MicroRNA-4463 facilitates the development of colon cancer by suppression of the expression of PPP1R12B.

PURPOSE: In the present work, we investigated the expression pattern of miR-4463 in the non-metastasis and metastasis colorectal cancer (CRC) patients and its regulation axis. METHODS: RT-qPCR assay was performed to assess miR-4463 expression in the serum and tissues of patients with non-metastasis and metastasis, and in the CRC cell lines. MTT assay, colony formation assay, transwell assay, and flow cytometry assay were used to examine the role of miR-4463 in CRC cell viability, proliferation, and migration. Bioinformatic analysis was used to identify the potential target gene of miR-4463, and the targeting relationship between miR-4463 and PPP1R12B was verified in vitro using dual luciferase assay. Western blotting assay was used to determine the protein level of the target gene PPP1R12B in CRC cells under the transfections of miR-4463 mimic, inhibitor and vectors overexpressing PPP1R12B. RESULTS: miR-4463 was markedly increased in the non-metastasis CRC tissues, and increased even higher in the metastasis CRC tissues, while miR-4463 expression had no significant difference in serum from non-metastasis and metastasis CRC samples. Besides, miR-4463 was upregulated in CRC cell lines. Functionally, miR-4463 promoted CRC cell proliferation, migration, and inhibiting cell apoptosis. Further analysis revealed that the miR-4463/PPP1R12B axis was responsible for the role of this miRNA. CONCLUSION: We reported the roles of miR-4463 in CRC proliferation and migration, supporting that miR-4463 could be a potential predictive diagnostic marker for colon cancer.

Traditional Chinese medicine reverses cancer multidrug resistance and its mechanism.

Chemotherapy is one of the most commonly used clinical treatments among the currently available cancer therapies. However, the phenomenon of Multidrug resistance (MDR) has become a challenge in the treatment process, weakening the impact of chemotherapy. Extensive research on elucidating the development of cancer MDR has identified the following mechanisms that play a critical role in the development of several MDR reversal agents: abnormal expression of cell membrane transporters, adaptation of cancer cells to the microenvironment, regulation of hypoxia, repair of DNA damage and reduction of apoptosis, the enhancement of the EMT process, the existence of cancer stem cells (CSCs), and the abnormal activation of key signaling pathways. However, they failed to demonstrate significant efficacy due to severe side effects during their clinical trials. Traditional Chinese medicines (TCMs) are known to play an important anti-cancer role since they have low toxicity, high efficacy, and safety and can reverse MDR. TCMs reversal agents can be divided into Chinese medicine monomers, synthetic monomers, analogs, or derivatives. Several studies have shown that TCMs can effectively overcome cancer MDR and can be effectively used for treating cancer patients.

The role of macrophages during breast cancer development and response to chemotherapy.

Macrophages play an important role in the immune system as a key host defense against pathogens. Non-polarized macrophages can differentiate into pro-inflammatory classical pathway-activated macrophages or anti-inflammatory alternative pathway-activated macrophages, both of which play central roles in breast cancer growth and progression in a process called polarization of macrophages. Classical pathway-activated and alternative pathway-activated macrophages can transform into each other and their transformational properties and orientation are determined by cytokines in the tumor microenvironment. Tumor-associated macrophages display many functions, such as tissue reforming, participating in inflammation and tumor growth in breast cancer progression. Some cytokines, such as interleukins and transcriptional activators, reside in the tumor microenvironment and influence tumor-associated macrophages. Chemotherapy is a common treatment for breast cancer and macrophages play an important role in mammary tumor cell migration, cancer invasion, and angiogenesis. This review summarizes the activities of tumor-associated macrophages in the mammary tumor, chemotherapeutic processes and some potential strategies for breast cancer therapy.

FAMLF is a target of miR-181b in Burkitt lymphoma.

