A multiple-oscillator mechanism underlies antigen-induced Ca2+ oscillations in Jurkat T-cells.

T-cell receptor stimulation triggers cytosolic Ca2+ signaling by inositol-1,4,5-trisphosphate (IP3)-mediated Ca2+ release from the endoplasmic reticulum (ER) and Ca2+ entry through Ca2+ release-activated Ca2+ (CRAC) channels gated by ER-located stromal-interacting molecules (STIM1/2). Physiologically, cytosolic Ca2+ signaling manifests as regenerative Ca2+ oscillations, which are critical for nuclear factor of activated T-cells-mediated transcription. In most cells, Ca2+ oscillations are thought to originate from IP3 receptor-mediated Ca2+ release, with CRAC channels indirectly sustaining them through ER refilling. Here, experimental and computational evidence support a multiple-oscillator mechanism in Jurkat T-cells whereby both IP3 receptor and CRAC channel activities oscillate and directly fuel antigen-evoked Ca2+ oscillations, with the CRAC channel being the major contributor. KO of either STIM1 or STIM2 significantly reduces CRAC channel activity. As such, STIM1 and STIM2 synergize for optimal Ca2+ oscillations and activation of nuclear factor of activated T-cells 1 and are essential for ER refilling. The loss of both STIM proteins abrogates CRAC channel activity, drastically reduces ER Ca2+ content, severely hampers cell proliferation and enhances cell death. These results clarify the mechanism and the contribution of STIM proteins to Ca2+ oscillations in T-cells.

Cellular Iron Deficiency Disrupts Thyroid Hormone Regulated Gene Expression in Developing Hippocampal Neurons.

BACKGROUND: Developing neurons have high thyroid hormone and iron requirements to support their metabolically demanding growth. Early-life iron and thyroid-hormone deficiencies are prevalent and often coexist, and each independently increases risk of permanently impaired neurobehavioral function in children. Early-life dietary iron deficiency reduces thyroid-hormone concentrations and impairs thyroid hormone-responsive gene expression in the neonatal rat brain, but it is unclear whether the effect is cell-intrinsic. OBJECTIVES: This study determined whether neuronal-specific iron deficiency alters thyroid hormone-regulated gene expression in developing neurons. METHODS: Iron deficiency was induced in primary mouse embryonic hippocampal neuron cultures with the iron chelator deferoxamine (DFO) beginning at 3 d in vitro (DIV). At 11DIV and 18DIV, thyroid hormone-regulated gene messenger ribonucleic acid (mRNA)concentrations indexing thyroid hormone homeostasis (Hairless, mu-crystallin, Type II deiodinase, solute carrier family member 1c1, and solute carrier family member 16a2) and neurodevelopment (neurogranin, Parvalbumin, and Krüppel-like factor 9) were quantified. To assess the effect of iron repletion, DFO was removed at 14DIV from a subset of DFO-treated cultures, and gene expression and adenosine 5'-triphosphate (ATP) concentrations were quantified at 21DIV. RESULTS: At 11DIV and 18DIV, neuronal iron deficiency decreased neurogranin, Parvalbumin, and mu-crystallin, and by 18DIV, solute carrier family member 16a2, solute carrier family member 1c1, Type II deiodinase, and Hairless were increased, suggesting cellular sensing of a functionally abnormal thyroid hormone state. Dimensionality reduction with Principal component analysis reveals that thyroid hormone homeostatic genes strongly correlate with and predict iron status. Iron repletion from 14-21DIV did not restore ATP concentration, and Principal component analysis suggests that, after iron repletion, cultures maintain a gene expression signature indicative of previous iron deficiency. CONCLUSIONS: These novel findings suggest there is an intracellular mechanism coordinating cellular iron/thyroid hormone activities. We speculate this is a part of the homeostatic response to acutely match neuronal energy production and growth signaling. However, the adaptation to iron deficiency may cause permanent deficits in thyroid hormone-dependent neurodevelopmental processes even after recovery from iron deficiency.

What, How, When, and Where: Spatiotemporal Water Quality Hazards of Cyanotoxins in Subtropical Eutrophic Reservoirs.

