Alzheimer's disease is a debilitating, progressive neurodegenerative disorder characterized by the progressive accumulation of abnormal proteins, including amyloid plaques and intracellular tau tangles, primarily within the brain. Lysosomes, crucial intracellular organelles responsible for protein degradation, play a key role in maintaining cellular homeostasis. Some studies have suggested a link between the dysregulation of the lysosomal system and pathogenesis of neurodegenerative diseases, including Alzheimer's disease. Restoring the normal physiological function of lysosomes hold the potential to reduce the pathological burden and improve the symptoms of Alzheimer's disease. Currently, the efficacy of drugs in treating Alzheimer's disease is limited, with major challenges in drug delivery efficiency and targeting. Recently, nanomaterials have gained widespread use in Alzheimer's disease drug research owing to their favorable physical and chemical properties. This review aims to provide a comprehensive overview of recent advances in using nanomaterials (polymeric nanomaterials, nanoemulsions, and carbon-based nanomaterials) to enhance lysosomal function in treating Alzheimer's disease. This review also explores new concepts and potential therapeutic strategies for Alzheimer's disease through the integration of nanomaterials and modulation of lysosomal function. In conclusion, this review emphasizes the potential of nanomaterials in modulating lysosomal function to improve the pathological features of Alzheimer's disease. The application of nanotechnology to the development of Alzheimer's disease drugs brings new ideas and approaches for future treatment of this disease.
Although abundant unconventional oil resources have been discovered in conglomerate and sandstone reservoirs in rift basins, the mechanism of differential pore evolution in conglomerates and sandstone reservoirs within different secondary structural zones of rift basins is not yet clear. The pore structures of conglomerate and sandstone reservoirs in the distinct secondary structural zones in the Chezhen Sag were quantified in three dimensions using high-resolution microcomputed tomography (micro-CT). Thin section and scanning electron microscopy observations were used to investigate the differential evolution mechanisms of conglomerate and sandstone reservoirs. Micro-CT analysis of the pore structures of conglomerate and sandstone reservoirs revealed that sandstone reservoirs are superior to conglomerate reservoirs with regard to the pore number and pore connectivity and that sandstone reservoirs are more heterogeneous than conglomerate reservoirs. Triangles dominate the pore and pore throat geometries of sandstone and conglomerate reservoirs, while the sandstone reservoir pores are more regular than conglomerate reservoir pores. The depositional environment, mineral composition, and diagenetic intensity jointly control the quality of the reservoirs. Because of the lengthy transportation distance of their parent rocks, the compositional maturity and sorting behavior of sandstone reservoirs in depression and gentle slope zones are better than those of conglomerate reservoirs in steep slope zones, and thus sandstone reservoirs have a higher initial porosity than conglomerate reservoirs. The rapid compaction experienced by the conglomerate reservoirs in steep slope zones in their early stages creates a closed diagenetic environment, making it difficult to effectively improve reservoir porosity through dissolution. However, the widely developed microfractures in the reservoirs provide channels for fluid migration, promote the development of dissolution pores, and form a tight reservoir dominated by secondary pores. With weak compaction and an open diagenetic environment, the primary pores in sandstone reservoirs in the gentle slope zone are preserved in large quantities. Meanwhile, dissolution expands the secondary pores of the reservoir, resulting in a high-quality reservoir having both primary and secondary pores. In addition, an approach based on primary, secondary, and total porosity was proposed in the study to efficiently evaluate reservoir quality and identify reservoir evolution mechanisms.
In this article, the history and taxonomy of Placoneis gastrum, the type species of the genus Placoneis, was discussed. We investigated the structure of pore occlusions in Placoneis and related genera. As a result, we propose a new classification for tectulum-like types of pore occlusions. The new classification is congruent with previously-published and newly-constructed phylogenies based on molecular data. Based on the different structures of the pore occlusions, species of Placoneis are transferred to Witkowskia gen. nov. Hence, 168 new combinations are introduced. A new diatom species, with a similar morphology to Placoneis flabellata, was discovered in Bac Kan Province, Vietnam. It is described in this article as Chudaevia densistriata sp. nov. Placoneis flabellata is transferred to Chudaevia gen. nov. We also illustrate Placoneis flabellata herein and compare it to Chudaevia densistriata sp. nov. An unknown diatom, similar to Placoneis coloradensis, was discovered in Chukotka, Russia. It is introduced as Placoneis elinae sp. nov. below. Additionally, we discuss the distribution of some species of Witkowskia gen. nov. and Chudaevia gen. nov.
