Annulment of Oil Licences in Nigeria’s Upstream Petroleum Sector: A Legal Critique of the Costs and Benefits

Owing to various reasons, tenable and untenable, successive governments in Nigeria have annulled licenses duly granted to identifiable upstream petroleum operators. With due sense of circumspect, when irregularities manifest in the process and the grant of substantive licences, such does not vest in the government an unfettered right to annul the licence. There are evidences of such occurrence in spite of established procedures regulating annulments, commonly referred to as revocation or cancellation. This paper is a critique of the annulment of oil licenses and the associated contractualregulatory dimensions. The validity of the Federal Government’s actions also comes to the fore, particularly in the light of renewed drive to attract investments into the upstream sector. Thus, as some benefits are accruable to the players, it is also important to appraise the consequential costs attributable to undue annulment of oil licenses. The paper adopts a descriptive analytical method of available facts, expounds requisite statutory provisions and utilizes judicial precedents to highlight the context of the study. It is imperative that the Federal Government adheres to established procedures on oil license annulment, as a contrary posture will amount to several negative outcomes

Patients with syphilis investigated for neurosyphilis—Inclusion criteria, clinical and diagnostic features.

<p>Patients with syphilis investigated for neurosyphilis—Inclusion criteria, clinical and diagnostic features.</p

Neurosyphilis in Africa: A systematic review

<div><p>Introduction</p><p>Neurological involvement is one of the most important clinical manifestations of syphilis and neurological disease occurs in both early and late syphilis. The impact of HIV co-infection on clinical neurosyphilis remains unclear. The highest prevalence of both syphilis and HIV is in Africa. Therefore it might be expected that neurosyphilis would be an important and not uncommon manifestation of syphilis in Africa and frequently occur in association with HIV co-infection; yet few data are available on neurosyphilis in Africa. The aim of this study is to review data on neurosyphilis in Africa since the onset of the HIV epidemic.</p><p>Methods</p><p>We searched the literature for references on neurosyphilis in Africa for studies published between the 1^st of January 1990 and 15^th February 2017. We included case reports, case series, and retrospective and prospective cohort and case-control studies. We did not limit inclusion based on the diagnostic criteria used for neurosyphilis. For retrospective and prospective cohorts, we calculated the proportion of study participants who were diagnosed with neurosyphilis according to the individual study criteria. Depending on the study, we assessed the proportion of patients with syphilis found to have neurosyphilis, and the proportion of patients with neurological syndromes who had neurosyphilis. Due to heterogeneity of data no formal pooling of the data or meta-analysis was undertaken.</p><p>Results</p><p>Amongst patients presenting with a neurological syndrome, three studies of patients with meningitis were identified; neurosyphilis was consistently reported to cause approximately 3% of all cases. Three studies on stroke reported mixed findings but were limited due to the small number of patients undergoing CSF examination, whilst neurosyphilis continued to be reported as a common cause of dementia in studies from North Africa. Ten studies reported on cases of neurosyphilis amongst patients known to have syphilis. Studies from both North and Southern Africa continue to report cases of late stage syphilis, including tabes dorsalis and neurosyphilis, in association with ocular disease.</p><p>Discussion</p><p>This is the first systematic review of the literature on neurosyphilis in Africa since the beginning of the HIV epidemic. Neurosyphilis continues to be reported as a manifestation of both early and late syphilis, but the methodological quality of the majority of the included studies was poor. Future well-designed prospective studies are needed to better delineate the incidence and clinical spectrum of neurosyphilis in Africa and to better define interactions with HIV in this setting.</p></div

Ultrastructural Colocalization of Ligand-BCR Complexes and AP2 in Clathrin-Coated Pits.

<p>A20µWT B cells or primary murine splenocytes were pulsed with anti-IgM-btn followed by anti-biotin-15 nm gold (arrow heads), incubated 2 minutes at 37° and then plasma membrane rips were prepared as previously reported <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054938#pone.0054938-Caballero1" target="_blank">[10]</a>. The exposed cytoplasmic face of the plasma membrane was stained with anti-AP2 and Protein A-5 nm gold (arrows). The percent of BCR-containing CCP that also stained for AP2 is indicated below each image. Inset: AP2 and BCR co-localization within electron dense membrane regions lacking discernable CCP architecture. Shown are representative images from 1 of 3 experiments, with 1,000+ BCR-bound gold particles or 100+ CCP photographed cumulatively.</p

C-terminal Deletions Localize the Motif that Drives AP2 Binding to the Membrane Proximal YxxØ Motif of CD79a.

<p>Binding of AP2µ-btn to bead-captured GST bearing the indicated C-terminal deletions of CD79a was determined as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054938#pone-0054938-g003" target="_blank">Figure 3</a>. Data is the mean of 3 independent experiments ± S.E.M. and data were normalized to the binding of AP2 to full length CD79a.</p

CD79b Y195 Controls BCR Internalization.

