Macular vascular density alteration patterns in paediatric optic neuritis patients with serum MOG antibody positivity detected by optic coherence tomography angiography.

PURPOSE: The retinal microvascular network plays a crucial role in inflammatory injury in paediatric optic neuritis (PON) with serum MOG antibody positivity (MOG + PON). This study compared retinal microvascular densities and structural alterations in MOG + PON eyes with paediatric isolated optic neuritis (PION) eyes and followed up with the final best-corrected visual acuity (BCVA) after 6 months. METHODS: A total of 29 children (52 eyes) with PON, including 15 MOG + PON cases (28 eyes), 6 PION cases (10 eyes), 2 neuromyelitis optica spectrum disorders associated PON(NMOSD-PON) cases (4 eyes), 6 MOG-associated disease (MOGAD) patients without ON-affected eyes (MOG + NPON) cases (10 eyes) and age- and gender-matched healthy controls (HCs) underwent superficial/deep retinal angiography density (SAD/DAD) by optical coherence tomography angiography (OCTA). Their BCVAs were followed up until 6 months after PON onsets. RESULTS: MOG + PON cases had better final BCVAs than PION and NMOSD-ON. MOG + PON (35.7 ± 10.3 %) and PION (40.1 ± 10.3 %) eyes experienced severe SAD reductions in contrast to MOGAD+NPON (48.7 ± 5.2 %) and HCs eyes (55.6 ± 8.2 %). However, DAD in MOG + PON eyes (48.5 ± 9.2 %) and MOG + NPON eyes (53.1 ± 3.3 %) increased compared to HC eyes (45.7 ± 9.6 %; p = 0.028 and 0.009, respectively). SAD reduction occurred in acute PON and was detected as early as 2 weeks after PON onset. CONCLUSIONS: MOG + PON eyes had better final BCVAs than PION eyes, which displayed superficial retinal microvascular perfusion reductions and deep microvascular perfusion increases. SAD could be a sensitive surrogate for PON attacks in children with MOGAD.

Individuals with anxiety and depression use atypical decision strategies in an uncertain world.

Previous studies on reinforcement learning have identified three prominent phenomena: (1) individuals with anxiety or depression exhibit a reduced learning rate compared to healthy subjects; (2) learning rates may increase or decrease in environments with rapidly changing (i.e. volatile) or stable feedback conditions, a phenomenon termed learning rate adaptation; and (3) reduced learning rate adaptation is associated with several psychiatric disorders. In other words, multiple learning rate parameters are needed to account for behavioral differences across participant populations and volatility contexts in this flexible learning rate (FLR) model. Here, we propose an alternative explanation, suggesting that behavioral variation across participant populations and volatile contexts arises from the use of mixed decision strategies. To test this hypothesis, we constructed a mixture-of-strategies (MOS) model and used it to analyze the behaviors of 54 healthy controls and 32 patients with anxiety and depression in volatile reversal learning tasks. Compared to the FLR model, the MOS model can reproduce the three classic phenomena by using a single set of strategy preference parameters without introducing any learning rate differences. In addition, the MOS model can successfully account for several novel behavioral patterns that cannot be explained by the FLR model. Preferences for different strategies also predict individual variations in symptom severity. These findings underscore the importance of considering mixed strategy use in human learning and decision-making and suggest atypical strategy preference as a potential mechanism for learning deficits in psychiatric disorders.

A novel strategy for waste activated sludge treatment: Recovery of structural extracellular polymeric substances and fermentative production of volatile fatty acids.

