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As David Mead remarks his recent UKCLG blog post on the scope of the Human Rights Act, there is ‘much more than meets the eye’ to the HRA’s hybrid public authority scheme. It is not just about the meaning of the term ‘functions of a public nature’ under s 6(3)(b). Hugely important though this issue is, its well-documented intractability may have obscured deeper issues relating to the inherent mechanics of the scheme itself. Two such issues are the meaning and scope of the notion of a private act under s 6(5) and the rights-status of hybrid public authorities when performing public as opposed to private functions. They are important not just in their own right but also as potential clues to the proper interpretation of s 6(3)(b). As I have argued elsewhere (at  PL 139), it is difficult to see how judges could ever determine the scope of that provision correctly without first being clear as to how the scheme of liability it triggers actually works, and what it does to the defendants to which it applies.
Using the recent ruling of Arnold J in Olympic Delivery Authority v Persons Unknown  EWCA 1012 (Ch) as a springboard, Mead offers some thoughts on each of the s 6(5) and rights-status issues. In this post I offer my own. My end point is agreement with his basic contention that Arnold J was mistaken to believe that the Olympic Delivery Authority (the ODA) enjoyed Convention rights of its own in that case. But our thinking on each point differs somewhat, as will be seen.
In ODA, in which the ODA successfully sought an injunction to prevent trespassers from unlawfully obstructing agents and contractors from entering land earmarked for Olympic development, Arnold J believed himself bound (at ) to balance the protesters’ rights under Arts 10 and 11 ECHR with ODA’s right to respect for property under Art 1 FP. Evidently, his Lordship therefore assumed that the ODA could not have been a ‘core’ public authority under s 6 HRA. These, of course, are obviously public bodies such as government departments, the NHS and the armed forces, all of whose activities are caught by the Convention. To be a rights-holder one must be a ‘victim’ under s 7(1) HRA, which in turn requires one to be a ‘person, non-governmental organisation or group of individuals’ under Art 34 ECHR (see s 7(7)). It is clear beyond doubt from the ruling of the House of Lords in Aston Cantlow PCC v Wallbank  UKHL 37 that core public authorities, being inherently governmental, can never satisfy the victim test. This is rooted in Strasbourg’s idea that Art 34 envisages a binary, institutional distinction between the individual and the state, with the result that governmental organisations are permanently precluded from filing their own Convention claims, even if they happen to be doing so in relation to activities that would straightforwardly be regarded as private (see e.g. Ayuntamiento de Mula v Spain App no 55346/00 (ECtHR, 1 February 2001)). The idea has been criticised (by Howard Davis, at  CLJ 315), but it remains the law.
Mead’s criticism of ODA is not based on the argument, easy enough to make, that the ODA is indeed a core public authority. Core public authorities are ‘selfless’ bodies created and controlled to serve the public interest over their own: see my earlier work at  PL 139, 148-150. They differ fundamentally from ‘selfish’ institutionally non-state bodies, who are constitutionally allowed their own interests and motivations, whether as human beings, charities, or profit-making organisations, and who can therefore do as they wish – as Laws J emphasised in R v Somerset County Council, ex p Fewings  1 All ER 513, 524 – within the confines of the law. This is evident from what has been said about core public authorities academically (by Dawn Oliver, at  PL 476), and judicially (in Aston Cantlow, which drew from Oliver’s work), and also from the scope of the governmental organisation concept in Strasbourg to which the core public authority concept equates. It is clear that core public authority status would apply to the ODA, which was established under s 3 of the Olympic and Paralympic Games Act 2006 and invested with the power ‘to take any action it thinks necessary or expedient’ in order to prepare, or to make or ensure that arrangements are made for the preparation of, the London Olympics (see s 4). In exercising its functions the ODA must obey any directions given by the Secretary of State (Sch 1, para 18(1)(b)), who appoints its members and chairman following consultation with the Mayor of London (Sch 1, para 1(1)). Despite its formal status under s 3(1) as a body corporate, the ODA is evidently not a constitutionally selfish private organisation. That it must exercise its functions with regard to ‘the desirability of maximising the benefits to be derived after the London Olympics from things done in preparation for them’ (s 4(3)(a)), for instance, is a further indicator of the public-interest purpose for which it was created and is so closely central government-controlled. The ODA’s status as a core public authority is the real reason it lacks Convention rights of its own.
