Dominant-negative chaperonin mutation ptCPN60α1S57F uncovers redundancy in chloroplast rRNA processing.

The biogenesis of functional forms of chloroplast ribosomal RNAs (rRNAs) is crucial for the translation of chloroplast mRNAs into polypeptides. However, the molecular mechanisms underlying the proper processing and maturation of chloroplast rRNA species are poorly understood. Through a genetic approach, we isolated and characterized an Arabidopsis mutant, α1-4, harboring a missense mutation in the plastid chaperonin-60α1 gene. Using allelism tests and transgenic manipulation, we determined functional redundancy among ptCPN60 subunits. The ptCPN60α1S57F mutation caused specific defects in the formation of chloroplast rRNA species, including 23S, 5S, and 4.5S rRNAs, but not 16S rRNAs. Allelism tests suggested that the dysfunctional ptCPN60α1S57F competes with other members of the ptCPN60 family. Indeed, overexpression of the ptCPN60α1S57F protein in wild-type plants mimicked the phenotypes observed in the α1-4 mutant, while increasing the endogenous transcriptional levels of ptCPN60α2, ß1, ß2, and ß3 in the α1-4 mutant partially mitigated the abnormal fragmentation processing of chloroplast 23S, 5S, and 4.5S rRNAs. Furthermore, we demonstrated functional redundancy between ptCPN60ß1 and ptCPN60ß2 in chloroplast rRNA processing through double-mutant analysis. Collectively, our data reveal a novel physiological role of ptCPN60 subunits in generating the functional rRNA species of the large 50S ribosomal subunit in Arabidopsis chloroplasts.

Preventing periprosthetic osteolysis in aging populations through lymphatic activation and stem cell-associated secretory phenotype inhibition.

With increases in life expectancy, the number of patients requiring joint replacement therapy and experiencing periprosthetic osteolysis, the most common complication leading to implant failure, is growing or underestimated. In this study, we found that osteolysis progression and osteoclast differentiation in the surface of the skull bone of adult mice were accompanied by significant expansion of lymphatic vessels within bones. Using recombinant VEGF-C protein to activate VEGFR3 and promote proliferation of lymphatic vessels in bone, we counteracted excessive differentiation of osteoclasts and osteolysis caused by titanium alloy particles or inflammatory cytokines LPS/TNF-α. However, this effect was not observed in aged mice because adipogenically differentiated mesenchymal stem cells (MSCs) inhibited the response of lymphatic endothelial cells to agonist proteins. The addition of the JAK inhibitor ruxolitinib restored the response of lymphatic vessels to external stimuli in aged mice to protect against osteolysis progression. These findings suggest that inhibiting SASP secretion by adipogenically differentiated MSCs while activating lymphatic vessels in bone offers a new method to prevent periprosthetic osteolysis during joint replacement follow-up.

A practical nomogram for preoperatively predicting lateral cervical lymph node metastasis in medullary thyroid carcinoma: a dual-center retrospective study.

Purpose: Lateral lymph node metastasis (LLNM) is very common in medullary thyroid carcinoma (MTC), but there is still controversy about how to manage cervical lateral lymph nodes, especially for clinically negative MTC. The aim of this study is to develop and validate a nomogram for predicting LLNM risk in MTC. Materials and methods: A total of 234 patients from two hospitals were retrospectively enrolled in this study and divided into LLNM positive group and LLNM negative group based on the pathology. The correlation between LLNM and preoperative clinical and ultrasound variables were evaluated by univariable and multivariable logistic regression analysis. A nomogram was generated to predict the risk of the LLNM of MTC patients, validated by external dataset, and evaluated in terms of discrimination, calibration, and clinical usefulness. Results: The training, internal, and external validation datasets included 152, 51, and 31 MTC patients, respectively. According to the multivariable logistic regression analysis, gender (male), relationship to thyroid capsule and serum calcitonin were independently associated with LLNM in the training dataset. The predictive nomogram model developed with the aforementioned variables showed favorable performance in estimating risk of LLNM, with the area under the ROC curve (AUC) of 0.826 in the training dataset, 0.816 in the internal validation dataset, and 0.846 in the external validation dataset. Conclusion: We developed and validated a model named MTC nomogram, utilizing available preoperative variables to predict the probability of LLNM in patients with MTC. This nomogram will be of great value for guiding the clinical diagnosis and treatment process of MTC patients.