Structural extracellular polymeric substances (SEPS) as valuable biopolymers, can be extracted from waste activated sludge (WAS). However, the extraction yield is typically low, and detailed information on SEPS characterizations, as well as proper treatment of the sludge after SEPS extraction, remains limited. This study aimed to optimize the conditions of heating-Na2CO3 extraction process to increase the yield of SEPS extracted from WAS. Subsequently, SEPS were characterized, and, for the first time, insights into their protein composition were uncovered by using proteomics. A maximum SEPS yield of 209 mg g-1 volatile solid (VS) was obtained under optimal conditions: temperature of 90 °C, heating time of 60 min, Na+ dosage of 8.0 mmol/g VS, and pH required to precipitation of 4.0, which was comparable to that from the aerobic granular sludge reported in literature. Proteomics analysis unveiled that the proteins in SEPS primarily originated from microorganisms involved in nitrogen fixation and organic matter degradation, including their intracellular and membrane-associated regions. These proteins exhibited various catalytic activities and played crucial roles in aggregation processes. Besides, the process of SEPS extraction significantly enhanced volatile fatty acid (VFA) production during the anaerobic fermentation of residual WAS after SEPS extraction. A maximum VFA yield of 420 ± 14 mg COD/g VSadded was observed in anaerobic fermentation of 10 d, which was 77.2 ± 0.1 % higher than that from raw sludge. Mechanism analysis revealed that SEPS extraction not only improved WAS disintegration and solubilization but also reduced the relative activity of methanogens during anaerobic fermentation. Moreover, SEPS extraction shifted the microbial population during anaerobic fermentation in the direction towards hydrolysis and acidification such as Fermentimonas sp. and Soehngenia sp. This study proposed a novel strategy based on SEPS extraction and VFA production for sludge treatment, offering potential benefits for resource recovery and improved process efficiency.

Polymorphism in the Drug Transporter Gene ABCB1 as a Potential Disease Modifier in Cortisol-Producing Adrenal Adenomas.

INTRODUCTION: Endogenous hypercortisolism presents with variable phenotypes. Etiological factors accounting for the level of hypercortisolism or varying severity of associated comorbidities are lacking. Recently, the adrenal ATP-binding cassette B1 (ABCB1) gene was identified as a modulator of glucocorticoid secretion. OBJECTIVE: To evaluate the effect of ABCB1 polymorphism rs2032582 on steroid metabolome and clinical phenotypes in patients with endogenous hypercortisolism. METHODS: In this cross-sectional cohort study, 137 patients prospectively enrolled in the German Cushing's registry were included (41 with ACTH-producing pituitary adenoma, 21 with cortisol-producing adrenal adenoma, and 75 with excluded hypercortisolism). In all patients, ABCB1 polymorphism was analyzed using a TaqMan genotyping assay, glucocorticoid metabolite excretion in 24-hour urine samples was analyzed by gas chromatography-mass spectrometry, and the clinical phenotype was assessed systematically. RESULTS: In patients with cortisol-producing adrenal adenomas, but not in patients with ACTH-producing pituitary adenomas, homozygous major allele GG of ABCB1 polymorphism rs2032582 was associated with higher overall cortisol metabolite secretion (median 13515 [IQR 10347; 25669] µg/24h vs. 9645 [6146; 10732] µg/24h in minor homo- and heterozygotes, p=0.036) and elevated major cortisol metabolites αTHF, THF and THE (9339 [6929; 17789] µg/24h vs. 6288 [4184; 7455] µg/24h, p=0.045). Moreover, these patients showed higher mean arterial pressure (116 [111; 131] mmHg in major homozygotes vs. 105 [96; 112] mmHg in minor homo- and heterozygotes, p=0.036). CONCLUSION: The genotype of drug transporter gene ABCB1 rs2032582 polymorphism is associated with the degree of cortisol metabolite secretion in cortisol-producing adrenal adenomas and could, therefore, represent a modifier of disease severity in this context.

High-density lipoprotein cholesterol trajectory and new-onset metabolic dysfunction-associated fatty liver disease incidence: a longitudinal study.