I begin with the rights-status issue, giving my views on the s 6(5) point below. I have argued before (at  PL 139) that hybrid public authorities do not lose Convention protection when acting in their public capacities. It is possible in a given case for a hybrid both to be attacked under the Convention and to defend itself using its own Convention rights. The issue has never been judicially resolved, as Mead observes, and a handful of commentators – notably Buxton LJ, in YL v Birmingham City Council  EWCA Civ 26, at  – have previously assumed that hybrid public authorities do indeed lack Convention protection when engaging in public activity. But under the HRA as presently drafted there is nevertheless a right answer. Whether a person can assert Convention rights under the HRA turns, as seen above, on whether Strasbourg would regard that person as a victim under Art 34 ECHR were a claim to be brought before the ECtHR in respect of the same act. What the issue therefore boils down to is the interpretation of the Strasbourg case-law on the meaning of Art 34. If a hybrid public authority is a governmental organisation under Art 34 and therefore not a victim in Strasbourg’s eyes when behaving publically, then it loses Convention protection under s 7 HRA. But if it is a victim under Art 34, then it follows that it must enjoy its own Convention rights domestically. This is apparent not just from Parliament’s clear intention to tie the standing questions under s 7 and Art 34 together, but also from the potentially very serious discrimination issue that would arise if we denied rights protection against Strasbourg’s wishes to hybrid public authorities acting in their public capacities. In Art 14 ECHR terms, it represents a classic example of denying Convention rights according to a person’s status in the domestic system. It is not a million miles, to borrow from some familiar examples, from denying Convention protection to those with red hair – or to fishing companies without the requisite number of British directors. Parliament could of course defy Strasbourg by legislating expressly for rights-stripping if it wished. But in the absence of any such move, the conclusion is irresistible: hybrid public authorities will enjoy Convention rights in their public capacities under the HRA if this is what would occur in Strasbourg under Art 34. Although I spare readers a lengthy re-rehearsal of my reasons for thinking that this would indeed occur (these can be found at  PL 139, 145-154), it is certainly worth reiterating the point made above, that Strasbourg has constructed a rigid and binary institutional divide between governmental and non-governmental bodies under Art 34. A body is either governmental in nature – constitutionally ‘selfless’ – or it is not. Under no circumstances will its Art 34 status change according to the nature of the activity it performs. Governmental organisations are governmental through and through; private organisations are private through and through, and therefore enjoy Convention protection at all times. So the point I am making on the rights-status issue is this: s 6(5) is irrelevant to the capacity of a hybrid public authority to enforce its own Convention rights. If the ODA were a hybrid public authority, which I have argued anyway is not the case, then it would be entitled to its rights in whichever capacity it acted. Whether it performed public functions or was otherwise engaged in public activity when seeking to enforce those rights is not the issue.
