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To explore the mortality of patients with fragile hip fractures and assess the death-associated risk factors.A total of 690 patients with osteoporotic hip fractures (age, 50-103 years) that were treated from January 2010 to December 2015 were enrolled and followed-up in this study and the clinical data were retrospectively collected. Three months, 1 year, and the total mortality were measured. Mortality-related risk factors were assessed including age, gender, surgery, the duration from injury to operation, pulmonary infection, and the number and type of complications. The mortality of each group was compared by chi-square test or corrected chi-square test for univariate analysis, and the factors with statistically significant mortality difference confirmed by univariate analysis were analyzed by binary logistic multivariate analysis.The 3-month mortality was 7.69%, the 1-year mortality was 15.60%, and the total mortality of the follow-up time was 24.06%. The 1-year and total mortality during the follow-up of the patients were higher in the75-year-old group than those in the ≤75-year-old group (p = 0.000, respectively); were higher in the male patients than that in the female patients (p = 0.042; p = 0.017, respectively); were significantly lower in the operation group than that in the non-operation group (p = 0.000, respectively); were significantly lower in the patients that underwent the operation in ≤5 days than the patients that underwent the operation within5 days (p = 0.008; p = 0.000, respectively); were significantly lower in patients with2 kinds of combined medical diseases than those with ≥2 kinds of chronic diseases (p = 0.000, respectively); were significantly lower in patients receiving anti-osteoporosis treatment than in patients not receiving anti-osteoporosis treatment (p = 0.000, p = 0.002, respectively). Binary logistic regression analysis showed that the independent risk factors affecting mortality included advanced age 75-years-old (OR = 5.653, p = 0.000), male (OR = 1.998, p = 0.001), non-surgical treatment (OR = 9.909, p = 0.000), the number of combined medical diseases ≥2 (OR = 1.522, p = 0.042), and non-anti-osteoporosis treatment (OR = 1.796, p = 0.002).Age, whether or not surgical treatment was performed, the number of medical diseases, and whether or not anti-osteoporosis treatment was performed were independent risk factors for 3-month and 1-year mortality in patients with fragile hip fractures.

Within urban green spaces, tree species diversity is believed to correlate with aboveground biomass, though there is some disagreement within the literature on the strength and directionality of the relationship. Therefore, we assessed the relationship between the biodiversity of woody species and the aboveground biomass of woody plant species in the tropical, coastal city of Haikou in southern China. To accomplish this, we obtained comprehensive tree and site data through field sampling of 190 urban functional units (UFUs, or work units) corresponding to six types of land uses governmental‐institutional, industrial‐commercial, park‐recreational, residential, transport infrastructure, and undeveloped area. Based on our field data, we investigated the relationship between tree species diversity and aboveground biomass using multiple regression, which revealed significant relationships across all five types of land uses. Aboveground biomass in green spaces was also correlated with anthropogenic factors, especially time since urban development, or site age, annual maintenance frequency by human caretakers, and human population density. Among these factors, maintenance is the strongest predictor of aboveground biomass in urban green space. Therefore, this study highlights the critical role of maintenance of urban green space in promoting both aboveground biomass and woody biodiversity in urban ecosystems and, consequently, on urban ecosystem services. Our findings contribute to a deeper understanding of the ecosystem services provided by communities of woody plant species in urban areas., We investigated the relationship between tree species diversity and aboveground biomass using multiple regression, which revealed significant relationships across all five types of land uses. Aboveground biomass in green spaces was also correlated with anthropogenic factors, especially time since urban development, or site age, annual maintenance frequency by human caretakers, and human population density. Among these factors, maintenance is the strongest predictor of aboveground biomass in urban green space. Therefore, this study highlights the critical role of maintenance of urban green space in promoting both aboveground biomass and woody biodiversity in urban ecosystems and, consequently, on urban ecosystem services. Our findings contribute to a deeper understanding of the ecosystem services provided by communities of woody plant species in urban areas.

