tbuckley/cabot-search huggingface dataset:
The economic origins of ultrasociality
Authors: John Gowdy, Lisi Krall
Journal: Behavioral and Brain Sciences (2015)

Ultrasociality refers to the social organization of a few species, including humans and some social insects, having a complex division of labor, city-states, and an almost exclusive dependence on agriculture for subsistence. We argue that the driving forces in the evolution of these ultrasocial societies were economic. With the agricultural transition, species could directly produce their own food and this was such a competitive advantage that those species now dominate the planet. Once underway, this transition was propelled by the selection of within-species groups that could best capture the advantages of (1) actively managing the inputs to food production, (2) a more complex division of labor, and (3) increasing returns to larger scale and larger group size. Together these factors reoriented productive life and radically altered the structure of these societies. Once agriculture began, populations expanded as these economic drivers opened up new opportunities for the exploitation of resources and the active management of inputs to food production. With intensified group-level competition, larger populations and intensive resource exploitation became competitive advantages, and the "social conquest of Earth" was underway. Ultrasocial species came to dominate the earth's ecosystems. Ultrasociality also brought a loss of autonomy for individuals within the group. We argue that exploring the common causes and consequences of ultrasociality in humans and the social insects that adopted agriculture can provide fruitful insights into the evolution of complex human society.
Disappearance of hepatic parenchymal nerves in human liver cirrhosis.
Authors: J A Lee, Q Ahmed, J E Hines, A D Burt
Journal: Gut (1992)

The normal human liver receives a substantial autonomic innervation that is thought to subserve motor, metabolic, and sensory functions. In this study an antibody to a neural axoplasmic protein (PGP 9.5) was used to visualise autonomic nerves in tissue from normal, precirrhotic, and cirrhotic livers. Nerve fibres were readily identified in the parenchyma and portal tracts of normal livers, and in those where the histological diagnosis was non-specific reactive hepatitis or acute liver injury. In precirrhotic and cirrhotic livers nerves in portal tracts and fibrous septae remained prominent, but the parenchymal innervation was reduced in precirrhotic livers and was absent from regenerating nodules in established cirrhosis. The causes and functional consequences of this parenchymal denervation in cirrhosis remain to be established.
MicroRNA-940 suppresses prostate cancer migration and invasion by regulating MIEN1
Authors: Smrithi Rajendiran, Anil V Parwani, Richard J Hare, Subhamoy Dasgupta, Rhonda K Roby, Jamboor K Vishwanatha
Journal: Molecular Cancer (2014)

MicroRNAs (miRNAs) are crucial molecules that regulate gene expression and hence pathways that are key to prostate cancer progression. These non-coding RNAs are highly deregulated in prostate cancer thus facilitating progression of the disease. Among the many genes that have gained importance in this disease, Migration and invasion enhancer 1 (MIEN1), a novel gene located next to HER2/neu in the 17q12 amplicon of the human chromosome, has been shown to enhance prostate cancer cell migration and invasion, two key processes in cancer progression. MIEN1 is differentially expressed between normal and cancer cells and tissues. Understanding the regulation of MIEN1 by microRNA may enable development of better targeting strategies. The miRNAs that could target MIEN1 were predicted by in silico algorithms and microarray analysis. The validation for miRNA expression was performed by qPCR and northern blotting in cells and by in situ hybridization in tissues. MIEN1 and levels of other molecules upon miRNA regulation was determined by Western blotting, qPCR, and immunofluorescence. The functional effects of miRNA on cells were determined by wound healing cell migration, Boyden chamber cell invasion, clonal and colony formation assays. For knockdown or overexpression of the miRNA or overexpression of MIEN1 3′UTR, cells were transfected with the oligomiRs and plasmids, respectively. A novel miRNA, hsa-miR-940 (miR-940), identified and validated to be highly expressed in immortalized normal cells compared to cancer cells, is a regulator of MIEN1. Analysis of human prostate tumors and their matched normal tissues confirmed that miR-940 is highly expressed in the normal tissues compared to its low to negligible expression in the tumors. While MIEN1 is a direct target of miR-940, miR-940 alters MIEN1 RNA, in a quantity as well as cell dependent context, along with altering its downstream effectors. The miR-940 inhibited migratory and invasive potential of cells, attenuated their anchorage-independent growth ability, and increased E-cadherin expression, implicating its role in mesenchymal-to-epithelial transition (MET). These results, for the first time, implicate miR-940, a regulator of MIEN1, as a promising novel diagnostic and prognostic tool for prostate cancer.
Units of measurement of central venous pressure
Authors: J R. Sneyd
Journal: BMJ (1995)

