Comparison of multiple treatments in the management of transplant-related thrombotic microangiopathy: a network meta-analysis.

Hematopoietic stem cell transplantation-associated thrombotic microangiopathy (TA-TMA) is a fatal post-transplant complication. It has a high mortality rate and worse prognosis, but treatment strategies remain controversial. We screened 6 out of 3453 studies on the treatment of TA-TMA. These investigations compared 5 treatment strategies with a network meta-analysis approach. The final outcome was the proportion of patients who responded to these therapies. There were significant differences in response rates for each treatment. Achieving analysis through direct and indirect evidence in the rank probabilities shows that rTM (recombinant human soluble thrombomodulin) is most likely to be rank 1 (64.98%), Eculizumab intervention rank 2 (48.66%), ISM (immunosuppression manipulation) rank 3 (32.24%), TPE (therapeutic plasma exchange) intervention rank 4 (69.56%), and supportive care intervention rank 5 (70.20%). Eculizumab and ISM have significantly higher efficacy than supportive care (odds ratio (OR): 18.04, 18.21 respectively); and TPE having lower efficacy than all other TA-TMA therapies exception to supportive care. In our study, rTM and Eculizumab may be the best choice when treating TA-TMA.

Peptide YY inhibits transcription and replication of hepatitis B virus by suppressing promoter/enhancer activity.

Hepatitis B virus (HBV) infection is a noteworthy cause of liver diseases, especially cirrhosis and hepatocellular carcinomas. However, the interaction between the host and HBV has not been fully elucidated. Peptide YY (PYY) is a 36-amino-acid gastrointestinal hormone that is mainly involved in the regulation of the human digestive system. This study found that PYY expression was reduced in HBV-expressing hepatocytes and HBV patients. Overexpression of PYY could significantly inhibit HBV RNA, DNA levels, and the secretion of HBsAg. In addition, PYY inhibits HBV RNA dependent on transcription through reducing the activities of CP/Enh I/II, SP1 and SP2. Meanwhile, PYY blocks HBV replication independent on core, polymerase protein and ε structure of pregenomic RNA. These results suggest that PYY can impair HBV replication by suppressing viral promoters/enhancers in hepatocytes. Our data shed light on a novel role for PYY as anti-HBV restriction factor.

Exploration of risk factors of platelet transfusion refractoriness and its impact on the prognosis of hematopoietic stem cell transplantation: a retrospective study of patients with hematological diseases.

Platelet transfusion refractoriness (PTR) is an intractable issue in hematological patients, which increases bleeding risks and hospitalization costs to a great extent. We reviewed 108 patients with hematological diseases including acute leukemia, myelodysplastic syndrome, aplastic anemia, and others who received allogeneic hematopoietic stem cell transplantation (HSCT) from January 2019 through December 2020. After multivariable logistic regression, we found that splenomegaly (odds ratio [OR] = 26.98, p < .001) and JAK mutation (OR = 17.32, p = .024) were independent risk factors for PTR. During the period of transplantation, patients in the PTR group had a significantly higher platelet transfusion demand, which was reflected in the increased number of platelet transfusions (10.23 ± 6.696 vs. 5.06 ± 1.904, p < .001). After multivariate adjustment, PTR turned out to be independently associated with worse overall survival (hazard ratio = 2.794, 95% confidence interval = 1.083-7.207, p = .034). In conclusion, we found that splenomegaly and JAK gene mutation were independent risk factors for PTR in patients with hematological diseases. A history of PTR prior to allo-HSCT indicates a poor prognosis.

