Biomechanical evaluation of a modified intramedullary nail for the treatment of unstable femoral trochanteric fractures.

Background: The Proximal Femoral Nail Antirotation (PFNA) device is the most commonly used implant to fix unstable femoral trochanteric fractures (UFTFs), but it has a relatively high incidence of complications. Due to this factor, the modified intramedullary nail (MIN) was created to treat patients with UFTFs. The aim was to exhibit the MIN and make a comparison with PFNA and InterTAN using biomechanical methods. Methods: An adult UFTF model was developed using Mimics software. The PFNA, InterTAN nail, and MIN models were drawn referring to the corresponding parameters and installed in the fracture models. Vertical, anteroposterior (AP) bending, and torsion loads of the femoral head were set in advance and loaded onto the fracture models. The value of maximal displacement and von Mises stress was evaluated via finite element analysis (FEA). Results: The MIN model had smaller values for maximal displacement than that of the PFNA model, and the increase in displacement was less pronounced for the MIN compared to PFNA under increasing vertical loads. For the indicator of von Mises stress, the MIN model showed lower stress compared with the PFNA model in vertical loads ranging from 300 N to 2100 N. Except for the maximal stress at implants under AP bending loads, the MIN demonstrated the most superior biomechanical properties under AP bending and torsional loads. Conclusion: The MIN offered obvious advantages in terms of mechanical stability and stress distribution among the three studied implants, providing a promising implant option for patients with UFTFs.

Multifunctional gold nanoparticles for osteoporosis: synthesis, mechanism and therapeutic applications.

Osteoporosis is currently the most prevalent bone disorder worldwide and is characterized by low bone mineral density and an overall increased risk of fractures. To treat osteoporosis, a range of drugs targeting bone homeostasis have emerged in clinical practice, including anti-osteoclast agents such as bisphosphonates and denosumab, bone formation stimulating agents such as teriparatide, and selective oestrogen receptor modulators. However, traditional clinical medicine still faces challenges related to side effects and high costs of these types of treatments. Nanomaterials (particularly gold nanoparticles [AuNPs]), which have unique optical properties and excellent biocompatibility, have gained attention in the field of osteoporosis research. AuNPs have been found to promote osteoblast differentiation, inhibit osteoclast formation, and block the differentiation of adipose-derived stem cells, which thus is believed to be a novel and promising candidate for osteoporosis treatment. This review summarizes the advances and drawbacks of AuNPs in their synthesis and the mechanisms in bone formation and resorption in vitro and in vivo, with a focus on their size, shape, and chemical composition as relevant parameters for the treatment of osteoporosis. Additionally, several important and promising directions for future studies are also discussed, which is of great significance for prevention and treatment of osteoporosis.

Azurin Regulates P21 and Enhances the Sensitivity of Osteosarcoma Cells to Cisplatin.

Background: Osteosarcoma (OS) is the most common bone malignancy, with a high mortality rate in adolescents. Despite advancements in therapeutic interventions, OS prognosis remains poor due to drug resistance. P21, a cyclin-dependent kinase inhibitor, plays a critical role in cell cycle regulation and has been implicated in OS pathogenesis. Cisplatin (DDP) is a conventional chemotherapeutic agent for OS, but its efficacy is often limited due to drug resistance. Azurin, a bacterial redox protein, has been reported to exhibit antitumor activity. However, its interaction with P21 in OS remains unexplored. In this study, we sought to investigate the impact of azurin on the cytotoxic effect of DDP against OS cells in relation to P21 expression. Methods: Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting were used to determine the level of p21 and apoptosis-related factors in U2OS cells. A Cell Counting Kit-8 (CCK-8) was used to examine the effects of azurin-p21 on the U2OS cell proliferation rate. Flow cytometry (FCM)was used to analyze the impact of azurin-P21 on the apoptosis/cell cycle. Enzyme-linked immunosorbent assay (ELISA) was used to analyze the effects of azurin-P21 on the secretion of oxygen free radicals, glutathione and glutathione peroxidase. Results: Azurin exhibited significant cytotoxic activity against U2OS cells expressing wild-type (WT) P21, with minimal impact on SAOS-2 and MG63 cells lacking endogenous P21. Azurin treatment resulted in increased expression of procaspase-3 and Bax, decreased expression of B-cell lymphoma-2 (Bcl-2) and a consequential increase in apoptosis. The depletion of P21 attenuated these effects, suggesting the crucial role of P21 in azurin-mediated cytotoxicity. Furthermore, azurin synergistically enhanced the cytotoxic effect of DDP against U2OS cells, which was mitigated by P21 depletion. Conclusions: Our findings demonstrated that azurin selectively induces apoptosis and cell cycle arrest in U2OS cells, which is mediated via P21. This study highlights the potential of azurin as a sensitizer for DDP in the treatment of OS. Future studies on DDP-resistant OS cells may further elucidate the clinical relevance of our findings.