a history of a sore throat, fever, and malaise.He had had two recent episodes of a sore throat treated with antibiotics.Examination showed oral candidiasis, enlarged asymmetrical cervical and axillary lymph nodes, a soft systolic murmur, and hepatosplenomegaly.Laboratory investigations showed anaemia (haemoglobin concentration 71 g/l), a platelet count of 128 x 106/l, a prolonged inter- national normalised ratio, hypoalbuminaemia, and renal failure.The result of an HIV antibody test was positive.The CD4 cell count was 100 x 106/l.Throat swabs for bacterial pathogens yielded negative results, and serial antistreptolysin 0 titres were not raised.An electrocardiogram was normal and echocardiography showed a dilated left ventricle.Staining of cerebrospinal fluid for acid fast bacilli yielded a positive result, and empirical antituberculous treatment was started.He initially responded, with appreciable improvement in clinical, haematological, and biochemical variables.Over the next five months he was admitted on three occasions with fever, arthralgia, progressive dyspnoea, and hypersplenism.On his final admis- sion he had clinical signs of congestive cardiac failure, with cardiomegaly and pulmonary oedema evident on chest radiography.Repeat echocardiography showed a dilated hypokinetic left ventricle with a normal mitral valve.Despite conventional treatment for heart failure he developed progres- sive biventricular failure and died.At postmortem examination the gross findings included pro- nounced left ventricular dilatation, a normal mitral valve, pulmonary oedema, enlarged peripheral and retroperitoneal lymph nodes, and hepatosplenomegaly.Cardiac sections showed Aschoff's bodies in the myocardium and subendocardium.This patient died of left ventricular failure secondary to rheumatic myocarditis.Patients with HIV infection are often unable to mount an appropriate serological response.'The absence of appreciable valve abnormalities agrees with a previous report of rheumatic heart disease in HIV infection.2Rheumatic heart disease should be considered in HIV positive patients from endemic areas who have evidence of heart disease.Clinical and laboratory features may be modified by immunodeficiency associated with HIV.
Prospective Study of Herpes Simplex Virus, Cytomegalovirus, and the Risk of Future Myocardial Infarction and Stroke
Authors: Paul M. Ridker, Charles H. Hennekens, Meir J. Stampfer, Fred Wang
Journal: Circulation (1998)

Background —It has been hypothesized that infection with either herpes simplex virus (HSV) or cytomegalovirus (CMV) is associated with atherogenesis. However, prospective data relating evidence of prior exposure to these agents with risks of future myocardial infarction (MI) and stroke are sparse. Methods and Results —In a prospective, nested case-control study of apparently healthy men, the baseline prevalence of antibodies directed against HSV or CMV was similar among 643 men who subsequently developed a first MI or thromboembolic stroke and among 643 age- and smoking-matched men who remained free of reported vascular disease over a 12-year follow-up period. Specifically, the relative risks for future MI and stroke were 0.94 (95% CI, 0.7 to 1.2) for HSV seropositivity and 0.72 (95% CI, 0.6 to 0.9) for CMV seropositivity, after adjustment for other cardiovascular risk factors. These findings were not materially altered in comparisons of early versus late events or in analyses stratified by smoking status. There was no evidence of association between HSV or CMV antibodies and plasma concentration of C-reactive protein, a marker of inflammation that predicts vascular risk in this cohort. Conclusions —Among apparently healthy middle-aged men, IgG antibodies directed against HSV or CMV do not appear to be a marker for increased atherothrombotic risk. The observed possible inverse relationship of CMV with MI and stroke was unexpected and may well be due to chance, because the direction of association is not compatible with the a priori hypothesis based on proposed biological mechanisms or previous cross-sectional and retrospective data.
The Northeast Indian Passageway: A Barrier or Corridor for Human Migrations?
Authors: R. Cordaux
Journal: Molecular Biology and Evolution (2004)

