Analysis Based on Clinical Data and Imaging - Factors Affecting the Prognosis of Patients with Optic Neuritis.

Objective: To analyze the risk factors that affect the prognosis of patients with optic neuritis through imaging examinations and clinical data analysis. Methods: 130 patients with optic neuritis admitted to our hospital from February 2018 to February 2022 were selected as the study subjects. They were divided into a poor prognosis group (n = 52) and a good prognosis group (n = 78) based on their prognosis. Imaging examination and clinical data analysis, along with the assessment of the predictive value of statistically significant continuous variables using ROC experiments and risk factors using logistic regression were performed. Results: The results showed that there was no statistically significant difference in general data such as gender and BMI between the two groups (P > .05). Compared with the group with good prognosis, the group with poor prognosis had higher age (34.47 ± 1.58 years vs 35.81 ± 2.60 years), onset to visit interval (1.81 ± 0.40 weeks vs 2.50 ± 0.64 weeks), VCAM-1 (608.70 ± 42.80 ng/mL vs 625.58 ± 35.62 ng/mL), recurrence rate (48.72% vs 69.23%), optic nerve atrophy rate (3.85% vs 15.38%), eye rotation pain rate (28.21% vs 30.77%), and MRI long T2 signal rate (21.79% vs 40.38%). The proportion of MRI T1 enhanced signals was relatively high (17.95% vs 34.62%) (P < .05). Age, the interval between onset and visit time, and AUC of VCAM-1 were 0.657, 0.785, and 0.621, and the optimal cutoff values were 35 years old, 2 weeks old, and 620.29 ng/mL; 95% CI was (0.596 0.738), (0.704 0.852), and (0.532 0.704), P < .05. Conclusion: Age (>35 years old), recurrence (yes), interval between onset and visit (>2 weeks), MRI long T2 signal (yes), and MRI T1 enhanced signal (yes) are all risk factors that affect the prognosis of patients with optic neuritis. Clinical attention should be paid to high-risk populations.

Efficient Aggressive Behavior Recognition of Pigs Based on Temporal Shift Module.

Aggressive behavior among pigs is a significant social issue that has severe repercussions on both the profitability and welfare of pig farms. Due to the complexity of aggression, recognizing it requires the consideration of both spatial and temporal features. To address this problem, we proposed an efficient method that utilizes the temporal shift module (TSM) for automatic recognition of pig aggression. In general, TSM is inserted into four 2D convolutional neural network models, including ResNet50, ResNeXt50, DenseNet201, and ConvNext-t, enabling the models to process both spatial and temporal features without increasing the model parameters and computational complexity. The proposed method was evaluated on the dataset established in this study, and the results indicate that the ResNeXt50-T (TSM inserted into ResNeXt50) model achieved the best balance between recognition accuracy and model parameters. On the test set, the ResNeXt50-T model achieved accuracy, recall, precision, F1 score, speed, and model parameters of 95.69%, 95.25%, 96.07%, 95.65%, 29 ms, and 22.98 M, respectively. These results show that the proposed method can effectively improve the accuracy of recognizing pig aggressive behavior and provide a reference for behavior recognition in actual scenarios of smart livestock farming.

Corroded iron stent increases fibrin deposition and promotes endothelialization after stenting.

Poststent restenosis is caused by insufficient endothelialization and is one of the most serious clinical complications of stenting. We observed a rapid endothelialization rate and increased fibrin deposition on the surfaces of the corroded iron stents. Thus, we hypothesized that corroded iron stents would promote endothelialization by increasing fibrin deposition on rough surfaces. To verify this hypothesis, we conducted an arteriovenous shunt experiment to analyze fibrin deposition in the corroded iron stents. We implanted a corroded iron stent in both the carotid and iliac artery bifurcations to elucidate the effects of fibrin deposition on endothelialization. Co-culture experiments were conducted under dynamic flow conditions to explore the relationship between fibrin deposition and rapid endothelialization. Our findings indicate that, from the generation of corrosion pits, the surface of the corroded iron stent was rough, and numerous fibrils were deposited in the corroded iron stent. Fibrin deposition in corroded iron stents facilitates endothelial cell adhesion and proliferation, which, in turn, promotes endothelialization after stenting. Our study is the first to elucidate the role of iron stent corrosion in endothelialization, pointing to a new direction for preventing clinical complications caused by insufficient endothelialization.

