Miracle-dz/UniFAR-FTUs huggingface dataset:
[Treatment of degenerative medial meniscus injury of knee joint by arthroscopy combined with small needle knife to release superficial medial collateral ligament of knee joint].

OBJECTIVE To explore the clinical effect of arthroscopic combined with small needle knife in the treatment of degenerative medial meniscus (MM) injury of knee joint by releasing the superficial layer of medial collateral ligament (SMCL). METHODS From February 2016 to November 2018, 56 patients (56 knees) with limited pain, strangulation and flexion in medial knee joint space were selected. X-ray Kellgren-Lawrence grading was I-II. MRI showed medial meniscus injury(III degree) of knee joint. There were 30 males(30 knees) and 26 females(26 knees). Arthroscopic MM plasty and small needle knife were used to release SMCL. The Lysholm knee score was used to evaluate the effect of operation. RESULTS All 56 patients were followed up, and the duration ranged from 3 to 24 months, with an average of 10 months. According to the Lysholm knee score standard, the final follow-up was compared with that of before operation. The results showed that the preoperative knee score was 37.24±1.32, the latest follow-up knee score was 85.72±5.28, the knee score was higher than that before the operation(P<0.05). CONCLUSIONS Arthroscopy combined with small needle knife release of superficial medial collateral ligament in the treatment of degenerative medial knee meniscus injury can effectively improve the mechanical balance of the knee joint, improve Lysholm knee score in patients with knee meniscus injury, and promote the recovery of knee joint function, which has clinical value.
Regulation of INF2-mediated actin polymerization through site-specific lysine acetylation of actin itself

Significance Tight regulation is required to control biochemical reactions in cells so that these reactions can be activated precisely when and where needed. Our work focuses on actin, a protein that polymerizes into filaments in at least 20 distinct processes in mammalian cells. We have previously shown that lysine acetylation, a relatively minor modification on actin, is crucial for regulating a specific population of actin filaments through a protein called INF2. Here we identify key acetylated lysines that control INF2 activity. INF2 mutations link to 2 human diseases, focal segmental glomerulosclerosis (a kidney disease) and Charcot–Marie–Tooth disease (a neuropathy), and our findings further the mechanistic understanding of these diseases. INF2 is a formin protein that accelerates actin polymerization. A common mechanism for formin regulation is autoinhibition, through interaction between the N-terminal diaphanous inhibitory domain (DID) and C-terminal diaphanous autoregulatory domain (DAD). We recently showed that INF2 uses a variant of this mechanism that we term “facilitated autoinhibition,” whereby a complex consisting of cyclase-associated protein (CAP) bound to lysine-acetylated actin (KAc-actin) is required for INF2 inhibition, in a manner requiring INF2-DID. Deacetylation of actin in the CAP/KAc-actin complex activates INF2. Here we use lysine-to-glutamine mutations as acetylmimetics to map the relevant lysines on actin for INF2 regulation, focusing on K50, K61, and K328. Biochemically, K50Q- and K61Q-actin, when bound to CAP2, inhibit full-length INF2 but not INF2 lacking DID. When not bound to CAP, these mutant actins polymerize similarly to WT-actin in the presence or absence of INF2, suggesting that the effect of the mutation is directly on INF2 regulation. In U2OS cells, K50Q- and K61Q-actin inhibit INF2-mediated actin polymerization when expressed at low levels. Direct-binding studies show that the CAP WH2 domain binds INF2-DID with submicromolar affinity but has weak affinity for actin monomers, while INF2-DAD binds CAP/K50Q-actin 5-fold better than CAP/WT-actin. Actin in complex with full-length CAP2 is predominately ATP-bound. These interactions suggest an inhibition model whereby CAP/KAc-actin serves as a bridge between INF2 DID and DAD. In U2OS cells, INF2 is 90-fold and 5-fold less abundant than CAP1 and CAP2, respectively, suggesting that there is sufficient CAP for full INF2 inhibition.
Traditional and modern research of 'taking pulse at cunkou alone' method

