This longitudinal study aimed to validate the biosocial theory of borderline personality disorder (BPD) by examining the transactional relationship between individual vulnerabilities and parental invalidation, and their links to BPD symptoms. We recruited a sample of 332 adolescents (mean age = 14.18 years; 58.3% female) residing in Singapore and administered self-report measures across three time-points (six months apart). Results from our path analytic model indicated that parental invalidation, impulsivity, and emotional vulnerability exhibited unique predictive associations with emotion dysregulation six months later. There was also a reciprocal prospective relationship between emotion regulation difficulties and BPD symptoms. Using random-intercepts cross-lagged panel models, we found partial evidence for a within-individual reciprocal relationship between parental invalidation and emotional vulnerability, and a unidirectional relationship of within-individual changes in impulsivity positively predicting changes in parental invalidation six months later. Overall, the study provided partial empirical support for the biosocial model in a Singaporean context.

The putative host galaxy of FRB 20171020A was first identified as ESO 601-G036 in 2018, but as no repeat bursts have been detected, direct confirmation of the host remains elusive. In light of recent developments in the field, we re-examine this host and determine a new association confidence level of 98%. At 37 Mpc, this makes ESO 601-G036 the third closest FRB host galaxy to be identified to date and the closest to host an apparently non-repeating FRB (with an estimated repetition rate limit of $<$$0.011$ bursts per day above $10^{39}$ erg). Due to its close distance, we are able to perform detailed multi-wavelength analysis on the ESO 601-G036 system. Follow-up observations confirm ESO 601-G036 to be a typical star-forming galaxy with H i and stellar masses of $\log_{10}\!(M_{\rm{H\,{\small I}}} / M_\odot) \sim 9.2$ and $\log_{10}\!(M_\star / M_\odot) = 8.64^{+0.03}_{-0.15}$, and a star formation rate of $\text{SFR} = 0.09 \pm 0.01\,{\rm M}_\odot\,\text{yr}^{-1}$. We detect, for the first time, a diffuse gaseous tail ($\log_{10}\!(M_{\rm{H\,{\small I}}} / M_\odot) \sim 8.3$) extending to the south-west that suggests recent interactions, likely with the confirmed nearby companion ESO 601-G037. ESO 601-G037 is a stellar shred located to the south of ESO 601-G036 that has an arc-like morphology, is about an order of magnitude less massive, and has a lower gas metallicity that is indicative of a younger stellar population. The properties of the ESO 601-G036 system indicate an ongoing minor merger event, which is affecting the overall gaseous component of the system and the stars within ESO 601-G037. Such activity is consistent with current FRB progenitor models involving magnetars and the signs of recent interactions in other nearby FRB host galaxies.

This study examined the intergenerational transmission of parental invalidation and whether parental difficulties in emotion regulation mediated the association between past experiences of invalidation and current invalidating parenting practices. We also aimed to investigate whether gender might influence the transmission of parental invalidation. We recruited a community sample of 293 dual-parent families (adolescent and their parents) based in Singapore. Parents and adolescents each completed measures of childhood invalidation, whereas parents additionally reported on their difficulties in emotion regulation. Results based on path analyses demonstrated that past parental invalidation experienced by fathers positively predicted current perceived invalidation by their children. The association between mothers’ childhood invalidation and current invalidating practices was fully mediated by mothers’ difficulties with emotion regulation. Further analyses revealed that parents’ current invalidating behaviors were not predicted by their past experiences of paternal or maternal invalidation. These findings point to the importance of considering the family invalidating environment as a whole when examining the influence of past experienced parental invalidation on emotion regulation and invalidating behaviors of second-generation parents. Our study provides empirical support for the intergenerational transmission of parental invalidation and highlights the need to address childhood experiences of parental invalidation in parenting programs.

Anxiety is the most prevalent psychological disorder among youth, and even following treatment, it confers risk for anxiety relapse and the development of depression. Anxiety disorders are associated with heightened response to negative affective stimuli in the brain networks that underlie emotion processing. One factor that can attenuate the symptoms of anxiety and depression in high-risk youth is parental warmth. The current study investigates whether parental warmth helps to protect against future anxiety and depressive symptoms in adolescents with histories of anxiety and whether neural functioning in the brain regions that are implicated in emotion processing and regulation can account for this link. Following treatment for anxiety disorder (Time 1), 30 adolescents (M age = 11.58, SD = 1.26) reported on maternal warmth, and 2 years later (Time 2) they participated in a functional neuroimaging task where they listened to prerecorded criticism and neutral statements from a parent. Higher maternal warmth predicted lower neural activation during criticism, compared with the response during neutral statements, in the left amygdala, bilateral insula, subgenual anterior cingulate (sgACC), right ventrolateral prefrontal cortex, and anterior cingulate cortex. Maternal warmth was associated with adolescents’ anxiety and depressive symptoms due to the indirect effects of sgACC activation, suggesting that parenting may attenuate risk for internalizing through its effects on brain function.