Iron corroded granules inhibiting vascular smooth muscle cell proliferation.

In-stent restenosis after interventional therapy remains a severe clinical complication. Current evidence indicates that neointimal hyperplasia induced by vascular smooth muscle cell (VSMC) proliferation is a major cause of restenosis. Thus, inhibiting VSMC proliferation is critical for preventing in-stent restenosis. The incidence of restenosis was reduced in nitrided iron-based stents (hereafter referred to as iron stents). We hypothesized that the corroded granules produced by the iron stent would prevent in-stent restenosis by inhibiting VSMC proliferation. To verify this hypothesis, we introduced a dynamic circulation device to analyze the components of corroded granules. To investigate the effects of corroded granules on VSMC proliferation, we implanted the corroded iron stent into the artery of the atherosclerotic artery stenosis model. Moreover, we explored the mechanism underlying the inhibition of VSMC proliferation by iron corroded granules. The results indicated that iron stent produced the corroded granules after implantation, and the main component of the corrosion granules was iron oxide. Remarkably, the corroded granules reduced the neointimal hyperplasia in an atherosclerotic artery stenosis model, and iron corroded granules decreased the neointimal hyperplasia by inhibiting VSMC proliferation. In addition, we revealed that corroded granules reduced VSMC proliferation by activating autophagy through the AMPK/mTOR signaling pathway. Importantly, safety of iron corroded granules was evaluated and proved to be satisfactory hemocompatibility in rabbit model. Overall, the role of corroded granules in restenosis prevention was described for the first time. This finding highlighted the implication of corroded granules produced by iron stent in inhibiting VSMC proliferation, pointing to a new direction to prevent in-stent restenosis.

In vitro Induction and Phenotypic Variations of Autotetraploid Garlic (Allium sativum L.) With Dwarfism.

Garlic (Allium sativum L.) is a compelling horticultural crop with high culinary and therapeutic values. Commercial garlic varieties are male-sterile and propagated asexually from individual cloves or bulbils. Consequently, its main breeding strategy has been confined to the time-consuming and inefficient selection approach from the existing germplasm. Polyploidy, meanwhile, plays a prominent role in conferring plants various changes in morphological, physiological, and ecological properties. Artificial polyploidy induction has gained pivotal attention to generate new genotype for further crop improvement as a mutational breeding method. In our study, efficient and reliable in vitro induction protocols of autotetraploid garlic were established by applying different antimitotic agents based on high-frequency direct shoot organogenesis initiated from inflorescence explant. The explants were cultured on solid medium containing various concentrations of colchicine or oryzalin for different duration days. Afterward, the ploidy levels of regenerated plantlets with stable and distinguished characters were confirmed by flow cytometry and chromosome counting. The colchicine concentration at 0.2% (w/v) combined with culture duration for 20 days was most efficient (the autotetraploid induction rate was 21.8%) compared to the induction rate of 4.3% using oryzalin at 60 µmol L-1 for 20 days. No polymorphic bands were detected by simple sequence repeat analysis between tetraploid and diploid plantlets. The tetraploids exhibited a stable and remarkable dwarfness effect rarely reported in artificial polyploidization among wide range of phenotypic variations. There are both morphological and cytological changes including extremely reduced plant height, thickening and broadening of leaves, disappearance of pseudostem, density reduction, and augmented width of stomatal. Furthermore, the level of phytohormones, including, indole propionic acid, gibberellin, brassinolide, zeatin, dihydrozeatin, and methyl jasmonate, was significantly lower in tetraploids than those in diploid controls, except indole acetic acid and abscisic acid, which could partly explain the dwarfness in hormonal regulation aspect. Moreover, as the typical secondary metabolites of garlic, organosulfur compounds including allicin, diallyl disulfide, and diallyl trisulfide accumulated a higher content significantly in tetraploids. The obtained dwarf genotype of autotetraploid garlic could bring new perspectives for the artificial polyploids breeding and be implemented as a new germplasm to facilitate investigation into whole-genome doubling consequences.

