Conjugated Molecules Based Multi-Component Artificial Photosynthesis System for Producing Multi-Objective Products.

The development of artificial photosynthesis systems that mimics natural photosynthesis can help address the issue of energy scarcity by efficiently utilizing solar energy. Here, it presents liposomes-based artificial photosynthetic nanocapsules (PSNC) integrating photocatalytic, chemical catalytic, and biocatalytic systems through one-pot method. The PSNC contains 5,10,15,20-tetra(4-pyridyl) cobalt-porphyrin, tridipyridyl-ruthenium nitrate, oligo-pphenyl-ethylene-rhodium complex, and creatine kinase, efficiently generating oxygen, nicotinamide adenine dinucleotide (NADH), and adenosine triphosphate with remarkable enhancements of 231%, 30%, and 86%, compared with that of molecules mixing in aqueous solution. Additionally, the versatile PSNC enables simulation of light-independent reactions, achieving a controllable output of various target products. The regenerated NADH within PSNC further facilitates alcohol dehydrogenase, yielding methanol with a notable efficiency improvement of 37%. This work introduces a promising platform for sustainable solar energy conversion and the simultaneous synthesis of multiple valuable products in an ingenious and straightforward way.

A Chalcone-based Fluorescence Probe for H2S Detecting Utilizing ESIPT Coupled ICT Mechanism.

The accurate and effective identification of hydrogen sulfide holds great significance for environmental monitoring. Azide-binding fluorescent probes are powerful tools for hydrogen sulfide detection. We combined the 2'-Hydroxychalcone scaffold with azide moiety to construct probe Chal-N3, the electron-withdrawing azide moiety was utilized to block the ESIPT process of 2'-Hydroxychalcone and quenches the fluorescence. The fluorescent probe was triggered with the addition of hydrogen sulfide, accompanied by great fluorescence intensity enhancement with a large Stokes shift. With excellent fluorescence properties including high sensitivity, specificity selectivity, and wider pH range tolerance, the probe was successfully applied to natural water samples.

BmPGPR-L4 is a negative regulator of the humoral immune response in the silkworm Bombyx mori.

Toll, immune deficiency and prophenoloxidase cascade represent vital immune signaling pathways in insects. Peptidoglycan recognition proteins (PGRPs) are innate immune receptors that activate and regulate the immune signaling pathways. Previously, we reported that BmPGPR-L4 was induced in the silkworm Bombyx mori larvae by bacteria and peptidoglycan challenges. Here, we focused on the function of BmPGRP-L4 in regulating the expression of antimicrobial peptides (AMPs). The hemolymph from BmPGRP-L4-silenced larvae exhibited an enhanced inhibitory effect on the growth of Escherichia coli, either by growth curve or inhibitory zone experiments. Coincidentally, most of the AMP genes were upregulated after RNAi of BmPGRP-L4. Oral administration of heat-inactivated E. coli and Staphylococcus aureus after RNAi of BmPGRP-L4 resulted in the increased expression of BmPGRP-L4 in different tissues of the silkworm larvae, revealing an auto-regulatory mechanism. By contrast, the expression of most AMP genes was downregulated by oral bacterial administration after RNAi of BmPGRP-L4. The above results demonstrate that BmPGRP-L4 recognizes bacterial pathogen-associated molecular patterns and negatively regulates AMP expression to achieve immunological homeostasis. As a negative regulator, BmPGPR-L4 is proposed to be involved in the feedback regulation of the immune signaling pathways of the silkworm to prevent excessive activation of the immune response.

The potential molecular markers of inflammatory response in KOA with AD based on single-cell transcriptome sequencing analysis and identification of ligands by virtual screening.