Diatoms , Phylogeny , Diatoms/classification , Vietnam , Russia , Species Specificity
Aim: To examine both predictive and clinicopathological importance underlying FOXD1 in malignant tumors, our study adopts meta-analysis. Methods: We searched from PubMed, Embase, WOS, Wanfang and CNKI. Stata SE15.1 was used to calculate the risk ratio (HR) as well as relative risk (RR) with 95% of overall CIs to assess FOXD1 and overall survival rate (OS), disease-free survival rate as well as clinicopathological parameters. Results: 3808 individuals throughout 17 trials showed high FOXD1 expression was linked to disadvantaged OS (p < 0.001) and disease-free survival (p < 0.001) and higher TNM stage (p < 0.001). Conclusion: Elevated FOXD1 had worse predictions and clinicopathological parameters in most cancers. The GEPIA database findings also support our results.
FOXD1 is a gene linked to a variety of cancers. In our article, we analyzed the results of several clinical trials in patients with different cancers. We found that when this gene is expressed in large amounts, it is often indicative of poor survival rates. From this study we can use FOXD1 to predict the course of the disease and at the same time study its upper and lower pathways to find therapeutic drugs to treat the cancer.
Purpose: This study sought to determine if the use of tranexamic acid (TXA) in preexisting thromboembolic risk patients undergoing total joint arthroplasty (TJA) was linked to an increased risk of death or postoperative complications. Methods: We conducted a comprehensive search for studies up to May 2023 in PubMed, Web of Science, EMBASE, and the Cochrane Library. We included randomized clinical trials, cohort studies, and case-control studies examining the use of TXA during TJA surgeries on high-risk patients. The Cochrane Risk of Bias instrument was used to gauge the excellence of RCTs, while the MINORS index was implemented to evaluate cohort studies. We used mean difference (MD) and relative risk (RR) as effect size indices for continuous and binary data, respectively, along with 95% CIs. Results: Our comprehensive study, incorporating data from 11 diverse studies involving 812 993 patients, conducted a meta-analysis demonstrating significant positive outcomes associated with TXA administration. The findings revealed substantial reductions in critical parameters, including overall blood loss (MD = -237.33; 95% CI (-425.44, -49.23)), transfusion rates (RR = 0.45; 95% CI (0.34, 0.60)), and 90-day unplanned readmission rates (RR = 0.86; 95% CI (0.76, 0.97)). Moreover, TXA administration exhibited a protective effect against adverse events, showing decreased risks of pulmonary embolism (RR = 0.73; 95% CI (0.61, 0.87)), myocardial infarction (RR = 0.47; 95% CI (0.40-0.56)), and stroke (RR = 0.73; 95% CI (0.59-0.90)). Importantly, no increased risk was observed for mortality (RR = 0.53; 95% CI (0.24, 1.13)), deep vein thrombosis (RR = 0.69; 95% CI (0.44, 1.09)), or any of the evaluated complications associated with TXA use. Conclusion: The results of this study indicate that the use of TXA in TJA patients with preexisting thromboembolic risk does not exacerbate complications, including reducing mortality, deep vein thrombosis, and pulmonary embolism. Existing evidence strongly supports the potential benefits of TXA in TJA patients with thromboembolic risk, including lowering blood loss, transfusion, and readmission rates.