As a main method of TCM pulse differentiation,'taking pulse at cunkou alone' method has a history over 2000 years,and has always been the main basis for TCM doctors in checking yin and yang,differentiating zangfu,discussing deficiency and excess,diagnosing the pathogenesis and designing the principle of treatment.This method is not only a scientific conclusion of ancient TCM doctors in their thousand-years of clinical practice,but also the most important TCM method worth to be developed.This paper analyzes the 'taking pulse at cunkou alone' method from its formation,position and traditional understandings,alone with modern research methods such as physiology and pathology,with the hope to develop this important differentiation method depending on the heritage of our antecedents,and the ever-expanding modern science and technology.
Metformin Inhibit Cervical Cancer Migration by Suppressing the FAK/Akt Signaling Pathway

Background: Metformin, an antidiabetic drug, has been previously reported to have anti-cancer activities. However, its role in the control of cancer cell migration remains elusive. Methods: To examine the possible effect of metformin on migration of cervical cancer cells. The related mechanisms were further determined by immunocytochemistry and Western’s blotting assay. Results: The results showed that metformin treatment substantially inhibited the migration ability of cervical cancer cells. Consistently, the filopodia and lamellipodia formation were depleted after exposure to metformin. The suppression of migration mediated through the regulatory proteins such as focal adhesion kinase (FAK), ATP-dependent tyrosine kinase (Akt), Rac1 and RhoA after metformin treatment. Conclusion: Metformin displays antimigration effects in cervical cancer cells by inhibiting filopodia and lamellipodia formation through the suppression of FAK, Akt and its downstream Rac1 and RhoA protein. We propose that metformin could be a novel potential candidate as an antimetastatic cancer drug in the cervical cancer management.
Systematic Review: Acupuncture vs Standard Pharmacological Therapy for Migraine Prevention

Standard pharmacological treatment of migraine has many shortcomings. Acupuncture is becoming a more widely used therapy for the prevention and treatment of migraine, but its effectiveness is still in question when compared to the pharmacological treatments even though very few of these have Class A and B evidence for migraine prevention. This is a systematic review of data from existing randomized trials that compare the effectiveness of acupuncture treatment with conventional migraine preventative medications.
Molecular causes of sex‐specific deficits in rodent models of neurodevelopmental disorders

Neurodevelopmental disorders (NDDs) such as intellectual disability and autism spectrum disorder consistently show a male bias in prevalence, but it remains unclear why males and females are affected with different frequency. While many behavioral studies of transgenic NDD models have focused only on males, the requirement by the National Institutes of Health to consider sex as a biological variable has promoted the comparison of male and female performance in wild‐type and mutant animals. Here, we review examples of rodent models of NDDs in which sex‐specific deficits were identified in molecular, physiological, and/or behavioral responses, showing sex differences in susceptibility to disruption of genes mutated in NDDs. Haploinsufficiency in genes involved in mechanisms such as synaptic function (GABRB3 and NRXN1), chromatin remodeling (CHD8, EMHT1, and ADNP), and intracellular signaling (CC2D1A and ERK1) lead to more severe behavioral outcomes in males. However, in the absence of behavioral deficits, females can still present with cellular and electrophysiological changes that could be due to compensatory mechanisms or differential allocation of molecular and cellular functions in the two sexes. By contrasting these findings with mouse models where females are more severely affected (MTHFR and AMBRA1), we propose a framework to approach the study of sex‐specific deficits possibly leading to sex bias in NDDs.
Lipid rafts and neurodegeneration: structural and functional roles in physiologic aging and neurodegenerative diseases

Lipid rafts are small, dynamic membrane areas characterized by the clustering of selected membrane lipids as the result of the spontaneous separation of glycolipids, sphingolipids, and cholesterol in a liquid-ordered phase. The exact dynamics underlying phase separation of membrane lipids in the complex biological membranes are still not fully understood. Nevertheless, alterations in the membrane lipid composition affect the lateral organization of molecules belonging to lipid rafts. Neural lipid rafts are found in brain cells, including neurons, astrocytes, and microglia, and are characterized by a high enrichment of specific lipids depending on the cell type. These lipid rafts seem to organize and determine the function of multiprotein complexes involved in several aspects of signal transduction, thus regulating the homeostasis of the brain. The progressive decline of brain performance along with physiological aging is at least in part associated with alterations in the composition and structure of neural lipid rafts. In addition, neurodegenerative conditions, such as lysosomal storage disorders, multiple sclerosis, and Parkinson’s, Huntington’s, and Alzheimer’s diseases, are frequently characterized by dysregulated lipid metabolism, which in turn affects the structure of lipid rafts. Several events underlying the pathogenesis of these diseases appear to depend on the altered composition of lipid rafts. Thus, the structure and function of lipid rafts play a central role in the pathogenesis of many common neurodegenerative diseases.
Potassium-presenting Zinc Oxide Surfaces Induce Vertical Phase Separation in Fullerene-free Organic Photovoltaics.

