Hierarchical Mn3O4/NiSe2-MnSe2: A Versatile Electrode Material for High-Performance All-Solid-State Hybrid Pseudocapacitors with Supreme Working Durability.

As highly efficient electrochemical energy storage devices are in indispensable demand for numerous modern-day technologies, herein sluggish precipitation followed by an anion exchange procedure has been developed to synthesize an oxide-selenide mixed phase (Mn3O4/NiSe2-MnSe2) novel electrode material with high surface area and porosity for high-performance all-solid-state hybrid pseudocapacitors (ASSHPC). Mn3O4/NiSe2-MnSe2 shows a rich Tyndall effect (in H2O) and possesses randomly arranged low-dimensional crystallites of nearly similar size and uniform shape. The electrochemical analyses of Mn3O4/NiSe2-MnSe2 corroborate good electrochemical reversibility during charge transfer, superior pseudocapacitive charge-storage efficiency, and very low charge transfer and series resistance, ion-diffusion resistance, and relaxation time, which endorse the quick pseudocapacitive response of the material. The Mn3O4/NiSe2-MnSe2||N-rGO ASSHPC device demonstrates excellent charge-storage physiognomies suggestive of rich electrochemical and electromicrostructural compatibility between the electrode materials in the fabricated assembly. The Mn3O4/NiSe2-MnSe2||N-rGO ASSHPC device delivers high mass and area specific capacitance/capacity, very low charge-transfer resistance (∼0.74 Ω), total series resistance (∼0.76 Ω), diffusion resistance, and a relaxation time constant, which endorse the quick pseudocapacitive response of the device. The device delivers higher energy and power density (∼34 W h kg-1 at ∼2994 W kg-1), rate efficiency (∼17 W h kg-1 at ∼11,995 W kg-1), and cyclic performance (∼97.2% specific capacity/capacitance retention after 9500 continuous GCD cycles). The superior Ragone and cyclic efficiencies of the ASSHPC device are ascribed to the multiple redox-active Ni and Mn ions which lead to the supplemented number of redox reactions; "electroactive-ion buffering pool"-like physiognomics of Mn3O4/NiSe2-MnSe2, which facilitate the electrolyte ion dissemination to the electroactive sites even at high rate redox condition; and ideal electro-microstructural compatibility between the electrode materials, which leads to assisted charge transfer and absolute ion dissemination during the charge-storage process.

Evaluation and comparison of performance of low-dose 128-slice CT scanner with different mAs values: A phantom study.

OBJECTIVE: Radiation dose in computed tomography (CT) has been the concern of physicists ever since the introduction of CT scan. The objective of this study was to evaluate the performance of low-dose 128-slice CT scanner with different mAs values. MATERIALS AND METHODS: Quantitative study was carried out at different values of mAs. Philips brilliance CT phantom with Philips ingenuity 128-slice low-dose CT scanner was chosen for this study. CT number linearity, CT number accuracy, slice thickness accuracy, high-contrast resolution, and low-contrast resolution were calculated and estimated computed tomography dose index volume (CTDIvol) for all the mAs values were recorded. Noise was calculated for all mAs values for comparison. RESULTS: Data analysis shows that image quality was acceptable for all protocols. High-contrast resolution for all protocols was 20 line pairs per centimeter. Low-contrast resolution for 50 mAs images was 4 mm and 3 mm for other mAs protocols. Images acquired using 100 mAs revealed ring artifacts. CTDIvol using 50 mAs was 33% of the CTDIvol using 150 mAs. The dose-length product at 100 mAs was reduced to 66% of the dose-length product at 150 mAs, and the same at 50 mAs was reduced to 33%. CONCLUSION: It is evident here that mAs has direct impact on the radiation dose to patient. With iDose4, mAs can be reduced to 50 mAs in multislice low-dose CT scan to reduce the radiation dose with minimal effect on image quality for slice thickness 4 mm. However, noise would dominate at tube current lower than 50 mAs for 120 kVp.