This leads neatly, then, to the s 6(5) question – more specifically, of how the concept of a private act relates to that of a public function under s 6(3)(b). This question is by far the thornier, not helped by the absence of any ministerial comment at all on the concept of a private act as the HRA passed through Parliament. Earlier cases such as Poplar Housing v Donoghue  EWCA Civ 595 tended to ignore the functions-acts distinction altogether. Ruling that a government-created registered social landlord was a hybrid public authority when providing accommodation to a tenant whom the landlord later sought to evict, the Court of Appeal (at ) listed a number of factors relevant to its conclusion – but made no effort whatsoever to explain whether these bore on the nature of the landlord’s function under s 6(3)(b) or its act under s 6(5). Later cases saw something of a judicial awakening in this respect, with a growing appreciation that the hybrid public authority question actually involves a two-stage test of both the function and the act (see Lord Hobhouse in Aston Cantlow and Lords Scott and Neuberger in YL v Birmingham City Council  UKHL 27), but this only brought the perplexing conceptual question of how ‘functions’ and ‘acts’ differ to the fore. The Court of Appeal’s ruling in R (Weaver) v London & Quadrant Housing Trust  EWCA Civ 587, which concerned the status under s 6 of a registered social landlord that in contrast to Poplar had not been created by government, is an interesting case in point. It is a glorious illustration of how easy it is in this context to become engulfed by a trap with a black hole-like capacity to swallow up virtually all trace of rationality and common sense. The trap’s unsuspecting victim was Elias LJ, who seized on the functions-acts distinction and reasoned that s 6(5), not s 6(3)(b), is effectively the operative provision when it comes to determining whether a particular hybrid public authority is bound in a given instance to respect Convention rights (at ). Since s 6(5) has the last word on the body’s liability, and since s 6(3)(b) says nothing of which of a hybrid’s functions must be public, his Lordship took the view that Parliament really only intended to cast s 6(3)(b) in a cameo role: as long as one of a body’s functions is public, then all that matters is the nature of the act complained of under s 6(5). If this act is public, then Convention challenge against the body can lie, regardless of whether the function pursuant to which the act is performed is public or private in nature. What we have under this approach, then, is an apparent broadening of s 6(3)(b): a hybrid body with a single public function on its books could theoretically perform a private function towards the complainant but nevertheless face Convention liability because under the all-important s 6(5) it performed a public act. The effort to open up s 6(3)(b) in this way, if that was indeed the intention, is laudable enough. I am not the only author to have argued (at  EHRLR 524) that the courts’ treatment of s 6(3)(b) is probably too narrow, after all. The approach has moreover been suggested before (by Jonny Landau, at  PL 630). But with the greatest respect to those who are tempted by it, the approach is seriously flawed. The idea that a public act could be performed pursuant to a private function is highly dubious in any event, as Lord Collins MR observed (at ). Elias LJ admitted himself (at ) that ‘Such situations are likely to be extremely rare.’ One might argue that with a clearer impression in mind of the functions-acts distinction the approach does become tenable, but this is where Weaver becomes even more puzzling. Joined by Lord Collins (at ), Elias LJ took the view (at ) that the nature of the act under s 6(5) strongly depends upon that of the function pursuant to which it is performed anyway. Acts that are ‘so bound up with’ a public function, he believed, would be public acts. So having showered s 6(5) in roses as the real star of the s 6 show, and having admonished (at ) the Divisional Court for failing at first instance to spot its Hollywood potential, his Lordship was in any event forced down the very same road trodden by judges in previous cases – of having to determine the nature of the function in question, around which everything else hinges. Having concluded that the function of allocating and managing housing stock was public, Elias LJ then ruled that the act of evicting the tenant was public as well. Even if the approach is theoretically viable, therefore, it gets the courts nowhere in practice. There is no escaping the need to determine the nature of the particular function performed towards the claimant in the case at hand. Indeed, it was disagreement over the nature of the function that split the court two to one, with Rix LJ dissenting.