Though toxins produced during harmful blooms of cyanobacteria present diverse risks to public health and the environment, surface water quality surveillance of cyanobacterial toxins is inconsistent, spatiotemporally limited, and routinely relies on ELISA kits to estimate total microcystins (MCs) in surface waters. Here, we employed liquid chromatography tandem mass spectrometry to examine common cyanotoxins, including five microcystins, three anatoxins, nodularin, cylindrospermopsin, and saxitoxin in 20 subtropical reservoirs spatially distributed across a pronounced annual rainfall gradient. Probabilistic environmental hazard analyses identified whether water quality values for cyanotoxins were exceeded and if these exceedances varied spatiotemporally. MC-LR was the most common congener detected, but it was not consistently observed with other toxins, including MC-YR, which was detected at the highest concentrations during spring with many observations above the California human recreation guideline (800 ng/L). Cylindrospermopsin was also quantitated in 40% of eutrophic reservoirs; these detections did not exceed a US Environmental Protection Agency swimming/advisory level (15,000 ng/L). Our observations have implications for routine water quality monitoring practices, which traditionally use ELISA kits to estimate MC levels and often limit collection of surface samples during summer months near reservoir impoundments, and further indicate that spatiotemporal surveillance efforts are necessary to understand cyanotoxins risks when harmful cyanobacteria blooms occur throughout the year.

Association of white matter hyperintensities and clinical vascular burden with depressive symptoms in Black older adults.

OBJECTIVES: Black older adults have a higher vascular burden compared to non-Hispanic White (NHW) older adults, which may put them at risk for a form of depression known as vascular depression (VaDep). The literature examining VaDep in Black older adults is sparse. The current study addressed this important gap by examining whether vascular burden was associated with depressive symptoms in Black older adults. METHODS: Participants included 113 Black older adults from the Healthy Brain Project, a substudy of the Health, Aging, and Body Composition Study. In multiple regression analyses, clinical vascular burden (sum of vascular conditions) and white matter hyperintensity (WMH) volume predicted depressive symptoms as measured by the Center for Epidemiologic Studies Depression Scale, controlling for demographic variables. Follow-up analyses compared the associations in the Black subsample and in 179 NHW older adults. RESULTS: Higher total WMH volume, but not clinically-defined vascular burden, predicted higher concurrent depressive symptoms and higher average depressive symptoms over 4 years. Similar associations were found between uncinate fasciculus (UF) WMHs and concurrent depressive symptoms and between superior longitudinal fasciculus WMHs and average depressive symptoms. The association between depressive symptoms and UF WMH was stronger in Black compared to NHW individuals. CONCLUSION: This research is consistent with the VaDep hypothesis and extends it to Black older adults, a group that has historically been underrepresented in the literature. Results highlight WMH in the UF as particularly relevant to depressive symptoms in Black older adults and suggest this group may be particularly vulnerable to the negative effects of WMH.

NPC1 deficiency impairs cerebellar postnatal development of microglia and climbing fiber refinement in a mouse model of Niemann-Pick disease type C.

Little is known about the effects of NPC1 deficiency in brain development and whether these effects contribute to neurodegeneration in Niemann-Pick disease type C (NPC). Degeneration of cerebellar Purkinje cells occurs at an earlier stage and to a greater extent in NPC; therefore, we analyzed the effect of NPC1 deficiency on microglia and on climbing fiber synaptic refinement during cerebellar postnatal development using the Npc1nmf164 mouse. Our analysis revealed that NPC1 deficiency leads to early phenotypic changes in microglia that are not associated with an innate immune response. However, the lack of NPC1 in Npc1nmf164 mice significantly affected the early development of microglia by delaying the radial migration, increasing the proliferation and impairing the differentiation of microglia precursor cells during postnatal development. Additionally, increased phagocytic activity of differentiating microglia was observed at the end of the second postnatal week in Npc1nmf164 mice. Moreover, significant climbing fiber synaptic refinement deficits along with an increased engulfment of climbing fiber synaptic elements by microglia were found in Npc1nmf164 mice, suggesting that profound developmental defects in microglia and synaptic connectivity might precede and predispose Purkinje cells to early neurodegeneration in NPC.

Infant epigenetic aging moderates the link between Black maternal childhood trauma and offspring symptoms of psychopathology.