Dysregulated T cell activation underpins the immunopathology of rheumatoid arthritis (RA), yet the machineries that orchestrate T cell effector program remain incompletely understood. Herein, we leveraged bulk and single-cell RNA sequencing data from RA patients and validated protein disulfide-isomerase A3 (PDIA3) as a potential therapeutic target. PDIA3 is remarkably upregulated in pathogenic CD4 T cells derived from RA patients and positively correlates with C-reactive protein (CRP) level and disease activity score 28 (DAS28). Pharmacological inhibition or genetic ablation of PDIA3 alleviates RA-associated articular pathology and autoimmune responses. Mechanistically, T cell receptor (TCR) signaling triggers intracellular calcium flux to activate NFAT1, a process that is further potentiated by Wnt5a under RA settings. Activated NFAT1 then directly binds to the Pdia3 promoter to enhance the expression of PDIA3, which complexes with STAT1 or PKM2 to facilitate their nuclear import for transcribing Th1 and Th17 lineage-related genes, respectively. This non-canonical regulatory mechanism likely occurs under pathological conditions as PDIA3 could only be highly induced following aberrant external stimuli. Together, our data support that targeting PDIA3 is a vital strategy to mitigate autoimmune diseases, such as RA, in clinical settings.
BACKGROUND: The specific effects of adverse childhood experiences (ACEs) in adulthood and senectitude were less known. We aim to examine the relationship between early ACEs and overall health condition as well as specific dimensions in the middle-aged and elderly population. METHODS: In the 2019-2021 Behavioral Risk Factor Surveillance System Study, robust Poisson regression models were used to estimate the relationship between ACE exposure and current health status among adults aged 45 ≥ years. RESULTS: Of the 195,472 participants, 53.8 % were female and the mean age was 65.0 years. Compared to populations without ACE, ACE exposures were more significantly associated with depression (PR: 2.03, 95 %CI: 1.94-2.21), frequent mental health (PR: 1.85, 95 %CI: 1.74-1.97) and subject cognitive decline (PR: 1.99, 95 %CI:1.85-2.14) than with physical health (PR: 1.37, 95 %CI: 1.32-1.44), with dose-response patterns. The association with mental disorder was especially significant among the elderly population. CONCLUSION: Early ACEs are associated with adverse health outcomes that persist into later life, particularly mental disorders and cognitive decline. Poor mental health may indirectly influence associations with ACEs and cognitive decline as well as physical health. Our findings emphasize the importance of lifelong psychological screening and support for the ACE-exposed middle-aged and elderly population.
Recently, the intestinal lymphatic transport based on Peyer's patches (PPs) is emerging as a promising absorption pathway for natural polysaccharides. Herein, the aim of this study is to investigate the PP-based oral absorption of a pectic polysaccharide from Smilax china L. (SCLP), as well as its uptake and transport mechanisms in related immune cells. Taking advantages of the traceability of fluorescently labeled SCLP, we confirmed that SCLP could be absorbed into PPs and captured by their mononuclear phagocytes (dendritic cells and macrophages) following oral administration. Subsequently, the systematic in vitro study suggested that the endocytic mechanisms of SCLP by model mononuclear phagocytes (BMDCs and RAW264.7 cells) mainly involved caveolae-mediated endocytosis, macropinocytosis and phagocytosis. More importantly, SCLP directly binds and interacts with toll-like receptor 2 (TLR2) and galectin 3 (Gal-3) receptor, and was taken up by mononuclear phagocytes in receptor-mediated manner. After internalization, SCLP was intracellularly transported primarily through endolysosomal pathway and ultimately localized in lysosomes. In summary, this work reveals novel information and perspectives about the in vivo fate of SCLP, which will contribute to further research and utilization of SCLP and other pectic polysaccharides.
Peyer's Patches , Smilax , Animals , Mice , RAW 264.7 Cells , Peyer's Patches/metabolism , Smilax/chemistry , Endocytosis , Pectins/chemistry , Pectins/metabolism , Macrophages/metabolism , Macrophages/drug effects , Phagocytosis/drug effects , Phagocytes/metabolism , Phagocytes/drug effects , Toll-Like Receptor 2/metabolism , Mice, Inbred BALB C , Male , Dendritic Cells/metabolism , Dendritic Cells/drug effects , Administration, Oral
Surface and underwater (S/U) acoustic targets recognition is an important application of passive sonar. It is difficult to distinguish them due to the mixture of underwater target radiation noise and marine environmental noise. In previous studies, although using a single hydrophone was able to identify S/U acoustic targets, there were still a few hydrophones that had poor accuracy. In this paper, S/U acoustic targets recognition using two hydrophones based on Gradient Boosting Decision Tree is proposed, and it is first found out as high as 100% accuracy could be achieved with the implementation of SACLANT 1993 data. The real experimental data are always rare and insufficient. The big training dataset is generated using environmental information by acoustic model named KRAKEN. Simulation and experimental data used in the model are heterogeneous, and the differences between these two kinds of data are assimilated by using vertical linear array feature extraction method. The model realizes the recognition of S/U acoustic targets based on channel information besides source spectrum information. By using the combination of two hydrophones, the surface and underwater targets recognition accuracy reached 1 and 0.9384, while they are only 0.4715 and 0.5620 using a single hydrophone, respectively.
