mg) once daily for endocrine therapy and docetaxel (100 mg) combined with prednisone (5 mg) twice a day. After treatment, the prostate-specific antigen (PSA) level decreased significantly, but the CEA, CA199, and CA125 levels began to increase progressively after a short decline. However, no solid tumor recurrence was observed in multiple reexaminations. It was not until 9 months after the elevation of tumor markers that multiple metastatic lesions appeared in the liver, which finally confirmed the diagnosis of metastatic SCNECP. After chemotherapy with etoposide 360 mg combined with carboplatin 200 mg, the tumor size was significantly reduced, and tumor markers decreased. However, the remission time was only 3 months. The patient's liver metastases continued to grow, and CEA, CA199, and CA125 levels continued to increase. Conclusion: During CPAC treatment, PSA levels continued to decrease, whereas CEA, CA199, and CA125 levels continued to increase. This suggests the possibility of the transformation of CPAC into SCNECP.

Exosomal miR-122-3p represses the growth and metastasis of MCF-7/ADR cells by targeting GRK4-mediated activation of the Wnt/ß-catenin pathway.

Breast cancer (BC) is a common cancer whose incidence continues to grow while its medical progress has stagnated. miRNAs are vital messengers that facilitate communications among different cancer cells. This study was to reveal the correlation of miR-122-3p expression with BC metastasis and Adriamycin (ADM) resistance and its mechanism of inhibiting BC metastasis. We found that expression of miR-122-3p is negatively correlated with BC metastasis and is lower in MCF-7/ADR cells. Overexpression of miR-122-3p in MCF-7/ADR cancer cells impairs their ability to migrate, invade, and stimulate blood vessel formation. Further research found that miR-122-3p directly binds to the 3' UTR of GRK4, reducing the phosphorylation of LRP6, which activates the Wnt/ß-catenin signaling pathway, facilitating BC development and metastasis. In addition, we observed that miR-122-3p is present in MCF-7  cells, and treatment of MCF-7/ADR cells with MCF-7-derived exosomes, but not with exosomes from miR-122-3p-deficient MCF-7 cells, has identical effects to miR-122-3p overexpression. Data from xenograft experiments further suggest that excess miR-122-3p and MCF-7-derived exosomes inhibit the growth and metastasis of MCF-7/ADR cancer cells in vivo. In conclusion our data reveal that exosomal miR-122-3p may negatively regulate BC growth and metastasis, potentially serving as a diagnostic and druggable target for BC treatment.

Fabrication and characterization of curcumin-loaded nanoparticles using licorice protein isolate from Radix Glycyrrhizae.

Licorice was widely used in food and herbal medicine. In its extract industry, a substantial amount of licorice protein was produced and discarded as waste. Herein, we extracted Licorice Protein Isolate (LPI) and explored its potential as a curcumin nanocarrier. Using a pH-driven method, we fabricated LPI-curcumin nanoparticles with diameters ranging from 129.30 ± 3.21 nm to 75.03 ± 1.19 nm, depending on the LPI/curcumin molar ratio. The formation of LPI-curcumin nanoparticles was primarily driven by hydrophobic interactions, with curcumin entrapped in LPI being in an amorphous form. These nanoparticles significantly enhanced curcumin properties in terms of solubility, photochemical stability, and stability under varying pH, storage, and physiological conditions. Moreover, the loaded curcumin exhibited a 2.58-fold increase in cellular antioxidant activity on RAW 264.7 cells and a 1.86-fold increase in antitumor activity against HepG2 cells compared to its free form. These findings suggested that LPI could potentially serve as a promising novel delivery material.

Hsa_circ_0022383 promote non-small cell lung cancer tumorigenesis through regulating the miR-495-3p/KPNA2 axis.

Hsa_circ_0022383 (circ_0022383) is a newly discovered circRNA. Its functions and relevant molecular mechanisms in tumorigenesis have not been reported. Here we aimed to explore how circ_0022383 regulates the tumorigenesis of non-small-cell lung cancer (NSCLC). We found thatcirc_0022383 expression was dramatically elevated in NSCLC tissues and cell lines. Upregulation of circ_0022383 was associated with poor prognosis in NSCLC patients. Silencing of circ_0022383 repressed cell proliferation and migration in vitro and inhibited oncogenesis and tumor metastasis in vivo. Moreover, our results discovered that circ_0022383 was mainly located in the cytoplasm of NSCLC cells. Mechanistically, circ_0022383 sponged miR-495-3p to modulate KPNA2 expression, thereby regulating NSCLC tumorigenesis and progression. In conclusion, our study demonstrates that circ_0022383 facilitates NSCLC tumorigenesis by regulating the miR-495-3p/KPNA2 axis, providing new insights into NSCLC development.