Rational design of S-scheme AgI/ZrTiO4-x heterojunctions for remarkably boosted norfloxacin degradation.

Emerging S-scheme heterojunction photocatalysts endowed with efficient charge separation and strong redox capacity have stimulated wide interests in dealing with environmental issues nowadays. In this work, we firstly fabricated the oxygen vacancy modified ZrTiO4-x nanocrystals, which was further combined with AgI to build the defective S-scheme AgI/ZrTiO4-x heterojunctions for visible-light photocatalytic norfloxacin degradation. The synthesized ZrTiO4-x nanocrystals and AgI/ZrTiO4-x heterojunctions displayed remarkably boosted norfloxacin degradation performance under visible-light irradiation. The reaction rate constant of the optimized AgI/ZrTiO4-x-5% heterojunction is as high as 0.01419 min-1, which is approximately 43.35 times that of AgI and 7.93 times that of ZrTiO4-x nanocrystals, and far superior to those of commercial TiO2 and commercial ZrO2. The high-performance photocatalytic norfloxacin degradation could be mainly attributed to the formation of S-scheme charge transfer pathways and oxygen vacancy defects. More significantly, AgI/ZrTiO4-x could also realize the effective photo-decomposition of other emerging pollutants. Finally, the visible-light photocatalytic performance and photocatalysis mechanism were investigated.

F-decoration-induced partially amorphization of nickel iron layered double hydroxides for high efficiency urea oxidation reaction.

The urea oxidation reaction (UOR) has been well-acknowledged as one of the promising alternatives for hydrogen production through electrochemical water splitting system because of the more favorable thermodynamic potential. But the shortage of cost-effective electrocatalysts with high catalytic activity and durability restricts its practical development. Herein, the partially amorphous fluorine-decorated nickel iron layered double hydroxides (NiFe-F) is constructed via a low-temperature fluoridation method. Our study found that HF acid etching of NiFe LDH precursor resulted in the partially amorphous feature and abundant oxygen vacancies, providing rich reaction sites. Simultaneously, the formation of ionic metal-F bond makes it easier to form high-valence metal oxygen hydroxide active sites. Specifically, the as-prepared NiFe-F-4 electrode demonstrates a superb mass activity of 1290 mA mg-1 at 1.6 V vs. RHE. Further experiments found that amorphous structure and F decorating decreased the activation energy of UOR from 30.71 kJ mol-1 (crystalline NiFe-F-4) to 20.17 kJ mol-1 (amorphous NiFe-F-4), leading to a rapid dynamic with a small Tafel slope of 31 mV dec-1. Moreover, NiFe-F-4 casts remarkable long-term durability for 40 h without performance decay. This work holds great promise to develop advanced electrocatalysts for pollution treatment of urea-rich wastewater and energy-saving H2 production.

A Prognostic Molecular Signature of N6-Methyladenosine Methylation Regulators for Soft-Tissue Sarcoma from The Cancer Genome Atlas Database.