The asymmetrical distribution of auxin supports high intensity blue light (HBL)-mediated phototropism. Flavonoids, secondary metabolites induced by blue light and TRANSPARENT TESTA GLABRA1 (TTG1), alter auxin transport. However, the role of TTG1 in HBL-induced phototropism in Arabidopsis (Arabidopsis thaliana) remains unclear. We found that TTG1 regulates HBL-mediated phototropism. HBL-induced degradation of CRYPTOCHROME 1 (CRY1) was repressed in ttg1-1, and depletion of CRY1 rescued the phototropic defects of the ttg1-1 mutant. Moreover, overexpression of CRY1 in a cry1 mutant background led to phototropic defects in response to HBL. These results indicated that CRY1 is involved in the regulation of TTG1-mediated phototropism in response to HBL. Further investigation showed that TTG1 physically interacts with CRY1 via its N-terminus and that the added TTG1 promotes the dimerization of CRY1. The interaction between TTG1 and CRY1 may promote HBL-mediated degradation of CRY1. TTG1 also physically interacted with blue light inhibitor of cryptochrome 1 (BIC1) and Light-Response Bric-a-Brack/Tramtrack/Broad 2 (LRB2), and these interactions either inhibited or promoted their interaction with CRY1. Exogenous gibberellins (GA) and auxins, two key plant hormones that crosstalk with CRY1, may confer the recovery of phototropic defects in the ttg1-1 mutant and CRY1-overexpressing plants. Our results revealed that TTG1 participates in the regulation of HBL-induced phototropism by modulating CRY1 levels, which are coordinated with GA or IAA signaling.
This study aimed to improve the eating quality of yellow-feathered broiler chicks by feeding them corn-soybean meal diets supplemented with 250, 500, and 1,000 mg/kg quercetin. we examined the impact of varying doses of dietary quercetin on the sensory quality of chicken breast meat as well as on the antioxidant enzymes, antioxidant-related signaling molecules, structure and thermal stability of myofibrillar protein (MPs), and microstructure of myogenic fibers in the meat during 24 h of postslaughter aging. Additionally, we investigated the potential correlations among antioxidant capacity, MP structure, and meat quality parameters. The results indicated that dietary supplementations with 500 and 1,000 mg/kg quercetin improved the physicochemical properties and eating quality of yellow-feathered broiler chicken breast meat during 12 to 24 h postslaughter. Additionally, quercetin improved the postslaughter oxidative stress status and reduced protein and lipid oxidation levels. It also increased hydrogen bonding interactions and α-helix content during 6 to 12 h postslaughter and decreased ß-sheet content during 12 to 24 h postslaughter in chicken breast MP. This resulted in improved postslaughter MP structure and thermal stability. The correlation results indicated that the enhancement of antioxidant capacity and MP structure enhanced the physicochemical and edible qualities of yellow-feathered broiler chicken breast meat. In conclusion, the current findings suggest that dietary supplementation with quercetin is an ideal approach for improving the eating quality of chicken meat, thereby broadening our understanding of theoretical and technological applications for improving the quality of chicken.