The northeast Indian passageway connecting the Indian subcontinent to East/Southeast Asia is thought to have been a major corridor for human migrations. Because it is also an important linguistic contact zone, it is predicted that northeast India has witnessed extensive population interactions, thus, leading to high genetic diversity within groups and heterogeneity among groups. To test this prediction, we analyzed 14 biallelic and five short tandem–repeat Y-chromosome markers and hypervariable region 1 mtDNA sequence variation in 192 northeast Indians. We find that both northeast Indian Y chromosomes and mtDNAs consistently show strikingly high homogeneity among groups and strong affinities to East Asian groups. We detect virtually no Y-chromosome and mtDNA admixture between northeast and other Indian groups. Northeast Indian groups are also characterized by a greatly reduced Y-chromosome diversity, which contrasts with extensive mtDNA diversity. This is best explained by a male founder effect during the colonization of northeast India that is estimated to have occurred within the past 4,000 years. Thus, contrary to the prediction, these results provide strong evidence for a genetic discontinuity between northeast Indian groups and other Indian groups. We, therefore, conclude that the northeast Indian passageway acted as a geographic barrier rather than as a corridor for human migrations between the Indian subcontinent and East/Southeast Asia, at least within the past millennia and possibly for several tens of thousand years, as suggested by the overall distinctiveness of the Indian and East Asian Y chromosome and mtDNA gene pools.
STUDIES ON THE INHIBITION OF PROTEOLYTIC ENZYMES BY SERUM
Authors: N. Raphael Shulman
Journal: The Journal of Experimental Medicine (1952)

The mechanism of the inhibition of trypsin, plasmin, and chymotrypsin by serum was studied using fibrin tagged with radioactive iodine as a substrate. Enzyme-inhibitor relationships were studied by: (a) varying the concentration of serum; (b) varying the concentration of enzyme; and (c) by diluting the enzyme-serum mixture. The results indicate that the inhibition of trypsin, plasmin, and chymotrypsin is a stoichiometric and irreversible reaction. By using the Lineweaver-Burk graphical method of analysis it was demonstrated that the inhibition of trypsin and chymotrypsin is a non-competitive reaction. This finding supports the conclusion that inhibition by serum is an irreversible type of reaction. The substrate was found to exert a retarding effect on the activity of plasmin. The possibility of a plasmin inhibitor in fibrinogen was suggested. The suitability of the various procedures used in evaluating serum proteolytic inhibition was discussed.
Hormones and breast cancer
Journal: Human Reproduction Update (2004)

The incidence of breast cancer in women varies with age, mammary gland mass and exposure to endogenous and exogenous hormones. Age is the single most important factor and if, as projected, 32% of women will be aged >60 years by 2050, world breast cancer incidence will exceed the current 106 per year. Hormonal influences that affect growth of the mammary gland increase the risk of breast cancer; for example earlier menarche and later menopause. Childbearing protects against later development of breast cancer, and breastfeeding further decreases the risk. The breast cancer risk declines more with increasing total duration of breastfeeding. Exposure to hormonal contraceptives has been evaluated in a combined reanalysis of data from 51 epidemiological studies. There is a small transient increase in the relative risk of breast cancer among users of oral contraceptives but, since use typically occurs at young ages when breast cancer is relatively rare, such an increase would have little effect on overall incidence rates. In contrast, exposure to menopause hormone treatment occurs when the baseline risk of breast cancer is higher, and epidemiological studies and randomized controlled trials consistently find an increase in breast cancer risk with exposure to combined estrogen and progestogen. Women with a family history of breast cancer in first degree relatives have an increased risk of breast cancer but there is no evidence to suggest that this differs according to a woman's use of oral contraceptives or menopause hormone treatment. Selective estrogen receptor modulators are useful in the treatment and/or prevention of breast cancer depending on the specific agonist or antagonist effects on estrogen target tissues.
HIV-1 Vaccine Development After STEP
Authors: Dan H. Barouch, Bette Korber
Journal: Annual Review of Medicine (2010)