BACKGROUND Soft-tissue sarcomas are a group of heterogeneous and rare mesenchymal tumors with aggressive behavior. We aimed to identify the molecular signatures of N6-methyladenosine (m6A) methylation regulators associated with patient prognosis using The Cancer Genome Atlas (TCGA) database. MATERIAL AND METHODS To evaluate the role of m6A in soft-tissue sarcomas, genomic and clinical data were downloaded from TCGA. The copy number variations (CNVs) and mutations of m6A regulators were analyzed. RESULTS Alterations of m6A regulators were common, and ALKBH5 showed the highest frequency of copy number gain, while ZC3H13 had the highest frequency of loss. CNVs and mutations were closely correlated with histology (P<0.001) and tumor size (P=0.040), and CNVs were correlated with mRNA expression. Furthermore, patients with gains of METTL16, RMB15, RMB15B, YTHDC, and YTHDF3 displayed poorer overall survival (OS), and patients with gains of RBM15 and YTHDC2 and loss of IGF2BP1 had poorer disease-free survival (DFS). Further analysis indicated that CNVs and mutations of KIAA1429, YTHDF3, and IGF2BP1 were independent risk factors predicting OS and DFS. Gain of "writers" with loss of "erasers" led to worse OS than gain of "writers". Genes involved in JAK2 oncogenic signature were enriched in cases of higher expressions of METTL16, YTHDC2, and YTHDF3. Similarly, the core serum response signature was enriched in patients with higher expressions of IGF2BP1, METTL16, RBM15, and YTHDC2. CONCLUSIONS Our study provides a useful molecular tool to predict the outcome of soft-tissue sarcomas and deepens our understanding of the molecular mechanisms of the development of the disease.

Expanding the strong absorption band by impedance matched mosquito-coil-like acoustic metamaterials.

A mosquito-coil-like acoustic artificial structure consisting of a spiral channel and a perforated plate with excellent impedance matching is proposed, which can realize strong sound absorption within a certain frequency range. Due to the difficulty in matching the impedance of the single-hole structure with that of the sound propagation medium, the sound absorption should be poor. To overcome this shortcoming caused by the mismatched impedance, some multi-hole microstructures are designed. Moreover, since single-chamber labyrinth can only achieve single-frequency perfect sound absorption, a labyrinthine channel is divided into several chambers with each length distributing by an arithmetic progression gradient. The sound absorption bandwidth can be extended by synergetic coupling resonance among multiple chambers. By selecting different structural parameters including the number of holes, the width of the labyrinthine channel, and the depth of labyrinthine channel, sound absorption of these mosquito-coil-like structures is investigated. The results suggest that the multi-hole structures are helpful in improving the impedance matching, while the synergetic coupling resonance among multiple chambers ensures that the sound absorption coefficient of the structure can be maintained at a high level within a certain frequency range. In addition, some mosquito-coil-like sound absorption structures are fabricated by 3D printing, then the sound absorptions under vertical sound incident conditions are measured, and the strong sound absorption ability in a wide band is experimentally demonstrated. Finally, a method is proposed for adjusting the sound absorptions by proportionally zooming in or out the structure, by which the sound absorptions of the acoustic structure can be effectively shifted to lower or higher frequencies.

Overexpression of HIF-2α-Dependent NEAT1 Promotes the Progression of Non-Small Cell Lung Cancer through miR-101-3p/SOX9/Wnt/ß-Catenin Signal Pathway.

BACKGROUND/AIMS: The present study aimed to explore the function of NEAT1 on non-small cell lung cancer (NSCLC), as well as its underlying mechanisms. METHODS: Quantitative realtime PCR (qRT-PCR) was used to measure NEAT1 expression in NSCLC tissues and cells. MTT assay and transwell assay were performed to detect cell proliferation, migration and invasion. Potential target genes were identified via luciferase reporter assay. Protein analysis was performed through western blotting. RESULTS: The expressions of NEAT1 were significantly higher in both of NSCLC tissues and cells than in normal controls. High expression of NEAT1 was significantly associated with TNM stage (P=0.000) and metastasis (P=0.000). NEAT1 knockdown inhibited the proliferation, migration and invasion of NSCLC cells. Hypoxia induction mediated by HIF-2α promoted EMT and NEAT1 expressions. Moreover, miR-101-3p was a target of NEAT1. We also found that SOX9 was a target of miR-101-3p. Oncogenic function of NEAT1 on NSCLC progression was mediated by miR-101-3p/SOX9/Wnt/ß-catenin signaling pathway. CONCLUSION: NEAT1 up-regulation induced by HIF-2α over-expression could promote the progression of NSCLC under hypoxic condition. Moreover, NEAT1 also takes part in NSCLC progression via miR-101-3p/SOX9/Wnt/ß-catenin axis.

The Effects of Adiponectin and Adiponectin Receptor 1 Levels on Macrovascular Complications Among Patients with Type 2 Diabetes Mellitus.

