Bank credit and economic activity in a developing economy

The importance of bank credit to financing economic activity and development has been the subject of empirical analysis for decades. This paper contributes to the debate by evaluating the effect of bank credit on economic activity using a developing economy data. The study period ranged from January 2007 to December 2017. Estimates from descriptive statistics show that the economic activity and bank credit series are negatively skewed and peaked, with non-normal distribution. The results generated for the Augmented Dickey unit root test showed that at the level form, all the variables are non-stationary but after first differencing the variables became stationary and integrated of order one (i.e. I(1)). The results obtained from the multiple regression model show that bank credit has a positive and significant effect on the economic activity. We, therefore, conclude that bank credit has a predictive influence on economic activity. One of the implications of this conclusion is that banking system regulators should formulate policies that enhance access to credit to the private sector while containing inflation.&nbsp

Nigeria’s fiscal health: an analysis of budget process, systems and trends [2014 – 2016]

Nigeria is an oil dependent economy which faced a lot of economic and political challenges between the periods under review, such as increased broad money supply, fall in the value of money market assets, decline in the unpaid FGN Bonds, unfavorable exchange rates, fall in oil prices, and the May 2015 general elections, amongst others. Nigeria’s fiscal stance was thus threatened, and it is in light of these that the paper, uses interactions between expenditure, revenue, debts, and deficits trends, to compute indices that capture its fiscal health. The study found that using compounded annual growth rates (CAGR), certain sectors with high CAGRs (Interior, Transport, Finance, Science & Technology, and Health) seemed to be prone to high fiscal mismanagement. Also, conservativeness in applying debt instruments are unavailable, and such measures are not tied to growth; revenue from increased taxation are not matched with requisite infrastructure; and debts are not adequately tied to capital projects, as established in Fiscal Responsibility Act. Amidst several, few recommendations are undoubtedly notable mainly; that overhead costs revealed in several line-items and are marked up should be eradicated; and huge recurrent expenditure, mainly personnel cost (about 75% of the total budget) mostly visible as remuneration “in kind” should be strictly removed from the line items and programmes at MDA level. Thus, Nigeria’s government should maintain expenditure ceilings; create solidified link between policy and budget; establish realistic fiscal targets and indicators; and allow more public participation in budget process

Regulation of human salt-sensitivite hypertension by myeloid cell renin-angiotensin-aldosterone system

Introduction: Salt sensitivity of blood pressure is a phenomenon in which blood pressure changes according to dietary sodium intake. Our previous studies found that high salt activates antigen presenting cells, resulting in the development of hypertension. The mechanisms by which salt-induced immune cell activation is regulated in salt sensitivity of blood pressure are unknown. In the current study, we investigated dietary salt-induced effects on the renin-angiotensin-aldosterone system (RAAS) gene expression in myeloid immune cells and their impact on salt sensitive hypertension in humans.Methods: We performed both bulk and single-cell sequencing analysis on immune cells with in vitro and in vivo high dietary salt treatment in humans using a rigorous salt-loading/depletion protocol to phenotype salt-sensitivity of blood pressure. We also measured plasma renin and aldosterone using radioimmunoassay.Results: We found that while in vitro high sodium exposure downregulated the expression of renin, renin binding protein and renin receptor, there were no significant changes in the genes of the renin-angiotensin system in response to dietary salt loading and depletion in vivo. Plasma renin in salt sensitive individuals tended to be lower with a blunted response to the salt loading/depletion challenge as previously reported.Discussion: These findings suggest that unlike systemic RAAS, acute changes in dietary salt intake do not regulate RAAS expression in myeloid immune cells

