Altered Growth Research Articles

Human peripancreatic adipose tissue paracrine signaling impacts insulin secretion, blood flow, and gene transcription.

Adipose tissue accumulation around non-adipose tissues is associated with obesity and metabolic disease. One relatively unstudied depot is peripancreatic adipose tissue (PAT) that accumulates in obesity and insulin resistance and may impact beta cell function. Pancreatic lipid accumulation and PAT content are negatively related to metabolic outcomes in humans, but these studies are limited by the inability to pursue mechanisms. We obtained PAT from human donors through the Human Pancreas Analysis Program to evaluate differences in paracrine signaling compared to subcutaneous adipose tissue (SAT), as well as effects of the PAT secretome on aortic vasodilation, human islet insulin secretion, and gene transcription using RNAseq. PAT had greater secretion of IFN-γ and most inflammatory eicosanoids compared to SAT. Secretion of adipokines negatively related to metabolic health were also increased in PAT compared to SAT. We found no overall effects of PAT compared to SAT on human islet insulin secretion, however, insulin secretion was suppressed after PAT exposure from men compared to women. Vasodilation was significantly dampened by PAT conditioned media, an effect explained almost completely by PAT from men and not women. Islets treated with PAT showed selective changes in lipid metabolism pathways while SAT altered cellular signaling and growth. RNAseq analysis showed changes in islet gene transcription impacted by PAT compared to SAT, with the biggest changes found between PAT based on sex. The PAT secretome is metabolically negative compared to SAT, and impacts islet insulin secretion, blood flow, and gene transcription in a sex dependent manner.

Decoding Apelin: Its Role in Metabolic Programming, Fetal Growth, and Gestational Complications.

Placental insufficiency and gestational diabetes, which are both serious pregnancy complications, are linked to altered fetal growth, whether restricted or excessive, and result in metabolic dysfunction, hypoxic/oxidative injury, and adverse perinatal outcomes. Although much research has been carried out in this field, the underlying pathogenetic mechanisms have not as yet been fully elucidated. Particularly because of the role it plays in cardiovascular performance, glucose metabolism, inflammation, and oxidative stress, the adipokine apelin was recently shown to be a potential regulator of fetal growth and metabolic programming. This review investigated the numerous biological actions of apelin in utero and aimed to shed more light on its role in fetal growth and metabolic programming. The expression of the apelinergic system in a number of tissues indicates its involvement in many physiological mechanisms, including angiogenesis, cell proliferation, energy metabolism, inflammation, and oxidative stress. Moreover, it appears that apelin has a major function in disorders such as diabetes mellitus, fetal growth abnormalities, fetal hypoxia, and preeclampsia. We herein describe in detail the regulatory effects exerted by the adipokine apelin on fetal growth and metabolic programming while stressing the necessity for additional research into the therapeutic potential of apelin and its mechanisms of action in pregnancy-related disorders.

Long-term exposure to environmentally relevant Bisphenol-A levels affects growth, swimming, condition factor, sex ratio and histology of juvenile zebrafish

Bisphenol A (BPA) is an environmental estrogen which perturbs hormone signaling pathways adversely affecting aquatic organisms. To evaluate the impact of developmental exposure to long term yet environmentally relevant low doses of BPA, wild-type juvenile zebrafish of 35 days post fertilization were treated with BPA (1 and 10 µg/L), treatment control (0.5% v/v methanol) and control for 60 days. Both BPA treatments led to significantly increased morality overtime. Length increment and specific growth rates became significantly high in BPA exposed zebrafish overtime. Obesogenic property of BPA was not evident with longexposure to low BPA doses. A significantly high and BPA dose-dependent female-biased sex ratios were observed following the juvenile exposure. Significantly low swimming speed was recorded in the fish of both BPA-treated tanks than that of control. Condition factor was significantly low in BPA exposed fish indicating the poor-wellness. There were numerous histopathological alterations of gonads, liver and kidney indicating impacts of juvenile exposure in zebrafish. Altered growth, swimming, mortality, feminization and histopathological changes in zebrafish induced by BPA indicate the risks associated with developmental exposures. The findings call for more comprehensive studies to comprehend the ecological risks imposed by low concentrations of environmental estrogens in urban aquatic ecosystems.