BACKGROUND/AIMS: The present study aimed to investigate the serum levels of adiponectin (APN) and adiponectin receptor 1 (AdipoR1) in patients with type 2 diabetes mellitus (T2DM) combined with macrovascular complications (MVC), as well as their correlation with clinical parameters. METHODS: A total of 60 T2DM patients were divided into 2 groups according to the presence of MVC: T2DM + MVC group (n=30) and T2DM group (n=30). Additionally, 30 healthy people were selected as control group (NC group). Clinical data and biological parameters were detected and recorded. T test was performed to compare the differences between two groups, and the results were corrected using Bonferroni method. Meanwhile, the correlation analysis and multiple stepwise regression analysis were used to analyze the association of APN and AdipoR1 with clinical factors. RESULTS: The levels of APN and AdipoR1 were significantly decreased in T2DM group and T2DM + MVC group compared with NC group, with the lowest value in T2DM + MVC group (all P<0.01). Serum APN levels were positively correlated with FINS and TG (r = 0.412, 0.316, respectively; both P<0.05), and negatively correlated with SBP, DBP and LDL-C (r = -0.292, -0.383, -0.334, respectively; all P<0.05). Serum levels of AdipoR1 were positively correlated with APN (r = 0.726, P<0.01), and negatively correlated with BMI, SBP, DBP, FBG, TC and LDL-C (r = -0.440, -0.446, -0.374, -0.444, -0.344, -0.709, respectively; all P<0.01). CONCLUSION: Serum levels of APN and AdipoR1 are significantly lower in T2DM group and T2DM + MVC group, showing lowest value in T2DM + MVC group. APN and AdipoR1 levels may influence glucose and lipid metabolism in T2DM patients.

Association of MCP-1 rs1024611 polymorphism with diabetic foot ulcers.

Monocyte chemotactant protein-1 (MCP-1), a pro-inflammatory cytokine, plays an important role in inflammatory process. In present study, we evaluated the association of MCP-1 gene rs1024611 polymorphism with risk and clinical characteristics of diabetic foot ulcers (DFUs).This study recruited 116 patients with DFUs, 135 patients with diabetes mellitus (DM) without complications (non-DFU), and 149 healthy controls (HCs). MCP-1 gene rs1024611 polymorphism was genotyped by direct sequencing. The expression of MCP-1 was analyzed using quantitative real-time polymerase chain reaction. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assume the association strength.Individuals with rs1024611 AG and GG genotypes exhibited significantly higher susceptibility to DFUs, in the comparison with HCs (AG vs AA, OR = 2.364, 95% CI = 1.021-5.470; GG vs AA, OR = 2.686, 95% CI = 1.154-6.255). Meanwhile, G allele was associated with increased DFUs susceptibility (OR = 1.457, 95% CI = 1.014-2.093). Besides, rs1024611 SNP was slightly correlated with increased DFUs susceptibility in patients with DM. GG genotype of rs1024611 was significantly correlated with higher epidermal thickness and lower dermis thickness in patients with DFUs (P < .01). Patients with DFU exhibited upregulation of MCP-1 mRNA, and GG genotype was correlated with enhanced MCP-1 expression in DFU and non-DFU groups.Rs1024611 polymorphism was significantly associated with MCP-1 expression and individual susceptibility to DFUs.

The Neuroprotective Effect of Puerarin in Acute Spinal Cord Injury Rats.

BACKGROUND: Acute spinal cord injury (SCI) leads to permanent disabilities. This study evaluated the neuroprotective effect of puerarin, a natural extract, in a rat model of SCI. METHODS: Acute SCI models were established in rats using a modified Allen's method. Locomotor function was evaluated using the BBB test. The histological changes in the spinal cord were observed by H&E staining. Neuron survival and glial cells activation were evaluated by immunostaining. ELISA and realtime PCR were used to measure secretion and gene expression of cytokines. TUNEL staining was used to examine cell apoptosis and western blot analysis was used to detect protein expression. RESULTS: Puerarin significantly increased BBB score in SCI rats, attenuated histological injury of spinal cord, decreased neuron loss, inhibited glial cells activation, alleviated inflammation, and inhibited cell apoptosis in the injured spinal cords. In addition, the downregulated PI3K and phospho-Akt protein expression were restored by puerarin. CONCLUSION: Puerarin accelerated locomotor function recovery and tissue repair of SCI rats, which is associated with its neuroprotection, glial cell activation suppression, anti-inflammatory and anti-apoptosis effects. These effects may be associated with the activation of PI3K/Akt signaling pathway.