Topologically Localized Vibronic Excitations in Second-Layer Graphene Nanoribbons.

It is of fundamental importance to characterize the intrinsic properties, like the topological end states, in the on-surface synthesized graphene nanoribbons (GNRs), but the strong electronic interaction with the metal substrate usually smears out their characteristic features. Here, we report our approach to investigate the vibronic excitations of the topological end states in self-decoupled second-layer GNRs, which are grown using an on-surface squeezing-induced spillover strategy. The vibronic progressions show highly spatially localized distributions at the second-layer GNR ends, which can be ascribed to the decoupling-extended lifetime of charging through resonant electron tunneling at the topological end states. In combination with theoretical calculations, we assign the vibronic progressions to specific vibrational modes that mediate the vibronic excitations. The spatial distribution of each resolved excitation shows evident characteristics beyond the conventional Franck-Condon picture. Our work by direct growth of second-layer GNRs provides an effective way to explore the interplay between the intrinsic electronic, vibrational, and topological properties.

Femoral artery and vein injuries in a child due to firecracker explosion: a case report.

Background: Traumatic vascular injuries in the pediatric patient population are uncommon, especially firecracker blast injuries. Extremities are more frequently affected. Vascular lesions in children have unique characteristics compared to adults, including small vessel diameters, continued growth and development, and susceptibility to vasospasm. There are no clear guidelines for vascular repair and postoperative drug therapy. This may present some challenges during treatment. The study's purpose is to retrospectively analyze a case of femoral artery and vein injuries in a child due to firecracker explosion, and to summarize the characteristics of femoral artery and vein rupture in children and the diagnostic and therapeutic experience. Case Description: We reported a 9-year-old boy with a firecracker injury to the perineum resulting in a left femoral artery and femoral vein rupture. In particular, the wound from firecracker explosion is located at the point of body projection of the spermatic cord, rather than the femoral artery and femoral vein. Emergency compression of the wound to stop bleeding provided an opportunity for subsequent surgical treatment. The intraoperative exploration revealed that the left femoral artery was mostly dissected along a 3-cm long section with a disfigured wall, and the left femoral vein was partially dissected with its anterior wall partially disrupted and missing. The child was subjected to left femoral artery autologous great saphenous vein interposition and left femoral vein repair with patch plasty. The patient had a successful surgery with good follow-up. Conclusions: Pediatric femoral arteriovenous injury is a rare and complex condition, often associated with critical complications, challenging surgical interventions, and a high risk of mortality and disability. The location of body wounds may contribute to delayed diagnosis of the condition, emphasizing the importance of timely physical examination for early diagnosis. Timely and accurate vascular repair is paramount for saving lives and minimizing the risk of limb amputation. Long-term postoperative follow-up is necessary to monitor the patency of the repaired vessels and promptly detect any complications.

Molecularly imprinted Photoelectrochemical sensor for Escherichia coli based on Cu:ZIF-8/KZ3TTz heterojunction.

Herein, a signal stable molecularly imprinted photoelectrochemical (MIP-PEC) sensing platform was designed to sensitively detect Escherichia coli by incorporating polythiophene film with Cu: ZIF-8/KZ3TTz heterojunction. Attributed to the formation of a staggered type II heterostructure between KZ3TTz and Cu: ZIF-8 semiconductors, the Cu: ZIF-8/KZ3TTz heterojunction exhibited stable and significant cathode PEC response. Impressively, selective MIP film was grown on the surface of Cu: ZIF-8/KZ3TTz/GCE by electro-polymerization of 2,2-Dimethyl-5-(3-thienyl)-1,3-dioxane-4,6-dione (DTDD) in the presence of E. coli. After removing E. coli, more electrons were transferred to the electrolyte solution through the imprinting cavity on the MIP film, which was eliminated by O2 in the electrolyte, causing further enhancement of the cathode PEC response. On the contrary, when the imprinted cavity was filled with E. coli, the cathodic PEC response gradually decreased due to steric hindrance effect. The sensor showed excellent linearity in the range of 101 to 108 CFU/mL with a detection limit of 4.09 CFU/mL (S/N = 3). This strategy offered a novel approach for pathogenic bacteria detection in food safety and environmental monitoring.

Self-supervised learning for improved calibrationless radial MRI with NLINV-Net.