Genetic Characterization of the Glucose-PTS in Streptococcus sanguinis, examining competitive fitness.

Ecological shifts in dental microbiome from homeostasis to dysbiosis have been hypothesized to underlie several oral diseases including dental caries. Streptococcus sanguinis, a commensal bacterium, is pivotal in maintaining oral health through its metabolic activities, including the production of ammonia and hydrogen peroxide (H2O2). This study aims to elucidate the genetic underpinnings of the glucose::phosphotransferase system (PTS) in the physiology and competitive fitness of S. sanguinis within the oral microbiome, by examining single nucleotide polymorphisms (SNPs) in the EIIABMan (manL) and HPr of PTS in S. sanguinis strain SK36. Employing genetic engineering, bioinformatic analysis, growth and metabolic assays, recreating and characterizing several unique ManL SNPs in SK36 that were identified among clinical strains of S. sanguinis. Mutations in ManL and HPr correlated with altered growth dynamics, H2O2 production, acid production, and pH homeostasis in a manner uncoupled from canonical regulators such as CcpA and Rex. These genetic variations likely contributed to S. sanguinis's competitiveness, although their ecological impact remains to be further elucidated. This research is part of the ongoing effort to understand the genetic mechanisms that contribute to microbial ecology in relation to health, knowledge from which may allow for enhanced diagnostics, pro-health formulations, and other microbial interventions.

Robust organ size in Arabidopsis is primarily governed by cell growth rather than cell division patterns.

Organ sizes and shapes are highly reproducible, or robust, within a species and individuals. Arabidopsis thaliana sepals, which are the leaf-like organs that enclose flower buds, have consistent size and shape, indicating robust development. Cell growth is locally heterogeneous due to intrinsic and extrinsic noise. To achieve robust organ shape, fluctuations in cell growth must average to an even growth rate, which requires that fluctuations are uncorrelated or anti-correlated in time and space. Here, we live image and quantify the development of sepals with an increased or decreased number of cell divisions (lgo mutant and LGO overexpression, respectively), a mutant with altered cell growth variability (ftsh4), and double mutants combining these. Changes in the number of cell divisions do not change the overall growth pattern. By contrast, in ftsh4 mutants, cell growth accumulates in patches of over- and undergrowth owing to correlations that impair averaging, resulting in increased organ shape variability. Thus, we demonstrate in vivo that the number of cell divisions does not affect averaging of cell growth, preserving robust organ morphogenesis, whereas correlated growth fluctuations impair averaging.

Assessment of Zygomaticomaxillary Suture Maturation in Patients With Unilateral Cleft Lip and Palate: Implications for Orthodontic Treatment Planning.

Introduction The zygomaticomaxillary suture (ZMS) is vital for craniofacial development and orthodontic treatment planning. Located at the junction of the zygomatic and maxillary bones, the ZMS undergoes significant changes during growth, affecting midfacial morphology and stability. Understanding ZMS maturation is essential for optimizing orthodontic interventions, especially in patients with cleft lip and palate (CLP), who often exhibit altered craniofacial growth patterns due to congenital deformities and surgical interventions. Methodology A retrospective analysis was conducted with 50 participants, including 25 patients with unilateral CLP and 25 age-matched controls. Clinical and radiographic data, including lateral cephalometric radiographs and cone-beam computed tomography (CBCT) scans, were collected to assess ZMS maturation stages. The stages, ranging from immature (stage 0) to fully mature (stage 4), were evaluated using established radiographic criteria. Statistical analyses, including Chi-square tests and logistic regression, were performed to compare the distribution of maturation stages between groups. Results Significant differences were observed in ZMS maturation stages between the cleft side, non-cleft side, and control group. The cleft side exhibited a higher prevalence of immature (stage 0) and early maturation (stage 1) stages compared to the control group, with mean values of 4 ± 1.2 and 5 ± 1.3, respectively. The control group showed a higher prevalence of fully mature (stage 4) sutures, with a mean value of 8 ± 1.4. The p-values for stages 0, 1, and 4 were 0.045, 0.034, and 0.039, respectively, indicating statistical significance. The findings highlight distinct maturation patterns in CLP patients, with delayed ZMS maturation on the cleft side. This suggests the need for tailored orthodontic interventions to accommodate prolonged growth phases in CLP patients. The study underscores the importance of detailed ZMS assessments for personalized treatment planning. Future research should focus on longitudinal studies to further understand CLP's impact on craniofacial development. Conclusion Assessing ZMS maturation provides critical insights for optimizing orthodontic and surgical treatment outcomes in CLP patients. By identifying specific developmental delays and tailoring interventions accordingly, clinicians can improve the effectiveness and stability of treatments. This study contributes to the growing body of evidence supporting individualized treatment plans based on precise developmental assessments.

