Dollarization in Sierra Leone: Evidence and Some Policy Options

This study aims to empirically investigate the determinants of dollarization in Sierra. It uses quarterly data from 1992Q1 to 2017Q4 and autoregressive distributed lag Bound Testing technique. Both the long and short run results revealed that inflation, exchange rate depreciation, financial deepening and war dummy were the main determinants of dollarization in Sierra Leone during the study period. The error correction term depicts that 53 percent of any disequilibrium in dollarization will be corrected within a year. A key policy recommendation is that policy makers should implement prudent policies that will ensure broader macroeconomic stability (including price stability and exchange rate stability) as a recipe for de-dollarization in Sierra Leone

Seven Different Glucose-6-phosphate Dehydrogenase Variants Including a New Variant Distributed in Lam Dong Province in Southern Vietnam.

We conducted a survey for glucose-6-phosphate dehydrogenase (G6PD) deficiency using blood samples from male outpatients of a local hospital in southern Vietnam. Most of the samples were from the Kinh (88.9%), the largest ethnic group in Vietnam, with a small number (11.1%) coming from the K'Ho, Chauma, Nung, and Tay minorities. We detected 25 G6PD-deficient cases among 1,104 samples (2.3%), and read the open reading frame of G6PD. A novel mutation (352T>C) predicting an aminoacid change of 118Tyr>His was found in a 1-year-old Kinh boy. His G6PD activity was estimated to be less than 10% residual activity, although he did not show chronic hemolytic anemia. Thus, we categorized this variant as Class II and named it G6PD Bao Loc. In the Kinh population, G6PD Viangchan (871G>A, 1311C>T, intron 11 nt93T>C), one of the most common variants in continental Southeast Asian populations, was the highest (6/19), followed by variants originating from the Chinese such as G6PD Canton (1376G>T) (5/19), G6PD Kaiping (1388G>A) (3/19), G6PD Gaohe (95A>G) (1/19), and G6PD Quing Yuan (392G>T) (1/19). In addition, G6PD Union (1360C>T) (2/19), which originated from the Oceania, was also detected. These findings suggest that the Kinh people are derived from various ancestries from continental Southeast Asia, China, and Oceania. In contrast, all of the 5 deficient cases in the K'Ho population were G6PD Viangchan, suggesting that they were very close to Southeast Asian populations such as the Khmer in Cambodia and the Lao in Laos. It is interesting that G6PD Mahidol (487G>A), another common variant in continental Southeast Asian populations in Myanmar, Thailand, and Malaysia, has not been detected from the Vietnamese

T-cell epitope polymorphisms of the Plasmodium falciparum circumsporozoite protein among field isolates from Sierra Leone: age-dependent haplotype distribution?

<p>Abstract</p> <p>Background</p> <p>In the context of the development of a successful malaria vaccine, understanding the polymorphisms exhibited by malaria antigens in natural parasite populations is crucial for proper vaccine design. Recent observations have indicated that sequence polymorphisms in the C-terminal T-cell epitopes of the <it>Plasmodium falciparum </it>circumsporozoite protein (Pf<it>csp</it>) are rather low and apparently stable in low endemic areas. This study sought to assess the pattern in a malaria endemic setting in Africa, using samples from Freetown, Sierra Leone.</p> <p>Methods</p> <p>Filter-paper blood samples were collected from subjects at a teaching hospital in Freetown during September–October 2006 and in April–May 2007. The C-terminal portion of the Pf<it>csp </it>gene spanning the Th2R and Th3R epitopes was amplified and directly sequenced; sequences were analysed with subject parameters and polymorphism patterns in Freetown were compared to that in other malaria endemic areas.</p> <p>Results and Discussion</p> <p>Overall, the genetic diversity in Freetown was high. From a total of 99 sequences, 42 haplotypes were identified with at least three accounting for 44.4% (44/99): the 3D7-type (19.2%), a novel type, P-01 (17.2%), and E12 (8.1%). Interestingly, all were unique to the African sub-region and there appeared to be predilection for certain haplotypes to distribute in certain age-groups: the 3D7 type was detected mainly in hospitalized children under 15 years of age, while the P-01 type was common in adult antenatal females (Pearson Chi-square = 48.750, degrees of freedom = 34, <it>P </it>= 0.049). In contrast, the single-haplotype predominance (proportion > 50%) pattern previously identified in Asia was not detected in Freetown.</p> <p>Conclusion</p> <p>Haplotype distribution of the T-cell epitopes of Pf<it>csp </it>in Freetown appeared to vary with age in the study population, and the polymorphism patterns were similar to that observed in neighbouring Gambia, but differed significantly at the sequence level from that observed in Asia. The findings further emphasize the role of local factors in generating polymorphisms in the T-cell epitopes of the <it>P. falciparum </it>circumsporozoite protein.</p