Energy restriction induced SIRT6 inhibits microglia activation and promotes angiogenesis in cerebral ischemia via transcriptional inhibition of TXNIP.

Energy restriction (ER) protects against cerebral ischemic injury, but the underlying mechanism remains largely unclear. Here, rats were fed ad libitum (AL) or on an alternate-day food deprivation intermittent fasting (IF) diet for 3 months, followed by middle cerebral artery occlusion (MCAO) surgery. The body weight, infarct volume, and neurological deficit score were accessed at the designated time points. ELISA, qRT-PCR, and Western blotting were used to determine cytokine secretion and the expression of SIRT6, TXNIP, and signaling molecules, respectively. Immunofluorescence evaluated microglial activation and angiogenesis in vivo. For in vitro study, oxygen-glucose deprivation/reoxygenation (OGD/R)-treated cell model was generated. MTT and tube formation assays were employed to determine cell viability and tube formation capability. ChIP assay detected chromatin occupancy of SIRT6 and SIRT6-mediated H3 deacetylation. We found that IF or ER mimetics ameliorated cerebral ischemic brain damage and microglial activation, and potentiated angiogenesis in vivo. ER mimetics or SIRT6 overexpression alleviated cerebral ischemia and reperfusion (I/R)-induced injury in vitro. SIRT6 suppressed TXNIP via deacetylation of H3K9ac and H3K56ac in HAPI cells and BMVECs. Downregulation of SIRT6 reversed ER mimetics-mediated protection during cerebral I/R in vitro. Our study demonstrated that ER-mediated upregulation of SIRT6 inhibited microglia activation and potentiated angiogenesis in cerebral ischemia via suppressing TXNIP.

Increased Number of Perivascular CD20-Positive B Lymphocytes in the Neuropathology of CLIPPERS: Findings of 6 Patients from Mainland China.

INTRODUCTION: Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) syndrome is a recently described chronic inflammatory disease of the central nervous system. There are few reports of CLIPPERS in the Chinese population to date. We summarized the clinical characteristics of 6 CLIPPERS patients to deepen the understanding of this disease. METHODS: The clinical manifestations and treatment of 6 CLIPPERS patients confirmed by pathology or clinical diagnosis in our hospital were retrospectively analyzed. RESULTS: The common clinical manifestations included ataxia, dysarthria, diplopia, dysphagia, dizziness, cognitive impairment, facial paresthesia, and paralysis. Most of the lesions showed typical symmetric "pepper powder"-like dot and nodular enhancement centered in the pontine and cerebellum except 1 patient with unilateral nodular enhancement. The brain histopathological examination of the 5 biopsied patients indicated that, with the exception of patient 4 with no lymphocyte infiltration, a large amount of perivascular lymphocytic infiltration was found in the other 4 patients, among whom only 1 patient was dominated by CD3+ T cell infiltration and the other 3 patients were dominated by CD20+ B cell infiltration. After treatment with intravenous methylprednisolone, all patients had significant clinical recovery associated with complete or significant MRI recovery, but they were prone to relapse after withdrawal or reduction of the corticosteroid. CONCLUSION: Our reports highlight the importance of neuropathological examinations when encountering atypical imaging manifestations, such as unilateral and large nodular Gd+ lesions, in order to establish a final diagnosis of CLIPPERS. In addition, the lymphocytic infiltration in the lesions of CLIPPERS may be dominated by CD20+ B cells instead of CD3+ T cells.

Histological, Physiological and Transcriptomic Analysis Reveal Gibberellin-Induced Axillary Meristem Formation in Garlic (Allium sativum).

