Ecological stoichiometry and homeostasis characteristics of plant-litter-soil system with vegetation restoration of the karst desertification control.

It is of great significance to clarify the ecologically chemical stoichiometric characteristics of plant-litter-soil in vegetation restoration process for elucidating the nutrient cycling law and soil nutrient management of karst ecosystem. The carbon (C), nitrogen (N) and phosphorus (P) contents of leaves, litter and soil and their stoichiometry were determined in loquat (Eribotrya japonica) plantations in a karst plateau canyon after 3, 6, 10 and 15 years of restoration. The homeostasis characteristics of leaf N, P, and N:P with the change in soil nutrients during restoration were revealed. The results showed that leaf C, N, and P contents initially increased and then decreased with increasing years of restoration at the same sampling time. The contents of nutrients in soil and litter varied with increasing restoration years, with the highest values mostly appearing in May and July. This could be due to greater moisture in May and July, which helps with nutrient absorption and transformation. The leaf N:P ratio of loquat with different restoration years was 35.76-47.39, with an average of 40.06. Therefore, loquat leaves may experience P limitation in the growth process. The relationships between N, P and N:P in leaves and soil indexes could be simulated by a homeostasis model. Except for the weak sensitivity of loquat leaf N in 10 years, the other indexes and treatments had a certain homeostasis. Plants maintain homeostasis by regulating physiological responses in vivo in response to soil nutrient changes, indicating that loquat has good adaptability in karst desertification environments, but attention should focus on the management of soil P in the field as part of the vegetation restoration process. Therefore, in future research, we should combine the soil water and fertilizer conditions of different growing seasons in karst rocky desertification areas and provide scientific field management to ensure that the results of rocky desertification management can play a role in rural revitalization.

Hexamethyldisilazane Lithium (LiHMDS)-Promoted Hydroboration of Alkynes and Alkenes with Pinacolborane.

Lithium-promoted hydroboration of alkynes and alkenes using commercially available hexamethyldisilazane lithium as a precatalyst and HBpin as a hydride source has been developed. This method will be appealing for organic synthesis because of its remarkable substrate tolerance and good yields. Mechanistic studies revealed that the hydroboration proceeds through the in situ-formed BH3 species, which acts to drive the turnover of the hydroboration of alkynes and alkenes.

Interdigitating dendritic cell sarcoma located in the adrenal gland: a case report and literature review.

We report a case of interdigitating dendritic cell sarcoma (IDCS) originating from the adrenal gland. A 57-year-old middle-aged woman with no previous history of malignancy came to our hospital after color Doppler ultrasound revealed a right adrenal mass. An abdominal computed tomography scan also showed an adrenal mass. Postoperative pathology confirmed the diagnosis of IDCS. After complete surgical removal of the adrenal tumor, the patient has been disease-free for 1 year. IDCS may have a good prognosis after surgical resection. To our knowledge, this is only the second reported case of IDCS in the adrenal region.

Application of Primary/Secondary Circulating Tumor Cells for the Prediction of Biochemical Recurrence in Nonmetastatic Prostate Cancer Patients following Radical Prostatectomy or Radiotherapy: A Meta-Analysis.

BACKGROUND: Circulating tumor cells (CTCs) have been regarded as an independent prognostic marker for metastatic castration-resistant prostate cancer (mCRPC). Its prognostic value, however, in nonmetastatic prostate cancer (NMPC) is still unclear. PURPOSE: To elucidate whether CTCs can predict the biochemical recurrence (BCR) in NMPC patients following radical prostatectomy (RP) or radiotherapy (RT). METHODS: PubMed, Cochrane Database, and Embase and the references in relevant studies were systematically searched. Studies that investigated the correlation of CTCs and BCR in NMPC patients after RP or RT were identified and reviewed. Overall odds ratio (OR) of BCR in such patients with/without CTCs was pooled. We also calculated and pooled overall prevalence of BCR in such CTC-positive patients. RESULTS: In total, 12 studies comprising 1917 participants were eligible for the meta-analysis and showed that the presence of secondary circulating tumor cells (SCTCs) is associated with a higher BCR rate of 59% (95% CI: 22%-88%) in patients with NMPC after RP or RT (OR = 6.12; 95% CI: 2.22-16.85; P < 0.001). However, regardless of the presence of primary circulating tumor cells (PCTCs), it has not been shown to be associated with higher BCR. CONCLUSIONS: Our research demonstrated that SCTC-positive patients are associated with higher BCR compared to SCTC-negative patients in NMPC. Therefore, it is recommended that NMPC patients undergo CTC surveillance intensively after RP or RT.