Response of Staphylococcus aureus physiology and Agr quorum sensing to low-shear modeled microgravity.

Staphylococcus aureus is commonly isolated from astronauts returning from spaceflight. Previous analysis of omics data from S. aureus low Earth orbit cultures indicated significantly increased expression of the Agr quorum sensing system and its downstream targets in spaceflight samples compared to ground controls. In this current study, the rotary cell culture system (RCCS) was used to investigate the effect of low-shear modeled microgravity (LSMMG) on S. aureus physiology and Agr activity. When cultured in the same growth medium and temperature as the previous spaceflight experiment, S. aureus LSMMG cultures exhibited decreased agr expression and altered growth compared to normal gravity control cultures, which are typically oriented with oxygenation membrane on the bottom of the high aspect rotating vessel (HARV). When S. aureus was grown in an inverted gravity control orientation (oxygenation membrane on top of the HARV), reduced Agr activity was observed relative to both traditional control and LSMMG cultures, signifying that oxygen availability may affect the observed differences in Agr activity. Metabolite assays revealed increased lactate and decreased acetate excretion in both LSMMG and inverted control cultures. Secretomics analysis of LSMMG, control, and inverted control HARV culture supernatants corroborated these results, with inverted and LSMMG cultures exhibiting a decreased abundance of Agr-regulated virulence factors and an increased abundance of proteins expressed in low-oxygen conditions. Collectively, these studies suggest that the orientation of the HARV oxygenation membrane can affect S. aureus physiology and Agr quorum sensing in the RCCS, a variable that should be considered when interpreting data using this ground-based microgravity model.IMPORTANCES. aureus is commonly isolated from astronauts returning from spaceflight and from surfaces within human-inhabited closed environments such as spacecraft. Astronaut health and immune function are significantly altered in spaceflight. Therefore, elucidating the effects of microgravity on S. aureus physiology is critical for assessing its pathogenic potential during long-term human space habitation. These results also highlight the necessity of eliminating potential confounding factors when comparing simulated microgravity model data with actual spaceflight experiments.

The role of microRNAs in pregnancies complicated by maternal diabetes.

With the global prevalence of diabetes increasing, more people of reproductive age are experiencing hyperglycaemic pregnancies. Maternal Type 1 (T1DM) or Type 2 (T2DM) diabetes mellitus, and gestational diabetes mellitus (GDM) are associated with maternal cardiovascular and metabolic complications. Pregnancies complicated by maternal diabetes also increase the risk of short- and long-term health complications for the offspring, including altered fetal growth and the onset of T2DM and cardiometabolic diseases throughout life. Despite advanced methods for improving maternal glucose control, the prevalence of adverse maternal and offspring outcomes associated with maternal diabetes remains high. The placenta is a key organ at the maternal-fetal interface that regulates fetal growth and development. In pregnancies complicated by maternal diabetes, altered placental development and function has been linked to adverse outcomes in both mother and fetus. Emerging evidence suggests that microRNAs (miRNAs) are key molecules involved in mediating these changes. In this review, we describe the role of miRNAs in normal pregnancy and discuss how miRNA dysregulation in the placenta and maternal circulation is associated with suboptimal placental development and pregnancy outcomes in individuals with maternal diabetes. We also discuss evidence demonstrating that miRNA dysregulation may affect the long-term health of mothers and their offspring. As such, miRNAs are potential candidates as biomarkers and therapeutic targets in diabetic pregnancies at risk of adverse outcomes.