Burkitt lymphoma (BL) is a highly malignant non-Hodgkin's lymphoma that is closely related to the abnormal expression of genes. Familial acute myelogenous leukemia related factor (FAMLF; GenBank accession No. EF413001.1) is a novel gene that was cloned by our research group, and miR-181b is located in the intron of the FAMLF gene. To verify the role of miR-181b and FAMLF in BL, RNAhybrid software was used to predict target site of miR-181b on FAMLF and real-time quantitative PCR (RQ-PCR) was used to detect expression of miR-181b and FAMLF in BL patients, Raji cells and unaffected individuals. miR-181b was then transfected into Raji and CA46 cell lines and FAMLF expression was examined by RQ-PCR and western blotting. Further, Raji cells viability and proliferation were detected by MTT and clone formation, and Raji cell cycle and apoptosis were detected by flow cytometry. The results showed that miR-181b can bind to bases 21-42 of the FAMLF 5' untranslated region (UTR), FAMLF was highly expressed and miR-181b was lowly expressed in BL patients compared with unaffected individuals. FAMLF expression was significantly and inversely correlated to miR-181b expression, and miR-181b negatively regulated FAMLF at posttranscriptional and translational levels. A dual-luciferase reporter gene assay identified that the 5' UTR of FAMLF mRNA contained putative binding sites for miR-181b. Down-regulation of FAMLF by miR-181b arrested cell cycle, inhibited cell viability and proliferation in a BL cell line model. Our findings explain a new mechanism of BL pathogenesis and may also have implications in the therapy of FAMLF-overexpressing BL.

FAMLF is a target of miR-181b in Burkitt lymphoma

Burkitt lymphoma (BL) is a highly malignant non-Hodgkin's lymphoma that is closely related to the abnormal expression of genes. Familial acute myelogenous leukemia related factor (FAMLF; GenBank accession No. EF413001.1) is a novel gene that was cloned by our research group, and miR-181b is located in the intron of the FAMLF gene. To verify the role of miR-181b and FAMLF in BL, RNAhybrid software was used to predict target site of miR-181b on FAMLF and real-time quantitative PCR (RQ-PCR) was used to detect expression of miR-181b and FAMLF in BL patients, Raji cells and unaffected individuals. miR-181b was then transfected into Raji and CA46 cell lines and FAMLF expression was examined by RQ-PCR and western blotting. Further, Raji cells viability and proliferation were detected by MTT and clone formation, and Raji cell cycle and apoptosis were detected by flow cytometry. The results showed that miR-181b can bind to bases 21–42 of the FAMLF 5′ untranslated region (UTR), FAMLF was highly expressed and miR-181b was lowly expressed in BL patients compared with unaffected individuals. FAMLF expression was significantly and inversely correlated to miR-181b expression, and miR-181b negatively regulated FAMLF at posttranscriptional and translational levels. A dual-luciferase reporter gene assay identified that the 5′ UTR of FAMLF mRNA contained putative binding sites for miR-181b. Down-regulation of FAMLF by miR-181b arrested cell cycle, inhibited cell viability and proliferation in a BL cell line model. Our findings explain a new mechanism of BL pathogenesis and may also have implications in the therapy of FAMLF-overexpressing BL.

Detection of quantitative trait loci for kernel oil and protein concentration in a B73 and Zheng58 maize cross.

Maize (Zea mays L.) is one of the most important food crops throughout the world, and provides oil and proteins to humans and livestock. Kernel oil and protein content in maize are two complex quantitative traits. In order to identify quantitative trait loci (QTL) controlling oil and protein concentration in maize kernels, and to evaluate their genetic effects, QTL analysis was conducted on an F3:4 population derived from a cross between an inbred line with a low oil and protein concentration (Zheng58) and an inbred line with a higher oil and protein concentration (B73). A total of 189 polymorphic simple sequence repeat markers were used to construct a linkage map. Eleven QTLs for kernel oil concentration were detected on nine chromosomes, except for chromosome 9. A single QTL explained 4.6 to 11.1% of the phenotypic variance. Ten QTLs for kernel protein concentration were also detected on nine chromosomes, except for chromosome 9. A single QTL explained 4.2 to 11.4% of the phenotypic variance. Interestingly, novel QTLs for oil concentration (qOIL08-01 and qOIL10-01) and QTLs for protein concentration (qPRO01-01 and qPRO05-01) were specific to the population studied, which could explain 7.1 to 11.1% of the phenotypic variance. These results will provide better understanding of the genetic basis of oil and protein concentrations in maize. The markers closely linked with the QTLs will facilitate breeding of maize varieties with high oil and protein concentrations through molecular marker-assisted selection.