PURPOSE: To develop a neural network architecture for improved calibrationless reconstruction of radial data when no ground truth is available for training. METHODS: NLINV-Net is a model-based neural network architecture that directly estimates images and coil sensitivities from (radial) k-space data via nonlinear inversion (NLINV). Combined with a training strategy using self-supervision via data undersampling (SSDU), it can be used for imaging problems where no ground truth reconstructions are available. We validated the method for (1) real-time cardiac imaging and (2) single-shot subspace-based quantitative T1 mapping. Furthermore, region-optimized virtual (ROVir) coils were used to suppress artifacts stemming from outside the field of view and to focus the k-space-based SSDU loss on the region of interest. NLINV-Net-based reconstructions were compared with conventional NLINV and PI-CS (parallel imaging + compressed sensing) reconstruction and the effect of the region-optimized virtual coils and the type of training loss was evaluated qualitatively. RESULTS: NLINV-Net-based reconstructions contain significantly less noise than the NLINV-based counterpart. ROVir coils effectively suppress streakings which are not suppressed by the neural networks while the ROVir-based focused loss leads to visually sharper time series for the movement of the myocardial wall in cardiac real-time imaging. For quantitative imaging, T1-maps reconstructed using NLINV-Net show similar quality as PI-CS reconstructions, but NLINV-Net does not require slice-specific tuning of the regularization parameter. CONCLUSION: NLINV-Net is a versatile tool for calibrationless imaging which can be used in challenging imaging scenarios where a ground truth is not available.

The expression of SOCS1 is regulated by promoter DNA methylation and is associated with mitochondria-mediated apoptosis of T-2 induced chondrocytes.

At present, the function of SOCS1 in Kashin-Beck disease (KBD) has not been reported. This study aims to explore the expression and mechanism of SOCS1 in KBD, and provide theoretical basis for the prevention and treatment of KBD. The expression of SOCS1 were measured by qRT-PCR and Western blot. ELISA was used to detect the content of SOCS1 in serum and synovial fluid. CCK-8 kits were selected to measure the cell viability. Methylation Specific PCR (MSP) assay is used to detect the methylation level of SOCS1 in chondrocytes. Flow cytometry was used to analyze the apoptosis rate of chondrocytes in different groups. The expression of apoptosis related proteins (caspase-3 and caspase-9) and Cytochrome c were detected using Western blot. The mitochondrial ROS, ATP and the activity of mitochondrial respiratory chain complexes were detected using commercial kits. The results showed that the expression of SOCS1 significantly increases in KBD patients and T-2 induced chondrocytes. Further research has found that the methylation levels of SOCS1 were significantly reduced in KBD patients and T-2 induced chondrocytes. Functional studies have found that SOCS1 silencing inhibited chondrocyte apoptosis and mitochondrial dysfunction. More importantly, SOCS1 regulated mitochondrial mediated chondrocyte apoptosis through the IGF-1/IGF-1R/FAK/Drp1 pathway. In conclusion, SOCS1 expression is increased and methylation levels are decreased in KBD, and is involved in regulating mitochondrial mediated apoptosis in T-2 induced chondrocytes through IGF-1/IGF-1R/FAK/Drp1 signaling. This study provides new theoretical basis for the treatment and prevention of KBD in clinical practice.

BaP/BPDE exposure causes human trophoblast cell dysfunctions and induces miscarriage by up-regulating lnc-HZ06-regulated IL1B.

Exposure to environmental BaP or its metabolite BPDE causes trophoblast cell dysfunctions to induce miscarriage (abnormal early embryo loss), which might be generally regulated by lncRNAs. IL1B, a critical inflammatory cytokine, is closely associated with adverse pregnancy outcomes. However, whether IL1B might cause dysfunctions of BaP/BPDE-exposed trophoblast cells to induce miscarriage, as well as its specific epigenetic regulatory mechanisms, is completely unexplored. In this study, we find that BPDE-DNA adducts, trophoblast cell dysfunctions, and miscarriage are closely associated. Moreover, we also identify a novel lnc-HZ06 and IL1B, both of which are highly expressed in BPDE-exposed trophoblast cells, in villous tissues of recurrent miscarriage patients, and in placental tissues of BaP-exposed mice with miscarriage. Both lnc-HZ06 and IL1B suppress trophoblast cell migration/invasion and increase apoptosis. In mechanism, lnc-HZ06 promotes STAT4-mediated IL1B mRNA transcription, enhances IL1B mRNA stability by promoting the formation of METTL3/HuR/IL1B mRNA ternary complex, and finally up-regulates IL1B expression levels. BPDE exposure promotes TBP-mediated lnc-HZ06 transcription, and thus up-regulates IL1B levels. Knockdown of either murine lnc-hz06 (which down-regulates Il1b levels) or murine Il1b could alleviate miscarriage in BaP-exposed mice. Collectively, this study not only discovers novel biological mechanisms and pathogenesis of unexplained miscarriage but also provides novel potential targets for treatment against BaP/BPDE-induced miscarriage.

