Regulation and function of endoplasmic reticulum autophagy in neurodegenerative diseases.

The endoplasmic reticulum, a key cellular organelle, regulates a wide variety of cellular activities. Endoplasmic reticulum autophagy, one of the quality control systems of the endoplasmic reticulum, plays a pivotal role in maintaining endoplasmic reticulum homeostasis by controlling endoplasmic reticulum turnover, remodeling, and proteostasis. In this review, we briefly describe the endoplasmic reticulum quality control system, and subsequently focus on the role of endoplasmic reticulum autophagy, emphasizing the spatial and temporal mechanisms underlying the regulation of endoplasmic reticulum autophagy according to cellular requirements. We also summarize the evidence relating to how defective or abnormal endoplasmic reticulum autophagy contributes to the pathogenesis of neurodegenerative diseases. In summary, this review highlights the mechanisms associated with the regulation of endoplasmic reticulum autophagy and how they influence the pathophysiology of degenerative nerve disorders. This review would help researchers to understand the roles and regulatory mechanisms of endoplasmic reticulum-phagy in neurodegenerative disorders.

Extracellular vesicles as therapeutic tools in regenerative dentistry.

Dental and maxillofacial diseases are always accompanied by complicated hard and soft tissue defects, involving bone, teeth, blood vessels and nerves, which are difficult to repair and severely affect the life quality of patients. Recently, extracellular vesicles (EVs) secreted by all types of cells and extracted from body fluids have gained more attention as potential solutions for tissue regeneration due to their special physiological characteristics and intrinsic signaling molecules. Compared to stem cells, EVs present lower immunogenicity and tumorigenicity, cause fewer ethical problems, and have higher stability. Thus, EV therapy may have a broad clinical application in regenerative dentistry. Herein, we reviewed the currently available literature regarding the functional roles of EVs in oral and maxillofacial tissue regeneration, including in maxilla and mandible bone, periodontal tissues, temporomandibular joint cartilage, dental hard tissues, peripheral nerves and soft tissues. We also summarized the underlying mechanisms of actions of EVs and their delivery strategies for dental tissue regeneration. This review would provide helpful guidelines and valuable insights into the emerging potential of EVs in future research and clinical applications in regenerative dentistry.

Engineering ratchet-based particle separation via extended shortcuts to isothermality.

Microscopic particle separation plays a vital role in various scientific and industrial domains. Conventional separation methods relying on external forces or physical barriers inherently exhibit limitations in terms of efficiency, selectivity, and adaptability across diverse particle types. To overcome these limitations, researchers are constantly exploring new separation approaches, among which ratchet-based separation is a noteworthy method. However, in contrast to the extensive numerical studies and experimental investigations on ratchet separation, its theoretical exploration appears weak, particularly lacking in the analysis of energy consumption involved in the separation processes. The latter is of significant importance for achieving energetically efficient separation. In this paper, we propose a nonequilibrium thermodynamic approach, extending the concept of shortcuts to isothermality, to realize controllable separation of overdamped Brownian particles with low energy cost. By utilizing a designed ratchet potential with temporal period τ, we find in the slow-driving regime that the average particle velocity v[over ¯]_{s}∝(1-D/D^{*})τ^{-1}, indicating that particles with different diffusion coefficients D can be guided to move in distinct directions with a preset D^{*}. It is revealed that an inevitable portion of the energy cost in separation depends on the driving dynamics of the ratchet, with an achievable lower bound W_{ex}^{(min)}∝L^{2}|v[over ¯]_{s}|. Here, L is the thermodynamic length of the driving loop in the parametric space. With a sawtooth potential, we numerically test the theoretical findings and illustrate the optimal separation protocol associated with W_{ex}^{(min)}. Finally, for practical considerations, we compare our approach with the conventional ratchets in terms of separation velocity and energy consumption. The scalability of the current framework for separating various particles in two-dimensional space is also demonstrated. This paper bridges the gap between thermodynamic process control and particle separation, paving the way for further thermodynamic optimization in ratchet-based particle separation.

