New Mexico State University Alamogordo

The granular dorsolateral prefrontal cortex (dlPFC) is an evolutionary specialization of primates that is centrally involved in cognition. We assessed more than 600,000 single-nucleus transcriptomes from adult human, chimpanzee, macaque, and marmoset dlPFC. Although most cell subtypes defined transcriptomically are conserved, we detected several that exist only in a subset of species as well as substantial species-specific molecular differences across homologous neuronal, glial, and non-neural subtypes. The latter are exemplified by human-specific switching between expression of the neuropeptide somatostatin and tyrosine hydroxylase, the rate-limiting enzyme in dopamine production in certain interneurons. The above molecular differences are also illustrated by expression of the neuropsychiatric risk gene FOXP2 , which is human-specific in microglia and primate-specific in layer 4 granular neurons. We generated a comprehensive survey of the dlPFC cellular repertoire and its shared and divergent features in anthropoid primates.

Except for ribavirin, no other antiviral drugs for treating hantaviral diseases have been identified. It is well established that ribavirin will inhibit the production of infectious Hantaan virus (HTNV); however, its mechanism of action is unknown. To characterize the inhibitory effect of ribavirin on HTNV, the levels of viral RNAs, proteins, and infectious particles were measured for 3 days posttreatment of HTNV-infected Vero E6 cells. HTNV-infected cells treated with ribavirin showed a slight reduction in the levels of cRNA, viral RNA, and mRNA populations on the first day postinfection. The amount of cRNA and viral RNA increased to that observed for untreated HTNV-infected cells on day 2, whereas mRNA levels were more greatly reduced on days 2 and 3. Despite the finding of S-segment mRNA, albeit low, three of the viral proteins-nucleocapsid (N) protein and glycoproteins G1 and G2-could not be detected by immunohistochemistry in ribavirin-treated cells. To test the hypothesis that these effects were caused by incorporation of ribavirin into nascent RNA and a resultant "error catastrophe" was occurring, we cloned and sequenced the S-segment cRNA/mRNA from ribavirin-treated or untreated cells from day 3. We found a high mutation frequency (9.5/1,000 nucleotides) in viral RNA synthesized in the presence of ribavirin. Hence, the transcripts produced in the presence of the drug were not functional. These results suggest that ribavirin's mechanism of action lies in challenging the fidelity of the hantavirus polymerase, which causes error catastrophe.

Several violent non-state groups also administer social services. Although earlier works stress the effects of social service provision on support and sympathy for violent groups, this article emphasizes a broader challenge. Namely, social welfare organizations threaten to rob the state of the legitimacy it derives through the social contract. Abolishing these organizations can cause humanitarian crises, radicalize populations, and erode domestic and international policy support. Ignoring them invites the continued erosion of state power. The way out of this dilemma is through a strategy of “displacement,” whereby the state eradicates non-state social services while concurrently extending its own welfare capacity.

Population-level right-handedness has historically been considered a hallmark of human evolution. Even though recent studies in chimpanzees (Pan troglodytes) have demonstrated population-level right-handedness for certain behaviors, some have questioned the validity and consistency of these findings by arguing that reported laterality effects are specific to certain colonies of apes and to those chimpanzees reared by humans. The authors report evidence of population-level right-handedness in 3 separate colonies of chimpanzees. Moreover, handedness in the 3 colonies was unrelated to the proportion of subjects that were raised by humans. This is the strongest evidence to date that population-level handedness is evident in chimpanzees and is not an artifact of human rearing.