Circ_ATAD3B inhibits cell proliferation of breast cancer via mediating the miR-570-3p/MX2 axis.

It has been discovered that some circular RNAs can serve as excellent therapeutic targets for breast cancer (BC). However, the biological role that circ ATAD3B plays in BC is not yet completely understood. As a result, the purpose of this work was to evaluate the function of circ_ATAD3B in the development of BC. Three different GEO datasets were used to compile the expression profiles of circRNAs related to BC (GSE101124, GSE165884, and GSE182471). CCK-8 and the production of clones, in addition to RT-PCR and western blot assays, were utilized in this study to evaluate the regulation of these three biological molecules in the process of BC carcinogenesis.circ_ATAD3B was the only potential BC-related circRNA that was significantly reduced in BC tumor tissues, and it functioned as a miR-570-3p sponge to suppress cell survival and proliferation, as stated by the aforementioned two algorithms. The expression of MX2 was boosted when circ_ATAD3B was used to sponge miR-570-3p. The inhibitory effect that circ_ATAD3B has on the malignant phenotype of BC cells was overcome by the expression of miR-570-3p through up-regulation and MX2 through down-regulation. The tumor suppressor circ_ATAD3B prevents cancer progression by regulating the miR-570-3p/MX2 pathway. Circ_ATAD3B may be a candidate for targeted therapy of breast cancer.

Deep learning for efficiently imaging through the localized speckle field of a multimode fiber.

Due to the occurrence of redundant speckle, multimode fiber (MMF) imaging is extremely challenging. Our work studies the relationship between the effective feature distribution of the speckle field and the local spatial position and area, and proves that the information distribution of the speckle is highly redundant. The effective feature refers to the phase and amplitude information of the optical field carrying the image point information and the co-exciting very redundant information due to mode dispersion, interference, coupling, and entrained noise through transmission. The neural network Swin-Unet can well learn the association information between global and local features, greatly simplifies the fitting of the MMF end-to-end global mapping relationship, and achieves high-fidelity reconstruction from the local speckle field to the global image. This work will contribute to the realization of MMF real-time large-field endoscopic imaging.

Pt1 enhanced C-H activation synergistic with Ptn catalysis for glycerol cascade oxidation to glyceric acid.

The selective oxidation of glycerol to glyceric acid, an important value-added reaction from polyols, is a typical cascade catalytic process. It is still of great challenge to simultaneously achieve high glycerol activity and glyceric acid selectivity, suffering from either deep oxidation and C-C cleavage or poor oxidation efficiency from glyceraldehyde to glyceric acid. Herein, this work, inspired by nature, proposes a cascade synergistic catalysis strategy by atomic and low-coordinated cluster Pt on well-defined Cu-CuZrOx, which involves enhanced C-H activation on atomic Pt1 and O-H activation on cluster Ptn in the oxidation of glycerol to glyceraldehyde, and cluster Ptn for C=O activation followed by O-H insertion and atomic Pt1 for C-H activation in the tandem oxidation of glyceraldehyde to glyceric acid. The enhanced C-H activation in the cascade process by atomic Pt1 is revealed to be essential for the high glycerol activity (90.0±0.1%) and the glyceric acid selectivity (80.2±0.2%).

Conjugation of human serum albumin and flucloxacillin provokes specific immune response in HLA-B*57:01 transgenic mice.

