Collateral Segments Research Articles

The Assessment of Blood Flow Velocities in Retinal Collaterals in Diabetic Retinopathy.

Diabetic retinopathy (DR) is a microvascular disease characterized by capillary dropout and resultant retinal ischemia which then leads to retinal vascular remodeling. Our goal was to assess blood flow velocities in retinal collateral vessels in healthy and diabetic subjects with various stages of DR. In our pilot study, we enrolled five eyes of five healthy subjects (H), five eyes of four subjects with diabetes and no retinopathy (DM), three eyes of three subjects with mild non-proliferative diabetic retinopathy (MDR), and five eyes of four subjects with proliferative diabetic retinopathy (PDR). Following routine ophthalmic examination, all subjects were imaged using a retinal function imager (RFI; Optical Imaging Inc., Rehovot, Israel). The built-in software of the RFI was used to identify and segment retinal collaterals with measurement of the blood flow velocities (BFV). One-way ANOVA was performed for BFV, followed by Newman-Keuls post hoc test. The level of significance was set at 5%. The total number of collateral segments involved in the study was 30, 31, 21, and 39 in the H, DM, MDR, and PDR groups, respectively. The BFVs in the collaterals were significantly lower in PDR (H: 1.86 ± 0.67, DM: 1.91 ± 0.71, MDR: 1.71 ± 0.53, PDR: 1.37 ± 0.58 mm/s). The PDR group showed a statistically significant difference in the comparisons to all groups (p = 0.012, p = 0.008, and p = 0.043 for the H, DM, and MDR groups, respectively), while no other comparisons between the groups were significant. We observed decreased BFV in retinal collaterals in PDR that may be due to the extensive capillary dropout and retinal ischemia. Further studies are needed for the noninvasive functional assessment of retinal microvascular changes in DR to better understand the underlying pathophysiology.

DNA Methyltransferase 1-Dependent DNA Hypermethylation Constrains Arteriogenesis by Augmenting Shear Stress Set Point.

BackgroundArteriogenesis is initiated by increased shear stress and is thought to continue until shear stress is returned to its original “set point.” However, the molecular mechanism(s) through which shear stress set point is established by endothelial cells (ECs) are largely unstudied. Here, we tested the hypothesis that DNA methyltransferase 1 (DNMT1)–dependent EC DNA methylation affects arteriogenic capacity via adjustments to shear stress set point.Methods and ResultsIn femoral artery ligation–operated C57BL/6 mice, collateral artery segments exposed to increased shear stress without a change in flow direction (ie, nonreversed flow) exhibited global DNA hypermethylation (increased 5‐methylcytosine staining intensity) and constrained arteriogenesis (30% less diameter growth) when compared with segments exposed to both an increase in shear stress and reversed‐flow direction. In vitro, ECs exposed to a flow waveform biomimetic of nonreversed collateral segments in vivo exhibited a 40% increase in DNMT1 expression, genome‐wide hypermethylation of gene promoters, and a DNMT1‐dependent 60% reduction in proarteriogenic monocyte adhesion compared with ECs exposed to a biomimetic reversed‐flow waveform. These results led us to test whether DNMT1 regulates arteriogenic capacity in vivo. In femoral artery ligation–operated mice, DNMT1 inhibition rescued arteriogenic capacity and returned shear stress back to its original set point in nonreversed collateral segments.ConclusionsIncreased shear stress without a change in flow direction initiates arteriogenic growth; however, it also elicits DNMT1‐dependent EC DNA hypermethylation. In turn, this diminishes mechanosensing, augments shear stress set point, and constrains the ultimate arteriogenic capacity of the vessel. This epigenetic effect could impact both endogenous collateralization and treatment of arterial occlusive diseases.