Uric acid reference values for children and adolescents should be stratified by pubertal stage.

BACKGROUND AND AIM: To establish reference values for hyperuricemia (HUA) in children and adolescents. METHODS AND RESULTS: The study enrolled 4807 students from "The Evaluation and Monitoring on School-based Nutrition and Growth in Shenzhen study." Utilizing quantile regression, associations between age, body mass index (BMI), pubertal stage, and serum uric acid (SUA) were examined, alongside the relationship between SUA and cardiovascular disease (CVD) risk factors. Reference values for SUA were explored using receiver operating characteristic analysis, considering sex and pubertal stage. The prevalence of HUA was 34.3 % for boys and 29 % for girls (using the adult HUA diagnostic criteria: >420 µmol/L for males, >360 µmol/L for females), increasing with higher BMI, age, and pubertal stage. Pubertal stage had the largest influence on SUA in boys, while nutritional status was the most significant factor affecting SUA in girls. Adjusting for age and pubertal stage, higher SUA levels correlated with an increased risk of CVD risk factors. Proposed reference values included >360 µmol/L for girls ages 6-17 years and prepubertal boys. For pubertal boys, reference values varied based on age: >392 µmol/L for ages 9-11 in early-middle puberty, >429 µmol/L for ages 12-14 in early-middle puberty, >478 µmol/L for ages 12-14 in late puberty, and >505 µmol/L for ages 15-17 in late puberty. CONCLUSIONS: Stratifying HUA reference values by pubertal stage, particularly for boys, is crucial. Long-term follow-up of individuals with high SUA levels may aid in refining SUA reference values.

Clinical Identification of Two Novel C. kroppenstedtii-like Species Isolated as Pathogens of Granulomatous Lobular Mastitis.

Granulomatous lobular mastitis (GLM) is a rare benign breast inflammatory disease that affects women of childbearing age. Corynebacterium species, especially Corynebacterium kroppenstedtii, was reported as the pathogen of GLM. A recent study showed that the C. kroppenstedtii complex is composed of C. kroppenstedtii and two novel species, C. parakroppenstedtii and C. pseudokroppenstedtii. The study presents seven C. kroppenstedtii-like strains isolated from GLM patients. However, they turned out to be six strains of C. parakroppenstedtii and one strain of C. pseudokroppenstedtii according to 16sRNA sequencing. In order to conduct a phylogenetic study, we further sequenced the fusA and rpoB genes, which were frequently employed in studies of Corynebacterium species. Novel Mass Spectral Peaks (MSPs) for C. parakroppenstedtii were created with Bruker MALDI-TOF MS. Then, the identification power of the MSPs was tested by C. parakroppenstedtii strains and remotely related Corynebacterum spp. The antibiotic sensitivity tests were performed according to the CLSI M45 guidelines. All of the strains were not resistant to ß-lactams, vancomycin or linezolid. However, applying erythromycin and clindamycin could be fruitless. Phenotypic identification using a Vitek2 ANC ID card proved all of the C. parakroppenstedtii strains were identified as Actinomycete naeslundii. The test of Ala-Phe-Pro arylamidase and urease could be employed as the characteristics to distinguish C. pseudokroppenstedtii from C. parakroppenstedtii. Here, we present the identification, antibiotic sensitivity tests (ASTs) and epidemiological investigation of two novel C. kroppenstedtii-like species with the purpose of improving the understanding of C. kroppenstedtii-like species and related diseases.

Inhibition of ATP1V6G3 prompts hepatic stellate cell senescence with reducing ECM by activating Notch1 pathway to alleviate hepatic fibrosis.