BACKGROUND: We aimed to investigate the associations of diabetes mellitus (DM) and C-reactive protein (CRP) with biological ageing acceleration and mortality risk. METHODS: We analyzed data from 41,634 adults with CRP and DM at baseline. Subjects were categorized into high CRP (>3 mg/L) and low CRP (≤3 mg/L) groups. The cross-sectional endpoints of the study were biological ageing indicators Klemera-Doubal method BioAge acceleration (KDMAccel) and Phenotypic age acceleration (PhenoAgeAccel), and the follow-up endpoints were all-cause mortality and cardiovascular mortality. RESULTS: In adults with high CRP, compared with those without DM, PhenoAgeAccel increased by 1.66 years (95 % CI: 1.38-1.93), and 8.74 years (95 % CI: 8.25-9.22) in adults with prediabetes and DM, respectively (p for interaction <0.001). Using the CRPlow/non-DM group as a reference, adults in the CRPhigh/non-DM, CRPlow/DM, and CRPhigh/DM groups had significantly advanced biological ageing. Compared to adults without DM, low CRP, and no ageing acceleration, the multivariable-adjusted HRs (95%CIs) of all-cause and cardiovascular mortality in those with DM, CRP, and ageing acceleration were 3.22 (2.79-3.72), and 3.57 (2.81-4.54), respectively. CONCLUSIONS: These findings suggest that the joint presence of low-grade inflammation and DM might be associated with higher odds of biological ageing acceleration and premature mortality.
BACKGROUND: Hepatocellular carcinoma (HCC) is plagued by failures across the cancer care continuum, leading to frequent late-stage diagnoses and high mortality. We evaluated the effectiveness of mailed outreach invitations plus patient navigation to promote HCC screening process completion in patients with cirrhosis. METHODS: Between April 2018 and September 2021, we conducted a multicentre pragmatic randomised clinical trial comparing mailed outreach plus patient navigation for HCC screening (n=1436) versus usual care with visit-based screening (n=1436) among patients with cirrhosis at three US health systems. Our primary outcome was screening process completion over a 36-month period, and our secondary outcome was the proportion of time covered (PTC) by screening. All patients were included in intention-to-screen analyses. RESULTS: All 2872 participants (median age 61.3 years; 32.3% women) were included in intention-to-screen analyses. Screening process completion was observed in 6.6% (95% CI: 5.3% to 7.9%) of patients randomised to outreach and 3.3% (95% CI: 2.4% to 4.3%) of those randomised to usual care (OR 2.05, 95% CI: 1.44 to 2.92). The intervention increased HCC screening process completion across most subgroups including age, sex, race and ethnicity, Child-Turcotte-Pugh class and health system. PTC was also significantly higher in the outreach arm than usual care (mean 37.5% vs 28.2%; RR 1.33, 95% CI: 1.31 to 1.35). Despite screening underuse, most HCC in both arms were detected at an early stage. CONCLUSION: Mailed outreach plus navigation significantly increased HCC screening process completion versus usual care in patients with cirrhosis, with a consistent effect across most examined subgroups. However, screening completion remained suboptimal in both arms, underscoring a need for more intensive interventions. TRIAL REGISTRATION NUMBER: NCT02582918.
The present study investigated the effects of different deep-frying times and temperatures on the amylose content, crystal structure, thermodynamics, and other properties of deep-fried dough sticks. Results showed that the change of amylose content in deep-fried dough sticks during the deep-frying process was positively correlated with time and temperature. Moreover, the deep-frying process of deep-fried dough sticks was accompanied by the formation of starch-lipid complexes that led to the destruction of starch structure. The degreased sample and the oil sample had the same absorption peaks at 2854 and 1746 cm-1, respectively. The melting enthalpy (ΔH) of the starch-lipid complex decreased significantly. In addition, the viscosity of starch reduced as the deep-frying time and temperature increased. Furthermore, it was found that the effect of increasing deep-frying temperature was greater than that of time. PRACTICAL APPLICATION: As a popular deep-fried food, the main component of deep-fried dough sticks is starch. Starch gelatinization, protein denaturation, and interaction among components occurred during deep-frying. At present, there are few studies focusing on the properties of starch in deep-fried dough sticks in the real deep-frying system. Therefore, this study provided a theoretical basis for subsequent research by measuring the effects of different deep-frying conditions on the properties of starch in deep-fried dough sticks.