The foregoing, I think, exposes three things about the meaning of s 6(5). First, it attests to the sheer difficulty of attempting to pin down the abstract distinction between functions and acts. The only real judicial guidance to have been given on the functions-acts distinction is by Lord Neuberger in YL (at ), that ‘functions’ are less specific than ‘acts’ and that various acts may be done in the performance of a particular function, but this is probably as precise, realistically, as it could get. Second, it emphasises that s 6(3)(b) retains the lead role – even if, as I mentioned at the start of this post, it is not the only issue worth worrying about in the hybrid public authority context. This follows not just from the difficulties seen in Weaver of trying to depart from this idea, but also from the very idea of a test that assigns public status to a body according to the function that it performs. A functional categorisation like this is alien to the institutionally-focussed governmental organisation jurisprudence in Strasbourg, as I argued above, so there will be no useful steer on the acts-functions distinction from here. The same is true of the meaning of a public function for the purposes of amenability to judicial review, which constitutes the only domestic body of case-law to provide any potential guidance to the courts on which functions are public and therefore attract legal duties, like Convention obligations, that apply primarily to the state. This is a tricky area in its own right and its link to s 6(3)(b) is equally unclear. I have my own views on both issues, but here is not the place to detail them. The point is that the amenability test itself may be functionally focussed, but there is no similar functions-acts distinction here either, so the courts are unassisted by this body of law as well. Clearly s 6(5) is designed to cut down the scope of hybrid public authority liability by reference to the nature of the particular act complained of, but quite how Parliament intended this to happen is manifestly unclear. All of this militates against reading s 6 in a way that renders s 6(5) the protagonist. There is no substitute for a more precise definition of a public function, difficult though it is to define, which should be able to do the vast majority of the work of determining when a private organisation should be a hybrid liable to Convention challenge and when it should not. Third, and finally, I think the foregoing suggests that in terms of the meaning of a private act under s 6(5), Elias LJ and Lord Collins were probably correct. Although Elias LJ’s specific idea that a public act could flow from a private function is difficult to swallow, the basic idea that an act should ordinarily take the same nature as its parent function is sensible. It strikes a fair balance between giving s 6(5) some sort of role by recognising a basic functions-acts distinction, on the one hand, and bogging the courts down in an artificial, complex and technical assessment of the precise distinction between public functions and public acts, on the other. On this approach, s 6(5) would only come into play if the defendant hybrid could cast real doubt over the idea that the act complained of did in fact result from – was ‘so bound up with’ – the particular public function in question. This might be because the act was more naturally seen as resulting from a private function, or perhaps because in reality it was simply a one-off act with no parent function at all. Not all acts, of course, will have parent functions: what is the function pursuant to which a fight in the street takes place, for example? To-double lock this more minor role for s 6(5), too, the courts would obviously have to treat defendants’ attempts to make use of that provision cautiously. It should not be open to a hybrid public authority care home, for instance, to wriggle too easily out of Convention liability by claiming that the abuse by nursing staff of residents fell outside of the public function of providing care and accommodation and was therefore a private act under s 6(5). The need to avoid simply emptying out the content of s 6(3)(b) is an important reason to ensure that it plays a proper role relative to that played by s 6(5).
Dr Alexander Williams is a Lecturer in Law and Co-Director of the Human Rights Centre at the University of Durham.
This entry was posted on October 28, 2013 by Constitutional Law Group in Human rights and tagged Human Rights Act, Human Rights Act Section 6, Public-Private Divide.

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Overview of fusion tags for recombinant proteins by E. N. Kosobokova; K. A. Skrypnik; V. S. Kosorukov (187-200).
Virtually all recombinant proteins are now prepared using fusion domains also known as “tags”. The use of tags helps to solve some serious problems: to simplify procedures of protein isolation, to increase expression and solubility of the desired protein, to simplify protein refolding and increase its efficiency, and to prevent proteolysis. In this review, advantages and disadvantages of such fusion tags are analyzed and data on both well-known and new tags are generalized. The authors own data are also presented.
Chlorophylls d and f and their role in primary photosynthetic processes of cyanobacteria by S. I. Allakhverdiev; V. D. Kreslavski; S. K. Zharmukhamedov; R. A. Voloshin; D. V. Korol’kova; T. Tomo; J.-R. Shen (201-212).
The finding of unique Chl d- and Chl f-containing cyanobacteria in the last decade was a discovery in the area of biology of oxygenic photosynthetic organisms. Chl b, Chl c, and Chl f are considered to be accessory pigments found in antennae systems of photosynthetic organisms. They absorb energy and transfer it to the photosynthetic reaction center (RC), but do not participate in electron transport by the photosynthetic electron transport chain. However, Chl d as well as Chl a can operate not only in the light-harvesting complex, but also in the photosynthetic RC. The long-wavelength (Qy) Chl d and Chl f absorption band is shifted to longer wavelength (to 750 nm) compared to Chl a, which suggests the possibility for oxygenic photosynthesis in this spectral range. Such expansion of the photosynthetically active light range is important for the survival of cyanobacteria when the intensity of light not exceeding 700 nm is attenuated due to absorption by Chl a and other pigments. At the same time, energy storage efficiency in photosystem 2 for cyanobacteria containing Chl d and Chl f is not lower than that of cyanobacteria containing Chl a. Despite great interest in these unique chlorophylls, many questions related to functioning of such pigments in primary photosynthetic processes are still not elucidated. This review describes the latest advances in the field of Chl d and Chl f research and their role in primary photosynthetic processes of cyanobacteria.