Although offspring of women exposed to childhood trauma exhibit elevated rates of psychopathology, many children demonstrate resilience to these intergenerational impacts. Among the variety of factors that likely contribute to resilience, epigenetic processes have been suggested to play an important role. The current study used a prospective design to test the novel hypothesis that offspring epigenetic aging - a measure of methylation differences that are associated with infant health outcomes - moderates the relationship between maternal exposure to childhood adversity and offspring symptomatology. Maternal childhood adversity was self-reported during pregnancy via the ACEs survey and the CTQ, which assessed total childhood trauma as well as maltreatment subtypes (i.e., emotional, physical, and sexual abuse). Offspring blood samples were collected at or shortly after birth and assayed on a DNA methylation microarray, and offspring symptomatology was assessed with the CBCL/1.5-5 when offspring were 2-4 years old. Results indicated that maternal childhood trauma, particularly sexual abuse, was predictive of offspring symptoms (ps = 0.003-0.03). However, the associations between maternal sexual abuse and offspring symptomatology were significantly attenuated in offspring with accelerated epigenetic aging. These findings further our understanding of how epigenetic processes may contribute to and attenuate the intergenerational link between stress and psychopathology.

Introduction to the Special Section on the International Society for Traumatic Stress Studies 38th Annual Meeting: Trauma as a transdiagnostic risk factor across the lifespan.

This article serves as an introduction to the special section in the Journal of Traumatic Stress related to the 38th annual meeting of the International Society for Traumatic Stress Studies, held in Atlanta, Georgia (USA) in November 2022. The theme of this meeting, "Trauma as a Transdiagnostic Risk Factor Across the Lifespan," provided an opportunity to recognize the far-reaching impact of trauma and how traumatic experiences can become embedded into the mind, body, and societal spirit. This introductory article outlines the importance of harnessing multiple perspectives to address these wide-ranging sequelae of trauma and provides an overview of the series of contributions to the special section.

Shift-and-persist coping and health among rural African American adolescents.

This study examines whether shift-and-persist coping, a coping strategy defined by accepting challenges and remaining hopeful for the future, is associated with psychosocial and physical health and/or moderates the effects of contextual stress (i.e., racial discrimination, financial strain) on health among African American adolescents living in the rural Southeastern United States. Participants (N = 299, 56% boys, Mage = 12.91) completed measures of shift-and-persist coping, contextual stress, and psychosocial and physical health. Shift-and-persist coping was generally associated with better health but did not buffer the effects of contextual stress. Results suggest that shift-and-persist coping may serve as a source of resilience among African American adolescents living in a context where many experience heightened contextual stress.

Racial Discrimination and Private Regard Among Black Early Adolescents: Testing Between- and Within-Person Associations Over Time.

The current study examined concurrent and longitudinal associations between experiences of racial discrimination and private regard (i.e., feelings about being Black and other Black people) among 346 Black early adolescents who completed four assessments over two years. Between-person (interpersonal) and within-person (intrapersonal) effects were tested to provide a rigorous and comprehensive examination of these associations. There was minimal evidence of significant between-person effects in which youth experiencing varying levels of racial discrimination differed in their private regard. However, at the within-person level, there were significant negative concurrent associations between racial discrimination and private regard, indicating that youths' positive racial identity was undermined at times when they were encountering higher levels of racial discrimination than they typically did. Results highlight significant intrapersonal links between racial discrimination and private regard and underscore the continued need for interventions to eliminate racial discrimination and to support Black youth experiencing it.

Childhood adversity predicts black young adults' DNA methylation-based accelerated aging: A dual pathway model.

We expand upon prior work (Gibbons et al., ) relating childhood stressor effects, particularly harsh childhood environments, to risky behavior and ultimately physical health by adding longer-term outcomes - deoxyribonucleic acid (DNA) methylation-based measures of accelerated aging (DNAm-aging). Further, following work on the effects of early exposure to danger (McLaughlin et al., ), we also identify an additional pathway from harsh childhood environments to DNAm-aging that we label the danger/FKBP5 pathway, which includes early exposure to dangerous community conditions that are thought to impact glucocorticoid regulation and pro-inflammatory mechanisms. Because different DNAm-aging indices provide different windows on accelerated aging, we contrast effects on early indices of DNAm-aging based on chronological age with later indices that focused on predicting biological outcomes. We utilize data from Family and Community Health Study participants (N = 449) from age 10 to 29. We find that harshness influences parenting, which, in turn, influences accelerated DNAm-aging through the risky cognitions and substance use (i.e., behavioral) pathway outlined by Gibbons et al. (). Harshness is also associated with increased exposure to threat/danger, which, in turn, leads to accelerated DNAm-aging through effects on FKBP5 activity and enhanced pro-inflammatory tendencies (i.e., the danger/FKBP5 pathway).