CD19+ B cell subsets in the peripheral blood and skin lesions of psoriasis patients and their correlations with disease severity.

T lymphocytes are important in the pathogenesis of psoriasis, and increasing evidence indicates that B cells also play an important role. The mechanisms of action, however, remain unclear. We evaluated the ratios of CD19+ B cells in peripheral blood mononuclear cells (PBMCs) from 157 patients with psoriasis (65 patients with psoriasis vulgaris, 32 patients with erythrodermic psoriasis, 30 patients with arthropathic psoriasis, and 30 patients with pustular psoriasis) and 35 healthy controls (HCs). Ratios of CD19+ B cells in skin lesions were compared with non-lesions in 7 erythrodermic psoriasis patients. The Psoriasis Area Severity Index (PASI) was used to measure disease severity. CD19+ B cell ratios in PBMCs from psoriasis vulgaris (at both the active and stationary stage) and arthropathic psoriasis patients were higher compared with HCs (P<0.01), but ratios were lower in erythrodermic and pustular psoriasis patients (P<0.01). CD19+ B cell ratios in erythrodermic psoriasis skin lesions were higher than in non-lesion areas (P<0.001). Different subsets of CD19+CD40+, CD19+CD44+, CD19+CD80+, CD19+CD86+, CD19+CD11b+, and CD19+HLA-DR+ B cells in PBMCs were observed in different psoriasis clinical subtypes. PASI scores were positively correlated with CD19+ B cell ratios in psoriasis vulgaris and arthropathic psoriasis cases (r=0.871 and r=0.692, respectively, P<0.01), but were negatively correlated in pustular psoriasis (r=-0.569, P<0.01). The results indicated that similar to T cells, B cells activation may also play important roles in different pathological stages of psoriasis.

Pterostilbene as treatment for severe acute pancreatitis.

Acute pancreatitis (AP) has a fast onset and progression, which lead to an unfavorable prognosis. Therefore, the development of novel drugs for its treatment is critical. As a homologous derivative of resveratrol, pterostilbene exerts a variety of effects including anti-inflammatory, antioxidant, and antitumor effects. This study investigated the potential of pterostilbene for treatment of severe AP (SAP) and related mechanisms. Effects of pterostilbene were evaluated in a Wistar rat model of AP. Serum levels of amylase (AMY), creatinine (Cr), and alanine aminotransferase (ALT) were quantified. Furthermore, serum levels of tumor necrosis factor (TNF)-a and interleukin (IL)-1b were quantified using enzyme-linked immunosorbent assay. Nuclear factor (NF)-kB expression in pancreatic tissues was quantified by real-time PCR and western blotting. The production of reactive oxygen species (ROS) was determined using a spectrometer, while superoxide dismutase (SOD) activity was assayed. In the AP rat model, the expression of inflammatory markers TNF-a and IL-1b, expression of NF-kB, and serum indices (AMY, Cr, and ALT) increased compared to the corresponding levels in the control group (P < 0.05). Pterostilbene reduced serum levels of TNF-a and IL-1b; decreased NF-kB gene expression, serum indices, and ROS generation; and increased SOD activity in a dose-dependent manner. In conclusion, pterostilbene can alleviate SAP-induced tissue damage by decreasing the inflammatory response and by promoting antioxidation leading to the protection of pancreatic tissues.

Wnt1 and SFRP1 as potential prognostic factors and therapeutic targets in cutaneous squamous cell carcinoma.