What is the context?Platelet transfusion refractoriness is a critical issue, and it greatly increases bleeding risks and hospitalization costs.Patients with hematological diseases tend to develop PTR.PTR results from immune and nonimmune factors and the latter account for 80­90%.At present, there are few studies focused on the inducing factors of PTR, and the specific mechanism is not clear.What is new?In this study, we investigated 108 patients with hematological disorders who received allogeneic HSCT from January 2019 to December 2020.We found that splenomegaly and JAK gene mutation were independent risk factors for PTR in patients with hematological diseases.PTR had a passive effect on the prognosis of patients after HSCT, as indicated by worse OS and a trend toward lower platelets after transplantation.PTR might affect megakaryocyte reconstitution after transplantation.What is the impact?This study provides evidence that hematological patients with splenomegaly should be alert to the occurrence of PTR, which often indicates a worse prognosis of transplantation.Spleen reduction and JAK inhibitors in the treatment of PTR are worth exploring.AbbreviationsPLT: platelets; PTR: platelet transfusion refractoriness; HSCT: hematopoietic stem cell transplantation; OR: odds ratio; HR: hazard ratio; CI: confidence interval; IQR: interquartile range; SD: standard deviation; HLA: human leukocyte antigen; HPA: human platelet antigen; OS: overall survival; RFS: relapse free survival; PI: post-transfusion increment; PPR: percentage platelet recovery; CCI: corrected count increment; ICU: intensive care unit; AA: aplastic anemia; MDS: myelodysplastic syndrome; AML: acute myeloid leukemia; ALL: acute lymphocytic leukemia; CML: chronic myeloid leukemia; CMML: chronic myelomonocytic leukemia; MPN: myeloproliferative neoplasm; SI: splenic irradiation; Abs: antibodies; CR: complete remission; DAC: decitabine; GVHD: graft-versus-host disease; BM: bone marrow; PB: peripheral blood.

Serum levels of galactose-deficient IgA1 in Chinese children with IgA nephropathy, IgA vasculitis with nephritis, and IgA vasculitis.

OBJECTIVE: IgA nephropathy (IgAN) and IgA vasculitis with nephritis (IgAV-N) are related diseases. Galactose-deficient IgA1 (Gd-IgA1) plays an important role in the pathology of IgAV-N and IgAN, so we aim to compare the serum levels of Gd-IgA1 in Chinese pediatric patients with IgAN, IgAV-N, and IgAV. METHODS: We retrospectively enrolled 52 patients with IgAN, 57 patients with IgAV-N, 26 patients with IgAV, and 40 healthy children. The serum levels of Gd-IgA1 were measured at the time of biopsy using a lectin-based ELISA method. RESULTS: Gd-IgA1 levels in IgAV-N patients and IgAN patients were higher than in healthy controls (303.94 ± 39.37 U/ml, 314.91 ± 47.79 U/ml vs. 273.57 ± 48.29 U/ml, P < 0.001), and Gd-IgA1 levels in IgAV-N patients were higher than in IgAV patients (303.94 ± 39/ml vs. 286. 21 ± 38.81 U/ml, P = 0.059), but the latter result is not statistically significant. The Gd-IgA1 levels in IgAV patients were comparable with those in healthy controls (286.21 ± 38.81 U/ml vs. 273.57 ± 48.29 U/ml, P = 0.267). Among the four groups, we did not observe significant correlations of Gd-IgA1 levels with eGFR, proteinuria, or the MEST-C score. CONCLUSION: Serum Gd-IgA1 maybe involved in the pathogenesis of the IgAV-N and IgAN. However, we found no statistically significant correlation between Gd-IgA1 levels and clinical and pathological features.

Mesangial C3 deposition and serum C3 levels predict renal outcome in IgA nephropathy.

BACKGROUND: Complement activation plays an important role in the pathogenesis of IgA nephropathy (IgAN). We aimed to evaluate the relationship between mesangial C3 deposition and histologic lesions and to investigate the role of mesangial C3 deposition and serum C3 reduction in predicting renal outcome in IgAN children. METHODS: We performed a retrospective cohort study in children with biopsy-proven IgAN. Mesangial C3 deposition (< 2+ vs. ≥ 2+) was detected by the immunofluorescence. Histopathologic kidney grades were determined by the Oxford classification. A decreased serum C3 concentration (hypoC3) was defined when C3 < 90 mg/dl. The endpoint was composite kidney outcome with either a 30% decline in glomerular filtration rates from baseline or kidney failure during the follow-up period. RESULTS: A total of 98 children were analyzed. Mesangial hypercellularity (M) was an independent factor associated with mesangial C3 deposition (HR 3.267; 95% CI 1.028-10.389; P = 0.045). After a median follow-up period of 25 months (interquartile range 18-36 months), 6 (6.1%) children reached the endpoint. Compared with other children, a significantly higher proportion of children with composite kidney outcomes had mesangial C3 deposition ≥ 2+ and hypoC3 (3.4% versus 27.3%, P = 0.002). After adjustment for clinicopathologic risk factors, mesangial C3 deposition ≥ 2+ and hypoC3 were associated with renal outcome (HR 9.772; 95% CI 1.264-75.518; P = 0.029). CONCLUSION: Mesangial C3 deposition was associated with M in IgAN. Mesangial C3 deposition and hypoC3 were risk factors for renal outcome in children with IgAN.

