The evolution of democratic peace in animal societies.

A major goal in evolutionary biology is to elucidate common principles that drive human and other animal societies to adopt either a warlike or peaceful nature. One proposed explanation for the variation in aggression between human societies is the democratic peace hypothesis. According to this theory, autocracies are more warlike than democracies because autocratic leaders can pursue fights for private gain. However, autocratic and democratic decision-making processes are not unique to humans and are widely observed across a diverse range of non-human animal societies. We use evolutionary game theory to evaluate whether the logic of democratic peace may apply across taxa; specifically adapting the classic Hawk-Dove model to consider conflict decisions made by groups rather than individuals. We find support for the democratic peace hypothesis without mechanisms involving complex human institutions and discuss how these findings might be relevant to non-human animal societies. We suggest that the degree to which collective decisions are shared may explain variation in the intensity of intergroup conflict in nature.

Leaders of war: modelling the evolution of conflict among heterogeneous groups.

War, in human and animal societies, can be extremely costly but can also offer significant benefits to the victorious group. We might expect groups to go into battle when the potential benefits of victory (V) outweigh the costs of escalated conflict (C); however, V and C are unlikely to be distributed evenly in heterogeneous groups. For example, some leaders who make the decision to go to war may monopolize the benefits at little cost to themselves ('exploitative' leaders). By contrast, other leaders may willingly pay increased costs, above and beyond their share of V ('heroic' leaders). We investigated conflict initiation and conflict participation in an ecological model where single-leader-multiple-follower groups came into conflict over natural resources. We found that small group size, low migration rate and frequent interaction between groups increased intergroup competition and the evolution of 'exploitative' leadership, while converse patterns favoured increased intragroup competition and the emergence of 'heroic' leaders. We also found evidence of an alternative leader/follower 'shared effort' outcome. Parameters that favoured high contributing 'heroic' leaders, and low contributing followers, facilitated transitions to more peaceful outcomes. We outline and discuss the key testable predictions of our model for empiricists studying intergroup conflict in humans and animals. This article is part of the theme issue 'Intergroup conflict across taxa'.

Cannulated screw versus Kirschner-wire fixation for Milch II lateral condyle fractures in a paediatric sawbone model: a biomechanical comparison.

PURPOSE: Lateral condyle fractures of the humerus are common in the paediatric population, accounting for up to 20% of elbow fractures. Traditional management involves internal fixation with Kirschner (K)-wires, however, this has been associated with complications and insufficiently rigid fixation. Recently, cannulated screws have been proposed as a more stable method of fixation. While cannulated screws have been thought to allow earlier range of movement and shorten time to union, data regarding the biomechanical performance and optimal screw placement is scarce. We hypothesize that cannulated screw fixation is superior to K-wire fixation and screw placement can enhance the stability of the construct. METHODS: Paediatric humerus sawbones with Milch II fractures were fixed with one of three methods. Fractures were reduced with either a single cannulated screw either through the centre of the capitellum (oblique), or placed up the lateral column across the growth plate (lateral), or fixed with two K-wires. Fixed sawbone fractures were then mechanically tested in two directions simulating in vivo forces. RESULTS: The lateral screw construct had a higher maximum force to failure, higher stiffness and absorbed higher energy as compared with the K-wire fixation and oblique screw under an anterior force. When loaded from the posterior direction, only the lateral column screw was better than K-wire fixation. CONCLUSIONS: Screw fixation is a biomechanically effective alternative to K-wire fixation, especially when placed up the lateral column of the distal humerus. Further clinical studies are required before transcapitellar screw fixation can be adopted.

Mortality risk and social network position in resident killer whales: sex differences and the importance of resource abundance.