Abstract 571: Non-reversed Increase In Shear Stress Magnitude Enhances Global Endothelial Cell Dna Methylation And Limits Extent of Collateral Artery Growth Following Femoral Arterial Ligation

Femoral artery ligation (FAL) in the mouse leads to increased flow across all collateral arteries with some collateral segments experiencing increased flow and reversed flow direction. We have recently shown that these “reversed flow” segments exhibit remarkably permanent, amplified arteriogenesis compared to those exposed to “non-reversed” flow. As the role of epigenetics in arteriogenesis remains unknown, we sought to determine the effect of biomimetic shear stress waveforms on DNA methylation and DNA methyltransferase 1 (DNMT1) expression in endothelial cells. Next generation sequencing of bisulfite converted genomic DNA was used to generate global DNA methylation profiles of ECs exposed to shear stress waveforms biomimetic of our “reversed” and “non-reversed” conditions. We found that the “non-reversed” waveform increased gene promoter hypermethylation in-vitro. Furthermore, DNMT1 mRNA expression was increased 1.25-fold in non-reversed conditions compared to reversed conditions as determined by RT-PCR (p≤0.05, n=8). We then tested the hypothesis that increased DNMT1 expression and subsequent DNA hypermethylation, elicited by a “non-reversed” flow waveform, limits steady state, long-term arteriogenic capacity in-vivo. Whole mount vascular casting was used to determine the lumenal diameter of both reversed and non-reversed collateral artery segments from mice treated with 5-AZA, a preferential inhibitor of DNMT1, or vehicle control 14 days post-FAL for an additional 14 days. We found that lumenal diameter was significantly enhanced in non-reversed collateral segments of 5-AZA treated mice (70.9±7.9μm vs. 50.1±3.4μm, p≤0.05, n=6) while there was no difference in reversed segments. Together, we conclude that a non-reversed, increased shear stress magnitude results in a rapid increase DNMT1 expression and DNA hypermethylation, limiting the extent of arteriogenesis in non-reversed collateral artery segments of the mouse gracilis muscle. However, inhibition of DNMT1 with 5-AZA enables for enhanced collateral growth. Further interrogation of the central relationships between hemodynamics, epigenetics, and collateral artery growth may lead to durable therapeutic options for arterial occlusive diseases.

Abstract 572: Inhibition of MicroRNA-199a-5p Enhances Perfusion Recovery and Arteriogenesis Following Femoral Arterial Ligation

We have recently reported that a subset of collateral artery segments in the mouse hindlimb are exposed to both a 2-fold increase in shear stress magnitude and reversed flow direction (“reversed” flow) following femoral arterial ligation (FAL). These segments experiencing a reversed flow subsequently undergo a disproportionate amplification of collateral growth (i.e. arteriogenesis) after FAL. Interestingly, a subset of microRNAs, including miR-199a-5p, are significantly down-regulated in endothelial cells exposed to a shear stress waveform biomimetic of this pro-arteriogenic “reversed flow” condition in-vitro. Here, we hypothesized that the inhibition of miR-199a-5p would lead to enhanced arteriogenesis and/or perfusion recovery following arterial occlusion. To test this hypothesis, Balb/c mice were treated with either anti-miR-199a-5p or non-targeting control locked-nucleic acid (LNA) immediately following FAL. Treatment efficacy was determined via RT-PCR for expression of miR-199a-5p and its downstream targets’ expression. Laser Doppler perfusion imaging and both whole mount and cross-sectional analysis of vascular casted gracilis muscles were used to assess vascular remodeling. We found that anti-miR-199a-5p LNA markedly reduced miR-199a-5p expression in the gracilis muscle by over 80%, 7 days post-FAL (n=4). By day 21 post-FAL, perfusion recovery was significantly improved in anti-miR-199a-5p treated mice (101.5±1.8% vs. 87.8±1.8%, p≤0.05, n=6). Moreover, both lumenal diameter (106.5±7.2μm vs. 78.4±2.9 μm, p≤0.0001, n=6) and wall area (1770±147μm 2 vs. 1163±41μm 2 , p≤0.0001, n=6) were significantly enhanced in anti-miR-199a-5p treated mice compared to controls. We therefore conclude that the inhibition of miR-199a-5p leads to enhanced perfusion recovery and arteriogenesis following arterial occlusion and could represent a novel strategy for therapeutic arteriogenesis.

Mechanisms of Amplified Arteriogenesis in Collateral Artery Segments Exposed to Reversed Flow Direction.

