Regional Assessment of Soybean Brown Stem Rot, Phytophthora sojae, and Heterodera glycines Using Area-Frame Sampling: Prevalence and Effects of Tillage

The prevalence of brown stem rot (caused by Phialophora gregata), Heterodera glycines, and Phytophthora sojae in the north central United States was investigated during the fall of 1995 and 1996. Soybean fields were randomly selected using an area-frame sampling design in collaboration with the National Agricultural Statistics Service. Soil and soybean stem samples, along with tillage information, were collected from 1,462 fields in Illinois, Iowa, Minnesota, Missouri, and Ohio. An additional 275 soil samples collected from Indiana were assessed for H. glycines. For each field, the incidence and prevalence of brown stem rot was assessed in 20 soybean stem pieces. The prevalence and recovery (expressed as the percentage of leaf disks colonized) of P. sojae and the prevalence and population densities of H. glycines were determined from the soil samples. The prevalence of brown stem rot ranged from 28% in Missouri to 73% in Illinois; 68 and 72% of the fields in Minnesota and Iowa, respectively, showed symptomatic samples. The incidence of brown stem rot was greater in conservation-till than in conventional-till fields in all states except Minnesota, which had few no-till fields. P. sojae was detected in two-thirds of the soybean fields in Ohio and Minnesota, whereas 63, 55, and 41% of the fields in Iowa, Missouri, and Illinois, respectively, were infested with the pathogen. The recovery rates of P. sojae were significantly greater (P ≤ 0.05) in conservation-till than in conventional-till fields in all states except Iowa. H. glycines was detected in 83% of the soybean fields in Illinois, 74% in Iowa, 71% in Missouri, 60% in Ohio, 54% in Minnesota, and 47% in Indiana. Both the prevalence and population densities of H. glycines were consistently greater in tilled than in no-till fields in all states for which tillage information was available

Knockdown of BACE1-AS Nonprotein-Coding Transcript Modulates Beta-Amyloid-Related Hippocampal Neurogenesis

Background. Alzheimer's disease (AD) is a devastating neurological disorder and the main cause of dementia in the elderly population worldwide. Adult neurogenesis appears to be upregulated very early in AD pathogenesis in response to some specific aggregates of beta-amyloid (Aβ) peptides, exhausting the neuronal stem cell pools in the brain. Previously, we characterized a conserved nonprotein-coding antisense transcript for β-secretase-1 (BACE1), a critical enzyme in AD pathophysiology. We showed that the BACE1-antisense transcript (BACE1-AS) is markedly upregulated in brain samples from AD patients and promotes the stability of the (sense) BACE1 transcript. In the current paper, we examine the relationship between BACE1, BACE1-AS, adult neurogenesis markers, and amyloid plaque formation in amyloid precursor protein (APP) transgenic mice (Tg-19959) of various ages. Results. Consistent with previous publications in other APP overexpressing mouse models, we found adult neurogenesis markers to be noticeably upregulated in Tg-19959 mice very early in the development of the disease. Knockdown of either one of BACE1 or BACE1-AS transcripts by continuous infusion of locked nucleic acid- (LNA-) modified siRNAs into the third ventricle over the period of two weeks caused concordant downregulation of both transcripts in Tg-19959 mice. Downregulation of BACE1 mRNA was followed by reduction of BACE1 protein and insoluble Aβ. Modulation of BACE1 and BACE1-AS transcripts also altered oligomeric Aβ aggregation pattern, which was in turn associated with an increase in neurogenesis markers at the RNA and protein level. Conclusion. We found alterations in the RNA and protein concentrations of several adult neurogenesis markers, as well as non-protein-coding BACE1-AS transcripts, in parallel with the course of β-amyloid synthesis and aggregation in the brain of Tg15999 mice. In addition, by knocking down BACE1 or BACE1-AS (thereby reducing Aβ production and plaque deposition), we were able to modulate expression of these neurogenesis markers. Our findings suggest a distortion of adult neurogenesis that is associated with Aβ production very early in amyloid pathogenesis. We believe that these alterations, at the molecular level, could prove useful as novel therapeutic targets and/or as early biomarkers of AD

Effects of �Satureja hortensis L.� on improving adult gastroesophageal reflux disease: A double-blind, randomized, controlled, clinical trial

Background: Gastro-esophageal reflux disease (GERD) is one of the most widespread gastrointestinal disorders. In addition, there is increasing evidence that not all patients respond to its current remedies. Objectives: The aim of this pilot study was to investigate the effect of �Satureja hortensis L.� on improving the symptoms of mild to moderate GERD in adults. Methods: In this double-blind, randomized, controlled, clinical trial, we evaluated the efficacy of �Satureja hortensis L.� compared to placebo in the symptoms of GERD in fifty-eight adultswith GERD who referred to Hazrat Rasool-e-Akram hospital in Tehran, Iran, in 2015. In order to assess GERD symptoms, a standardized questionnaire of frequency scale (FSSG) was used before and after the intervention. Results: Regarding within-group changes, a significant decrease was observed in FSSG, dysmotility-like symptoms and acid reflux related scores in both groups of the study after the intervention compared to baseline (P < 0.001). Regarding between-group analysis, no significant differences were observed between the two groups in terms of FSSG total scores (0.05 < P). Conclusions: According to the results of the current study, Satureja hortensis L. with the dose of 500mgthree times per day failed to improve the symptoms of GERD in adults compared to placebo. The significant reductions in the GERD scores in both groups seem to be related to the lifestyle modification that was prescribed to both groups. © 2018, Iranian Red Crescent Medical Journal