BACKGROUND: Although high-density lipoprotein cholesterol (HDL-C) exerts a significant influence on the development of metabolic dysfunction-associated fatty liver disease (MAFLD), the association of dynamic changes in HDL-C levels with the risk of MAFLD remains unclear. Thus, the aim of the current study was to explore the association between the changing trajectories of HDL-C and new-onset MAFLD. The findings of this study may provide a theoretical basis for future personalized intervention and prevention targeting MAFLD. METHODS: A total of 1507 participants who met the inclusion criteria were recruited from a community-based physical examination population in Nanjing, China from 2017 to 2021. Group-based trajectory models were constructed to determine the heterogeneous HDL-C trajectories. The incidence of MAFLD in each group in 2022 was followed up, and the Cox proportional hazards regression model was applied to investigate the associations between different HDL-C trajectories and the risk of new-onset MAFLD. RESULTS: The incidences of MAFLD in the low-stable, moderate-stable, moderate-high-stable, and high-stable groups of HDL-C trajectory were 26.5%, 13.8%, 7.2% and 2.6%, respectively. The incidence rate of MAFLD in the order of the above trajectory groups exhibited a decreasing trend (χ2 = 72.55, Ptrend<0.001). After adjusting for confounders, the risk of MAFLD onset in HDL-C low-stable group was still 5.421 times (95%CI: 1.303-22.554, P = 0.020) higher than that in the high-stable group. Subgroup analyses of the combined (moderate high-stable and high-stable groups combined), moderate-stable and low-stable groups showed that sex, age, and overweight/obesity did not affect the association between HDL-C trajectory and MAFLD risk. CONCLUSIONS: Persistently low HDL-C level is a risk factor for the onset of MAFLD. Long-term monitoring of HDL-C levels and timely intervention for those experiencing persistent declines are crucial for early prevention of MAFLD.

Senescence-associated secretory phenotype regulation by dual drug delivery biomimetic nanoplatform for enhanced tumor chemotherapy.

Many chemotherapies, which are still the main clinical treatment for primary tumors, will induce persistent DNA damage in non-tumor stromal cells, especially cancer-associated fibroblasts (CAFs), and activate them to secrete senescence-associated secretory phenotype (SASP). The transition could further result in the formation of tumor immunosuppressive microenvironment and cause drug resistance of neighboring tumor cells. To solve this dilemma, a multi-functional biomimetic drug delivery system (named mPtP@Lipo) was rationally developed by combining CAFs reshaper ginsenoside 20(S)-protopanaxadiol (PPD) and cisplatin prodrug (PtLA) to inhibit tumor progression and the formation of SASP. To achieve effective delivery of these molecules deep into the desmoplastic tumor, fibroblast membrane was fused with liposomes as a targeting carrier. In vitro and in vivo results showed that mPtP@Lipo could penetrate deep into the tumor, reverse CAFs phenotype and inhibit SASP formation, which then blocked the immunosuppressive progress and thus reinforced anti-tumor immune response. The combination of chemotherapeutics and CAFs regulator could achieve both tumor inhibition and tumor immune microenvironment remodeling. In conclusion, mPtP@Lipo provides a promising strategy for the comprehensive stromal-desmoplastic tumor treatment.

Does artificial intelligence affect the ecological footprint? -Evidence from 30 provinces in China.

Artificial intelligence (AI) technology serves as a powerful tool to optimize energy efficiency and lessen ecological footprints. Using data from 30 provinces in China over the period from 2018 to 2022, this study investigates how regional AI development affects the per capita ecological footprint and explores the underlying mechanisms. The results show that: (1) Regional AI development can significantly decrease the ecological footprint, and this conclusion remains robust after a series of robustness checks. (2) Mediation effect analysis indicates that AI technology mainly decreases the ecological footprint by improving energy utilization efficiency. (3) The panel threshold model results show that AI's influence on the ecological footprint has a single energy efficiency threshold. Only when regional energy efficiency exceeds a certain threshold can AI fully exert its suppressive effect on the ecological footprint. (4) Regional heterogeneity analysis shows that the reduction effect of AI on the ecological footprint is more pronounced in the central and eastern regions of China. This paper helps clarify the specific impact of AI technology development on the ecological footprint and provides scientific evidence for regional technology development, energy efficiency improvement, and ecological environment policy formulation.

The irregular developmental duration mainly caused by the broad-complex in Chilo suppressalis.

