The Impediments to Nigeria Understanding Oil Production Volumes, Losses and Potential Solutions

The issue of the quantity of oil produced or missing has traditionally been played down in Nigeria. This is evident as no one in or outside Nigeria is able to quote a totally reliable production volume or loss figure. The aim of this study is thus to search for the root causes as to why there are difficulties in ascertaining the quantity of crude oil produced or missing per day and for potential solutions. The research assesses the present situation and problems requiring solution concerning Nigerian oil and gas measurement control. This is achieved through an intensive review of each of the notified bodies responsible for Nigeria’s oil and gas measurement control, using secondary resources. The bodies reviewed in this study are the Department of Petroleum Resources and the Weights and Measures Department. The study has identified knowledge impediments among the designated bodies. Also discovered were inadequate measurement equipment and absence of measurement guidelines, thus, no mechanisms were in place to address any mismeasurements or losses that are discovered. Provision of comprehensive training to the regulatory body to provide it with the necessary “teeth” to ensure effective delivery of it regulatory function has therefore been recommended as the key solution

Consequences of perinatal treatment with l-arginine and antioxidants for the renal transcriptome in spontaneously hypertensive rats

Treating spontaneously hypertensive rats (SHR) with l-arginine, taurine, and vitamins C and E (ATCE) during nephrogenesis (2 weeks before to 4 weeks after birth) persistently lowers blood pressure. Hypothetically, differential gene expression in kidney of SHR vs. normotensive Wistar–Kyoto rats (WKY) is partially corrected by maternal ATCE in SHR. Differential gene expression in 2-days, 2-weeks, and 48-week-old rats was studied using oligonucleotide chips. Transcription factor binding sites (TFBS) of differentially expressed genes were analyzed in silico. Differential gene expression varied between SHR+ATCE and SHR, suggesting both direct and indirect effects; but, few genes were modulated toward WKY level and there was little overlap between ages. TFBS analysis suggests less Elk-1-driven gene transcription in both WKY and SHR+ATCE vs. SHR at 2 days and 2 weeks. Concluding, in SHR, persistent antihypertensive effects of maternal ATCE are not primarily due to persistent corrective transcription. Less Elk-1-driven transcription at 2 days and 2 weeks may be involved

Geometric Variations of Modular Head-Stem Taper Junctions of Total Hip Replacements

Taper degradation in Total Hip Replacements (THR) has been identified as a clinical concern, and the degradation occurring at these interfaces has received increased interest in recent years. Wear and corrosion products produced at the taper junction are associated with adverse local tissue responses, leading to early failure and revision surgery. Retrieval and in-vitro studies have found that variations in taper design affect degradation. However, there is a lack of consistent understanding within the literature of what makes a good taper interface. Previous studies assessed different design variations using their global parameters assuming a perfect cone such as: taper length, cone angle and diameters. This study assessed geometrical variations of as-manufactured head and stem tapers and any local deviations from their geometry. The purpose of this study was to provide a greater insight into possible engagement, a key performance influencing parameter predicted by Morse taper connection theory. This was achieved by taking measurements of twelve different commercially available male tapers and six female tapers using a coordinate measurement machine (CMM). The results suggested that engagement is specific to a particular head-stem couple. This is subject to both their micro-scale deviations, superimposed on their macro-scale differences. Differences in cone angles between female and male tapers from the same manufacturer was found to create a predominately proximal contact. However, distally mismatched couples are present in some metal-on-metal head-stem couples. On a local scale, different deviation patterns were observed from the geometry which appeared to be linked to the manufacturing process. Future work will look at using this measurement methodology to fully characterise an optimal modular taper junction for a THR prosthesis

Perinatal L-arginine and antioxidant supplements reduce adult blood pressure in spontaneously hypertensive rats