Gut microbiota-derived butyrate selectively interferes with growth of carbapenem-resistant Escherichia coli based on their resistance mechanism

ABSTRACT We investigated consequences of resistance acquisition in Escherichia coli clinical isolates during anaerobic (continuous culture) growth and examined their sensitivity to butyrate, a hallmark metabolite of healthy gut microbiota. Strains were stratified based on carrying either a carbapenemase (CARB) or displaying porin malfunctioning (POR). POR displayed markedly altered growth efficiencies, lower membrane stability and increased sensitivity to butyrate compared with CARB. Major differences in global gene expression between the two groups during anaerobic growth were revealed involving increased expression of alternative substrate influx routes, the stringent response and iron acquisition together with lower expression of various stress response systems in POR. Longitudinal analyses during butyrate wash-in showed common responses for all strains as well as specific features of POR that displayed strong initial “overshoot” reactions affecting various stress responses that balanced out over time. Results were partly reproduced in a mutant strain verifying porin deficiencies as the major underlying mechanism for results observed in clinical isolates. Furthermore, direct competition experiments confirmed butyrate as key for amplifying fitness disadvantages based on porin malfunctioning. Results provide new (molecular) insights into ecological consequences of resistance acquisition and can assist in developing measures to prevent colonization and infection based on the underlying resistance mechanism.

EsxA, a type VII secretion system-dependent effector, reveals a novel function in the sporulation of Bacillus cereus ATCC14579

BackgroundBacillus cereus is a Gram-positive, spore-forming bacterium that produces a spectrum of effectors integral to bacterial niche adaptation and the development of various infections. Among those is EsxA, whose secretion depends on the EssC component of the type VII secretion system (T7SS). EsxA’s roles within the bacterial cell are poorly understood, although postulations indicate that it may be involved in sporulation. However, the T7SS repertoire in B. cereus has not been reported, and its functions are unestablished.MethodsWe used the type strain, B. cereus ATCC14579, to generate ΔessC mutant through homologous recombination using the homing endonuclease I-SceI mediated markerless gene replacement. Comparatively, we analyzed the culture supernatant of type strain and the ΔessC mutant through Liquid chromatography-tandem mass spectrometry (LC-MS/MS). We further generated T7SSb-specific gene mutations to explore the housekeeping roles of the T7SSb-dependent effectors. The sporulation process of B. cereus ATCC14579 and its mutants was observed microscopically through the classic Schaeffer-Fulton staining method. The spore viability of each strain in this study was established by enumerating the colony-forming units on LB agar.ResultsThrough LC-MS/MS, we identified a pair of nearly identical (94%) effector proteins named EsxA belonging to the sagEsxA-like subfamily of the WXG100 protein superfamily in the culture supernatant of the wild type and none in the ΔessC mutant. Homology analysis of the T7SSb gene cluster among B. cereus strains revealed diversity from the 3’ end of essC, encoding additional substrates. Deletions in esxA1 and esxA2 neither altered cellular morphology nor growth rate, but the ΔesxA1ΔesxA2 deletion resulted in significantly fewer viable spores and an overall slower sporulation process. Within 24 h culture, more than 80% of wild-type cells formed endospores compared to less than 5% in the ΔesxA1ΔesxA2 mutant. The maximum spore ratios for the wild type and ΔesxA1ΔesxA2 were 0.96 and 0.72, respectively. Altogether, these results indicated that EsxA1 and EsxA2 work cooperatively and are required for sporulation in B. cereus ATCC14567.ConclusionB. cereus ATCC14579 possesses two nearly identical T7SSb-dependent effectors belonging to the sagEsxA-like proteins. Simultaneous deletion of genes encoding these effectors significantly delayed and reduced sporulation, a novel finding for EsxA.