Flucloxacillin (FLX) induces adverse liver reactions, which has been reported to be related to human leukocyte antigen (HLA)-B*57:01. In a previous study, abacavir-induced hypersensitivity was induced in HLA-B*57:01-transgenic mice (B*57:01-Tg), originally constructed by our group (Susukida et al., 2021). In this study, B*57:01-Tg mice were used to reproduce FLX-induced liver injury. However, treatment of B*57:01-Tg mice with FLX alone did not increase serum ALT levels. Immune-deficient B*57:01-Tg/PD-1-/-mice were produced by mating B*57:01-Tg with PD-1-/- mice. The immune response of B*57:01-Tg/PD-1-/- mice was further modulated by co-administration of CpG-oligodeoxynucleotides and anti-CD4 mAb. Nevertheless, immune regulation in B*57:01-Tg mice did not contribute to the onset of FLX-induced liver injury or immune activation. Moreover, we generated an FLX-human serum albumin (HSA) conjugate and showed that FLX covalently bound to HSA in a time-dependent manner. The FLX-HSA conjugate was administered to the B*57:01-Tg mice. The immune response was investigated using flow cytometry, revealing the phenotype of CD44highCD62Llow in CD8+ T cells (TEM cells). Administration of the FLX-HSA conjugate resulted in an HLA-B*57:01 restricted immune response as shown by the stimulation of TEM cells in the draining lymph nodes. In conclusion, administration of FLX alone to B*57:01-Tg mice did not induce liver injury or immune activation. Immune system sensitivity does not play a decisive role in this process. The conjugation of FLX and HSA results in specific TEM cell stimulation, which suggests that HLA-B*57:01 drives a stronger interaction with CD8+ T cells. These results suggest that patients carrying HLA-B*57:01 could be more susceptible to a conjugate of FLX and albumin and drive CD8+ T cell activation, which may be a vital risk factor for FLX-induced liver injury. In addition, the application of the FLX-HSA adduct may be an effective method for the construction of FLX-induced idiosyncratic liver injury in mice.

Genome-Wide Association and Transcriptome-Wide Association Studies Identify Novel Susceptibility Genes Contributing to Colorectal Cancer.

Background: Colorectal cancer (CRC) is among the most common cancers diagnosed worldwide. Although genome-wide association studies have effectively identified the genetic basis of CRC, there is still unexplained variability in genetic risk. Transcriptome-wide association studies (TWAS) integrate summary statistics from CRC genome-wide association studies (GWAS) with gene expression data to prioritize these GWAS findings and uncover additional gene-trait correlations. Methods: First, we carried out a post-GWAS analysis using summary statistics from a large-scale GWAS of CRC (n = 4,562 cases, n = 382,756 controls). Second, combined with the expression weight sets from GTEx (v7), susceptibility genes were identified with the FUSION software. Colocalization, conditional and fine-mapping analyses, phenome-wide association study (pheWAS), and Mendelian randomization were employed to further characterize the observed correlations. Results: In the post-GWAS analyses, we first identified new genome-wide significant associations: three genomic risk loci were identified at 8q24.21 (rs6983267, P = 6.98 × 10-12), 15q13.3 (rs58658771, P = 1.40 × 10-10), and 18q21.1 (rs6507874, P = 1.91 × 10-14). In addition, the TWAS also identified four loci statistically significantly associated with CRC risk, largely explained by expression regulation, including six candidate genes (DUSP10, POU5F1B, C11orf53, COLCA1, COLCA2, and GREM1-AS1). We further discovered evidence that low expression of COLCA2 is correlated with CRC risk with Mendelian randomization. Conclusions: We discovered novel CRC risk loci and candidate functional genes by merging gene expression and GWAS summary data, offering new insight into the molecular processes underlying CRC development. This makes it easier to prioritize potential genes for follow-up functional research in CRC.

The combination of decitabine and aspirin inhibits tumor growth and metastasis in non-small cell lung cancer.

OBJECTIVE: Combination therapy has become the hallmark of lung cancer treatment, as it reduces the dosage intensity of individual drugs while increasing their efficacy. In the current study, we analyzed the combinatorial effect of decitabine and aspirin on non-small cell lung cancer (NSCLC) cell growth. METHODS: In this study, we investigated the combinatorial effect of decitabine and aspirin by MTT, colony formation, and Transwell assays. We also explored the underlying molecular mechanism via a series of in vitro and in vivo experiments. RESULTS: The combination of decitabine and aspirin regulated cell viability and migration in vitro. Moreover, the combination therapy suppressed tumor cell growth by inhibiting the ß-catenin/STAT3 signaling pathway. Our study also found that the regimen increased the phosphorylation of ß-catenin and decreased the expression of STAT3 and ß-catenin. CONCLUSION: The combined administration of decitabine and aspirin significantly reduced tumor growth compared with single-agent treatment and the control in vivo. The study results indicated that decitabine and aspirin could suppress NSCLC cell growth and metastasis via the ß-catenin/STAT3 signaling pathway.