Injury to long axonal projections is a central pathological feature at the early phase of intracerebral hemorrhage (ICH). It has been reported to contribute to persistent functional disability following ICH. However, the molecular mechanisms that drive axonal degeneration remain unclear. Autologous blood was injected into the striatum to mimic the pathology of ICH. Observed significant swollen axons with characteristic retraction bulbs were found around the striatal hematoma at 24 h after ICH. Electronic microscopic examination revealed highly disorganized microtubule and swollen mitochondria in the retraction bulbs. MEC17 is a specific α-tubulin acetyltransferase, ablation of acetylated α-tubulin in MEC17-/- mice aggravated axonal injury, axonal transport mitochondria dysfunction, and motor dysfunction. In contrast, treatment with tubastatin A (TubA), which promotes microtubule acetylation, significantly alleviated axonal injury and protected the integrity of the corticospinal tract and fine motor function after ICH. Moreover, results showed that 41% mitochondria were preferentially bundled to the acetylated α-tubulin in identifiable axons and dendrites in primary neurons. This impaired axonal transport of mitochondria in primary neurons of MEC17-/- mice. Given that opening of mitochondrial permeability transition pore (mPTP) induces mitochondrial dysfunction and impairs ATP supply thereby promoting axonal injury, we enhanced the availability of acetylated α-tubulin using TubA and inhibited mPTP opening with cyclosporin A. The results indicated that this combined treatment synergistically protected corticospinal tract integrity and promoted fine motor control recovery. These findings reveal key intracellular mechanisms that drive axonal degeneration after ICH and highlight the need to target multiple factors and respective regulatory mechanisms as an effective approach to prevent axonal degeneration and motor dysfunction after ICH.

The use of diverse datasets in phylogenetic studies aiming for understanding evolutionary histories of species can yield conflicting inference. Phylogenetic conflicts observed in animal and plant systems have often been explained by hybridization, incomplete lineage sorting (ILS), or horizontal gene transfer. Here, we employed target enrichment data, species tree and species network approaches to infer the backbone phylogeny of the family Caprifoliaceae, while distinguishing among sources of incongruence. We used 713 nuclear loci and 46 complete plastome sequence data from 43 samples representing 38 species from all major clades to reconstruct the phylogeny of the family using concatenation and coalescence approaches. We found significant nuclear gene tree conflict as well as cytonuclear discordance. Additionally, coalescent simulations and phylogenetic species network analyses suggested putative ancient hybridization among subfamilies of Caprifoliaceae, which seems to be the main source of phylogenetic discordance. Ancestral state reconstruction of six morphological characters revealed some homoplasy for each character examined. By dating the branching events, we inferred the origin of Caprifoliaceae at approximately 66.65 Ma in the late Cretaceous. By integrating evidence from molecular phylogeny, divergence times, and morphology, we herein recognize Zabelioideae as a new subfamily in Caprifoliaceae. This work shows the necessity of using a combination of multiple approaches to identify the sources of gene tree discordance. Our study also highlights the importance of using data from both nuclear and chloroplast genomes to reconstruct deep and shallow phylogenies of plants.

Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating cerebrovascular disease with high mortality and morbidity. In recent years, a large number of studies have focused on the mechanism of early brain injury (EBI) and delayed cerebral ischemia (DCI), including vasospasm, neurotoxicity of hematoma and neuroinflammatory storm, after aSAH. Despite considerable efforts, no novel drugs have significantly improved the prognosis of patients in phase III clinical trials, indicating the need to further re-examine the multifactorial pathophysiological process that occurs after aSAH. The complex pathogenesis is reflected by the destruction of the dynamic balance of the energy metabolism in the nervous system after aSAH, which prevents the maintenance of normal neural function. This review focuses on the fluid metabolic pathways of the central nervous system (CNS), starting with ruptured aneurysms, and discusses the dysfunction of blood circulation, cerebrospinal fluid (CSF) circulation and the glymphatic system during disease progression. It also proposes a hypothesis on the metabolic disorder mechanism and potential therapeutic targets for aSAH patients. Cover Image for this issue: https://doi.org/10.1111/jnc.15384.