The number of cloves in a garlic bulb is controlled by axillary meristem differentiation, which directly determines the propagation efficiency. Our previous study showed that injecting garlic plants with gibberellins (GA3) solution significantly increased clove number per bulb. However, the physiological and molecular mechanism of GA-induced axillary bud formation is still unknown. Herein, dynamic changes in histology, phytohormones, sugars and related genes expression at 2, 4, 8, 16 and 32 days after treatment (DAT) were investigated. Histological results indicated two stages (axillary meristem initiation and dormancy) were in the period of 0-30 days after GA3 treatment. Application of GA3 caused a significant increase of GA3 and GA4, and the downregulation of AsGA20ox expression. Furthermore, the change trends in zeatin riboside (ZR) and soluble sugar were the same, in which a high level of ZR at 2 DAT and high content of soluble sugar, glucose and fructose at 4 DAT were recorded, and a low level of ZR and soluble sugar arose at 16 and 32 DAT. Overall, injection of GA3 firstly caused the downregulation of AsGA20ox, a significant increase in the level of ZR and abscisic acid (ABA), and the upregulation of AsCYP735 and AsAHK to activate axillary meristem initiation. Low level of ZR and soluble sugar and a high level of sucrose maintained axillary meristem dormancy.

Micro-structural white matter abnormalities and cognitive impairment in asymptomatic carotid plaque patients: A DTI study using TBSS analysis.

BACKGROUND: It has been shown that symptomatic or severe carotid atherosclerosis is closely related to cognitive impairment and brain white matter damage. However, there is still a lack of effective and non-invasive imaging biomarkers to identify early high-risk cerebrovascular diseases. Therefore, the purpose of this study is to explore the integrity of brain white matter and cognitive impairment in patients with asymptomatic carotid plaques by using imaging technology. METHODS: All subjects were from a project of Stroke Risk Screening and Prevention and were defined as stroke high-risk patients (with three or more stroke risk factors). Tract-based spatial statistics (TBSS) based on diffusion tensor imaging (DTI) was used to analyze the whole brain white matter abnormalities in 61 patients with carotid artery plaque and in 40 healthy controls. At the same time, the general clinical data between the two groups were compared, such as age, gender, smoking, hypertension and cognitive function scores etc. Furthermore, the plaque group was divided into the have-hyperintensities group and the no-hyperintensities group to compare their microstructure of white matter injuries. RESULTS: The cognitive scores of plaque group were significantly lower than that of control group. We found that when plaque group and control group were compared, no white matter fiber tracts with difference was found in FA, MD, AD and RD. However, the decrease of FA and the increase of RD were found in some white matter regions (P < 0.05) when comparing the have-hyperintensities group and the no-hyperintensities group. These white matter regions included anterior thalamic radiation, corticospinal tract, cingulum (cingulate gyrus), forceps minor, inferior fronto-occipital fasciculus, superior longitudinal fasciculus, uncinate fasciculus. What's more, there were significant differences in blood pressure between the two groups. CONCLUSION: The cognitive function of patients with early high-risk cerebrovascular diseases (asymptomatic carotid plaques) has a downward trend. TBSS based on DTI can help to find out the actual damage of brain white matter in patients with early carotid plaque, and reflect the early pathological changes from the micro level.

Altered brain volume and its relationship to characteristics of carotid plaques in asymptomatic patients.

Carotid plaque is an aggregate marker of exposure to vascular risk factors, which are linked to structural brain changes. We investigated prestroke global and regional changes in brain volume in a carotid plaque population of cognitively healthy individuals and the association between carotid plaque characteristics and these changes.A total of 76 participants were divided into healthy control (HC, n = 28), vulnerable plaque (n = 27) and stable plaque groups (n = 21). All subjects underwent carotid ultrasound and brain magnetic resonance imaging (MRI). Voxel-based morphometry (VBM) was used to examine differences in regional gray matter volumes (rGMVs) among the different groups.The plaque group had a significantly lower mean total cerebral brain volume (TCBV) than the HC group (P = .03). Carotid intima-media thickness (CIMT) was negatively correlated with TCBV (r = -0.311, P = .006) and rGMV in the right thalamus (r = -0.589, P = .001). The rGMVs of the right middle occipital gyrus and bilateral lingual gyrus were significantly different between the unstable and stable groups. The gray-scale median (GSM) of the plaque and the total plaque risk score (TPRS) were correlated with the volume of the right middle occipital gyrus (r=-0.478, P = .001; r = 0.541, P = .001) and bilateral lingual gyrus (r = -0.419, P = .003; r = 0.288, P = .04).Carotid plaque is related to the volume of the brain parenchyma and right thalamus. The rGMVs of the right middle occipital gyrus and bilateral lingual gyrus differed between the vulnerable plaque and stable plaque groups, and the characteristics of carotid plaques may serve as indexes that reflect these changes.