The Wnt signaling pathway plays a key role in insurgence and progression of many different forms of cancer. Some crucial components of the Wnt pathway have been proposed to be novel targets for cancer therapy. To date, the Wnt signaling pathway has not been studied in cutaneous squamous cell carcinoma (CSCC). This study was designed to investigate the expression of Wnt1 and SFRP1 from the Wnt pathway in CSCC. Tissue samples were obtained from 35 patients with CSCC and 30 controls admitted to the Xinjiang Uygur Autonomous Region People's Hospital at Urumchi City, China. Gene and protein expressions of Wnt1 and SFRP1 were quantified by immunohistochemistry and western blotting. Wnt1 expression was significantly higher (P < 0.05) in CSCC samples than in normal skin cells of the control subjects; in contrast, SFRP1 expression was significantly lower in CSCC tissues than that in tissues of control subjects (P < 0.05). Moreover, Wnt1 expression (P < 0.05) was found to be correlated with histopathological differentiation in CSCC, and negatively correlated with SFRP1 expression in CSCC (rs = -0.473, P = 0.015). Therefore, we concluded that Wnt1 and SFRP1 play important roles in the development of CSCC and could be potent markers for diagnosis, prevention, and therapy of CSCC.

Proteomic analysis of mycelial proteins from Magnaporthe oryzae under nitrogen starvation.

Magnaporthe oryzae is an important model system in studies of plant pathogenic fungi, and nitrogen is a key nutrient source affecting microbial growth and development. In order to understand how nitrogen stress causes changes in mycelial proteins, we analyzed differentially expressed mycelial proteins from the M. oryzae virulent strain CH-63 using two-dimensional electrophoresis and mass spectrometry in complete medium or under nitrogen starvation conditions. A total of 975 ± 70 and 1169 ± 90 protein spots were detected in complete medium and under nitrogen starvation conditions, respectively. Forty-nine protein spots exhibited at least 2-fold up-regulation or down-regulation at the protein level according to PDQuest7.4. Moreover, 43 protein spots were successfully identified by matrix-assisted laser desorption/ionization-time-of-flight/time-of-flight mass spectrometry. Among these spots, 6 proteins were functionally unknown and 37 proteins were categorized into 5 groups according to their functions, including development, metabolism, biosynthesis, and biological process. These 37 proteins were further analyzed for their enriched metabolic pathways by KOBAS2.0, and 14 proteins were found to be involved in glycolysis, tricarboxylic acid cycle, and nitrogen metabolism. Taken together, the regulation of M. oryzae growth under the nitrogen starvation conditions appears to be complex because of the various proteins and enzymes involved.

Tetradecyl 2,3-dihydroxybenzoate promotes functional recovery after spinal cord injury in adult rats.

Tetradecyl 2,3-dihydroxybenzoate (ABG001) is a small molecule separated from gentian extract that has a similar effect to nerve growth factor. It is not clear whether it can promote functional recovery in animals suffering from a central nervous system injury. In order to explore the role of ABG001 in restoration of tissue structure and motor function of rats with spinal cord injury (SCI), ABG001 (0.4 mg/kg) was administered intraperitoneally. Subsequently, behavioral assessments and morphological studies were performed to detect recovery of hind limb motor function and neuroregeneration. The results showed that compared with DMSO group, the rats in the ABG treatment group had better performance in BBB score and grip strength test (P < 0.05), the area of necrosis was smaller (P < 0.05), GFAP expression was significantly reduced (P < 0.01), and Map-2 expression was significantly increased (P < 0.01). Additionally, after ABG treatment, the number of fluorogold positive cells transported reversely to red nucleus increased (P < 0.05). The results suggest that ABG001 can promote recovery of hind limb motor function in rats with SCI, which may be related to its functions of inhibiting glial cell proliferation and promoting neuroregeneration.

AMFR gene silencing inhibits the differentiation of porcine preadipocytes.