Structure and functions of linker histones by A. V. Lyubitelev; D. V. Nikitin; A. K. Shaytan; V. M. Studitsky; M. P. Kirpichnikov (213-223).
Linker histones such as variants H1, H5, and other similar proteins play an important role in regulation of chromatin structure and dynamics. However, interactions of linker histones with DNA and proteins, as well as specific functions of their different variants, are poorly studied. This is because they acquire tertiary structure only when interacting with a nucleosome, and because of limitations of currently available methods. However, deeper investigation of linker histones and their interactions with other proteins will address a number of important questions — from structure of compacted chromatin to regulation of early embryogenesis. In this review, structures of histone H1 variants and its interaction with chromatin DNA are considered. A possible functional significance of different H1 variants, a role of these proteins in maintaining interphase chromatin structure, and interactions of linker histones with other cellular proteins are also discussed.
Age-related changes in antioxidant and glutathione S-transferase enzyme activities in the Asian clam by J. Vranković (224-232).
Aging is accompanied by increased production of free oxygen radicals and impairment of normal cellular functions. The aim of this work was to provide preliminary data on age-related differences in the activities of antioxidant enzymes and phase II biotransformation enzyme glutathione S-transferase (GST) in a wild population of the Asian clam Corbicula fluminea. The antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), and GST were assessed in visceral mass of four age classes (0+-, 1+-, 2+-, and 3+-year-old) of C. fluminea clams. Age-related changes were seen in antioxidant enzyme status: levels of total SOD (totSOD) (P < 0.05), MnSOD, and CuZnSOD (P < 0.05) activities increased progressively during aging from younger to older clams. Changes in CAT and GR activities with advancing age were found, the levels being the highest in age class II, then being lower in age classes III and IV (P < 0.05). Activities of GPX and GST were lower in the senescent individuals (2+- and 3+-year-old clams) compared with young individuals (0+- and 1+-year-old clams). Overall, the decline of glutathione-dependent enzyme activities, coupled with higher and lower activities of totSOD and CAT, respectively, as the individual grows older, may render the older animals more susceptible to oxidative stress. Data reported here are not intended to be exhaustive since they concern only age/size structure of the population at one locality, so more detailed studies on both the developmental stages and levels of antioxidant enzymes of this new alien species in Serbian rivers are required.
Interaction of nucleotide excision repair protein XPC—RAD23B with DNA containing benzo[a]pyrene-derived adduct and apurinic/apyrimidinic site within a cluster by L. V. Starostenko; E. A. Maltseva; N. A. Lebedeva; P. E. Pestryakov; O. I. Lavrik; N. I. Rechkunova (233-241).
The combined action of reactive metabolites of benzo[a]pyrene (B[a]P) and oxidative stress can lead to cluster-type DNA damage that includes both a bulky lesion and an apurinic/apyrimidinic (AP) site, which are repaired by the nucleotide and base excision repair mechanisms — NER and BER, respectively. Interaction of NER protein XPC—RAD23B providing primary damage recognition with DNA duplexes containing a B[a]P-derived residue linked to the exocyclic amino group of a guanine (BPDE-N2-dG) in the central position of one strand and AP site in different positions of the other strand was analyzed. It was found that XPC—RAD23B crosslinks to DNA containing (+)-trans-BPDE-N2-dG more effectively than to DNA containing cis-isomer, independently of the AP site position in the opposite strand; protein affinity to DNA containing one of the BPDE-N2-dG isomers depends on the AP site position in the opposite strand. The influence of XPC—RAD23B on hydrolysis of an AP site clustered with BPDE-N2-dG catalyzed by the apurinic/apyrimidinic endonuclease 1 (APE1) was examined. XPC—RAD23B was shown to stimulate the endonuclease and inhibit the 3′–5′ exonuclease activity of APE1. These data demonstrate the possibility of cooperation of two proteins belonging to different DNA repair systems in the repair of cluster-type DNA damage.