Liver fibrosis is characterized by an excessive reparative response to various etiological factors, with the activated hepatic stellate cells (aHSCs) leading to extracellular matrix (ECM) accumulation. Senescence is a stable growth arrest, and the senescence of aHSCs is associated with the degradation of ECM and the regression of hepatic fibrosis, making it a promising approach for managing hepatic fibrosis. The role and specific mechanisms by which V-Type Proton ATPase Subunit G 3 (ATP6V1G3) influences senescence in activated HSCs during liver fibrosis remain unclear. Our preliminary results reveal upregulation of ATP6V1G3 in both human fibrotic livers and murine liver fibrosis models. Additionally, ATP6V1G3 inhibition induced senescence in aHSCs in vitro. Moreover, suppressing Notch1 reversed the senescence caused by ATP6V1G3 inhibition in HSCs. Thus, targeting ATP6V1G3, which appears to drive HSCs senescence through the Notch1 pathway, emerges as a potential therapeutic strategy for hepatic fibrosis.

Weight-Specific Grip Strength as a Novel Indicator Associated with Cardiometabolic Risk in Children: The EMSNGS Study.

CONTEXT: Handgrip strength (HGS) is an important indicator of sarcopenia and adverse health outcomes. However, evaluating HGS in children presents challenges, and its association with metabolism remains incompletely understood. OBJECTIVE: To establish grip strength reference values for Chinese children and adolescents, as well as to evaluate the relationship between HGS and cardiometabolic risk. METHODS: Data were collected from 4 072 participants aged 6-18 as part of the Evaluation and Monitoring on School-based Nutrition and Growth in Shenzhen (EMSNGS) study. HGS was measured, and relative HGS (RHGS) was normalized by body mass index. Age- or weight-specific HGS and RHGS were derived using the generalized additive model of location, scale, and shape (GAMLSS) model, and participants' values were categorized into quartiles, defining low strength as the lowest quartile. The cardiometabolic risk index (CMRI) z-score was calculated, with high risk defined as a z-score of ≥ 1. RESULTS: Both boys and girls exhibited similar increases in age- and weight-specific grip strength. Low grip strength, classified by weight-specific HGS and RHGS, was linked to higher CMRI z-scores compared to classifications based on age-specific references in both sexes. A dose-dependent relationship was observed between weight-specific grip strength and cardiometabolic risk, particularly in boys. Compared to the middle category (P25th-P75th), the odds ratios for high cardiometabolic risks associated with low grip strength increased in both sexes. CONCLUSION: This study established grip strength reference values for Chinese youth, introduced the concept of weight-specific HGS and RHGS, and demonstrated a dose-dependent relationship between weight-specific grip strength and cardiometabolic risk. These findings highlighted the association between low muscle strength and increased cardiometabolic risk.

An inhalable nanoparticle enabling virulence factor elimination and antibiotics delivery for pneumococcal pneumonia therapy.

Streptococcus pneumoniae (S. pneumoniae) is a major cause of community-acquired pneumonia. Current standard clinical therapies mainly focus on combating S. pneumoniae through antibiotics. However, the limited delivery of antibiotics and the undetoxified hydrogen peroxide (H2O2) virulence factor secreted by S. pneumoniae impede the therapeutic outcomes. Here we report an inhalable catalase (CAT)-tannic acid (TA) nanoassembly for local antibiotic (levofloxacin) delivery and simultaneously neutralizing the secreted H2O2 virulence factors to treat pneumococcal pneumonia. After aerosol inhalation, the inhalable formulation (denoted as CT@LVX) effectively accumulates in lung tissues through TA-mediated mucoadhesion. CAT can reduce alveolar epithelial cells apoptosis by catalyzing the decomposition of accumulated H2O2 in the infected lung tissues. In synergy with antibiotic LVX-mediated S. pneumoniae elimination, CT@LVX significantly decreases lung injury companied with reduced inflammatory, resulting in 100 % survival of mice with pneumonia. In a clinically isolated S. pneumoniae strain-induced pneumonia mouse model, CT@LVX also shows superior outcomes compared to the traditional antibiotic treatment, highlighting its potential clinical application prospects.