Alzheimer's disease (AD) and osteoarthritis (OA) are both senile degenerative diseases. Clinical studies have found that OA patients have a significantly increased risk of AD in their later life. This study hypothesized that chronic aseptic inflammation might lead to AD in KOA patients. However, current research has not yet clarified the potential mechanism between AD and KOA. Therefore, this study intends to use KOA transcriptional profiling and single-cell sequencing analysis technology to explore the molecular mechanism of KOA affecting AD development, and screen potential molecular biomarkers and drugs for the prediction, diagnosis, and prognosis of AD in KOA patients. It was found that the higher the expression of TXNIP, MMP3, and MMP13, the higher the risk coefficient of AD was. In addition, the AUC of TXNIP, MMP3, and MMP13 were all greater than 0.70, which had good diagnostic significance for AD. Finally, through the virtual screening of core proteins in FDA drugs and molecular dynamics simulation, it was found that compound Cobicistat could be targeted to TXNIP, Itc could be targeted to MMP3, and Isavuconazonium could be targeted to MMP13. To sum up, TXNIP, MMP3, and MMP13 are prospective molecular markers in KOA with AD, which could be used to predict, diagnose, and prognosis.

Myricitrin promotes osteogenesis and prevents ovariectomy bone mass loss via the PI3K/AKT signalling pathway.

This study aimed to explore the effect of myricitrin on osteoblast differentiation in mice immortalised bone marrow mesenchymal stem cells (imBMSCs). Additionally, ovariectomy (OVX) mice were employed to examine the effect of myricitrin on bone trabecular loss in vivo. The effect of myricitrin on the proliferation of imBMSCs was evaluated using a cell counting kit-8 assay. Alizarin red staining, alkaline phosphatase staining were performed to elucidate osteogenesis. Furthermore, qRT-PCR and western blot determined the expression of osteo-specific genes and proteins. To screen for candidate targets, mRNA transcriptome genes were sequenced using bioinformatics analyses. Western blot and molecular docking analysis were used to examine target signalling markers. Moreover, rescue experiments were used to confirm the effect of myricitrin on the osteogenic differentiation of imBMSCs. OVX mice were also used to estimate the delay capability of myricitrin on bone trabecular loss in vivo using western blot, micro-CT, tartaric acid phosphatase (Trap) staining, haematoxylin and eosin staining, Masson staining and immunochemistry. In vitro, myricitrin significantly enhanced osteo-specific genes and protein expression and calcium deposition. Moreover, mRNA transcriptome gene sequencing and molecular docking analysis revealed that this enhancement was accompanied by an upregulation of the PI3K/AKT signalling pathway. Furthermore, copanlisib, a PI3K inhibitor, partially reversed the osteogenesis promotion induced by myricitrin. In vivo, western blot, micro-CT, hematoxylin and eosin staining, Masson staining, Trap staining and immunochemistry revealed that bone trabecular loss rate was significantly alleviated in the myricitrin low- and high-dose groups, with an increased expression of osteopontin, osteoprotegerin, p-PI3K and p-AKT compared to the OVX group. Myricitrin enhances imBMSC osteoblast differentiation and attenuate bone mass loss partly through the upregulation of the PI3K/AKT signalling pathway. Thus, myricitrin has therapeutic potential as an antiosteoporosis drug.

Effects of CX3CR1 and CXCR2 antagonists on running-dependent intramuscular neutrophil recruitments and myokine upregulation.