437 Fetal Programming in Sheep: Epigenetic modifications in offspring from poorly nourished dams

Abstract Poor maternal nutrition (restricted- and over-feeding) during gestation can negatively impact the efficiency of livestock production by generating offspring with decreased muscle mass, increased adiposity, and impaired metabolism. The mechanisms behind these altered phenotypes are not well-characterized. The effects of poor maternal nutrition during gestation on offspring growth and development begin in utero and contribute to metabolic dysregulation of offspring into maturity and across subsequent generations, demonstrating long-term negative effects on the livestock. Fetal programming results in epigenetic modifications that can involve changes in offspring gene expression and downstream function, with no alteration on the DNA sequence. Using a sheep model of poor maternal nutrition, we have previously shown that F1 offspring from restricted- and over-fed dams are smaller at 10 mo of age relative to offspring from control-fed dams. Additionally, we observed that this phenotype persisted in the F2 offspring from restricted-fed granddams, while F2 offspring from over- and control-fed granddams were of similar body weight. We have recently demonstrated that F1 offspring from poorly nourished ewes have differential methylation patterns and altered gene expression in liver tissue demonstrating a potential mechanism that contributes to persistent altered growth. We have also begun evaluating the effects of maternal nutrient restriction on the development of fetal small intestine, a key facilitator of nutrient transport. Poor maternal nutrition during gestation alters development of offspring small intestine and further understanding of developmental programming in key metabolic tissues can aid in the development of nutritional strategies to improve efficiency of livestock production.

Adiponectin and Leptin during Pregnancy: A Systematic Review of Their Association with Pregnancy Disorders, Fetal Growth and Placental Function

During pregnancy, the adipokines leptin and adiponectin can affect placental nutrient transport and inflammatory pathways, potentially leading to altered fetal growth and pregnancy complications including gestational diabetes mellitus (GDM) and preeclampsia (PE). The aim of this systematic review is to gather and analyze research on maternal circulating leptin and adiponectin levels and their relationship to adverse pregnancy and birth outcomes. Additionally, it seeks to determine whether these hormones are linked to alterations in placental transporters and cell signaling pathways. PubMed and MEDLINE were systematically searched to include studies published between 2012 and 2022. All primary data studies reporting serum adiponectin and/or leptin, placental mRNA and protein levels of related transporters, and adverse birth outcomes were eligible. The current systematic review encompasses a total of 14 articles. Abnormal serum maternal leptin and adiponectin levels were associated with changes in fetal growth and placental cellular signaling and nutrient transporters. A majority of studies associated elevated maternal leptin and reduced adiponectin with fetal overgrowth, although this relationship was not consistent and may be complicated when other pathologies are present. The effects of maternal leptin and adiponectin on fetal growth may be driven by placental adaptation in nutrient transporters and mitochondria. Future studies should determine if the placental effects of leptin and adiponectin that have been found in models have mechanistic roles in human pregnancy.

Leishmania major telomerase RNA knockout: From altered cell proliferation to decreased parasite infectivity

This study focuses on the biological impacts of deleting the telomerase RNA from Leishmania major (LeishTER), a parasite responsible for causing leishmaniases, for which no effective treatment or prevention is available. TER is a critical player in the telomerase ribonucleoprotein complex, containing the template sequence copied by the reverse transcriptase component during telomere elongation. The success of knocking out both LeishTER alleles was confirmed, and no off-targets were detected. LmTER−/− cells share similar characteristics with other TER-depleted eukaryotes, such as altered growth patterns and partial G0/G1 cell cycle arrest in early passages, telomere shortening, and elevated TERRA expression. They also exhibit increased γH2A phosphorylation, suggesting that the loss of LeishTER induces DNA damage signaling. Moreover, pro-survival autophagic signals and mitochondrion alterations were shown without any detectable plasma membrane modifications. LmTER−/− retained the ability to transform into metacyclics, but their infectivity capacity was compromised. Furthermore, the overexpression of LeishTER was also deleterious, inducing a dominant negative effect that led to telomere shortening and growth impairments. These findings highlight TER's vital role in parasite homeostasis, opening discussions about its potential as a drug target candidate against Leishmania.

