Dendrite initiation and propagation in lithium metal solid-state batteries.

All-solid-state batteries with a Li anode and ceramic electrolyte have the potential to deliver a step change in performance compared with today's Li-ion batteries1,2. However, Li dendrites (filaments) form on charging at practical rates and penetrate the ceramic electrolyte, leading to short circuit and cell failure3,4. Previous models of dendrite penetration have generally focused on a single process for dendrite initiation and propagation, with Li driving the crack at its tip5-9. Here we show that initiation and propagation are separate processes. Initiation arises from Li deposition into subsurface pores, by means of microcracks that connect the pores to the surface. Once filled, further charging builds pressure in the pores owing to the slow extrusion of Li (viscoplastic flow) back to the surface, leading to cracking. By contrast, dendrite propagation occurs by wedge opening, with Li driving the dry crack from the rear, not the tip. Whereas initiation is determined by the local (microscopic) fracture strength at the grain boundaries, the pore size, pore population density and current density, propagation depends on the (macroscopic) fracture toughness of the ceramic, the length of the Li dendrite (filament) that partially occupies the dry crack, current density, stack pressure and the charge capacity accessed during each cycle. Lower stack pressures suppress propagation, markedly extending the number of cycles before short circuit in cells in which dendrites have initiated.

A prophage encoded ribosomal RNA methyltransferase regulates the virulence of Shiga-toxin-producing Escherichia coli (STEC).

Shiga toxin (Stx) released by Shiga toxin producing Escherichia coli (STEC) causes life-threatening illness. Its production and release require induction of Stx-encoding prophage resident within the STEC genome. We identified two different STEC strains, PA2 and PA8, bearing Stx-encoding prophage whose sequences primarily differ by the position of an IS629 insertion element, yet differ in their abilities to kill eukaryotic cells and whose prophages differ in their spontaneous induction frequencies. The IS629 element in ϕPA2, disrupts an ORF predicted to encode a DNA adenine methyltransferase, whereas in ϕPA8, this element lies in an intergenic region. Introducing a plasmid expressing the methyltransferase gene product into ϕPA2 bearing-strains increases both the prophage spontaneous induction frequency and virulence to those exhibited by ϕPA8 bearing-strains. However, a plasmid bearing mutations predicted to disrupt the putative active site of the methyltransferase does not complement either of these defects. When complexed with a second protein, the methyltransferase holoenzyme preferentially uses 16S rRNA as a substrate. The second subunit is responsible for directing the preferential methylation of rRNA. Together these findings reveal a previously unrecognized role for rRNA methylation in regulating induction of Stx-encoding prophage.

FgSnt1 of the Set3 HDAC complex plays a key role in mediating the regulation of histone acetylation by the cAMP-PKA pathway in Fusarium graminearum.

The cAMP-PKA pathway is critical for regulating growth, differentiation, and pathogenesis in fungal pathogens. In Fusarium graminearum, mutants deleted of PKR regulatory-subunit of PKA had severe defects but often produced spontaneous suppressors. In this study eleven pkr suppressors were found to have mutations in FgSNT1, a component of the Set3C histone deacetylase (HDAC) complex, that result in the truncation of its C-terminal region. Targeted deletion of the C-terminal 98 aa (CT98) in FgSNT1 suppressed the defects of pkr in growth and H4 acetylation. CT98 truncation also increased the interaction of FgSnt1 with Hdf1, a major HDAC in the Set3 complex. The pkr mutant had no detectable expression of the Cpk1 catalytic subunit and PKA activities, which was not suppressed by mutations in FgSNT1. Cpk1 directly interacted with the N-terminal region of FgSnt1 and phosphorylated it at S443, a conserved PKA-phosphorylation site. CT98 of FgSnt1 carrying the S443D mutation interacted with its own N-terminal region. Expression of FgSNT1S443D rescued the defects of pkr in growth and H4 acetylation. Therefore, phosphorylation at S443 and suppressor mutations may relieve self-inhibitory binding of FgSnt1 and increase its interaction with Hdf1 and H4 acetylation, indicating a key role of FgSnt1 in crosstalk between cAMP signaling and Set3 complex.

Cardiac injury in hospitalized patients with severe fever and thrombocytopenia syndrome.