Measuring the Biological Embedding of Racial Trauma Among Black Americans Utilizing the RDoC Approach.

The NIMH Research Domain Criteria (RDoC) initiative aims to understand the mechanisms influencing psychopathology through a dimensional approach. Limited research thus far has considered potential racial/ethnic differences in RDoC constructs that are influenced by developmental and contextual processes. A growing body of research has demonstrated that racial trauma is a pervasive chronic stressor that impacts the health of Black Americans across the life course. In this review article, we examine the ways that an RDOC framework could allow us to better understand the biological embedding of racial trauma among Black Americans. We also specifically examine the Negative Valence System domain of RDoC to explore how racial trauma is informed by and can help expand our understanding of this domain. We end the review by providing some additional research considerations and future research directives in the area of racial trauma that build on the RDoC initiative.

Childhood adversity is linked to adult health among African Americans via adolescent weight gain and effects are genetically moderated.

Identifying the mechanisms linking early experiences, genetic risk factors, and their interaction with later health consequences is central to the development of preventive interventions and identifying potential boundary conditions for their efficacy. In the current investigation of 412 African American adolescents followed across a 20-year period, we examined change in body mass index (BMI) across adolescence as one possible mechanism linking childhood adversity and adult health. We found associations of childhood adversity with objective indicators of young adult health, including a cardiometabolic risk index, a methylomic aging index, and a count of chronic health conditions. Childhood adversities were associated with objective indicators indirectly through their association with gains in BMI across adolescence and early adulthood. We also found evidence of an association of genetic risk with weight gain across adolescence and young adult health, as well as genetic moderation of childhood adversity's effect on gains in BMI, resulting in moderated mediation. These patterns indicated that genetic risk moderated the indirect pathways from childhood adversity to young adult health outcomes and childhood adversity moderated the indirect pathways from genetic risk to young adult health outcomes through effects on weight gain during adolescence and early adulthood.

Racial discrimination, depressive symptoms, and sleep problems among Blacks in the rural South.

OBJECTIVES: Experiences of racial discrimination are common for Black Americans and have been associated with depression and sleep disturbance, factors likely involved in the insidious development of health disparities. The current study replicates these associations and examines longitudinal linkages. METHOD: Black American couples (men: N = 248, Mage = 40, SD = 9; women: N = 277, Mage = 37, SD = 7) and their children, aged 9 to 14 (N = 276, Mage = 11, SD = 1), completed measures of experiences of racial discrimination, depressive symptoms, and sleep problems at baseline and 8-month follow-up. In separate analyses for men, women, and youth, we examined concurrent and prospective associations of racial discrimination with depressive symptoms and sleep problems, then used longitudinal indirect effect models to examine whether depressive symptoms in response to racial discrimination led to increased sleep problems, or vice versa. RESULTS: Racial discrimination was associated concurrently with depressive symptoms and sleep problems for all family members. Prospective associations were also found with depressive symptoms and sleep problems in fathers and youth, and sleep problems in mothers. Longitudinal models showed significant indirect effects of racial discrimination on change in sleep problems through depressive symptoms for fathers and mothers, and a similar, but nonsignificant, pattern in youth. There were no indirect effects on change in depressive symptoms through sleep problems. CONCLUSIONS: Persistent associations of racial discrimination with depressive symptoms and sleep problems reflect a lasting impact of racial discrimination. Because discrimination's effects on depression may contribute to increased sleep problems over time, interventions that buffer the effects of discrimination on depressive symptoms may also reduce sleep problems. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Seminoma in an adult striped dolphin Stenella coeruleoalba: tomographic, macroscopical, histological and immunohistochemical study.

Testicular neoplasms have been extensively described and characterized in domestic animals, but reports in wildlife species, including marine mammals, are scarce. This case report describes a testicular seminoma in an adult striped dolphin Stenella coeruleoalba stranded along the coasts of the Canary Islands. Post-mortem computerized tomography (CT) showed a prominent enlargement of the cranial pole of the right testicle, displacing the intestinal loops. Necropsy gross findings confirmed the presence of a testicular mass, bulging at the cut surface, with multiple well-delimitated whitish nodular lesions. Histologically, intratubular and diffuse neoplastic germinative cell proliferation was described. Complementary immunohistochemical assessments for vimentin and CD117 antibodies were negative. To the authors' knowledge, this is the first seminoma described in a S. coeruleoalba. We suggest that post-mortem (PM) pre-necropsy CT in dolphins is a useful tool for anatomic-guided pathology in such cases.