Despite more than 25 years of concerted worldwide research, the development of a safe and effective HIV-1 vaccine remains elusive. Prototype antibody-based and T cell-based HIV-1 vaccines have failed to show efficacy in clinical trials to date. Next-generation HIV-1 vaccine candidates are in various stages of preclinical and clinical development, but key scientific obstacles pose major challenges for the field. Critical hurdles include the enormous global diversity of the virus and the challenges associated with generating broadly reactive neutralizing antibody and cellular immune responses. We review the current state of the HIV-1 vaccine field and outline strategies that are being explored to overcome these roadblocks.
ADOLESCENT RESILIENCE: A Framework for Understanding Healthy Development in the Face of Risk
Authors: Stevenson Fergus, Marc A. Zimmerman
Journal: Annual Review of Public Health (2004)

▪ Abstract Adolescent resilience research differs from risk research by focusing on the assets and resources that enable some adolescents to overcome the negative effects of risk exposure. We discuss three models of resilience—the compensatory, protective, and challenge models—and describe how resilience differs from related concepts. We describe issues and limitations related to resilience and provide an overview of recent resilience research related to adolescent substance use, violent behavior, and sexual risk behavior. We then discuss implications that resilience research has for intervention and describe some resilience-based interventions.
Risk factors of recurrent hamstring injuries: a systematic review
Authors: HM de Visser, M Reijman, MP Heijboer, PK Bos
Journal: British Journal of Sports Medicine (2011)

Background Although recurrent hamstring injury is a frequent problem with a significant impact on athletes, data on factors determining the risk for a recurrent hamstring injury are scarce. Objective To systematically review the literature and provide an overview of risk factors for re-injury of acute hamstring muscle injuries. Study design Prospective studies on risk factors for re-injury following acute hamstring injuries were systematically reviewed. Medical databases and reference lists of the included articles were searched. Two reviewers independently selected potential studies and assessed methodological quality; one reviewer extracted the data. A best-evidence synthesis of all studied risk factors was performed. Results Of the 131 articles identified, five prospective follow-up studies fulfilled our inclusion criteria. These studies reported a recurrence incidence of 13.9–63.3% in the same playing season up to 2 years after initial injury. Limited evidence for three risk factors and one protective factor for recurrent hamstring injury was found; patients with a recurrent hamstring injury had an initial injury with a larger volume size as measured on MRI (47.03 vs 12.42 cm 3 ), more often had a Grade 1 initial trauma (Grade 0: 0–30.4%; Grade 1: 60.9–100%; Grade 2: 8.7%) and more often had a previous ipsilateral anterior cruciate ligament (ACL) reconstruction (66.6% vs 17.1%) independent of graft selection. Athletes in a rehabilitation programme with agility/stabilisation exercises rather than strength/stretching exercises had a lower risk for re-injury (7.7% vs 70%). No significant relationship with re-injury was found for 11 related determinants. There was conflicting evidence that a larger cross-sectional area is a risk factor for recurrent hamstring injury. Conclusions There is limited evidence that athletes with a larger volume size of initial trauma, a Grade 1 hamstring injury and a previous ipsilateral ACL reconstruction are at increased risk for recurrent hamstring injury. Athletes seem to be at lower risk for re-injury when following agility/stabilisation exercises.
An analysis of pre-operative Pao2 in a general surgical population
Authors: M. L. Diament, K. N. V. Palmer
Journal: Thorax (1969)

Two hundred and thirty one patients awaiting elective surgery were divided on the basis of spirometric examination into normal (group A) and those with increased airway resistance (group B). The mean arterial oxygen tension for the 151 normal subjects was 96·3 (± 11·6) mm. Hg. There was a significant inverse correlation of Pao<sub>2</sub> with age and dynamic lung volumes. The 80 patients in group B were significantly older and their mean Pao<sub>2</sub> was 88·7 (± 12·9) mm. Hg. There was, however, no correlation between Pao<sub>2</sub> and age in this group, probably because the increased airway resistance had a greater influence in lowering the arterial oxygen tension than did the age factor alone.
Chest drain insertion-- training is the key, Seldinger or otherwise
Authors: T. R. Naicker, D. T. McLeod
Journal: Thorax (2011)

