Correction: Up-Regulation of 91H Promotes Tumor Metastasis and Predicts Poor Prognosis for Patients with Colorectal Cancer.

[This corrects the article DOI: 10.1371/journal.pone.0103022.].

Targeting inhibitor of apoptosis proteins (IAPs) enhances susceptibility of oral squamous carcinoma cells to cisplatin.

PURPOSE: Oral Squamous Cell Carcinoma (OSCC) is the 6th most common cancer worldwide. It is generally aggressive and closely associated with chemoresistance and poor survival. There is accumulating evidence for the involvement of inhibitors of apoptosis proteins (IAPs), including IAP1 and XIAP, in mediating chemotherapy resistance in OSCC. Various strategies for targeting IAPs have been designed and tested in recent years and several small molecule IAP inhibitors are in clinical trials as monotherapies as well as in combination with radiotherapy and chemotherapy. The purpose of this study was to evaluate and compare the efficacy and biological activity of three IAP inhibitors both as stand-alone and sensitising agents to cisplatin in a preclinical model of squamous cell carcinoma of the tongue. METHODS: Cisplatin-sensitive SCC4 and -resistant SCC4cisR cells were utilised in this study. Apoptosis was evaluated by flow cytometric analysis of Annexin V/Propidium Iodide-stained cells. Expression of IAP proteins was determined by western blotting and knockdown of cIAP1, livin and XIAP was conducted by transfection of cells with siRNA. RESULTS: We establish for the first time the therapeutic efficacy of the Smac mimetic, BV6 and the XIAP inhibitor Embelin, for OSCC. Both of these IAP targeting agents synergistically enhanced cisplatin-mediated apoptotic cell death in resistant cells which was mediated in part by depletion of XIAP. In addition, knockdown of XIAP using siRNA enhanced cisplatin-mediated cell death, demonstrating the importance of targeting XIAP in this sensitisation. CONCLUSION: These findings provide pre-clinical evidence that IAP inhibition may be a valuable therapeutic option in OSCC.

Clinical application of artificial intelligence-assisted three-dimensional planning in direct anterior approach hip arthroplasty.

PURPOSE: The objective of this study was to investigate the efficacy of an artificial intelligence-assisted 3D planning system (AIHIP) in total hip arthroplasty by direct anterior approach and assess the reliability of the AIHIP preoperative program in terms of both interobserver and intraobserver agreement. METHODS: A retrospective analysis was conducted on patients who underwent unilateral primary THA via direct anterior approach from June 2019 to March 2022. Participants were randomly assigned to receive either the AIHIP system (n = 220) or the 2D template (control group) (n = 220) for preoperative planning. The primary outcome aimed to evaluate the correspondence between the prosthesis selected intro-operation and the one planned preoperatively, as well as to calculate the intraclass correlation coefficient (ICC). Secondary outcomes included operation time, intraoperative blood loss, fluoroscopy times, Harris hip score (HHS), lower limb length difference (LLD), femoral offset (FO), and bilateral femoral offset difference. RESULTS: No significant differences were observed in gender, age, body mass index (BMI), aetiology, and American Society of Anesthesiologists (ASA) score between the two groups. Both planning methods exhibited good intraobserver agreement for component planning (ICC: 0.941-0.976). Interobserver agreement for component planning was comparable between the two methods (ICC: 0.882-0.929). In the AIHIP group, the accuracy of acetabular cup and femoral stem prosthetics planning significantly improved, with accuracies within the size range of ± 0 and ± 1 being 76.8% and 90.5% and 79.5% and 95.5%, respectively. All differences between two groups were statistically significant (p < 0.05). Patients receiving AIHIP preoperative planning experienced shorter operation times, reduced intraoperative blood loss, fewer fluoroscopy times, and lower leg length discrepancy (LLD) (p < 0.05). Moreover, they demonstrated a higher Harris hip score (HHS) at three days post-surgery (p < 0.05). However, no significant differences were found in femoral offset (FO), difference of bilateral femoral offsets, and HHS at 1 month after the operation. CONCLUSION: Utilizing AIHIP for preoperative planning of direct anterior approach THA can significantly enhance the accuracy of prosthetic sizing with good reliability, decrease operation time, reduce intraoperative blood loss, and more effectively restore the length of both lower limbs. This approach has greater clinical application value.