Optical Excitation of a Nanoparticle Cu/p-NiO Photocathode Improves Reaction Selectivity for CO2 Reduction in Aqueous Electrolytes.

We report the light-induced modification of catalytic selectivity for photoelectrochemical CO2 reduction in aqueous media using copper (Cu) nanoparticles dispersed onto p-type nickel oxide (p-NiO) photocathodes. Optical excitation of Cu nanoparticles generates hot electrons available for driving CO2 reduction on the Cu surface, while charge separation is accomplished by hot-hole injection from the Cu nanoparticles into the underlying p-NiO support. Photoelectrochemical studies demonstrate that optical excitation of plasmonic Cu/p-NiO photocathodes imparts increased selectivity for CO2 reduction over hydrogen evolution in aqueous electrolytes. Specifically, we observed that plasmon-driven CO2 reduction increased the production of carbon monoxide and formate, while simultaneously reducing the evolution of hydrogen. Our results demonstrate an optical route toward steering the selectivity of artificial photosynthetic systems with plasmon-driven photocathodes for photoelectrochemical CO2 reduction in aqueous media.

Chitin/MoS2 Nanosheet Dielectric Composite Films with Significantly Enhanced Discharge Energy Density and Efficiency.

High-performance dielectric nanomaterials have received increasing attention due to their important applications in the field of energy storage. Among various dielectric materials, polymer nanocomposite is one of the most promising candidates. However, the problems of environmental pollution caused by polymer-based dielectric materials have been extensively studied in recent years, which need to be solved urgently, leading to the search for new biodegradable dielectric materials. Herein, we report composite materials based on biodegradable and renewable chitin and molybdenum disulfide (MoS2) nanosheets for the first time. The MoS2 nanosheets were first fabricated by glycerol/urea system and then KOH/urea aqueous solution was used to directly dissolve chitin at low temperature together with the dispersion of the MoS2 nanosheets in a simple green process. The two-dimensional MoS2 nanosheets possess high polarization strength, and a large specific surface area can enhance the interfacial polarization with chitin; meanwhile, it can serve as a charge breakdown barrier to hinder the propagation of electrical tree branches. The results also show that the dielectric constant and breakdown strength of the chitin/MoS2 nanocomposites were increased, while the dielectric loss remained low. When the MoS2 content was 5 wt %, the charge and discharge efficiencies of the composite film were more than 80%, and the breakdown strength also reached 350 MV m-1, thus resulting in a high discharge energy density of 4.91 J cm-3, which was more than twice of the neat chitin (2.17 J cm-3). Furthermore, the nanocomposite films exhibited good thermal stability. Therefore, these chitin-based nanocomposite films are promising as high-performance biomass-based dielectric capacitors.

Light-Induced Thermal Gradients in Ruthenium Catalysts Significantly Enhance Ammonia Production.

Industrial scale catalytic chemical synthesis demands both high reaction rates and high product yields. In exothermic chemical reactions, these conflicting objectives require a complex balance of optimized catalysts, high temperatures, high pressures, and multiple recycling steps, as in the energy-intensive Haber-Bosch process for ammonia synthesis. Here we report that illumination of a conventional ruthenium-based catalyst produces ammonia with high reaction rates and high conversion yields. Indeed, using continuous wave light-emitting diodes that simulate concentrated solar illumination, ammonia is copiously produced without any external heating or elevated pressures. The possibility of nonthermal plasmonic effects are excluded by carefully comparing the catalytic activity under direct and indirect illumination. Instead, thermal gradients, created and controlled by photothermal heating of the illuminated catalyst surface, are shown to be responsible for the high reaction rates and conversion yields. This nonisothermal environment enhances both by balancing the conflicting requirements of kinetics and thermodynamics, heralding the use of optically controlled thermal gradients as a universal, scalable strategy for the catalysis of many exothermic chemical reactions.