Chilo suppressalis, a critical rice stem borer pest, poses significant challenges to rice production due to its overlapping generations and irregular developmental duration. These characteristics complicate pest management strategies. According to the dynamic analysis of the overwintering adults of C. suppressalis in fields, it indicates that the phenomenon of irregular development of C. suppressalis exists widely and continuously. This study delves into the potential role of the Broad-Complex (Br-C) gene in the developmental duration of C. suppressalis. Four isoforms of Br-C, named CsBr-C Z1, CsBr-C Z2, CsBr-C Z4, and CsBr-C Z7, were identified. After CsBr-Cs RNAi, the duration of larva development spans extended obviously. And, the average developmental duration of dsCsBr-Cs feeding individuals increased obviously. Meanwhile, the average developmental duration of the dsCsBr-C Z2 feeding group was the longest among all the RNAi groups. After dsCsBr-Cs feeding continuously, individuals pupated at different instars changed obviously: the proportion of individuals pupated at the 5th instar decreased and pupated at the 7th instar or higher increased significantly. Moreover, the pupation rate of dsCsBr-Cs (except dsCsBr-C Z7) were significantly lower than that of dsGFP. The same results were obtained from the mutagenesis in CsBr-C genes mediated by CRISPR/Cas9. The average developmental duration of CsBr-Cs knockout individuals was significantly prolonged. And, the instar of pupation in knockout individuals was also delayed significantly. In conclusion, this work showed that CsBr-Cs played a crucial role in pupal commitment and affected the developmental duration of C. suppressalis significantly.

PPARγ Agonist Pioglitazone Prevents Hypoxia-induced Cardiac Dysfunction by Reprogramming Glucose Metabolism.

The heart relies on various defense mechanisms, including metabolic plasticity, to maintain its normal structure and function under high-altitude hypoxia. Pioglitazone, a peroxisome proliferator-activated receptor γ (PPARγ), sensitizes insulin, which in turn regulates blood glucose levels. However, its preventive effects against hypoxia-induced cardiac dysfunction at high altitudes have not been reported. In this study, pioglitazone effectively prevented cardiac dysfunction in hypoxic mice for 4 weeks, independent of its effects on insulin sensitivity. In vitro experiments demonstrated that pioglitazone enhanced the contractility of primary cardiomyocytes and reduced the risk of QT interval prolongation under hypoxic conditions. Additionally, pioglitazone promoted cardiac glucose metabolic reprogramming by increasing glycolytic capacity; enhancing glucose oxidation, electron transfer, and oxidative phosphorylation processes; and reducing mitochondrial reactive ROS production, which ultimately maintained mitochondrial membrane potential and ATP production in cardiomyocytes under hypoxic conditions. Notably, as a PPARγ agonist, pioglitazone promoted hypoxia-inducible factor 1α (HIF-1α) expression in hypoxic myocardium. Moreover, KC7F2, a HIF-1α inhibitor, disrupted the reprogramming of cardiac glucose metabolism and reduced cardiac function in pioglitazone-treated mice under hypoxic conditions. In conclusion, pioglitazone effectively prevented high-altitude hypoxia-induced cardiac dysfunction by reprogramming cardiac glucose metabolism.

The WFS1-ZnT3-Zn2+ Axis Regulates the Vicious Cycle of Obesity and Depression.

Obesity, a growing global health concern, is closely linked to depression. However, the neural mechanism of association between obesity and depression remains poorly understood. In this study, neural-specific WFS1 deficiency exacerbates the vicious cycle of obesity and depression in mice fed a high-fat diet (HFD), positioning WFS1 as a crucial factor in this cycle. Through human pluripotent stem cells (hESCs) neural differentiation, it is demonstrated that WFS1 regulates Zn2+ homeostasis and the apoptosis of neural progenitor cells (NPCs) and cerebral organoids by inhibiting the zinc transporter ZnT3 under the situation of dysregulated lipid metabolism. Notably, riluzole regulates ZnT3 expression to maintain zinc homeostasis and protect NPCs from lipotoxicity-induced cell death. Importantly, riluzole, a therapeutic molecule targeting the nervous system, in vivo administration prevents HFD-induced obesity and associated depression. Thus, a WFS1-ZnT3-Zn2+ axis critical is demonstrated for the vicious cycle of obesity and depression and that riluzole may have the potential to reverse this process against obesity and depression.

Platelets promote primary hepatocellular carcinoma metastasis through TGF-ß1-mediated cancer cell autophagy.

