Profile Of The Nigerian Sickle Cell Anaemia Patients Above 30 Years Of Age

A CAJM article on the profiles of Nigerian sickle cell anaemic patients.Haemoglobin S occurs with greatest prevalence in tropical Africa and clinicians have generally associated sickle cell disease with high morbidity and mortality.1-3 The heterozygous frequency in Nigeria is usually about 25% but in some areas it reaches 32.5%.4 Patients with sickle cell anaemia (SCA) constitute about 2 to 3% of the Nigerian population. While the disease appears benign in some patients, it runs a crippling course in others. There are a few reports of patients surviving till the fourth or fifth decade but this is a very rare occurrence in Nigeria. Thus, patients over the age of 30 years form a very small proportion of the patients. It has been implied that inherited and acquired factors influence the pathogenesis and clinical symptoms of the disease.1 Hence, this results either in death in the early years in some patients or cases discovered late in life as a result of chance survey 1 With improvement in the living standard and increasing availability of health care, it has been observed that more patients with sickle cell anaemia in Nigeria survive into adolescence and maturity, and they are able to reproduce and some are in gainful employment

Plasma lipid profiles change with increasing numbers of mild traumatic brain injuries in rats

Mild traumatic brain injury (mTBI) causes structural, cellular and biochemical alterations which are difficult to detect in the brain and may persist chronically following single or repeated injury. Lipids are abundant in the brain and readily cross the blood-brain barrier, suggesting that lipidomic analysis of blood samples may provide valuable insight into the neuropathological state. This study used liquid chromatography-mass spectrometry (LC-MS) to examine plasma lipid concentrations at 11 days following sham (no injury), one (1×) or two (2×) mTBI in rats. Eighteen lipid species were identified that distinguished between sham, 1× and 2× mTBI. Three distinct patterns were found: (1) lipids that were altered significantly in concentration after either 1× or 2× F mTBI: cholesterol ester CE (14:0) (increased), phosphoserine PS (14:0/18:2) and hexosylceramide HCER (d18:0/26:0) (decreased), phosphoinositol PI(16:0/18:2) (increased with 1×, decreased with 2× mTBI); (2) lipids that were altered in response to 1× mTBI only: free fatty acid FFA (18:3 and 20:3) (increased); (3) lipids that were altered in response to 2× mTBI only: HCER (22:0), phosphoethanolamine PE (P-18:1/20:4 and P-18:0/20:1) (increased), lysophosphatidylethanolamine LPE (20:1), phosphocholine PC (20:0/22:4), PI (18:1/18:2 and 20:0/18:2) (decreased). These findings suggest that increasing numbers of mTBI induce a range of changes dependent upon the lipid species, which likely reflect a balance of damage and reparative responses