Potential impact of platelet-to-lymphocyte ratio on prognosis in patients with colorectal cancer: A systematic review and meta-analysis.

Background: Numerous studies have confirmed that inflammation promotes the occurrence, development and prognosis of colorectal cancer (CRC). Objective: This study focuses on the potentially prognostic value of the platelet-to-lymphocyte ratio (PLR) in CRC patients. Data Sources: This study was registered at PROSPERO (ID: CRD42020219215). Relative studies were searched on PubMed, Cochrane Library, Embase, Web of Science, and clinical trial databases by two back-to-back reviewers. Study Selection and Intervention: Studies were screened according to the predetermined inclusion and exclusion criteria, comparing prognosis differences between low PLR levels and high PLR levels for CRC patients. Main Outcome Measures: Studies were integrated and compared to analyze the value of PLR in predicting overall survival (OS), progression-free survival (PFS), cancer-specific survival (CSS), disease-free survival (DFS) and recurrence-free survival (RFS) of CRC. Results: Outcomes were compared using Review Manager (version 5.4) software from Cochrane Collaboration. A total of 27 literary works, including 13,330 patients, were incorporated into our study. The final results showed that higher PLR levels had worse OS (hazard ratio [HR] = 1.40, 95% confidence interval [CI] = 1.21-1.62, P < 0.00001), DFS (HR = 1.44, 95% CI = 1.09-1.90, P = 0.01) and RFS (HR = 1.48, 95% CI = 1.13-1.94, P = 0.005) than lower PLR levels, respectively. However, there was no evidence of significance for PFS (HR = 1.14, 95% CI = 0.84-1.54, P = 0.40) and CSS (HR = 1.16, 95% CI = 0.88-1.53, P = 0.28) in the final meta-analysis. Limitations: Our study has the following limitations. First of all, we only included literature published in English, which means that some publication bias may be inevitable. In addition, our study used aggregate data, not individual data; furthermore, we did not define the exact cut-off value representing the PLR level. Conclusion: An elevated PLR seems to be an adverse prognostic factor affecting survival outcomes in patients with CRC. Meanwhile, more prospective studies are required to confirm our conclusion.PROSPERO ID: CRD42020219215.

Synthesis of Oxide Interface-Based Two-Dimensional Electron Gas on Si.

Two-dimensional electron gas (2DEG) at the interface of amorphous Al2O3/SrTiO3 (aAO/STO) heterostructures has received considerable attention owing to its convenience of fabrication and relatively high mobility. The integration of these 2DEG heterostructures on a silicon wafer is highly desired for electronic applications but remains challanging up to date. Here, conductive aAO/STO heterostructures have been synthesized on a silicon wafer via a growth-and-transfer method. A scanning transmission electron microscopy image shows flat and close contact between STO membranes and a Si wafer. Electron energy loss spectroscopic measurements reveal the interfacial Ti valence state evolution, which identifies the formation of 2D charge carriers confined at the interface of aAO/STO. This work provides a feasible strategy for the integration of 2DEG on a silicon wafer and other desired substrates for potential functional and flexible electronic devices.

Retraction Notice to: YTHDF1 Facilitates the Progression of Hepatocellular Carcinoma by Promoting FZD5 mRNA Translation in an m6A-Dependent Manner.

[This retracts the article DOI: 10.1016/j.omtn.2020.09.036.].

Identification of autophagy related genes in predicting the prognosis and aiding 5- fluorouracil therapy of colorectal cancer.