The epithelial sodium channel in inflammation and blood pressure modulation

A major regulator of blood pressure and volume homeostasis in the kidney is the epithelial sodium channel (ENaC). ENaC is composed of alpha(α)/beta(β)/gamma(γ) or delta(δ)/beta(β)/gamma(γ) subunits. The δ subunit is functional in the guinea pig, but not in routinely used experimental rodent models including rat or mouse, and thus remains the least understood of the four subunits. While the δ subunit is poorly expressed in the human kidney, we recently found that its gene variants are associated with blood pressure and kidney function. The δ subunit is expressed in the human vasculature where it may influence vascular function. Moreover, we recently found that the δ subunit is also expressed human antigen presenting cells (APCs). Our studies indicate that extracellular Na+ enters APCs via ENaC leading to inflammation and salt-induced hypertension. In this review, we highlight recent findings on the role of extra-renal ENaC in inflammation, vascular dysfunction, and blood pressure modulation. Targeting extra-renal ENaC may provide new drug therapies for salt-induced hypertension

Oligoclonal CD8+ T Cells Play a Critical Role in the Development of Hypertension

Recent studies have emphasized a role of adaptive immunity, and particularly T cells, in the genesis of hypertension. We sought to determine the T-cell subtypes that contribute to hypertension and renal inflammation in angiotensin II-induced hypertension. Using T-cell receptor spectratyping to examine T-cell receptor usage, we demonstrated that CD8(+) cells, but not CD4(+) cells, in the kidney exhibited altered T-cell receptor transcript lengths in Vβ3, 8.1, and 17 families in response to angiotensin II-induced hypertension. Clonality was not observed in other organs. The hypertension caused by angiotensin II in CD4(-/-) and MHCII(-/-) mice was similar to that observed in wild-type mice, whereas CD8(-/-) mice and OT1xRAG-1(-/-) mice, which have only 1 T-cell receptor, exhibited a blunted hypertensive response to angiotensin II. Adoptive transfer of pan T cells and CD8(+) T cells but not CD4(+)/CD25(-) cells conferred hypertension to RAG-1(-/-) mice. In contrast, transfer of CD4(+)/CD25(+) cells to wild-type mice receiving angiotensin II decreased blood pressure. Mice treated with angiotensin II exhibited increased numbers of kidney CD4(+) and CD8(+) T cells. In response to a sodium/volume challenge, wild-type and CD4(-/-) mice infused with angiotensin II retained water and sodium, whereas CD8(-/-) mice did not. CD8(-/-) mice were also protected against angiotensin-induced endothelial dysfunction and vascular remodeling in the kidney. These data suggest that in the development of hypertension, an oligoclonal population of CD8(+) cells accumulates in the kidney and likely contributes to hypertension by contributing to sodium and volume retention and vascular rarefaction

Hypertension and increased endothelial mechanical stretch promote monocyte differentiation and activation: roles of STAT3, interleukin 6 and hydrogen peroxide

Aims: Monocytes play an important role in hypertension. Circulating monocytes in humans exist as classical, intermediate and non-classical forms. Monocyte differentiation can be influenced by the endothelium, which in turn is activated in hypertension by mechanical stretch. We sought to examine the role of increased endothelial stretch and hypertension on monocyte phenotype and function. Methods and Results: Human monocytes were cultured with confluent human aortic endothelial cells undergoing either 5% or 10% cyclical stretch. We also characterized circulating monocytes in normotensive and hypertensive humans. In addition, we quantified accumulation of activated monocytes and monocyte-derived cells in aortas and kidneys of mice with Angiotensin II-induced hypertension. Increased endothelial stretch enhanced monocyte conversion to CD14++CD16+ intermediate monocytes and monocytes bearing the CD209 marker and markedly stimulated monocyte mRNA expression of interleukin (IL)-6, IL-1β, IL-23, chemokine (C-C motif) ligand 4 and tumor necrosis factor α. STAT3 in monocytes was activated by increased endothelial stretch. Inhibition of STAT3, neutralization of IL-6 and scavenging of hydrogen peroxide prevented formation of intermediate monocytes in response to increased endothelial stretch. We also found evidence that nitric oxide inhibits formation of intermediate monocytes and STAT3 activation. In vivo studies demonstrated that humans with hypertension have increased intermediate and non-classical monocytes and that intermediate monocytes demonstrate evidence of STAT3 activation. Mice with experimental hypertension exhibit increased aortic and renal infiltration of monocytes, dendritic cells and macrophages with activated STAT3. Conclusions: These findings provide insight into how monocytes are activated by the vascular endothelium during hypertension. This is likely in part due to a loss of nitric oxide signaling and increased release of IL-6 and hydrogen peroxide by the dysfunctional endothelium and a parallel increase in STAT activation in adjacent monocytes. Interventions to enhance bioavailable nitric oxide, reduce IL-6 or hydrogen peroxide production or to inhibit STAT3 may have anti-inflammatory roles in hypertension and related conditions