Growth hormone receptor (GHR), the cognate receptor of growth hormone (GH), is a membrane bound receptor that belongs to the class I cytokine receptor superfamily. GH binding GHR induces cell differentiation and maturation, initiates the anabolism inside the cells and promotes cell proliferation. Recently, GHR has been reported to be associated with various types of cancer. However, the underlying mechanism of GHR in gastric cancer has not been defined. Our results showed that silence of GHR inhibited the growth of SGC‐7901 and MGC‐803 cells, and tumour development in mouse xenograft model. Flow cytometry showed that GHR knockout significantly stimulated gastric cancer cell apoptosis and caused G1 cell cycle arrest, which was also verified by Western blot that GHR deficiency induced the protein level of cleaved‐PARP, a valuable marker of apoptosis. In addition, GHR deficiency inhibited the activation of PI3K/AKT signalling pathway. On the basis of the results, that GHR regulates gastric cancer cell growth and apoptosis through controlling G1 cell cycle progression via mediating PI3K/AKT signalling pathway. These findings provide a novel understanding for the role of GHR in gastric cancer.

Dexmedetomidine (Dex) possesses analgesic and anaesthetic values and reported being used in cerebral ischaemic injury therapeutics. Accumulating studies have determined the effect of microRNAs (miRNAs) on the cerebral ischaemic injury. Thus, the present study aimed to unravel the molecular mechanism of miR‐381 and Dex in cerebral ischaemic injury. For this purpose, the cerebral ischaemic injury rat model was established by induction of middle cerebral artery occlusion (MCAO) and expression of miR‐381 and IRF4 was determined. Thereafter, MCAO rats were treated with Dex, miR‐381 mimic, miR‐381 inhibitor and oe‐IRF4 respectively, followed by evaluation of neurological function. Furthermore, neuron cells were isolated from the hippocampus of rats and subjected to oxygen‐glucose deprivation (OGD). Then, OGD‐treated neuron cells and primary neuron cells were examined by gain‐ and loss‐of‐function assay. Neuron cell apoptosis was detected using TUNEL staining and flow cytometry. The correlation between interferon regulatory factor 4 (IRF4) and interleukin (IL)‐9 was detected. Our results showed down‐regulated miR‐38 and up‐regulated IRF4 in MCAO rats. Besides, IRF4 was targeted by miR‐381 in neuron cells. Dex and overexpressed miR‐381, or silenced IRF4 improved the neurological function and inhibited neuron cell apoptosis in MCAO rats. Additionally, in MCAO rats, Dex was found to increase the miR‐381 expression and reduced IRF4 expression to decrease the IL‐9 expression, which suppressed the inflammatory response and cell apoptosis both in vivo and in vitro. Importantly, our study demonstrated that Dex elevated the expression of miR‐381, which ultimately results in the inhibition of inflammation response in rats with cerebral ischaemic injury.

Background The purpose of this study was to analyze the clinical characteristics and prognostic survival of patients with neuroendocrine tumors of the thymus (NETTs), and to develop and validate a nomogram model for predicting the prognosis of patients. Methods We conducted a retrospective analysis of patients with neuroendocrine tumors of the thymus in the Surveillance, Epidemiology, and End Results (SEER) database in the United States between 1988 and 2016. Cox scale risk regression analysis, the Kaplan‐Meier method and log‐rank test were used to carry out the significance test to determine the independent prognostic factors, from which a nomogram for NETTs was established. C‐index and calibration curve were used to evaluate the prediction accuracy of the model. External validation of the nomogram was performed using data from our center. Results A total of 254 patients with NETTs were collected in the SEER database. In the multivariable analysis, T stage, tumor grade, surgery, and chemotherapy were found to be independent factors affecting the prognosis of patients (all P, The neuroendocrine tumors of the thymus is a rare invasive tumor with a poor prognosis, and visualization models are needed to provide patients with appropriate individualized treatment strategies.In this study, we established and validated a new Nomogram model to predict the survival of patients with neuroendocrine tumors of the thymus.