Antidepressant Effects of Rhodomyrtone in Mice with Chronic Unpredictable Mild Stress-Induced Depression.

Background: Rhodomyrtone is one of the main active compounds derived from Rhodomyrtus tomentosa, which belongs to the Myrtaceae family. In the current study, we investigated the properties of rhodomyrtone as a potential drug candidate for the treatment of stress-caused depression. Methods: We assessed the function of rhodomyrtone in chronic unpredictable mild stress, a well-validated depression model in mice. Depression-like behavior tests, including a sucrose performance test, social interaction test, and forced swimming test, were used to validate the antidepressant effects of rhodomyrtone. The Morris water maze was used to evaluate the mice's learning and memory ability. Spine density, glycogen synthase kinase-3ß, brain-derived neurotrophic factor, postsynaptic density protein 95, and apoptosis-associated protein were detected to reveal the underlying mechanism. Results: Rhodomyrtone was found to prevent source consumption decrease, decreased social behaviors, and increase immobility in the forced swimming test, suggesting a protective effect of rhodomyrtone against depression-like behaviors. Additionally, rhodomyrtone prevented the impairment of spatial memory in mice exposed to chronic unpredictable mild stress. Rhodomyrtone administration also reversed dendritic spine density defects in chronic unpredictable mild stress. Furthermore, rhodomyrtone inhibited the increase of glycogen synthase kinase-3ß activity and reversed the decrease of brain-derived neurotrophic factor and postsynaptic density protein 95 in chronic unpredictable mild stress mice. Elevated expression of apoptosis-associated protein Bax and cleaved-caspase 3 was also reversed by rhodomyrtone treatment. Conclusions: These results suggested that the antidepressant effect of rhodomyrtone involves the regulation of neurogenesis, neuronal survival, and synaptic plasticity in the hippocampus.

A clinicopathological comparison between IgA nephropathy and Henoch-Schönlein purpura nephritis in children: use of the Oxford classification.

BACKGROUND: There is controversy over whether IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis (HSPN) are the same diseases. This study focuses on the clinicopathological comparison between HSPN and IgAN in children. METHODS: Children with IgAN and HSPN who had a diagnostic renal biopsy were enrolled. This study collected the clinical data of patients at biopsy, re-evaluated the pathological lesions of patients according to the Oxford Classification (MEST-C), and made a retrospective comparison between IgAN and HSPN on different stratifications of the course (Tc) and proteinuria. RESULTS: A total of 142 children with IgAN and 57 children with HSPN were enrolled. Various stratification showed the same result, which suggested that IgAN showed more mesangial proliferation (M). HSPN showed more segmental glomerulosclerosis in the Tc > 12 m group than IgAN (S 60.0% vs. 9.10%, P = 0.008). In the non-nephrotic-range and nephrotic-range proteinuria group, there were no significant differences in MEST-C scores between IgAN and HSPN. CONCLUSION: M is more common in IgAN. HSPN had more S than IgAN over the course of more than 12 months. These results indicate the differences in the pathogenesis in IgAN and HSPN. We propose early biopsy and active treatment of HSPN within 12 months to delay the development of chronic lesions.

Plasmon-Enhanced Catalysis: Distinguishing Thermal and Nonthermal Effects.

In plasmon-enhanced heterogeneous catalysis, illumination accelerates reaction rates by generating hot carriers and hot surfaces in the constituent nanostructured metals. In order to understand how photogenerated carriers enhance the nonthermal reaction rate, the effects of photothermal heating and thermal gradients in the catalyst bed must be confidently and quantitatively characterized. This is a challenging task considering the conflating effects of light absorption, heat transport, and reaction energetics. Here, we introduce a methodology to distinguish the thermal and nonthermal contributions from plasmon-enhanced catalysts, demonstrated by illuminated rhodium nanoparticles on oxide supports to catalyze the CO2 methanation reaction. By simultaneously measuring the total reaction rate and the temperature gradient of the catalyst bed, the effective thermal reaction rate may be extracted. The residual nonthermal rate of the plasmon-enhanced reaction is found to grow with a superlinear dependence on illumination intensity, and its apparent quantum efficiency reaches ∼46% on a Rh/TiO2 catalyst at a surface temperature of 350 °C. Heat and light are shown to work synergistically in these reactions: the higher the temperature, the higher the overall nonthermal efficiency in plasmon-enhanced catalysis.