The human oncoprotein MDM2 induces replication stress eliciting early intra-S-phase checkpoint response and inhibition of DNA replication origin firing.

Conventional paradigm ascribes the cell proliferative function of the human oncoprotein mouse double minute2 (MDM2) primarily to its ability to degrade p53. Here we report that in the absence of p53, MDM2 induces replication stress eliciting an early S-phase checkpoint response to inhibit further firing of DNA replication origins. Partially synchronized lung cells cultured from p53-/-:MDM2 transgenic mice enter S phase and induce S-phase checkpoint response earlier than lung cells from p53-/- mice and inhibit firing of DNA replication origins. MDM2 activates chk1 phosphorylation, elevates mixed lineage lymphoma histone methyl transferase levels and promotes checkpoint-dependent tri-methylation of histone H3 at lysine 4, known to prevent firing of late replication origins at the early S phase. In the absence of p53, a condition that disables inhibition of cyclin A expression by MDM2, MDM2 increases expression of cyclin D2 and A and hastens S-phase entry of cells. Consistently, inhibition of cyclin-dependent kinases, known to activate DNA replication origins during firing, inhibits MDM2-mediated induction of chk1 phosphorylation indicating the requirement of this activity in MDM2-mediated chk1 phosphorylation. Our data reveal a novel pathway, defended by the intra-S-phase checkpoint, by which MDM2 induces unscheduled origin firing and accelerates S-phase entry of cells in the absence of p53.

Exploration on natural product anibamine side chain modification toward development of novel CCR5 antagonists and potential anti-prostate cancer agents.

Prostate cancer is one of the leading causes of death among males in the world. Prostate cancer cells have been shown to express upregulated chemokine receptor CCR5, a G protein-coupled receptor (GPCR) that relates to the inflammation process. Anibamine, a natural product containing a pyridine ring and two aliphatic side chains, was shown to carry a binding affinity of 1 µM at CCR5 as an antagonist with potential anti-cancer activity. However, it is not drug-like according to the Lipinski's rule of five mainly due to its two long aliphatic side chains. In our effort to improve its drug-like property, a series of anibamine derivatives were designed and synthesized by placement of aromatic side chains through an amide linkage to the pyridine ring. The newly synthesized compounds were tested for their CCR5 affinity and antagonism, and potential anti-proliferation activity against prostate cancer cell lines. Basal cytotoxicity was finally studied for compounds showing potent anti-proliferation activity. It was found that compounds with hydrophobic substitutions on the aromatic systems seemed to carry more promising CCR5 binding and prostate cancer cell proliferation inhibition activities.

MDM2 overexpression, activation of signaling networks, and cell proliferation.

Frequent overexpression of MDM2 in human cancers suggests that the protein confers a survival advantage to cancer cells. However, overexpression of MDM2 in normal cells seems to restrict cell proliferation. This review discusses the cell growth regulatory functions of MDM2 in normal and genetically defective cells to assess how cancer cells evade the growth-restricting consequence of MDM2 overexpression. Similar to oncoproteins that induce a DNA damage response and oncogene induced senescence in non-transformed cells, MDM2 induces G1-arrest and intra-S phase checkpoint responses that control untimely DNA replication in the face of genetic challenges.

Mammalian SWI/SNF complex activity regulates POU2F3 and constitutes a targetable dependency in small cell lung cancer.

Small cell lung cancers (SCLC) are comprised of heterogeneous subtypes marked by lineage-specific transcription factors, including ASCL1, NEUROD1, and POU2F3. POU2F3-positive SCLC, ∼12% of all cases, are uniquely dependent on POU2F3 itself; as such, approaches to attenuate POU2F3 expression may represent new therapeutic opportunities. Here using genome-scale screens for regulators of POU2F3 expression and SCLC proliferation, we define mSWI/SNF complexes, including non-canonical BAF (ncBAF) complexes, as top dependencies specific to POU2F3-positive SCLC. Notably, clinical-grade pharmacologic mSWI/SNF inhibition attenuates proliferation of all POU2F3-positive SCLCs, while disruption of ncBAF via BRD9 degradation is uniquely effective in pure non-neuroendocrine POU2F3-SCLCs. mSWI/SNF maintains accessibility over gene loci central to POU2F3-mediated gene regulatory networks. Finally, chemical targeting of SMARCA4/2 mSWI/SNF ATPases and BRD9 decrease POU2F3-SCLC tumor growth and increase survival in vivo . Taken together, these results characterize mSWI/SNF-mediated global governance of the POU2F3 oncogenic program and suggest mSWI/SNF inhibition as a therapeutic strategy for SCLC.

