This study investigated hair metals as potential biomarkers in Parkinson's disease (PD) and their link to gut-mediated iron metabolism. In 60 PD patients and matched controls, hair analysis revealed a distinct profile: significantly lower iron and copper, higher manganese and arsenic, and unchanged zinc levels, with combined metals showing diagnostic value (e.g., Cu AUC = 0.79). Using an MPTP-induced mouse model, we linked lower hair iron to gut pathophysiology, finding impaired intestinal barrier integrity, downregulated host iron absorption genes (DMT1 and FPN), and upregulated microbial iron-acquisition genes (e.g., fepG). These results suggest that gastrointestinal dysfunction and gut microbiota dysbiosis may contribute to systemic iron deficiency in PD. Hair multi-metal analysis shows promise as a diagnostic adjunct, reflecting the involvement of the gut-brain axis and highlighting a potential target for intervention.

Background: Aggregation and pathological phosphorylation of α‑synuclein (α‑syn) are central drivers of Parkinson’s disease (PD) progression. Identifying natural compounds capable of directly targeting α‑syn remains a major challenge in PD drug discovery.Purpose: This study investigated whether bisphenol F (BPF), a naturally occurring polyphenolic compound found in multiple medicinal plants, exerts neuroprotective effects in PD by directly binding to α‑syn and modulating its pathological aggregation.Methods: Network pharmacology and molecular docking were used to predict BPF–target interactions and identify α‑syn as a core hub target. Binding affinity was validated using surface plasmon resonance (SPR) and cellular thermal shift assay (CETSA). Functional assays—including native PAGE, Western blotting, cell viability, climbing assays, and survival analysis—were performed in A53T‑α‑syn–overexpressing SH‑SY5Y cells and a Drosophila PD model.Results: BPF showed favorable drug‑likeness, high predicted oral absorption, and strong BBB penetration potential. Network analysis identified SNCA as a major hub target. SPR confirmed direct BPF–α‑syn binding (KD in the micromolar range), and CETSA demonstrated increased thermal stability of α‑syn upon BPF treatment. BPF significantly inhibited α‑syn oligomerization and S129 phosphorylation in vitro. In vivo, BPF improved climbing ability and extended lifespan in α‑syn transgenic Drosophila without detectable toxicity.Conclusion: BPF directly binds to α‑syn, suppresses its pathological aggregation and phosphorylation, and ameliorates PD‑like motor deficits in vivo. These findings identify BPF as a promising natural α‑syn–targeting candidate for disease‑modifying PD therapy.

Accurate and efficient grade assessment of tumor budding (TB) in hematoxylin and eosin-stained whole slide images (H&E-stained WSIs) of colorectal cancer (CRC) remains challenging. This study proposes a full-automated TB annotation approach to assist in manual grade assessment by extracting tumor invasive front boundaries, annotating TBs in tumor invasive front patches, and transferring annotations to WSIs. Our approach demonstrates exceptional performance in tumor invasive front boundary extraction, achieving AUCs of 0.988, 0.921, and 0.929 on three different validation datasets. For TB annotations in tumor invasive front patches, the approach shows better recalls of 0.850, 0.753, and 0.720 on the same datasets. The average time of TB grade assisted by the approach in each WSI from different datasets is limited to 21 s, 15 s, and 18 s, respectively. These results demonstrate that this approach significantly improves assessment efficiency while guaranteeing accuracy, offering a reliable tool for CRC clinicopathological diagnosis.