Our study clarifies the role of the autocrine motility factor receptor (AMFR) gene in porcine preadipocyte differentiation. AMFR-siRNA was transfected into porcine preadipocytes and the preadipocytes were induced to differentiation. Subsequently, qRT-PCR was conducted to examine changes in mRNA expression of a series of genes in porcine preadipocytes, including AMFR, sterol-regulatory element-binding protein-1a (SREBP1a), SREBP2, insulin-induced gene 1 (Insig1), and Insig2. Expression changes in the mRNA of genes regulating adipocyte differentiation were also analyzed using qRT-PCR, including peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein alpha (C/EBPα), and Kruppel-like factor 2 (KLF2). Western blot analysis was conducted to examine the changes in AMFR protein expression in porcine preadipocytes. Additionally, morphological changes in differentiated porcine preadipocytes were examined by oil red O staining, and changes in optical density (OD) values were measured using an ultraviolet spectrophotometer. At 24 h after transfection with AMFR-siRNA, AMFR mRNA expression significantly reduced (P < 0.01), and AMFR protein expression markedly decreased (P < 0.05). The mRNA expression of SREBP1a, SREBP2, Insig1, and C/EBPα was significantly reduced (P < 0.01), whereas the expression of KLF2 mRNA was significantly elevated (P < 0.01). After induction of preadipocyte differentiation, the number of lipid droplets decreased in the AMFR-silenced group, and the OD value markedly reduced (P < 0.05). In addition, the expression of C/EBPα mRNA significantly decreased (P < 0.05), whereas the expression of KLF2 mRNA considerably increased (P < 0.05). Taken together, silencing of the AMFR gene inhibits the differentiation of porcine preadipocytes.

Association of APOA1 gene polymorphisms (rs670, rs5069, and rs2070665) with dyslipidemia in the Kazakhs of Xinjiang.

The aim of this study was to investigate the potential association between apolipoprotein A1 (APOA1) gene rs670, rs5069, and rs2070665 polymorphisms and dyslipidemia in the Kazakh population of Xinjiang, China. Matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS) was used to identify APOA1 (rs670, rs5069, and rs2070665) genotypes in 736 subjects (341 dyslipidemia patients and 395 control subjects). The frequencies of the CC genotype for rs1421085 were found to be 7.2% (obese group), 4.4% (overweight group), and 5.6% (control group). Polymorphisms of the three loci of the APOA1 gene in Kazakh subjects met Hardy-Weinberg equilibrium. The frequencies of the A allele for rs670 were found to be 14.3% (dyslipidemia group) and 12.7% (control group). The frequencies of the T allele for rs5069 and rs2070665 were: dyslipidmia group (7.2 and 30.1%, respectively) and control group (7.7 and 32.5%, respectively). Frequency distributions of the 3 types of genotypes and alleles of the three loci showed no statistically significant difference (P > 0.05). Significant differences were observed in lipoprotein (α) [Lp(α)] between patients with the rs2070665 CT + TT and CC genotypes (P < 0.05); however, none of the other relevant indicators differed significantly between the two genotypes. No significant association was identified between rs670 or rs5069 and the lipid-related metabolic indices assessed in the study. These findings indicate that the polymorphisms in the APOA1 gene (rs670, rs5069, and rs2070665) are not associated with dyslipidemia in the Kazakh population assessed in this study.

A new method for estimating the number of non-differentially expressed genes.

Control of the false discovery rate is a statistical method that is widely used when identifying differentially expressed genes in high-throughput sequencing assays. It is often calculated using an adaptive linear step-up procedure in which the number of non-differentially expressed genes should be estimated accurately. In this paper, we discuss the estimation of this parameter and point out defects in the original estimation method. We also propose a new estimation method and provide the error estimation. We compared the estimation results from the two methods in a simulation study that produced a mean, standard deviation, range, and root mean square error. The results revealed that there was little difference in the mean between the two methods, but the standard deviation, range, and root mean square error obtained using the new method were much smaller than those produced by the original method, which indicates that the new method is more accurate and robust. Furthermore, we used real microarray data to verify the conclusion. Finally we provide a suggestion when analyzing differentially expressed genes using statistical methods.