D1-Tyr246 and D2-Tyr244 in photosystem II: Insights into bicarbonate binding and electron transfer from QA•− to QB

In photosystem II (PSII), D1-Tyr246 and D2-Tyr244 are symmetrically located at the binding site of the bicarbonate ligand of the non-heme Fe complex. Here, we investigated the role of the symmetrically arranged tyrosine pair, D1-Tyr246 and D2-Tyr244, in the function of PSII, by generating four chloroplast mutants of PSII from Chlamydomonas reinhardtii: D1-Y246F, D1-Y246T, D2-Y244F, and D2-Y244T. The mutants exhibited altered photoautotrophic growth, reduced PSII protein accumulation, and impaired O2-evolving activity. Flash-induced fluorescence yield decay kinetics indicated a significant slowdown in electron transfer from QA•− to QB in all mutants. Bicarbonate reconstitution resulted in enhanced O2-evolving activity, suggesting destabilization of bicarbonate binding in the mutants. Structural analyses based on a quantum mechanical/molecular mechanical approach identified the existence of a water channel that leads to incorporation of bulk water molecules and destabilization of the bicarbonate binding site. The water intake channels, crucial for bicarbonate stability, exhibited distinct paths in the mutants. These findings shed light on the essential role of the tyrosine pair in maintaining bicarbonate stability and facilitating efficient electron transfer in native PSII.

Impact of Nickel Toxicity on Growth, Fruit Quality and Antioxidant Response in Zucchini Squash (Cucurbita pepo L.).

The impact of trace metal elements (TMEs) on plants is one current pollution problem, the severity of which is increasing with industrial development, population growth and inappropriate agricultural practices. The latter can have irreversible effects on ecosystems, including species extinction, trophic chain contamination and altered human health, particularly in the case of consumed plants such as zucchini squash (Cucurbita pepo L.). This study aims to investigate the effects of nickel on various physiological and biochemical parameters of zucchini growth, with a particular focus on how this toxic metal impacts the quality of fruit that is consumed by humans. To achieve this, plants aged 45 days were grown for one month on solid media loaded with different concentrations of Ni (0, 100, 300 and 500 µM). The results showed that exposure of plants to Ni resulted in significantly altered growth and higher accumulation of Ni in the shoots (1314 µg·g-1 DW) than in roots and fruits. Concerning non-enzymatic antioxidants, the results showed that Ni toxicity significantly increased total polyphenols, especially in shoots at 300 µM Ni, while flavonoid content decreased in the roots and shoots in response to Ni treatment. Our results also show that nickel tolerance in C. pepo is ensured by a combination of several mechanisms such as an increase in the content of proline. This species can survive and tolerate, to different degrees, toxic cations at concentrations up to 500 µM but with visible symptoms of toxicity such as chlorosis of the leaves. Indeed, based on thresholds of hyperaccumulation, we can qualify Cucurbita pepo as a hyperaccumulator species of nickel.

PCIS1, Encoded by a Pentatricopeptide Protein Co-expressed Gene, Is Required for Splicing of Three Mitochondrial nad Transcripts in Angiosperms.