Severe fever with thrombocytopenia syndrome (SFTS), an emerging infectious disease with a high fatality rate. Cardiac injury in SFTS patients is a major concern. This study aimed to evaluate the prevalence of cardiac injury and its association with mortality in hospitalized patients infected with novel Bunyavirus. Cardiac injury was defined as the presence of any of the following abnormalities: (1) blood levels of cardiac biomarkers (creatine kinase-MB, troponin-I, B-type natriuretic peptide or N-terminal pro-B-type natriuretic peptide); (2) new abnormalities in electrocardiography. The 203 SFTS patients were included in the final analysis. The proportion of SFTS patients developing cardiac injury during hospitalization was 71.4% (145/203). Compared with the uninjured group, the cardiac injury group had the severity of cardiac injury was underscored by higher median hospital costs (31420 vs. 12911, p < 0.001), higher proportion of intensive care units admissions (13.1% vs. 3.4%, p = 0.041), and higher hospital mortality rate (33.8% vs. 6.9%, p < 0.001). Multivariable-adjusted Cox proportional hazards regression analysis showed that cardiac injury was associated with higher mortality during hospitalization (hazards ratio, 7.349; 95% CI: 2.352-22.960). Cardiac injury is common among hospitalized SFTS patients, and it is associated with higher risk of mortality.

Neurophysiological features of STN LFP underlying sleep fragmentation in Parkinson's disease.

BACKGROUND: Sleep fragmentation is a persistent problem throughout the course of Parkinson's disease (PD). However, the related neurophysiological patterns and the underlying mechanisms remained unclear. METHOD: We recorded subthalamic nucleus (STN) local field potentials (LFPs) using deep brain stimulation (DBS) with real-time wireless recording capacity from 13 patients with PD undergoing a one-night polysomnography recording, 1 month after DBS surgery before initial programming and when the patients were off-medication. The STN LFP features that characterised different sleep stages, correlated with arousal and sleep fragmentation index, and preceded stage transitions during N2 and REM sleep were analysed. RESULTS: Both beta and low gamma oscillations in non-rapid eye movement (NREM) sleep increased with the severity of sleep disturbance (arousal index (ArI)-betaNREM: r=0.9, p=0.0001, sleep fragmentation index (SFI)-betaNREM: r=0.6, p=0.0301; SFI-gammaNREM: r=0.6, p=0.0324). We next examined the low-to-high power ratio (LHPR), which was the power ratio of theta oscillations to beta and low gamma oscillations, and found it to be an indicator of sleep fragmentation (ArI-LHPRNREM: r=-0.8, p=0.0053; ArI-LHPRREM: r=-0.6, p=0.0373; SFI-LHPRNREM: r=-0.7, p=0.0204; SFI-LHPRREM: r=-0.6, p=0.0428). In addition, long beta bursts (>0.25 s) during NREM stage 2 were found preceding the completion of transition to stages with more cortical activities (towards Wake/N1/REM compared with towards N3 (p<0.01)) and negatively correlated with STN spindles, which were detected in STN LFPs with peak frequency distinguishable from long beta bursts (STN spindle: 11.5 Hz, STN long beta bursts: 23.8 Hz), in occupation during NREM sleep (ß=-0.24, p<0.001). CONCLUSION: Features of STN LFPs help explain neurophysiological mechanisms underlying sleep fragmentations in PD, which can inform new intervention for sleep dysfunction. TRIAL REGISTRATION NUMBER: NCT02937727.

The impacts of venous outflow profiles on outcomes among large vessel occlusion patients receiving endovascular treatment in the late window.

OBJECTIVES: To investigate the association between venous outflow (VO) profiles and outcomes among acute ischemic stroke caused by anterior circulation large vessel occlusion (AIS-LVO) patients who had undergone endovascular treatment (EVT) in the late window of 6-24 h from stroke onset. METHODS: This was a post-hoc analysis of our preceding RESCUE-BT trial, with findings validated in an external cohort. Baseline computed tomographic angiography (CTA) was performed to assess VO using the Cortical Vein Opacification Score (COVES). The primary clinical outcome was functional independence at 90 days (modified Rankin Scale score of 0-2). The adjusted odd ratio (aOR) and confidence interval (CI) were obtained from multivariable logistic regressions. RESULTS: A total of 440 patients were included in the present study. After identifying the cutoff of COVES by marginal effects approach, enrolled patients were divided into the favorable VO group (COVES 4-6) and the poor VO (COVES 0-3) group. Multivariable logistic regression analysis showed that favorable VO (aOR 2.25; 95% CI 1.31-3.86; p = 0.003) was associated with functional independence. Similar results were detected in the external validation cohort. Among those with poor arterial collateralization, favorable VO was still an independent predictor of functional independence (aOR 2.09; 95% CI 1.06-4.10; p = 0.032). CONCLUSION: The robust VO profile indicated by COVES 4-6 could promote the frequency of functional independence among AIS-LVO patients receiving EVT in the late window, and the prognostic value of VO was independent of the arterial collateral status. CLINICAL RELEVANCE STATEMENT: The robust venous outflow profile was a valid predictor for functional independence among AIS-LVO patients receiving EVT in the late window (6-24 h) and the predictive role of venous outflow did not rely on the status of arterial collateral circulation.