Previous research has revealed that platelets promote tumor metastasis by binding to circulating tumor cells (CTCs). However, the role of platelets in epithelial-mesenchymal transition (EMT) of cancer cells at the primary tumor site, the crucial initial step of tumor metastasis, remains to be elucidated. Here, we found that platelet releasate enhanced EMT and motility of hepatocellular carcinoma (HCC) cells via AMPK/mTOR-induced autophagy. RNA-seq indicated that platelet releasate altered TGF-ß signaling pathway of cancer cells. Inhibiting TGFBR or deleting platelet TGF-ß1 suppressed AMPK/mTOR pathway activation and autophagy induced by platelet releasate. Compared with Pf4cre-; Tgfb1fl/fl mice, HCC orthotopic models established on Pf4cre+; Tgfb1fl/fl mice showed reduced TGF-ß1 in primary tumors, which corresponded with decreased cancer cell EMT, autophagy, migration ability and tumor metastasis. Inhibition of autophagy via Atg5 knockdown in cancer cells negated EMT and metastasis induced by platelet-released TGF-ß1. Clinically, higher platelet count correlated with increased TGF-ß1, LC3 and N-cad expression in primary tumors of HCC patients, suggesting a link between platelets and HCC progression. Our study indicates that platelets promote cancer cell EMT in the primary tumor and HCC metastasis through TGF-ß1-induced HCC cell autophagy via the AMPK/mTOR pathway. These findings offer novel insights into the role of platelets in HCC metastasis and the potential therapeutic targets for HCC metastasis.

Conjugation of TLR7 and TLR7/8 agonists onto weak protein antigen via versatile oxime ligation for enhanced vaccine efficacy.

Protein-based subunit vaccines are weakly immunogenic, and developing self-adjuvanting vaccines with adjuvant conjugated to antigen is a promising approach for generating optimal immune responses. Here, we report a novel adjuvant-protein conjugate vaccine based on versatile oxime ligation technique. Firstly, the adjuvant properties of a series of TLR7 and TLR7/8 small molecule agonists in self-adjuvanting vaccines were systematically compared by coupling them to proteins in consistent ratio via p-carboxybenzaldehyde (p-CBA) for the first time. All conjugate vaccines induced cytokine secretion in murine and human macrophages in vitro, and promoted specific antibody production in vivo. Notably, a conjugate containing imidazoquinoline TLR7/8 agonist (TLR7/8a1) showed the greatest enhancement in Th1/2 balanced antibody response. To minimize the interference with the protein antigenic integrity, we further developed a systematic glycoconjugation strategy to conjugate this TLR7/8a1 onto the glycan chains of SARS-CoV-2 S1 glycoprotein via oxime ligation, in which S1 containing different numbers of aldehyde groups were obtained by differential periodate oxidation. The resulting TLR7/8a1-S1 conjugate triggered a potent humoral and cellular immunity in vivo. Together these data demonstrate the promise of these TLR7 and TLR7/8 agonists as effective built-in adjuvants, and the versatile oxime ligation strategy might broaden potential applications in designing different conjugate vaccines.

Effect of Genetic Risk on the Relationship Between rs-fMRI Complexity and Tau and Amyloid PET in Alzheimer's Disease.

Reduced functional magnetic resonance imaging (fMRI)-complexity in Alzheimer's disease (AD) progression has been demonstrated and found to be associated with tauopathy and cognition. However, association of fMRI-complexity with amyloid and influence of genetic risk (APOEɛ4) remain unknown. Here we investigate the association between fMRI-complexity, tau-PET, and amyloid-PET as well as influence of APOE genotype using multivariate generalized linear models. We show that fMRI-complexity has a strong association with tau but not amyloid deposition and that the presence of an APOEɛ4 allele enhances this effect. Thus fMRI-complexity provides a surrogate marker of impaired brain functionality in AD progression.

Understanding hepatitis E vaccination intention among women of childbearing-age: A theory-based cross-sectional study.