Collateral arteriogenesis, the growth of existing arterial vessels to a larger diameter, is a fundamental adaptive response that is often critical for the perfusion and survival of tissues downstream of chronic arterial occlusion(s). Shear stress regulates arteriogenesis; however, the arteriogenic significance of reversed flow direction, occurring in numerous collateral artery segments after femoral artery ligation, is unknown. Our objective was to determine if reversed flow direction in collateral artery segments differentially regulates endothelial cell signaling and arteriogenesis. Collateral segments experiencing reversed flow direction after femoral artery ligation in C57BL/6 mice exhibit increased pericollateral macrophage recruitment, amplified arteriogenesis (30% diameter and 2.8-fold conductance increases), and remarkably permanent (12 weeks post femoral artery ligation) remodeling. Genome-wide transcriptional analyses on human umbilical vein endothelial cells exposed to reversed flow conditions mimicking those occurring in vivo yielded 10-fold more significantly regulated transcripts, as well as enhanced activation of upstream regulators (nuclear factor κB [NFκB], vascular endothelial growth factor, fibroblast growth factor-2, and transforming growth factor-β) and arteriogenic canonical pathways (protein kinase A, phosphodiesterase, and mitogen-activated protein kinase). Augmented expression of key proarteriogenic molecules (Kruppel-like factor 2 [KLF2], intercellular adhesion molecule 1, and endothelial nitric oxide synthase) was also verified by quantitative real-time polymerase chain reaction, leading us to test whether intercellular adhesion molecule 1 or endothelial nitric oxide synthase regulate amplified arteriogenesis in flow-reversed collateral segments in vivo. Interestingly, enhanced pericollateral macrophage recruitment and amplified arteriogenesis was attenuated in flow-reversed collateral segments after femoral artery ligation in intercellular adhesion molecule 1(-/-) mice; however, endothelial nitric oxide synthase(-/-) mice showed no such differences. Reversed flow leads to a broad amplification of proarteriogenic endothelial signaling and a sustained intercellular adhesion molecule 1-dependent augmentation of arteriogenesis. Further investigation of the endothelial mechanotransduction pathways activated by reversed flow may lead to more effective and durable therapeutic options for arterial occlusive diseases.

Reversal of flow direction enhances endothelial cell arteriogenic signaling (670.9)

The key initiating stimulus for arteriogenesis in the presence of an arterial occlusion is altered shear stress along collateral arterial pathways that bypass the occlusion. Femoral artery occlusion in the mouse leads to increased flow across all collateral arteries with some collateral segments also experiencing a reversal of flow direction. We have recently shown that these “flow reversed” segments exhibited a 4‐fold increase in leukocyte recruitment and demonstrated enhanced arteriogenesis in the gracilis collateral network. To test if endothelial cell sensitivity to the flow‐direction change was a key element of the enhanced arteriogenesis, we applied the measured the in vivo hemodynamic changes of the gracilis collateral network to cultured human umbilical vein endothelial cells (HUVECs) and performed genome‐wide transcriptional profiling and pathways analysis. Endothelial cells demonstrated a 10‐fold greater number of genes sensitive to the additional flow‐reversal stimulus, as well as a broad amplification of the gene expression patterns of cells only exposed to an increase in shear stress magnitude. Further, the addition of flow‐reversal activated many of the signaling pathways known to be key mediators of collateral growth (e.g. p38 MAPK, VEGF, HGF, PKC, and NF‐κB) when compared to steady shear stress control. These were not activated with increased shear stress alone. Microarray results were further validated by RT‐PCR of a subset of known pro‐arteriogenic genes (KLF2, eNOS, and ICAM‐1) which demonstrated an increased expression with flow reversal. These results are consistent with an increase in shear stress alone as insufficient to fully achieve the maximal activation of the arteriogenic pathway. Incorporation of directional reversal may, therefore, provide a more physiological stimulus for interrogating the central pathways that drive arteriogenesis thus leading toward novel, more effective therapeutic options.Grant Funding Source: Supported by NIH 5R01HL074082, NIH1R21HL098632, AHA 09PRE2060385 AHA 10GRNT3490001, NSF GRFP DGE‐131

Innate collateral vessels in the absence of ischemia undergo shear stress similar to normal arterial segments of the same diameter (1079.12)