<p><u>Panel A</u>, Amino acid sequences of the cytoplasmic domains of CD79a and CD79b. YxxØ putative AP2 binding motifs underlined. <u>Panel B</u>, Confocal laser scanning microscopic analysis of the endocytosis of indicated MHC class II-CD79 chimeric proteins. Plasma membrane is yellow (anti-MHC class II-Alexa 488+ post-endocytic labeling of external MHC class II-CD79 with an Alexa 594-labeled antibody). Internalized MHC class II-CD79 is green (anti-MHC class II-Alexa 488 only). <u>Panel C</u>, Quantification of MHC class II-CD79 endocytosis. 100+ cells from across 3 independent experiments were scored for internalization. Reported is the percent of cells showing internalized MHC class II-CD79 for each construct. Statistical comparisons were made between the construct with both CD79 cytoplasmic domains and cells expressing other constructs.</p

AP2-mediated CD79-driven Endocytosis is Regulated in Cis via ITAM-embedded DCSM and QTAT motifs.

<p><u>Panel A</u>, Binding of AP2-btn to bead-captured GST bearing the indicated CD79a or CD79b cytoplasmic domains with the indicated mutations was determined as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054938#pone-0054938-g003" target="_blank">Figure 3</a>. Binding is expressed as a percentage of wild type CD79a binding and represents the mean of 3 independent experiments ± SEM. Statistical comparisons were measured between the non-mutated CD79a or CD79b_DCSM cytoplasmic domains and other samples. <u>Panels B and C</u>, Endocytosis of the indicated MHC class II-CD79 fusion proteins was analyzed and quantitated as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054938#pone-0054938-g001" target="_blank">Figure 1</a>. Statistical comparisons were made between the reporter protein expressing the wild type CD79a or CD79b cytoplasmic domains and other reporter proteins. <u>Panel D</u>, Diagrammatic representation of <i>cis</i> and <i>trans</i> regulation of BCR AP2 binding and endocytosis. The open arrows indicate <i>cis</i> regulation by the DCSM and QTAT regulatory motifs. The closed arrows represent <i>trans</i> regulation of the endocytic activity of each cytoplasmic domain by the presence of the partner cytoplasmic domain.</p

AP2µ Binds to Isolated CD79a but not CD79b.

<p><u>Panel A</u>, Amino acid sequences of CD79a and CD79b cytoplasmic domains. YxxØ putative AP2 binding motifs underlined. <u>Panel B</u>, AP2µ expressed as a Gal4 activation domain fusion protein was assayed for specific interaction with the cytoplasmic domain of either CD79a or CD79b fused to the Gal4 DNA binding domain. Growth on histidine deficient (His-) plates indicates an AP2–CD79 interaction. The cytoplasmic domain of TGN38 contains a known AP2 binding YxxØ motif and served as a positive control, while the cytoplasmic domain of OCA2 contains a dileucine motif (which does not bind AP2µ) and served as a negative control. Data are representative of 2 experiments. <u>Panel C</u>, Diagram of the GST-CD79 cytoplasmic domain–AP2µ direct binding assay. <u>Panel D</u>, The cytoplasmic domains of CD79a and CD79b were expressed as GST fusion proteins in BL21 <i>E. coli</i> cells. GST-fusion proteins were captured from cell lysates on glutathione beads and the resulting matrix was tested for binding to <i>in vitro</i> translated, biotin-labeled AP2µ. The AP2 binding motif from TGN38, (SDYQRL)₃, and a non-AP2-binding derivation containing a tyrosine to glycine substitution, (SDGQRL)₃, fused to GST served as positive and negative controls, respectively. Binding is expressed as a percentage of (SDYQRL)₃–AP2 interactions. Data is the mean of 3 independent experiments ± S.E.M. Statistical comparisons were measured between SDYQRL and other samples.</p

Receptor Endocytosis of Isolated CD79a but not CD79b.

<p>Endocytosis of the indicated MHC class II-CD79 fusion proteins was analyzed (<u>Panel A</u>) and quantitated (<u>Panel B</u>) as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054938#pone-0054938-g001" target="_blank">Figure 1</a>. Statistical comparisons were made between the reporter proteins with both CD79 cytoplasmic domains and other reporter proteins.</p

AP2µ Directly Binds the YxxØ Motif Centered on the Membrane-Proximal Tyrosine of Isolated CD79a.

<p><u>Panel A</u>, The binding of AP2µ-btn to bead-captured GST bearing 21 amino acid peptides centered on the five CD79 YxxØ motifs was determined as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054938#pone-0054938-g003" target="_blank">Figure 3</a>. Binding is expressed as a percentage of CD79a–AP2 interactions and represents the mean of 3 independent experiments ± SEM. Statistical comparisons were measured between CD79a and other samples. <u>Panel B</u>, For both CD79a and CD79b, a positive or negative regulatory motif lies within +/−10 amino acids of the tyrosine residue of the membrane-proximal YxxØ AP2 binding motif. In this example, the motif is arbitrarily depicted as being downstream of the YxxØ motif.</p