Group II introns are large catalytic RNAs, which reside mainly within genes encoding respiratory complex I (CI) subunits in angiosperms' mitochondria. Genetic and biochemical analyses led to the identification of many nuclear-encoded factors that facilitate the splicing of the degenerated organellar introns in plants. Here, we describe the analysis of the pentatricopeptide repeat (PPR) co-expressed intron splicing-1 (PCIS1) factor, which was identified in silico by its co-expression pattern with many PPR proteins. PCIS1 is well conserved in land plants but has no sequence similarity with any known protein motifs. PCIS1 mutant lines are arrested in embryogenesis and can be maintained by the temporal expression of the gene under the embryo-specific ABI3 promoter. The pABI3::PCIS1 mutant plants display low germination and stunted growth phenotypes. RNA-sequencing and quantitative RT-PCR analyses of wild-type and mutant plants indicated that PCIS1 is a novel splicing cofactor that is pivotal for the maturation of several nad transcripts in Arabidopsis mitochondria. These phenotypes are tightly associated with respiratory CI defects and altered plant growth. Our data further emphasize the key roles of nuclear-encoded cofactors that regulate the maturation and expression of mitochondrial transcripts for the biogenesis of the oxidative phosphorylation system, and hence for plant physiology. The discovery of novel splicing factors other than typical RNA-binding proteins suggests further complexity of splicing mechanisms in plant mitochondria.

Transcriptomic analysis for the gamma-ray-induced sweetpotato mutants with altered stem growth pattern.

Sweetpotato faces breeding challenges due to physiological and genomic issues. Gamma radiation is a novel approach for inducing genetic variation in crops. We analyzed the transcriptomic changes in gamma ray-induced sweetpotato mutants with altered stem development compared with those in the wild-type 'Tongchaeru' cultivar. RNA sequencing analyses were performed to identify changes in the expression of genes related to stem development. Transcriptomic analysis identified 8,931 upregulated and 6,901 downregulated genes, including the upregulation of the auxin-responsive SMALL AUXIN UP RNA (SAUR) and three PHYTOCHROME INTERACTING FACTOR 4 (PIF4) genes. PIF4 is crucial for regulating the expression of early auxin-responsive SAUR genes and stem growth in Arabidopsis thaliana. In the mutant, several genes related to stem elongation, including PIF4 and those involved in various signaling pathways such as auxin and gibberellin, were upregulated. Our results suggest that gamma ray-induced mutations influence auxin-dependent stem development by modulating a complex regulatory network involving the expression of PIF4 and SAUR genes, and other signaling pathways such as gibberellin and ethylene signaling genes. This study enhances our understanding of the regulatory mechanisms underlying stem growth in sweetpotato, providing valuable insights for genomics-assisted breeding efforts.

Magnetic Resonance Imaging Assessment of Pulmonary Vascularity in Preterm Infants with Bronchopulmonary Dysplasia

Introduction: Pulmonary hypertension often complicates bronchopulmonary dysplasia (BPD) and infants with BPD plus pulmonary hypertension experience higher mortality rates. Current methods to evaluate pulmonary hypertension fail to evaluate the primary cause of this disease. We hypothesize that preterm infants with BPD experience altered pulmonary vascular growth and that magnetic resonance imaging (MRI) can be used to assess vascularity in BPD. Methods: In this observational cohort study, preterm infants with BPD (n = 33) and controls (n = 6) received a postnatal chest MRI that included a 2-dimensional time-of-flight acquisition. Semi-automatic segmentation was performed to measure vascularity parameters including vascular volume and density (vascular density = vascular volume/lung volume). Results: Vascular volume on MRI increases with post-menstrual age (877.2 mm3/week); however, the vascular density does not significantly change. Vascular volume is higher in infants with more severe BPD (p < 0.002), but vascular density did not significantly change when comparing mild, moderate, and severe BPD. Vascular density in infants with severe BPD requiring tracheostomy trended lower when compared to infants not requiring tracheostomy (0.18 mm3/mm3 vs. 0.27 mm3/mm3, p = 0.06). Vascular density increases with increasing days of inhaled nitric oxide (iNO) therapy in infants with severe BPD (0.02 mm3/mm3/week of iNO, rho = +0.56, p = 0.03). Conclusion: Neonatal MRI can be used to assess pulmonary vascularity in preterm infants with BPD. Infants with BPD experience altered vascular growth and while higher vascular volume is associated with more severe BPD, lower vascular density trends toward worse clinical outcomes. Vascular density increases with iNO therapy in severe BPD.