Diagnosis of Alzheimer's disease by feature weighted-LSTM: a preliminary study of temporal features in brain resting-state fMRI.

The long short-term memory network (LSTM) is widely used in time series data processing as a temporal recursive network. The resting-state functional magnetic resonance data shows that not only are there temporal variations in the resting state, but there are also interactions between brain regions. To integrate the temporal and spatial characteristics of brain regions, this paper proposes a model called feature weighted-LSTM (FW-LSTM). The feature weight is defined by spatial characteristics calculating the frequency of connectivity of each brain region and further integrated into the LSTM. Thus, it can comprehensively model both temporal and spatial changes in rs-fMRI brain regions. The FW-LSTM model on the Alzheimer's disease neuroimaging initiative (ADNI) dataset is used to extract the time-varying characteristics of 90 brain regions for Alzheimer's disease (AD) classification. The model performances are 77.80%, 76.41%, and 78.81% in accuracy, sensitivity, and specificity. It outperformed the one-dimensional convolutional neural networks (1D-CNN) model and LSTM model, which only used temporal features of brain regions.

Deep learning image transmission through a multimode fiber based on a small training dataset.

An improved deep neural network incorporating attention mechanism and DSSIM loss function (AM_U_Net) is used to recover input images with speckles transmitted through a multimode fiber (MMF). The network is trained on a relatively small dataset and demonstrates an optimal reconstruction ability and generalization ability. Furthermore, a bimodal fusion method is developed based on S polarization and P polarization speckles, greatly improving the recognition accuracy. These findings prove that AM_U_Net has remarkable capabilities for information recovery and transfer learning and good tolerance and robustness under different MMF transmission conditions, indicating its significant application potential in medical imaging and secure communication.

Resonance prediction and inverse design of multi-core selective couplers based on neural networks.

Resonance analysis and structural optimization of multi-channel selective fiber couplers currently rely on numerical simulation and manual trial and error, which is very repetitive and time consuming. To realize fast and accurate resonance analysis and calculation, we start with dual-core structures and establish forward classification and regression neural networks to classify and predict different resonance properties, including resonance types, operating wavelength, coupling coefficient, coupling length, 3 dB bandwidth, and conversion efficiency. The pre-trained forward neural networks for dual-core fibers can also realize accurate and fast prediction for multi-core fibers if the mode energy exchange occurs only between one surrounding core and the central core. For the inverse design, a tandem neural network has been constructed by cascading the pre-trained forward neural network and the inverse network to solve the non-uniqueness problem and provide an approach to search for appropriate and desired multi-core structures. The proposed forward and inverse neural networks are efficient and accurate, which provides great convenience for resonance analysis and structural optimization of multi-channel fiber structures and devices.

The PD1 inhibitory pathway and mature dendritic cells contribute to abacavir hypersensitivity in human leukocyte antigen transgenic PD1 knockout mice.

Based on recent genome-wide association studies, abacavir-induced hypersensitivity is highly associated with human leukocyte antigen (HLA)-B*57:01 allele. However, the underlying mechanism of this occurrence is unclear. To investigate the underlying mechanism, we developed HLA-B*57:01 transgenic mice and found that application of abacavir could cause CD8 T cell activation with elevation in PD1 expression; however, severe skin hypersensitivity was not observed. To eliminate the immunosuppressive effect of PD1, HLA-B*57:01 transgenic/PD1 knockout (01Tg/PD1) mice were generated by mating HLA-B*57:01 transgenic mice and PD1 knockout mice. Thereafter, 01Tg/PD1 mice were treated with abacavir. Similar to the above results, severe skin hypersensitivity was not observed. Therefore, we treated 01Tg/PD1 mice with an anti-CD4 antibody to deplete CD4 T cells, followed by abacavir topically and orally. Severe abacavir-induced skin hypersensitivity was observed in 01Tg/PD1 mice after depletion of CD4 T cells, in addition to significant CD8 T cell activation and dendritic cell maturation. Taken together, we succeeded in reproducing severe skin hypersensitivity in a mouse model. And we found that through the combined depletion of PD1 and CD4 T cells, CD8 T cells could be activated and could proceed to clonal proliferation, which is promoted by mature dendritic cells, thereby eventually inducing severe skin hypersensitivity.

