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on and/or activities may be effective for HCC treatment.
TBX3 is a liver-specific target of the Wnt/β-catenin pathway and thought to be an oncogene in promoting liver cancer development. Herein, we demonstrate that TBX3 is in fact a tumor suppressor gene that restricts liver tumor growth. Strategies which increase TBX3 expression and/or activities may be effective for HCC treatment.The term non-alcoholic fatty liver disease (NAFLD) was originally coined to describe hepatic fat deposition as part of the metabolic syndrome. However, a variety of rare hereditary liver and metabolic diseases, intestinal diseases, endocrine disorders and drugs may underlie, mimic, or aggravate NAFLD. In contrast to primary NAFLD, therapeutic interventions are available for many secondary causes of NAFLD. Accordingly, secondary causes of fatty liver disease should be considered during the diagnostic workup of patients with fatty liver disease, and treatment of the underlying disease should be started to halt disease progression. find more Common genetic variants in several genes involved in lipid handling and metabolism modulate the risk of progression from steatosis to fibrosis, cirrhosis and hepatocellular carcinoma development in NAFLD, alcohol-related liver disease and viral hepatitis. Hence, we speculate that genotyping of common risk variants for liver disease progression may be equally useful to gauge the likelihood of developing advanced liver disease in patients with secondary fatty liver disease.Cadmium (Cd) was a serious heavy metal pollutant. Cd exposure will cause damage to reproductive organs. It was largely unknown whether Cd exposure caused inflammation and apoptosis in epididymis. In this study, we established models of Cd exposure in swine, and the apoptotic level of epididymis was detected by in situ TUNEL fluorescence staining assay, the results showed that Cd exposure significantly increased TUNEL-apoptosis index. Furthermore, the results of qRT-PCR and Western blot showed that Cd activated the proto-oncogenic serine/threonine kinase-1 (RAF1)/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) signal pathway (RAF1/MEK/ERK) and led to the subsequent up-regulation of the nuclear factor-κB (NF-κB), tumor necrosis factor α (TNF-α), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), caused inflammation in epididymis. NF-κB inflammation pathway also mediated the tumor protein P53 (P53) and indirectly activated the Cytochrome c (Cytc), B-cell lymphoma-2 (Bcl-2), Bcl-2-Associated X protein (Bax), Caspase 3, Caspase 9. In summary, we believed that the RAF1/MEK/ERK pathway came into play in the apoptosis of epididymal tissues exposed to Cd by activating the NF-κB Inflammation pathway, followed by activation of the mitochondrial apoptotic pathway. This study provides more abundant data for exploring the reproductive toxicity of Cd.Deafness is the most common sensory disorder in the world. Ototoxic drugs are common inducing factors of sensorineural hearing loss, and cochlear hair cell (HC) damage is the main concern of the present studies. Cisplatin is a widely used, highly effective antitumor drug, but some patients have experienced irreversible hearing loss as a result of its application. This hearing loss is closely related to HC apoptosis and autophagy. U0126 is a specific inhibitor of the extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) signaling pathway and has neuroprotective effects. For example, the neuroprotective effect of U0126 on ischemic stroke has been widely recognized. In neural cells, U0126 can prevent death due to excess glutamate, dopamine, or zinc ions. However, no studies of U0126 and ototoxic drug-induced injury have been reported to date. In the present study, we found that U0126 pretreatment significantly reduced the apoptosis and autophagy of HCs in auditory House Ear Institute-Organ of Corti 1 (HEI-OC1) cells and cochlear HCs. In addition, U0126 reduced the cisplatin-induced production of reactive oxygen species as well as the cisplatin-induced decrease in the mitochondrial membrane potential. These findings suggest that U0126 may be a potential therapeutic candidate for the prevention of cisplatin-induced ototoxicity.Eukaryotic translation initiation factor 4E (eIF4E) and protein arginine methyltransferase 5 (PRMT5) are frequently overexpressed in colorectal cancer (CRC) tissues and associated with poor prognosis. Ribavirin, the only clinically approved drug known to target eIF4E, is an anti-viral molecule currently used in hepatitis C therapy. The potential of ribavirin to treat CRC remains largely unknown. Ribavirin treatment in CRC cell lines drastically inhibited cell proliferation and colony formation, induced S phase arrest and reduced cyclin D1, cyclin A/E and proliferating cell nuclear antigen (PCNA) levels in vitro, and suppressed tumorigenesis in mouse model of colitis-associated CRC. Mechanistically, ribavirin treatment significantly reduced PRMT5 and eIF4E protein levels and the accumulation of symmetric dimethylation of histone 3 at arginine 8 (H3R8me2s) and that of histone 4 at arginine 3 (H4R3me2s). Importantly, inhibition of PRMT5 by ribavirin resulted in promoted H3R8 methylation in eIF4E promoter region. Our results demonstrate the anti-cancer efficacy of ribavirin in CRC and suggest that the anti-cancer efficacy of ribavirin may be mediated by downregulating PRMT5 levels but not its enzymatic activity.
Many workers are exposed to lead dust in lead-‑zinc mines. Exposure to this heavy toxic metal and its compounds can cause irreversible adverse health effects.

To assess possible hematotoxic, nephrotoxic, and hepatotoxic potentials of low levels of lead in a group of mine workers exposed to this heavy metal in an unusual work schedule.

A total of 73 exposed and 70 non-exposed employees were interviewed. Demographic data, and occupational and medical history of the employees were obtained by questionnaires. Air monitoring was performed to determine the workers' time-weighted average (TWA) exposure to lead dust. The threshold limit value (TLV) for lead was adjusted for unusual work schedules according to the model developed by the University of Montreal and the Institute de Recherche en Sante et en Securite du Travail (IRSST). Blood samples were collected for complete blood count, liver and kidney function tests. Data were analyzed using version 21.0 of the SPSS software.

The TWA exposure of workers was 24μg/m
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