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The purpose of this study was to identify molecular mechanisms by which the liver influences total lesion burden in a nonhuman primate model (NHP) of cardiovascular disease with acute and chronic feeding of a high cholesterol, high fat (HCHF) diet. Baboons (47 females, 64 males) were fed a HCHF diet for 2 years (y); liver biopsies were collected at baseline, 7 weeks (w) and 2y, and lesions were quantified in aortic arch, descending aorta, and common iliac at 2y. Unbiased weighted gene co-expression network analysis (WGCNA) revealed several modules of hepatic genes correlated with lesions at different time points of dietary challenge. Pathway and network analyses were performed to study the roles of hepatic module genes. More significant pathways were observed in males than females. In males, we found modules enriched for genes in oxidative phosphorylation at baseline, opioid signaling at 7w, and EIF2 signaling and HNF1A and HNF4A networks at baseline and 2y. One module enriched for fatty acid β oxidation pathway genes was found in males and females at 2y. To our knowledge, this is the first study of a large NHP cohort to identify hepatic genes that correlate with lesion burden. Correlations of baseline and 7w module genes with lesions at 2y were observed in males but not in females. Pathway analyses of baseline and 7w module genes indicate EIF2 signaling, oxidative phosphorylation, and μ-opioid signaling are possible mechanisms that predict lesion formation induced by HCHF diet consumption in males. Our findings of coordinated hepatic transcriptional response in male baboons but not female baboons indicate underlying molecular mechanisms differ between female and male primate atherosclerosis.

Although COVID-19 infection has been associated with a number of clinical and environmental risk factors, host genetic variation has also been associated with the incidence and morbidity of infection. The CRP gene codes for a critical component of the innate immune system and CRP variants have been reported associated with infectious disease and vaccination outcomes. We investigated possible associations between COVID-19 outcome and a limited number of candidate gene variants including rs1205. The Strong Heart and Strong Heart Family studies have accumulated detailed genetic, cardiovascular risk and event data in geographically dispersed American Indian communities since 1988. Genotypic data and 91 COVID-19 adjudicated deaths or hospitalizations from 2/1/20 through 3/1/23 were identified among 3,780 participants in two subsets. Among 21 candidate variants including genes in the interferon response pathway, APOE, TMPRSS2, TLR3, the HLA complex and the ABO blood group, only rs1205, a 3' untranslated region variant in the CRP gene, showed nominally significant association in T-dominant model analyses (odds ratio 1.859, 95%CI 1.001-3.453, p = 0.049) after adjustment for age, sex, center, body mass index, and a history of cardiovascular disease. Within the younger subset, association with the rs1205 T-Dom genotype was stronger, both in the same adjusted logistic model and in the SOLAR analysis also adjusting for other genetic relatedness. A T-dominant genotype of rs1205 in the CRP gene is associated with COVID-19 death or hospitalization, even after adjustment for relevant clinical factors and potential participant relatedness. Additional study of other populations and genetic variants of this gene are warranted.

Reported associations between leukocyte telomere length (LTL) attrition, diet and cardiovascular disease (CVD) are inconsistent. This study explores effects of prolonged exposure to a high cholesterol high fat (HCHF) diet on LTL in a baboon model of atherosclerosis. We measured LTL by qPCR in pedigreed baboons fed a chow (n = 105) or HCHF (n = 106) diet for 2 years, tested for effects of diet on LTL, and association between CVD risk factors and atherosclerotic lesions with LTL. Though not different at baseline, after 2 years median LTL is shorter in HCHF fed baboons (P < 0.0001). Diet predicts sex- and age-adjusted LTL and LTL attrition (P = 0.0009 and 0.0156, respectively). Serum concentrations of CVD biomarkers are associated with LTL at the 2-year endpoint and LTL accounts approximately 6% of the variance in aortic lesions (P = 0.04). Although heritable at baseline (h 2  = 0.27, P = 0.027) and after 2 years (h 2  = 0.46, P = 0.0038), baseline LTL does not predict lesion extent after 2 years. Atherogenic diet influences LTL, and LTL is a potential biomarker for early atherosclerosis. Prolonged exposure to an atherogenic diet decreases LTL and increases LTL attrition, and shortened LTL is associated with early-stage atherosclerosis in pedigreed baboons.