Identification of key genes and pathways at the downstream of S100PBP in pancreatic cancer cells by integrated bioinformatical analysis.

BACKGROUND: The aim of the present study was to identify key genes and pathways downstream of S100PPBP in pancreatic cancer cells. METHODS: The microarray datasets GSE35196 (S100PBP knockdown) and GSE35198 (S100PBP overexpression) were downloaded from the Gene Expression Omnibus (GEO). Differentially expressed genes (DEGs) were obtained separately from GEO2R, and heatmaps showing clustering analysis of DEGs were generated using R software. Gene Ontology and pathway enrichment analyses were performed for identified DEGs using the Database for Annotation, Visualization, and Integrated Discovery and Kyoto Encyclopedia of Genes and Genomes, respectively. A protein-protein interaction (PPI) network was created using the Search Tool for the Retrieval of Interacting Genes and Cytoscape software. Relevant expression datasets of key identified genes were downloaded from The Cancer Genome Atlas, and overall survival (OS) analysis was performed with R software. Finally, Gene Expression Profiling Interactive Analysis was used to evaluate the expression of key DEGs in pancreatic cancer tissues. RESULTS: A total of 34 DEGs (11 upregulated and 23 downregulated) were screened out from the two datasets. Gene Ontology enrichment analysis revealed that the identified DEGs were mainly functionally enriched in ATPase activity, production of siRNA involved in RNA interference, and production of miRNAs involved in gene silencing by miRNA. The pathway enrichment analysis of the identified DEGs showed enrichment mainly in apoptosis, non-homologous end-joining, and miRNA pathways in cancer. The protein-protein interaction network was composed of 21 nodes and 30 edges. After survival analysis and gene expression analysis, 4 genes associated with poor prognosis were selected, including LMNB1, PRKRA, SEPT2, and XRCC5. CONCLUSIONS: LMNB1, PRKRA, SEPT2, and XRCC5 could be key downstream genes of the S100PBP gene in the inhibition of pancreatic cancer cell adhesion.

Examination of clinically-derived p210 BCR/ABL1 RhoGEF mutations in a murine bone marrow transplantation model of CML.

Expression of the p210 BCR/ABL1 fusion protein has been described in virtually all patients with chronic myelogenous leukemia (CML). Previous studies have identified a guanine nucleotide exchange factor (RhoGEF) domain within BCR that is retained in p210 BCR/ABL1. Missense mutations at residues T654 (T654K) and F547 (F547L) within this domain have been reported in a CML patient in blast crisis (BC). In this study, we have evaluated p210 BCR/ABL1 constructs that contain these substitutions in a murine bone marrow transplantation (BMT) model of CML. The mutants exhibit normal expression and tyrosine kinase activity but altered signaling. When examined in the BMT assay, mice that express the mutants exhibit earlier onset of disease but have significantly extended lifespans relative to mice that express unmodified p210 BCR/ABL1. While mice that express p210 BCR/ABL1 exhibit neutrophilia that progresses to a less differentiated phenotype at death, disease in the mutant mice is characterized by eosinophilia with no maturation arrest. This observation was confirmed in vitro using myeloid cells and was associated with enhanced p53 phosphorylation and G1/S arrest. These results suggest that residues within the RhoGEF domain of p210 BCR/ABL1 can influence disease progression.

Expression of Krüppel-like factor 9 in breast cancer patients and its effect on prognosis.

