Plant-parasitic nematodes (PPN) are among the most economically and ecologically damaging pests, causing severe losses of crop production worldwide. Chemical-based nematicides have been widely used, but these may have adverse effects on human health and the environment. Hence, biological control agents (BCAs) have become an alternative option for controlling PPN, since they are environmentally friendly and cost effective. Lately, a major effort has been made to evaluate the potential of a commercial grade strain of plant growth-promoting rhizobacteria (PGPR) as BCAs, because emerging evidence has shown that PGPR can reduce PPN in infested plants through direct and/or indirect antagonistic mechanisms. Direct antagonism occurs by predation, release of antinematicidal metabolites and semiochemicals, competition for nutrients, and niche exclusion. However, the results of direct antagonism may be inconsistent due to unknown endogenous and exogenous factors that may prevent PGPR from colonizing plant’s roots. On the other hand, indirect antagonism may occur from the induced systemic resistance (ISR) that primes whole plants to better fight against various biotic and abiotic constraints, actuating faster and/or stronger defense responses (adaption), enhancing their promise as BCAs. Hence, this review will briefly revisit (i) two modes of PGPR in managing PPN, and (ii) the current working models and many benefits of ISR, in the aim of reassessing current progresses and future directions for isolating more effective BCAs and/or developing better PPN management strategy.
CRISPR-Cas mediated genome engineering has revolutionized functional genomics. However, understanding of DNA repair following Cas-mediated DNA cleavage remains incomplete. Using Cas12a ribonucleoprotein genome editing in the fungal pathogen, Magnaporthe oryzae, we detail non-canonical DNA repair outcomes from hundreds of transformants. Sanger and nanopore sequencing analysis reveals significant variation in DNA repair profiles, ranging from small INDELs to kilobase size deletions and insertions. Furthermore, we find the frequency of DNA repair outcomes varies between loci. The results are not specific to the Cas-nuclease or selection procedure. Through Ku80 deletion analysis, a key protein required for canonical non-homologous end joining, we demonstrate activity of an alternative end joining mechanism that creates larger DNA deletions, and uses longer microhomology compared to C-NHEJ. Together, our results suggest preferential DNA repair pathway activity in the genome that can create different mutation profiles following repair, which could create biased genome variation and impact genome engineering and genome evolution.
Patient: Male, 52 Final Diagnosis: Clindamycin induced acute kidney injury Symptoms: Nausea • fatigue • anorexia • hematuria • decreased urine output Medication: Clindamycin Clinical Procedure: None Specialty: Nephrology and Internal Medicine Objective: Mistake in diagnosis Background: Medications are one of the most common causes of acute kidney injury (AKI). Elderly patients with diabetes mellitus and chronic kidney disease seem to be at particularly high risk for development of medication-induced AKI. Among antibiotics, the most commonly implicated agents are aminoglycosides, cephalosporins, trimethoprim-sulfamethoxazole, acyclovir, and amphotericin. Despite its widespread use, clindamycin has been rarely associated with AKI. Case Report: A 52-year-old male patient with type II insulin dependent diabetes mellitus without diabetic nephropathy was treated with clindamycin for chronic osteomyelitis. Five days following initiation of therapy, he developed nausea, poor appetite, decrease in urine output, and profound generalized weakness. His symptoms were initially attributed to gastrointestinal side effects of clindamycin and he was advised to take it with food and to hydrate himself vigorously. Despite this change, his symptoms progressed and he developed hematuria and AKI which prompted hospital admission. Extensive workup for AKI that included evaluation for pre-renal, intrinsic renal, and post-renal etiologies failed to point to other etiologies apart from clindamycin-induced AKI. Following cessation of medication and temporary renal replacement therapy (RRT), his renal function returned to baseline. Conclusions: We present a case of clindamycin-induced AKI that was diagnosed after a delay due to uremia symptoms being mistakenly attributed to gastrointestinal side effects of clindamycin. Although rare, clindamycin can be a cause of AKI and clinician should be aware of this association in order to recognize and treat it in timely manner.
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