The last couple of decades have highlighted the importance of studying hybridization, particularly among primate species, as it allows us to better understand our own evolutionary trajectory. Here, we report on genetic ancestry estimates using dense, full genome data from 881 olive ( Papio anubus ), yellow ( Papio cynocephalus ), or olive-yellow crossed captive baboons from the Southwest National Primate Research Center. We calculated global and local ancestry information, imputed low coverage genomes (n = 830) to improve marker quality, and updated the genetic resources of baboons available to assist future studies. We found evidence of historical admixture in some putatively purebred animals and identified errors within the Southwest National Primate Research Center pedigree. We also compared the outputs between two different phasing and imputation pipelines along with two different global ancestry estimation software. There was good agreement between the global ancestry estimation software, with R 2 > 0.88, while evidence of phase switch errors increased depending on what phasing and imputation pipeline was used. We also generated updated genetic maps and created a concise set of ancestry informative markers (n = 1,747) to accurately obtain global ancestry estimates.

This article illustrates the application of the labeling or societal reaction theory regarding the events of September 11, 2001. It explains the various types of labels that society assigned to ``September 11'' and how societal reactions led to governmental and law enforcement changes. Pertinent opinion polls were analyzed to indicate the power of labeling which, in turn, was used to demonstrate how the USA PATRIOT Act was passed during heightened societal reaction. [PUBLICATION ABSTRACT]

Baboons (genus Papio) are broadly studied in the wild and in captivity. They are widely used as a non-human primate model for biomedical studies, and the Southwest National Primate Research Center (SNPRC) at Texas Biomedical Research Institute has maintained a large captive baboon colony for more than 50 years. Unlike other model organisms though, the genomic resources for baboons are severely lacking. This has hindered the progress of studies using baboons as a model for basic biology or human disease. Here, we describe a dataset of 100 high-coverage whole-genome sequences obtained from the mixed colony of olive (P. anubis) and yellow (P. cynocephalus) baboons housed at the SNPRC. These data provide a comprehensive catalog of common genetic variation in baboons, as well as a fine-scale genetic map. We show how the data can be used to learn about ancestry and admixture, and to correct errors in the colony records. Finally, we investigated the consequences of inbreeding within the SNPRC colony and found clear evidence for increased rates of juvenile mortality and increased homozygosity of putatively deleterious alleles in inbred individuals.

The purpose of this study was to identify molecular mechanisms by which the liver influences total lesion burden in a nonhuman primate model (NHP) of cardiovascular disease with acute and chronic feeding of a high cholesterol, high fat (HCHF) diet. Baboons (47 females, 64 males) were fed a HCHF diet for 2 years (y); liver biopsies were collected at baseline, 7 weeks (w) and 2y, and lesions were quantified in aortic arch, descending aorta, and common iliac at 2y. Unbiased weighted gene co-expression network analysis (WGCNA) revealed several modules of hepatic genes correlated with lesions at different time points of dietary challenge. Pathway and network analyses were performed to study the roles of hepatic module genes. More significant pathways were observed in males than females. In males, we found modules enriched for genes in oxidative phosphorylation at baseline, opioid signaling at 7w, and EIF2 signaling and HNF1A and HNF4A networks at baseline and 2y. One module enriched for fatty acid β oxidation pathway genes was found in males and females at 2y. To our knowledge, this is the first study of a large NHP cohort to identify hepatic genes that correlate with lesion burden. Correlations of baseline and 7w module genes with lesions at 2y were observed in males but not in females. Pathway analyses of baseline and 7w module genes indicate EIF2 signaling, oxidative phosphorylation, and μ-opioid signaling are possible mechanisms that predict lesion formation induced by HCHF diet consumption in males. Our findings of coordinated hepatic transcriptional response in male baboons but not female baboons indicate underlying molecular mechanisms differ between female and male primate atherosclerosis.