The septin protein Sep4 facilitates host infection by plant fungal pathogens via mediating initiation of infection structure formation.

Many phytopathogenic fungi use infection structures (IFSs, i.e., appressoria and infection cushions) to penetrate host cuticles. However, the conserved mechanisms that mediate initiation of IFS formation in divergent pathogens upon sensing the presence of host plants remain obscure. Here, we demonstrate that a conserved septin gene SEP4 plays crucial roles in this process. Disruption of SEP4 in the plant grey mould fungus Botrytis cinerea completely blocked IFS formation and abolished the virulence of ΔBcsep4 mutants on unwounded hosts. During IFS formation, mutants lacking SEP4 could produce reactive oxygen species (ROS) normally. Inhibition of ROS production in strains harbouring the SEP4 gene resulted in disordered assembly of Sep4 and the subsequent failure to form infection cushions, suggesting that proper Sep4 assembly regulated by ROS is required for initiation of IFS formation and infection. Moreover, loss of SEP4 severely impaired mutant conidiation, melanin and chitin accumulation in hyphal tips and lesion expansion on wounded hosts, but significantly promoted germ tube elongation and sclerotium production. SEP4-mediated fungal pathogenic development, including IFS formation, was validated in the hemibiotroph Magnaporthe oryzae. Our findings indicate that Sep4 plays pleiotropic roles in B. cinerea development and specifically facilities host infection by mediating initiation of IFS formation in divergent plant fungal pathogens in response to ROS signaling.

Granulocyte-macrophage colony-stimulating factor increases tumor growth and angiogenesis directly by promoting endothelial cell function and indirectly by enhancing the mobilization and recruitment of proangiogenic granulocytes.

Granulocyte-macrophage colony-stimulating factor has been widely used as an adjuvant therapy for cancer patients exhibiting myelosuppression induced by chemotherapy or radiotherapy. However, the effects of granulocyte-macrophage colony-stimulating factor on tumor growth, as well as its precise mechanism, are still controversial due to inconsistent evidence. This study investigated the effect of exogenous granulocyte-macrophage colony-stimulating factor on the growth of B16 melanoma, S180 sarcoma, and U14 cervical carcinoma in mice. The angiogenesis and recruitment of bone-marrow-derived cells were analyzed in tumor tissues. Interactions among granulocyte-macrophage colony-stimulating factor, bone-marrow-derived cells, and B16 tumor cells were investigated in vitro. Proangiogenic types of bone-marrow-derived cells in blood were assessed both in vivo and in vitro. The results showed that granulocyte-macrophage colony-stimulating factor markedly facilitated the growth of B16 and S180 tumors, but not U14 tumors. Granulocyte-macrophage colony-stimulating factor increased the densities of blood vessels and the number of bone-marrow-derived cells in B16 tumor tissues. The granulocyte-macrophage colony-stimulating factor-induced enhancement of tumor cell proliferation was mediated by bone-marrow-derived cells in vitro. Meanwhile, a distinct synergistic effect on endothelial cell function between granulocyte-macrophage colony-stimulating factor and bone-marrow-derived cells was observed. After separating two types of bone-marrow-derived cells, granulocyte-macrophage colony-stimulating factor-induced enhancement of tumor growth and angiogenesis in vivo was mediated by proangiogenic cells in granulocytes, but not monocytes, with CD11b+, vascular endothelial growth factor receptor 2, and C-X-C chemokine receptor 4 granulocytes possibly involved. These data suggest that granulocyte-macrophage colony-stimulating factor contributes to the growth and angiogenesis of certain types of tumor, and these mechanisms are probably mediated by proangiogenic cells in granulocytes. Applying granulocyte-macrophage colony-stimulating factor may attenuate the antitumor effects of chemotherapy and radiotherapy in certain types of tumor.