BACKGROUND: Investigating the unexplored territory of lncRNA m6A modification in colorectal cancer (CRC) vasculature, this study focuses on LINC01106 and YTHDF1. METHODS: Clinical assessments reveal upregulated LINC01106 promoting vascular generation via the miR-449b-5p-VEGFA pathway. RESULTS: YTHDF1, elevated in CRC tissues, emerges as an adverse prognostic factor. Functional experiments showcase YTHDF1's inhibitory effects on CRC cell dynamics. Mechanistically, Me-CLIP identifies m6A-modified LINC01106, validated as a YTHDF1 target through Me-RIP. CONCLUSIONS: This study sheds light on the YTHDF1-mediated m6A modification of LINC01106, presenting it as a key player in suppressing CRC vascular generation.
Cancer is a leading cause of mortality globally, characterized by intricate molecular alterations, including epigenetic changes such as glycosylation. This study presents a comprehensive pan-cancer analysis of Polypeptide N-Acetylgalactosaminyltransferase 7 (GALNT7), an enzyme involved in mucin-type O-linked protein glycosylation. GALNT7 has previously been linked to various cancers, but a unified analysis across cancer types is lacking. Leveraging data from TCGA, GTEx, and other sources, we scrutinized GALNT7's expression, prognostic relevance, links to immune-related genes, immune cell infiltration, and its involvement in tumor genetic heterogeneity across 33 cancer types. GALNT7 exhibited diverse expression patterns across cancer types, showcasing its potential as an oncogenic factor, with its expression levels linked to both positive and negative prognoses, highlighting the context-specific nature of its role in cancer progression. We delved into the intricate interplay between GALNT7 and immune genes, unveiling positive and negative correlations, underscoring complex interactions in the tumor microenvironment. GALNT7 was found to impact immune cell infiltration, which could have implications for treatment strategies. Additionally, GALNT7 displayed associations with genetic tumor aspects, encompassing genomic instability, DNA repair issues, and genetic mutations, hinting at its pivotal role in shaping the genetic landscape of diverse cancers. Enrichment analysis uncovered potential functions of GALNT7 beyond glycosylation, such as its participation in signaling pathways and its association with various diseases, notably cancer. This comprehensive analysis elucidates the multifaceted role of GALNT7 in cancer biology, underlining its potential as a therapeutic target and biomarker across various cancer types. These findings provide valuable insights for future research and the development of personalized cancer treatment strategies.
Background: In the two common inflammatory skin diseases, Atopic Dermatitis (AD) and Psoriasis (Ps), keratinocytes (KCs) respond to immune insults through activation of proinflammatory transcription factors (TFs) and their translocation to the cell's nucleus. Therein, the TFs induce expression of genes encoding mediators of skin inflammation. The Nuclear Transport Checkpoint Inhibitors (NTCIs) were developed to regulate nuclear translocation of activated TFs, the essential step of inflammatory response. This new class of cell-penetrating peptide therapeutics controls inflammation caused by allergic, autoimmune, metabolic, and microbial insults. In preclinical model of AD, the treatment with NTCI, cSN50.1 peptide, suppressed the expression of Thymic Stromal Lymphopoietin (TSLP), the key gene in the development of allergic inflammation, among the 15 genes silenced by the NTCI. Here, we report the mechanism of anti-inflammatory action of NTCI in human skin-derived KCs. Objectives: We aimed to determine whether the NTCI treatment can protect human KCs from harmful inflammatory insults. Methods: Human primary KCs were pretreated with NTCI and challenged with the mix of cytokines Tumour Necrosis Factor alpha (TNF-α) and Interleukin (IL)-17A, or with Phorbol 12-Myristate 13-Acetate (PMA), and analysed for nuclear content of TFs and the expression of genes encoding mediators of inflammation. Results: The nuclear import of TFs, Nuclear Factor ĸB (NF-ĸB) and Signal Transduction and Activator of Transcription 3 (STAT3), was inhibited in cells treated with NTCI. The expression of TSLP, along with genes encoding the core mediators of inflammation (TNF, IL1B, and IL6) was suppressed by NTCI. Noteworthy, NTCI silenced genes encoding Granulocyte-Macrophage Colony-Stimulating Factor (CSF2), and chemokine IL-8 (CXCL8), responsible for skin infiltration by the eosinophils and other myelomonocytic cells. Conclusion: The control of inflammatory response in human KCs by NTCI is attributed to the inhibition of nuclear import of proinflammatory TFs. The protection of human KCs by NTCI, adds new perspectives to the completed Phase two clinical trial of the NTCI (AMTX-100 CF) for AD (NCT04313400).