Expression of Krüppel-like factor 9 (KLF9) in breast cancer tissue and its influence on prognosis was investigated. Sixty-eight patients with breast cancer admitted in Ningde Hospital Affiliated to Fujian Medical University from February 2014 to August 2015 were collected, and the expression level of KLF9 in cancerous tissue (n=68) and normal tissue (n=68) of the patients was measured by quantitative real-time PCR (RT-qPCR). The relationship between the expression and clinical pathological features and prognosis of patients was analyzed. The expression level of KLF9 in cancerous tissue was significantly lower than that in normal tissue (P<0.05). The expression in breast cancer tissue was not significantly correlated with age, height, menstrual status, lymph node metastasis or pathological differentiation (P>0.05), but was significantly correlated with tumor size and clinical stage (P<0.05). The 1-, 2-, and 3-year survival rates in the high expression group were significantly higher than those in the low expression group (P<0.001). Univariate Cox regression analysis was carried out according to the 3-year survival of the patients, and the results showed that tumor size (P=0.009), lymph node metastasis (P=0.002), pathological differentiation (P=0.015), clinical stage (P=0.013), and KLF9 (P=0.018) were factors affecting the survival of breast cancer patients. Subsequently, multivariate Cox regression analysis of the indicators with differences showed that those indicators were independent predictors of survival of breast cancer patients. In conclusion, KLF9 expression is low in breast cancer tissue, and its expression level is related to tumor size and clinical stage. Moreover, tumor size >5 cm, lymph node metastasis, low pathological differentiation, high clinical stage and low expression of KLF9 are all important factors that cause death of patients.

Association of urinary incontinence and depression or anxiety: a meta-analysis.

OBJECTIVE: We explored the relationship between urinary incontinence (UI) and depression or anxiety. METHODS: We searched the Cochrane Library, Embase, and PubMed for articles on the association between depression, anxiety, and UI. We calculated pooled 95% confidence intervals (CIs) and odds ratios (ORs). RESULTS: Twelve articles (31,462 participants) were included. The UI group had significantly higher depression and anxiety levels than the non-UI group (OR = 1.73, 95%CI: 1.64-1.82, I2 = 75.5%). In subgroup analysis, depression and anxiety were significantly higher in participants with UI than in those without UI (OR = 1.95, 95%CI: 1.82-2.10, I2 = 64.3% and OR = 1.54, 95%CI: 1.43-1.65, I2 = 59.2%, respectively). In subgroup analysis by age, participants with UI had significantly higher depression and anxiety, regardless of age, than the non-UI group (OR = 1.59, 95%CI: 1.29-1.95, I2 = 59.1% and OR = 1.98, 95%CI: 1.62-2.43, I2 = 75.5%, respectively). CONCLUSION: Patients with UI had significantly higher depression and anxiety levels than those without UI. Depression and anxiety were higher in patients with UI than in those without UI, regardless of age. Larger sample sizes and more high-quality studies are needed to validate our findings.

Effect of endostatin on Wnt pathway of stem-like cells in bladder cancer in tumor microenvironment.

Wnt/ß-catenin signaling pathway modulates miscellaneous biological events in cells including gene expression, cell growth, apoptosis, metabolism and transition. The aim of this study was to investigate the effect of endostatin on Wnt signaling pathway of stem-like cells in bladder cancer in tumor microenvironment. The qRT-PCR assay and western blot were conducted to evaluate related factors expressions of Wnt signaling pathway in both bladder cancer 5637 cells and stem cells. Loss of function assays were carried out to detect the influence of endostatin on the proliferation, migration, cell proliferation and apoptosis of bladder cancer cells. We demonstrated that endostatin triggered the degradation of ß-catenin, a key mediator of Wnt signaling. The activation of the endostatin blocked ß-catenin function and inhibited cell growth and migration of bladder cancer. In order to verify that the Wnt/ß-catenin signaling pathway was inhibited by endostain in 5637 bladder cancer cells and stem cells, the Wnt/ß-catenin signaling pathway-associated molecules, including DKK1, LRP5, TCF4, ß-catenin, cyclin D1, and c-Myc, were evaluated in 5637 bladder cancer cells and stem cells. The western blotting results showed that expressions of these molecules were remarkably increased in the 5637 bladder cancer cells and stem cells compared to the control group. In summary, our study demonstrated that endostatin inhibited angiogenesis. The downregulation of the Wnt/ß-catenin pathway may be engaged in the suppression of angiogenesis by endostatin in bladder cancer cells and cancer stem cells.

Radical prostatectomy after previous transurethral resection of the prostate: oncological, surgical and functional outcomes-a meta-analysis.

