Acute methanol intoxication is a severe affection associated to high rates of mortality and morbidity, we report the cases of two men in circumstances of fall in prices had consumed an adulterated whiskey. The first patient was 55-year-old man, he developed polyneuropathy and cognitive impairment after a fraudulent adulteration of alcoholic drinks (whisky). Neuroimaging findings showed typical bilateral lesions in basal ganglia and atypical hyperintensities in the occipital, temporal, and frontal areas which have been rarely reported. The second patient was a 29-year-old man, he developed confusion wish had been resolved in three days. We describe the clinical presentations and we highlight the importance of intensive detoxification protocols to improve clinical outcomes.

Heparanase inhibition represents a new and interesting target for addressing cancer as well as other inflammatory-based diseases. This target is still largely underexploited. Heparanase activity releases from the extracellular matrix (ECM) and tumor microenvironment a multitude of heparan sulphate (HS)-bound growth factors, cytokines, chemokines, and enzymes that affect cells and tissue functions such as inflammation, wound healing and tumor invasion. A pro-metastatic and pro-angiogenic role for this enzyme has been widely demonstrated in many primary human tumors since high levels of heparanase correlate with lymph node and distant metastasis, elevated microvessel density and reduced survival of cancer patients. Heparanase is up regulated in many human hematologic and solid tumors. Two HS mimetics, PG545 and Roneparstat, are in active clinical development, the former in solid tumors, and the latter in Multiple Myeloma (MM).
These progresses together with increasing and sound preclinical data suggesting a significant potential for anti-heparanase therapy in many types of tumors, underscores the need to explore the full potential of this novel and safe therapeutic approach. This paper reviews the role of heparanase as novel therapeutic target in cancer and illustrates Roneparstat as a concrete example of such potential.

We applaud the military for keeping us safe, revere our armed forces for facilitating the unparalleled freedom we enjoy, and are humbled by the men and women who serve to maintain our democracy. We hold parades in their honor and provide unique employment strategies for our soldiers upon return to civilian life.

Cancer is responsible for millions of deaths worldwide. The relative lack of effective treatments for cancer makes extremely urgent the development of more efficient and selective new drugs. In contrast to the major part of commonly used chemotherapeutic drugs, the antineoplastic phospholipids (ALP) do not have DNA as a target. Such phospholipids are responsible for modifying the cell membrane turnover, inducing cell death by apoptosis, with high selectivity for tumor cells. The central hypothesis is that the antitumor effects of ALP are due to the inhibition of CTP: phosphocholinecytidylyltransferase (Pcyt-1) enzyme in the phospholipid biosynthetic pathway, known as Kennedy's pathway. The inhibition of the Pcyt-1 blocks the synthesis of phosphatidylcholine and causes the accumulation of ceramide, commonly associated with apoptosis. Moreover, important substrates, which are produced by this pathway are compromised and blocks the cell cycle progression, and consequently the correct cytokinesis. Mainly of them are also responsible for inducing a topological impairment of the trans-membrane protein domains, mostly located in mitochondria. Such fact affects the cellular bioenergetics, eventually triggering death by apoptosis. Besides, it impairs lipids signaling, which are directly associated with the regulation of mitogen-activated protein kinase (MAPKs) responsible for mediating signaling pathways. Therefore, the inhibition of Kennedy's pathway constitutes a promising strategy for the identification of novel antitumor compounds, and Pcyt-1, which is a key enzyme of such signaling/pathway, becomes the main potential target, with innovative character, for the development of antitumor drugs.

Long-term methotrexate (MTX) administration has the potential to cause hepatotoxicity that is claimed to be due to decrease the folate levels and/or oxidative stress.
Objectives: To study the protective effect of a-tocopherol and\or N-acetylcysteine against methotrexate-induced hepatotoxicity in chronically-treated patients with rheumatoid arthritis.
Subjects and methods: The study was carried on 250 subjects, whom were divided into five groups (50 subject each) as follows: Group I: Normal apparently healthy, Group II: Newly diagnosed as rheumatoid patients whom will be treated with MTX alone over one year, Group III: Newly diagnosed as rheumatoid patients whom will be treated with MTX with a-tocopherol over one year, Group IV: Newly diagnosed as rheumatoid patients whom will be treated with MTX with N-acetylcysteine over one year, Group V: Newly diagnosed as rheumatoid patients whom will be treated with MTX with a-tocopherol + N-acetylcysteine over one year. All subjects were investigated for liver function tests (ALT, AST, ALP, GDH) in the beginning of the study and every 3 months of the period of the study.
Results: It was found that long-term MTX therapy induced significant elevation of GDH started from 6th month of treatment while the other parameters (ALT, AST & ALP) started to be significantly increased from the 9th month of therapy. Co-administration of a-tocopherol or N-acetylcysteine induced significant improvement of all parameters. Co-administration of both anti-oxidants lead to improvement which was statistically significant more than each drug alone.
Conclusion: The co-administration of MTX with a-tocopherol and/or N-acetylcysteine may protect against MTX-induced hepatotoxicity in chronically-treated patients with rheumatoid arthritis which seems to be multifactorial.