Advances in research on the impacts of anti-submarine sonar on beaked whales.

Mass stranding events (MSEs) of beaked whales (BWs) were extremely rare prior to the 1960s but increased markedly after the development of naval mid-frequency active sonar (MFAS). The temporal and spatial associations between atypical BW MSEs and naval exercises were first observed in the Canary Islands, Spain, in the mid-1980s. Further research on BWs stranded in association with naval exercises demonstrated pathological findings consistent with decompression sickness (DCS). A 2004 ban on MFASs around the Canary Islands successfully prevented additional BW MSEs in the region, but atypical MSEs have continued in other places of the world, especially in the Mediterranean Sea, with examined individuals showing DCS. A workshop held in Fuerteventura, Canary Islands, in September 2017 reviewed current knowledge on BW atypical MSEs associated with MFAS. Our review suggests that the effects of MFAS on BWs vary among individuals or populations, and predisposing factors may contribute to individual outcomes. Spatial management specific to BW habitat, such as the MFAS ban in the Canary Islands, has proven to be an effective mitigation tool and mitigation measures should be established in other areas taking into consideration known population-level information.

Muscle Pathology in Free-Ranging Stranded Cetaceans.

Despite the profound impact that skeletal muscle disorders may pose for the daily activities of wild terrestrial and marine mammals, such conditions have been rarely described in cetaceans. In this study, the authors aimed to determine the nature and prevalence of skeletal muscle lesions in small and large odontocetes and mysticetes ( n = 153) from 19 different species. A macroscopic evaluation of the epaxial muscle mass and a histologic examination of the longissimus dorsi muscle were performed in all cases. The only macroscopically evident change was variable degrees of atrophy of the epaxial muscles ( longissimus dorsi, multifidus, spinalis) in emaciated specimens. The histopathological study revealed single or combined morphological changes in 91.5% of the cases. These changes included the following: degenerative lesions (75.2%), muscle atrophy (37.9%), chronic myopathic changes (25.5%), parasitic infestation (9.2%), and myositis (1.9%). The skeletal muscle is easily sampled during a necropsy and provides essential microscopic information that reflects both local and systemic conditions. Thus, skeletal muscle should be systematically sampled, processed, and examined in all stranded cetaceans.

Coinfection by Streptococcus phocae and cetacean morbillivirus in a short-beaked common dolphin Delphinus delphis.

We describe gross, histopathological, and immunohistochemical features of Streptococcus phocae and cetacean morbillivirus coinfection in a short-beaked common dolphin Delphinus delphis. Major gross findings were cutaneous purulent nodules in the tail fluke, vegetative mitral valve endocarditis, and presumed postpartum pyometra. Histologic examination revealed bacterial septicemia characterized by widespread intravascular coccoid bacterial emboli. These were associated with fibrinonecrotizing to pyogranulomatous dermatitis and panniculitis, embolic pneumonia, neutrophilic and lymphoplasmacytic meningochoroiditis, random neutrophilic hepatitis, lymphoplasmacytic myocarditis and epicarditis, necrotizing adrenalitis, suppurative endometritis, and multicentric reactive lymphadenopathy. Bacteriology and molecular analysis with sequencing of the 16S rRNA gene identified S. phocae from lung, brain, and adrenal gland tissue. Immunohistochemical analysis for morbillivirus detection revealed positive immunolabeling in the epithelium of the choroid plexus of the fourth ventricle. Published reports on S. phocae infection in cetaceans are rare, and pathological details are limited. The present case indicates that S. phocae has potential pathogenic capacity in common dolphins. The pathogenesis is proposed to have involved cutaneous penetration after a skin trauma, leading to initial cutaneous disease and eventual systemic infection.

Characterization of EST3: a metagenome-derived esterase with suitable properties for biotechnological applications.