Effects of �Satureja hortensis L.� on improving adult gastroesophageal reflux disease: A double-blind, randomized, controlled, clinical trial

Background: Gastro-esophageal reflux disease (GERD) is one of the most widespread gastrointestinal disorders. In addition, there is increasing evidence that not all patients respond to its current remedies. Objectives: The aim of this pilot study was to investigate the effect of �Satureja hortensis L.� on improving the symptoms of mild to moderate GERD in adults. Methods: In this double-blind, randomized, controlled, clinical trial, we evaluated the efficacy of �Satureja hortensis L.� compared to placebo in the symptoms of GERD in fifty-eight adultswith GERD who referred to Hazrat Rasool-e-Akram hospital in Tehran, Iran, in 2015. In order to assess GERD symptoms, a standardized questionnaire of frequency scale (FSSG) was used before and after the intervention. Results: Regarding within-group changes, a significant decrease was observed in FSSG, dysmotility-like symptoms and acid reflux related scores in both groups of the study after the intervention compared to baseline (P < 0.001). Regarding between-group analysis, no significant differences were observed between the two groups in terms of FSSG total scores (0.05 < P). Conclusions: According to the results of the current study, Satureja hortensis L. with the dose of 500mgthree times per day failed to improve the symptoms of GERD in adults compared to placebo. The significant reductions in the GERD scores in both groups seem to be related to the lifestyle modification that was prescribed to both groups. © 2018, Iranian Red Crescent Medical Journal

A novel frame-shift deletion in FANCF gene causing autosomal recessive Fanconi anemia: A case report

Background: Fanconi anemia (FA) is a heterogeneous genetic disorder characterized by congenital anomalies, early-onset bone marrow failure, and a high predisposition to cancers. Up to know, different genes involved in the DNA repair pathway, mainly FANCA genes, have been identified to be affected in patients with FA. Case presentation: Here, we report clinical, laboratory and genetic findings in a 3.5-year-old Iranian female patient, a product of a consanguineous marriage, who was suspicious of FA, observed with short stature, microcephaly, skin hyperpigmentation, anemia, thrombocytopenia and hypo cellular bone marrow. Therefore, Next Generation Sequencing was performed to identify the genetic cause of the disease in this patient. Results revealed a novel, private, homozygous frameshift mutation in the FANCF gene (NM-022725: c. 534delG, p. G178 fs) which was confirmed by Sanger sequencing in the proband. Conclusion: Such studies may help uncover the exact pathomechanisms of this disorder and establish the genotype-phenotype correlations by identification of more mutations in this gene. It is the first report of a mutation in the FANCF gene in Iranian patients with Fanconi anemia. This new mutation correlates with a hematological problem (pancytopenia), short stature, and microcephaly and skin hyperpigmentation. Until now, no evidence of malignancy was detected

Upregulation of Haploinsufficient Gene Expression in the Brain by Targeting a Long Non-coding RNA Improves Seizure Phenotype in a Model of Dravet Syndrome

AbstractDravet syndrome is a devastating genetic brain disorder caused by heterozygous loss-of-function mutation in the voltage-gated sodium channel gene SCN1A. There are currently no treatments, but the upregulation of SCN1A healthy allele represents an appealing therapeutic strategy. In this study we identified a novel, evolutionary conserved mechanism controlling the expression of SCN1A that is mediated by an antisense non-coding RNA (SCN1ANAT). Using oligonucleotide-based compounds (AntagoNATs) targeting SCN1ANAT we were able to induce specific upregulation of SCN1A both in vitro and in vivo, in the brain of Dravet knock-in mouse model and a non-human primate. AntagoNAT-mediated upregulation of Scn1a in postnatal Dravet mice led to significant improvements in seizure phenotype and excitability of hippocampal interneurons. These results further elucidate the pathophysiology of Dravet syndrome and outline a possible new approach for the treatment of this and other genetic disorders with similar etiology

Stabilization of ribozyme-like cis-noncoding rRNAs induces apoptotic and nonapoptotic death in lung cells

Bidirectional non-protein-coding RNAs are ubiquitously transcribed from the genome. Convergent sense and antisense transcripts may regulate each other. Here, we examined the convergent cis-noncoding rRNAs (nc-rRNAs) in A5 and E9 lung cancer models. Sense nc-rRNAs extending from rDNA intergenic region to internal transcribed spacer of around 10 kb in length were identified. nc-rRNAs in sense direction exhibited in vitro characteristics of ribozymes, namely, degradation upon incubation with MgCl2 and stabilization by complementary oligonucleotides. Detection of endogenous cleavage-ligation products carrying internal deletion of hundreds to thousands nucleotides by massively parallel sequencing confirmed the catalytic properties. Transfection of oligonucleotides pairing with antisense nc-rRNAs stabilized both target and complementary transcripts, perturbed rRNA biogenesis, and induced massive cell death via apoptotic and/or nonapoptotic mechanisms depending on cell type and treatment. Oligonucleotides targeting cellular sense transcripts are less responsive. Spontaneously detached cells, though rare, also showed accumulation of nc-rRNAs and perturbation of rRNA biogenesis. Direct participation of nc-rRNAs in apoptotic and nonapoptotic death was demonstrated by transfection of synthetic nc-rRNAs encompassing the rDNA promoter. In sum, convergent cis-nc-rRNAs follow a feed-forward mechanism to regulate each other and rRNA biogenesis. This opens an opportunity to disrupt rRNA biogenesis, commonly upregulated in cancers, via inhibition of ribozyme-like activities in nc-rRNAs