Bulk heterojunction (BHJ) structure based organic photovoltaics (OPVs) have recently showed great potential for achieving high power conversion efficiencies (PCEs). An ideal BHJ structure would feature a large donor/acceptor interfacial area for efficient exciton dissociation and gradient distributions with high donor and acceptor concentrations near the anode and cathode, respectively, for efficient charge extraction. However, the random mixing of donor and acceptor in BHJ often suffers the severe charge recombination in the interface, resulting in poor charge extraction. Herein, we propose a new approach-treating the surface of the zinc oxide (ZnO) as electron transport layer with potassium hydroxide-to induce vertical phase separation of an active layer incorporating the non-fullerene acceptor IT-4F. Density functional theory calculations suggested that the binding energy difference between IT-4F and the PBDB-T-2Cl, to the potassium(K)-presenting ZnO interface is twice stronger than that for IT-4F and PBDB-T-2Cl to the untreated ZnO surface, such that it would induce more IT-4F moving toward the K-presenting ZnO interface than the untreated ZnO interface thermodynamically. Benefiting from efficient charge extraction, the best PCEs increased to 12.8% from 11.8% for PBDB-T-2Cl:IT-4F based devices, to 12.6% from 11.6% for PBDB-T-2Cl:Y1-4F based devices, to 13.5% from 12.2% for PBDB-T-2Cl:Y6 based devices, and to 15.7% from 15.1% for PM6:Y6 based devices.
Structural and functional relationships between plasmodesmata and plant endoplasmic reticulum-plasma membrane contact sites consisting of three synaptotagmins.

Synaptotagmin 1 (SYT1) has been recognised as a tethering factor of plant endoplasmic reticulum (ER)-plasma membrane (PM) contact sites (EPCSs) and partially localises to around plasmodesmata (PD). However, other components of EPCSs associated with SYT1 and functional links between the EPCSs and PD have not been identified. We explored interactors of SYT1 by immunoprecipitation and mass analysis. The dynamics, morphology and spatial arrangement of the ER in Arabidopsis mutants lacking the EPCS components were investigated by using confocal microscopy and electron microscopy. PD permeability of EPCS mutants was assessed using a virus movement protein and free GFP as indicators. We identified two additional components of the EPCSs, SYT5 and SYT7, that interact with SYT1. The mutants of the three SYTs were defective in the anchoring of the ER to the PM. The ER near the PD entrance appeared to be weakly squeezed in the triple mutant compared to the wild type. The triple mutant suppressed cell-to-cell movement of the virus movement protein, but not GFP diffusion. We revealed major additional components of EPCS associated with SYT1 and suggested that the EPCSs arranged around the PD squeeze the ER to regulate active transport via PD.
Six-DOF Spacecraft Optimal Trajectory Planning and Real-Time Attitude Control: A Deep Neural Network-Based Approach

This brief presents an integrated trajectory planning and attitude control framework for six-degree-of-freedom (6-DOF) hypersonic vehicle (HV) reentry flight. The proposed framework utilizes a bilevel structure incorporating desensitized trajectory optimization and deep neural network (DNN)-based control. In the upper level, a trajectory data set containing optimal system control and state trajectories is generated, while in the lower level control system, DNNs are constructed and trained using the pregenerated trajectory ensemble in order to represent the functional relationship between the optimized system states and controls. These well-trained networks are then used to produce optimal feedback actions online. A detailed simulation analysis was performed to validate the real-time applicability and the optimality of the designed bilevel framework. Moreover, a comparative analysis was also carried out between the proposed DNN-driven controller and other optimization-based techniques existing in related works. Our results verify the reliability of using the proposed bilevel design for the control of HV reentry flight in real time.
Minimalist analogue robot discovers animal-like walking gaits