Macrophages promote the transition from myocardial ischemia reperfusion injury to cardiac fibrosis in mice through GMCSF/CCL2/CCR2 and phenotype switching.

Following acute myocardial ischemia reperfusion (MIR), macrophages infiltrate damaged cardiac tissue and alter their polarization phenotype to respond to acute inflammation and chronic fibrotic remodeling. In this study we investigated the role of macrophages in post-ischemic myocardial fibrosis and explored therapeutic targets for myocardial fibrosis. Male mice were subjected to ligation of the left coronary artery for 30 min. We first detected the levels of chemokines in heart tissue that recruited immune cells infiltrating into the heart, and found that granulocyte-macrophage colony-stimulating factor (GMCSF) released by mouse cardiac microvascular endothelial cells (MCMECs) peaked at 6 h after reperfusion, and c-c motif chemokine ligand 2 (CCL2) released by GMCSF-induced macrophages peaked at 24 h after reperfusion. In co-culture of BMDMs with MCMECs, we demonstrated that GMCSF derived from MCMECs stimulated the release of CCL2 by BMDMs and effectively promoted the migration of BMDMs. We also confirmed that GMCSF promoted M1 polarization of macrophages in vitro, while GMCSF neutralizing antibodies (NTABs) blocked CCL2/CCR2 signaling. In MIR mouse heart, we showed that GMCSF activated CCL2/CCR2 signaling to promote NLRP3/caspase-1/IL-1ß-mediated and amplified inflammatory damage. Knockdown of CC chemokine receptor 2 gene (CCR2-/-), or administration of specific CCR2 inhibitor RS102895 (5 mg/kg per 12 h, i.p., one day before MIR and continuously until the end of the experiment) effectively reduced the area of myocardial infarction, and down-regulated inflammatory mediators and NLRP3/Caspase-1/IL-1ß signaling. Mass cytometry confirmed that M2 macrophages played an important role during fibrosis, while macrophage-depleted mice exhibited significantly reduced transforming growth factor-ß (Tgf-ß) levels in heart tissue after MIR. In co-culture of macrophages with fibroblasts, treatment with recombinant mouse CCL2 stimulated macrophages to release a large amount of Tgf-ß, and promoted the release of Col1α1 by fibroblasts. This effect was diminished in BMDMs from CCR2-/- mice. After knocking out or inhibiting CCR2-gene, the levels of Tgf-ß were significantly reduced, as was the level of myocardial fibrosis, and cardiac function was protected. This study confirms that the acute injury to chronic fibrosis transition after MIR in mice is mediated by GMCSF/CCL2/CCR2 signaling in macrophages through NLRP3 inflammatory cascade and the phenotype switching.

Validity of the Chinese version of the weekly calendar planning activity (WCPA) on assessing executive function in adults with stroke.

The weekly calendar planning activity (WCPA) is a performance-based assessment of executive function (EF) via a cognitively-based instrumental activity of daily life (C-IADL). This study aimed to examine the validity of the Chinese version of the WCPA in adults with stroke and to explore the characteristics of cognitive strategy use among the population. Fifty-eight hospitalized patients with stroke aged 26-82 years and 53 controls completed the WCPA, two neuropsychological tests and instrumental activity of daily life (IADL) scale. Participants with stroke were subdivided into a stroke cognitive impaired group (Stroke-CI) and a general stroke group (Stroke-NCI) based on the Montreal Cognitive Assessment. Results showed that the WCPA was able to discriminate between Stroke-CI with controls and the Stroke-NCI group with controls. We found significant limitations in stroke patients' ability to use strategies. Concurrent and ecological validities were demonstrated through correlations between the neuropsychological test scores, IADL and the WCPA performance. This study provides initial evidence for the validity of the Chinese version of the WCPA-10 for adults with stroke and suggests the need to use performance-based tests even in patients with normal cognitive screening test results. The WCPA could provide useful information for strategy-based interventions for adults with stroke.