Cell death after spinal cord ischemia/reperfusion (I/R) can occur through necrosis, apoptosis, and autophagy, resulting in changes to the immune environment. However, the molecular mechanism of this immune regulation is not clear. Accumulating evidence indicates that microRNAs (miRs) play a crucial role in the pathogenesis of spinal cord I/R injury. Here, we hypothesized miR-22-3p may be involved in spinal cord I/R injury by interacting with interferon regulatory factor (IRF) 5. Rat models of spinal cord I/R injury were established by 12-min occlusion of the aortic arch followed by 48-hr reperfusion, with L4-6 segments of spinal cord tissues collected. MiR-22-3p agomir, a lentivirus-delivered siRNA specific for IRF5, or a lentivirus expressing wild-type IRF5 was injected intrathecally to rats with I/R injury to evaluate the effects of miR-22-3p and IRF5 on hindlimb motor function. Macrophages isolated from rats were treated with miR-22-3p mimic or siRNA specific for IRF5 to evaluate their effects on macrophage polarization. The levels of IL-1β and TNF-α in spinal cord tissues were detected by ELISA. miR-22-3p was down-regulated, whereas IRF5 was up-regulated in rat spinal cord tissues following I/R. IRF5 was a target gene of miR-22-3p and could be negatively regulated by miR-22-3p. Silencing IRF5 or over-expressing miR-22-3p relieved inflammation, elevated Tarlov score, and reduced the degree of severity of spinal cord I/R injury. Increased miR-22-3p facilitated M2 polarization of macrophages and inhibited inflammation in tissues by inhibiting IRF5, thereby attenuating spinal cord I/R injury. Taken together, these results demonstrate that increased miR-22-3p can inhibit the progression of spinal cord I/R injury by repressing IRF5 in macrophages, highlighting the discovery of a promising new target for spinal cord I/R injury treatment.

Nowadays, the pathogenesis of minimal change disease (MCD) is still not well‐known, and the current understanding on MCD is mainly based on data derived from children, and very few adults. Here, we comprehensively analysed the correlation between the changes of peripheral basophils and the incidence rate and relapse of adult‐onset MCD. The results showed that in patients at the onset of MCD, the ratio and activation of basophils were all higher than those of healthy controls (all P

Understanding the causes of the Sino‐Japanese disjunctions in plant taxa has been a central question in eastern Asian biogeography, with vicariance or long‐distance dispersal often invoked to explain such patterns. Diabelia Landrein (Caprifoliaceae; Linnaeoideae) comprises four shrubby species with a Sino‐Japanese disjunct distribution. The species diversification time within Diabelia, covering a long geological history of the formation process of the Sino‐Japanese flora, dated back to the middle Oligocene, therefore, Diabelia would be an ideal model to elucidate the biogeographic patterns of Sino‐Japanese disjunctions with climate fluctuation. In this study, we analyzed complete plastome sequence data for 28 individuals representing all four species of Diabelia. These 28 plastomes were found to be highly similar in overall size (156 243–157 578 bp), structure, gene order, and content. Our phylogenomic analysis of the plastomes supported a close relationship between Diabelia ionostachya (Nakai) Landrein & R.L. Barrett var. wenzhouensis (S.L. Zhou ex Landrein) Landrein from eastern China and Diabelia spathulata (Siebold & Zucc.) Landrein var. spathulata from Japan. Diabelia serrata (Siebold & Zucc.) Landrein was identified as sister to a population of Diabelia sanguinea (Makino) Landrein from Tochigi in central Japan and D. spathulata Landrein, from Toyama, central Japan. Most Diabelia lineages were estimated to have differentiated 8–28 Mya. Our results indicate that two independent vicariance events could explain the disjunction between Japan and Korea in the mid to late Miocene, and between Zhejiang and Japan in the early Miocene.

Motivation: Assessing biodiversity status and trends in plant communities is critical for understanding, quantifying and predicting the effects of global change on ecosystems. Vegetation plots record the occurrence or abundance of all plant species co-occurring within delimited local areas. This allows species absences to be inferred, information seldom provided by existing global plant datasets. Although many vegetation plots have been recorded, most are not available to the global research community. A recent initiative, called ‘sPlot’, compiled the first global vegetation plot database, and continues to grow and curate it. The sPlot database, however, is extremely unbalanced spatially and environmentally, and is not open-access. Here, we address both these issues by (a) resampling the vegetation plots using several environmental variables as sampling strata and (b) securing permission from data holders of 105 local-to-regional datasets to openly release data. We thus present sPlotOpen, the largest open-access dataset of vegetation plots ever released. sPlotOpen can be used to explore global diversity at the plant community level, as ground truth data in remote sensing applications, or as a baseline for biodiversity monitoring. Main types of variable contained: Vegetation plots (n=95,104) recording cover or abundance of naturally co-occurring vascular plant species within delimited areas. sPlotOpen contains three partially overlapping resampled datasets (c.50,000 plots each), to be used as replicates in global analyses. Besides geographical location, date, plot size, biome, elevation, slope, aspect, vegetation type, naturalness, coverage of various vegetation layers, and source dataset, plot-level data also include community-weighted means and variances of 18 plant functional traits from the TRY Plant Trait Database. Spatial location and grain: Global, 0.01–40,000m². Time period and grain: 1888–2015, recording dates. Major taxa and level of measurement: 42,677 vascular plant taxa, plot-level records. Software format: Three main matrices (.csv), relationally linked.