Mutation Analysis of 2009 Pandemic Influenza A(H1N1) Viruses Collected in Japan during the Peak Phase of the Pandemic

BACKGROUND: Pandemic influenza A(H1N1) virus infection quickly circulated worldwide in 2009. In Japan, the first case was reported in May 2009, one month after its outbreak in Mexico. Thereafter, A(H1N1) infection spread widely throughout the country. It is of great importance to profile and understand the situation regarding viral mutations and their circulation in Japan to accumulate a knowledge base and to prepare clinical response platforms before a second pandemic (pdm) wave emerges. METHODOLOGY: A total of 253 swab samples were collected from patients with influenza-like illness in the Osaka, Tokyo, and Chiba areas both in May 2009 and between October 2009 and January 2010. We analyzed partial sequences of the hemagglutinin (HA) and neuraminidase (NA) genes of the 2009 pdm influenza virus in the collected clinical samples. By phylogenetic analysis, we identified major variants of the 2009 pdm influenza virus and critical mutations associated with severe cases, including drug-resistance mutations. RESULTS AND CONCLUSIONS: Our sequence analysis has revealed that both HA-S220T and NA-N248D are major non-synonymous mutations that clearly discriminate the 2009 pdm influenza viruses identified in the very early phase (May 2009) from those found in the peak phase (October 2009 to January 2010) in Japan. By phylogenetic analysis, we found 14 micro-clades within the viruses collected during the peak phase. Among them, 12 were new micro-clades, while two were previously reported. Oseltamivir resistance-related mutations, i.e., NA-H275Y and NA-N295S, were also detected in sporadic cases in Osaka and Tokyo

An Update on the Surveillance of Livestock Diseases and Antimicrobial Use in Sierra Leone in 2021-An Operational Research Study.

In Sierra Leone, in 2020, a study by the Livestock and Veterinary Services Division (Ministry of Agriculture and Forestry) on the surveillance system of animal diseases and antimicrobial use found poor reporting. Of the expected weekly districts reports, &lt;1% were received and only three of the 15 districts had submitted reports occasionally between 2016 and 2019. Following this, staff-capacity-building on reporting was undertaken. In 2021, we reassessed the improvement in reporting and used the reports to describe livestock diseases and antimicrobials utilized in their treatment. Between March and October 2021, 88% of expected weekly reports from all 15 districts were received. There were minor deficiencies in completeness and consistency in the terminology used for reporting animal disease and antimicrobials. Available reports showed that 25% of the livestock had an infectious disease, and a quarter of the sick animals had received an antimicrobial drug. Most animals received antimicrobials belonging to World Organization for Animal Health's "veterinary critically important" category (77%) and World Health Organization's "critically" (17%) and "highly important" (60%) categories for human health. These indicate a significant improvement in the animal health surveillance system and highlight the need for enhanced antimicrobial stewardship to prevent misuse of antimicrobials that are significant in animal and human health