The precise differentiation of recurrent glioma from treatment-related changes, such as pseudoprogression or radiation necrosis, is essential for treatment planning and remains a significant challenge. Fibroblast activation protein (FAP) expressed by cancer-associated fibroblasts can be targeted with PET tracers for in vivo visualization and quantification. This study aims to evaluate the diagnostic and prognostic effectiveness of FAP expression in patients with potential recurrent glioma by directly comparing [gallium-68] FAP inhibitor-04 and [fluorine-18] fluoroethyl-L-tyrosine PET/CT imaging. Thirty glioma patients showing signs of possible recurrence during routine MRI follow-up after treatment were enrolled. PET-based semiquantitative parameters, clinical factors, and survival data were collected for analysis. Paired comparison of SUVmax, TBRmax, MTV, and TLU originating from two PET imaging studies indicated significant differences in TBRmax, MTV, and TLU, with P values of 0.000, 0.001, and 0.000, respectively. Univariate logistic regression analysis revealed a marginally non-significant difference in efficacy (P = 0.053) of the initial pathological diagnosis. In multivariate logistic regression analysis, PET parameters, initial pathological data, age, and gender were used to develop the predictive models step by step. Although trends towards significance were observed in the MTVFAPI:MTVFET ratio, no PET parameters reached statistical significance. The MTVFAPI:MTVFET ratio improved the area under the receiver operating characteristic curve (AUC). When PET parameters and initial pathological diagnosis were included, the MTVFAPI:MTVFET ratio significantly enhanced the model’s AUC (P = 0.040) from 0.709 (0.465–0.953, 95

BACKGROUND:Clinical-biological diagnosis of Alzheimer's disease (AD) is gaining increasing recognition. Beyond diagnosis, biological profiles can be of great benefit for disease monitoring and prognosis, although evidence from real-world memory clinics is still limited. METHOD:211 subjects with cognitive concerns and 31 cognitive unimpaired (CU) volunteers visiting our memory clinic with longitudinal follow-up were enrolled (mean (SD) interval: 1.89 (1.19) years). All participants received AD pathological evaluations (core 1: amyloid-PET or plasma p-tau 217; core 2: Florzolotau tau-PET) at baseline. Biomarkers were assessed by binary amyloid and tau status, and quantitative tau burden in key regions (medial temporal lobe (MTL), neocortical areas (NEO)). Clinical progression served as the primary outcome (increase in CDR or annual MMSE decline ≥ 6). The prognostic values of biomarkers were compared with basic demographic characteristics (a combination of significant risks in Cox Proportional Hazard Models) by receiver operating characteristic analysis. RESULT:91 (37.6%) participants were classified as clinical progression (0 CU (0%), 0 SCD (0%), 41 MCI (31.5%) and 50 (56.8%) AD dementia). Only age (older, HR = 1.03, 95%CI 1.01-1.07, P = 0.005) and sex (female, HR = 1.61, 95%CI 1.02-2.52, P = 0.039) showed the significant risks for clinical progression. In the entire cohort, incorporating any of the above biomarkers individually into the basic model (AUC = 0.57) significantly improved the prognostic value (AUC = 0.73-0.80, all P < 0.001), with quantitative tau burden in NEO showing the best added value. Combining both amyloid and tau biomarkers into the basic model further slightly improved the prognosis (AUC = 0.77-0.82), with the one with binary amyloid status plus quantitative tau burden in NEO showing the best added value. In the A+ subcohort, prognostic value was significantly increased by incorporating the quantitative tau burden (MTL: AUC = 0.71, P < 0.001; NEO: AUC = 0.73, P < 0.001) into the basic model (AUC = 0.50), while binary tau status didn't achieve significant improvement (AUC = 0.60, P = 0.125). CONCLUSION:AD core biomarkers are promising in improving clinical prognosis, among which quantitative tau burden is preferable to binary assessment, especially in the AD continuum.