Effects of IL-10 and glucose on expression of OPG and RANKL in human periodontal ligament fibroblasts.

The effects of interleukin-10 (IL-10) and glucose on mRNA and protein expression of osteoprotegerin (OPG), and its ligand, receptor activator of nuclear factor-κB ligand (RANKL), were investigated in human periodontal ligament fibroblasts (HPDLFs). Primary HPDLFs were treated with different concentrations of IL-10 (0, 1, 10, 25, 50, and 100 ng/mL) or glucose (0, 5.5, 10, 20, 30, and 40 mmol/L). Changes in mRNA and protein expression were examined using the reverse-transcription polymerase chain reaction (RT-PCR) and Western blot analysis, respectively. After IL-10 treatment, mRNA and protein levels of OPG were increased, while mRNA and protein levels of RANKL were decreased (P<0.05), both in a concentration-dependent manner. Glucose stimulation had the opposite concentration-dependent effect to that of IL-10 on OPG and RANKL expression. IL-10 upregulated OPG expression and downregulated RANKL expression, whereas high glucose upregulated RANKL and downregulated OPG in HDPLFs. Abnormal levels of IL-10 and glucose may contribute to the pathogenesis of periodontal disease.

Effects of IL-10 and glucose on expression of OPG and RANKL in human periodontal ligament fibroblasts

The effects of interleukin-10 (IL-10) and glucose on mRNA and protein expression of osteoprotegerin (OPG), and its ligand, receptor activator of nuclear factor-κB ligand (RANKL), were investigated in human periodontal ligament fibroblasts (HPDLFs). Primary HPDLFs were treated with different concentrations of IL-10 (0, 1, 10, 25, 50, and 100 ng/mL) or glucose (0, 5.5, 10, 20, 30, and 40 mmol/L). Changes in mRNA and protein expression were examined using the reverse-transcription polymerase chain reaction (RT-PCR) and Western blot analysis, respectively. After IL-10 treatment, mRNA and protein levels of OPG were increased, while mRNA and protein levels of RANKL were decreased (P<0.05), both in a concentration-dependent manner. Glucose stimulation had the opposite concentration-dependent effect to that of IL-10 on OPG and RANKL expression. IL-10 upregulated OPG expression and downregulated RANKL expression, whereas high glucose upregulated RANKL and downregulated OPG in HDPLFs. Abnormal levels of IL-10 and glucose may contribute to the pathogenesis of periodontal disease.

CD19+ B cell subsets in the peripheral blood and skin lesions of psoriasis patients and their correlations with disease severity

T lymphocytes are important in the pathogenesis of psoriasis, and increasing evidence indicates that B cells also play an important role. The mechanisms of action, however, remain unclear. We evaluated the ratios of CD19+ B cells in peripheral blood mononuclear cells (PBMCs) from 157 patients with psoriasis (65 patients with psoriasis vulgaris, 32 patients with erythrodermic psoriasis, 30 patients with arthropathic psoriasis, and 30 patients with pustular psoriasis) and 35 healthy controls (HCs). Ratios of CD19+ B cells in skin lesions were compared with non-lesions in 7 erythrodermic psoriasis patients. The Psoriasis Area Severity Index (PASI) was used to measure disease severity. CD19+ B cell ratios in PBMCs from psoriasis vulgaris (at both the active and stationary stage) and arthropathic psoriasis patients were higher compared with HCs (P<0.01), but ratios were lower in erythrodermic and pustular psoriasis patients (P<0.01). CD19+ B cell ratios in erythrodermic psoriasis skin lesions were higher than in non-lesion areas (P<0.001). Different subsets of CD19+CD40+, CD19+CD44+, CD19+CD80+, CD19+CD86+, CD19+CD11b+, and CD19+HLA-DR+ B cells in PBMCs were observed in different psoriasis clinical subtypes. PASI scores were positively correlated with CD19+ B cell ratios in psoriasis vulgaris and arthropathic psoriasis cases (r=0.871 and r=0.692, respectively, P<0.01), but were negatively correlated in pustular psoriasis (r=-0.569, P<0.01). The results indicated that similar to T cells, B cells activation may also play important roles in different pathological stages of psoriasis.