ATAD2 overexpression is associated with progression and prognosis in colorectal cancer.

OBJECTIVES: ATPase family AAA domain-containing 2 plays an important role in tumor progression including cell cycle, proliferation, apoptosis and chemoresistance. However, the expression of ATPase family AAA domain-containing 2 in colorectal cancer and its significance are still unclear. The aim of this study was to examine the expression of ATPase family AAA domain-containing 2 in colorectal cancer. METHODS: Immunohistochemistry was used to determine the expression of ATPase family AAA domain-containing 2 in 155 colorectal cancer and 30 matched adjacent noncancerous tissues. The correlation of ATPase family AAA domain-containing 2 expression with clinicopathological variables was assessed using chi-square test. Patient survival was analyzed using the Kaplan-Meier and log-rank tests. Cox regression was performed for the multivariate analysis of prognostic factors. RESULTS: High expression of ATPase family AAA domain-containing 2 was detected in 58.1% of the colorectal cancers and was significantly associated with advanced tumor-node-metastasis stage (P = 0.044), poor differentiation (P = 0.028), deep infiltration (P < 0.001), lymphovascular invasion (P = 0.006), lymph node metastasis (P = 0.024) and recurrence (P = 0.022). Patients with high ATPase family AAA domain-containing 2 expression had significantly poorer overall survival and disease-free survival (both P < 0.001) when compared with patients with low expression of ATPase family AAA domain-containing 2. The multivariate analysis showed that ATPase family AAA domain-containing 2 was an independent factor for both overall survival (P = 0.003; hazard ratio (HR): 2.356; 95% confidence interval (CI): 1.335-4.158) and disease-free survival (P = 0.001; HR: 2.643; 95% CI: 1.489-4.693). CONCLUSIONS: These results showed that ATPase family AAA domain-containing 2 overexpression was associated with progression and prognosis of colorectal cancer.

An integrated overview of spatiotemporal organization and regulation in mitosis in terms of the proteins in the functional supercomplexes.

Eukaryotic cells may divide via the critical cellular process of cell division/mitosis, resulting in two daughter cells with the same genetic information. A large number of dedicated proteins are involved in this process and spatiotemporally assembled into three distinct super-complex structures/organelles, including the centrosome/spindle pole body, kinetochore/centromere and cleavage furrow/midbody/bud neck, so as to precisely modulate the cell division/mitosis events of chromosome alignment, chromosome segregation and cytokinesis in an orderly fashion. In recent years, many efforts have been made to identify the protein components and architecture of these subcellular organelles, aiming to uncover the organelle assembly pathways, determine the molecular mechanisms underlying the organelle functions, and thereby provide new therapeutic strategies for a variety of diseases. However, the organelles are highly dynamic structures, making it difficult to identify the entire components. Here, we review the current knowledge of the identified protein components governing the organization and functioning of organelles, especially in human and yeast cells, and discuss the multi-localized protein components mediating the communication between organelles during cell division.

The maize DWARF1 encodes a gibberellin 3-oxidase and is dual localized to the nucleus and cytosol.

The maize (Zea mays) gibberellin (GA)-deficient mutant dwarf1 (d1) displays dwarfism and andromonoecy (i.e. forming anthers in the female flower). Previous characterization indicated that the d1 mutation blocked three steps in GA biosynthesis; however, the locus has not been isolated and characterized. Here, we report that D1 encodes a GA 3-oxidase catalyzing the final step of bioactive GA synthesis. Recombinant D1 is capable of converting GA20 to GA1, GA20 to GA3, GA5 to GA3, and GA9 to GA4 in vitro. These reactions are widely believed to take place in the cytosol. However, both in vivo GFP fusion analysis and western-blot analysis of organelle fractions using a D1-specific antibody revealed that the D1 protein is dual localized in the nucleus and cytosol. Furthermore, the upstream gibberellin 20-oxidase1 (ZmGA20ox1) protein was found dual localized in the nucleus and cytosol as well. These results indicate that bioactive GA can be synthesized in the cytosol and the nucleus, two compartments where GA receptor Gibberellin-insensitive dwarf protein1 exists. Furthermore, the D1 protein was found to be specifically expressed in the stamen primordia in the female floret, suggesting that the suppression of stamen development is mediated by locally synthesized GAs.