Tau PET is increasingly recognized for its prognostic and disease-monitoring value in Alzheimer’s disease (AD); however, real-world evidence in heterogeneous memory clinic populations remains limited, especially for novel tau positron emission tomography (PET) with 18F-Florzolotau. We prospectively enrolled 340 individuals (patients with cognitive complaints and community volunteers) undergoing baseline amyloid PET and tau PET with 18F-Florzolotau, with subsets for clinical follow-up (n = 260; median interval 1.45 [0.96–2.56] years) and repeat tau PET (n = 64; median interval 2.27 [1.47–2.88] years). The incremental prognostic role of tau PET beyond demographic and clinical characteristics was assessed using binary clinical outcomes and continuous cognitive declines. The monitoring utility of tau PET was evaluated through tau accumulation rates versus clinical outcomes, and cognition-tau correlations. Cross-sectionally, tau standardized uptake value ratios (SUVRs) increased with cognitive impairment severity and correlated with domain-specific deficits. Longitudinally, baseline tau SUVRs provided incremental prognostic value, with higher neocortical SUVR as the sole independent predictor beyond demographic and clinical characteristics, particularly in AD spectrum (HR = 1.62, p = 0.018). Accelerated tau deposition was observed in motor regions including the precentral gyrus (β = 0.07 SUVR/year, p = 0.007) and supplementary motor area (β = 0.08 SUVR/year, p = 0.017) in those clinically progressive individuals than stable counterparts. Critically, these motor regions showed stronger cognition-tau correlations than canonical tau-vulnerable regions (medial temporal lobe and neocortex), establishing them as superior monitoring biomarkers. 18F-Florzolotau PET provides significant prognostic value and enables AD progression tracking. Motor cortices offered enhanced sensitivity for monitoring clinical deterioration in symptomatic stages, supporting their integration into stage-specific frameworks.

Pyroptosis has emerged as a promising mechanism for eliciting robust antitumor immunity; however, the current pyroptosis inducers lack tumor‐selectivity and feedback of therapeutic effect. In this study, we developed a series of twisted intramolecular charge transfer luminogens (TICTgens) for precisely regulating and in situ monitoring of tumor cell pyroptosis in vitro and in vivo. The outperformed TICTgen HCM displayed second near‐infrared (NIR‐II) fluorescence emission and exceptional viscosity sensitivity. Upon 671 nm laser irradiation, HCM induced the generation of type‐I/II reactive oxygen species (ROS) and hyperthermia effect, which cumulatively triggered mitochondrial damage and pyroptosis of tumor cells. HCM was systemically delivered via intracellular acidity‐sensitive nanoparticles (namely PDPA@HCM NPs) to effectively trigger pyroptosis‐driven antitumor immunity. Notably, HCM performed NIR‐II fluorescence and photoacoustic (PA) imaging of pyroptosis‐induced mitochondrial dysfunction by measuring viscosity change, thus enabling in situ monitoring of pyroptosis‐mediated antitumor immunotherapy. In combination with immune checkpoint blockade therapy, the PDPA@HCM NPs dramatically regressed colorectal tumor growth in a mouse model. Overall, this study demonstrated that the TICTgens could serve as a versatile platform for pyroptosis induction and monitoring of pyroptosis‐based cancer immunotherapy.

Clinical‐biological diagnosis of Alzheimer's disease (AD) is gaining increasing recognition. Beyond diagnosis, biological profiles can be of great benefit for disease monitoring and prognosis, although evidence from real‐world memory clinics is still limited. 211 subjects with cognitive concerns and 31 cognitive unimpaired (CU) volunteers visiting our memory clinic with longitudinal follow‐up were enrolled (mean (SD) interval: 1.89 (1.19) years). All participants received AD pathological evaluations (core 1: amyloid‐PET or plasma p ‐tau 217; core 2: Florzolotau tau‐PET) at baseline. Biomarkers were assessed by binary amyloid and tau status, and quantitative tau burden in key regions (medial temporal lobe (MTL), neocortical areas (NEO)). Clinical progression served as the primary outcome (increase in CDR or annual MMSE decline ≥ 6). The prognostic values of biomarkers were compared with basic demographic characteristics (a combination of significant risks in Cox Proportional Hazard Models) by receiver operating characteristic analysis. 91 (37.6%) participants were classified as clinical progression (0 CU (0%), 0 SCD (0%), 41 MCI (31.5%) and 50 (56.8%) AD dementia). Only age (older, HR = 1.03, 95%CI 1.01‐1.07, P = 0.005) and sex (female, HR = 1.61, 95%CI 1.02‐2.52, P = 0.039) showed the significant risks for clinical progression. In the entire cohort, incorporating any of the above biomarkers individually into the basic model (AUC = 0.57) significantly improved the prognostic value (AUC = 0.73‐0.80, all P < 0.001), with quantitative tau burden in NEO showing the best added value. Combining both amyloid and tau biomarkers into the basic model further slightly improved the prognosis (AUC = 0.77‐0.82), with the one with binary amyloid status plus quantitative tau burden in NEO showing the best added value. In the A+ subcohort, prognostic value was significantly increased by incorporating the quantitative tau burden (MTL: AUC = 0.71, P < 0.001; NEO: AUC = 0.73, P < 0.001) into the basic model (AUC = 0.50), while binary tau status didn’t achieve significant improvement (AUC = 0.60, P = 0.125). AD core biomarkers are promising in improving clinical prognosis, among which quantitative tau burden is preferable to binary assessment, especially in the AD continuum.

Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by dopaminergic (DA) neuron loss and neuroinflammation. Current therapies fail to halt disease progression, which underscores the need for new treatments. This study investigated the neuroprotective effects and mechanisms of Gastrodia elata polysaccharide (GEP) in MPTP-induced PD mice. GEP was administered for two weeks, and motor function was assessed using behavioral tests. Immunohistochemical and Western Blot analyses evaluated DA neuron survival, microglial activation, and NLRP3 inflammasome components. GEP-medicated serum (GMS) was applied to SH-SY5Y neuroblastoma cells exposed to neuroinflammatory conditions, and metabolomic analysis identified key metabolites. GEP improved motor function, reduced DA neuron loss, and increased tyrosine hydroxylase expression. It suppressed microglial activation, decreased NLRP3 inflammasome components, and lowered pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). GMS reduced ROS levels, enhanced mitochondrial membrane potential, and promoted autophagy in SH-SY5Y cells. Metabolomic analysis revealed elevated dopamine levels in GMS, linked to NLRP3 inflammasome inhibition, and reduced neuroinflammation. GMS also activated the PINK1/Parkin pathway to promote mitochondrial autophagy and prevent apoptosis. GEP alleviates PD symptoms by targeting neuroinflammation, mitochondrial dysfunction, and dopamine regulation, which highlights its potential as a therapeutic candidate. Further research is needed to explore its long-term efficacy and clinical applications.

Background:Cancer-associated fibroblasts (CAFs) within the tumor microenvironment (TME) can interact with tumor parenchymal cells to promote tumor growth and migration. Fibroblast activation protein (FAP) expressed by CAFs can be targeted with positron emission tomography (PET) tracers, but studies on FAP expression patterns in intracranial tumors remain scarce. We aimed to evaluate FAP expression patterns in intracranial tumors with gallium-68 FAP inhibitor-04 (68Ga-FAPi-04) and immunohistochemical staining and to observe the interactions between CAFs and tumor cells with a head-to-head comparison of 68Ga-FAPi-04 and fluoride-18 fluoroethyl-L-tyrosine (18F-FET) for PET quantification analysis. Methods:We prospectively enrolled 22 adult patients with intracranial mass lesions. 68Ga-FAPi-04 and 18F-FET PET-computed tomography (PET/CT) brain imaging were applied before surgery. Maximal tumor-to-brain ratio (TBRmax), metabolic tumor volume (MTV), and total lesion tracer uptake (TLU) was obtained, and different thresholds were used for 68Ga-FAPi-04-positive lesion delineation owing to the lack of relevant guidelines. The MTV and TLU ratios of both tracers were calculated. Linear regression was applied to observe the differential efficacy of semiquantitative PET parameters. Results:A total of 22 patients with a mean age of 50±13 years (range, 27-69 years) were enrolled. Heterogeneous patterns of 68Ga-FAPi-04 uptake [median of maximal standardized uptake value (SUVmax) =3.8; range, 0.1-19.1] were found. More malignant tumors, including brain metastasis, glioblastoma, and medulloblastoma, generally exhibited more significant 68Ga-FAPi-04 uptake than did the less malignant tumors, while the SUVmax and TBRmax exhibited nonsignificant differences across three intracranial lesion groups of primary brain tumor, brain metastasis, and noncancerous disease (SUVmax: P=0.092; TBRmax: P=0.189). Immunohistochemistry staining showed different stromal FAP expression status in various intracranial lesions. In 15 patients with positive 68Ga-FAPi-04 intracranial tumor uptake, the MTVFAPi:MTVFET ratio had differential efficacy in various types of intracranial tumors [95% confidence interval (CI): 0.572-7.712; P=0.027], and further quantification analyses confirmed the differential ability of the MTVFAPi:MTVFET ratio (95% CI: -0.045 to 11.013, P=0.052; 95% CI: 0.044-17.903, P=0.049; 95% CI: -1.131 to 30.596, P=0.065) with different isocontour volumetric thresholds. Conclusions:This head-to-head study demonstrated heterogeneous FAP expression in intracranial tumors. The FAP expression volume percentage in tumor parenchyma may therefore offer benefit with respect to differentiating between intracranial tumor types.