Investigation on the association between NLRP3 gene polymorphisms and susceptibility to primary gout.

We conducted a case-control study to investigate the association between 3 common NALP3 polymorphisms (rs10754558, rs7512998, and rs12137901) and the susceptibility to primary gout. A total of 320 patients with primary gout and 320 controls were included in this study. The genotyping of NALP3 rs10754558, rs7512998, and rs12137901 were conducted by polymerase chain reaction-restriction fragment length polymorphism. Comparison analysis showed that primary gout patients were more likely to have higher body mass index, prevalence of hypertension, blood glucose, triglycerides, urea nitrogen, and uric acid (P < 0.05). Logistic regression analysis revealed no significant association between the NALP3 rs10754558, rs7512998, and rs12137901 polymorphisms and the risk of gouty arthritis. In conclusion, we found no significant association between NALP3 gene polymorphisms and the risk of primary gout.

Effect of CYP1A1 and GSTM1 genetic polymorphisms on bone tumor susceptibility.

Tumor gene polymorphisms are often associated with individual susceptibility to genetic diseases. Cytochrome P4501A1 (CYP1A1) and glutathione S-transferase mu 1 (GSTM1) gene polymorphisms are closely related to the susceptibility of the body to chemical carcinogens in the environment. Therefore, we explored the relationship between CYP1A1 and GSTM1 gene polymorphisms and susceptibility to bone tumors. Multiplex-polymerase chain reaction (PCR), allelic-specific PCR, and PCR-restriction fragment length polymorphism techniques were used to analyze CYP1A1 and GSTM1 gene polymorphisms in 52 bone tumor patients and 100 healthy subjects. The allelic variation frequency of the CYP1A1 gene at exon 7 (Ile 462 Val) in bone tumor patients was 0.462, which was significantly higher than that in the normal controls (0.223). The frequency of the absence of the GSTM1 homozygous genotype in the patients (0.65) was also markedly higher than that in the control group (0.41). Subjects with CYP1A1 Val/Val homozygous mutations and absence of the GSTM1 homozygous genotype were at markedly increased risk of developing bone tumors [ORs 4.15 (95%CI: 1.268-13.30) and 2.35 (95%CI: 1.15-4.85), respectively]. The OR for the combined effect of the CYP1A1 and GSTM1 gene polymorphisms was 8.55 (95%CI: 1.75-41.50). CYP1A1 and GSTM1 polymorphisms are genetic risk factors in patients with bone tumors, and the allelic variation of these genes increases the risk of bone tumor occurrence.

Effects of choice of month of treatment and parity order on bovine superovulation traits.

In this study, the performance of 300 Changbaishan Black cattle treated for superovulation from June to September was evaluated to determine the optimal conditions and herds for bovine embryo production. Data analysis revealed that cattle treated in July and August had higher numbers of available embryos (NAE), M1 embryos (NM1), and total embryos (NTE), as well as a higher percentage of M1 embryos (PM1). The temperature and precipitation observed during July and August were greater than those seen in the other two months; strong correlations were observed between these traits and the choice of month of treatment. In addition, multiparous cattle showed a better performance, higher NTE, NAE, NM1, and PM1 values, higher percentages of available embryos, and a lower percentage of degenerated embryos. The co-efficient correlation analysis showed that the month chosen for the treatment did not affect the superovulation traits of nulliparous cattle; however, the choice of the month affected multiparous cattle. Multiparous and nulliparous cattle exhibited many significant differences when treated in July and in August. In addition, the superovulatory traits of multiparous cattle, and not the nulliparous cattle, were strongly correlated to the choice of month of treatment. The results suggested that superovulation is more effective during a period with appropriate environmental temperature and humidity, and that multiparous cattle are more suitable for morula production.