Single-Stranded RNA Origami-Based Epigenetic Immunomodulation.

The integration of functional modules at the molecular level into RNA nanostructures holds great potential for expanding their applications. However, the quantitative integration of nucleoside analogue molecules into RNA nanostructures and their impact on the structure and function of RNA nanostructures remain largely unexplored. Here, we report a transcription-based approach to controllably integrate multiple nucleoside analogues into a 2000 nucleotide (nt) single-stranded RNA (ssRNA) origami nanostructure. The resulting integrated ssRNA origami preserves the morphology and biostability of the original ssRNA origami. Moreover, the integration of nucleoside analogues introduced new biomedical functions to ssRNA origamis, including innate immune recognition and regulation after the precise integration of epigenetic nucleoside analogues and synergistic effects on tumor cell killing after integration of therapeutic nucleoside analogues. This study provides a promising approach for the quantitative integration of functional nucleoside analogues into RNA nanostructures at the molecular level, thereby offering valuable insights for the development of multifunctional ssRNA origamis.

Kinase Inhibitors and Kinase-Targeted Cancer Therapies: Recent Advances and Future Perspectives.

Over 120 small-molecule kinase inhibitors (SMKIs) have been approved worldwide for treating various diseases, with nearly 70 FDA approvals specifically for cancer treatment, focusing on targets like the epidermal growth factor receptor (EGFR) family. Kinase-targeted strategies encompass monoclonal antibodies and their derivatives, such as nanobodies and peptides, along with innovative approaches like the use of kinase degraders and protein kinase interaction inhibitors, which have recently demonstrated clinical progress and potential in overcoming resistance. Nevertheless, kinase-targeted strategies encounter significant hurdles, including drug resistance, which greatly impacts the clinical benefits for cancer patients, as well as concerning toxicity when combined with immunotherapy, which restricts the full utilization of current treatment modalities. Despite these challenges, the development of kinase inhibitors remains highly promising. The extensively studied tyrosine kinase family has 70% of its targets in various stages of development, while 30% of the kinase family remains inadequately explored. Computational technologies play a vital role in accelerating the development of novel kinase inhibitors and repurposing existing drugs. Recent FDA-approved SMKIs underscore the importance of blood-brain barrier permeability for long-term patient benefits. This review provides a comprehensive summary of recent FDA-approved SMKIs based on their mechanisms of action and targets. We summarize the latest developments in potential new targets and explore emerging kinase inhibition strategies from a clinical perspective. Lastly, we outline current obstacles and future prospects in kinase inhibition.

Comprehensive analysis of the exosomal circRNA-miRNA-mRNA network in breast cancer.

BACKGROUND: Exosomal circular RNAs (circRNAs) played critical roles in tumor development and progression and might be novel biomarkers in the diagnosis and treatment of various cancers. However, the biological functions and clinical implications of exosomal circRNAs in breast cancer are unclear. METHODS: Expression profiles of exosomal circRNAs the in exoRBase 2.0 database were used to identify differentially expressed exosomal circRNAs in breast cancer. The LASSO and SVM-RFE algorithms followed by multivariate logistic regression analysis were performed to construct the diagnostic model. The target genes of circRNAs were selected by combing differential expression analysis and CSCD, TargetScan and ENCORI databases. Univariate and multivariate survival analysis were conducted to construct a survival-associated exosomal circRNA-miRNA-mRNA network. GSVA and CIBERSORT algorithms were used to evaluate the cancer hallmarks and immune cells in breast cancer and Spearman correlation analysis was used to investigate their correlations with the circRNA-miRNA-mRNA network. RESULTS: In total, 347 upregulated and three downregulated exosomal circRNAs were identified in breast cancer patients. The diagnostic model based on 14 exosomal circRNAs showed a high area under the curve (AUC) value in both the training (AUC = 0.98) and validation (AUC = 0.94) dataset. In total, 70 miRNAs and 1147 mRNAs were selected as the downstream targets of circRNAs and were revealed to participate in tumor-associated pathways, including the PI3K-AKT, MAPK, RAS and RAP1 pathways, as well as calcium signaling pathways, in addition to transcriptional misregulations. The constructed survival-associated exosomal circRNA-miRNA-mRNA network contained nine exosomal circRNAs, 12 miRNAs and 10 mRNAs, and showed complicated correlations and interactions within networks. Cancer hallmark pathways, including the TGF-ß, KRAS and MYC signaling pathways, tumor angiogenesis, epithelial-mesenchymal transition, DNA repair and G2M checkpoint, as well as immune cells, including CD4+ and CD8+ T cells, dendritic cells, mast cells, macrophage cells, memory B cells and natural killer cells, were closely correlated with the circRNA-miRNA-mRNA network. CONCLUSIONS: The present study is the first to systematically analyze the exosomal circRNAs in breast cancer. We established an exosomal circRNA diagnostic model and constructed a survival-associated exosomal circRNA-miRNA-mRNA network. Our results revealed the complicated functions and potential mechanisms of the exosomal circRNA-miRNA-mRNA network in breast cancer, which need to be validated further in future studies.

