Environmental and ecological studies in northern Alborz (Golestan Province)

Caspian Sea with an area of 400 thousand square kilometers is the largest lake in the world. The Caspian Sea about 1200 km from north to south on the longest section and an average width of 320 km. Along the coastline around the Caspian Sea is about 6500 kilometers. Caspian Sea is about 78,000 cubic kilometers of water volume that is 44% of stocks of blue lakes around the world. Caspian Sea basin, which is composed of seven major basins of the main watershed from west to east are: juniper, Talsh- Anzali, large Sefidrood between Haraz Sefid and, Hraz- Gharehsou, Nagorno Sv- Gorgan and Atrak in the basin of Aras no limits to the beach. Aras sub-basin is located in the North West and Iran, the second largest sub-basin of the Caspian Sea. Talysh-Anzali on the Caspian Sea basin West and the seventh largest sub-basin of the Caspian Sea. White basin is located in the South East of the Caspian Sea and the extent of the sub-basin of the Caspian Sea. Haraz located in the south Caspian Sea basin and the ninth largest sub-basin of the Caspian Sea. Gorgan is located in the South East of the Caspian Sea basin and the fourth largest sub-basin of the Caspian Sea. In these areas, about 28 percent of the total fish production in the northern waters of aquatic allocated

Nonalcoholic Steatohepatitis and HCC in a Hyperphagic Mouse Accelerated by Western Diet.

Background & aimsHow benign liver steatosis progresses to nonalcoholic steatohepatitis (NASH), fibrosis, and hepatocellular carcinoma (HCC) remains elusive. NASH progression entails diverse pathogenic mechanisms and relies on complex cross-talk between multiple tissues such as the gut, adipose tissues, liver, and the brain. Using a hyperphagic mouse fed with a Western diet (WD), we aimed to elucidate the cross-talk and kinetics of hepatic and extrahepatic alterations during NASH-HCC progression, as well as regression.MethodsHyperphagic mice lacking a functional Alms1 gene (Foz/Foz) and wild-type littermates were fed WD or standard chow for 12 weeks for NASH/fibrosis and for 24 weeks for HCC development. NASH regression was modeled by switching back to normal chow after NASH development.ResultsFoz+WD mice were steatotic within 1 to 2 weeks, developed NASH by 4 weeks, and grade 3 fibrosis by 12 weeks, accompanied by chronic kidney injury. Foz+WD mice that continued on WD progressed to cirrhosis and HCC within 24 weeks and had reduced survival as a result of cardiac dysfunction. However, NASH mice that were switched to normal chow showed NASH regression, improved survival, and did not develop HCC. Transcriptomic and histologic analyses of Foz/Foz NASH liver showed strong concordance with human NASH. NASH was preceded by an early disruption of gut barrier, microbial dysbiosis, lipopolysaccharide leakage, and intestinal inflammation. This led to acute-phase liver inflammation in Foz+WD mice, characterized by neutrophil infiltration and increased levels of several chemokines/cytokines. The liver cytokine/chemokine profile evolved as NASH progressed, with subsequent predominance by monocyte recruitment.ConclusionsThe Foz+WD model closely mimics the pathobiology and gene signature of human NASH with fibrosis and subsequent HCC. Foz+WD mice provide a robust and relevant preclinical model of NASH, NASH-associated HCC, chronic kidney injury, and heart failure