Regulation of the immune tolerance system determines the susceptibility to HLA-mediated abacavir-induced skin toxicity.

Idiosyncratic drug toxicity (IDT) associated with specific human leukocyte antigen (HLA) allotype is a rare and unpredictable life-threatening adverse drug reaction for which prospective mechanistic studies in humans are difficult. Here, we show the importance of immune tolerance for IDT onset and determine whether it is susceptible to a common IDT, HLA-B*57:01-mediated abacavir (ABC)-induced hypersensitivity (AHS), using CD4+ T cell-depleted programmed death-1 receptor (PD-1)-deficient HLA-B*57:01 transgenic mice (B*57:01-Tg/PD-1-/-). Although AHS is not observed in B*57:01-Tg mice, ABC treatment increases the proportion of cytokine- and cytolytic granule-secreting effector memory CD8+ T cells in CD4+ T cell-depleted B*57:01-Tg/PD-1-/- mice, thereby inducing skin toxicity with CD8+ T cell infiltration, mimicking AHS. Our results demonstrate that individual differences in the immune tolerance system, including PD-1highCD8+ T cells and regulatory CD4+ T cells, may affect the susceptibility of humans to HLA-mediated IDT in humans.

Efficacy of Concurrent Chemoradiotherapy With S-1 vs Radiotherapy Alone for Older Patients With Esophageal Cancer: A Multicenter Randomized Phase 3 Clinical Trial.

IMPORTANCE: Most older patients with esophageal cancer cannot complete the standard concurrent chemoradiotherapy (CCRT). An effective and tolerable chemoradiotherapy regimen for older patients is needed. OBJECTIVE: To evaluate the efficacy and toxic effects of CCRT with S-1 vs radiotherapy (RT) alone in older patients with esophageal cancer. DESIGN, SETTING, AND PARTICIPANTS: A randomized, open-label, phase 3 clinical trial was conducted at 23 Chinese centers between June 1, 2016, and August 31, 2018. The study enrolled 298 patients aged 70 to 85 years. Eligible participants had histologically confirmed esophageal cancer, stage IB to IVB disease based on the 6th edition of the American Joint Committee on Cancer (stage IVB: only metastasis to the supraclavicular/celiac lymph nodes) and an Eastern Cooperative Oncology Group performance status of 0 to 1. Data analysis was performed from August 1, 2020, to March 10, 2021. INTERVENTIONS: Patients were stratified according to age (<80 vs ≥80 years) and tumor length (<5 vs ≥5 cm) and randomly assigned (1:1) to receive either CCRT with S-1 or RT alone. MAIN OUTCOMES AND MEASURES: The primary end point was the 2-year overall survival rate using intention-to-treat analysis. RESULTS: Of the 298 patients enrolled, 180 (60.4%) were men. The median age was 77 (interquartile range, 74-79) years in the CCRT group and 77 (interquartile range, 74-80) years in the RT alone group. A total of 151 patients (50.7%) had stage III or IV disease. The CCRT group had a significantly higher complete response rate than the RT group (41.6% vs 26.8%; P = .007). Surviving patients had a median follow-up of 33.9 months (interquartile range: 28.5-38.2 months), and the CCRT group had a significantly higher 2-year overall survival rate (53.2% vs 35.8%; hazard ratio, 0.63; 95% CI, 0.47-0.85; P = .002). There were no significant differences in the incidence of grade 3 or higher toxic effects between the CCRT and RT groups except that grade 3 or higher leukopenia occurred in more patients in the CCRT group (9.5% vs 2.7%; P = .01). Treatment-related deaths were observed in 3 patients (2.0%) in the CCRT group and 4 patients (2.7%) in the RT group. CONCLUSIONS AND RELEVANCE: In this phase 3 randomized clinical trial, CCRT with S-1 was tolerable and provided significant benefits over RT alone in older patients with esophageal cancer. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02813967.

Hydrophobin HGFI assisted immunobiologic sensor based on a cascaded taper integrated ultra-long-period fiber grating.