MEPS Marine Ecology Progress Series Contact the journal Facebook Twitter RSS Mailing List Subscribe to our mailing list via Mailchimp HomeLatest VolumeAbout the JournalEditorsTheme Sections MEPS 329:99-113 (2007) - doi:10.3354/meps329099 Predicting the distribution of the scyphomedusa Chrysaora quinquecirrha in Chesapeake Bay M. B. Decker1,*, C. W. Brown2, R. R. Hood3, J. E. Purcell4, T. F. Gross5, J. C. Matanoski3,6, R. O. Bannon7, E. M. Setzler-Hamilton8,† 1Department of Ecology and Evolutionary Biology, Yale University, New Haven, Connecticut 06520, USA 2National Oceanic and Atmospheric Administration, Cooperative Institute of Climate Studies, University of Maryland, College Park, Maryland 20742-2465, USA 3Horn Point Laboratory, University of Maryland Center for Environmental Science, PO Box 775, Cambridge, Maryland 21613, USA 4Shannon Point Marine Center, 1900 Shannon Point Road, Anacortes, Washington 98221, USA 5Chesapeake Bay Research Consortium, 645 Contees Wharf Rd., Edgewater, Maryland 21037, USA 6New Mexico State University-Alamogordo, 2400 North Scenic Drive, Alamogordo, New Mexico 88310, USA 7University of Rhode Island, Graduate School of Oceanography, Box 200, South Ferry Road, Narragansett, Rhode Island 02882, USA 8Chesapeake Biological Laboratory, University of Maryland Center for Environmental Science, PO Box 38, Solomons, Maryland 20688, USA *Email: marybeth.decker@yale.edu. †Deceased ABSTRACT: Jellyfish blooms are important events controlling plankton dynamics in coastal waters worldwide, yet factors that influence bloom development are not well understood. We used the scyphomedusa Chrysaora quinquecirrha as a model to examine physical factors that control jellyfish populations and to develop an ecological forecasting system. Over 700 in situ observations collected from Chesapeake Bay and its tributaries during 1987–2000 were used to develop habitat models that predict the probability of occurrence and the likely concentration of medusae as a function of sea-surface temperature and salinity. Medusae were found within a relatively narrow range of temperature (26 to 30°C) and salinity (10 to 16). Regression analyses reveal that a combination of temperature and salinity is a significant predictor of medusa occurrence. Assessments of the predictive performance of these models using medusae and environmental data collected at independent survey sites (n = 354) indicated that model-predicted medusa occurrence and concentration correspond well with observations. Our models can be forced with near-real time and retrospective estimates of temperature and salinity to generate probability of occurrence maps of C. quinquecirrha medusa presence and abundance in order to better understand how this top predator varies in space and time, and how this species could potentially affect energy flow through the Chesapeake Bay system. KEY WORDS: Gelatinous zooplankton · Scyphozoa · Jellyfish · Temperature · Salinity · Climate · Predictive model · Forecasting · Nowcasting Full text in pdf format PreviousNextExport citation RSS - Facebook - Tweet - linkedIn Cited by Published in MEPS Vol. 329. Online publication date: January 11, 2007 Print ISSN: 0171-8630; Online ISSN: 1616-1599 Copyright © 2007 Inter-Research.

Metabolite concentrations reflect the physiological states of tissues and cells. However, the role of metabolic changes in species evolution is currently unknown. Here, we present a study of metabolome evolution conducted in three brain regions and two non-neural tissues from humans, chimpanzees, macaque monkeys, and mice based on over 10,000 hydrophilic compounds. While chimpanzee, macaque, and mouse metabolomes diverge following the genetic distances among species, we detect remarkable acceleration of metabolome evolution in human prefrontal cortex and skeletal muscle affecting neural and energy metabolism pathways. These metabolic changes could not be attributed to environmental conditions and were confirmed against the expression of their corresponding enzymes. We further conducted muscle strength tests in humans, chimpanzees, and macaques. The results suggest that, while humans are characterized by superior cognition, their muscular performance might be markedly inferior to that of chimpanzees and macaque monkeys.

Cognitive defects in autism spectrum disorder (ASD) include socialization and communication: key behavioral capacities that separate humans from other species. Here, we analyze gene expression in the prefrontal cortex of 63 autism patients and control individuals, as well as 62 chimpanzees and macaques, from natal to adult age. We show that among all aberrant expression changes seen in ASD brains, a single aberrant expression pattern overrepresented in genes involved synaptic-related pathways is enriched in nucleotide variants linked to autism. Furthermore, only this pattern contains an excess of developmental expression features unique to humans, thus resulting in the disruption of human-specific developmental programs in autism. Several members of the early growth response (EGR) transcription factor family can be implicated in regulation of this aberrant developmental change. Our study draws a connection between the genetic risk architecture of autism and molecular features of cortical development unique to humans.

Serum concentrations of dehydroepiandrosterone (DHA), DHA sulfate, and cortisol were measured in 52 chimpanzees (aged 0.5--10 yr), 76 Macaca mulatta (aged 0.25--5 yr), and 80 Macaca nemestrina (aged 0.5--9 yr). Sexual maturation was assessed by age and by the presence of menarche or the appearance of perineal turgescence in the females and by measurement of serum testosterone in the males. In an additional group of 10 young adult female M. mulatta, four repeated determinations of these same steroids at 30-min intervals demonstrated that the stress of capture and venipuncture caused a significant rise in serum levels of not only cortisol but also of DHA and DHA sulfate. The chimpanzees demonstrated an age-related rise in serum concentrations of DHA and DHA sulfate relative to cortisol which began before the onset of puberty and thus closely resembled human adrenarche. In M. mulatta, serum DHA levels showed no change with age, while DHA sulfate values decreased progressively both before and during puberty. The pattern in M. nemestrina was similar, with stable DHA and declining DHA sulfate levels before and during puberty. However, in the oldest group (aged 6--9 yr) of mature M. nemestrina, there was a significant postpubertal rise of both DHA and DHA sulfate with no change in serum cortisol. These data suggest that monkeys, just as higher primates, may show increasing adrenal secretion of C19 steroids at around 6--9 yr. This adrenarchal process appears to be completely independent of sexual maturation and probably merely reflects the influence of progressive adrenal growth and the resulting impact of changing intraadrenal steroid concentrations upon steroidogenesis in the zona reticularis.