OBJECTIVES: The purpose of this study was to investigate the HEV vaccination intention, its determinants, and overall influence mechanisms among childbearing-age women. METHOD: The current study was cross-sectional and conducted online from June 25, 2023 to September 25, 2023 in Nanjing, China. Logistic regression models were constructed to identify the intention-associated background factors. Technology Acceptance Model (TAM) and Theory of Planned Behavior (TPB) were integrated and expanded as TAM-TPB model to further investigate the determinants and overall influence mechanism of HEV vaccination intention among this population using structural equation modeling. RESULTS: A total of 423 eligible participants were included in this study. High general HEV knowledge was independently associated with an increased intention to get HEV vaccination (OR = 1.97, 95 % CI: 1.11-3.58, P = 0.023). All the hypotheses proposed in the theoretical TAM-TPB model were supported, with perceived ease of use, perceived usefulness, attitude, subjective norm, and perceived behavioral control positively affecting the intention of HEV vaccination (all P values <0.05), while perceived risk (P = 0.003) exhibited an inverse association with HEV vaccination intention. The model achieved an acceptable fit, and the total explained variance of HEV vaccination intention was as high as 86.20 %. Moreover, no significant common method bias was observed. CONCLUSION: This is the first theory-based study that explored the HEV vaccination intention, its determinants, and overall influence mechanism among childbearing-age women. The results of the current study are of great importance for improving the understanding of the HEV vaccination intention among females of childbearing age.

Pain, obesity, adenosine salvage disruption, and smoking behavior mediate the effect of gut microbiota on sleep disorders: results from network Mendelian randomization and 16S rDNA sequencing.

Objectives: The objective of this study is to investigate the indirect causalities between gut microbiota and sleep disorders. Methods: In stage 1, we utilized 196 gut microbiota as the exposure factor and conducted a two-sample univariable Mendelian randomization (MR) analysis on five sleep disorders: insomnia, excessive daytime sleepiness (EDS), sleep-wake rhythm disorders (SWRD), obstructive sleep apnea (OSA), and isolated REM sleep behavior disorder (iRBD). In stage 2, we validated the MR findings by comparing fecal microbiota abundance between patients and healthy controls through 16S rDNA sequencing. In stage 3, we explored the indirect pathways by which the microbiota affects sleep, using 205 gut microbiota metabolic pathways and 9 common risk factors for sleep disorders as candidate mediators in a network MR analysis. Results: In stage 1, the univariable MR analysis identified 14 microbiota potentially influencing five different sleep disorders. In stage 2, the results from our observational study validated four of these associations. In stage 3, the network MR analysis revealed that the Negativicutes class and Selenomonadales order might worsen insomnia by increasing pain [mediation: 12.43% (95% CI: 0.47, 24.39%)]. Oxalobacter could raise EDS by disrupting adenosine reuptake [25.39% (1.84, 48.95%)]. Allisonella may elevate OSA risk via obesity promotion [36.88% (17.23, 56.54%)], while the Eubacterium xylanophilum group may lower OSA risk by decreasing smoking behavior [7.70% (0.66, 14.74%)]. Conclusion: Triangulation of evidence from the MR and observational study revealed indirect causal relationships between the microbiota and sleep disorders, offering fresh perspectives on how gut microbiota modulate sleep.

Reduction of eEF2 kinase alleviates the learning and memory impairment caused by acrylamide.

BACKGROUND: The impact of acrylamide (ACR) on learning and memory has garnered considerable attention. However, the targets and mechanisms are still unclear. RESULTS: Elongation factor 2 (eEF2) was significantly upregulated in the results of serum proteomics. Results from in vitro and in vivo experiments indicated a notable upregulation of Eukaryotic elongation factor 2 kinase (eEF2K), the sole kinase responsible for eEF2 phosphorylation, following exposure to ACR (P < 0.05). Subsequent in vitro experiments using eEF2K siRNA and in vivo experiments with eEF2K-knockout mice demonstrated significant improvements in abnormal indicators related to ACR-induced learning and memory deficits (P < 0.05). Proteomic analysis of the hippocampus revealed Lpcat1 as a crucial downstream protein regulated by eEF2K. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses indicated that eEF2K may play a role in the process of ACR-induced learning and memory impairment by affecting ether lipid metabolism. CONCLUSIONS: In summary, eEF2K as a pivotal treatment target in the mechanisms underlying ACR-induced learning and memory impairment, and studies have shown that it provides robust evidence for potential clinical interventions targeting ACR-induced impairments.