Background: Cancer-associated fibroblasts (CAFs) within the tumor microenvironment (TME) can interact with tumor parenchymal cells to promote tumor growth and migration. Fibroblast activation protein (FAP) expressed by CAFs can be targeted with positron emission tomography (PET) tracers, but studies on FAP expression patterns in intracranial tumors remain scarce. We aimed to evaluate FAP expression patterns in intracranial tumors with gallium-68 FAP inhibitor-04 (68Ga-FAPi-04) 68 Ga-FAPi-04) and immunohistochemical staining and to observe the interactions between CAFs and tumor cells with a head-to-head comparison of 68 Ga- FAPi-04 and fluoride-18 fluoroethyl-L-tyrosine (18F-FET) 18 F-FET) for PET quantification analysis. Methods: We prospectively enrolled 22 adult patients with intracranial mass lesions. 68 Ga-FAPi-04 and 18 F-FET PET-computed tomography (PET/CT) brain imaging were applied before surgery. Maximal tumor-to-brain ratio (TBRmax), metabolic tumor volume (MTV), and total lesion tracer uptake (TLU) was obtained, and different thresholds were used for 68 Ga-FAPi-04-positive lesion delineation owing to the lack of relevant guidelines. The MTV and TLU ratios of both tracers were calculated. Linear regression was applied to observe the differential efficacy of semiquantitative PET parameters. Results: A total of 22 patients with a mean age of 50 +/- 13 years (range, 27-69 years) were enrolled. Heterogeneous patterns of 68 Ga-FAPi-04 uptake [median of maximal standardized uptake value (SUVmax) =3.8; range, 0.1-19.1] were found. More malignant tumors, including brain metastasis, glioblastoma, and medulloblastoma, generally exhibited more significant 68 Ga-FAPi-04 uptake than did the less malignant tumors, while the SUVmax and TBRmax exhibited nonsignificant differences across three intracranial lesion groups of primary brain tumor, brain metastasis, and noncancerous disease (SUVmax: P=0.092; TBRmax: P=0.189). Immunohistochemistry staining showed different stromal FAP expression status in various intracranial lesions. In 15 patients with positive 68 Ga-FAPi-04 intracranial tumor uptake, the MTVFAPi:MTVFET FAPi :MTV FET ratio had differential efficacy in various types of intracranial tumors [95% confidence interval (CI): 0.572-7.712; P=0.027], and further quantification analyses confirmed the differential ability of the MTVFAPi:MTVFET FAPi :MTV FET ratio (95% CI: -0.045 to 11.013, P=0.052; 95% CI: 0.044-17.903, P=0.049; 95% CI: -1.131 to 30.596, P=0.065) with different isocontour volumetric thresholds. Conclusions: This head-to-head study demonstrated heterogeneous FAP expression in intracranial tumors. The FAP expression volume percentage in tumor parenchyma may therefore offer benefit with respect to differentiating between intracranial tumor types.