Muscle contractile activity stimulates intramuscular recruitment of immune cells including neutrophils emerging to serve as a prerequisite for exerting proper muscular performance, although the underlying mechanisms and their contributions to myokine upregulation remain ill-defined. We previously reported that pharmacological inhibition of CX3CR1, a fractalkine receptor, dampens gnawing-dependent neutrophil recruitment into masseter muscles along with compromising their masticatory activity. By using a running exercise model, we herein demonstrated that hindlimb muscles require collaborative actions of both CX3CR1- and CXCR2-mediated signals for achieving neutrophil recruitment, upregulation of myokines including interleukin (IL)-6, enhanced GLUT4 translocation, and adequate endurance capability. Mechanistically, we revealed that a combination of CX3CR1 and CXCR2 antagonists, i.e., AZD8797 and SB2205002, inhibits exercise-inducible ICAM-1 and fractalkine upregulations in the area of the endothelium and muscle-derived CXCL1 upregulation, both of which apparently contribute to the intramuscular neutrophil accumulation in working muscles. Intriguingly, we also observed that 2 h of running results in intramuscular augmentation of innate lymphoid type 2 cells (ILC2s) markers, i.e., Bcl11b mRNA levels and anti-GATA-3-antibody-positive signals, and that these effects are completely abolished by administration of the combination of CX3CR1 and CXCR2 antagonists. Taken together, our findings strongly suggest that the exercise-evoked regional interplay among working myofibers, the adjacent endothelium, and recruited immune cells including neutrophils and possibly ILC2s, mediated through these local factors, plays a key role in the organization of the intramuscular microenvironment supporting the performance of hindlimb muscles during running.NEW & NOTEWORTHY This study provides compelling evidence that running-dependent intramuscular neutrophil recruitment requires both CX3CR1- and CXCR2-mediated signals that prime not only myofiber-derived myokine upregulations but also endothelium ICAM-1 and fractalkine expressions. The results revealed the importance of the exercise-evoked regional interplay among working myofibers, the adjacent endothelium, and recruited immune cells, including neutrophils and possibly ILC2s, which plays a key role in the organization of the intramuscular microenvironment supporting the performance of hindlimb muscles during running.

Speeding Up Entanglement Generation by Proximity to Higher-Order Exceptional Points.

Entanglement is a key resource for quantum information technologies ranging from quantum sensing to quantum computing. Conventionally, the entanglement between two coupled qubits is established at the timescale of the inverse of the coupling strength. In this Letter, we study two weakly coupled non-Hermitian qubits and observe entanglement generation at a significantly shorter timescale by proximity to a higher-order exceptional point. We establish a non-Hermitian perturbation theory based on constructing a biorthogonal complete basis and further identify the optimal condition to obtain the maximally entangled state. Our study of speeding up entanglement generation in non-Hermitian quantum systems opens new avenues for harnessing coherent nonunitary dissipation for quantum technologies.

Exceptional points enhance sensing in an optical microcavity.

Sensors play an important part in many aspects of daily life such as infrared sensors in home security systems, particle sensors for environmental monitoring and motion sensors in mobile phones. High-quality optical microcavities are prime candidates for sensing applications because of their ability to enhance light-matter interactions in a very confined volume. Examples of such devices include mechanical transducers, magnetometers, single-particle absorption spectrometers, and microcavity sensors for sizing single particles and detecting nanometre-scale objects such as single nanoparticles and atomic ions. Traditionally, a very small perturbation near an optical microcavity introduces either a change in the linewidth or a frequency shift or splitting of a resonance that is proportional to the strength of the perturbation. Here we demonstrate an alternative sensing scheme, by which the sensitivity of microcavities can be enhanced when operated at non-Hermitian spectral degeneracies known as exceptional points. In our experiments, we use two nanoscale scatterers to tune a whispering-gallery-mode micro-toroid cavity, in which light propagates along a concave surface by continuous total internal reflection, in a precise and controlled manner to exceptional points. A target nanoscale object that subsequently enters the evanescent field of the cavity perturbs the system from its exceptional point, leading to frequency splitting. Owing to the complex-square-root topology near an exceptional point, this frequency splitting scales as the square root of the perturbation strength and is therefore larger (for sufficiently small perturbations) than the splitting observed in traditional non-exceptional-point sensing schemes. Our demonstration of exceptional-point-enhanced sensitivity paves the way for sensors with unprecedented sensitivity.

Rosuvastatin suppresses TNF-α-induced matrix catabolism, pyroptosis and senescence via the HMGB1/NF-κB signaling pathway in nucleus pulposus cells.