An individual's ecological environment affects their mortality risk, which in turn has fundamental consequences for life-history evolution. In many species, social relationships are likely to be an important component of an individual's environment, and therefore their mortality risk. Here, we examine the relationship between social position and mortality risk in resident killer whales (Orcinus orca) using over three decades of social and demographic data. We find that the social position of male, but not female, killer whales in their social unit predicts their mortality risk. More socially integrated males have a significantly lower risk of mortality than socially peripheral males, particularly in years of low prey abundance, suggesting that social position mediates access to resources. Male killer whales are larger and require more resources than females, increasing their vulnerability to starvation in years of low salmon abundance. More socially integrated males are likely to have better access to social information and food-sharing opportunities which may enhance their survival in years of low salmon abundance. Our results show that observable variation in the social environment is linked to variation in mortality risk, and highlight how sex differences in social effects on survival may be linked to sex differences in life-history evolution.

Platelet activating factor-induced apoptosis is inhibited by ectopic expression of the platelet activating factor G-protein coupled receptor.

The pro-inflammatory lipid mediator platelet activating factor (PAF: 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) accumulates in ischemia, epilepsy, and human immunodeficiency virus-1-associated dementia and is implicated in neuronal loss. The present study was undertaken to establish a role for its G-protein coupled receptor in regulating neurotoxicity. PC12 cells do not express PAF receptor mRNA as demonstrated by northern analysis and RT-PCR. In the absence of the G-protein coupled receptor, PAF (0.1-1 micro m) triggered chromatin condensation, DNA strand breaks, oligonucleosomal fragmentation, and nuclear disintegration characteristic of apoptosis. Lyso-PAF (0.001-1 micro m), the immediate metabolite of PAF, did not elicit apoptotic death. Concentrations of PAF or lyso-PAF that exceeded critical micelle concentration had physicochemical effects on plasma membrane resulting in necrosis. Apoptosis but not necrosis was inhibited by the PAF antagonist BN52021 (1-100 micro m) but not CV3988 (0.2-20 micro m). Ectopic PAF receptor expression protected PC12 transfectants from ligand-induced apoptosis. PAF receptor-mediated protection was inhibited by CV3988 (1 micro m). These data provide empirical evidence that: (i) PAF can initiate apoptosis independently of its G-protein coupled receptor; (ii) PAF signaling initiated by its G-protein coupled receptor is cytoprotective to PC12 cells; (iii) the pro- and anti-apoptotic effects of PAF on PC12 cells can be pharmacologically distinguished using two different PAF antagonists.

Acquired resistance to Ah receptor agonists in a population of Atlantic killifish (Fundulus heteroclitus) inhabiting a marine superfund site: in vivo and in vitro studies on the inducibility of xenobiotic metabolizing enzymes.

New Bedford Harbor (NBH), MA, is a federal Superfund site that is heavily contaminated with polychlorinated biphenyls (PCBs) and other halogenated aromatic hydrocarbons (HAHs), including some potent aryl hydrocarbon receptor (AhR) agonists. A population of Atlantic killifish (Fundulus heteroclitus) continues to inhabit this site, despite accumulating extraordinarily high concentrations of PCBs (272 microg/g dry weight). To determine if NBH killifish have developed resistance to HAHs that act through the AhR, we examined the inducibility of cytochrome P4501A1 (CYP1A1), UDP glucuronosyl transferase (UGT), and glutathione S-transferase (GST) in fish from NBH and a reference site, Scorton Creek (SC, Cape Cod, MA; PCB concentrations 0.177 microg/g dry weight). 2,3,7,8-Tetrachlorodibenzofuran (TCDF) induced CYP1A1 mRNA, protein, and activity in SC fish in all tissues examined (liver, heart, gut, gill, kidney, spleen, and gonad). In contrast, NBH fish expressed low levels of CYP1A1 and showed no induction of CYP1A1 mRNA, protein, or activity by TCDF, or induction that was lower in magnitude or required higher doses of inducer. p-Nitrophenol UGT activity was not induced by TCDF in either population, while GST activity with 1-chloro-2,4-dinitrobenzene as substrate was induced only in NBH fish in one experiment. Inducibility of CYP1A1 by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or beta-naphthoflavone (BNF) was measured in primary hepatocyte cultures prepared from SC and NBH fish. TCDD induced CYP1A1 activity (ethoxyresorufin O-deethylase) to the same degree in hepatocytes from both populations, demonstrating the functionality of the AhR signaling pathway in NBH fish. However, hepatocytes from NBH fish were 14-fold less sensitive to TCDD than were those from SC fish. The nonhalogenated AhR agonist BNF also induced CYP1A1 in cells from both populations, although with only a 3-fold difference in sensitivity (NBH < SC). These results indicate that chronic exposure to high levels of HAHs has led to a reduction in the sensitivity of NBH killifish to AhR agonists. The resistance is systemic and pretranslational, and exhibits compound-specific differences in magnitude. These findings suggest an alteration in the AhR signal transduction pathway in NBH fish.

