Primary myelofibrosis (PMF) is a type of myeloproliferative neoplasm (MPN) that portends a poor prognosis and has limited options for treatment. PMF is often driven by clonal mutations in one of three genes that regulate the JAK-STAT signaling pathway, leading to hyperactivation of this signaling pathway and over-proliferation of megakaryocytes (MKs) and their precursors. PMF presents with debilitating symptoms such as splenomegaly and weight loss.

In the respiratory management of preterm infants of less than 33 weeks gestational age and very low birth weight infants, it is essential to understand changes in chest X-ray and blood gas findings in addition to observing their clinical symptoms.

Non-Alcoholic Fatty Liver Disease (NAFLD) is the growing epidemic which is rapidly increasing in USA. Elderly people are the most affected population which suffers from NAFLD. The earliest stage of NAFLD, hepatic steatosis has no evidence of liver injury, but is characterized by an accumulation of triglycerides in hepatocytes. Hepatic steatosis progresses in age-dependent manner to non-alcoholic steatohepatitis (NASH) and cirrhosis. Mechanisms of development of age associated NAFLD are not well understood and approaches to treat this disease are not developed. Recent studies within last three years; however, provided several lines of evidence showing that although hepatic steatosis strongly correlates with development of NAFLD, it might be not a cause of next steps of NAFLD: fibrosis and NASH. Moreover, some reports suggest that hepatic steatosis might play a protective role in development of fibrosis and NASH. Recent studies of NAFLD in animal models showed that the increase of liver proliferation is the first event in high-fat diet-induced NAFLD.

According to the global epidemiological report on chronic kidney disease (CKD) published by The Lancet, CKD is recognized as a global public health problem with high morbidity and mortality [1]. Diabetic nephropathy (DN) is the most main microvascular complication of diabetes and is one of the leading causes of end-stage renal disease (ESRD) and CKD [2].

The liver plays a pivotal role in intermediary metabolism, biosynthesis, and pharmacotherapy. As such, chemical influences can result in detrimental effects. Anatomically, the liver is centrally placed, with loose capillary fenestrations, which makes it susceptible to chemical assault. Epidemiological evidence shows that chemical-induced liver injury is a major cause of acute liver failure, fibrosis and cirrhosis. In preclinical studies, drug-induced liver injury is a major reason why many interesting lead molecules and novel compounds fail to transcend beyond the laboratory.