The emergence of 5-Fluorouracil (5-FU) resistance is the barrier to effective clinical outcomes for colorectal cancer (CRC) patients. Autophagy was found to be involved in protecting tumor cells from 5-FU. However, the specific role of autophagy-related genes in CRC 5-FU resistance remains unclear. In this study, HSPB8 among 34 differentially expressed ARGs in CRC was identified to be the hub ARGs in 5-FU resistant which was down-regulated in CRC samples when compared with normal samples but up-regulated in CRC samples with relatively higher lymphatic invasion, later stages and poor prognosis of CRC. Mechanistic analysis demonstrated that due to the recruitment of CAFs, HSPB8 expression was enhanced in CRC cells so that HSPB8 could act together with its co-chaperone BAG3 in autophagy drived 5-FU resistance. Furthermore, the augmented expression level of HSPB8 was found to be significantly correlated to the immune cell infiltration such as Treg cells, macrophages, monocyte and dendritic cells and so on. Our results suggested CAFs driving HSPB8 induced CRC 5-FU resistance by promoting tumor autophagy would provide a new strategy in seeking potential CRC therapeutic target.

Upregulated LINC01088 facilitates malignant phenotypes and immune escape of colorectal cancer by regulating microRNAs/G3BP1/PD-L1 axis.

PURPOSE: Long intergenic non-coding RNA LINC01088 is a newly discovered long non-coding RNA (lncRNA). Its biological function in colorectal cancer (CRC) remains unknown. METHODS: Here, 36 paired CRC and para-cancerous tissues were collected. In vitro, fluorescence in situ hybridization (FISH) assay, qPCR, western blotting analysis and cellular functional experiments, RNA immunoprecipitation (RIP) assay and dual-luciferase reporter system analysis were performed. In vivo, xenograft tumor mouse models were generated. Besides, patient-derived intestinal organoid (PDO) was generated ex vivo. RESULTS: We found that LINC01088 was significantly upregulated in colorectal cancer tissues and CRC cell lines compared to adjacent normal tissues and colonic epithelial cells. High LINC01088 levels were correlated with adverse outcomes in patients with CRC. LINC01088 was mainly located in the cytoplasm. LINC01088 knockdown suppressed the proliferation, migration, invasion, and immune escape of colorectal cancer cells. Mechanistically, LINC01088 bound directly to miR-548b-5p and miR-548c-5p that were significantly upregulated Ras GTPase-activating protein-binding proteins 1 (G3BP1) and programmed death ligand 1 (PD-L1) expression, altering CRC cell phenotypes. In mouse xenograft models, LINC01088 knockdown restrained CRC tumor growth and lung metastasis. Furthermore, G3BP1 overexpression reversed LINC01088-knockdown-mediated inhibitory effects on tumor growth. Notably, LINC01088 knockdown downregulated PD-L1 expression, while G3BP1 overexpression restored PD-L1 expression in xenograft tumors. Besides, LINC01088 knockdown repressed CRC organoid growth ex vivo. CONCLUSION: Overall, these findings suggested that LINC01088 directly targeted miR-548b-5p and miR-548c-5p, promoting G3BP1 and PD-L1 expression, which facilitated colorectal cancer progression and immune escape.

YTHDF1 Facilitates the Progression of Hepatocellular Carcinoma by Promoting FZD5 mRNA Translation in an m6A-Dependent Manner.

Hepatocellular carcinoma (HCC), one of the most aggressive malignancies, ranks as the fourth leading cause of cancer-related deaths worldwide. Emerging evidence indicates that RNA N6-methyladenosine (m6A) plays a critical role in tumor progression. However, the biological function of YTHDF1 in HCC remains unclear. Here, we found that YTHDF1 expression was strikingly elevated in HCC tissues and cell lines and significantly associated with prognosis of HCC patients. Moreover, YTHDF1 expression was transcriptionally regulated by USF1 and c-MYC in HCC. Functional studies showed that YTHDF1 can promote HCC cell proliferation and metastasis both in vitro and in vivo. Multi-omics analysis revealed that YTHDF1 can accelerate the translational output of FZD5 mRNA in an m6A-dependent manner and function as an oncogene through the WNT/ß-catenin pathway. Taken together, our study revealed an essential role of YTHDF1 in the progression of HCC cells, which indicated that targeting YTHDF1 may be a potential therapeutic strategy in HCC.