Self-Supervised Learning for Improved Calibrationless Radial MRI with NLINV-Net.

PURPOSE: To develop a neural network architecture for improved calibrationless reconstruction of radial data when no ground truth is available for training. METHODS: NLINV-Net is a model-based neural network architecture that directly estimates images and coil sensitivities from (radial) k-space data via non-linear inversion (NLINV). Combined with a training strategy using self-supervision via data undersampling (SSDU), it can be used for imaging problems where no ground truth reconstructions are available. We validated the method for (1) real-time cardiac imaging and (2) single-shot subspace-based quantitative T1 mapping. Furthermore, region-optimized virtual (ROVir) coils were used to suppress artifacts stemming from outside the FoV and to focus the k-space based SSDU loss on the region of interest. NLINV-Net based reconstructions were compared with conventional NLINV and PI-CS (parallel imaging + compressed sensing) reconstruction and the effect of the region-optimized virtual coils and the type of training loss was evaluated qualitatively. RESULTS: NLINV-Net based reconstructions contain significantly less noise than the NLINV-based counterpart. ROVir coils effectively suppress streakings which are not suppressed by the neural networks while the ROVir-based focussed loss leads to visually sharper time series for the movement of the myocardial wall in cardiac real-time imaging. For quantitative imaging, T1-maps reconstructed using NLINV-Net show similar quality as PI-CS reconstructions, but NLINV-Net does not require slice-specific tuning of the regularization parameter. CONCLUSION: NLINV-Net is a versatile tool for calibrationless imaging which can be used in challenging imaging scenarios where a ground truth is not available.

Propofol improves sleep deprivation-induced sleep structural and cognitive deficits via upregulating the BMAL1 expression and suppressing microglial M1 polarization.

BACKGROUND: Sleep deprivation (SD) is a growing global health problem with many deleterious effects, such as cognitive impairment. Microglia activation-induced neuroinflammation may be an essential factor in this. Propofol has been shown to clear sleep debt after SD in rats. This study aims to evaluate the effects of propofol-induced sleep on ameliorating sleep quality impairment and cognitive decline after 48 h SD. METHODS: Almost 8-12-week-old rats were placed in the SD system for 48 h of natural sleep or continuous SD. Afterwards, rats received propofol (20 mg·kg-1·h-1, 6 h) via the tail or slept naturally. The Morris water maze (MWM) and Y-maze test assessed spatial learning and memory abilities. Rat EEG/EMG monitored sleep. The expression of brain and muscle Arnt-like protein 1 (BMAL1), brain-derived neurotrophic factor (BDNF) in the hippocampus and BMAL1 in the hypothalamus were assessed by western blot. Enzyme-linked immunosorbent assay detected IL-6, IL-1ß, arginase 1 (Arg1), and IL-10 levels in the hippocampus. Immunofluorescence was used to determine microglia expression as well as morphological changes. RESULTS: Compared to the control group, the sleep-deprived rats showed poor cognitive performance on both the MWM test and the Y-maze test, accompanied by disturbances in sleep structure, including increased total sleep time, and increased time spent and delta power in non-rapid eye movement sleep. In addition, SD induces abnormal expression of the circadian rhythm protein BMAL1, activates microglia, and causes neuroinflammation and nerve damage. Propofol reversed these changes and saved sleep and cognitive impairment. Furthermore, propofol treatment significantly reduced hippocampal IL-1ß and IL-6 levels, increased BDNF, Arg1, and IL-10 levels, and switched microglia surface markers from the inflammatory M1 type to the anti-inflammatory M2 type. CONCLUSION: Propofol reduces SD-induced cognitive impairment and circadian rhythm disruption, possibly by lowering neuronal inflammation and switching the microglia phenotype from an M1 to an M2 activated state, thus exerting neuroprotective effects.