266 nm ultraviolet communication under unknown interference using UVC micro-LED.

Ultraviolet C (UVC) micro light-emitting diode (LED) can achieve symbol communication rate up to 100Msps at distance 40 meters without transmitter-side lens to guarantee certain communication mobility. We consider what we believe to be a new scenario where high speed UV communciation is realized under unknown low-rate interference. The signal amplitude properties are characterized, and the interference intensity is categorized into three cases, namely weak, medium and high interference intensity. The achievable transmission rates for the three cases are derived, where the achievable transmission rate for medium interference intensity can approach those in weak interference intensity and strong interference intensity cases. We provide Gaussian approximation and related log-likelihood ratio (LLR) calculation, which are fed into the subsequent message-passing decoder. In the experiment, the data is transmitted with symbol rate 20 Msps under unknown interference with symbol rate 1 Msps, received by one photomultiplier tube (PMT). Experimental results show that the proposed interference symbol estimation approach shows negligibly higher bit error rate (BER) compared with those with perfect knowledge on the interference symbols.

Resource-efficient channel estimation for DCO-OFDM based VLC systems.

We consider a resource-efficient pilot design for visible light communication (VLC) system employing direct-current offset orthogonal frequency division multiplexing (DCO-OFDM). Firstly, we experimentally verify that the normalized channel gain vectors remain approximately the same at different locations under a line-of-sight (LOS) path between the transmitter and the receiver. Then, under the constant normalized subcarrier gain assumption, it is proved that a single pilot subcarrier is optimal to maximize the achievable rate without signal clipping. The impact of power budget and statistical channel characteristics is investigated regarding the optimal pilot position and the related achievable rate. We extend the pilot position optimization to a general case considering the light-emitting diode (LED) and power amplifier (PA) with a limited linear dynamic range. Assuming double-sided clipping, the impact of LED upper saturation voltage and statistical channel characteristics on the optimal pilot position and the achievable rate is investigated via the Bussgang theorem. Finally, under constant normalized link gain assumption, we propose a blind channel estimation approach based on the covariance of frequency-domain outputs. The convergence of the proposed channel estimation approaches based on constant normalized link gain is verified experimentally.

Ultraviolet communication with a large scattering angle via artificial agglomerate fog.

Considering strong signal attenuation of the large-angle non-line-of-sight (NLOS) link achieved due to the ultraviolet (UV) scattering properties, we propose to increase the UV communication link gain under a large scattering angle via generating agglomerate fog within a certain range as a secondary light source. In this study, a channel model with locally strong scatterers from agglomerate fog is proposed based on Monte Carlo ray-tracing approaches. Mie theory is adopted to calculate the atmospheric channel parameters, to further evaluate the link gain of a channel under non-uniform atmosphere. The performance of scattering system in the presence of fog conditions depends on the relative positions of the light source to the fog and to the receiver. The link gain results reveal the transmission capabilities for different scattering channel geometries, and give the optimal spray point location within a 10 m communication range. We further establish a foggy NLOS system using an agglomerate fog generator to verify our research in the real environment. The results show that the received signal strength of the NLOS link can be effectively enhanced by constructing scatterers in the atmospheric channel, which significantly decreases the bit-error rate (BER).

Enhanced efficacy of combined fluzoparib and chidamide targeting in natural killer/T-cell lymphoma.