IGF2 loss of imprinting enhances colorectal cancer stem cells pluripotency by promoting tumor autophagy.

Cancer stem cells (CSCs) are believed to be the driving force behind the tumor growth. We performed this study to further explore the role of IGF2 epigenetic on CRC stem cells pluripotency which showed that IGF2 LOI CRC cells usually had a higher CD133 expression and sphere forming efficiency than MOI cells. IGF2 LOI CSCs were also found to have a higher level of autophagy than MOI CSCs. Moreover, IGF2/IR-A signal was determined to play a more important role in CSCs formation than IGF2/IGF1R. At last, by using miRNA-195 mimics, we fortunately found the increased IR-A expression might be due to the degradation of miRNA-195 in CRC. In conclusion, our results might reveal that IGF2 LOI could promote CRC stem cells pluripotency by promoting CSCs autophagy. For the degradation of miRNA-195, IGF2 showed a higher ability in interacting with overexpressed IR-A rather than IGF1R which would further activate CSCs autophagy. All these findings might provide a novel mechanistic insight into CRC diagnosis and therapy.

Analysis of METTL3 and METTL14 in hepatocellular carcinoma.

N6-methyladenosine (m6A) RNA methylation is the most prevalent modification of messenger RNAs (mRNAs) and catalyzed by a multicomponent methyltransferase complex (MTC), among which methyltransferase-like 3 (METTL3) and METTL14 are two core molecules. However, METTL3 and METTL14 play opposite regulatory roles in hepatocellular carcinoma (HCC). Based on The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database, we conducted a multi-omics analysis of METTL3 and METTL14 in HCC, including RNA-sequencing, m6ARIP-sequencing, and ribosome-sequencing profiles. We found that the expression and prognostic value of METTL3 and METTL14 are opposite in HCC. Besides, after METTL3 and METTL14 knockdown, most of the dysregulated mRNAs, signaling pathways and biological processes are distinct in HCC, which partly explains the contrary regulatory role of METTL3 and METTL14. Intriguingly, these mRNAs whose stability or translation efficiency are influenced by METTL3 or METTL14 in an m6A dependent manner, jointly regulate multiple signaling pathways and biological processes, which supports the cooperative role of METTL3 and METTL14 in catalyzing m6A modification. In conclusion, our study further clarified the contradictory role of METTL3 and METTL14 in HCC.

Dual blockade of CD47 and HER2 eliminates radioresistant breast cancer cells.

Although the efficacy of cancer radiotherapy (RT) can be enhanced by targeted immunotherapy, the immunosuppressive factors induced by radiation on tumor cells remain to be identified. Here, we report that CD47-mediated anti-phagocytosis is concurrently upregulated with HER2 in radioresistant breast cancer (BC) cells and RT-treated mouse syngeneic BC. Co-expression of both receptors is more frequently detected in recurrent BC patients with poor prognosis. CD47 is upregulated preferentially in HER2-expressing cells, and blocking CD47 or HER2 reduces both receptors with diminished clonogenicity and augmented phagocytosis. CRISPR-mediated CD47 and HER2 dual knockouts not only inhibit clonogenicity but also enhance macrophage-mediated attack. Dual antibody of both receptors synergizes with RT in control of syngeneic mouse breast tumor. These results provide the evidence that aggressive behavior of radioresistant BC is caused by CD47-mediated anti-phagocytosis conjugated with HER2-prompted proliferation. Dual blockade of CD47 and HER2 is suggested to eliminate resistant cancer cells in BC radiotherapy.

Long non-coding RNA 91H regulates IGF2 expression by interacting with IGF2BP2 and promotes tumorigenesis in colorectal cancer.