Mammalian SWI/SNF complex activity regulates POU2F3 and constitutes a targetable dependency in small cell lung cancer.

Small cell lung cancers (SCLCs) are composed of heterogeneous subtypes marked by lineage-specific transcription factors, including ASCL1, NEUROD1, and POU2F3. POU2F3-positive SCLCs, ∼12% of all cases, are uniquely dependent on POU2F3 itself; as such, approaches to attenuate POU2F3 expression may represent new therapeutic opportunities. Here using genome-scale screens for regulators of POU2F3 expression and SCLC proliferation, we define mSWI/SNF complexes as top dependencies specific to POU2F3-positive SCLC. Notably, chemical disruption of mSWI/SNF ATPase activity attenuates proliferation of all POU2F3-positive SCLCs, while disruption of non-canonical BAF (ncBAF) via BRD9 degradation is effective in pure non-neuroendocrine POU2F3-SCLCs. mSWI/SNF targets to and maintains accessibility over gene loci central to POU2F3-mediated gene regulatory networks. Finally, clinical-grade pharmacologic disruption of SMARCA4/2 ATPases and BRD9 decreases POU2F3-SCLC tumor growth and increases survival in vivo. These results demonstrate mSWI/SNF-mediated governance of the POU2F3 oncogenic program and suggest mSWI/SNF inhibition as a therapeutic strategy for POU2F3-positive SCLCs.

Downscaling Global Gridded Crop Yield Data Products and Crop Water Productivity Mapping Using Remote Sensing Derived Variables in the South Asia.

Local scale crop yield and crop water productivity information is critical for informed decision making, crop yield forecasting and crop model calibration applications. In this study, we have attempted to downscale coarse resolution primary season rice yield datasets to a local scale of 500 m using a minimum-median downscaling approach. Sixteen mainland countries in south and southeast Asia region were considered as study region to downscale global rice yield datasets for 2000-2015. Four medium resolution remote sensing derived vegetation indices such as Normalised Difference Vegetation Index (NDVI), Enhanced Vegetation Index (EVI), Leaf Area Index (LAI), and Gross Primary Product (GPP) were used to downscale coarse resolution global rice yield datasets. A kharif season district level rice yield data from International Crops Research Institute for the Semi-Arid Tropics (ICRISAT), India was used as a reference dataset to evaluate the downscaled rice yields at the district scale. The proposed downscaling approach performance was satisfactory with a mean absolute error (MAE) range of 0.85-1.2 t/ha which lies in the error range of 10-15% with respect to actual range of reference rice yield datasets. Furthermore, crop water productivity maps at 500 m scale were also developed with the downscaled rice yield and Moderate Resolution Imaging Spectroradiometer (MODIS) Evapotranspiration (ET) data products. Statistical analysis shows that the rice yield and crop water productivity values across different climate zones were statistically significant. Tropical zone-based crop yield and crop water productivity values were showing higher variation when compared to other climate zones with a range of 1-10 t/ha and 1-12.5 kg/m3, respectively. Supplementary Information: The online version contains supplementary material available at 10.1007/s42106-022-00223-2.