Some species, including humans, have structural collateral vessels, CV, that can further develop in the presence of coronary stenosis by increasing pressure difference across them. Question is how CV's are maintained in the absence of ischemia.The coronary network of 6 healthy canine hearts was reconstructed in 3D from images obtained with an imaging cryomicrotome after filling with fluorescent replica material (resolution 0.020 mm). CV's were automatically detected. The full coronary network was reconstructed. For all segments, including CV's, diameter and perfused tissue mass, PTM, was derived and shear stress, SS, calculated.Innate collateral connections ranged from 286 to 1015 µm in diameter and were distributed over the myocardial wall with some higher density at the subendocardium: density 2.5 ‐ 5.0 per gram tissue. Highly correlating fractal relations were found between PTM and diameter for normal tree segments and for CV's which fully overlapped. SS in the CV's was equal to neighboring tree segments of similar diameter.Results indicate that collateral segments have the same function in distributing blood, and do so at the same SS, as normal tree segments. Hence, functionally CV's are not different from normal vascular segments and are therefore maintained. CV's form substrate for collateral growth in ischemia.Grant Funding Source: FP7‐ICT‐2007‐224495: euHeart

Innate collateral segments are predominantly present in the subendocardium without preferential connectivity within the left ventricular wall

Functional collateral vessels often stem from outward remodelling of pre-existing connections between perfusion territories. Knowledge of the distribution and morphology of innate collateral connections may help in identifying myocardial areas with protection against risk for ischaemia. The coronary network of six healthy canine hearts was investigated with an imaging cryomicrotome. Innate collateral connections ranged from 286 to 1015 μm in diameter. Left ventricular collateral density (number per gram of tissue) was about five in the subendocardium vs. 2.5 in the mid-myocardium (P < 0.01) and 1.3 in the epicardium (P < 0.01). Subendocardial collateral connections were oriented parallel to the long axis of the heart. For the major coronary arteries, five times more intracoronary than intercoronary connections were found, while their median diameter and interquartile range were not significantly different, at 96.1 (16.9) vs. 94.7 (18.9) μm. Collateral vessels connecting crowns from sister branches from a stem are denoted intercrown connections and those within crowns intracrown connections. The number of intercrown connections was related to the mean tissue weight of the crowns (y = 0.73x - 0.33, r2 = 0.85, P < 0.0001). This relation was likewise found to describe intercoronary connections. The median collateral diameter and length were independent of the tissue volumes bridged. We conclude that connectivity and morphology of the innate collateral network are distributed with no preference for intra- or intercrown connections, independent of stem diameter, including epicardial arteries. This renders all sites of the myocardium equally protected in case of coronary artery disease. The orientation of subendocardial collateral vessels indicates the longitudinal direction of subendocardial collateral flow.

Shear stress reversal amplifies arteriogenesis in the mouse ischemic hindlimb model and augments a pro‐arteriogenic ICAM‐1hi/KLF2hi endothelial phenotype

Femoral artery occlusion in the mouse leads to increased flow across all collateral arteries with some collateral segments also experiencing a reversal of flow direction. We have recently shown that these “flow reversal” segments exhibit an amplified arteriogenesis response (i.e. 22% and 33% diameter increases in “flow reversed” over “non‐reversed” segments by days 3 and 7, respectively) and a 4‐fold increase in pericollateral CD45+cells (day 3). Thus, we hypothesize that these “flow reversed” collateral segments could provide clues for how to amplify arteriogenesis therapeutically. To this end, we studied the expression of markers of a pro‐arteriogenic endothelial phenotype in response to an in vitro shear stress protocol mimicking the in vivo hemodynamics. We observed rapid endothelial cell repolarization and 30% increases in KLF2 (regulator of pro‐arteriogenic eNOS), eNOS, and ICAM‐1 (pro‐arteriogenic regulator of monocyte adhesion) mRNA expression in reversed conditions compared to non‐reversed. These results are consistent with the hypothesis that, when coupled with increased shear stress magnitude, the reversal of shear stress direction leads to enhanced arteriogenesis by activating KLF2 and ICAM‐1. Sources of research support: NIH HL098632 and AHA10GRNT3490001.