INTRODUCTION:We aimed to evaluate the feasibility of the 2024 Alzheimer's Association Workgroup's integrated clinical-biological staging scheme in outpatient settings within a tertiary memory clinic. METHODS:The 2018 syndromal cognitive staging system, coupled with a binary biomarker classification, was implemented for 236 outpatients with cognitive concerns. The 2024 numeric clinical staging framework, incorporating biomarker staging, was specifically applied to 154 individuals within the Alzheimer's disease (AD) continuum. RESULTS:The 2024 staging scheme accurately classified 95.5% AD. Among these, 56.5% exhibited concordant clinical and biological stages (canonical), 34.7% demonstrated more advanced clinical stages than biologically expected (susceptible), and 8.8% displayed the inverse pattern (resilient). The susceptible group was characterized by a higher burden of neurodegeneration and inflammation than anticipated from tau, whereas the resilient group showed the opposite. DISCUSSION:The 2024 staging scheme is generally feasible. A discrepancy between clinical and biological stages is relatively frequent among symptomatic patients with AD. HIGHLIGHTS:The 2024 AA staging scheme is generally feasible in a tertiary memory clinic. A discrepancy between clinical and biological stages is relatively frequent in AD. The mismatch may be influenced by a non-specific pathological process involved in AD. Individual profiles like aging and lifestyles may contribute to such a mismatch. Matched and mismatched cases converge toward similar clinical outcomes.

Background: Reactive astrocytes play important roles in the development of Alzheimer’s disease (AD) and primary tauopathies. Here, we aim to investigate the relationship between reactive astrocytes, tau and amyloid beta, microgliosis and glucose metabolism by using multitracer imaging in widely used tauopathy and familial AD mouse models. Results: Positron emission tomography (PET) imaging using [ 18 F]SMBT-1 (monoamine oxidase-B), [ 18 F]florbetapir (amyloid-beta), [ 18 F]PM-PBB3 (tau), [ 18 F]DPA-714 (translocator protein) and [ 18 F]fluorodeoxyglucose (FDG) was carried out in 3- and 7-month-old rTg4510 tau mice, 5×FAD familial AD mice and aged-matched wild-type mice. We found increased regional [ 18 F]SMBT-1, [ 18 F]DPA-714 uptake, and hypoglucose metabolism in the brains of 7-month-old rTg4510 mice with tau accumulation as well as in 7-month-old 5×FAD mice with higher amyloid-beta and tau accumulation compared to age-matched wild-type mice. Conclusion: In summary, these findings provide in-vivo evidence for reactive astrocytes, microglial activation, and cerebral hypoglucose metabolism in animal models of tauopathy and familial AD.