Allele specific gain-of-function activity of p53 mutants in lung cancer cells.

p53 mutations are mostly single amino acid changes resulting in expression of a stable mutant protein with "gain of function" (GOF) activity having a dominant oncogenic role rather than simple loss of function of wild-type p53. Knock-down of mutant p53 in human lung cancer cell lines with different endogenous p53 mutants results in loss of GOF activity as shown by lowering of cell growth rate. Two lung cancer cell lines, ABC1 and H1437, carrying endogenous mutants p53-P278S and -R267P, show reduction in growth rate on knock-down on p53 levels. However, whereas reduction of the p53 level induces loss of tumorigenicity in nude mice for ABC1 cells, it escalates tumorigenicity for H1437 cells. We have tested their transactivation potential on p53 target gene promoters by performing transient transcriptional assays in the p53-null H1299 lung cancer cell line. Interestingly, while the mutant p53 target promoter Axl was activated by both the mutants, the p21 promoter was activated by p53-R267P and wild-type p53 but not by p53-P278S; showing a clear difference in transcriptional activity between the two mutants. Our results demonstrate allele specificity between GOF p53 mutants and attempt to show that the specificity is dependent on the transactivation property of GOF p53; it also suggests importance of p21 activation in tumor suppression by p53.

p53 mutants induce transcription of NF-κB2 in H1299 cells through CBP and STAT binding on the NF-κB2 promoter and gain of function activity.

Cancer cells with p53 mutations, in general, grow more aggressively than those with wild-type p53 and show "gain of function" (GOF) phenotypes such as increased growth rate, enhanced resistance to chemotherapeutic drugs, increased cell motility and tumorigenicity; although the mechanism for this function remains unknown. In this communication we report that p53-mediated NF-κB2 up-regulation significantly contributes to the aggressive oncogenic behavior of cancer cells. Lowering the level of mutant p53 in a number of cancer cell lines resulted in a loss of GOF phenotypes directly implicating p53 mutants in the process. RNAi against NF-κB2 in naturally occurring cancer cell lines also lowers GOF activities. In H1299 cells expressing mutant p53, chromatin immunoprecipitation (ChIP) assays indicate that mutant p53 induces histone acetylation at specific sites on the regulatory regions of its target genes. ChIP assays using antibodies against transcription factors putatively capable of interacting with the NF-κB2 promoter show increased interaction of CBP and STAT2 in the presence of mutant p53. Thus, we propose that in H1299 cells, mutant p53 elevates expression of genes capable of enhancing cell proliferation, motility, and tumorigenicity by inducing acetylation of histones via recruitment of CBP and STAT2 on the promoters causing CBP-mediated histone acetylation.

Outcomes With Early Cardiac Catheterization in Out of Hospital Cardiac Arrest Survivors and Utility of a Prognostic Scoring System.

Objectives A retrospective study in patients presenting out of hospital cardiac arrest (OHCA) to assess the impact of early cardiac catheterization on survival and cerebral performance category (CPC) on discharge. Background The role of early coronary angiography in OHCA patients remains controversial. The cardiac arrest hospital prognosis (CAHP) scoring system has not been validated in the US population. Methods Inclusion criteria were OHCA patients with a sustained return of spontaneous circulation (ROSC), presumed cardiac cause of arrest, and elements to calculate CAHP score. We compared in-hospital mortality rates and final inpatient CPC in patients who underwent early cardiac catheterization to those with delayed or no cardiac catheterization. We assessed the performance of the CAHP score in the entire OHCA population using receiver-operator curve (ROC) analysis. Results A hundred and fifty-eight patients were included, of which 39 underwent early cardiac catheterization. The mortality rate of the early catheterization group was lower than the delayed or no catheterization group (41% vs 61.3%, p=0.02); the Early cardiac catheterization group had more favorable final hospital CPC scores overall (53.8% vs 24.3%, p<0.001). However, when risk-adjusted, there was no benefit in early catheterization for mortality or CPC level in any of the CAHP score subgroups. CAHP scores showed good discrimination with c-statistics of 0.85 for mortality and 0.90 for the CPC category. Conclusion Early use of cardiac catheterization in OHCA patients with sustained ROSC was not associated with lower mortality rates or higher rates of favorable neurologic recovery when adjusted for baseline risk factors in each of the different CAHP score-based sub-groups. This was despite a higher proportion of patients with STEMI in the early catheterization group. We demonstrated a good fit between observed outcomes and outcomes predicted by the CAHP scoring system.