Yushaniadezhui (Poaceae, Bambusoideae), a new bamboo species from Yunnan, China.

A new bamboo species, Yushaniadezhui, from Kunming, Yunnan, China is described and illustrated in this paper. The new species used to be misidentified as Y.polytricha. Based on careful comparison of morphological features and molecular phylogeny evidence, we confirmed its identity as a new member of the genus Yushania. Yushaniadezhui resembles Y.maculata, Y.polytricha and Y.weixiensis in several aspects, such as culm height and branch complement structure. However, the glabrous culm leaf sheaths and internodes, the absence of auricles and oral setae on most foliage leaves, except the one-year-old foliage leaves, the pubescence on the adaxial surface of the one-year-old foliage leaves and its limestone habitat preference can readily distinguish this new species from its related taxa. Moreover, we emphasise that individuals from various populations and molecular markers with different inheritance patterns for phylogeny reconstruction should be included in new species discovery, especially in plant groups with complex evolutionary histories.

PET/CT Recognition of Costal Cartilage Infection After Breast Implant Surgery.

BACKGROUND: Postoperative infection of breast implants can lead to implant removal and other complications. This study aimed to investigate the presence of costal cartilage infection following breast implant surgery and the diagnostic role of PET/CT in identifying this rare complication. PATIENTS AND METHODS: A retrospective study included 16 patients with persistent infections after breast implant removal surgery. Patients underwent PET/CT scans before surgery, and surgical plans were made based on PET/CT findings. Surgical procedures were guided by PET/CT, and specimens were collected for pathological examination and microbiological culture. Follow-up assessments were performed at 1, 3, and 12 months postoperatively. RESULTS: Among the 16 patients, 11 were diagnosed with costal cartilage infection, whereas 5 had subcutaneous soft tissue infections. PET/CT accurately identified costal cartilage infection in all cases and localized the infected costal cartilage in the majority of cases. Microbiological culture results showed various pathogens. All patients were cured with one or staged surgery. CONCLUSION: Costal cartilage infection following breast implant surgery is a significant concern. PET/CT plays a crucial role in the accurate diagnosis and localization of infected costal cartilage, aiding in appropriate surgical management. Patients should be closely monitored for the possibility of costal cartilage infection when experiencing persistent symptoms after breast implant surgery.

Risk analysis of blood pressure changes on cardiovascular disease in Chinese population.

The study aimed to assess the impact of changes in blood pressure on cardiovascular events in the Chinese population. It enrolled 33 179 Chinese participants aged ≥35 years (57.1% women) without CVD at baseline. BP status was defined according to the 2017 ACC/AHA hypertension guidelines. The type of BP change was defined as change in BP status from baseline to the end of follow-up, included stable BP <130/80, <130/80 to ≥130/80, ≥130/80 to <130/80 mm Hg, persistent BP ≥130/80 mm Hg. The hazard ratio (HR) of incident CVD by change in BP category was estimated using Cox proportional hazards and Fine-Gray models. During median follow-up of 3.17 years, 2023 CVD events occurred. Compared with BP <120/80, 120-129/<80 mm Hg at baseline (HR = 1.66, 95% CI: 1.09-2.53), 130-139/80-89 mm Hg (HR = 1.35, 95% CI: 0.94-1.95), and ≥140/90 mm Hg (HR = 2.46, 95% CI: 1.78-3.40) were risk factors for CVD. Compared with the group with stable BP <130/80 mm Hg, the risk of CVD was 1.88 (95% CI: 1.40-2.53) in the group with persistent BP ≥130/80 mm Hg and 1.40 (95% CI: 1.01-1.94) in the group of BP decreased to <130/80 mm Hg. These results showed that BP 120-129/<80, 130-139/80-89, and ≥140/90 mm Hg were associated with a high risk of CVD. Over time, persistent BP ≥130/80 mm Hg increased the risk of CVD, but a return to <130/80 mm Hg from hypertension decreased the risk of CVD.