FTO promotes gefitinib-resistance by enhancing PELI3 expression and autophagy in non-small cell lung cancer.

The established recognition of N6-methyladenosine (m6A) modification as an indispensable regulatory agent in human cancer is widely accepted. However, the understanding of m6A's role and the mechanisms underlying its contribution to gefitinib resistance is notably limited. Herein, using RT-qPCR, Western blot, Cell proliferation and apoptosis, as well as RNA m6A modification assays, we substantiated that heightened FTO (Fat Mass and Obesity-associated protein) expression substantially underpins the emergence of gefitinib resistance in NSCLC cells. This FTO-driven gefitinib resistance is hinged upon the co-occurrence of PELI3 (Pellino E3 Ubiquitin Protein Ligase Family Member 3) expression and concurrent autophagy activation. Manipulation of PELI3 expression and autophagy activation, including its attenuation, was efficacious in both inducing and overcoming gefitinib resistance within NSCLC cells, as validated in vitro and in vivo. In summary, this study has successfully elucidated the intricate interplay involving FTO-mediated m6A modification, its consequential downstream effect on PELI3, and the concurrent involvement of autophagy in fostering the emergence of gefitinib resistance within the therapeutic context of NSCLC.

GPR50 regulates neuronal development as a mitophagy receptor.

Neurons rely heavily on high mitochondrial metabolism to provide sufficient energy for proper development. However, it remains unclear how neurons maintain high oxidative phosphorylation (OXPHOS) during development. Mitophagy plays a pivotal role in maintaining mitochondrial quality and quantity. We herein describe that G protein-coupled receptor 50 (GPR50) is a novel mitophagy receptor, which harbors the LC3-interacting region (LIR) and is required in mitophagy under stress conditions. Although it does not localize in mitochondria under normal culturing conditions, GPR50 is recruited to the depolarized mitochondrial membrane upon mitophagy stress, which marks the mitochondrial portion and recruits the assembling autophagosomes, eventually facilitating the mitochondrial fragments to be engulfed by the autophagosomes. Mutations Δ502-505 and T532A attenuate GPR50-mediated mitophagy by disrupting the binding of GPR50 to LC3 and the mitochondrial recruitment of GPR50. Deficiency of GPR50 causes the accumulation of damaged mitochondria and disrupts OXPHOS, resulting in insufficient ATP production and excessive ROS generation, eventually impairing neuronal development. GPR50-deficient mice exhibit impaired social recognition, which is rescued by prenatal treatment with mitoQ, a mitochondrially antioxidant. The present study identifies GPR50 as a novel mitophagy receptor that is required to maintain mitochondrial OXPHOS in developing neurons.

Different Contributions of embB and ubiA Mutations to Variable Level of Ethambutol Resistance in Mycobacterium tuberculosis Isolates.

Objective: To explore the association between the variant mutations within embB and ubiA, and the degree of ethambutol (EMB) resistance of Mycobacterium tuberculosis (M. tuberculosis) isolates. Methods: A total of 146 M. tuberculosis isolates were used to determine the minimum inhibitory concentrations (MICs) of EMB with a 96-well microplate-based assay. The mutations within embB and ubiA among these isolates were identified with DNA sequencing. Moreover, a multivariate regression model and a computer model were established to assess the effects of mutations on EMB resistance. Results: Our data showed that overall 100 isolates exhibited 28 mutated patterns within the sequenced embB and ubiA. Statistical analysis indicated that embB mutations Met306Val, Met306Ile, Gly406Ala, and Gln497Arg, were strongly associated with EMB resistance. Of these mutations, Met306Val and Gln497Arg were significantly associated with high-level EMB resistance. Almost all multiple mutations occurred in high-level EMB-resistant isolates. Although the mutation within ubiA accompanied with embB mutation presented exclusively in EMB-resistant isolates, four single ubiA mutations (Ala39Glu, Ser173Ala, Trp175Cys, and Val283Leu) leading to protein instability were observed in EMB-susceptible isolates. Conclusion: This study highlighted the complexity of EMB resistance. Some individual mutations and multiple mutations within embB and ubiA contributed to the different levels of EMB resistance.