Knowledge, attitudes and practices of Ugandan men regarding prostate cancer

Background: The incidence of prostate cancer in Uganda is one of the highest recorded in Africa. Prostate cancer is the most common cancer among men in Uganda. Objective: This study assessed the current knowledge, attitudes and practices of adult Ugandan men regarding prostate cancer. Subjects and Methods: We conducted a descriptive cross-sectional study using interviewer administered questionnaires and focus group discussions among 545 adult men aged 18–71 years, residing in Kampala, the capital of Uganda. Quantitative data were analyzed with SPSS version 20. Qualitative data were collected using audio recorded focus group discussions, transcribed and analyzed by clustering into themes. Results: The majority of the respondents (324, 59.4%) were aged 18–28 years, 295 (54.1%) had heard about prostate cancer and 250 (45.9%) had never heard about it. The commonest source of information about prostate cancer was the mass media. Only 12.5% of the respondents obtained information about prostate cancer from a health worker, 37.4% did not know the age group that prostate cancer affects and 50.2% could not identify any risk factor for prostate cancer. Participants in the focus group discussions confused prostate cancer with gonorrhea and had various misconceptions about the causes of prostate cancer. Only 10.3% of the respondents had good knowledge of the symptoms of prostate cancer and only 9% knew about serum prostate specific antigen (PSA) testing. Although 63.5% thought they were susceptible to prostate cancer, only 22.9% considered getting and only 3.5% had ever undergone a serum PSA test. Conclusion: There was generally poor knowledge and several misconceptions regarding prostate cancer and screening in the study population. Community based health education programs about prostate cancer are greatly needed for this population

High CD8 T-cell receptor clonality and altered CDR3 properties are associated with elevated isolevuglandins in adipose tissue during diet-induced obesity

Adipose tissue (AT) CD4+ and CD8+ T cells contribute to obesity-associated insulin resistance. Prior studies identified conserved T-cell receptor (TCR) chain families in obese AT, but the presence and clonal expansion of specific TCR sequences in obesity has not been assessed. We characterized AT and liver CD8+ and CD4+ TCR repertoires of mice fed a low-fat diet (LFD) and high-fat diet (HFD) using deep sequencing of the TCRβ chain to quantify clonal expansion, gene usage, and CDR3 sequence. In AT CD8+ T cells, HFD reduced TCR diversity, increased the prevalence of public TCR clonotypes, and selected for TCR CDR3 regions enriched in positively charged and less polarized amino acids. Although TCR repertoire alone could distinguish between LFD- and HFD-fed mice, these properties of the CDR3 region of AT CD8+ T cells from HFD-fed mice led us to examine the role of negatively charged and nonpolar isolevuglandin (isoLG) adduct-containing antigen-presenting cells within AT. IsoLG-adducted protein species were significantly higher in AT macrophages of HFD-fed mice; isoLGs were elevated in M2-polarized macrophages, promoting CD8+ T-cell activation. Our findings demonstrate that clonal TCR expansion that favors positively charged CDR3s accompanies HFD-induced obesity, which may be an antigen-driven response to isoLG accumulation in macrophages