Robots based on simplified or abstracted biomechanical concepts can be a useful tool for investigating how and why animals move the way they do. In this paper we present an extremely simple quadruped robot, which is able to walk with no form of software or controller. Instead, individual leg movements are triggered directly by switches on each leg which detect leg loading and unloading. As the robot progresses, pitching and rolling movements of its body result in a gait emerging with a consistent leg movement order, despite variations in stride and stance time. This gait has similarities to the gaits used by walking primates and grazing livestock, and is close to the gait which was recently theorised to derive from animal body geometry. As well as presenting the design and construction of the robot, we present experimental measurements of the robot’s gait kinematics and ground reaction forces determined using high speed video and a pressure mat, and compare these to gait parameters of animals taken from literature. Our results support the theory that body geometry is a key determinant of animal gait at low speeds, and also demonstrate that steady state locomotion can be achieved with little to no active control.
Ionomic and transcriptomic analyses of two cotton cultivars (Gossypium hirsutum L.) provide insights into the ion balance mechanism of cotton under salt stress

Soil salinity is a major abiotic stress factor that limits cotton production worldwide. To improve salt tolerance in cotton, an in-depth understanding of ionic balance is needed. In this study, a pot experiment using three levels of soil salinity (0%, 0.2%, and 0.4%, represented as CK, SL, and SH, respectively) and two cotton genotypes (salt-tolerant genotype: L24; salt-sensitive genotype: X45) was employed to investigate how sodium chloride (NaCl) stress effects cotton growth, ion distribution, and transport, as well as to explore the related mechanism. The results showed that SL treatment mainly inhibited shoot growth, while SH treatment caused more extensive impairment to roots and shoots. The growth inhibition ratio of NaCl stress on X45 was more marked than that of L24. Under NaCl stress, the Na concentration in the roots, stems and leaves significantly increased, whereas the K, Cu, B, and Mo concentration in roots, as well as Mg and S concentrations in the leaves, significantly decreased. Under salt stress conditions, salt-tolerant cotton plants can store Na in the leaves, and as a result, a larger amount of minerals (e.g., Cu, Mo, Si, P, and B) tend to transport to the leaves. By contrast, salt-sensitive varieties tend to accumulate certain minerals (e.g., Ca, P, Mg, S, Mn, Fe, Cu, B, Mo, and Si) in the roots. Most genes related to ion transport and homeostasis were upregulated in L24, but not in X45. The expression level of GhSOS1 in X45 was higher than L24, but GhNHX1 in L24 was higher than X45. Our findings suggest that the two varieties response to salt stress differently; for X45 (salt-sensitive), the response is predominantly governed by Na+ efflux, whereas for L24 (salt-tolerant), vacuolar sequestration of Na+ is the major mechanism. The expression changes of the genes encoding the ion transporters may partially explain the genotypic difference in leaf ion accumulation under salt stress conditions.
Multistage GAN for Fabric Defect Detection

Fabric defect detection is an intriguing but challenging topic. Many methods have been proposed for fabric defect detection, but these methods are still suboptimal due to the complex diversity of both fabric textures and defects. In this paper, we propose a generative adversarial network (GAN)-based framework for fabric defect detection. Considering existing challenges in real-world applications, the proposed fabric defect detection system is capable of learning existing fabric defect samples and automatically adapting to different fabric textures during different application periods. Specifically, we customize a deep semantic segmentation network for fabric defect detection that can detect different defect types. Furthermore, we attempted to train a multistage GAN to synthesize reasonable defects in new defect-free samples. First, a texture-conditioned GAN is trained to explore the conditional distribution of defects given different texture backgrounds. Given a novel fabric, we aim to generate reasonable defective patches. Then, a GAN-based fusion network fuses the generated defects to specific locations. Finally, the well-trained multistage GAN continuously updates the existing fabric defect datasets and contributes to the fine-tuning of the semantic segmentation network to better detect defects under different conditions. Comprehensive experiments on various representative fabric samples are conducted to verify the detection performance of our proposed method.
Unisexual hybrids break through an evolutionary dead end by two‐way backcrossing