The treatment of natural killer/T-cell lymphoma (NKTCL) presents an onerous challenge, and a search for new therapeutic targets is urgently needed. Poly ADP-ribose polymerase inhibitors (PARPi) were initially used to treat breast and ovarian cancers with BRCA1/2 mutations. Their excellent antitumor efficacy led to a series of clinical trials conducted in other malignancies. However, the exploration of PARPi and their potential use in combination treatments for NKTCL remains unexplored. We treated NKTCL cell lines with fluzoparib (a novel inhibitor of PARP) and chidamide (a classical inhibitor of HDACs) to explore their cytotoxic effects in vitro. Then, their antitumor efficacy in vivo was confirmed in YT-luciferin xenograft mouse models. Fluzoparib or chidamide alone inhibited NKTCL cell proliferation in a dose-dependent manner. Cotreatment with both drugs synergistically induced excessive accumulation of DNA double-strand breaks and massive apoptotic cell death by inhibiting the DNA damage repair pathway, as shown by the decreased protein levels of p-ATM, p-BRCA1, p-ATR, and Rad51. Moreover, the combination treatment apparently increased the level of intracellular reactive oxygen species (ROS) to enhance apoptosis, and pretreatment with an ROS scavenger reduced the proapoptotic effect by 30-60% in NKTCL cell lines. In vivo, this combined regimen also showed synergistic antitumor effects in xenograft mouse models. The combination of fluzoparib and chidamide showed synergistic effects against NKTCL both in vitro and in vivo and deserves further exploration in clinical trials.

Absence of fluctuation and inverted circadian rhythm of blood pressure increase the risk of cognitive dysfunction in cerebral small vessel disease patients.

BACKGROUND AND PURPOSE: Cerebral small vessel disease (CSVD) is a common cause of stroke and senile vascular cognitive impairment, imposing a heavy burden on public health care systems worldwide. Hypertension and 24-hour blood pressure variability (BPV), known to be significant risk factors for cognitive dysfunction, have been found to be associated with cognitive function in CSVD patients in previous studies. However, as a derived part of BPV, there are few studies on the relationship between circadian rhythm of blood pressure and cognitive dysfunction in CSVD patients, and the relationship between them is still unclear. Thus, this study aimed to investigate whether the disturbance of circadian rhythm of blood pressure can affect the cognitive function of patients with CSVD. METHODS: A total of 383 CSVD patients hospitalized in the Geriatrics Department of the Lianyungang Second People's Hospital between May 2018 and June 2022 were enrolled in this study. The clinical information and parameters of 24-hour ambulatory blood pressure monitoring were compared between the cognitive dysfunction group (n = 224) and the normal group (n = 159). Finally, a binary logistic regression model was used to assess the relationship between circadian rhythm of blood pressure and cognitive dysfunction in patients with CSVD. RESULTS: (1) Patients in the cognitive dysfunction group were older, had lower blood pressure on admission, and had a greater number of previous cardiovascular and cerebrovascular diseases (P < 0.05). (2) More patients in the cognitive dysfunction group had circadian rhythm abnormalities in blood pressure, especially the non-dipper and reverse-dipper types (P < 0.001). (3) In the elderly, there was a statistical difference in the circadian rhythm of blood pressure between the cognitive dysfunction group and the normal group, but this phenomenon did not exist in the middle-aged. (4) Binary logistic regression analysis showed that after adjusting for confounding factors, the risk of cognitive dysfunction in CSVD patients with non-dipper type was 4.052 times higher than that of dipper type (95% CI, 1.782-9.211; P = 0.001), and reverse-dipper type was 8.002 times higher than those with dipper type (95% CI, 3.367-19.017; P<0.001). CONCLUSIONS: The disturbance of circadian rhythm of blood pressure may affect the cognitive function of patients with CSVD, and the risk of cognitive dysfunction in non-dipper and reverse-dipper types are higher.

ACCI could be a poor prognostic indicator for the in-hospital mortality of patients with SFTS.