Characterization of prostaglandin endoperoxide H synthase-1 enzyme expression during differentiation of the megakaryocytic cell line MEG-01.

OBJECTIVE: Because the prostaglandin endoperoxide H synthase-1 (PGHS-1)-dependent formation of thromboxane A(2) is an important modulator of platelet function, this pathway represents a pharmacologic target for the inhibition of platelet function by aspirin. The objective of our research was to study how PGHS-1 expression is regulated in platelets. MATERIALS AND METHODS: Because platelets are anucleated, their protein content is a consequence of gene expression in precursor cells known as megakaryocytes. We used the immortalized human megakaryoblastic cell line MEG-01 as a model to study the expression of PGHS-1, because MEG-01 cells can be induced to differentiate into platelet-like structures by adding nanomolar concentrations of 12-0-tetradecanoylphorbol-13-acetate (TPA). We determined the expression profiles of PGHS-1 protein and mRNA in the cells comprising the three different populations of MEG-01 cultures: nucleated floating, nucleated attached, and platelet-like structures. RESULTS: We determined that PGHS-1 protein levels were higher in the nucleated adherent population than in the nucleated floating population. PGHS-1 protein levels were greatest in the anucleated platelet-like population. In contrast, we found that PGHS-1 mRNA levels were highest in the cells that comprised the nucleated adherent population. Addition of TPA induced the expression of PGHS-1 protein and mRNA in all three populations but did not change the relationship of the amount of PGHS-1 protein or mRNA expressed in a given population relative to the other two fractions. We measured the expression of PGHS-1 protein on a cell-by-cell basis in the nucleated MEG-01 populations. We found that the percentage of MEG-01 cells expressing PGHS-1 protein in the adherent population was greater than in the floating population. We measured a time-dependent increase in the percentage of cells that expressed PGHS-1 over a period of 8 days after singular addition of TPA (1.6x10(-8)M). Importantly, we observed that TPA treatment stimulated floating MEG-01 to adhere to the surface of the tissue culture vessel and that, after such treatment, only floating MEG-01 cells suffered a compromised viability. We found that a high percentage of control cells expressed glycoprotein IIb/IIIa and that TPA treatment did not significantly alter this percentage. We did not detect glycoprotein Ib in control cells but did measure a slight increase in the percentage of MEG-01 cells that expressed this antigen in the TPA-treated population. CONCLUSION: We established a correlation between the level of PGHS-1 expression and the overall level of differentiation of MEG-01 cells. PGHS-1 protein expression, which increases consistently over the full course of differentiation, now may be used as an additional and perhaps better index by which to survey megakaryocytes.

The presence of an unusual PKC isozyme profile in rat liver cells.

We have previously shown that protein kinase C (PKC) is involved in the mitogenic response of T51B cells to epidermal growth factor. In fact, epidermal growth factor was an excellent mitogen, even after prolonged pretreatment of cells with TPA, suggesting that the PKC isoform implicated in proliferation is not down-regulated by 12-O-tetradecanoyl phorbol-13-acetate (TPA). We have now determined that the PKC isozymes -alpha, -beta, -delta, -epsilon, and -zeta are present in T51B cells. All five isoforms are associated with the plasma membrane and the cytoplasm and are either in or around the nucleus. PKC-beta I has a slightly different subcellular profile from that of the other isoforms in that it is clearly and strongly associated with the nuclear membrane. Also, a unique and novel pattern is obtained from immunoblots with anti-PKC-beta I. PKC-beta I is detected as a single band of 70 kDa in the cytosolic fraction and as a doublet of 65 and 77 kDa in the membrane fraction. PKC-alpha, -delta, and -epsilon were down-regulated by pretreatment of cells with TPA, while PKC-zeta was unaffected. Of particular interest was the fact that TPA did not down-regulate PKC-beta I. In fact, the amount of this isoform associated with the plasma membrane increased. These findings indicate that it is probably PKC-beta I that is involved in the mitogenic response of T51B cells to epidermal growth factor. Since PKC-zeta is also not down-regulated by TPA, the possible involvement of this isoform needs to be resolved.