Lactational performance varies widely among mammalian species. Lactation plays a variable role in the overall reproductive strategy. The fraction of total growth and development of the young contributed by lactation is minimal in such species as guinea pigs but is a very high proportion in some marsupials and primates. Although the overall daily capacity for transfer of energy for many species is rather constant at about 125 kcal/kg body weight.70, the proportions of nutritive constituents in milk differ greatly among species and vary during lactation.

The terminal investment hypothesis (Williams [1966] Adaptation and Natural Selection; Princeton, NJ: Princeton University Press) holds that reproductive effort should increase over time in iteroparous species in which reproductive value declines with age. Attempts to model this hypothesis and test it in various species have produced mixed results. Clutton-Brock ([ 1984] Am. Nat. 123:212-229) argued that simply testing for changes in propagule size with age fails to recognize that the costs of producing offspring of a given size may increase over the lifespan, hence absence of a positive correlation does not defeat the hypothesis. However, this interpretation is weakened by evidence of sequential increases in propagule size independent of age, as such changes reveal a capacity to increase absolute investment over time. Humans and chimpanzees meet the preconditions of the terminal investment hypothesis. Surveying the obstetrics literature, we show that the majority of published studies indicate that parity has a positive effect on birth weight, but age has no effect. Analyzing 436 captive chimpanzee births, we document a positive influence of parity and a negative influence of age. We therefore conclude that, though it is yet to be replaced by a more compelling alternative, the terminal investment hypothesis is not supported in these two species, as absence of a positive effect of age on birth weight cannot be interpreted in a manner congruent with the hypothesis.

Sudden cardiac death (SCD), presumed secondary to fatal arrhythmias, is a common cause of mortality in captive chimpanzees at the Alamogordo Primate Facility. Over the 6-year period at the Alamogordo Primate Facility between 2001 and 2006, 13 animals were defined as sudden cardiac death (11 male and 2 female) on the basis of clinical presentation which was 38% of all deaths. All animals had annual physical exams, including electrocardiograms and serial blood pressures. Six of the 13 animals underwent a complete cardiac evaluation by a veterinary cardiologist and all six of these animals were diagnosed with various degrees of cardiomyopathy. Systemic hypertension was noted in two of the 13 cases and antemortem cardiac arrhythmias were seen in all 13 animals. Histological examination of the hearts revealed myocardial fibrosis in 12 chimpanzees. Most of the animals (10/13) that died of sudden cardiac death had cardiomegaly (increased heart weight/body weight ratio) and some degree of myocardial fibrosis noted. Additional data as well as serial diagnostic evaluations will be needed to identify the possible causes of sudden cardiac death in captive chimpanzees.

The clinical and necropsy records of 36 (25 male and 11 female) chimpanzees age 10 to 40 y old that died over a 6-y period (2001 to 2006) were reviewed. All animals had annual physical exams that included electrocardiograms and serial blood pressures. Nine of the 36 animals had a complete cardiac evaluation by a board certified veterinary cardiologist, and 7 of the 36 animals (19%) were diagnosed with some form of cardiomyopathy. Systemic hypertension was noted in 3 cases. Cardiac arrhythmias (ventricular ectopy) were seen in 15 (12 male and 3 female) of the 36 animals (42%). Sudden cardiac death (SCD) occurred in 13 (11 male and 2 female) chimps (36%) and was the leading cause of death (n = 13), followed by renal failure (n = 9) and septicemia (n = 3). Histologic examination of the hearts revealed interstitial myocardial fibrosis (IMF) in 29 chimpanzees (81%), and all of the animals that died suddenly due to cardiac causes had IMF to varying degrees. More data will be needed to identify the possible causes of IMF in captive chimpanzees, and IMF may be associated with arrhythmias and SCD in these animals.

Human immunodeficiency virus (HIV)-1 IIIB infection of chimpanzees leads to a compartmentalized, nonpathogenic in vivo and in vitro relationship with the virus. The absence of an acquired immunodeficiency syndrome (AIDS)-like disease in over 100 chimpanzees persistently infected may be related to some or all of the findings reported here. Further characterizing these possible host adapative mechanisms may be critical in both understanding pathogenesis, as well as elucidating novel mechanisms for therapeutic and/or the preventive strategies for AIDS in humans.