This study aims to evaluate the predictive role of age-adjusted Charlson comorbidity index (ACCI) scores for in-hospital prognosis of severe fever in thrombocytopenia syndrome (SFTS) patients. A total of 192 patients diagnosed with SFTS were selected as the study subjects. Clinical data were retrospectively collected. Receiver operating characteristic curves were used to evaluate the diagnostic value of ACCI for the mortality of SFTS patients, and Cox regression models were used to assess the association between predictive factors and prognosis. The 192 SFTS patients were divided into two groups according to the clinical endpoints (survivors/non-survivors). The results showed that the mortality of the 192 hospitalized SFTS patients was 26.6%. The ACCI score of the survivor group was significantly lower than that of the non-survivor group. Multivariate Cox regression analysis showed that the increased ACCI score was a significant predictor of poor prognosis in SFTS. Kaplan-Meier survival analysis showed that SFTS patients with an ACCI >2.5 had shorter mean survival times, indicating a poor prognosis. Our findings suggest that ACCI, as an easy-to-use clinical indicator, may offer a simple and feasible approach for clinicians to determine the severity of SFTS.

Collimating illumination of a refractive lens using an annularly stitched surface for extended LED sources.

We report a design method based on an annularly stitched aspherical surface for highly collimated optical systems with extended light sources. The annularly stitched aspherical surface is constructed as a circular central zone and one or more annular zones, which are rotationally symmetric and provide flexibility to satisfy the requirements of a practical design. An extended LED light source can be considered, and a backward ray-tracing process is used to construct the initial lens model. The specific optimization has been added step by step to modify the stitched surface to redistribute the light rays emitted from the extended source. The smoothness of the stitched surface is considered in the design and optimization process to guarantee the processability of the system. A prototype has been fabricated and tested, which demonstrates the validity of this method.

Effects of underwater swing nodes on water-to-air visible light communication.

In water-to-air visible light communication (W2A-VLC), the dynamics of underwater nodes and a wavy water surface should not be neglected. This paper investigates the link performance by combining the dynamic effects of an underwater light-emitting diode (LED) transmitter with a wavy water surface. Monte Carlo simulation is first adopted to evaluate the underwater LED dynamics. Experimental tests are then conducted to measure and analyze the influence of underwater dynamic parameters on link performance, which shows results consistent with theoretical prediction. It is demonstrated that the swing angle dominates the stability and reliability of the W2A-VLC link under a dynamic water surface, providing some insight into the design of underwater optical transmitters.

Mitochondrial dynamics-related genes DRP1 and OPA1 contributes to early diagnosis of cognitive impairment in diabetes.

BACKGROUND AND AIM: DRP1 and OPA1 play important roles in mitochondrial fusion and fission. However, the role of DRP1 and OPA1 amplification in mitochondrial cognitive impairment has not been reported. This study aimed to investigate the relationship between DRP1 and OPA1 and the risk of cognitive impairment. METHODS: In this study, 45 elderly patients with diabetes admitted to the Lianyungang Second People's Hospital from September 2020 to January 2021 were included. The patients were divided into normal group, mild cognitive impairment group and dementia group by using MMSE score, and the clinical characteristics of the three groups were compared. The amplification multiples of the two genes' DNA were calculated by ΔΔCT and defined as 2- K. Spearman rank correlation was used to analyze the correlation between the DNA amplification multiples of patients' DRP1 and OPA1 and AD8 and MoCA scores. The sensitivity and specificity of DNA amplification multiples of DRP1 and OPA1 to predict clinical outcomes of diabetic cognitive impairment were evaluated using Receiver operator characteristic (ROC) curves. Multiple logistic regression was used to evaluate the relationship between DNA amplification factor of DRP1 and OPA1 and cognitive function. RESULTS: DRP1(2- K) and OPA1(2- K) significantly increased and decreased in dementia and MCI groups compared with the normal group (P ≤ 0.001). The DNA amplification factor of DRP1 was positively correlated with AD8 score and negatively correlated with MoCA score (P < 0.001). The DNA amplification factor of OPA1 was positively correlated with the MoCA score (P = 0.0002). Analysis of ROCs showed that the DNA amplification factor of OPA1 had a higher predictive value for dementia (P < 0.0001), and that it had a higher predictive value when used in combination with DRP1. Multiple logistic regression results showed that increased DNA amplification in DRP1 was associated with increased risk of dementia (OR 1.149;95%CI,1.035-1.275), and increased DNA amplification in OPA1 was associated with decreased risk of MCI (OR 0.004;95%CI,0.000-0.251) and dementia (OR 0.000;95%CI,0.000-0.134). CONCLUSION: DNA amplification multiples of DRP1 and OPA1 are associated with the risk of dementia in elderly patients and may serve as potential biomarkers.