Use of Laser in Sleep Disorders: A Review on Low Laser Uvulopalatoplasty.

METHODS: A comprehensive and systematic literature review was conducted using PubMed, Google Scholar, Cochrane Central Register of Controlled Trials, Embase, Web of Science, the US National Institutes of Health Trials Registry, WHO Library, and Medline. The search strategies were developed to cover publications from January 2010 through March 2020. The past 10 years of the search were performed to report the data following systematic review and meta-analysis protocol (PRISMA-P) 2015 statement. RESULTS: With the help of keywords, the total number of abstracts identified was 946. These abstracts were further reviewed as per inclusion and exclusion criteria, and 106 abstracts were identified to match the selection criteria. Further review of full articles resulted in 12 articles that matched the inclusion criteria for the study. CONCLUSION: Er:YAG can be a good alternative and least invasive therapy for managing snoring and obstructive sleep apnea. Er:YAG therapy is considered to nonsurgical intervention with minimum side effects and can be performed chairside.

Raman Spectroscopy Can Distinguish Glyphosate-Susceptible and -Resistant Palmer Amaranth (Amaranthus palmeri).

The non-judicious use of herbicides has led to a widespread evolution of herbicide resistance in various weed species including Palmer amaranth, one of the most aggressive and troublesome weeds in the United States. Early detection of herbicide resistance in weed populations may help growers devise alternative management strategies before resistance spreads throughout the field. In this study, Raman spectroscopy was utilized as a rapid, non-destructive diagnostic tool to distinguish between three different glyphosate-resistant and four -susceptible Palmer amaranth populations. The glyphosate-resistant populations used in this study were 11-, 32-, and 36-fold more resistant compared to the susceptible standard. The 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) gene copy number for these resistant populations ranged from 86 to 116. We found that Raman spectroscopy could be used to differentiate herbicide-treated and non-treated susceptible populations based on changes in the intensity of vibrational bands at 1156, 1186, and 1525 cm-1 that originate from carotenoids. The partial least squares discriminant analysis (PLS-DA) model indicated that within 1 day of glyphosate treatment (D1), the average accuracy of detecting herbicide-treated and non-treated susceptible populations was 90 and 73.3%, respectively. We also found that glyphosate-resistant and -susceptible populations of Palmer amaranth can be easily detected with an accuracy of 84.7 and 71.9%, respectively, as early as D1. There were relative differences in the concentration of carotenoids in plants with different resistance levels, but these changes were not significant. The results of the study illustrate the utility of Raman spectra for evaluation of herbicide resistance and stress response in plants under field conditions.

The oncogenicity of tumor-derived mutant p53 is enhanced by the recruitment of PLK3.

p53 mutations with single amino acid changes in cancer often lead to dominant oncogenic changes. Here, we have developed a mouse model of gain-of-function (GOF) p53-driven lung cancer utilizing conditionally active LSL p53-R172H and LSL K-Ras-G12D knock-in alleles that can be activated by Cre in lung club cells. Mutation of the p53 transactivation domain (TAD) (p53-L25Q/W26S/R172H) eliminating significant transactivation activity resulted in loss of tumorigenicity, demonstrating that transactivation mediated by or dependent on TAD is required for oncogenicity by GOF p53. GOF p53 TAD mutations significantly reduce phosphorylation of nearby p53 serine 20 (S20), which is a target for PLK3 phosphorylation. Knocking out PLK3 attenuated S20 phosphorylation along with transactivation and oncogenicity by GOF p53, indicating that GOF p53 exploits PLK3 to trigger its transactivation capability and exert oncogenic functions. Our data show a mechanistic involvement of PLK3 in mutant p53 pathway of oncogenesis.

Optimal Use of a Panoramic Radiograph as a Screening Tool for Condylar Resorption in Patients Undergoing Active Orthodontic Treatment: A Case Series.