The dopaminergic innervation of the striatum has been implicated in learning processes and in the development of human speech and language. Several lines of evidence suggest that evolutionary changes in dopaminergic afferents of the striatum may be associated with uniquely human cognitive and behavioral abilities, including the association of the human-specific sequence of the FOXP2 gene with decreased dopamine in the dorsomedial striatum of mice. To examine this possibility, we quantified the density of tyrosine hydroxylase-immunoreactive axons as a measure of dopaminergic innervation within five basal ganglia regions in humans, great apes, and New and Old World monkeys. Our results indicate that humans differ from nonhuman primate species in having a significant increase in dopaminergic innervation selectively localized to the medial caudate nucleus. This region of the striatum is highly interconnected, receiving afferents from multiple neocortical regions, and supports behavioral and cognitive flexibility. The medial caudate nucleus also shows hyperactivity in humans lacking a functional FOXP2 allele and exhibits altered dopamine concentrations in humanized Foxp2 mice. Additionally, striatal dopaminergic input was not altered in chimpanzees that used socially learned attention-getting sounds versus those that did not. This evidence indicates that the increase in dopamine innervation of the medial caudate nucleus in humans is a species-typical characteristic not associated with experience-dependent plasticity. The specificity of this increase may be related to the degree of convergence from cortical areas within this region of the striatum and may also be involved in human speech and language. J. Comp. Neurol. 524:2117-2129, 2016. © 2015 Wiley Periodicals, Inc.

Although transcriptomic profiling has become the standard approach for exploring molecular differences in the primate brain, very little is known about how the expression levels of gene transcripts relate to downstream protein abundance. Moreover, it is unknown whether the relationship changes depending on the brain region or species under investigation. We performed high-throughput transcriptomic (RNA-Seq) and proteomic (liquid chromatography coupled with tandem mass spectrometry) analyses on two regions of the human and chimpanzee brain: The anterior cingulate cortex and caudate nucleus. In both brain regions, we found a lower correlation between mRNA and protein expression levels in humans and chimpanzees than has been reported for other tissues and cell types, suggesting that the brain may engage extensive tissue-specific regulation affecting protein abundance. In both species, only a few categories of biological function exhibited strong correlations between mRNA and protein expression levels. These categories included oxidative metabolism and protein synthesis and modification, indicating that the expression levels of mRNA transcripts supporting these biological functions are more predictive of protein expression compared with other functional categories. More generally, however, the two measures of molecular expression provided strikingly divergent perspectives into differential expression between human and chimpanzee brains: mRNA comparisons revealed significant differences in neuronal communication, ion transport, and regulatory processes, whereas protein comparisons indicated differences in perception and cognition, metabolic processes, and organization of the cytoskeleton. Our results highlight the importance of examining protein expression in evolutionary analyses and call for a more thorough understanding of tissue-specific protein expression levels.

In the absence of disease, ageing in the human brain is accompanied by mild cognitive dysfunction, gradual volumetric atrophy, a lack of significant cell loss, moderate neuroinflammation, and an increase in the amyloid beta (A β ) and tau proteins. Conversely, pathologic age-related conditions, particularly Alzheimer's disease (AD), result in extensive neocortical and hippocampal atrophy, neuron death, substantial A β plaque and tau-associated neurofibrillary tangle pathologies, glial activation and severe cognitive decline. Humans are considered uniquely susceptible to neurodegenerative disorders, although recent studies have revealed A β and tau pathology in non-human primate brains. Here, we investigate the effect of age and AD-like pathology on cell density in a large sample of postmortem chimpanzee brains ( n = 28, ages 12–62 years). Using a stereologic, unbiased design, we quantified neuron density, glia density and glia:neuron ratio in the dorsolateral prefrontal cortex, middle temporal gyrus, and CA1 and CA3 hippocampal subfields. Ageing was associated with decreased CA1 and CA3 neuron densities, while AD pathologies were not correlated with changes in neuron or glia densities. Differing from cerebral ageing and AD in humans, these data indicate that chimpanzees exhibit regional neuron loss with ageing but appear protected from the severe cell death found in AD. This article is part of the theme issue ‘Evolution of the primate ageing process’.