91H, a long non-coding antisense transcripts located on the position of the H19/IGF2 locus had been suggested to play a critical role in tumour development. However, little study had proved the mechanism in colorectal cancer (CRC). Hence, we performed this study to deeply explore the mechanism of lncRNA 91H in tumour progression. The expression of lncRNA 91H was first detected in CRC tissues and cells which was higher in vitro and in vivo than normal cells or tissues and CRC patients with high lncRNA 91H expression usually had a high risk in tumour metastasis (p < .05). Then, monodansylcadaverine (MDC) staining, scratch wound, migration and invasion assays were conducted which showed to that reduced lncRNA 91H would greatly affect tumour migration, invasion and autophagy. Finally, by RNA pull down and RNA-binding protein immunoprecipitation (RIP) assay, a significant interaction was found between lncRNA 91H and IGF2BP2 which was proved to play an important role in CRC IGF2 expression. All these results suggested lncRNA 91H promotes IGF2 expression by interacting with IGF2BP2 which would provide a new strategy in finding potential CRC diagnostic biomarkers and therapeutic targets.

Exosomal lncRNA 91H is associated with poor development in colorectal cancer by modifying HNRNPK expression.

BACKGROUND: Exosomes mediated transfer of lncRNA 91H may play a critical role in the development of CRC. However, few studies have proved the mechanism. So we performed this study to deeply explore the biological functions of exosomal 91H in the development and progression of CRC. METHODS: The association between lncRNA 91H and exosomes was detected in vitro and vivo. Then RNA pulldown and RIP were used to detect how lncRNA 91H affect CRC IGF2 express. At last, clinic pathological significance of exosomal 91H was evaluated by Cox proportional hazards model. RESULTS: We found that serum lncRNA 91H expression was closely related to cancer exosomes in vitro and vivo which may enhance tumor-cell migration and invasion in tumor development by modifying HNRNPK expression. Then the clinic pathological significance of exosomal 91H was evaluated which demonstrated that CRC patients with high lncRNA 91H expression usually showed a higher risk in tumor recurrence and metastasis than patients with low lncRNA 91H expression (P < 0.05). CONCLUSION: All these data suggested that exosomal lncRNA 91H enhancing CRC metastasis by modifying HNRNPK expression might be an early plasma-based biomarker for CRC recurrence or metastasis. Further large-scale studies are needed to confirm our findings.

Age-specific sex difference in the incidence of hepatocellular carcinoma in the United States.

BACKGROUND: Hepatocellular carcinoma possesses a notable sex difference in incidence, and a protective role of estrogens has been hypothesized. METHODS: Using data from 13 cancer registries in the Surveillance, Epidemiology, and End Results Program, we describe the age-specific sex difference in the incidence of hepatocellular carcinoma in the United States during 1992-2013. We used a curve fitting by non-linear regression to quantitatively characterize the age-specific incidence rate of hepatocellular carcinoma by sex. RESULTS: A total of 44,287 incident cases of hepatocellular carcinoma (33,196 males and 11,091 females) were included, with an overall male-to-female ratio in age-standardized rate of 3.55. The sex ratio was below 2 at ages <25 years, increased with age from ages 25-29 years until peaking at 5.40 at ages 50-54 years, and declined thereafter. We also observed additional peaks in the age-specific sex ratio curves at ages 25-34 years across racial/ethnic groups. Modelling of age-specific incidence rates indicated a 15-year delayed increase with age in females compared with males in Asian and Pacific Islanders, and an 11-year delay in Hispanic whites. CONCLUSIONS: The age-dependent patterns in the sex difference in the incidence of hepatocellular carcinoma support the hypothesis of a protective role of estrogens. The underlying reasons for the sex difference in hepatocellular carcinoma remain to be further explored in analytic epidemiological studies.

Association of Genetic Polymorphisms in the LncRNAs with Gastric Cancer Risk in a Chinese Population.