Objective:To investigate the changes of serum mannose-binding lectin (MBL) and regulatory T cell(Treg) and their cytokines in patients with vitiligo at different stages and types, and their correlation with their activity.Methods:A total of 50 patients with vitiligo diagnosed in Zhongshan Hospital Fudan University from October 2020 to June 2021 were selected. According to the clinical staging criteria of vitiligo, they were divided into stable stage (25 cases) and progressive stage (25 cases). According to the clinical classification principle, they were divided into segmental type (14 cases) and non-segmental type (36 cases). Another 25 healthy subjects were selected as the control group. The changes of MBL, CD4 + CD25 + CD127 -Treg, related factors cytotoxic T lymphocyte-associated antigen-4 (CTLA-4), interleukin (IL)-10 and transforming growth factor-β(TGF-β) in peripheral blood of patients with vitiligo were compared among the control group and different stages and types, and the correlation between vitiligo disease activity score (VIDA) and related indicators was analyzed. Results:Compared with the control group, the levels of serum MBL, CD4 + CD25 + CD127 -Treg cells and related factor CD4 + CD25 + CD152 + (CTLA-4) in peripheral blood mononuclear cell(PBMC) of patients with stable and progressive vitiligo were significantly lower, while the level of TGF-β was significantly higher[ng/mL: (4.76±0.56)vs(4.32±0.56)vs(3.80±0.43), %: (7.51±3.28)vs(6.21±1.52)vs(4.02±0.68), %: (4.04±1.84)vs(4.00±2.04)vs(2.36±1.08), ng/mL: (32.17±14.49)vs(50.79±22.40)vs(66.40±27.04), F=20.78, 17.12, 7.88, 15.27, all P values <0.05]. However, there was no significant difference in IL-10 expression among the groups( P>0.05). Compared with the stable phase, the CTLA-4 levels of MBL, Treg cells and related factors decreased significantly, while the level of TGF-β increased significantly ( P=0.001, 0.001, 0.003). Compared with the control group, the levels of serum MBL and CD4 + CD25 + CD127 -Treg cells in patients with segmental vitiligo and non-segmental vitiligo were significantly lower, and the expression of TGF-β was significantly higher[ng/mL: (4.76±0.56)vs(3.95±0.61)vs(4.14±0.55), %: (7.51±3.28)vs(5.49±1.48)vs(4.97±1.65), ng/mL: (30.89±17.88)vs(58.08±30.14)vs(59.32±23.99), F=12.26, 9.19, 11.96, all P values <0.05)]. There was no significant difference in the expression of CD4 + CD25 + CD152 + (CTLA-4) and IL-10 among the groups ( P>0.05). VIDA score was negatively correlated with MBL and Treg, and positively correlated with TGF-β in patients with vitiligo( r=-0.28、-0.36、0.31, all P values <0.05). Conclusion:MBL, Treg and their cytokines CTLA-4 and TGF-β are closely related to the pathogenesis and activity of vitiligo.

目的 探讨子宫肌瘤在妊娠期间的生长模式.方法 回顾性分析2019年1月至2022年9月在复旦大学附属妇产科医院产检并分娩的202例妊娠合并子宫肌瘤患者的临床资料,分别在早孕期、中孕期、晚孕期测量子宫肌瘤3条径线,比较不同妊娠阶段子宫肌瘤的体积变化,分析与肌瘤体积变化相关的影响因素;同时统计不良妊娠事件的发生情况并分析与其相关的危险因素.结果 与早孕期相比,子宫肌瘤体积在中孕期增加(172.54±281.95)％,在晚孕期增加(117.56± 245.92)％.与中孕期相比,子宫肌瘤体积在晚孕期减少(9.84±62.66)％.肌瘤体积变化与年龄、孕前体质量指数(BMI)、孕次、产次、早孕期肌瘤最大径线、肌瘤数量无显著相关(P＞0.05).不良妊娠事件包括28例(13.86％)子宫肌瘤红色变性、3例(1.49％)产后出血和4例(1.98％)早产.年龄、孕前BMI、早孕期肌瘤最大径线、肌瘤数量对肌瘤红色变性的发生均无显著影响(P＞0.05).结论 子宫肌瘤在妊娠期间呈体积先增后减的生长模式,中孕期显著增长,晚孕期缩小,但终体积仍大于早孕期.

Background Gaining more information about the reciprocal associations between different biomarkers within the ATN (Amyloid/Tau/Neurodegeneration) framework across the Alzheimer’s disease (AD) spectrum is clinically relevant. We aimed to conduct a comprehensive head-to-head comparison of plasma and positron emission tomography (PET) ATN biomarkers in subjects with cognitive complaints. Methods A hospital-based cohort of subjects with cognitive complaints with a concurrent blood draw and ATN PET imaging ( 18 F-florbetapir for A, 18 F-Florzolotau for T, and 18 F-fluorodeoxyglucose [ 18 F-FDG] for N) was enrolled ( n = 137). The β-amyloid (Aβ) status (positive versus negative) and the severity of cognitive impairment served as the main outcome measures for assessing biomarker performances. Results Plasma phosphorylated tau 181 (p-tau181) level was found to be associated with PET imaging of ATN biomarkers in the entire cohort. Plasma p-tau181 level and PET standardized uptake value ratios of AT biomarkers showed a similarly excellent diagnostic performance for distinguishing between Aβ+ and Aβ− subjects. An increased tau burden and glucose hypometabolism were significantly associated with the severity of cognitive impairment in Aβ+ subjects. Additionally, glucose hypometabolism – along with elevated plasma neurofilament light chain level – was related to more severe cognitive impairment in Aβ− subjects. Conclusion Plasma p-tau181, as well as 18 F-florbetapir and 18 F-Florzolotau PET imaging can be considered as interchangeable biomarkers in the assessment of Aβ status in symptomatic stages of AD. 18 F-Florzolotau and 18 F-FDG PET imaging could serve as biomarkers for the severity of cognitive impairment. Our findings have implications for establishing a roadmap to identifying the most suitable ATN biomarkers for clinical use.