Intervertebral disc degeneration is mainly caused by irregular matrix metabolism in nucleus pulposus cells and involves inflammatory factors such as TNF-α. Rosuvastatin, which is widely used in the clinic to reduce cholesterol levels, exerts anti-inflammatory effects, but whether rosuvastatin participates in IDD remains unclear. The current study aims to investigate the regulatory effect of rosuvastatin on IDD and the potential mechanism. In vitro experiments demonstrate that rosuvastatin promotes matrix anabolism and suppresses catabolism in response to TNF-α stimulation. In addition, rosuvastatin inhibits cell pyroptosis and senescence induced by TNF-α. These results demonstrate the therapeutic effect of rosuvastatin on IDD. We further find that HMGB1, a gene closely related to cholesterol metabolism and the inflammatory response, is upregulated in response to TNF-α stimulation. HMGB1 inhibition or knockdown successfully alleviates TNF-α-induced ECM degradation, senescence and pyroptosis. Subsequently, we find that HMGB1 is regulated by rosuvastatin and that its overexpression abrogates the protective effect of rosuvastatin. We then verify that the NF-κB pathway is the underlying pathway regulated by rosuvastatin and HMGB1. In vivo experiments also reveal that rosuvastatin inhibits IDD progression by alleviating pyroptosis and senescence and downregulating HMGB1 and p65. This study might provide new insight into therapeutic strategies for IDD.

Research Progress of Perovskite-Based Bifunctional Oxygen Electrocatalyst in Alkaline Conditions.

In light of the depletion of conventional energy sources, it is imperative to conduct research and development on sustainable alternative energy sources. Currently, electrochemical energy storage and conversion technologies such as fuel cells and metal-air batteries rely heavily on precious metal catalysts like Pt/C and IrO2, which hinders their sustainable commercial development. Therefore, researchers have devoted significant attention to non-precious metal-based catalysts that exhibit high efficiency, low cost, and environmental friendliness. Among them, perovskite oxides possess low-cost and abundant reserves, as well as flexible oxidation valence states and a multi-defect surface. Due to their advantageous structural characteristics and easily adjustable physicochemical properties, extensive research has been conducted on perovskite-based oxides. However, these materials also exhibit drawbacks such as poor intrinsic activity, limited specific surface area, and relatively low apparent catalytic activity compared to precious metal catalysts. To address these limitations, current research is focused on enhancing the physicochemical properties of perovskite-based oxides. The catalytic activity and stability of perovskite-based oxides in Oxygen Reduction Reaction/Oxygen Evolution Reaction (ORR/OER) can be enhanced using crystallographic structure tuning, cationic regulation, anionic regulation, and nano-processing. Furthermore, extensive research has been conducted on the composite processing of perovskite oxides with other materials, which has demonstrated enhanced catalytic performance. Based on these different ORR/OER modification strategies, the future challenges of perovskite-based bifunctional oxygen electrocatalysts are discussed alongside their development prospects.

Clinical and Pathological Features of Congenital Hepatic Hemangioma in Children: A Retrospective Analysis.

Objective: We reviewed our experience with congenital hepatic hemangiomas (CHH) to assess the effectiveness of our treatment strategies. Methods: Clinical and pathologic features of children with CHH were reviewed. Results: Twenty-two cases of CHH were collected, 17 were resected and 5 were followed until resolution. In 17 with alpha-feto-protein (AFP) levels, 9 were elevated with 5 decreasing to normal before surgery. In six with tumors under 3 cm, five regressed between 1 and 13 months, one required removal 5 years after initial diagnosis. Postoperative histopathology of 17 cases showed abnormal vascular hyperplasia without lobular architecture. CD34 was expressed in all tumors, glucose transporter 1(Glut1) was negative. Conclusion: If the tumor is less than 3 cm, AFP is normal and there are no obvious complications, the lesion can be followed with regular assessment imaging. Surgical resection is an option in tumors less than 3 cm which have not regressed over time.

Topological Quantum State Control through Exceptional-Point Proximity.

We study the quantum evolution of a non-Hermitian qubit realized as a submanifold of a dissipative superconducting transmon circuit. Real-time tuning of the system parameters to encircle an exceptional point results in nonreciprocal quantum state transfer. We further observe chiral geometric phases accumulated under state transport, verifying the quantum coherent nature of the evolution in the complex energy landscape and distinguishing between coherent and incoherent effects associated with exceptional point encircling. Our work demonstrates an entirely new method for control over quantum state vectors, highlighting new facets of quantum bath engineering enabled through dynamical non-Hermitian control.