BACKGROUND: The current study aimed to carry out a comprehensive meta-analysis on the existing evidence to quantify and compare the oncological, surgical and functional outcomes following radical prostatectomy between TURP group and Non-TURP group. METHODS: A systematic literature search was conducted using EMBASE, PubMed and Cochrane databases to identify relevant studies published in English up to March 2019. A meta-analysis was conducted using Review Manager. RESULTS: There were 13 studies included in the present study. Our results suggest that TURP group demonstrates a significantly higher positive surgical margin rate, bladder neck reconstruction rate and overall complication rate compared with Non-TURP group (OR = 1.31, 95% CI 1.09-1.58, P = 0.004, I2 = 0%; OR = 14.36, 95% CI 2.93-70.45, P = 0.001, I2 = 81%; OR = 2.63, 95% CI 1.87-3.71, P < 0.00001, I2 = 0%); whereas TURP group demonstrates a significantly lower nerve sparing rate compared with Non-TURP group (OR = 0.30, 95% CI 0.22-0.43, P < 0.00001, I2 = 40%); the operation time, blood loss and 1-year urinary continence rate are same between TURP group and Non-TURP group (MD = 4.25, 95% CI - 0.13 to 8.63, P = 0.06, I2 = 34%; MD = 27.29, 95% CI - 10.31 to 64.90, P = 0.15, I2 = 39%; OR = 0.68, 95% CI 0.43-1.06, P = 0.09, I2 = 0%). CONCLUSION: This meta-analysis demonstrates that Non-TURP group may have a great advantage over TURP group in terms of positive surgical margin rate, bladder neck reconstruction rate, overall complication rate and sparing rate. The operation time, blood loss and 1-year urinary continence rate are comparable between TURP group and Non-TURP group. Therefore, important information should be given to those patients at risk of prostate cancer that TURP procedure may increase perioperative complications in case of a following radical prostatectomy. In the meantime, our meta-analysis found that each of these four subgroups (RARP, LRP, ORP and RARP/ORP) has its own advantages or disadvantages in every pool results. So when radical prostatectomy is performed on patients with TURP history, the appropriate operation method should be selected as per the conditions of patients, doctors and hospitals.

Retraction note to: Lentivirus-Mediated Short-Hairpin RNA Targeting Protein Phosphatase 4 Regulatory Subunit 1 Inhibits Growth in Breast Cancer.

[This retracts the article on p. 218 in vol. 18, PMID: 26472971.].

Erratum: Lentivirus-Mediated Short-Hairpin RNA Targeting Protein Phosphatase 4 Regulatory Subunit 1 Inhibits Growth in Breast Cancer.

[This corrects the article on p. 218 in vol. 18, PMID: 26472971.].

Lentivirus-Mediated Short-Hairpin RNA Targeting Protein Phosphatase 4 Regulatory Subunit 1 Inhibits Growth in Breast Cancer.

PURPOSE: Protein phosphatase 4 regulatory subunit 1 (PP4R1), as an interaction partner of the catalytic serine/threonine-protein phosphatase 4 catalytic subunit has been shown to involve in cellular processes and nuclear factor κB signaling. However, the functions of PP4R1 in human breast cancers remain unclear. This study is designed to explore the effect of PP4R1 knockdown on the biological characteristics of breast cancer cells. METHODS: A lentivirus-mediated short hairpin RNA (shRNA) was designed to knockdown the expression of PP4R1 in ZR-75-30 breast cancer cells. The efficiency of lentivirus-mediated shRNA infection was determined using fluorescence microscopy to observe lentivirus-mediated green fluorescent protein expression and confirmed to be over 80%. PP4R1 expression in infected ZR-75-30 cells was detected by quantitative real-time polymerase chain reaction and western blot analysis. Cell proliferation and colony formation ability were measured by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and colony formation assay, respectively. Flow cytometry was used to measure cell cycle progression and cell apoptosis. In addition, apoptosis makers, including poly-ADP-ribose polymerase (PARP) and caspase-3, were investigated in PP4R1-silenced ZR-75-30 cells by western blot assay. RESULTS: We successfully constructed lentivirus-mediated shRNA to target PP4R1 in ZR-75-30 cells. MTT assay and colony formation assay showed the loss of PP4R1 suppressed the proliferation of ZR-75-30 cells. Flow cytometry analysis indicated cell cycle arrest and increased cell apoptosis in PP4R1 knockdown cells. Further, the apoptosis response in cells depleted of PP4R1 was illustrated by downregulation of PARP and upregulation of caspase-3. CONCLUSION: Our results suggest that PP4R1 could promote breast cancer cell proliferation and might play a vital role in breast cancer occurrence.