Accelerated Arteriogenesis In Collateral Arterial Segments Exposed To Flow Reversal After Femoral Arterial Ligation

Elevated fluid shear stress is known to be a key stimulus for driving arteriogenesis; however, the role that flow‐reversal (FR) plays in arteriogenesis is largely unknown. We hypothesized that FR in spatially distinct regions of collateral arteries (CAs) can lead to spatially distinct variations in CA growth.METHODSUnilateral femoral artery ligation (FAL) was performed in C57Bl6 mice. Gracilis muscles were harvested at 1, 7, 14, and 28 days after FAL and immunolabeled for smooth muscle α‐actin to visualize CAs. As determined by intravital microscopy, FAL increased flow across the length of the primary gracilis CAs with distinct regions of flow reversal (FR) and non‐flow reversal (NFR).RESULTSBoth FR and NFR CA segments showed significant growth as compared to the unligated (control) leg arterial diameters at days 7, 14, and 28 (p&lt;0.001). However, CA regions experiencing FR showed significantly greater expansion of lumenal diameter (arteriogenesis) compared to the NFR regions at days 7 and 14 (p&lt;0.005). This increase became non‐significant by day 28. At day 7, CD45+ leukocyte density was significantly greater around FR CA segments as compared to NFR segments (6.3±3.9 versus 3.9±2.1 CD45+ cells/collaterals, p&lt;0.05, respectively). Further, pericollateral CD45+ cell density significantly correlated with CA diameter in ligated (R2=0.41, p&lt;0.05), but not in unligated CAs (R2=0.0024, p=0.64).CONCLUSIONSThese data suggest that there are spatial variations in CA growth, CD45+ cell recruitment, and changes in hemodynamics along the length of a given CA after FAL. Together, our data suggest differences in mechanotransduction along a CA lead to differentialgrowth, with increased leukocyte accumulation as a potential mechanism. Supported by NIH HL074082, NIH R21HL098632, AHA 09PRE2060385, AHA 10GRNT3490001.

High‐resolution spatial quantification of canine coronary collaterals in endo‐ and epicardial layers

Ischemia and subsequent infarction may occur when blood supply to the heart is impeded by coronary artery disease. Stimulating coronary collateral formation may provide a therapeutic option in patients that cannot be successfully revascularized by conventional surgery. However, detailed information on the mechanism of collateral formation is needed.In this study an imaging cryomicrotome was used to acquire high resolution data of collateral connections. Coronary arteries in 5 canine hearts were prepared with fluorescent cast material and cut serially at 20μm slices. After each cut, the surface of the remaining material was imaged. Skeletonization of the 3D vasculature allowed defining connectivity and collateral connection identification. On average, 800 collaterals were identified for each heart, diameters ranging from 40 – 200 μm. The number of collaterals was approximately twofold higher in the endocardium compared to the epicardium, even though the measured volume of the endocardium was on average 2.5 times smaller than the epicardial volume. The diameter and length distributions of the collateral segments appeared equal for the two myocardial layers. These characteristics may provide a better understanding of the mechanisms of collateral formation. Supported by the Netherlands Organization for Health Research and Development (ZonMw 91105008and 91611171), and by FP7‐ICT 2007224495 (euHeart).

Animal models of arteriogenesis

Arteriogenesis is the process of growth of collateral arteries after the stenosis of a feeding artery. The mechanism varies among species. In dogs, occlusion of a coronary artery leads to the growth of muscular vessels, whereas in pigs only capillary vessels grow. Ligation of rabbit and mouse femoral arteries induce collateral artery growth in non‐ischemic areas. The vascular response is restricted to collateral segments and collateral ending branches remain quiescent. Collateral neo‐formation is a rare event. Leukocyte recruitment and vascular proliferation dominate the process in both species, but only rabbit collateral arteries develop a neo‐intima layer. Two experimental models illustrate the crucial roles of leukocytes and shear stress in arteriogenesis: Infusion of the leukocyte chemoattractant protein MCP‐1, and surgical creation of an arterio‐venous shunt, both after femoral ligation result in an exacerbated development of collateral arteries. In a hamster model of Bland‐White‐Garland syndrome (origin of the left coronary artery from the pulmonary artery), collateral arteries connecting the right and left coronary arteries appear spontaneously, creating a left‐to‐right shunt that allows perfusion of the left heart. This model supports the idea that shear stress regulates not only the growth, but also de formation of new collateral arteries during the postnatal life.