Unisexual vertebrates (i.e., those produced through clonal or hemiclonal reproduction) are typically incapable of purging deleterious mutations, and, as a result, are considered short‐lived in evolutionary terms. In hemiclonal reproduction (hybridogenesis), one parental genome is eliminated during oogenesis, producing haploid eggs containing the genome of a single parent. Hemiclonal hybrids are usually produced by backcrossing hemiclonal hybrids with males of the paternal species. When hemiclonal hybrids from a genus of greenlings (Hexagrammos) are crossed with males of the maternal species, the progeny are phenotypically similar to the maternal species and produce recombinant gametes by regular meiosis. The present study was conducted to determine if the hemiclonal genome is returned to the gene pool of the maternal species in the wild. Using a specific cytogenetic marker to discriminate between such progeny and the maternal species, we observed that Hexagrammos hybrids mated with maternal and paternal ancestors at the same frequency. This two‐way backcrossing in which clonal genomes are returned to the gene pool where they can undergo recombination plays an important role in increasing the genetic variability of the hemiclonal genome and reducing the extinction risk. In this way, hybrid lineages may have survived longer than predicted through occasional recombinant generation.
Microsecond-timescale simulations suggest 5-HT–mediated preactivation of the 5-HT3A serotonin receptor

Significance The pentameric ligand-gated ion channel 5-HT3A exhibits a transient preactive state that provides valuable insight into its binding and activation mechanisms. In this preactive state, the allosteric regulation of the channel structure, and thereby function, upon ligand binding occur at timescales that are too fast to be measured experimentally. This study demonstrates the power of microsecond-timescale MD simulations in detecting these transitional preactive states upon ligand binding and describing their effects on channel function at the molecular scale. Such a mechanistic understanding of the channel function is a critical element in the design of therapeutics for the regulation of 5-HT3A, which are needed to reverse the effects of numerous pathological conditions. Aided by efforts to improve their speed and efficiency, molecular dynamics (MD) simulations provide an increasingly powerful tool to study the structure–function relationship of pentameric ligand-gated ion channels (pLGICs). However, accurate reporting of the channel state and observation of allosteric regulation by agonist binding with MD remains difficult due to the timescales necessary to equilibrate pLGICs from their artificial and crystalized conformation to a more native, membrane-bound conformation in silico. Here, we perform multiple all-atom MD simulations of the homomeric 5-hydroxytryptamine 3A (5-HT3A) serotonin receptor for 15 to 20 μs to demonstrate that such timescales are critical to observe the equilibration of a pLGIC from its crystalized conformation to a membrane-bound conformation. These timescales, which are an order of magnitude longer than any previous simulation of 5-HT3A, allow us to observe the dynamic binding and unbinding of 5-hydroxytryptamine (5-HT) (i.e., serotonin) to the binding pocket located on the extracellular domain (ECD) and allosteric regulation of the transmembrane domain (TMD) from synergistic 5-HT binding. While these timescales are not long enough to observe complete activation of 5-HT3A, the allosteric regulation of ion gating elements by 5-HT binding is indicative of a preactive state, which provides insight into molecular mechanisms that regulate channel activation from a resting state. This mechanistic insight, enabled by microsecond-timescale MD simulations, will allow a careful examination of the regulation of pLGICs at a molecular level, expanding our understanding of their function and elucidating key structural motifs that can be targeted for therapeutic regulation.
Length‐dependent MRI of hereditary neuropathy with liability to pressure palsies

Hereditary neuropathy with liability to pressure palsies (HNPP) is caused by heterozygous deletion of the peripheral myelin protein 22 (PMP22) gene. Patients with HNPP present multifocal, reversible sensory/motor deficits due to increased susceptibility to mechanical pressure. Additionally, age‐dependent axonal degeneration is reported. We hypothesize that length‐dependent axonal loss can be revealed by MRI, irrespective of the multifocal phenotype in HNPP.