Growth, mortality and stock assessment of Arius arius (Hamilton, 1822) from Hooghly-Matlah estuary, West Bengal

The growth, mortality, and stock assessment of Arius arius were estimated based on monthly length-frequency analysis data collected from the Hooghly-Matlah estuary of West Bengal, India from April 2017 to March 2018. The estimated growth parameters were as L∞ = 278 mm, K = 0.97 yr-1, and t0 = -0.0889 years. The different mortality coefficients Z, M, and F were obtained as 5.25 yr-1, 1.79 yr-1, and 3.46 yr-1, respectively. The calculated exploitation ratio (E) was found as 0.66, and the M/K value as 1.845 indicating overexploitation of the fish. The recruitment was found throughout the year with two peaks and the value of Lc was found at 56.00 mm. The estimated virtual population analysis (VPA) indicated that the highest fishing mortality (F) of 3.4499 was observed at the 190-200 mm length class, followed by 3.2393 from the 180-190 mm length class. The fishery was found at the overexploitation level and measures are needed to regulate it for promoting its sustainability

Efficacy of MSC for steroid-refractory acute GVHD associates with MSC donor age and a defined molecular profile

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Detection of high levels of mutations involved in anti-malarial drug resistance in Plasmodium falciparum and Plasmodium vivax at a rural hospital in southern Ethiopia

<p>Abstract</p> <p>Background</p> <p>In Ethiopia, malaria is caused by <it>Plasmodium falciparum </it>and <it>Plasmodium vivax</it>, and anti-malarial drug resistance is the most pressing problem confronting control of the disease. Since co-infection by both species of parasite is common and sulphadoxine-pyrimethamine (SP) has been intensively used, resistance to these drugs has appeared in both <it>P. falciparum </it>and <it>P. vivax </it>populations. This study was conducted to assess the prevalence of anti-malarial drug resistance in <it>P. falciparum </it>and <it>P. vivax </it>isolates collected at a rural hospital in southern Ethiopia.</p> <p>Methods</p> <p>A total of 1,147 patients with suspected malaria were studied in different months across the period 2007-2009. <it>Plasmodium falciparum dhfr </it>and <it>dhps </it>mutations and <it>P. vivax dhfr </it>polymorphisms associated with resistance to SP, as well as <it>P. falciparum pfcrt </it>and <it>pfmdr1 </it>mutations conferring chloroquine resistance, were assessed.</p> <p>Results</p> <p>PCR-based diagnosis showed that 125 of the 1147 patients had malaria. Of these, 52.8% and 37.6% of cases were due to <it>P. falciparum </it>and <it>P. vivax </it>respectively. A total of 10 cases (8%) showed co-infection by both species and two cases (1.6%) were infected by <it>Plasmodium ovale</it>. <it>Pfdhfr </it>triple mutation and <it>pfdhfr/pfdhps </it>quintuple mutation occurred in 90.8% (95% confidence interval [CI]: 82.2%-95.5%) and 82.9% (95% CI: 72.9%-89.7%) of <it>P. falciparum </it>isolates, respectively. <it>Pfcrt </it>T76 was observed in all cases and <it>pfmdr1 </it>Y86 and <it>pfmdr1 </it>Y1246 in 32.9% (95% CI: 23.4%-44.15%) and 17.1% (95% CI: 10.3-27.1%), respectively. The <it>P. vivax dhfr </it>core mutations, N117 and R58, were present in 98.2% (95% CI: 89.4-99.9%) and 91.2% (95% CI: 80.0-96.7%), respectively.</p> <p>Conclusion</p> <p>Current molecular data show an extraordinarily high frequency of drug-resistance mutations in both <it>P. falciparum </it>and <it>P. vivax </it>in southern Ethiopia. Urgent surveillance of the emergence and spread of resistance is thus called for. The level of resistance indicates the need for implementation of entire population access to the new first-line treatment with artemether-lumefantrine, accompanied by government monitoring to prevent the emergence of resistance to this treatment.</p

A systematic review and meta-analysis of evidence for correlation between molecular markers of parasite resistance and treatment outcome in falciparum malaria