Small kernel 1 encodes a pentatricopeptide repeat protein required for mitochondrial nad7 transcript editing and seed development in maize (Zea mays) and rice (Oryza sativa).

RNA editing modifies cytidines (C) to uridines (U) at specific sites in the transcripts of mitochondria and plastids, altering the amino acid specified by the DNA sequence. Here we report the identification of a critical editing factor of mitochondrial nad7 transcript via molecular characterization of a small kernel 1 (smk1) mutant in Zea mays (maize). Mutations in Smk1 arrest both the embryo and endosperm development. Cloning of Smk1 indicates that it encodes an E-subclass pentatricopeptide repeat (PPR) protein that is targeted to mitochondria. Loss of SMK1 function abolishes the C â†’ U editing at the nad7-836 site, leading to the retention of a proline codon that is edited to encode leucine in the wild type. The smk1 mutant showed dramatically reduced complex-I assembly and NADH dehydrogenase activity, and abnormal biogenesis of the mitochondria. Analysis of the ortholog in Oryza sativa (rice) reveals that rice SMK1 has a conserved function in C â†’ U editing of the mitochondrial nad7-836 site. T-DNA knock-out mutants showed abnormal embryo and endosperm development, resulting in embryo or seedling lethality. The leucine at NAD7-279 is highly conserved from bacteria to flowering plants, and analysis of genome sequences from many plants revealed a molecular coevolution between the requirement for C â†’ U editing at this site and the existence of an SMK1 homolog. These results demonstrate that Smk1 encodes a PPR-E protein that is required for nad7-836 editing, and this editing is critical to NAD7 function in complex-I assembly in mitochondria, and hence to embryo and endosperm development in maize and rice.

The requirement of WHIRLY1 for embryogenesis is dependent on genetic background in maize.

Plastid gene expression is essential to embryogenesis in higher plants, but the underlying mechanism is obscure. Through molecular characterization of an embryo defective 16 (emb16) locus, here we report that the requirement of plastid translation for embryogenesis is dependent on the genetic background in maize (Zea mays). The emb16 mutation arrests embryogenesis at transition stage and allows the endosperm to develop largely normally. Molecular cloning reveals that Emb16 encodes WHIRLY1 (WHY1), a DNA/RNA binding protein that is required for genome stability and ribosome formation in plastids. Interestingly, the previous why1 mutant alleles (why1-1 and why1-2) do not affect embryogenesis, only conditions albino seedlings. The emb16 allele of why1 mutation is in the W22 genetic background. Crosses between emb16 and why1-1 heterozygotes resulted in both defective embryos and albino seedlings in the F1 progeny. Introgression of the emb16 allele from W22 into A188, B73, Mo17, Oh51a and the why1-1 genetic backgrounds yielded both defective embryos and albino seedlings. Similar results were obtained with two other emb mutants (emb12 and emb14) that are impaired in plastid protein translation process. These results indicate that the requirement of plastid translation for embryogenesis is dependent on genetic backgrounds, implying a mechanism of embryo lethality suppression in maize.

Characteristic expression of rice pathogenesis-related proteins in rice leaves during interactions with Xanthomonas oryzae pv. oryzae.

Pathogenesis-related (PR) proteins play an important role in the disease resistance response. To better understand the function of rice PR proteins, we examined the expressions of ten PR proteins in rice leaves at different developmental stages with or without the interaction between rice and Xanthomonas oryzae pv. oryzae (Xoo). The results showed that most of the PR proteins were expressed in rice leaves in normal growth conditions, suggesting that they play a role in rice growth. Six out of ten PR proteins (PR1, PR2, PR3, PR4b, PR8, and PR-pha) showed enhanced expression in Xa21-mediated resistance responses at late stages after inoculation with Xoo. The remaining four PR proteins (PR5, PR6, PR15, and PR16) did not show changes in expression in the resistance response. The expressions of PR proteins in the resistance reaction were further compared with those in the susceptible reaction and a mock treatment. Interestingly, several of the PR proteins were expressed at the highest levels in the susceptible reaction and at the lowest levels in the mock treatment. Among the other four PR proteins, PR5 and PR16 showed changes in the abundance only in the susceptible response, while PR6 and PR15 showed no detectable difference in expression. These data provide fundamental knowledge about the expression of PR proteins in the interaction between rice and Xoo.