Cancer-associated fibroblast-derived colony-stimulating factor 2 confers acquired osimertinib resistance in lung adenocarcinoma via promoting ribosome biosynthesis.

Acquired resistance is a major obstacle to the therapeutic efficacy of osimertinib in lung adenocarcinoma (LUAD), but the underlying mechanisms are still not fully understood. Cancer-associated fibroblasts (CAFs) are the most abundant stromal cell type in LUAD tumor-microenvironment (TME) and have emerged as a key player in chemoresistance. However, the function of CAFs in osimertinib resistance is still unclear. Here, we showed that CAFs derived from osimertinib-resistant LUAD tissues (CAFOR) produced much more colony-stimulating factor 2 (CSF2) than those isolated from osimertinib-sensitive tissues. CAFOR-derived CSF2 activated the Janus kinase 2 (JAK2)/Signal transducer and activator of transcription 3 (STAT3) signaling pathway and upregulated lnc-CSRNP3 in LUAD cells. Lnc-CSRNP3 then promoted the expression of nearby gene CSRNP3 by recruiting chromodomain helicase DNA binding protein 9 (CHD9) and inhibited the phosphatase activity of the serine/threonine protein phosphatase 1 catalytic subunit α (PP1α), thereby induced osimertinib resistance by enhancing ribosome biogenesis. Collectively, our study reveals a critical role for CAFs in the development of osimertinib resistance and identifies the CSF2 pathway as an attractive target for monitoring osimertinib efficacy and overcoming osimertinib resistance in LUAD.

Intermittent fasting alleviates postoperative cognitive dysfunction by reducing neuroinflammation in aged mice.

Elderly individuals undergoing surgical procedures are often confronted with the peril of experiencing postoperative cognitive dysfunction (POCD). Prior research has demonstrated the exacerbating effect of sevoflurane anesthesia on neuroinflammation, which can further deteriorate the condition of POCD in elderly patients. Intermittent fasting (IF) restricts food consumption to a specific time window and has been demonstrated to ameliorate cognitive dysfunction induced by neuropathic inflammation. We subjected 18-month-old male mice to 16 hours of fasting and 8 hours of unrestricted eating over a 24-hour period for 0, 1, 2, and 4 weeks, followed by abdominal exploration under sevoflurane anesthesia. In this study, we aim to explore the potential impact of IF on postoperative cognitive function in aged mice undergoing sevoflurane surgery through the preoperative implementation of IF measures. The findings indicate two weeks of IF leads to a significant enhancement of learning and memory capabilities in mice following surgery. The cognitive performance, as determined by the novel object recognition and Morris water maze tests, as well as the synaptic plasticity, as measured by in vivo electrophysiological recordings, has demonstrated marked improvements. Furthermore, the administration of IF markedly enhances the expression of synaptic-associated proteins in hippocampal neurons, concomitant with a decreasing expression of pro-inflammatory factors and a reduced density of microglial cells within the hippocampal brain region. To summarize, the results of this study indicate that IF may mitigate inflammation in the hippocampal area of the brain. Furthermore, IF appears to provide a safeguard against cognitive impairment and synaptic plasticity impairment brought on by sevoflurane anesthesia.

Modulation of cardiac resident macrophages immunometabolism upon high-fat-diet feeding in mice.

Background: A high-fat diet (HFD) contributes to various metabolic disorders and obesity, which are major contributors to cardiovascular disease. As an essential regulator for heart homeostasis, cardiac resident macrophages may go awry and contribute to cardiac pathophysiology upon HFD. Thus, to better understand how HFD induced cardiac dysfunction, this study intends to explore the transcriptional and functional changes in cardiac resident macrophages of HFD mice. Methods: C57BL/6J female mice that were 6 weeks old were fed with HFD or normal chow diet (NCD) for 16 weeks. After an evaluation of cardiac functions by echocardiography, mouse hearts were harvested and cardiac resident CCR2- macrophages were sorted, followed by Smart sequencing. Bioinformatics analysis including GO, KEGG, and GSEA analyses were employed to elucidate transcriptional and functional changes. Results: Hyperlipidemia and obesity were observed easily upon HFD. The mouse hearts also displayed more severe fibrosis and diastolic dysfunction in HFD mice. Smart sequencing and functional analysis revealed metabolic dysfunctions, especially lipid-related genes and pathways. Besides this, antigen-presentation-related gene such as Ctsf and inflammation, particularly for NF-κB signaling and complement cascades, underwent drastic changes in cardiac resident macrophages. GO cellular compartment analysis was also performed and showed specific organelle enrichment trends of the involved genes. Conclusion: Dysregulated metabolism intertwines with inflammation in cardiac resident macrophages upon HFD feeding in mice, and further research on crosstalk among organelles could shed more light on potential mechanisms.