Molecular assays are often implemented by weed scientists for detection of herbicide-resistant individuals; however, the utility of these assays can be limited if multiple mechanisms of evolved resistance exist. Waterhemp resistant to protoporphyrinogen oxidase (PPO)– inhibiting herbicides is conferred by a target-site mutation in PPX2L (a gene coding for PPO), resulting in the loss of a glycine at position 210 (ΔG210). This ΔG210 mutation of PPX2L is the only known mechanism responsible for PPO-inhibitor resistance (PPO-R) in waterhemp from five states (Illinois, Indiana, Iowa, Kansas, and Missouri); however, a limited number of populations have been tested, especially in Illinois. To verify the ubiquity of the ΔG210 in PPO-R waterhemp populations in Illinois, a previously published allele-specific PCR (asPCR) was used for the detection of the ΔG210 mutation to associate this mutation with phenotypic resistance in 94 Illinois waterhemp populations. The ΔG210 mutation was detected in all populations displaying phenotypic resistance to lactofen (220 g ai ha−1), indicating the deletion is likely the only mechanism of resistance. With evidence that the ΔG210 mutation dominates PPO-R waterhemp biotypes, molecular detection techniques have considerable utility. Unfortunately, the previously published asPCR is time consuming, very sensitive to PCR conditions, and requires additional steps to eliminate the possibility of false negatives. To overcome these limitations, a streamlined molecular method using the TaqMan® technique was developed, utilizing allele-specific, fluorescent probes for high-throughput, robust discrimination of each allele (resistant and susceptible) at the 210th amino acid position of PPX2L.

DNA microarrays are one of the new tools of genomics that have become quite commonplace in plant science research within the past decade. Essentially, DNA microarrays are an extension of the more traditional molecular biology technique of northern blotting. Unlike northern blotting, however, in which the expression of a single gene is monitored, DNA microarrays allow for the simultaneous monitoring of thousands of genes—or, in fact, potentially all of an organism's genes—in a single experiment. Most of the currently available plant microarrays are designed for crops species or the model plant, Arabidopsis; however, a microarray for at least one major weed species is currently available. Furthermore, cDNA-based microarrays prepared for one species can be used to investigate gene expression in related species. As the technology is maturing it is becoming much more accessible, and now is the time to begin utilizing microarrays in weed science research. Questions related to herbicide activity are particularly well suited for a microarray approach. Additionally, gene-expression profiling via microarrays can be used to address questions relating to weed biology, weed–crop competition, allelopathy, parasitic weeds, and biological control of weeds.

Recent advances in sequencing technologies (next-generation sequencing) offer dramatically increased sequencing throughput at a lower cost than traditional Sanger sequencing. This technology is changing genomics research by allowing large scale sequencing experiments in nonmodel systems. Waterhemp is an important weed in the midwestern United States with characteristics that makes it an interesting ecological model. However, very few genomic resources are available for this species. One half of a 70 by 75 picotiter plate of 454-pyrosequencing was performed on total DNA isolated from waterhemp, generating 158,015 reads of an average length of 271 bp, or a total of nearly 43 Mbp of sequence. Included in this sequence was a nearly complete sequence of the chloroplast genome, sequences of several important herbicide resistance genes, leads for simple sequence repeat (SSR) markers, and a sampling of the repeated elements (e.g., transposons) present in this species. Here we present the waterhemp genomic data gleaned from this sequencing experiment and illustrate the value of next-generation sequencing technology to weed science research.

Resistance to protoporphyrinogen oxidase (PPO)-inhibiting herbicides in waterhemp has been shown previously to be the result of a unique mechanism. Specifically, a three–base-pair (3-bp) deletion in the PPX2L gene, a gene encoding both plastid- and mitochondria-targeted PPO enzymes, confers herbicide resistance in this species. Furthermore, when this unique mechanism was initially characterized it was presumed that waterhemp contained three PPX genes, PPX1, PPX2S, and PPX2L, and that the resistant biotypes were missing PPX2S. Here, allele testing and examination of genetic sequence data demonstrate that there are likely only two PPX genes in waterhemp, PPX1 and PPX2L. Next, to determine the prevalence of this mechanism of resistance in Illinois waterhemp, we developed an allele-specific polymerase chain reaction (PCR) marker that amplifies only the 3-bp deletion allele, ΔG210, of PPX2L. By utilizing this marker, we show that the ΔG210 PPX2L allele correlated with whole-plant resistance to PPO inhibitors in each of four other waterhemp populations evaluated from Illinois.

A population of common ragweed from Delaware was not controlled in the field by herbicides that inhibit acetolactate synthase (ALS) or protoporphyrinogen oxidase (PPO). Research was conducted to ascertain if this population was resistant to these herbicidal modes of action and, if so, to determine the resistance mechanism(s). Resistance was confirmed by dose-response studies on greenhouse-grown plants with multiple ALS- and PPO-inhibiting herbicides. DNA sequence data revealed that resistance to ALS-inhibiting herbicides was due to the previously reported W574L ALS mutation. To assist in determining the mechanism of resistance to PPO-inhibiting herbicides, an F2 population was derived from a cross between the resistant biotype (Del-R) and a sensitive biotype (DV1-S). This population segregated in the ratio of three resistant : one sensitive when treated with fomesafen, indicating that resistance to PPO-inhibiting herbicides was conferred by a single, (incompletely) dominant, nuclear gene. Sequences of the target-site genes, PPX1 and PPX2, for PPO-inhibiting herbicides were obtained through the screening of a common ragweed cDNA library and subsequent cDNA extension (5′-RACE). Molecular marker analysis with the F2 population revealed that the PPX2 gene cosegregated with resistance to PPO-inhibiting herbicides. A mutation substituting an arginine codon for a leucine codon at a conserved location (R98L) of the PPX2 gene was suspected of being responsible for resistance. By using a transgenic Escherichia coli system, it was demonstrated that the R98L mutation was sufficient to confer resistance to PPO-inhibiting herbicides. The level of resistance to acifluorfen conferred by the R98L mutation in the E. coli system was about 31-fold, similar to the level of resistance seen in the whole-plant dose-response study. Last, a DNA-based assay was developed to identify the presence or absence of the common ragweed PPX2 R98L mutation. The R98L PPX2 mutation is the second mechanism identified for evolved resistance to PPO-inhibiting herbicides.