Imbalance of circulating CD4(+)CXCR5(+)FOXP3(+) Tfr-like cells and CD4(+)CXCR5(+)FOXP3(-) Tfh-like cells in myasthenia gravis.

Follicular regulatory T (Tfr) cells are defined as a specialized subset of regulatory T cells (Tregs) that act to control the overactivation of follicular helper T (Tfh) cells and B cells in germinal centers. Accumulating evidence has demonstrated that the dysregulation of either Tfr cells or Tfh cells results in abnormal germinal center responses that contribute to the pathogenesis of autoimmune diseases. However, the role that Tfr cells and Tfh cells play in myasthenia gravis (MG) remains unclear. This study revealed a significantly decreased frequency of CD4(+)CXCR5(+)FOXP3(+) Tfr-like cells and an increased frequency of CD4(+)CXCR5(+)FOXP3(-) Tfh-like cells in the peripheral blood of MG patients compared with healthy controls. Moreover, the Tfr-like/Tfh-like ratio was inversely correlated with the clinical severity of the MG patients. Interestingly, glucocorticoid (GC) treatment can restore the imbalance of circulating Tfr-like/Tfh-like cells, and this restoration is accompanied by reduced clinical symptoms. These results suggested, for the first time, that an imbalance of circulating Tfr-like and Tfh-like cells may be involved in the immunopathogenesis of MG and may provide novel insight for the development of MG therapies.

[Association between tumor necrosis factor superfamily member 4 gene polymorphism and risk of asymptomatic carotid vulnerable plaque in a Chinese population].

OBJECTIVE: Vulnerable plaque of carotid artery is one of the risk factors of atherosclerotic cerebral infarction. Detection and treatment of vulnerable atherosclerotic plaque of carotid artery before symptoms of cerebral infarction is an effective way to prevent atherosclerotic cerebral infarction. Tumor necrosis factor superfamily member 4 (TNFSF4) plays a key role in the process of atherosclerosis, a common risk factor for both myocardial and cerebral infarctions. Studies have indicated that the single nucleotide polymorphism (SNP) rs3850641 in TNFSF4 is associated with higher risk of myocardial infarction and SNP rs3861950 in TNFSF4 is associated with higher risk of atherosclerosis cerebral infarction (ACI) ,but little is known about the association between TNFSF4 variations and vulnerable plaque of carotid artery. METHODS: A case-control study involving 510 patients with asymptomatic vulnerable plaque of carotid artery and 485 age and sex matched healthy subjects without vulnerable plaque of carotid artery was conducted in Hunan province. Asymptomatic vulnerable plaque of carotid artery means vulnerable plaque of carotid artery without cerebral infarction. Two SNPs of TNFSF4, rs3850641 and rs3861950, were genotyped by the TaqMan SNP genotyping method, and verified partly by Genomic DNA Sequencing. RESULTS: The results revealed a significant allelic association between rs3861950 and asymptomatic vulnerable plaque of carotid artery in case group (χ(2)=9.13, P=0.003; OR=1.41, 95%CI: 1.12-1.76). Compared with control subjects, the difference in genotype was significant in case group (χ(2)=25.28, P<0.000 1). However, there was no significant association between rs3850641 and asymptomatic vulnerable plaque of carotid artery (OR=1.16, 95%CI: 0.92-1.46; χ(2)=1.47, P=0.225). CONCLUSION: TNFSF4 gene polymorphism rs3861950 was associated with the risk of vulnerable plaques of carotid artery in a Chinese population, which might be middle phenotype indicating higher risk of cerebral infarction.