Abnormal Degraded Tapetum 1 (ADT1) is required for tapetal cell death and pollen development in rice.

The timely degradation of tapetum, the innermost somatic anther cell layer in flowering plants, is critical for pollen development. Although several genes involved in tapetum development have been characterized, the molecular mechanisms underlying tapetum degeneration remain elusive. Here, we showed that mutation in Abnormal Degraded Tapetum 1 (ADT1) resulted in overaccumulation of Reactive Oxygen Species (ROS) and abnormal anther development, causing earlier tapetum Programmed Cell Death (PCD) and pollen abortion. ADT1 encodes a nuclear membrane localized protein, which is strongly expressed in the developing microspores and tapetal cells during early anther development. Moreover, ADT1 could interact with metallothionein MT2b, which was related to ROS scavenging and cell death regulation. These findings indicate that ADT1 is required for proper timing of tapetum PCD by regulating ROS homeostasis, expanding our understanding of the regulatory network of male reproductive development in rice.

Exploring the potential mechanisms of Danshen against COVID-19 via network pharmacology analysis and molecular docking.

Danshen, a prominent herb in traditional Chinese medicine (TCM), is known for its potential to enhance physiological functions such as blood circulation, immune response, and resolve blood stasis. Despite the effectiveness of COVID-19 vaccination efforts, some individuals still face severe complications post-infection, including pulmonary fibrosis, myocarditis arrhythmias and stroke. This study employs a network pharmacology and molecular docking approach to investigate the potential mechanisms underlying the therapeutic effects of candidate components and targets from Danshen in the treatment of complications in COVID-19. Candidate components and targets from Danshen were extracted from the TCMSP Database, while COVID-19-related targets were obtained from Genecards. Venn diagram analysis identified common targets. A Protein-Protein interaction (PPI) network and gene enrichment analysis elucidated potential therapeutic mechanisms. Molecular docking evaluated interactions between core targets and candidate components, followed by molecular dynamics simulations to assess stability. We identified 59 potential candidate components and 123 targets in Danshen for COVID-19 treatment. PPI analysis revealed 12 core targets, and gene enrichment analysis highlighted modulated pathways. Molecular docking showed favorable interactions, with molecular dynamics simulations indicating high stability of key complexes. Receiver operating characteristic (ROC) curves validated the docking protocol. Our study unveils candidate compounds, core targets, and molecular mechanisms of Danshen in COVID-19 treatment. These findings provide a scientific foundation for further research and potential development of therapeutic drugs.

Development and Validation of Nomograms for Predicting Pneumonia in Patients with COVID-19 and Lung Cancer.

Background: COVID-19 has spread worldwide, becoming a global threat to public health and can lead to complications, especially pneumonia, which can be life-threatening. However, in lung cancer patients, the prediction of pneumonia and severe pneumonia has not been studied. We aimed to develop effective models to assess pneumonia after SARS-CoV-2 infection in lung cancer patients to guide COVID-19 management. Methods: We retrospectively recruited 621 lung cancer patients diagnosed with COVID-19 via SARS-CoV-2 RT-PCR analysis in two medical centers and divided into training and validation group, respectively. Univariate and multivariate logistic regression analysis were used to identify independent risk factors of all-grade pneumonia and ≥ grade 2 pneumonia in the training group. Nomograms were established based on independent predictors and verified in the validation group. C-index, ROC curves, calibration curve, and DCA were used to evaluate the nomograms. Subgroup analyses in immunotherapy or thoracic radiotherapy patients were then conducted. Results: Among 621 lung cancer patients infected with SARS-CoV-2, 203 (32.7%) developed pneumonia, and 66 (10.6%) were ≥ grade 2. Multivariate logistic regression analysis showed that diabetes, thoracic radiotherapy, low platelet and low albumin at diagnosis of COVID-19 were significantly associated with all-grade pneumonia. The C-indices of the prediction nomograms in the training group and validation group were 0.702 and 0.673, respectively. Independent predictors of ≥ grade 2 pneumonia were age, KPS, thoracic radiotherapy, platelet and albumin at COVID 19 diagnosis, with C-indices of 0.811 and 0.799 in the training and validation groups. In the thoracic radiotherapy subgroup, 40.8% and 11% patients developed all-grade and ≥grade 2 pneumonia, respectively. The rates in the immunotherapy subgroup were 31.3% and 6.6%, respectively. Conclusion: We developed nomograms predicting the probability of pneumonia in lung cancer patients infected with SARS-CoV-2. The models showed good performance and can be used in the clinical management of COVID-19 in lung cancer patients. Higher-risk patients should be managed with enhanced protective measures and appropriate intervention.