MSMEG_5850, a global TetR family member supports Mycobacterium smegmatis to survive environmental stress.

A Mycobacterium smegmatis transcriptional regulator, MSMEG_5850, and its ortholog in M. tuberculosis, rv0775 were annotated as putative TetR Family Transcriptional Regulators. Our previous study revealed MSMEG_5850 is involved in global transcriptional regulation in M. smegmatis and the presence of gene product supported the survival of bacteria during nutritional starvation. Phylogenetic analysis showed that MSMEG_5850 diverged early in comparison to its counterparts in virulent strains. Therefore, the expression pattern of MSMEG_5850 and its counterpart, rv0775, was compared during various in-vitro growth and stress conditions. Expression of MSMEG_5850 was induced under different environmental stresses while no change in expression was observed under mid-exponential and stationary phases. No expression of rv0775 was observed under any stress condition tested, while the gene was expressed during the mid-exponential phase that declined in the stationary phase. The effect of MSMEG_5850 on the survival of M. smegmatis under stress conditions and growth pattern was studied using wild type, knockout, and supplemented strain. Deletion of MSMEG_5850 resulted in altered colony morphology, biofilm/pellicle formation, and growth pattern of M. smegmatis. The survival rate of wild-type MSMEG_5850 was higher in comparison to knockout under different environmental stresses. Overall, this study suggested the role of MSMEG_5850 in the growth and adaptation/survival of M. smegmatis under stress conditions.

The developmental phenotype of motor delay in extremely preterm infants following early-life respiratory adversity is influenced by brain dysmaturation in the parietal lobe

BackgroundResearch indicates that preterm infants requiring prolonged mechanical ventilation often exhibit suboptimal neurodevelopment at follow-up, coupled with altered brain development as detected by magnetic resonance imaging (MRI) at term-equivalent age (TEA). However, specific regions of brain dysmaturation and the subsequent neurodevelopmental phenotype following early-life adverse respiratory exposures remain unclear. Additionally, it is uncertain whether brain dysmaturation mediates neurodevelopmental outcomes after respiratory adversity. This study aims to investigate the relationship between early-life adverse respiratory exposures, brain dysmaturation at TEA, and the developmental phenotype observed during follow-up in extremely preterm infants.Methods89 infants born < 29 weeks’ gestation from 2019 to 2021 received MRI examinations at TEA for structural and lobe brain volumes, which were adjusted with sex-and-postmenstrual-age expected volumes for volume residuals. Assisted ventilation patterns in the first 8 postnatal weeks were analyzed using kmlShape analyses. Patterns for motor, cognition, and language development were evaluated from corrected age 6 to 12 months using Bayley Scales of Infant Development, third edition. Mediation effects of brain volumes between early-life respiratory exposures and neurodevelopmental phenotypes were adjusted for sex, gestational age, maternal education, and severe brain injury.ResultsTwo distinct respiratory trajectories with varying severity were identified: improving (n = 35, 39%) and delayed improvement (n = 54, 61%). Compared with the improving group, the delayed improvement group exhibited selectively reduced brain volume residuals in the parietal lobe (mean − 4.9 cm3, 95% confidence interval − 9.4 to − 0.3) at TEA and lower motor composite scores (− 8.7, − 14.2 to − 3.1) at corrected age 12 months. The association between delayed respiratory improvement and inferior motor performance (total effect − 8.7, − 14.8 to − 3.3) was partially mediated through reduced parietal lobe volume (natural indirect effect − 1.8, − 4.9 to − 0.01), suggesting a mediating effect of 20%.ConclusionsEarly-life adverse respiratory exposure is specifically linked to the parietal lobe dysmaturation and neurodevelopmental phenotype of motor delay at follow-up. Dysmaturation of the parietal lobe serves as a mediator in the connection between respiratory adversity and compromised motor development. Optimizing respiratory critical care may emerge as a potential avenue to mitigate the consequences of altered brain growth and motor developmental delay in this extremely preterm population.