Condylar resorption of temporomandibular joint findings in the panoramic radiographs is an indication of bone resorption suggesting possible degenerative joint disease that warrants early screen and subsequent referral to a dedicated specialist. This case series reports three patients that underwent the active orthodontic treatment for the duration of approximately 24-36 months. The patients were asymptomatic at the initial examination. The clinical examination was negative for clicking; the range of motion on opening, lateral excursion, and protrusion was normal. Neither of these patients had a history of rheumatic disease or bruxism. During the later stages of orthodontic treatment, two of the three patients reported mild pain and clicking during mastication, which was also confirmed chairside on clinical evaluation. Patients were referred to the orofacial pain specialist, were they were prescribed specific medication for the symptoms, along with cognitive behavioral therapy, and were further evaluated for splint therapy. Panoramic radiographs taken before the start of the treatment, during the treatment and at the completion of the orthodontic treatments indicate the progression in the resorption of mandibular condyle in all three patients suggesting possible degeneration that warrants further investigation and therapy.

Symbiotic nitrogen fixation and endophytic bacterial community structure in Bt-transgenic chickpea (Cicer arietinum L).

Symbiotic nitrogen fixation (SNF) of transgenic grain legumes might be influenced either by the site of transgene integration into the host genome or due to constitutive expression of transgenes and antibiotic-resistant marker genes. The present investigation confirmed proper nodulation of five tested Bt-chickpea events (IPCa2, IPCa4, IPCT3, IPCT10, and IPCT13) by native Mesorhizobium under field environment. Quantitative variations for nodulation traits among Bt-chickpea were determined and IPCT3 was found superior for nodule number and nodule biomass. Diversity, as well as richness indices, confirmed the changes in bacterial community structure of root and root-nodules from Bt-chickpea events IPCa2 and IPCT10. Especially, Gram-positive bacteria belonging to Firmicutes and Actinobacteria were selectively eliminated from root colonization of IPCa2. Richness indices (CHAO1 and ACE) of the root-associated bacterial community of IPCa2 was 13-14 times lesser than that of parent cv DCP92-3. Root nodule associated bacterial community of IPCT10 was unique with high diversity and richness, similar to the roots of non-Bt and Bt-chickpea. It indicated that the root nodules of IPCT10 might have lost their peculiar characteristics and recorded poor colonization of Mesorhizobium with a low relative abundance of 0.27. The impact of Bt-transgene on bacterial community structure and nodulation traits should be analyzed across the years and locations to understand and stabilize symbiotic efficiency for ecosystem sustainability.

DNA replication in progenitor cells and epithelial regeneration after lung injury requires the oncoprotein MDM2.

Depletion of epithelial cells after lung injury prompts proliferation and epithelial mesenchymal transition (EMT) of progenitor cells, and this repopulates the lost epithelial layer. To investigate the cell proliferative function of human oncoprotein MDM2, we generated mouse models targeting human MDM2 expression in either lung Club or alveolar cells after doxycycline treatment. We report that MDM2 expression in lung Club or alveolar cells activates DNA replication specifically in lung progenitor cells only after chemical- or radiation-induced lung injury, irrespective of their p53 status. Activation of DNA replication by MDM2 triggered by injury leads to proliferation of lung progenitor cells and restoration of the lost epithelial layers. Mouse lung with no Mdm2 allele loses its ability to replicate DNA, whereas loss of 1 Mdm2 allele compromises this function, demonstrating the requirement of endogenous MDM2. We show that the p53-independent ability of MDM2 to activate Akt signaling is essential for initiating DNA replication in lung progenitor cells. Furthermore, MDM2 activates the Notch signaling pathway and expression of EMT markers, indicative of epithelial regeneration. This is the first report to our knowledge demonstrating a direct p53-independent participation of MDM2 in progenitor cell proliferation and epithelial repair after lung injury, distinct from a p53-degrading antiapoptotic effect preventing injury.