Estimation of total collagen and types I and III collagen in canine rotator cuff tendons.

The collagen composition of the supraspinatus, infraspinatus, and subscapularis tendons, which form part of the rotator cuff of the shoulder, was determined. Tendons were obtained from adult, male beagle dogs and total collagen was estimated by measurement of hydroxyproline. There was little variation in collagen content among the three major cuff tendons and the quantity approximated that cited in the literature for other tendons. However, the collagen content in the insertion zone of the supraspinatus tendon was significantly higher than in the tendon proper. NaCl fractionation of supraspinatus collagen indicated that type I was the predominant collagen but significant amounts of type III and possibly some type II and type V were also present. Interestingly, there appeared to be more type III collagen in the insertion zone than in the tendon proper, cyanogen bromide digestion and peptide mapping confirmed this finding. The differential collagen composition of the supraspinatus tendon may contribute to the high incidence of tear that is associated with this rotator cuff tendon.

Evolutionary relationships of cultivated psychrophilic and barophilic deep-sea bacteria.

Evolutionary relationships of cultivated barophilic bacteria were determined. All psychrophilic and barophilic isolates were affiliated with one of five genera of the gamma subdivision of the class Proteobacteria ((gamma)-Proteobacteria): Shewanella, Photobacterium, Colwellia, Moritella, and a new group containing strain CNPT3. The data indicate that the barophilic phenotype has evolved independently in different (gamma)-Proteobacteria genera.

Case recognition and interview utterances: effect of GHQ feedback.

Eighty-four audiotaped clinical interviews of seven general practitioners (GPs) with high scoring patients on the General Health Questionnaire (GHQ-28) were analysed at baseline and compared with a similar number at feedback during which doctors were presented with the GHQ-28 scores of their patients. At feedback, there was a significant reduction in the use of physical utterances (deviance 35.150, df 1, P < 0.001), an increase in the use of directive questions, a reduction in closed questions, and more advice and more psychological utterances were made. The five doctors who improved had a mean rise in identification index (ID) of 0.25 +/- 0.12. Such benefit was more apparent among doctors with lower IDs at baseline. There was no significant correlation in the magnitude of rise in ID and change in psychological utterances. Most doctors were not aware of the impact of the GHQ on their interview technique and case recognition ability.

Asymmetrical role-taking: comparing battered and nonbattered women.

Franks's social psychological model of oppressive situations and asymmetric role-taking offers a new way of understanding the predicaments faced by battered women. Unlike individualistic or single-factor explanations, the model suggests that women faced with a particular combination of situational pressures and relationship inequities are especially vulnerable to distressful emotions and self-esteem difficulties. Survey data from 66 battered women using domestic violence services and 80 nonbattered women were collected to test the major propositions of the model. Battered women's social situations were oppressive and characterized by powerlessness, social isolation, and economic dependency. Batterers were poor empathizers. Predictions about self-blame and identification with the aggressor were not confirmed. The practical value of this theoretical approach with its emphasis on enhancing women's power base and increasing men's interpersonal sensitivity is developed.

Modifications in cytokeratin and actin in cultured liver cells derived from griseofulvin-fed mice.