Axons in cat visual cortex are topologically self-similar.

The axonal arbors of the different types of neocortical and thalamic neurons appear highly dissimilar when viewed in conventional 2D reconstructions. Nevertheless, we have found that their one-dimensional metrics and topologies are surprisingly similar. To discover this, we analysed the axonal branching pattern of 39 neurons (23 spiny, 13 smooth and three thalamic axons) that were filled intracellularly with horseradish peroxidase (HRP) during in vivo experiments in cat area 17. The axons were completely reconstructed and translated into dendrograms. Topological, fractal and Horton-Strahler analyses indicated that axons of smooth and spiny neurons had similar complexity, length ratios (a measure of the relative increase in the length of collateral segments as the axon branches) and bifurcation ratios (a measure of the relative increase in the number of collateral segments as the axon branches). We show that a simple random branching model (Galton-Watson process) predicts with reasonable accuracy the bifurcation ratio, length ratio and collateral length distribution of the axonal arbors.

Feedback connections from area MT of the squirrel monkey to areas V1 and V2

Area MT/V5 is reciprocally connected with both V1 and V2; but, despite extensive anatomical and physiological investigations, detailed information on the feedback component of these connections is still not available. The present report uses serial section reconstruction of single axons, labeled by anterograde tracers injected in area MT of squirrel monkeys, to characterize these connections further. As with other feedback systems, MT axons terminating in both areas V1 (n = 9) and V2 (n = 6) are widely divergent. In area V1, MT fields are larger than those from V2 and are about comparable to those from V4 or TEO. Terminations in V1, unlike other feedback connections described so far, terminate in several laminar combinations: only layer 1 (n = 2); only layer 4B (n = 3); layers 1 and 4B (n = 1); and layers 1, 4B, and 6 (n = 3). In V2, they occur mainly in layers 1 and 5 or 6. Terminations have two patterns even within a single axon: strung along collateral segments and grouped within small clusters. There are no apparent differences in the size, shape, or density of terminal specializations in V1 or V2, and, consistently with previous double-labeling experiments (Kennedy and Bullier [1985] J Neurosci 5:2815-2830), some axons can branch to both areas. This result, along with the laminar evidence for subtypes of feedback connections, argues against an exclusively hierarchical organization based on "pairwise" connectivity. For V1 and MT, there may be directly reciprocal loops between feedforward and feedback projecting neurons, but this is less likely to be so for V2 and MT.

Beta-adrenergic receptors on canine coronary collateral vessels: characterization and function

The present studies were performed to examine the role of beta-adrenergic receptors in modulating smooth muscle tone in mature coronary collaterals. To examine the beta-adrenergic receptor population present, radioligand binding-cover slip autoradiographic studies were performed on sections of native canine coronary vessels and sections of coronary collaterals developed after placement of Ameroid constrictors. Specific binding of the nonselective beta-adrenergic antagonist [125I]iodopindolol to vascular smooth muscle in segments of both collaterals and native coronary arteries was saturable and stereospecific. Maximal binding and the potency of beta-adrenergic subtype-selective antagonists were similar in all segments. Beta-adrenergic relaxation of native coronary vessels and collateral vessels were studied in isolated organ chambers after preconstriction with prostaglandin F2 alpha. Both native coronary arteries and collateral segments demonstrated beta-adrenergic-mediated relaxation with affinities for both agonists and antagonists compatible with a mixed population of beta 1- and beta 2-adrenergic receptors. These studies indicate that during development, the new collateral vascular smooth muscle expresses a functional population of beta-adrenergic receptors, comparable to that in native vessels.

Some quantitative results on Golgi impregnated axons in rat visual cortex using a computer assisted video digitizer.

Axonal fiber distributions of pyramidal cells in the visual cortex of the albino rat have been investigated using the rapid Golgi method and modern data collecting techniques. Three dimensional coordinate information was extracted from Golgi-impregnated axonal networks using a computer-assisted video digitizer. Computer programs used this data to generate various statistical distributions. In particular, angular distributions of the initial collateral segments and their endpoints were examined and found to reveal anisotropies. Inspection of the spatial distributions of the endpoints indicated a clustering at two distinct levels with respect to the pyramidal cell from which they originate. Dynamic graphic displays of the three dimensional data have been obtained and presented in the form of computer tracings of various orthogonal projections.