Decoherence-Induced Exceptional Points in a Dissipative Superconducting Qubit.

Open quantum systems interacting with an environment exhibit dynamics described by the combination of dissipation and coherent Hamiltonian evolution. Taken together, these effects are captured by a Liouvillian superoperator. The degeneracies of the (generically non-Hermitian) Liouvillian are exceptional points, which are associated with critical dynamics as the system approaches steady state. We use a superconducting transmon circuit coupled to an engineered environment to observe two different types of Liouvillian exceptional points that arise either from the interplay of energy loss and decoherence or purely due to decoherence. By dynamically tuning the Liouvillian superoperators in real time we observe a non-Hermiticity-induced chiral state transfer. Our study motivates a new look at open quantum system dynamics from the vantage of Liouvillian exceptional points, enabling applications of non-Hermitian dynamics in the understanding and control of open quantum systems.

Diagnosing autism spectrum disorder in children using conventional MRI and apparent diffusion coefficient based deep learning algorithms.

OBJECTIVE: To develop and validate deep learning (DL) methods for diagnosing autism spectrum disorder (ASD) based on conventional MRI (cMRI) and apparent diffusion coefficient (ADC) images. METHODS: A total of 151 ASD children and 151 age-matched typically developing (TD) controls were included in this study. The data from these subjects were assigned to training and validation datasets. An additional 20 ASD children and 25 TD controls were acquired, whose data were utilized in an independent test set. All subjects underwent cMRI and diffusion-weighted imaging examination of the brain. We developed a series of DL models to separate ASD from TD based on the cMRI and ADC data. The seven models used include five single-sequence models (SSMs), one dominant-sequence model (DSM), and one all-sequence model (ASM). To enhance the feature detection of the models, we embed an attention mechanism module. RESULTS: The highest AUC (0.824 ~ 0.850) was achieved when applying the SSM based on either FLAIR or ADC to the validation and independent test sets. A DSM using the combination of FLAIR and ADC showed an improved AUC in the validation (0.873) and independent test sets (0.876). The ASM also showed better diagnostic value in the validation (AUC = 0.838) and independent test sets (AUC = 0.836) compared to the SSMs. Among the models with attention mechanism, the DSM achieved the highest diagnostic performance with an AUC, accuracy, sensitivity, and specificity of 0.898, 84.4%, 85.0%, and 84.0% respectively. CONCLUSIONS: This study established the potential of DL models to distinguish ASD cases from TD controls based on cMRI and ADC images. KEY POINTS: • Deep learning models based on conventional MRI and ADC can be used to diagnose ASD. • The model (DSM) based on the FLAIR and ADC sequence achieved the best diagnostic performance with an AUC of 0.836 in the independent test sets. • The attention mechanism further improved the diagnostic performance of the models.

Dilated Optic Nerve Sheath Diameter Predicts Poor Outcome in Acute Spontaneous Intracerebral Hemorrhage.

BACKGROUND AND PURPOSE: Optic nerve sheath diameter (ONSD) enlargement occurs in patients with intracerebral hemorrhage (ICH). However, the relationship between ONSD and prognosis of ICH is uncertain. This study aimed to investigate the predictive value of ONSD on poor outcome of patients with acute spontaneous ICH. METHODS: We studied 529 consecutive patients with acute spontaneous ICH who underwent initial CT within 6 h of symptom onset between October 2016 and February 2019. The ONSDs were measured 3 mm behind the eyeball on initial CT images. Poor outcome was defined as having a Glasgow Outcome Scale (GOS) score of 1-3, and favorable outcome was defined as having a GOS score of 4-5 at discharge. RESULTS: The ONSD of the poor outcome group was significantly greater than that of the favorable outcome group (5.87 ± 0.86 vs. 5.21 ± 0.69 mm, p < 0.001). ONSD was related to hematoma volume (r = 0.475, p < 0.001). Adjusting other meaningful predictors, ONSD (OR: 2.83; 95% CI: 1.94-4.15) was associated with poor functional outcome by multivariable logistic regression analysis. Receiver operating characteristic curve showed that the ONSD improved the accuracy of ultraearly hematoma growth in the prediction of poor outcome (AUC: 0.790 vs. 0.755, p = 0.016). The multivariable logistic regression model with all the meaningful predictors showed a better predictive performance than the model without ONSD (AUC: 0.862 vs. 0.831, p = 0.001). CONCLUSIONS: The dilated ONSD measured on initial CT indicated elevated intracranial pressure and poor outcome, so appropriate intervention should be taken in time.