Silica nanoparticle design for colorectal cancer treatment: Recent progress and clinical potential.

Colorectal cancer (CRC) is the third most common cancer worldwide and the second most common cause of cancer death. Nanotherapies are able to selectively target the delivery of cancer therapeutics, thus improving overall antitumor efficiency and reducing conventional chemotherapy side effects. Mesoporous silica nanoparticles (MSNs) have attracted the attention of many researchers due to their remarkable advantages and biosafety. We offer insights into the recent advances of MSNs in CRC treatment and their potential clinical application value.

Assessment of aortic dilatation in Chinese children and adolescents with Turner syndrome: a single center experience.

BACKGROUND: Patients with Turner syndrome (TS) face an increased risk of developing aortic dilatation (AD), but diagnosing AD in children presents greater complexity compared to adults. This study aimed to investigate the application of various assessment indicators of AD in Chinese children and adolescents with TS. METHODS: This study included TS patients admitted to Shenzhen Children's Hospital from 2017 to 2022. Cardiovascular lesions were diagnosed by experienced radiologists. Patients without structural heart disease were divided into different body surface area groups, then the Chinese TS population Z-score (CHTSZ-score) of the ascending aorta was calculated and compared with other indicators such as aortic size index (ASI), ratio of the ascending to descending aortic diameter (A/D ratio), and TSZ-score (Quezada's method). RESULTS: A total of 115 TS patients were included, with an average age of 10.0 ± 3.7 years. The incidences of the three most serious cardiovascular complications were 9.6% (AD), 10.4% (coarctation of the aorta, CoA), and 7.0% (bicuspid aortic valve, BAV), respectively. The proportion of developing AD in TS patients aged ≥ 10 years was higher than that in those < 10 years old (16.6% vs. 1.8%, P = 0.009), and the proportion of patients with CoA or BAV who additionally exhibited AD was higher than those without these conditions (31.6% vs. 5.2%, P < 0.001). The ASI, A/D ratio, TSZ-score, and CHTSZ-score of the 11 patients with AD were 2.27 ± 0.40 cm/m2, 1.90 ± 0.37, 1.28 ± 1.08, and 3.07 ± 2.20, respectively. Among the AD patients, only 3 cases had a TSZ-score ≥ 2, and 2 cases had a TSZ-score ≥ 1. However, based on the assessment using the CHTSZ-score, 6 patients scored ≥ 2, and 5 patients scored ≥ 1. In contrast, the TSZ-score generally underestimated the aortic Z-scores in Chinese children with TS compared to the CHTSZ-score. CONCLUSIONS: The applicability of ASI and A/D ratio to children with TS is questionable, and racial differences can affect the assessment of TSZ-score in the Chinese population. Therefore, establishing the CHTSZ-score specifically tailored for Chinese children and adolescents is of paramount importance.

Abnormal Bone Turnover Observed in Obese Children based on Puberty Stage-Specific Bone Turnover Marker Reference.

CONTEXT: Childhood and adolescence are critical periods for lifelong bone health. The impact of obesity on these phases is controversial, which may be due to the lack of standards for age-, sex-, and puberty-specific bone turnover markers (BTMs) that could sensitively reflect bone metabolism. OBJECTIVE: To generate age-, sex, and puberty stage-specific BTM reference curves in children and adolescents and to explore the effect of obesity on bone metabolism in the Chinese population. METHODS: Our study was part of the Evaluation and Monitoring on School-based Nutrition and Growth in Shenzhen study. A total of 800 participants aged 6∼18 years with normal body mass index (BMI) were selected to establish BTM reference curves for boys and girls at different ages under different pubertal development stages. Additionally, 200 participants with obesity (BMI > 95th percentile) were matched with healthy children from the original cohort at a 1:1 ratio. All participants underwent bone mineral density assessment, and serum levels of procollagen type 1 N-propeptide (P1NP) and ß-C-telopeptide of type I collagen (CTX) were measured. RESULTS: The BTM values presented significant age, sex, and puberty stage differences. Analysis of serum BTMs based on the established reference revealed a higher percentage of low-level P1NP in boys with obesity (P = .005); no significant difference was observed in girls. However, the obese group showed a significantly higher proportion of high ß-CTX levels for girls, not boys (P = .022). CONCLUSION: We provide age-, sex-, and puberty stage-specific P1NP and ß-CTX reference curves. According to these, obesity appeared to be a negative factor for bone formation in boys and for bone resorption in girls.