Identifying Exotic Hidden-Charm Pentaquarks.

The LHCb Collaboration at the Large Hadron Collider at CERN discovered two pentaquark states P_{c}(4380) and P_{c}(4450). These two hidden-charm states are interpreted as the loosely bound Σ_{c}(2455)D^{*} and Σ_{c}^{*}(2520)D^{*} molecular states in the boson exchange interaction model, which provides an explanation for why the experimental width of P_{c}(4450) is much narrower than that of P_{c}(4380). The discovery of the new resonances P_{c}(4380) and P_{c}(4450), indeed, opens a new page for hadron physics. The partners of P_{c}(4380) and P_{c}(4450) should be pursued in future experiments.

[Genetic analysis and identification of candidate genes for a narrow leaf mutant (zy17) in rice].

Control of organ size by cell proliferation and cell expansion is a fundamental process in plant development, but little is known about the genetic and molecular mechanisms that determine organ size in plants. To understand the genetic and molecular mechanisms of organ growth control, we isolate a set of mutants with altered leaf size and identify the narrow leaf mutant, zhaiye 17 (zy17) (zhaiye means narrow leaf in Chinese). zy17 exhibits narrow leaves, slightly short plants, small panicles, reduced panicle branches and decreased grain numbers per panicle compared with the wild type. Our cytological analyses show that the narrow leaf phenotype of zy17 is caused by the reduced number of cells, indicating that ZY17 regulates cell proliferation. Genetic analyses show that the zy17 mutant phenotypes are controlled by a single gene. Using the whole genome resequencing approach and linkage analysis, we identify Os02g22390, Os02g28280 and Os02g29530 as candidate genes. Os02g22390 encodes a retrotransposon protein with the mutation occurring in the intronic region; Os02g28280 encodes a protein with unknown function with a base substitution resulting in non-synonymous mutation; Os02g29530 encodes a protein containing the PFAM domain related to glycosyltransferase, with a 2 bp deletion mutation causing a premature termination. Further studies on these three candidate genes will be helpful for understanding the molecular mechanism of organ size control in rice.

Biomimetic design of platelet-rich plasma controlled release bacterial cellulose/hydroxyapatite composite hydrogel for bone tissue engineering.

Bacterial cellulose (BC) hydrogel is renowned in the field of tissue engineering for its high biocompatibility, excellent mechanical strength, and eco-friendliness. Herein, we present a biomimetic mineralization method for preparing BC/hydroxyapatite (HAP) composite hydrogel scaffolds with different mineralization time and ion concentration of the mineralized solution. Spherical HAP reinforcement enhanced bone mineralization, thereby imparting increased bioactivity to BC matrix materials. Subsequently, platelet-rich plasma (PRP) was introduced into the scaffold. The PRP-loaded hydrogel enhanced the release of growth factors, which promoted cell adhesion, growth, and bone healing. After 3 weeks of MC3T3-E1 cell-induced osteogenesis, PRP positively affected cell differentiation in BC/HAP@PRP scaffolds. Overall, these scaffolds exhibited excellent biocompatibility, mineralized nodule formation, and controlled release in vitro, demonstrating great potential for application in bone tissue repair.

NLRC3 is a potential prognostic biomarker that is correlated with immune cell infiltration in lung adenocarcinoma.

The NLR family CARD domain containing 3 (NLRC3) gene has been reported to have a crucial effect on immunity, inflammation, and tumorigenesis. However, the clinical relevance of NLRC3 in lung adenocarcinoma (LUAD) remains unclear. This study analyzed both RNA sequencing data and corresponding clinical outcomes obtained from public databases to identify (i) NLRC3 as a tumor suppressor in LUAD and (ii) its predictive value for the likelihood of patient responsiveness to immunotherapy. The results showed that NLRC3 expression was reduced in LUAD and was lower in advanced-stage tumors. Additionally, reduced NLRC3 expression was correlated with worse patient prognosis. The protein level of NLRC3 was also observed to have prognostic significance. Moreover, downregulation of NLRC3 was found to suppress the chemotaxis and infiltration of antitumor lymphocyte subpopulations as well as natural killer cells. Mechanistic analysis indicated that NLRC3 may be involved in immune infiltration by regulating chemokines and their receptors in LUAD. Furthermore, NLRC3 functions as a molecular switch in macrophages, whereby it mediates the polarization of M1 macrophages. Patients with high NLRC3 expression were also found to exhibit a more promising response to immunotherapy. In conclusion, NLRC3 could serve as a potential prognostic biomarker for LUAD, help predict the immunotherapeutic response of patients, and guide personalized strategies for the treatment of LUAD.