The Gentry of a Traditional Peasant Community Undergoing Rapid Technological Change: An Iranian Case Study

The subject of this paper is a patrilineage that lives in two communities six kilometers apart in the north-eastern part of Iran. Traditionally this lineage together with its collateral sections has acted as a gentry for an area composed of eighteen villages. They were and still are (both the lineage and its collateral segments) referred to as the “landlords” (arbāb) of the area although their traditional economic status and political influence has been undermined by the Iranian land reform of 1962. The number of adults (above the age of fifteen) comprising the lineage is roughly between forty and fifty and is composed of the descendants of three brothers. These three brothers are in turn descended from one of three other brothers in the next ascending generation; the descendants of the latter set of brothers comprise the entire maximal lineage, the great majority of which lives in the two above-mentioned communities. Most members of the lineage between the ages of fifteen and twenty count the latter set of brothers as of the great-grandparental generation and the former set of brothers as of the grandparental generation.

Segmentary Opposition and the Theory of Games: A Study of Pathan Organization

THE PRESENT ESSAY relates to the extensive discussion in the anthropological literature on the role of unilineal descent groups in politics, i.e. the theory of lineage systems (cf. Fortes I953). It is, however, concerned with the analysis of a divergent case: a political system in which ramifying patrilineal descent is of prominent importance in politics, yet where larger lineage groups do not emerge as corporate units.' The case analysed is the acephalous political system of the Yusufzai Pathans of the Northwest Frontier Province, Pakistan. To elucidate this case, it will be necessary to present considerable detail on their organization. This consists of field material, collected in the course of the year I954. Further material has been, and will be, published elsewhere (Barth I956; Mss). In the analysis of this data, I shall utilize some of the elementary concepts and procedures of the Theory of Games (cf. Neumann and Morgenstern I947; Stone I948), as well as the relevant anthropological theory relating to descent groups and corporate groups. The argument of the essay depends on a distinction between the purely structural arrangement of units defined by a unilineal descent charter, and the manner in which these units are made relevant in corporate action. In the description of lineage systems in the literature, this distinction is not often made. The analysis of the solidarity of unilineal descent groups usually relies on a Durkheimian conception of mechanical solidarity. In such a framework, solidarity derives from likeness. The descent charter defines a hierarchy of homologous groups, and thus directs the fusion of political interests within a merging series of such groups. This particular expression of the descent group charter has been incorporated into our whole conception of lineage organizations, as if it were a necessary derivative of the descent structure. The present case study describes a different political application of unilineal descent. Descent units are arranged in a recognizable manner by patrilineal genealogies, and hold joint rights to large territories. But close collaterals in the system do not join in corporate groups in opposition to more distant collaterals. The genealogical charter is none the less relevant to the structure of the corporate groups that do emerge; essentially, it defines rivals and allies in a system of two opposed political blocs. Closely related descent units are consistent rivals; each establishes a net of political alliances with the rivals of allies of their own rivals. In this fashion a pervasive factional split into two grand alliances of descent segments emerges, with close collateral segments consistently in opposite moieties. Clearly, though this is a unlineal descent system of a kind, the analysis of the internal solidarity of the political units which emerge can not be contained in a schema based on the concept of mechanical solidarity. Among the Yusufzai Pathans, the recruitment of corporate political units depends on the exercise of individual choices between alternative allegiances. Thus descent charters do not unequivocally define corporate units; these charters are made relevant to political action indirectly through their strategic implications for the choices of individuals. Therefore, the manner of recruitment of Pathan political groups can not be understood directly in terms of the descent system; it requires some analysis of the bases of individual choices and the sources of the internial solidarity of the groups which do emerge. The 'Theory of Games' is designed precisely for the analysis of such strategic choices, and will be utilized in the latter part of this essay. The essay thus falls roughly into three parts: I, a descriptive and comparative account of Yusufzai Pathan uniline al descent groups and political organization; II, an attempted analysis wof