\"3 While there are various policy rationales underlying the attorney/client privilege, the most fundamental is the promotion of frank communication between a client and his or her attorney, in order to help ensure that an advocacy on behalf of his/her client is not impaired by the client's lack of disclosure.4 Typically, the privilege belongs to - and thus, can only be waived by - the client.5 Where the client is a corporate entity rather than an individual, the attomey/client privilege is held by the corporation itself, and the rules surrounding the protection of individual communications made by corporate officers, directors or employees are more nuanced.6 For example, the effect of the privilege remaining with the corporation allows a board of directors to waive the attomey/client privilege over discussions between a prior board and its counsel, or discussions between a senior officer and the corporation's counsel.7 In addition, where a corporation is sold, the purchaser could become the new owner of the corporation's privilege regarding matters pre-dating the sale.8 In bankruptcy cases, the debtor's pre-petition privilege becomes part of the estate and, like all estate assets, must be used to maximize recovery for stakeholders. The U.S. Supreme Court has made it clear that upon the commencement of a bankruptcy case, the debtor's pre-petition privilege is controlled by the debtor in possession, who simply \"retains\" the privilege, or by a bankruptcy trustee, who steps into the debtor's shoes.9 In CFTC v. Weintraub, the Commodity Futures Trading Commission (CFTC) filed a complaint against a corporation for violating the Commodity Exchange Act.10 Thereafter, the corporation's sole director and officer executed a consent decree with the CFTC, which required a receiver's appointment to file for bankruptcy on the corporation's behalf.\" When the trustee issued a subpoena for documents to counsel of a former special committee of the BCE board, counsel to the former special committee objected, arguing that communications between the former special committee and its counsel were protected by the former special committee's attorney/client privilege, which was controlled by the former special committee, not the trustee.21 Hon. Richard Casey of the U.S. District Court for the Southern District of New York agreed, holding that the special committee was intended to be a separate entity from the board of directors, and that the special committee's privilege was thus distinct from the corporation's and did not transfer to the litigation trustee.22 In so finding, Judge Casey acknowledged the holding in Weintraub, but noted that Weintraub specifically exempted from its holding the privileges of parties that are legally distinct from the corporation or its board.23 The issue was revisited by Hon. Ronnie Abrams, also of the U.S. District Court for the Southern District of New York, in In re China Medical Technologies Inc.24 In this case, a liquidator appointed in the debtor's chapter 15 proceedings sought discovery of privileged communications between the debtors' pre-petition audit committee and the audit committee's law firm.25 Relying in part on BCE West, the law firm argued that the communications were protected by a privilege distinct from that belonging to the debtor.26 Judge Abrams rejected the BCE West holding, finding that BCE West failed to adequately address the policy considerations that were crucial to the Supreme Court's decision in Weintraub.21 Although Judge Abrams acknowledged that the audit committee \"was 'independent' in some sense,\" she also found that the committee was merely a representative of the board of directors, and that it ceased to exist upon the debtor's bankruptcy.28 Therefore, Judge Abrams held that the considerations articulated by the Supreme Court in Weintraub dictated that the former audit committee's attorney/client privilege transferred to - and thus could be waived by - the liquidator.29 Weintraulrs Application to the Tribune Special Committee Judge Sullivan's recent ruling in the Tribune action further addresses the question of whether a special committee's pre-petition privilege transfers to a bankruptcy or litigation trustee.30 In Tribune, the confirmed reorganization plan provided for the appointment of a litigation trustee in order to pursue certain preserved causes of action relating to the debtors' pre-petition leveraged buyout (LBO). The litigation trustee moved to compel the production of such documents, arguing that the confirmation order approving the transfer agreement transferred the special committee's attorney/client privilege to the litigation trustee and was res judicata, and that even in the absence of such an order, the special committee's attorney/client privilege belonged to the litigation trustee under the Supreme Court's ruling in Weintraub.34 In response, the former special committee members and their counsel argued that the transfer agreement was ineffective to transfer the special committee's privilege, as it was signed only by the debtors, which did not control the special committee's privilege.35 The special committee also cited Delaware cases outside of the bankruptcy context in which special committees were found to have attorney/client privileges that could not be waived by the corporations whose boards of directors had appointed them.36 Judge Sullivan ruled in favor of the litigation trustee on each of these arguments, and held that the special committee's attorney/client privilege belonged to the litigation trustee.

Steady-state expression quantitative trait loci (eQTLs) explain only a fraction of disease-associated loci identified through genome-wide association studies (GWAS), while eQTLs involved in gene-by-environment (GxE) interactions have rarely been characterized in humans due to experimental challenges. Using a baboon model, we found hundreds of eQTLs that emerge in adipose, liver, and muscle after prolonged exposure to high dietary fat and cholesterol. Diet-responsive eQTLs exhibit genomic localization and genic features that are distinct from steady-state eQTLs. Furthermore, the human orthologs associated with diet-responsive eQTLs are enriched for GWAS genes associated with human metabolic traits, suggesting that context-responsive eQTLs with more complex regulatory effects are likely to explain GWAS hits that do not seem to overlap with standard eQTLs. Our results highlight the complexity of genetic regulatory effects and the potential of eQTLs with disease-relevant GxE interactions in enhancing the understanding of GWAS signals for human complex disease using nonhuman primate models.Competing Interest StatementThe authors have declared no competing interest.Footnotes* typos corrected; figures remade for high quality; supplemental files updated; text revised for clarity