Clinical significance of the anteromedial talus osteophyte in anteromedial ankle impingement in chronic lateral ankle instability.

PURPOSE: The aim of this study was to evaluate the relation between anteromedial ankle osteophytes (AMAO) and anteromedial ankle impingement (AMAI) in chronic lateral ankle instability (CLAI) through visualization and quantification. METHODS: Forty-three patients with unilateral CLAI between September 2018 and March 2020 accepted arthroscopic repair of an anterior talofibular ligament (ATFL) and were split into two groups: AMAI (AMAI including intraoperative AMAO resection) and pure CLAI (with AMAO but without AMAI, no AMAO resection). The AMAO protrusion lengths in each direction were measured and compared after all of the ankles were reconstructed. All patients were assessed preoperatively and at 2-year follow-up with ankle dorsiflexion, the American Orthopedic Foot and Ankle Society (AOFAS) ankle-hindfoot score, and visual analog scale (VAS) score. RESULTS: Intelligent analysis showed that a large extent of osteophytes was found at the dorsomedial surface of the talar neck in AMAI group. The upper and inner bound protrusion distances of AMAO in AMAI group were greater than in the pure CLAI group. There was no significant difference in anterior bound protrusion distance of AMAO between the two groups. Preoperatively, the ankle dorsiflexion of AMAI group (7.6 ± 1.4°) was considerably lower than that of pure CLAI group (22.4 ± 1.9°) (p < 0.001). When compared to the pure CLAI group, the AMAI group had a substantially worse AOFAS score (62.2 ± 6.7 vs 71.1 ± 9.1; p < 0.001) and VAS score (6.0 ± 1.0 vs 4.9 ± 0.8; p < 0.05). However, there was no significant difference in postoperative ankle dorsiflexion, AOFAS score, or VAS score between the two groups. CONCLUSION: AMAO is formed mostly on the dorsomedial surface of the talar neck in CLAI with AMAI, and the upper and inner bound protrusion lengths of AMAO were shown to be significantly correlated with the existence of AMAI in CLAI.

A meta-analysis of risk factors associated with platelet transfusion refractoriness.

BACKGROUND: Platelet transfusion refractoriness (PTR) remains an intractable issue in clinical practice, and is common in hematological patients. At present, it is believed that both immune and non-immune factors play a role. We conducted a meta-analysis of various risk factors which may contribute to PTR. METHODS: PubMed, Embase, Cochrane library, and Web of Science were selected as research database platforms. Citations included were further assessed for quality and bias using the Newcastle-Ottawa Scale. All analyses were performed using Review Manager Version 5.4 and STATA 16.0. RESULTS: The preliminary search revealed 1069 publications, and 17 (5929 patients in total) were ultimately included in the quantitative analysis. The following variables were associated with the occurrence of PTR: fever (OR = 2.26, 95%CI 2.00-2.55, p < 0.00001), bleeding (OR = 2.10, 95%CI 1.36-3.24, p = 0.0008), female sex (OR = 2.06, 95%CI 1.13-3.75, p = 0.02), antibiotic use (OR = 2.94, 95%CI 1.54-5.59, p = 0.001), and infection (OR = 2.19, 95%CI 1.20-4.03, p = 0.01). Antibodies involved in immune activation were a higher risk factor (OR = 4.17, 95%CI 2.36-7.36, p < 0.00001), and splenomegaly was nearly significant (OR = 1.73, 95%CI 0.97-3.07, p = 0.06). CONCLUSIONS: We identified some important risk factors for PTR, but further research is needed to identify the many other possible elements that may contribute to or mediate PTR.