Background: Genome-wide association studies have identified that polymorphisms in 8q24 confer susceptibility to gastric cancer. Polymorphisms in the lncRNA PRNCR1, PCAT1, and CCAT2 transcribed from the 8q24 locus have a potential risk for gastric cancer. Methods: To evaluate whether there is such an association in Chinese population, a case-control study enrolled 494 patients and 494 healthy controls was carried out. Sequenom MassARRAY platform was used for genotyping. Results: This study showed that rs16901946 G allele was associated with increased risk of gastric cancer (AG: adjusted OR = 1.33, 95% CI =1.02-1.73, p=0.033; GG: adjusted OR = 2.07; 95% CI = 1.11-3.86, p=0.023, AG/GG: adjusted OR = 1.39, 95% CI = 1.08-1.1.79, p=0.011; additive model: adjusted OR = 1.37; 95% CI = 1.10-1.70, p=0.004). Stratified analysis revealed that the increased risk was more evident in the cohort of younger subjects (adjusted OR = 1.84, 95% CI = 1.18-2.87, p=0.007), males (adjusted OR = 1.55, 95% CI = 1.15-2.08, p=0.004), positive Helicobacter pylori infection (adjusted OR = 1.44, 95% CI = 1.02-2.03, p=0.041), gastric cardia adenocarcinoma (adjusted OR = 1.61, 95% CI = 1.10-2.35, p=0.014), and tumor stage T1-T2 (adjusted OR = 1.58, 95% CI = 1.10-2.28, p=0.013). Conclusions: Our study suggested that rs16901946 G allele carriers have an increased risk of gastric cancer, and the risk could be enhanced by the interactions between the polymorphism and age, sex, Helicobacter pylori infection.

Nucleotide excision repair pathway gene polymorphisms are linked to breast cancer risk in a Chinese population.

Polymorphisms in nucleotide excision repair (NER) pathway genes are associated with the risk of breast cancer, but the relevance of these associations appeared to vary according to the ethnicity of the subjects. To systemically evaluate the potential associations between NER polymorphisms and breast cancer risk in a Chinese population, we carried out a case-control study on 450 breast cancer patients and 430 healthy controls. Sequenom MassARRAY was used for genotyping, and immunohistochemistry was performed to detect estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER-2) expression in tumor tissue. Our results showed that ERCC1 rs11615 (additive model: ORadjusted: 1.36, 95% CI: 1.08-1.71, p = 0.009), XPC rs2228000 (additive model: ORadjusted: 1.39, 95% CI: 1.13-1.72, p = 0.002) and ERCC2/XPD rs50872 (additive model: ORadjusted: 1.32, 95% CI: 1.04-1.67, p = 0.021) were associated with an increased risk of breast cancer. Stratified analysis revealed three polymorphisms (rs11615, rs1800975, and rs50872) to be associated with breast cancer in menopausal females. Three polymorphisms were associated with specific breast cancer grades (rs11615 with grade 3, rs2228000 and rs50872 with grade 1-2). Two polymorphisms (rs2228001 and rs50872) were associated with the risk of breast cancer with negative lymph node involvement. rs1800975 and rs50872 were associated with the risk of ER- and PR- breast cancer, whereas rs11615 was associated with the risk of ER+ and PR+ breast cancer. We found that carriers of the T allele of ERCC1 rs11615, XPC rs2228000 and rs50872, particularly in postmenopausal females, have an increased risk of breast cancer.

The association of Phosphatase and tensin homolog (PTEN) deletion and prostate cancer risk: A meta-analysis.