Cardiovascular disease is a primary cause of morbidity and mortality in captive chimpanzees. Four years of blood pressure (BP) data were analyzed from a captive former laboratory population of 201 healthy adult chimpanzees with assessment of age and obesity on elevated BP. Five different measures of obesity were compared: abdominal girth, basal metabolic rate, body-mass index (BMI), body weight, and surface area. Systolic BP varied by sex. Obesity did not influence male BP. For females, obesity was a significant determinant of BP. The best measure of female obesity was basal metabolic rate and the worst was BMI. Median systolic BP of healthy weight females (<54.5 kg) was significantly lower (128 mmHg) than overweight or obese females (140 mmHg), but both were lower than all males (147 mmHg). For diastolic BP, neither sex nor any of the five obesity measures was significant. But age was highly significant, with geriatric chimpanzees (>30 years) having higher median diastolic BP (74 mmHg) than young adults of 10-29 years of age (65 mmHg). By these criteria, 80% of this population is normotensive, 7% prehypertensive, and 13% hypertensive. In summary, systolic BP intervals required adjustment for obesity among females but not males. Diastolic BP required adjustment for advanced age (≥30 years). Use of these reference intervals can facilitate timely clinical care of captive chimpanzees.

We retrospectively reviewed 107 diabetic patients who received a split thickness skin graft (STSG) for treatment of a non-healing diabetic foot or leg ulcer to describe healing times based on patient characteristics, comorbidities or complications. The minimum follow-up was 6 months from the time of STSG application. The mean time to healing among all patients was 5.1 weeks (3 to 16 weeks). The mean healing time for patients with complications was 12.0 weeks (10 to 16 weeks) while the mean healing time for those without complications was 4.9 weeks (3 to 10 weeks). Overall complication rate was 2.8%. Patients with a STSG take of less than 95% had a mean healing time of 7.9 weeks compared to 4.8 weeks for those with a STSG take of 100% (p<0.001). The use of autologous STSG for treatment of non-healing diabetic foot and leg wounds is a viable method for soft tissue closure and may present a low complication rate and a satisfactory rate of healing.

BACKGROUND: It has been proposed that anatomical differences in human and great ape guts arose in response to species-specific diets and energy demands. To investigate functional genomic consequences of these differences, we compared their physiological levels of phytanic acid, a branched chain fatty acid that can be derived from the microbial degradation of chlorophyll in ruminant guts. Humans who accumulate large stores of phytanic acid commonly develop cerebellar ataxia, peripheral polyneuropathy, and retinitis pigmentosa in addition to other medical conditions. Furthermore, phytanic acid is an activator of the PPAR-alpha transcription factor that influences the expression of genes relevant to lipid metabolism. RESULTS: Despite their trace dietary phytanic acid intake, all great ape species had elevated red blood cell (RBC) phytanic acid levels relative to humans on diverse diets. Unlike humans, chimpanzees showed sexual dimorphism in RBC phytanic acid levels, which were higher in males relative to females. Cultured skin fibroblasts from all species had a robust capacity to degrade phytanic acid. We provide indirect evidence that great apes, in contrast to humans, derive significant amounts of phytanic acid from the hindgut fermentation of plant materials. This would represent a novel reduction of metabolic activity in humans relative to the great apes. CONCLUSION: We identified differences in the physiological levels of phytanic acid in humans and great apes and propose this is causally related to their gut anatomies and microbiomes. Phytanic acid levels could contribute to cross-species and sex-specific differences in human and great ape transcriptomes, especially those related to lipid metabolism. Based on the medical conditions caused by phytanic acid accumulation, we suggest that differences in phytanic acid metabolism could influence the functions of human and great ape nervous, cardiovascular, and skeletal systems.

Continuous advances in pediatric cardiology, surgery, and critical care have significantly improved survival rates for children and adults with congenital heart disease. Paradoxically, the resulting increase in longevity has expanded the prevalence of both repaired and unrepaired congenital heart disease and has escalated the need for diagnostic and interventional procedures. Because of this expansion in prevalence, anesthesiologists, pediatricians, and other health care professionals increasingly encounter patients with congenital heart disease or other pediatric cardiac diseases who are presenting for surgical treatment of unrelated, noncardiac disease. Patients with congenital heart disease are at high risk for mortality, complications, and reoperation after noncardiac procedures. Rigorous study of risk factors and outcomes has identified subsets of patients with minor, major, and severe congenital heart disease who may have higher-than-baseline risk when undergoing noncardiac procedures, and this has led to the development of risk prediction scores specific to this population. This scientific statement reviews contemporary data on risk from noncardiac procedures, focusing on pediatric patients with congenital heart disease and describing current knowledge on the subject. This scientific statement also addresses preoperative evaluation and testing, perioperative considerations, and postoperative care in this unique patient population and highlights relevant aspects of the pathophysiology of selected conditions that can influence perioperative care and patient management.