The predilection site of intracerebral hemorrhage (ICH) is in the basal ganglia, which is rich in white matter (WM) fiber bundles, such as cerebrospinal tract in the internal capsule. ICH induced damage to this area can easily lead to severe neurological dysfunction and affects the prognosis and quality of life of patients. At present, the pathophysiological mechanisms of white matter injury (WMI) after ICH have attracted researchers' attention, but studies on the repair and recovery mechanisms and therapy strategies remain rare. In this review, we mainly summarized the WM recovery and treatment strategies after ICH by updating the WMI‐related content by reviewing the latest researches and proposing the bottleneck of the current research.

Phylogenetic relationships in Dipsacales have long been a major challenge. Although considerable progress has been made during the past two decades, questions remain; the uncertain systematic positions of Heptacodium, Triplostegia, and Zabelia, in particular, impede our understanding of Dipsacales evolution. Here we use 75 complete plastomic sequences to reconstruct the phylogeny of Dipsacales, of which 28 were newly generated. Two primary clades were recovered that form the phylogenetic backbone of Dipsacales. Seven of the primary clades correspond to the recognized families Adoxaceae, Caprifoliaceae s. str., Diervillaceae, Dipsacaceae, Linnaeaceae, Morinaceae, and Valerianaceae, and one corresponds to Zabelia, which was found to be the closest relative of Morinaceae in all analyses. Additionally, our results, with greatly increased confidence in most branches, show that Heptacodium and Triplostegia are members of Caprifoliaceae s. str. and Dipsacaceae, respectively. The results of our study indicate that the complete plastomic sequences provide a fully-resolved and well-supported representation of the phylogenetic relationships within Dipsacales.

Objectives The arthroscopic “lateral gutter drive‐through” (LGDT) sign is reported to diagnose popliteus tendon (PT) injury with high sensitivity and specificity. However, no study has provided a postoperative evaluation of combined posterior cruciate ligament (PCL) and posterolateral corner (PLC) injuries using the LGDT test. Methods From January 2012 to January 2015, a total of 80 consecutive patients who underwent combined PCL reconstruction and PLC surgeries were identified. Fifty eligible patients were included in this study for evaluation with subjective scoring systems, physical examinations, posterior and varus stress radiographs, and second‐look arthroscopic surgeries during hardware removal operation. Results Forty‐nine patients were available for a mean of 31.5 ± 9.3 months follow‐up (range, 24.0–81.0 months). In terms of PLC injury pattern, there were 27 type A, 10 type B, and 12 type C patients, with 21 acute cases and 28 chronic cases. At the final follow‐up, subjective scores were all significantly improved. The side‐to‐side difference (SSD) of posterior tibial translation (PTT) improved from 18.4 ± 9.2 mm (range, 12.9–25.6 mm) to 5.2 ± 5.0 mm (range, −5.0−18.5 mm, P

