Effects of Cadmium on Kidney Function of the Freshwater Turtles Mauremys reevesii.

This research studied the effects of cadmium on kidney function of the freshwater turtles Mauremys reevesii. Turtles were injected intraperitoneally with 0, 7.5, 15, and 30 mg kg-1 cadmium separately for once. The samples were gathered to check the kidney index, the contents of TP in kidney tissue, and the levels of CRE and BUN in the plasma of the turtles. Results showed that the concentration of TP was overall decreased with the extension of cadmium exposure time and the increasing of the exposure dose of cadmium. The CRE content in the plasma of each treatment group increased with the prolongation of exposure time in a dose-dependent, and the BUN levels of all poisoned groups showed a trend of increasing. The kidney index of treated turtles increased. In summary, cadmium could induce the increase of turtle kidney index, the content of CRE and BUN in plasma, and the decrease of TP content in the kidney.

Identification of RNA-splicing factor Lsm12 as a novel tumor-associated gene and a potent biomarker in Oral Squamous Cell Carcinoma (OSCC).

BACKGROUND: Oral squamous cell carcinoma (OSCC) is one of the common cancers worldwide. The lack of specific biomarkers and therapeutic targets leads to delayed diagnosis and hence the poor prognosis of OSCC patients. Thus, it is urgent to identify effective biomarkers and therapeutic targets for OSCC. METHODS: We established the golden hamster carcinogenic model of OSCC induced by 7,12-dimethylbenz(a) anthrancene (DMBA) and used mRNA microarrays to detect the differentially expressed genes (DEGs). DEGs were validated in OSCC clinical tissue microarrays using immunohistochemistry method. Whole transcriptome sequencing was performed to obtain an overview of biological functions of Lsm12. PCR assay and sequencing were employed to investigate the alternative splicing of genes regulated by Lsm12. Cell proliferation, colony formation, Transwell migration and invasion assay and in vivo tumor formation assay were performed to investigate the roles of Lsm12 and two transcript variants of USO1 in OSCC cells. RESULTS: Lsm12 was identified to be significantly up-regulated in the animal model of OSCC tumorigenesis, which was validated in the clinical OSCC samples. In the paired normal tissues, Lsm12 staining was negative (91%, 92/101) or weak, while in OSCC tissues, positive rate is 100% and strong staining spread over the whole tissues in 93 (93/101, 92%) cases. Lsm12 overexpression significantly promoted OSCC cell growth, colony formation, migration and invasion abilities, while Lsm12 knockdown showed the opposite trends on these phenotypes and obviously inhibited the tumor formation in vivo. Furthermore, Lsm12 overexpression caused the inclusion of USO1 exon 15 and Lsm12 knockdown induced exon 15 skipping. Exon 15-retained USO1 significantly promoted the malignant phenotypes of OSCC cells when compared with the exon 15-deleted USO1. CONCLUSIONS: We identified Lsm12, a novel tumorigenesis-related gene, as an important regulator involved in OSCC tumorigenesis. Lsm12 is a novel RNA-splicing related gene and can regulate the alternative splicing of USO1 exon 15 which was associated closely with OSCC carcinogenesis. Our findings thus provide that Lsm12 might be a potent biomarker and potential therapeutic target for OSCC.

Lipid peroxidation of kidney of the turtle Mauremys reevesii caused by cadmium.

This research was designed to investigate lipid peroxidation of the kidney of turtle (Mauremys reevesii) caused by cadmium. Turtles were injected intraperitoneally with cadmium at the concentration of 0 (control), 7.5, 15, and 30 mg/kg, and 5 turtles were taken from each group after exposure for 1 week (1 w), 2 weeks (2 w), and 3 weeks (3 w). Superoxide dismutase (SOD) and catalase (CAT) activities as well as glutathione (GSH) and malonyldialdehyde (MDA) contents in the homogenate of kidney tissue were analyzed. The results demonstrated that a short time of low dose of cadmium could stimulate the increase of SOD activity in the kidney of turtles, but a long time of high dose of cadmium could induce the decrease of SOD activity in the kidney of turtles. Cadmium could decrease CAT activity and GSH content in turtle kidney, but increased MDA content in turtle kidney. There were some other effects on the turtles, such as depression and diarrhea. The experimental results indicate that cadmium causes temporary oxidative stress on the kidney of turtles.

Oxidative stress in liver of turtle Mauremys reevesii caused by cadmium.

The research was designed to examine oxidative stress of the liver of turtle Mauremys reevesii caused by cadmium (Cd). Turtles were injected intraperitoneally with cadmium at the concentration of 7.5, 15, and 30 mg/kg, and 5 turtles were taken from each group after exposure for 1 week (1 w), 2 weeks (2 w), and 3 weeks (3 w). The activities of SOD and CAT as well as the contents of GSH and MDA in liver tissues were detected by using a kit. The results showed that the difference between the control group and the Cd-treated group was statistically significant with the increase of Cd concentration and the prolongation of exposure time, which suggested that Cd caused oxidative stress on the liver of turtles.