NLRP3 inflammasome activation triggers severe inflammatory liver injury in N, N-dimethylformamide-exposed mice.

N,N-dimethylformamide (DMF) is a widely utilized chemical solvent with various industrial applications. Previous studies have indicated that the liver is the most susceptible target to DMF exposure, whereas the underlying mechanisms remain to be elucidated. This study aimed to investigate the role of NLRP3 inflammasome in DMF-induced liver injury in mice by using two NLRP3 inflammasome inhibitors, Nlrp3-/- mice, Nfe2l2-/- mice, and a macrophage-depleting agent. RNA sequencing revealed that endoplasmic reticulum (ER) stress and NLRP3 inflammasome-associated pathways were activated in the mouse liver after acute DMF exposure, which was validated by Western blotting. Interestingly, DMF-induced liver injury was effectively suppressed by two inflammasome inhibitors, MCC950 and Dapansutrile. In addition, knockout of Nlrp3 markedly attenuated DMF-induced liver injury without affecting the metabolism of DMF. Furthermore, silencing Nfe2l2 aggravated the liver injury and the NLRP3 inflammasome activation in mouse liver. Finally, the depletion of hepatic macrophages by clodronate liposomes significantly reduced the liver damage caused by DMF. These results suggest that NLRP3 inflammasome activation is the upstream molecular event in the development of acute liver injury induced by DMF.

Desmoglein 2 and desmocollin 2 depletions promote malignancy through distinct mechanisms in triple-negative and luminal breast cancer.

BACKGROUND: Aberrant expressions of desmoglein 2 (Dsg2) and desmocollin 2(Dsc2), the two most widely distributed desmosomal cadherins, have been found to play various roles in cancer in a context-dependent manner. Their specific roles on breast cancer (BC) and the potential mechanisms remain unclear. METHODS: The expressions of Dsg2 and Dsc2 in human BC tissues and cell lines were assessed by using bioinformatics analysis, immunohistochemistry and western blotting assays. Wound-healing and Transwell assays were performed to evaluate the cells' migration and invasion abilities. Plate colony-forming and MTT assays were used to examine the cells' capacity of proliferation. Mechanically, Dsg2 and Dsc2 knockdown-induced malignant behaviors were elucidated using western blotting assay as well as three inhibitors including MK2206 for AKT, PD98059 for ERK, and XAV-939 for ß-catenin. RESULTS: We found reduced expressions of Dsg2 and Dsc2 in human BC tissues and cell lines compared to normal counterparts. Furthermore, shRNA-mediated downregulation of Dsg2 and Dsc2 could significantly enhance cell proliferation, migration and invasion in triple-negative MDA-MB-231 and luminal MCF-7 BC cells. Mechanistically, EGFR activity was decreased but downstream AKT and ERK pathways were both activated maybe through other activated protein tyrosine kinases in shDsg2 and shDsc2 MDA-MB-231 cells since protein tyrosine kinases are key drivers of triple-negative BC survival. Additionally, AKT inhibitor treatment displayed much stronger capacity to abolish shDsg2 and shDsc2 induced progression compared to ERK inhibition, which was due to feedback activation of AKT pathway induced by ERK inhibition. In contrast, all of EGFR, AKT and ERK activities were attenuated, whereas ß-catenin was accumulated in shDsg2 and shDsc2 MCF-7 cells. These results indicate that EGFR-targeted therapy is not a good choice for BC patients with low Dsg2 or Dsc2 expression. Comparatively, AKT inhibitors may be more helpful to triple-negative BC patients with low Dsg2 or Dsc2 expression, while therapies targeting ß-catenin can be considered for luminal BC patients with low Dsg2 or Dsc2 expression. CONCLUSION: Our finding demonstrate that single knockdown of Dsg2 or Dsc2 could promote proliferation, motility and invasion in triple-negative MDA-MB-231 and luminal MCF-7 cells. Nevertheless, the underlying mechanisms were cellular context-specific and distinct.