BACKGROUND: Hepatocytes from mice fed griseofulvin (GF) for 8 months form Mallory bodies (MBs), which represent a pathologic state of intermediate filaments (IFs). The cellular mechanisms that lead to MB formation are not known. EXPERIMENTAL DESIGN: This study was aimed to investigate if MB formation could be related to modification in cytokeratin (CK) metabolism. Primary cultures of hepatocytes from control and GF livers were studied. Immunofluorescence microscopy was used to study the organization of the cytoskeleton in these cells. The hepatocytes were labeled with [35S]methionine or [32P]orthophosphate to study, respectively, the level of amino acid incorporation into IF proteins (CK 8 and CK 18) and their phosphorylation levels. The response to the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate stimulation of the phosphorylation of CK 8 and CK 18 was also elicited in contrast to control hepatocytes. RESULTS: We found that there was a change in the organization of actin and the IF network in the hepatocytes from GF-treated animals. This was associated with an increase in labeled amino acid incorporation into CK 8 and CK 18 as well as in actin. Although there was no significant difference in the absolute level of CK phosphorylation, we found modifications in the phosphorylated isomers of CK 8, the more phosphorylated isomers becoming more prominent. The treatment of the hepatocytes with 12-O-tetradecanoyl-phorbol-13-acetate did not induce changes in the level of CK phosphorylation in GF-pretreated hepatocytes. CONCLUSIONS: These results suggest that the modification of the IF network and MB formation are the consequences of increased CK synthesis and the modification of phosphorylation. They could alter the normal interaction of the IFs with different cellular components, which results in conformational changes of CKs and the reorganization of the IF network to the form of MBs.

Long-term exposure to epidermal growth factor results in apoptosis in T51B cells.

The major objective of this research was the development of an in vitro model for liver homeostasis that would allow the future study of early events in cell proliferation and cell death. The model that was set up involves growing T51B rat liver epithelial cells with a single dose of 1 nM epidermal growth factor (EGF). This results in a period of hyperplasia where the cells reach double the control cell numbers 2 days after EGF addition. This is then followed by a decrease in cell numbers and the cell density returns to around the confluent control level 5 days after EGF addition. The model was investigated to ascertain whether the decrease in cell numbers 3-5 days after EGF addition was due to an increase in apoptosis. The results from light and electron microscopy studies, electrophoresis of T51B cell DNA, and quantification of nuclear fragmentation indicated that the cells do die via an increase in apoptosis. The electron microscopy studies also show that healthy T51B cells can phagocytose apoptotic bodies. This suggests that the model is more physiological than other in vitro models of apoptosis. This work describes the development and characterization an in vitro model of liver homeostasis that closely parallels in vivo systems where animals are given mitogenic stimuli.

The epidermal growth factor mitogenic signal is modulated by protein kinase C in T51B rat liver cells.

The regulation of cell proliferation involves a complex interplay between several signal transduction pathways. The effect of EGF on DNA synthesis in serum starved quiescent, synchronized T51B cells was investigated by [3H]thymidine incorporation and flow cytometry. 1 nM EGF or readdition of serum initiated G1 progression and entry into S phase by 18 h and DNA synthesis reached a maximum by 28 h. Low concentrations of EGF markedly stimulated DNA synthesis, but EGF was not as potent as readdition of serum. The effect of EGF on DNA synthesis was only partially blocked by the tyrosine inhibitors genistein and tyrphostin, suggesting that other signalling pathways play a role in EGF-stimulated mitogenesis. 1 nM EGF caused a rapid, transient increase in the activity of membrane-associated protein kinase C (PKC) followed by a longer sustained increase that continued into S phase. TPA (12-O-tetradecanoyl-phorbol-13-acetate) did not mimic EGF, rather it caused a slight stimulation of membrane-associated PKC activity within 1 h followed by a dramatic downregulation of PKC within 4 h. TPA was without effect on DNA synthesis alone, but when added along with EGF or serum TPA caused a significant enhancement of DNA synthesis. Pretreatment of quiescent, serum-deprived T51B cells with TPA reduced the basal level of DNA synthesis; however, under these conditions EGF became as potent a mitogen as serum. We hypothesize that EGF via activation of PKC regulates the activity of its receptor by switching from high affinity to low affinity states. Downregulation of PKC by long term treatment with TPA removes this regulation thus rendering T15B cells more sensitive to exogenous EGF.