A new type of cascaded taper integrated ultra-long-period fiber grating (ULPFG) based immunobiologic sensor has been developed that benefits from the self-assembled monolayer of class I hydrophobin HGFI. Due to the cascaded arc, discharge tapers constitute an ultra-long-period and circular symmetrical refractive index modulation along fiber axial direction, and by local integration in one period, the mode coupling would generate to the higher harmonic of LP02, LP03 and LP04 modes in the wavelength range from 1300 nm to 1620 nm. The hydrophobic characteristic of the ULPFG surface is modified employing the HGFI, and the antibody molecule probes could be absorbed strongly on the HGFI nano-film, furthermore, the performances of immunobiologic sensing are investigated employing multiple control groups of matched and mismatched antigen molecule targets. The results show that it possesses higher sensing sensitivity of 4.5 nm/(µg/ml), faster response time about of 35 min, lower stability error of 8.8%, and excellent immuno-specificity. Moreover, this proposed ULPFG sensor has the advantages of low cost, simple fabrication and label-free, which is a powerful tool in the trace biomedical detection field.

Serum Phosphate and 1-Year Outcome in Patients With Acute Ischemic Stroke and Transient Ischemic Attack.

Objective: To determine the association between serum phosphate level and 1-year clinical outcomes in patients with acute ischemic stroke and transient ischemic attack. Methods: We included 7,353 patients with acute ischemic stroke and transient ischemic attack from the China National Stroke Registry III for analysis. Participants were divided into 4 groups according to serum phosphate quartiles. Composite end point included recurrent stroke, myocardial infarction, other ischemic vascular events, and all-cause mortality. Poor functional outcome is defined as modified Rankin Scale score of 3 to 6. Multivariable Cox regression or logistic regression was used to evaluate the independent association of serum phosphate with 1-year all-cause mortality, recurrent stroke, composite end point and poor functional outcome. Results: The mean age of the included 7,353 patients was 62.5 years, and 68.6% of them were men. Plotting hazard ratios over phosphate levels suggested a U-shaped association especially for recurrent stroke and composite end point, and therefore the third quartile group was set as reference group. Compared with the third quartile of phosphate (1.06-1.20 mmol/L), the adjusted hazard ratios/odds ratios (95% CI) of the lowest quartile (<0.94 mmol/L) were 0.98 (0.67-1.42) for all-cause mortality, 1.31 (1.05-1.64) for stroke recurrence, 1.26 (1.02-1.57) for composite end point, and 1.27 (1.01-1.61) for poor functional outcome, and the adjusted odds ratio of the highest quartile (≥1.2 mmol/L) was 1.40 (1.11-1.77) for poor functional outcome. Conclusions: Serum phosphate may be an independent predictor of stroke recurrence, composite end point and poor functional outcome after ischemic stroke.

Serum calcium and long-term outcome after ischemic stroke: Results from the China National stroke registry III.

BACKGROUND AND AIMS: Serum calcium abnormality is associated with adverse cardiovascular outcomes, but the effects of serum calcium level on stroke outcomes remain unknown. We aimed to assess the relationship between serum calcium level and 1-year outcomes in patients with acute ischemic stroke and transient ischemic attack. METHODS: We included 9375 stroke patients from the China National Stroke Registry III for analysis. Participants were divided into 4 groups according to albumin corrected-calcium quartiles. Composite end point comprised recurrent stroke, myocardial infarction, other ischemic vascular events, and all-cause mortality. Multivariable Cox or logistic regression was used to evaluate the independent association of albumin corrected-calcium with all-cause mortality, recurrent stroke, composite end point, and poor functional outcome (modified Rankin Scale score ≥3). RESULTS: Compared with the lowest calcium quartile (<2.16 mmol/L), the adjusted hazard ratio (95% CI) of the top quartile (≥2.31 mmol/L) was 1.56 (1.11-2.18) for all-cause mortality, 1.06 (0.87-1.28) for recurrent stroke and 1.08 (0.90-1.01) for composite end point, and the adjusted odds ratio for poor functional outcome was 1.18 (0.96-1.44). The addition of serum calcium to conventional risk factors improved risk prediction of all-cause mortality, leading to a small but significant increase in C-statistics and reclassification with non-significant integrated discrimination improvement (C-statistics, p = 0.02; net reclassification index 11.8%, p = 0.038; integrated discrimination improvement 0.08%, p = 0.42). CONCLUSIONS: High serum calcium levels at baseline were associated with all-cause mortality at 1-year after ischemic stroke, suggesting that serum calcium may be a potential prognostic biomarker and therapeutic target for ischemic stroke.