Bromodomain-containing protein 7 regulates matrix metabolism and apoptosis in human nucleus pulposus cells through the BRD7-PI3K-YAP1 signaling axis.

Intervertebral disc degeneration (IDD) results from dysregulated metabolism of the extracellular matrix of the nucleus pulposus (NP) and involves the participation of inflammatory factors such as TNF-α. Bromodomain-containing protein 7 (BRD7) shows considerable potential for anti-inflammatory applications. Herein, we investigated the role of BRD7 in IDD. The immunohistochemistry results demonstrated decreased BRD7 expression in severely degenerated human NP tissues compared to those showing mild degeneration. Lentiviruses and adenoviruses were used to knock down or overexpress BRD7 and YAP1, respectively. Our results revealed that BRD7 knockdown promoted matrix degradation and suppressed PI3K and YAP1 expression, while BRD7 overexpression alleviated matrix degradation and promoted YAP1 and PI3K expression. In addition, PI3K inhibition augmented matrix degradation, enhanced apoptosis, and reduced YAP1 expression, whereas YAP1 overexpression promoted matrix synthesis, suppressed apoptosis and promoted PI3K expression. Besides, BRD7 overexpression reversed the reductions in sulfated glycosaminoglycan levels induced by TNF-α, but this effect was blocked by PI3K or YAP1 inhibitors. Moreover, YAP1 and PI3K were shown to interact through coimmunoprecipitation analysis. In summary, our results demonstrate that BRD7 can regulate matrix metabolism and apoptosis in human NP cells through the BRD7-PI3K-YAP1 signaling axis. This study might provide new insights into the prevention and treatment of IDD.

Composite indices of femoral neck strength predicts the collapse of steroid-associated osteonecrosis of the femoral head: a retrospective study.

PURPOSES: The purpose of this study was to investigate the predictive effect exerted by composite indices of femoral neck strength (compressive strength index (CSI), bending strength index (BSI) and impact strength index (ISI) on the femoral head collapse in steroid-associated ONFH patients. METHODS: Nonoperative steroid-associated osteonecrosis of the femoral head (ONFH) patients from 2017 to 2019 were selected. The patients fell into the collapsed group and the non-collapsed group according to whether the femoral head collapsed. CSI, BSI and ISI were calculated. Moreover, bone turnover markers were measured. The statistical analysis was conducted on the predictive effects of composite indices of femoral neck strength and bone turnover index on ONFH collapse. RESULTS: A total of 62 patients were included. The mean CSI, BSI and ISI were significantly lower in the collapsed group than those in the non-collapsed group (P < 0.05). CSI, ISI,t-P1NP and ß-CTx were suggested as the protective risk factors for the femoral head collapse in ONFH patients. The ISI area under the curve values was 0. 878.The mean survival time of the hips of patients with ISI greater than 0.435 was greater (P < 0.05) than that of patients with ISI less than 0.435. CONCLUSION: The composite indices of femoral neck strength can predict steroid-associated ONFH femoral head collapse more effectively than the bone turnover markers. The ISI value of 0.435 is a potential cut-off value, lower than this value can predict the early collapse of steroid-associated ONFH.

Efficacy of Triple and Talonavicular Arthrodesis for the Treatment of III-V Müller-Weiss Disease.