Metagenomic libraries from diverse environments have been extensive sources of many lipases and esterases; nevertheless, most of these enzymes remain biochemically uncharacterized. We previously built a metagenomic fosmid library from a microbial consortium specialized for diesel oil degradation and tested it for lipolytic activity. In the present study, we identified the PL14.H10 clone that was subcloned and sequenced, which enabled the identification of the EST3 protein. This enzyme exhibited 74 % amino acid identity with the uncharacterized alpha/beta hydrolase from Parvibaculum lavamentivorans [GenBank: WP012110575.1] and was classified into lipolytic enzyme family IV. Biochemical characterization revealed that EST3 presents high activity in a wide range of temperature with highest activity from 41 to 45 °C. Also, this thermostable esterase acts from mild acidic to alkaline conditions with an optimum pH of 6.0. The enzyme exhibited activity against p-nitrophenyl esters of different chain lengths and highest catalytic efficiency against p-nitrophenyl caprylate. The activity of the protein was increased in the presence of 0.5 mM of Mn(+2), Li(+), EDTA, and 1 % of CTAB and exhibited half of the activity in the presence of 10 % methanol and ethanol. Moreover, the homology model of EST3 was built and compared to other esterases, revealing a substrate channel that should fit a wide range of substrates. Taken together, the data presented in this work reveal the unique and interesting characteristics of EST3 that might be explored for further use in biotechnological applications.

Verminous Arteritis Due to Crassicauda sp. in Cuvier's Beaked Whales (Ziphius Cavirostris).

The vascular system of Cuvier's beaked whales (CBW) (Ziphius cavirostris; family Ziphiidae), an extremely deep, prolonged-diving cetacean, is increasingly receiving anatomic and physiologic study due to possible anthropogenic interactions; however, vascular pathology rarely has been reported in this species. Thirteen CBW stranded in the Canary Islands from June 2008 to June 2014 were autopsied. A careful dissection of the thoracic and abdominal vasculature was performed on these animals. All had moderate to severe and extensive chronic fibrosing arteritis with aneurysms, hemorrhages, and thrombosis primarily involving the mesenteric and gastroepiploic arteries and the thoracic and abdominal aorta. Microscopically, the lesions varied from subacute subintimal hemorrhages and severe neutrophilic, eosinophilic, and histiocytic dissecting arteritis with intralesional nematode larvae to marked, chronic, fibrosing arteritis with thickening and distortion of the vascular wall with calcification and occasional cartilage metaplasia. In addition, adult nematodes in renal arteries and veins, renal parenchyma and/or ureter were identified morphologically as Crassicauda sp. Nucleic acid sequenced from renal nematodes from 2 animals yielded closest nucleotide identity to C. magna The pathogenesis is proposed to involve a host response to larval migration from the intestine to the kidney through the mesenteric arteries, abdominal aorta, and renal arteries. Severe consequences for such lesions are possible and could vary from reduced vascular compliance to chronic renal disease and predisposition to the development of disseminated intravascular coagulation and multiorgan failure. Severe chronic arteritis in CBW is associated with renal parasitism by Crassicauda spp.

Maternal dietary fat intake during pregnancy is associated with infant temperament.

Research with rodents and nonhuman primates suggests that maternal prenatal dietary fat intake is associated with offspring behavioral functioning indicative of risk for psychopathology. The extent to which these findings extend to humans remains unknown. The current study administered the Automated Self-Administered 24 hr Dietary Recall Questionnaire three times in pregnancy (n = 48) to examine women's dietary fat intake in relation to infant temperament assessed using the Infant Behavior Questionnaire at 4-months old. The amount of saturated fat that the mother consumed was considered as a moderator of the association between total fat intake and child temperament. Results from a series of multiple linear regressions indicate that greater total fat intake was associated with poorer infant regulation and lower surgency. However, this second effect was moderated by maternal saturated fat intake, such that total fat intake was only related to infant surgency when mothers consumed above the daily recommended allowance of saturated fat. Under conditions of high total fat and high saturated fat, infants were rated as lower on surgency; under conditions of low total fat yet high saturated fat, infants were rated as higher on surgency. There were no associations between maternal prenatal fat intake and infant negative reactivity. These findings provide preliminary evidence that pregnant women's dietary fat intake is associated with infants' behavioral development, though future research is needed to address this report's limitations: a relatively small sample size, the use of self-report measures, and a lack of consideration of maternal and infant postnatal diet.