Evaluation of jawbone morphology and bone density indices in panoramic radiographs of selective serotonin reuptake inhibitor users: a preliminary study.

OBJECTIVES:: To assess the influence of selective serotonin reuptake inhibitor (SSRI) use on jawbone and bone mineral density by retrospective analysis of panoramic radiographs. METHODS:: Radiographic and clinical records were sourced from the Division of Orthodontics and TMJD, Eastman Institute for Oral Health, University of Rochester. Randomly selected adults (20-65 years) were categorized into: "Active" (with history of SSRI use of >6 months) and a "Control" group. Panoramic indices: Klemetti index (KI), panoramic mandibular index, antegonial notching index, condylar pathology, mandibular cortical width (MCW)⁠ and mean ramus height were recorded. Frequency-weighted Χ2 tests and multinomial regression controlling for age and gender were applied to categorical indices (KI, condylar pathology, antegonial notching index). Multivariate generalized linear modeling was applied to mean ramus height, MCW and panoramic mandibular index. Multiple regression analyses determined: (a) panoramic indices that best predicted SSRI use, and (b) independent predictors of KI category. RESULTS:: 64 SSRI users and 48 Controls were assessed. SSRI users had significantly higher odds of having worse KI status than normal [mildly to moderately eroded cortex: odds ratio (OR) = 2.926, 95% CI (1.07-8.04) and severely eroded cortex: OR = 19.86, 95% CI (3.91-100.69)], more frequent flat condylar anatomy (right side: p = 0.009, left side: p < 0.001) but greater ramus height (p = 0.001) and mandibular cortical width (p = 0.032). Age, gender, SSRI use each significantly impacted KI. Only SSRI use significantly impacted condylar pathology, ramus height and MCW. KI category (OR = 1.3) was the best panoramic predictor of SSRI use. Conversely, KI category C3 was significantly predicted by SSRI use (OR = 31.2, p = 0.002), female gender (17.5, p = 0.006), and severe antegonial notching (OR = 1289, p < 0.001). CONCLUSIONS:: SRRI use was significantly associated with worse panoramic morphometric indices: KI, condylar pathology, ramus height, and MCW, where KI was its strongest predictor. Worse KI was independently predicted by SSRI use.

Target-site mutation accumulation among ALS inhibitor-resistant Palmer amaranth.

BACKGROUND: Palmer amaranth (Amaranthus palmeri S. Wats) is one of the most common and troublesome weeds in the USA. Palmer amaranth resistance to acetolactate synthase (ALS) inhibitors is widespread in the USA, as in Arkansas. The cross-resistance patterns and mechanism of resistance are not known. Experiments were conducted to determine cross-resistance to ALS inhibitors and identify target-site mutations in 20 Palmer amaranth localities from 13 counties in Arkansas. RESULTS: All Palmer amaranth localities tested had plants cross-resistant to imazethapyr, flumetsulam, primisulfuron, pyrithiobac and trifloxysulfuron. The dose of trifloxysulfuron that caused 50% control was 21-56-fold greater for resistant accessions than for susceptible ones. All but three resistant plants analyzed had one or two relative copies of ALS; one plant had seven relative copies. All resistant plants tested (18 localities) carried the Trp574Leu mutation, which is known to confer broad resistance to ALS inhibitors, supporting the cross-resistance pattern observed. Besides the Trp574Leu mutation, 30% of localities had individuals with one additional resistance-conferring mutation including Ala122Thr, Pro197Ala or Ser653Asn. CONCLUSION: The Trp574Leu mutation in ALS is the primary mechanism of resistance to ALS inhibitors in Palmer amaranth from Arkansas, USA. In some localities, multiple mutations have accumulated in one plant. All localities tested contained plants with resistance to five families of ALS inhibitors. Localities with extremely high resistance to ALS inhibitors, and those outside the subset we studied, may harbor non-target site resistance mechanisms. ALS inhibitors are generally no longer effective on Palmer amaranth in these localities from the US mid-south. © 2018 Society of Chemical Industry.