Regulation of vesicle transport and cell motility by Golgi-localized Dbs.

DBS/MCF2L has been recently identified as a risk locus for osteoarthritis. It encodes a guanine nucleotide exchange factor (Dbs) that has been shown to regulate both normal and tumor cell motility. In the current study, we have determined that endogenous Dbs is predominantly expressed as 2 isoforms, a 130 kDa form (Dbs-130) that is localized to the Golgi complex, and an 80 kDa form (Dbs-80) that is localized to the endoplasmic reticulum (ER). We have previously described an inhibitor that binds to the RhoGEF domain of Dbs and blocks its transforming activity. Here we show that the inhibitor localizes to the Golgi, where it specifically interacts with Dbs-130. Inhibition of endogenous Dbs-130 activity is associated with reduced levels of activated Cdc42, enlarged Golgi, and resistance to Brefeldin A-mediated Golgi dispersal, suggesting a role for Dbs in vesicle transport. Cells treated with the inhibitor exhibit normal protein transport from the ER to the Golgi, but are defective in transport from the Golgi to the plasma membrane. Inhibition of Dbs-130 in MDA-MB-231 human breast tumor cells limits motility in both transwell and wound healing assays, but appears to have no effect on the organization of the microtubule cytoskeleton. The reduced motility is associated with a failure to reorient the Golgi toward the leading edge. This is consistent with the Golgi localization, and suggests that the Dbs-130 regulates aspects of the secretory pathway that are required to support cell polarization during directed migration.

Energy-regulated molecules maintain young status in the trophocytes and fat cells of old queen honeybees.

Queen honeybees (Apis mellifera) have much longer lifespans than worker bees. Energy-regulated molecules in the trophocytes and fat cells of workers during aging have been determined, but are unknown in queen bees. In the present study, energy-regulated molecules were evaluated in the trophocytes and fat cells of young and old queen bees. Adenosine monophosphate-activated protein kinase α2 (AMPK-α2), phosphorylated AMPK-α2 (pAMPK-α2), and cAMP-specific phosphodiesterases activity increased with aging. The pAMPK-α2/AMPK-α2 ratio and AMPK activity; adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) concentrations; the ADP/ATP ratio and the AMP/ATP ratio; the cyclic adenosine monophosphate concentration; forkhead box protein O expression; Silent information regulator T1 (SirT1) expression and activity; and peroxisome proliferator-activated receptor-α (PPAR-α) expression were not significantly different between young and old queen bees. These results show that energy-regulated molecules maintain a youthful status in the trophocytes and fat cells of queen bees during aging. These cells seem to have longevity-promoting mechanisms and may clarify the secret of longevity in queen bees.

Inactivation of Rb and E2f8 synergizes to trigger stressed DNA replication during erythroid terminal differentiation.

Rb is critical for promoting cell cycle exit in cells undergoing terminal differentiation. Here we show that during erythroid terminal differentiation, Rb plays a previously unappreciated and unorthodox role in promoting DNA replication and cell cycle progression. Specifically, inactivation of Rb in erythroid cells led to stressed DNA replication, increased DNA damage, and impaired cell cycle progression, culminating in defective terminal differentiation and anemia. Importantly, all of these defects associated with Rb loss were exacerbated by the concomitant inactivation of E2f8. Gene expression profiling and chromatin immunoprecipitation (ChIP) revealed that Rb and E2F8 cosuppressed a large array of E2F target genes that are critical for DNA replication and cell cycle progression. Remarkably, inactivation of E2f2 rescued the erythropoietic defects resulting from Rb and E2f8 deficiencies. Interestingly, real-time quantitative PCR (qPCR) on E2F2 ChIPs indicated that inactivation of Rb and E2f8 synergizes to increase E2F2 binding to its target gene promoters. Taken together, we propose that Rb and E2F8 collaborate to promote DNA replication and erythroid terminal differentiation by preventing E2F2-mediated aberrant transcriptional activation through the ability of Rb to bind and sequester E2F2 and the ability of E2F8 to compete with E2F2 for E2f-binding sites on target gene promoters.