Gradient inflammation in the pancreatic stump after pancreaticoduodenectomy: Two case reports and review of literature.

BACKGROUND: Postoperative pancreatic fistula (POPF) contributes significantly to morbidity and mortality after pancreaticoduodenectomy (PD). However, the underlying mechanisms remain unclear. This study explored this pathology in the pancreatic stumps and elucidated the mechanisms of POPF following PD. CASE SUMMARY: Pathological analysis and 16S rRNA gene sequencing were performed on specimens obtained from two patients who underwent complete pancreatectomy for grade C POPF after PD. Gradient inflammation is present in the pancreatic stump. The apoptosis was lower than that in the normal pancreas. Moreover, neutrophil-dominated inflammatory cells are concentrated in the ductal system. Notably, neutrophils migrated through the ductal wall in acinar duct metaplasia-formed ducts. Additionally, evidence indicates that gut microbes migrate from the digestive tract. Gradient inflammation occurs in pancreatic stumps after PD. CONCLUSION: The mechanisms underlying POPF include high biochemical activity in the pancreas, mechanical injury, and digestive reflux. To prevent POPF and address pancreatic inflammation and reflux, breaking the link with anastomotic dehiscence is practical.

Photouranium-Catalyzed C-F Activation Hydroxylation via Water Splitting.

The C-F bond is the strongest covalent single bond (126 kcal/mol) in carbon-centered bonds, in which the highest electronegativity of fluorine (χ = 4) gives rise to the shortest bond length (1.38 Å) and the smallest van der Waals radius (rw = 1.47 Å), resulting in enormous challenges for activation and transformation. Herein, C-F conversion was realized via photouranium-catalyzed hydroxylation of unactivated aryl fluorides using water as a hydroxyl source to deliver multifunctional phenols under ambient conditions. The activation featured cascade sequences of single electron transfer (SET)/hydrogen atom transfer (HAT)/oxygen atom transfer (OAT), highly integrated from the excited uranyl cation. The *UO22+ prompted water splitting under mild photoexcitation, caging the active oxygen in a peroxo-bridged manner for the critical OAT process and releasing hydrogen via the HAT process.

Narrative Review of Traditional Chinese Medicine in the Treatment of Postmenopausal Osteoporosis.

An increasing percentage of people in China are suffering from osteoporosis, particularly postmenopausal osteoporosis (PMOP), as the country rapidly evolves into an aging culture. Patients with osteoporosis are inclined to endure fractures, as well as deformities and impairments, which drastically decrease people's quality of life. The benefits of Traditional Chinese medicine (TCM) treatment have continued to become increasingly apparent as reports of adverse responses to Western medications increased. The main advantage of traditional Chinese medicine treatment is that pharmacological interactions may be employed to lessen adverse effects while increasing therapeutic efficacy. In addition, there are various exercise therapies created by medical doctors in the past generations, such as: Wuqinxi, Taijiquan, Baduanjin, Yijinjing, etc. Chinese medicine and exercise treatment for postmenopausal osteoporosis have garnered a lot of attention recently both domestically and internationally, and investigations demonstrate that these therapies have considerable therapeutic effects. The pathophysiology of postmenopausal osteoporosis, advancements of herbal therapy options, and exercise treatment options are all thoroughly addressed in this article.