目的 分析中成药的药品不良反应(ADR)规律和特点,促进临床合理使用中成药.方法 收集复旦大学附属中山医院青浦分院2008年1月至2020年12月上报至国家药品不良反应监测中心的ADR报告,通过帕累托图来分析发生ADR的患者年龄、累及器官/系统、药品种类以及不合理因素.结果 共收集ADR报告401份,帕累托图分析结果显示,50岁以上中老年患者较多(208例,51.87％),主要累及器官/系统以皮肤及附件系统、消化系统(354例,67.82％),品种以理血类中成药(165例,41.15％)为主,不合理因素主要为用法用量不适宜(45例,38.46％).结论 临床用药应全面考虑ADR影响因素和用药合理性,以减少ADR的发生.

Purpose: 18F-Florzolotau is a novel second-generation tau radiotracer that shows higher binding affinity and selectivity and no off-target binding. The proportion loss of functional connectivity strength (PLFCS) is a new indicator for representing brain functional connectivity (FC) alteration. This study aims to estimate the relationship between the regional tau accumulation and brain FC abnormality in Alzheimer’s disease (AD) and mild cognitive impairment (MCI) patients based on Florzolotau PET and fMRI. Methods: 22 NC (normal control), 31 MCI and 42 AD patients who have already been scanned with 18F-Florzolotau PET were recruited in this study. (We calculated the PLFCS and standardized uptake value ratio (SUVR) of each node based on the Brainnetome atlas (BNA) template. The SUVR of 246 brain regions was calculated with the cerebellum as the reference region. Further functional connection strength (FCs), PLFCS and SUVR of each brain region were obtained in three groups for comparison.) For each patient, PLFCS and standardized uptake value ratio (SUVR) were calculated based on the Brainnetome atlas (BNA) template. These results, as well as functional connection strength (FCs), were then compared between different groups. Multiple permutation tests were used to determine the target nodes between NC and cognitive impairment (CI) groups (MCI and AD). The relationship between PLFCS and neuropsychological scores or cortical tau deposit was investigated via Pearson correlation analysis. Results: Higher PLFCS and FCs in AD and MCI groups were found compared to the NC group. The PLFCS of 129 brain regions were found to be different between NC and CI groups, and 8 of them were correlated with tau SUVR, including superior parietal lobule (MCI: r = 0.4360, p = 0.0260, AD: r = −0.3663, p = 0.0280), middle frontal gyrus (AD: MFG_R_7_2: r = 0.4106, p = 0.0129; MFG_R_7_5: r = 0.4239, p = 0.0100), inferior frontal gyrus (AD: IFG_R_6_2: r = 0.3589, p = 0.0316), precentral gyrus (AD: PrG_R_6_6: r = 0.3493, p = 0.0368), insular gyrus (AD: INS_R_6_3: r = 0.3496, p = 0.0366) and lateral occipital cortex (AD: LOcC _L_4_3: r = −0.3433, p = 0.0404). Noteworthily, the opposing relationship was found in the superior parietal lobule in the MCI and AD groups. Conclusions: Brain functional connectivity abnormality is correlated with tau pathology in AD and MCI.