An alternative method for inferring Pandy's test using cerebrospinal fluid total protein.

Background: Pandy's test is used to assess the globulin level in cerebrospinal fluid (CSF). As a semi-quantitative manual method, the practicality and clinical value of Pandy's test has been challenged. Objective: We tend to summarize the relationship between CSF total protein (CSF-TP) quantification and Pandy's results, providing a formula to estimate Pandy's results merely by CSF-TP value. Methods: This retrospective study involved 1090 cases hospitalized in Huashan Hospital during 1/1/2023 to 20/4/2023. All samples were divided into six group based on their Pandy's results. Their corresponding CSF-TP quantitative results were subsequently analyzed and summarized. Another 364 patients were also gathered for verification. Results: The turbidity of samples won't affect examiners'ocular inspection and interpretation of Pandy's tests in positive groups. The results of Pandy's tests can be deduced based on CSF-TP quantitative results according to following rules: CSF-TP quantitative results 0-614 mg/L for Pandy negative (-), 615-1322 mg/L for extremely weak positive (±), 1323-2953 mg/L for weak positive (1+), 2954-6561 mg/L for medium positive results (2+), 6562-13007 mg/L for strong positive results (3+) and CSF-TP results >13007 for strongest positive (4+). The quantitative range above was experimentally verified as effective and correct by calculating the agreement rate through another 364 samples and the R ratio of each Pandy group was greater than 90 %. Conclusion: There is an excellent correlation between CSF-TP and Pandy's test. Therefore, CSF-TP quantification test through PROT Slides can be used to infer the results of Pandy's test to accelerate the abolish of this traditional manual test.

Position-Aware Indoor Human Activity Recognition Using Multisensors Embedded in Smartphones.

Composite indoor human activity recognition is very important in elderly health monitoring and is more difficult than identifying individual human movements. This article proposes a sensor-based human indoor activity recognition method that integrates indoor positioning. Convolutional neural networks are used to extract spatial information contained in geomagnetic sensors and ambient light sensors, while transform encoders are used to extract temporal motion features collected by gyroscopes and accelerometers. We established an indoor activity recognition model with a multimodal feature fusion structure. In order to explore the possibility of using only smartphones to complete the above tasks, we collected and established a multisensor indoor activity dataset. Extensive experiments verified the effectiveness of the proposed method. Compared with algorithms that do not consider the location information, our method has a 13.65% improvement in recognition accuracy.

Recent approaches for the synthesis of heterocycles from amidines via a metal catalyzed C-H functionalization reaction.

Transition metal catalyzed C-H bond activation has become one of the most important tools for constructing new chemical bonds. Introducing directing groups to the substrates is the key to a successful reaction, these directing groups can also be further transformed in the reaction. Amidines with their unique structure and reactivity are ideal substrates for transition metal-catalyzed C-H transformations. This review describes the major advances and mechanistic investigations of the C-H activation/annulation tandem reactions of amidines until early 2024, focusing on metal-catalyzed C-H activation of amidines with unsaturated compounds, such as alkynes, ketone, vinylene carbonate, cyclopropanols and their derivatives. Meanwhile this manuscript also explores the reaction of amidines with different carbene precursors, for example diazo compounds, azide, triazoles, pyriodotriazoles, and sulfoxonium ylides as well as their own C-H bond activation/cyclization reactions. A bright outlook is provided at the end of the manuscript.