Effect of thrombin inhibitors on positive feedback in the coagulation cascade by N. B. Ustinov; E. G. Zav’yalova; A. M. Kopylov (242-248).
The coagulation cascade is a series of sequential reactions of limited proteolysis of protein factors resulting in generation of thrombin. Thrombin mediates both positive and negative feedback in regulating this cascade by taking part in activation of several factors. Some thrombin inhibitors, by affecting positive feedback, inhibit generation of thrombin itself. In the current study, we used two thrombin inhibitors: argatroban, a low molecular weight reversible competitive inhibitor that binds to the active site, and bivalirudin, a bivalent oligopeptide that blocks the active site and binding center of protein substrates (exosite I). Appearance rate and total amount of thrombin were measured in a thrombin generation assay (TGA) using a fluorescent substrate. We found that argatroban slows the appearance of thrombin and lowers its amount. Bivalirudin also slows appearance of thrombin, but it does not decrease its amount, perhaps because the region being bound to the active site undergoes hydrolysis so that the inhibitor stops binding to thrombin. Many reactions of the coagulation cascade proceed on the surface of phospholipid micelles (PLMs). In the case of argatroban, PLMs do not affect the results of the TGA, whereas for bivalirudin they lower its inhibitory activity. It seems that PLMs stabilize protein complexes (wherein thrombin exosite I is hindered) mediating positive feedback in the coagulation cascade, e.g. complexes of thrombin with factor V and VIII.
Identification of a region of the polypeptide chain of Na,K-ATPase α-subunit interacting with 67-kDa melittin-like protein by Yu. V. Kamanina; E. A. Klimanova; E. A. Dergousova; I. Yu. Petrushanko; O. D. Lopina (249-254).
It was shown earlier that a 67-kDa protein purified from mouse kidney using polyclonal antibodies against melittin (a peptide from bee venom) interacted with Na,K-ATPase from rabbit kidney. In this study, a 43-kDa proteolytic fragment of Na,K-ATPase α-subunit interacting with the 67-kDa melittin-like protein was found. The α-subunit was hydrolyzed by trypsin in the presence of 0.5 mM ouabain (E2-conformation of Na,K-ATPase). A proteolytic fragment interacting with the 67-kDa melittin-like protein that was identified by mass-spectrometry is a region of the cytoplasmic domain of Na,K-ATPase α-subunit located between amino acid residues 591 and 775. The fragment includes a conservative DPPRA motif that occurs in many P-type ATPases. It was shown earlier that this motif of H,K-ATPase from gastric mucosa binds to melittin. We suggest that namely this motif of P-type ATPases is able to interact with proteins containing melittin-like modules.
Tankyrase activity in organs and tissues of mice by A. N. Kuimov; A. S. Zhozhikashvili; V. N. Manskikh; L. V. Platonova; T. G. Dyuzheva (255-262).
Tankyrase, one of the NAD+ ADP-ribosyltransferases, is a target for drugs developed for their anticancer and other pharmacological activities. We designed an assay for estimation of the inhibition or activation of the enzyme in pre-clinical studies. In mice, the highest specific activity of tankyrase was observed in thymus, spleen, pancreas, and bone marrow. In murine liver, tankyrase is active in ontogenesis and during reparative regeneration; however, the basal activity is hardly detectable in normal liver and most of other organs of adult animals. We suggest that tankyrase is a part of the tissue growth and repair machinery, while its age-dependent inhibition, when an organism stops growing, turns on phenoptosis.
DNA with damage in both strands as affinity probes and nucleotide excision repair substrates by N. V. Lukyanchikova; I. O. Petruseva; A. N. Evdokimov; V. N. Silnikov; O. I. Lavrik (263-274).
