Pests and diseases affecting potato landraces and bred varieties grown in Peru under indigenous farming system

The major pests and diseases were identified and quantified on thirteen potato landraces and three bred varieties cultivated in Peru. Late blight (Phytophthora infestans) was the primary biotic constraint affecting plants before flowering with an average severity of 24%. No other pathogens caused severe foliar disease, but black scurf (Rhizoctonia solani) was relatively common on tubers of some genotypes with incidence ranging from 4.30 to 33.33%. The viruses most generally considered important in potato seed degeneration, PVY and PLRV, were extremely rare, with 1.11 and 0.12 % incidence, respectively. Other viruses considered mild, such as PVX and PVS, were more common, with incidence of 28.23 and 22.29 %, respectively. Potato flea beetle (Epitrix spp.), potato leaf beetle (Diabrotica spp.) and Andean potato weevil (Premnotrypes spp.) were common, with incidence of 28.14, 18.75 and 13.61%, respectively. Potato landraces known as Ishkupuru, Lengua de vaca, Chaulina, Chaulina Tajacaja and Negro cayash were identified as potentially resistant to P. infestan

The Bulgeless Seyfert/LINER Galaxy NGC 3367: Disk, Bar, Lopsidedness and Environment

NGC3367 is a nearby isolated active galaxy that shows a radio jet, a strong bar and evidence of lopsidedness. We present a quantitative analysis of the stellar and gaseous structure of the galaxy disk and a search for evidence of recent interaction based on new UBVRI Halpha and JHK images and on archival Halpha Fabry-Perot and HI VLA data. From a coupled 1D/2D GALFIT bulge/bar/disk decomposition an (B/D ~ 0.07-0.1) exponential pseudobulge is inferred in all the observed bands. A NIR estimate of the bar strength = 0.44 places NGC 3367 bar among the strongest ones. The asymmetry properties were studied using (1) optical and NIR CAS indexes (2) the stellar (NIR) and gaseous (Halpha, HI) A_1 Fourier mode amplitudes and (3) the HI integrated profile and HI mean intensity distribution. While the average stellar component shows asymmetry values close to the average found in the Local Universe for isolated galaxies, the young stellar component and gas values are largely decoupled showing significantly larger A_1 mode amplitudes suggesting that the gas has been recently perturbed. Our search for (1) faint stellar structures in the outer regions (up to u_R ~ 26 mag arcsec^{-2}), (2) (Halpha) star-forming satellite galaxies and (3) regions with different colors (stellar populations) along the disk all failed. Such an absence is interpreted using recent numerical simulations to constrain a tidal event with an LMC like galaxy to some dynamical times in the past or to a current very low mass, gas rich accretion. We conclude that a cold accretion mode (gas and small/dark galaxies) may be responsible of the nuclear activity and peculiar (young stars and gas) morphology regardless of the highly isolated environment. Black hole growth in bulgeless galaxies may be triggered by cosmic smooth mass accretion.Comment: 27 pages, 12 figures, accepted for publication in The Astronomical Journa

Vulvar myiasis during pregnancy.

Myiasis is a parasitic infestation caused by the larvae of several fly species. Diagnosis and treatment are simple. The location of this infestation at the vulvar area is, however, an extremely rare occurrence. The authors present two cases of vulvar myiasis affecting pregnant women. The first case is a 19-year-old pregnant girl with vulvar myiasis and concomitant syphilis, vaginal trichomoniasis and genital candidiasis. The patient was also HIV-positive. The second case is a 17-year-old pregnant girl with vulvar myiasis associated with extensive vulvar condyloma acuminatum lesions

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Mortality from gastrointestinal congenital anomalies at 264 hospitals in 74 low-income, middle-income, and high-income countries: a multicentre, international, prospective cohort study

Background: Congenital anomalies are the fifth leading cause of mortality in children younger than 5 years globally. Many gastrointestinal congenital anomalies are fatal without timely access to neonatal surgical care, but few studies have been done on these conditions in low-income and middle-income countries (LMICs). We compared outcomes of the seven most common gastrointestinal congenital anomalies in low-income, middle-income, and high-income countries globally, and identified factors associated with mortality. // Methods: We did a multicentre, international prospective cohort study of patients younger than 16 years, presenting to hospital for the first time with oesophageal atresia, congenital diaphragmatic hernia, intestinal atresia, gastroschisis, exomphalos, anorectal malformation, and Hirschsprung's disease. Recruitment was of consecutive patients for a minimum of 1 month between October, 2018, and April, 2019. We collected data on patient demographics, clinical status, interventions, and outcomes using the REDCap platform. Patients were followed up for 30 days after primary intervention, or 30 days after admission if they did not receive an intervention. The primary outcome was all-cause, in-hospital mortality for all conditions combined and each condition individually, stratified by country income status. We did a complete case analysis. // Findings: We included 3849 patients with 3975 study conditions (560 with oesophageal atresia, 448 with congenital diaphragmatic hernia, 681 with intestinal atresia, 453 with gastroschisis, 325 with exomphalos, 991 with anorectal malformation, and 517 with Hirschsprung's disease) from 264 hospitals (89 in high-income countries, 166 in middle-income countries, and nine in low-income countries) in 74 countries. Of the 3849 patients, 2231 (58·0%) were male. Median gestational age at birth was 38 weeks (IQR 36–39) and median bodyweight at presentation was 2·8 kg (2·3–3·3). Mortality among all patients was 37 (39·8%) of 93 in low-income countries, 583 (20·4%) of 2860 in middle-income countries, and 50 (5·6%) of 896 in high-income countries (p<0·0001 between all country income groups). Gastroschisis had the greatest difference in mortality between country income strata (nine [90·0%] of ten in low-income countries, 97 [31·9%] of 304 in middle-income countries, and two [1·4%] of 139 in high-income countries; p≤0·0001 between all country income groups). Factors significantly associated with higher mortality for all patients combined included country income status (low-income vs high-income countries, risk ratio 2·78 [95% CI 1·88–4·11], p<0·0001; middle-income vs high-income countries, 2·11 [1·59–2·79], p<0·0001), sepsis at presentation (1·20 [1·04–1·40], p=0·016), higher American Society of Anesthesiologists (ASA) score at primary intervention (ASA 4–5 vs ASA 1–2, 1·82 [1·40–2·35], p<0·0001; ASA 3 vs ASA 1–2, 1·58, [1·30–1·92], p<0·0001]), surgical safety checklist not used (1·39 [1·02–1·90], p=0·035), and ventilation or parenteral nutrition unavailable when needed (ventilation 1·96, [1·41–2·71], p=0·0001; parenteral nutrition 1·35, [1·05–1·74], p=0·018). Administration of parenteral nutrition (0·61, [0·47–0·79], p=0·0002) and use of a peripherally inserted central catheter (0·65 [0·50–0·86], p=0·0024) or percutaneous central line (0·69 [0·48–1·00], p=0·049) were associated with lower mortality. // Interpretation: Unacceptable differences in mortality exist for gastrointestinal congenital anomalies between low-income, middle-income, and high-income countries. Improving access to quality neonatal surgical care in LMICs will be vital to achieve Sustainable Development Goal 3.2 of ending preventable deaths in neonates and children younger than 5 years by 2030

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field