Bioinformatic Analysis Predicts Microglial Dysfunction in Murine Aging

Age-related disease is a growing concern as the global geriatric population increases. Neurodegenerative diseases scale unfavorably in prevalence with aging and inflict disastrous consequences to human health and well-being. These disorders are challenging to investigate because they arise from complex molecular origins. The neuroimmune system is a common factor among these diseases and microglia play an important role in maintaining homeostasis in the central nervous system. Aging progressively impairs microglia by decreasing their ability to adapt and respond to noxious environmental stimuli or injury. Microglial dysfunction aggravates neurodegenerative pathology when microglia are unable to regulate neuroinflammation effectively. We investigated aging microglial dysfunction by using mass spectrometry-based proteomics and bioinformatic analysis. In our first set of experiments, we isolated microglia from young and aged rats, identified differentially expressed proteins between the two age groups, and determined functional enrichment among canonical microglial signaling cascades in our AGING comparison. Aged microglia possessed an elevated pro-inflammatory phenotype characterized by metabolic irregularity. We then examined how polyphenol supplementation modified dysfunctional signaling in aging microglia. We fed aged rats a 30-day polyphenol diet and evaluated changes in their microglial proteomes relative to their age-matched counterparts fed a control diet. Polyphenol supplementation mitigated activation in neuroinflammatory pathways and reversed aberrant trends we observed in aging microglia. In our second set of experiments, we modeled aging dysfunction in microglia by disrupting the nutrient-sensing mTORC2 pathway in vivo. We generated mice expressing both Cre-recombinase under the Cx3cr1 promoter and loxP sites flanking exon 11 of the RICTOR gene. Tamoxifen treatment induced microglial-specific RICTOR depletion. We then identified differentially expressed proteins in male and female RICTOR-KO microglia and performed bioinformatics. We confirmed that RICTOR-deficient microglia expressed a pro-inflammatory phenotype that paralleled trends we observed in aging microglia. Disrupting mTORC2 signaling activated inflammatory canonical pathways and evoked metabolic dysfunction in male and female microglia. Our experimental results highlight the potential molecular underpinnings of aging in microglia

Bioinformatic Analysis Predicts Microglial Dysfunction in Murine Aging

Age-related disease is a growing concern as the global geriatric population increases. Neurodegenerative diseases scale unfavorably in prevalence with aging and inflict disastrous consequences to human health and well-being. These disorders are challenging to investigate because they arise from complex molecular origins. The neuroimmune system is a common factor among these diseases and microglia play an important role in maintaining homeostasis in the central nervous system. Aging progressively impairs microglia by decreasing their ability to adapt and respond to noxious environmental stimuli or injury. Microglial dysfunction aggravates neurodegenerative pathology when microglia are unable to regulate neuroinflammation effectively. We investigated aging microglial dysfunction by using mass spectrometry-based proteomics and bioinformatic analysis. In our first set of experiments, we isolated microglia from young and aged rats, identified differentially expressed proteins between the two age groups, and determined functional enrichment among canonical microglial signaling cascades in our AGING comparison. Aged microglia possessed an elevated pro-inflammatory phenotype characterized by metabolic irregularity. We then examined how polyphenol supplementation modified dysfunctional signaling in aging microglia. We fed aged rats a 30-day polyphenol diet and evaluated changes in their microglial proteomes relative to their age-matched counterparts fed a control diet. Polyphenol supplementation mitigated activation in neuroinflammatory pathways and reversed aberrant trends we observed in aging microglia. In our second set of experiments, we modeled aging dysfunction in microglia by disrupting the nutrient-sensing mTORC2 pathway in vivo. We generated mice expressing both Cre-recombinase under the Cx3cr1 promoter and loxP sites flanking exon 11 of the RICTOR gene. Tamoxifen treatment induced microglial-specific RICTOR depletion. We then identified differentially expressed proteins in male and female RICTOR-KO microglia and performed bioinformatics. We confirmed that RICTOR-deficient microglia expressed a pro-inflammatory phenotype that paralleled trends we observed in aging microglia. Disrupting mTORC2 signaling activated inflammatory canonical pathways and evoked metabolic dysfunction in male and female microglia. Our experimental results highlight the potential molecular underpinnings of aging in microglia

Molecular Analysis of Plasmodium ovale Variants

Complete DNA sequences of the small subunit ribosomal RNA (SSUrRNA) gene and partial sequences of three other loci were obtained from three variant-type and three classic-type Plasmodium ovale isolates from Southeast Asia and compared with GenBank-available data. Three different SSUrRNA sequences (Pov 1–3) were found in each variant-type isolate, and two different SSUrRNA sequences (Poc 1–2) in each classic-type isolate. Pov 1–3 were closer to sequences previously found in the Cameroon and MAL/MAI isolates, whereas Poc 1–2 were closer to sequences previously found in two clones of the Nigerian I/CDC strain. The 3′ half of Pov 1–3 was identical to the partial sequence of the SSUrRNA gene from the London School (LS) strain. Results support grouping P. ovale into two groups, the classic type (including the Nigerian I/CDC strain) and the variant type (Cameroon, MAL/MAI, and LS isolates)