Nucleotide excision repair (NER) is a multistep process of recognition and elimination of a wide spectrum of damages that cause significant distortions in DNA structure, such as UV-induced damage and bulky chemical adducts. A series of model DNAs containing new bulky fluoro-azidobenzoyl photoactive lesion dCFAB and well-recognized nonnucleoside lesions nFlu and nAnt have been designed and their interaction with repair proteins investigated. We demonstrate that modified DNA duplexes dCFAB/dG (probe I), dCFAB/nFlu+4 (probe II), and dCFAB/nFlu−3 (probe III) have increased (as compared to unmodified DNA, umDNA) structure-dependent affinity for XPC—HR23B (Kd um > Kd I > Kd II ≈ Kd III ) and differentially crosslink to XPC and proteins of NER-competent extracts. The presence of dCFAB results in (i) decreased melting temperature (ΔTm = −3°C) and (ii) 12° DNA bending. The extended dCFAB/dG-DNA (137 bp) was demonstrated to be an effective NER substrate. Lack of correlation between the affinity to XPC—HR23B and substrate properties of the model DNA suggests a high impact of the verification stage on the overall NER process. In addition, DNAs containing closely positioned, well-recognized lesions in the complementary strands represent hardly repairable (dCFAB/nFlu+4, dCFAB/nFlu−3) or irreparable (nFlu/nFlu+4, nFlu/nFlu−3, nAnt/nFlu+4, nAnt/nFlu−3) structures. Our data provide evidence that the NER system of higher eukaryotes recognizes and eliminates damaged DNA fragments on a multi-criterion basis.
Dynamics of antagonistic potency of Rhodobacter capsulatus PG lipopolysaccharide against endotoxin-induced effects by D. S. Kabanov; D. A. Serov; S. V. Zubova; S. V. Grachev; I. R. Prokhorenko (275-283).
The dynamics of antagonistic potency of lipopolysaccharide (LPS) isolated from Rhodobacter capsulatus PG on the synthesis of proinflammatory (TNF-α, IL-1β, IL-8, IL-6, IFN-γ) and antiinflammatory (IL-10, IL-1Ra) cytokines induced by highly stimulatory endotoxins from Escherichia coli or Salmonella enterica have been studied. Using human whole blood, we have shown that R. capsulatus PG LPS inhibited most pronouncedly the endotoxin-induced synthesis of TNF-α, IL-1β, IL-8, and IL-6 during the first 6 h after endotoxin challenge. Similarly, the endotoxin-induced release of IFN-γ was abolished by R. capsulatus PG LPS as well (24 h). In contrast to the above-mentioned cytokines, the relatively weak antagonistic activity of R. capsulatus PG LPS against endotoxin-triggered production of IL-6 and IL-8 was revealed. Since R. capsulatus PG LPS displays more potent antagonistic activity against deleterious effects of S. enterica LPS than those of E. coli LPS in the cases of such cytokines as IL-1β (6 and 24 h), IL-6 and IL-8 (4 h), we conclude that the effectiveness of protective action of antagonist is mostly determined by the primary lipid A structure of the employed agonist.
Mathematical model of self-oscillations of activity of Kai proteins by Sh. K. Bayramov (284-288).
A non-autocatalytic mathematical model of self-oscillations in vitro in solutions of cyanobacterial Kai proteins (KaiA, KaiB, KaiC) and ATP is suggested. This model describes the process of phosphorylation/dephosphorylation of KaiC protein, which is accelerated by KaiA and inhibited by KaiB. The method of metabolic control analysis is used to show that frequency (period) as well as amplitude of self-oscillations of components of Kai proteins are temperature-compensated.
Isoferulic acid action against glycation-induced changes in structural and functional attributes of human high-density lipoprotein by D. S. Jairajpuri; Z. S. Jairajpuri (289-295).