<p>Abstract</p> <p>Background</p> <p>An assessment of the correlation between anti-malarial treatment outcome and molecular markers would improve the early detection and monitoring of drug resistance by <it>Plasmodium falciparum</it>. The purpose of this systematic review was to determine the risk of treatment failure associated with specific polymorphisms in the parasite genome or gene copy number.</p> <p>Methods</p> <p>Clinical studies of non-severe malaria reporting on target genetic markers (SNPs for <it>pfmdr1</it>, <it>pfcrt</it>, <it>dhfr</it>, <it>dhps</it>, gene copy number for <it>pfmdr1</it>) providing complete information on inclusion criteria, outcome, follow up and genotyping, were included. Three investigators independently extracted data from articles. Results were stratified by gene, codon, drug and duration of follow-up. For each study and aggregate data the random effect odds ratio (OR) with 95%CIs was estimated and presented as Forest plots. An OR with a lower 95^thconfidence interval > 1 was considered consistent with a failure being associated to a given gene mutation.</p> <p>Results</p> <p>92 studies were eligible among the selection from computerized search, with information on <it>pfcrt </it>(25/159 studies), <it>pfmdr1 </it>(29/236 studies), <it>dhfr </it>(18/373 studies), <it>dhps </it>(20/195 studies). The risk of therapeutic failure after chloroquine was increased by the presence of <it>pfcrt </it>K76T (Day 28, OR = 7.2 [95%CI: 4.5–11.5]), <it>pfmdr1 </it>N86Y was associated with both chloroquine (Day 28, OR = 1.8 [95%CI: 1.3–2.4]) and amodiaquine failures (OR = 5.4 [95%CI: 2.6–11.3, p < 0.001]). For sulphadoxine-pyrimethamine the <it>dhfr </it>single (S108N) (Day 28, OR = 3.5 [95%CI: 1.9–6.3]) and triple mutants (S108N, N51I, C59R) (Day 28, OR = 3.1 [95%CI: 2.0–4.9]) and <it>dhfr</it>-<it>dhps </it>quintuple mutants (Day 28, OR = 5.2 [95%CI: 3.2–8.8]) also increased the risk of treatment failure. Increased <it>pfmdr1 </it>copy number was correlated with treatment failure following mefloquine (OR = 8.6 [95%CI: 3.3–22.9]).</p> <p>Conclusion</p> <p>When applying the selection procedure for comparative analysis, few studies fulfilled all inclusion criteria compared to the large number of papers identified, but heterogeneity was limited. Genetic molecular markers were related to an increased risk of therapeutic failure. Guidelines are discussed and a checklist for further studies is proposed.</p

Diversity of Plasmodium falciparum Chloroquine Resistance Transporter (pfcrt) Exon 2 Haplotypes in the Pacific from 1959 to 1979

Nearly one million deaths are attributed to malaria every year. Recent reports of multi-drug treatment failure of falciparum malaria underscore the need to understand the molecular basis of drug resistance. Multiple mutations in the Plasmodium falciparum chloroquine resistance transporter (pfcrt) are involved in chloroquine resistance, but the evolution of complex haplotypes is not yet well understood. Using over 4,500 archival human serum specimens collected from 19 Pacific populations between 1959 and 1979, the period including and just prior to the appearance of chloroquine treatment failure in the Pacific, we PCR-amplified and sequenced a portion of the pfcrt exon 2 from 771 P. falciparum-infected individuals to explore the spatial and temporal variation in falciparum malaria prevalence and the evolution of chloroquine resistance. In the Pacific, the prevalence of P. falciparum varied considerably across ecological zones. On the island of New Guinea, the decreases in prevalence of P. falciparum in coastal, high-transmission areas over time were contrasted by the increase in prevalence during the same period in the highlands, where transmission was intermittent. We found 78 unique pfcrt haplotypes consisting of 34 amino acid substitutions and 28 synonymous mutations. More importantly, two pfcrt mutations (N75D and K76T) implicated in chloroquine resistance were present in parasites from New Hebrides (now Vanuatu) eight years before the first report of treatment failure. Our results also revealed unexpectedly high levels of genetic diversity in pfcrt exon 2 prior to the historical chloroquine resistance selective sweep, particularly in areas where disease burden was relatively low. In the Pacific, parasite genetic isolation, as well as host acquired immune status and genetic resistance to malaria, were important contributors to the evolution of chloroquine resistance in P. falciparum