We welcome Maskell et al 's timely editorial highlighting the shortfalls of safe chest drain insertion.1 Modernising Medical Careers states that competence in chest drain insertion should be achieved as a part of core medical training but does not set out how this might be practically achieved. The authors suggest that chest drain insertion should not be a generic skill but be confined to respiratory teams. Where there is a large presence of chest …
Financial Anatomy of Biomedical Research
Authors: Hamilton Moses, E. Ray Dorsey, David H. M. Matheson, Samuel O. Thier
Journal: JAMA (2005)

Public and private financial support of biomedical research have increased over the past decade. Few comprehensive analyses of the sources and uses of funds are available. This results in inadequate information on which to base investment decisions because not all sources allow equal latitude to explore hypotheses having scientific or clinical importance and creates a barrier to judging the value of research to society.To quantify funding trends from 1994 to 2004 of basic, translational, and clinical biomedical research by principal sponsors based in the United States.Publicly available data were compiled for the federal, state, and local governments; foundations; charities; universities; and industry. Proprietary (by subscription but openly available) databases were used to supplement public sources.Total actual research spending, growth rates, and type of research with inflation adjustment.Biomedical research funding increased from 37.1 billion dollars in 1994 to 94.3 billion dollars in 2003 and doubled when adjusted for inflation. Principal research sponsors in 2003 were industry (57%) and the National Institutes of Health (28%). Relative proportions from all public and private sources did not change. Industry sponsorship of clinical trials increased from 4.0 dollars to 14.2 billion dollars (in real terms) while federal proportions devoted to basic and applied research were unchanged. The United States spent an estimated 5.6% of its total health expenditures on biomedical research, more than any other country, but less than 0.1% for health services research. From an economic perspective, biotechnology and medical device companies were most productive, as measured by new diagnostic and therapeutic devices per dollar of research and development cost. Productivity declined for new pharmaceuticals.Enhancing research productivity and evaluation of benefit are pressing challenges, requiring (1) more effective translation of basic scientific knowledge to clinical application; (2) critical appraisal of rapidly moving scientific areas to guide investment where clinical need is greatest, not only where commercial opportunity is currently perceived; and (3) more specific information about sources and uses of research funds than is generally available to allow informed investment decisions. Responsibility falls on industry, government, and foundations to bring these changes about with a longer-term view of research value.
Tumor Suppressor VHL Functions in the Control of Mitotic Fidelity
Authors: Michael P. Hell, Maria Duda, Thomas C. Weber, Holger Moch, Wilhelm Krek
Journal: Cancer Research (2013)

The von Hippel-Lindau (VHL) tumor suppressor protein pVHL is commonly mutated in clear cell renal cell carcinoma (ccRCC) and has been implicated in the control of multiple cellular processes that might be linked to tumor suppression, including promoting proper spindle orientation and chromosomal stability. However, it is unclear whether pVHL exerts these mitotic regulatory functions in vivo as well. Here, we applied ischemic kidney injury to stimulate cell division in otherwise quiescent mouse adult kidneys. We show that in the short term (5.5 days after surgery), Vhl-deficient kidney cells demonstrate both spindle misorientation and aneuploidy. The spindle misorientation phenotype encompassed changes in directed cell division, which may manifest in the development of cystic lesions, whereas the aneuploidy phenotype involved the occurrence of lagging chromosomes but not chromosome bridges, indicative of mitotic checkpoint impairment. Intriguingly, in the long term (4 months after the ischemic insult), Vhl-deficient kidneys displayed a heterogeneous pattern of ccRCC precursor lesions, including cysts, clear cell-type cells, and dysplasia. Together, these data provide direct evidence for a key role of pVHL in mediating oriented cell division and faithful mitotic checkpoint function in the renal epithelium, emphasizing the importance of pVHL as a controller of mitotic fidelity in vivo.