Embryo cross-transplantation and cross-fostering between spontaneously hypertensive rats (SHR) and normotensive rats (WKY) suggest that perinatal environment modulates the genetically determined phenotype. In SHR the balance between NO and reactive oxygen species (ROS) is disturbed. We hypothesized that increasing NO and diminishing ROS in perinatal life would ameliorate hypertension in adult SHR. Pregnant SHR and WKY and their offspring received L-arginine plus antioxidants ( vitamin C, vitamin E, and taurine) during the last 2 weeks of pregnancy and then until either 4 or 8 weeks after birth. Systolic blood pressure (SBP) and urinary excretion of protein, nitrates (NOx), and thiobarbituric acid reactive substances (TBARS) were measured. At 48 weeks of age rats were euthanized for glomerular counts. Perinatal supplements reduced SBP persistently in SHR and prevented the SBP increase observed in aging WKY. Initially NOx excretion was lower and TBARS excretion higher in SHR than WKY. There was a direct effect on NOx excretion in supplemented pregnant SHR and their offspring, but no increase was observed after stopping the supplements. TBARS excretion was only depressed up to 14 weeks by the supplements despite persistent differences in SBP. Consistent effects on nephron number were absent. Mild proteinuria, present in control SHR at 48 weeks, was prevented in all supplemented rats. Perinatal supplementation of NO substrate and antioxidants results in persistent reduction of SBP and renal protection in SHR, although effects on NOx and TBARS were only transient. This suggests a critical role for perinatal pro- and antioxidant balance in programming BP later in life

Temporary losartan or captopril in young SHR induces malignant hypertension despite initial normotension

Temporary losartan or captopril in young SHR induces malignant hypertension despite initial normotension.BackgroundExposure of normotensive rats to angiotensin-converting enzyme (ACE) inhibitors in early life causes hypertrophy of intrarenal arteries. Similar defects have been found in knockout mice lacking angiotensinogen, ACE, or angiotensin II type 1 (AT1) receptors. On the other hand, transient inhibition of the renin-angiotensin system from 2weeks of age in spontaneously hypertensive rats (SHR), either with ACE inhibitors or with AT1 receptor antagonists partially prevents the increase in blood pressure. However, permanent treatment of SHR from conception onwards with ACE inhibitors completely prevents hypertension. Although these studies demonstrated protection from hypertension-induced changes in the heart and large arteries, renal arteries were not studied and follow-up did not extend beyond 6months of age. We postulated that while brief exposure to ACE inhibitors or AT1 receptor antagonists in young SHR would temporarily decrease blood pressure, it would also be associated with development of intrarenal arterial malformation, and ultimately have deleterious effects.MethodsDirect effects on intrarenal arterial morphology of an ACE inhibitor (captopril, 100mg/kg/day) and an AT1 receptor antagonist (losartan, 50mg/kg/day), administered from the last week of gestation until 8weeks of age were examined in SHR. After stopping treatment at 8weeks, we continued to monitor blood pressure until spontaneous death.ResultsSystolic blood pressure at 8weeks was normalized by captopril and losartan (SHR control 187 ± 8mm Hg; captopril 118 ± 5mm Hg; and losartan 120 ± 9mm Hg). However, by 30weeks, blood pressure had increased to control SHR levels. At 4weeks, the media of renal arteries and arterioles was hypertrophied. Marked smooth muscle cell hyperplasia of cortical arteries resulted in significantly increased wall thickness by 8weeks, despite similar external diameter. Arterial wall structure was disrupted, with fragmentation of elastic fibers and irregular distribution of collagen type I fibers. After stopping treatment, the rats gradually began to show poor health and all had died by 1year of age, while all 1-year-old control SHR females were in good health. The cause of morbidity and mortality in the rats treated in early life was clearly malignant hypertension. Severe hypertrophy of renal arterioles was found, as well as cerebral hemorrhage.ConclusionDespite initial normalization of blood pressure interference with the renin-angiotensin system during a crucial stage of development in SHR can initiate marked smooth muscle cell hyperplasia and disruption of the wall structure of the intrarenal arteries. Subsequent progression of this intrarenal process after cessation of treatment suggests an independent process that eventually results in malignant hypertension and early death