BACKGROUND: The prevalence of multiple nosocomial infections (MNIs) is on the rise, however, there remains a limited comprehension regarding the associated risk factors, cumulative risk, probability of occurrence, and impact on length of stay (LOS). METHOD: This multicenter study includes all hospitalized patients from 2020 to July 2023 in two sub-hospitals of a tertiary hospital in Guangming District, Shenzhen. The semi-Markov multi-state model (MSM) was utilized to analyze risk factors and cumulative risk of MNI, predict its occurrence probability, and calculate the extra LOS of nosocomial infection (NI). RESULTS: The risk factors for MNI include age, community infection at admission, surgery, and combined use of antibiotics. However, the cumulative risk of MNI is lower than that of single nosocomial infection (SNI). MNI is most likely to occur within 14 days after admission. Additionally, SNI prolongs LOS by an average of 7.48 days (95% Confidence Interval, CI: 6.06-8.68 days), while MNI prolongs LOS by an average of 15.94 days (95% CI: 14.03-18.17 days). Furthermore, the more sites of infection there are, the longer the extra LOS will be. CONCLUSION: The longer LOS and increased treatment difficulty of MNI result in a heavier disease burden for patients, necessitating targeted prevention and control measures.
Cross Infection , Length of Stay , Humans , Cross Infection/epidemiology , Length of Stay/statistics & numerical data , Risk Factors , Male , Female , Middle Aged , China/epidemiology , Aged , Adult , Prevalence , Tertiary Care Centers , Anti-Bacterial Agents/therapeutic use
Crafting an inorganic semiconductor heterojunction with defect engineering and morphology modulation is a strategic approach to produce clean energy by the highly efficient light-driven splitting of water. In this paper, a novel Z-scheme sulfur-vacancy containing Zn3In2S6 (Vs-Zn3In2S6) nanosheets/In2O3 hollow hexagonal prisms heterostructrue (Vs-ZIS6INO) was firstly constructed by an oil bath method, in which Vs-Zn3In2S6 nanosheets grew on the surfaces of In2O3 hollow hexagonal prisms to form a hollow core-shell structure. The obtained Vs-ZIS6INO heterostructrue exhibited much enhanced activity of the production of H2 and H2O2 by the light-driven water splitting. In particular, under visible light irradiation (λ > 420 nm), the rate of generation of H2 of Vs-ZIS6INO sample containing 30 wt% Vs-Zn3In2S6 (30Vs-ZIS6INO) could reach 3721 µmol g-1h-1, which was 87 and 6 times higher than those of Zn3In2S6 (43 µmol g-1h-1) and Vs-Zn3In2S6 (586 µmol g-1h-1), respectively. Meanwhile, 30Vs-ZIS6INO could exhibit the rate of H2O2 production of 483 µmol g-1h-1 through the dual pathways of indirect 2e- oxygen reduction (ORR) and water oxidation (WOR) without adding any sacrifice agents, far exceeding In2O3 (7 µmol g-1h-1) and Vs-Zn3In2S6 (58 µmol g-1h-1). The excellent photocatalytic activities of H2 and H2O2 generations of Vs-ZIS6INO sample might result from the synergistic effect of the sulfur vacancy, hollow core-shell structure, and Z-scheme heterostructure, which accelerated the electron delocalization, enhanced the absorption and conversion of solar energy, reduced the carrier diffusion distance, and ensured high REDOX ability. In addition, the possible photocatalytic mechanisms for the production of H2 and H2O2 were discussed in detail. This study provided a new idea and reference for constructing the novel and efficient inorganic semiconductor heterostructures by coordinating vacancy defect and morphology design to adequately utilize water splitting for the production of clean energy.