In the present study, PeSTZ1, a cysteine-2/histidine-2-type zinc finger transcription factor, was isolated from the desert poplar, Populus euphratica, which serves as a model stress adaptation system for trees. PeSTZ1 was preferentially expressed in the young stems and was significantly up-regulated during chilling and freezing treatments. PeSTZ1 was localized to the nucleus and bound specifically to the PeAPX2 promoter. To examine the potential functions of PeSTZ1, we overexpressed it in poplar 84K hybrids (Populus alba × Populus glandulosa), which are known to be stress-sensitive. Upon exposure to freezing stress, transgenic poplars maintained higher photosynthetic activity and dissipated more excess light energy (in the form of heat) than wild-type poplars. Thus, PeSTZ1 functions as a transcription activator to enhance freezing tolerance without sacrificing growth. Under freezing stress, PeSTZ1 acts upstream of ASCORBATE PEROXIDASE2 (PeAPX2) and directly regulates its expression by binding to its promoter. Activated PeAPX2 promotes cytosolic APX that scavenges reactive oxygen species (ROS) under cold stress. PeSTZ1 may operate in parallel with C-REPEAT-BINDING FACTORS to regulate COLD-REGULATED gene expression. Moreover, PeSTZ1 up-regulation reduces malondialdehyde and ROS accumulation by activating the antioxidant system. Taken together, these results suggested that overexpressing PeSTZ1 in 84K poplar enhances freezing tolerance through the modulation of ROS scavenging via the direct regulation of PeAPX2 expression.

Neural stem/progenitor cells (NSPCs) are a promising candidate for the cell-replacement therapy after central nervous system (CNS) injury. However, the short of sufficient NSPCs migration and integration into the lesions is an essential challenge for cell-based therapy after CNS injury due to the disturbance of local environmental homeostasis. Chondroitin sulfate proteoglycan (CSPG) is obviously accumulated at the lesions and destroyed local homeostasis after CNS injury. The previous study has demonstrated that the CSPG is a dominating ingredient inhibiting axonal regrowth of newly born neurons after CNS injury. NSPCs, a strain of special neural subtypes, hold the capacity of leading processes formation to regulate NSPCs migration, which has the same mechanism as axonal regrowth. Hence, it is worth investigating the effect of CSPG on NSPCs migration and its underlying mechanism. Here, different concentration of CSPG was used to evaluate its effect on NSPCs migration. The results showed that the CSPG suppressed NSPCs migration in a dose-dependent manner from 10 to 80 µg/mL with phase-contrast microscopy after 24 hours. Meanwhile, transwell assays were performed to certify the above results. Our data indicated that the 40 µg/mL CSPG obviously suppressed NSPCs migration via decreasing filopodia formation using immunofluorescence staining. Furthermore, data indicated that the 40 µg/mL CSPG upregulated protein tyrosine phosphatase receptor σ (PTPσ) expression and decreased α-actinin4 (ACTN4) expression through immunofluorescence, reverse transcription polymerase chain reaction, and Western blot assays. While the inhibitory effect was attenuated using PTPσ-specific small interfering RNA. In addition, data demonstrated that the 40 µg/mL CSPG facilitated NSPCs differentiation into glial fibrillary acidic protein-positive cells and inhibited NSPCs directing into MAP2- and MBP-positive cells. Collectively, these data demonstrated that the CSPG suppressed NSPCs migration through PTPσ/ACTN4 signaling pathway. Meanwhile, CSPG facilitated NSPCs differentiation into astrocytes and inhibited NSPCs directing into neurons and oligodendrocytes.

Long noncoding RNA (lncRNA) LINC-PINT expression is inhibited in many types of cancer cells, suggesting its role as a tumor suppressor. However, the functionality of LINC-PINT in gastric cancer and the clinical values are unknown. In the present study, we found that lncRNA LINC-PINT was downregulated, while microRNA-21 (miR-21) was upregulated in tumor tissues than in adjacent healthy tissues of gastric cancer patients. A significant and inverse correlation between expression levels of lncRNA LINC-PINT and miR-21 was found in both tumor tissues and adjacent healthy tissues. The low expression level of LINC-PINT and high expression level of the miR-21 tumor were correlated with poor prognosis. LINC-PINT overexpression casued miR-21 inhibition in cells of human gastric cancer cell lines, while miR-21 overexpression did not alter LINC-PINT expression. LINC-PINT overexpression led to inhibited, while miR-21 overexpression led to promoted proliferation, migration, and invasion of gastric cancer cells. Effects of LINC-PINT overexpression on cellular behaviors of gastric cancer cells were attenuated by miR-21 overexpression. Therefore, LINC-PINT may participate in gastric cancer through the crosstalk with miR-21.