OBJECTIVE: Phosphatase and tensin homolog (PTEN) deleted on chromosome 10, a tumor suppressor that negatively regulates the phosphoinositide-3-kinase(PI3K) which has been implicated in a number of human malignancies including prostate cancer. However the prognostic value of PTEN deletion in prostate cancer patient's diagnosis and the mechanism of PTEN deletion in prostate cancer development still remain unclear. METHOD: A meta-analysis of 26 published studies including 8097 prostate cancer patients was performed. RESULTS: Compared to PTEN normal patients, PTEN deletion patients showed a higher aggressive Gleason score(OR: 1.284, 95%CI=1.145-1.439) and pathological stage(OR: 1.628, 95%CI=1.270-2.087) which generally had a higher risk in prostate replace(HR: 1.738, 95%CI=1.264-2.390). Significant association between PTEN deletion and ERG rearrangements in prostate cancer development was also proved that compared to PTEN normal patients, patients with PTEN deletion showed a higher risk in ERG rearrangements(OR: 1.345, 95%CI=1.102-1.788). CONCLUSION: This study indicated that patients with PTEN deletion were associated with higher pathological stage or Gleason score and a higher risk in prostate cancer replace potentially represent a novel clinically relevant event to identify individuals at increased risk for the occurrence, progression and prognosis of prostate cancer. Prostate cancer patients with PTEN deletion usually had a higher risk in ERG rearrangements than other patients may be a potential new area for identifying poor prognosis patients and selecting patients for targeted therapies which required confirmation through adequately designed prospective studies.

Association of Clostridium difficile infection in hospital mortality: A systematic review and meta-analysis.

BACKGROUND: The purpose of this study was to evaluate whether Clostridium difficile infection (CDI) contributed to hospital mortality and whether the correlation between intensive care units (ICUs) and surgical wards in hospital CDI risk still remain controversial. METHODS: By meta-analysis, 12 eligible studies involving 8,509 cases and 247,285 controls were identified via PubMed and Embase. RESULTS: CDI patients had a higher risk of hospital mortality than non-CDI patients (odds ratio [OR], 1.899; 95% confidence interval [CI], 1.269-2.840), especially in 30-day mortality (OR, 2.521; 95% CI, 1.800-3.531). No correlation was found between hospital CDI and Charlson comorbidity index (OR, 0.830; 95% CI, 0.559-1.231). Patients treated in the ICU have an increased risk of hospital CDI (OR, 1.820; 95% CI, 1.161-2.851). However, the risk of CDI in patients who used to have surgery in surgical wards was not different to patients in the other departments (OR, 1.054; 95% CI, 0.838-1.325). Moreover, CDI patients in studies from the most recent 5 years have a higher risk of hospital mortality (OR, 2.171; 95% CI, 1.426-3.304). CONCLUSION: Hospital CDI was associated with an increased risk of hospital mortality, especially in 30-day mortality. In addition, when compared with past years, CDI patients have a higher risk of hospital mortality in the most recent 5 years. Given the rapid dissemination of this organism worldwide, there is a need to aggressively develop and evaluate primary preventive strategies targeting CDI among hospitalized patients, especially in ICUs.

Evaluation the susceptibility of five polymorphisms in microRNA-binding sites to female breast cancer risk in Chinese population.

Polymorphisms in microRNA (miRNA) binding site have been widely discussed to be associated with cancer risk; however, the associations were unclear in Chinese population. To investigate the associations of five polymorphisms (rs11097457, rs1434536, rs1970801, rs1044129, rs11169571) in miRNA binding sites with breast cancer risk, a total of 435 female patients with breast cancer and 439 age- and gender-matched tumor-free individuals were enrolled in this case-control study. Sequenom MassARRAY was applied to detect the polymorphisms, and the immunohistochemistry assay was used to measure the expression of estrogen receptor (ER) and progesterone receptor (PR) and CerbB-2. The data showed that these polymorphisms were not associated with breast cancer risk or clinical characters of breast cancer in all participants and sub-group with the exception that, in the sub-group of women with their first menstruation after 14 years old, those who carried rs1970801 T allele (genotype TT/GT) were associated with decreased breast cancer risk. In short, this case-control study provided the evidence that women with their first menstruation after 14 years old and carried rs1970801 T allele (genotype TT/GT) were associated with decreased breast cancer risk.