Müller-Weiss Disease (MWD) is a rare foot disease with unclear etiology but frequently occurred in women. Due to the resistance to conservative treatment, surgical therapy has gradually occupied a necessary position in the clinical management of MWD. Joint fusion surgery is a commonly used treatment for MWD, which could effectively alleviate pain, correct deformation, and restore function. A total of 12 MWD patients (III-V stage) were enrolled in this study. All patients showed no significant improvement in conservative treatment and further received the triple and talonavicular arthrodesis. All patients were followed up with an average follow-up of 16.8 ± 1.19 months (mean ± SD). The triple and talonavicular arthrodesis significantly ameliorated the pain and walking dysfunction in the affected foot. The American Orthopedic Foot Andankle Society (AOFAS) scores dramatically increased from 43.4 ± 16.1 to 85.3 ± 6.2. Meanwhile, the conducting of triple and talonavicular arthrodesis improved the X-ray length (15.5 ± 0.8 vs. 14.3 ± 0.9 cm) and arch height (18.6 ± 0.9 vs. 10.2 ± 0.7 mm) and reduced the Meary-Tomeno angle (1.3 ± 2.5 vs. 2.14 ± 4.8°). The triple and talonavicular arthrodesis achieved a satisfying therapeutic effect on MWD patients at the III-V stage, which improved patients' outcomes and the quality of life.

Quantitative Ischemic Characteristics and Prognostic Analysis of Crossed Cerebellar Diaschisis in Hyperacute Ischemic Stroke.

OBJECTIVES: Crossed cerebellar diaschisis (CCD) is a secondary phenomenon caused by supratentorial brain injury, characterized by hypoperfusion and hypometabolism of the contralateral cerebellum. This study aimed to investigate the correlation between the quantitative data of initial supratentorial ischemia and CCD, and to further explore the prognosis value of CCD in the hyperacute phase. MATERIALS AND METHODS: The imaging and clinical data of 109 patients with hyperacute ischemic stroke were analyzed retrospectively, univariate analysis and multivariate logistic regression were used to observe the relationship between the volume and degree of initial supratentorial ischemia and CCD, respectively, and to further analyze the effects of CCD in the hyperacute phase on neurological function and clinical prognosis. RESULTS: The degree and volume of initial supratentorial ischemia was significantly correlated with hyperacute CCD. The volume of ischemic penumbra (OR=1.021 [95% CI: 1.009-1.033], P<0.001) and the reduction rate of cerebral blood volume (CBV) (OR=1.338 [95% CI: 1.073-1.668], P=0.01) were the main influencing factors of CCD; patients with hyperacute CCD had higher admission and discharge National Institutes of Health Stroke Scale (NIHSS) (P=0.046 and P=0.01), and more hemorrhagic transformation (P=0.021), but there was no significant difference in the final infarction volume (P=0.347) and the 90-day modified Rankin Scale (mRS) (P=0.757). CONCLUSION: Patients with CCD had larger initial supratentorial ischemic volume and more severe ischemic degree in the hyperacute ischemic stroke, more short-term neurological impairment, and worse short-term treatment effect, however, but the long-term functional prognosis was not be affected.

Repair of articular cartilage defect using adipose-derived stem cell-loaded scaffold derived from native cartilage extracellular matrix.

The purpose of this study was to investigate the feasibility of adipose-derived stem cells (ADSCs) as the seed cells of cartilage tissue engineering. ADSCs were isolated from adipose tissue that was harvested under sterile conditions from the inguen fold of porcines and cultured in vitro. Acellular cartilage extracellular matrix (ACECM) scaffolds of pigs were then constructed. Moreover, inflammatory cells, as well as cellular and humoral immune responses, were detected using hematoxylin and eosin staining staining, immunohistochemical staining, and western blot analysis. The results showed that the cartilage complex constructed by ADSCs and ACECM through tissue engineering successfully repaired the cartilage defect of the pig knee joint. The in vivo repair experiment showed no significant difference between chondrocytes, ADSCs, and induced ADSCs, indicating that ADSCs do not require in vitro induction and have the potential for chondrogenic differentiation in the environment around the knee joint. In addition, pig-derived acellular cartilage scaffolds possess no obvious immune inflammatory response when used in xenotransplantation. ADSCs may serve as viable seed cells for cartilage tissue engineering.