Ubiquitin-mediated interaction of p210 BCR/ABL with ß-catenin supports disease progression in a murine model for chronic myelogenous leukemia.

We have identified a ubiquitin-binding domain within the NH2-terminal sequences of p210 BCR/ABL and determined that the binding site co-localizes with the binding site for ß-catenin. The domain does not support the auto- or trans-kinase activity of p210 BCR/ABL or its ability to interact with GRB2 and activate ERK1/2 signaling. Expression of p210 BCR/ABL, but not a ß-catenin-binding mutant, in hematopoietic cells is associated with the accumulation of p-ß-catenin (Tyr654) and increased TCF/LEF-mediated transcription. In a bone marrow transplantation model, the interaction between ß-catenin and p-ß-catenin (Tyr654) is detectable in mice transplanted with p210 BCR/ABL, but not the mutant. Whereas mice transplanted with p210 BCR/ABL exhibit myeloid disease with expansion of monocytes and neutrophils, mice transplanted with the mutant predominantly exhibit expansion of neutrophils, polycythemia, and increased lifespan. The increased disease latency is associated with expansion of megakaryocyte-erythrocyte progenitors, a decrease in common myeloid progenitors, and reduced ß-catenin signaling in the bone marrow of the diseased mice. These observations support a model in which p210 BCR/ABL may influence lineage-specific leukemic expansion by directly binding and phosphorylating ß-catenin and altering its transcriptional activity. They further suggest that the interaction may play a role in chronic phase disease progression.

Concomitant inactivation of Rb and E2f8 in hematopoietic stem cells synergizes to induce severe anemia.

The retinoblastoma (Rb) tumor suppressor plays important roles in regulating hematopoiesis, particularly erythropoiesis. In an effort to understand whether Rb function can be mediated by E2F transcription factors in a BM-derived hematopoietic system in mice, we uncovered a functional synergy between Rb and E2F8 to promote erythropoiesis and to prevent anemia. Specifically, whereas Mx1-Cre-mediated inactivation of Rb or E2f8 in hematopoietic stem cells only led to mild erythropoietic defects, concomitant inactivation of both genes resulted in marked ineffective erythropoiesis and mild hemolysis, leading to severe anemia despite the presence of enhanced extramedullary erythropoiesis. Interestingly, although ineffective erythropoiesis was already present in the RbΔ/Δ mice and exacerbated in the RbΔ/Δ;E2f8Δ/Δ mice, hemolysis was exclusively manifested in the double-knockout mice. Using an adoptive transfer system and an erythroid-specific knockout system, we have shown that the synergy of Rb and E2f8 deficiency in triggering severe anemia is intrinsic to the erythroid lineage. Surprisingly, concomitant inactivation of Rb and E2f7, a close family member of E2f8, did not substantially worsen the erythropoietic defect resulted from Rb deficiency. The results of the present study reveal the specificity of E2F8 in mediating Rb function in erythropoiesis and suggest critical and overlapping roles of Rb and E2f8 in maintaining normal erythropoiesis and in preventing hemolysis.

Fank1 interacts with Jab1 and regulates cell apoptosis via the AP-1 pathway.

Regulation of apoptosis at various stages of differentiation plays an important role in spermatogenesis. Therefore, the identification and characterisation of highly expressed genes in the testis that are involved in apoptosis is of great value to delineate the mechanism of spermatogenesis. Here, we reported that Fank1, a novel gene highly expressed in testis, functioned as an anti-apoptotic protein that activated the activator protein 1 (AP-1) pathway. We found that Jab1 (Jun activation domain-binding protein 1), a co-activator of AP-1, specifically interacted with Fank1. Reporter analyses showed that Fank1 activated AP-1 pathway in a Jab1-dependent manner. Fank1 overexpression also increased the expression and activation of endogenous c-Jun. Further study showed that Fank1 inhibited cell apoptosis by upregulating and activating endogenous c-Jun and its downstream target, Bcl-3. This process was shown to be Jab1 dependent. Taken together, our results indicated that by interacting with Jab1, Fank1 could suppress cell apoptosis by activating the AP-1-induced anti-apoptotic pathway.