Effects of cadmium on the activities of ALT and AST as well as the content of TP in plasma of freshwater turtle Mauremys reevesii.

Cadmium (Cd) is one of the toxic metals in the aquatic environment. This study was designed to examine the effects of Cd on the activities of ALT and AST and the concentrations of TP in plasma of freshwater turtle Mauremys reevesii. Experiment turtles were exposed to Cd at the concentration of 15 mg/kg by intraperitoneal injection. The activities of ALT and AST and the concentrations of TP were investigated. Compared with the controls, the activities of ALT and AST in plasma of the treated turtles significantly increased. The concentrations of TP were comparable between the treated turtles and the controls except that were higher than the control turtles in 14 days (14 d) and 56 days (56 d). As a result that turtles exposed to Cd were led to liver function damage.

Effects of cadmium on the gene transcription of the liver in the freshwater turtle (Chinemys reevesii).

This study investigated the related gene transcription of liver in freshwater turtle Chinemys reevesii exposed to cadmium (Cd). After acclimation, healthy turtles were selected for experiments. They were randomly divided into four experimental groups and each group had 5 animals. The turtles were treated with 0 mg/kg, 7.5 mg/kg, 15 mg/kg, and 30 mg/kg Cd chloride separately by intraperitoneal injection. Liver samples were collected for examination of the transcription of related genes at 2 weeks after Cd exposure. The transcription of mRNA of MT, SOD, CAT, PNKP, and GPX4 genes in turtle liver cells were analyzed. Results showed that Cd promoted MT mRNA transcription in turtle's liver at low dose (7.5 mg/kg) and inhibited MT mRNA transcription in turtle's liver at middle dose (15 mg/kg) and high dose (30 mg/kg). Cd inhibited the transcription of SOD, CAT, and PNKP mRNA in turtle's liver, and the inhibition was obvious at high dose (30 mg/kg). Cd promoted GPX4 mRNA transcription in turtle's liver, especially at low dose (7.5 mg/kg). In conclusion, Cd had different effects on the mRNA transcription of liver cells in the freshwater turtle Chinemys reevesii exposed to Cd.

Effects of cadmium on oxidative stress activities in plasma of freshwater turtle Chinemys reevesii.

Cadmium (Cd) has been recently found in high concentrations in the aquatic environment. This study was designed to examine the effects of Cd on the oxidative stress activities in plasma of freshwater turtle Chinemys reevesii. Experimental turtles were exposed to Cd at the concentration of 15 mg/kg by intraperitoneal injection, and redox status was investigated. Compared to the controls, superoxide dismutase (SOD) and catalase activities in plasma of the treated animals significantly decreased in week 1, week 2, and week 4. However, SOD activities gradually increased from week 4 to week 8. The treated animals had higher content of MDA and lower content of GSH in plasma over the observation period. In conclusion, our results showed that Cd decreased the antioxidant capacity and increased the level of oxidative damage product in plasma, which suggest that Cd causes oxidative stress and damage in the animal under the experimental conditions.

Elevated interleukin-18 serum levels in chronic schizophrenia: Association with psychopathology.

BACKGROUND: Schizophrenia is associated with various abnormalities in the immune system including elevated levels of Interleukin-18 (IL-18), a potent inflammatory cytokine in T-helper 1 (Th1) responses. The aim of this study was to assess the clinical significance of serum IL-18 levels in various stages of schizophrenia. METHODS: We measured serum IL-18 levels using a sandwich enzyme-linked immunosorbent assay (ELISA) from 78 never-medicated first-episode schizophrenia, 79 medicated chronic schizophrenia and 78 healthy control subjects. The symptoms of schizophrenia were assessed by the Positive and Negative Syndrome Scale (PANSS). RESULTS: The chronic patients had significantly greater serum IL-18 levels than both first-episode patients and controls. Serum IL-18 was also positively correlated with the PANSS general psychopathology subscore in chronic schizophrenic patients. CONCLUSIONS: Our results showed elevated IL-18 pathway activity may be involved in the psychopathology of schizophrenia.

[Clinical investigation of a family with brachydactyly type A1 and the identification of the disease gene].

OBJECTIVE: To determine the inheritance mode and pathogenesis of a family with brachydactyly type A1 in Jining, Shandong province via clinical feature and disease gene analysis. METHODS: Family survey and clinical examinations were performed to determine the inheritance mode; microsatellite polymorphic markers and polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP)were employed for linkage analysis and mutation screening respectively. RESULTS: The brachydactyly type of the family was type A1 (BDA1), and autosomal dominant inheritance. A missense mutation (G298A) of the indian hedgehog gene (IHH) was identified in the patients of this family. CONCLUSION: A missense mutation G298A of the IHH gene might be the molecular basis for the brachydactyly type A1 in this family from Shandong province.