Glycation-induced high-density lipoprotein (HDL) modification by aldehydes can result in loss of its antiinflammatory/antioxidative properties, contributing to diabetes-associated cardiovascular diseases. Isoferulic acid, a major active ingredient of Cimicifuga heracleifolia, shows antiinflammatory, antiviral, antioxidant, and antidiabetic properties. Thus, this study investigated the antiglycation effect of isoferulic acid against compositional modifications of HDL and loss of biological activity of HDL-paraoxonase induced on incubation with different aldehydes. Protective effect of isoferulic acid was assessed by subjecting purified HDL from human plasma to glycation with methylglyoxal, glyoxal, or glycolaldehyde and varying concentrations of isoferulic acid. The effect of isoferulic acid was analyzed by determining amino group number, tryptophan and advanced glycation end-product fluorescence, thermal denaturation studies, carboxymethyl lysine content, and activity of HDL-paraoxonase. Concentration-dependent inhibitory action of isoferulic acid was observed against extensive structural perturbations, decrease in amino group number, increase in carboxymethyl lysine content, and decrease in the activity of HDL-paraoxonase caused by aldehyde-associated glycation in the HDL molecule. Isoferulic acid, when taken in concentration equal to that of aldehydes, was most protective, as 82-88% of paraoxonase activity was retained for all studied aldehydes. Isoferulic acid shows antiglycation action against aldehyde-associated glycation in HDL, which indicates its therapeutic potential for diabetic patients, especially those with micro-/macrovascular complications.

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1. GEORGE1 PROCTOR was born 1788 in London England, and died September 20, 1839 in New London PEI. He married JANE CANTELO April 26, 1818, daughter of JAMES CANTELO and MARY SALMON. She was born 1797 in Isle of Wight England, and died December 4, 1882 in New Glasgow PEI.
2. i. JAMES WILLIAM2 PROCTOR, b. May 31, 1819; d. September 27, 1914.
ii. GEORGE EDWIN PROCTOR, b. December 1823; d. December 21, 1825.
3. iii. MARY JANE PROCTOR, b. December 1825; d. 1898.
iv. EDWIN CORMACK PROCTOR, b. January 6, 1831; m. REBECCA MOUNTAIN, February 16, 1854, Kensington PEI; b. 1835, Kensington PEI.
v. GEORGE MOORE PROCTOR, b. May 21, 1833; m. CATHERINE WALSH.
4. vi. SARA CANTELO PROCTOR, b. July 9, 1827, Kings Co. PEI, Canada New Glasgow; d. May 22, 1913, Vancouver, BC.
2. JAMES WILLIAM2 PROCTOR (GEORGE1) was born May 31, 1819, and died September 27, 1914. He married ELLEN WALSH 1846.
5. i. EDMOND3 PROCTOR, b. September 1848, Hemlock Hills PEI; d. 1937, Charlottetown, Mt Edward Road.
ii. WILLIAM PROCTOR, b. 1847; d. 1937, Charlottetown PEI; m. KATHERINE.
iii. JAMES PROCTOR, b. 1857; d. Crystal Maine USA; m. CATHERINE, Cambridge MASS USA.
6. iv. SEMEON PROCTOR, b. 1853; d. January 1938, Crystal Maine USA.
v. KEM PROCTOR, b. 1861; d. 1947, Stanley Bridge PEI; m. PAT WALSH.
7. vi. JANE MARY E. PROCTOR, b. 1851.
8. vii. JOHN C. PROCTOR, b. 1852; d. 1927, New Glasgow PEI.
3. MARY JANE2 PROCTOR (GEORGE1) was born December 1825, and died 1898. She married GEORGE STEVENSON, son of JOHN STEVENSON and MARGARET NESBIT. He was born 1815, and died 1910 in Peoples Cemetery New Glasgow PEI.
i. GEORGE HENRY3 STEVENSON, b. 1842; d. 1864.
ii. EDWIN MORMICK STEVENSON, b. 1853; d. 1871.
iii. SARAH ADA STEVENSON, b. 1864; d. 1866.
iv. HIRAM WALLACE STEVENSON, b. 1861; d. 1879.
vi. MARGARET STEVENSON, b. 1844; m. GREGOR; b. MASS USA.
4. SARA CANTELO2 PROCTOR (GEORGE1) was born July 9, 1827 in Kings Co. PEI, Canada New Glasgow, and died May 22, 1913 in Vancouver, BC. She married WILLIAM ARTHUR January 22, 1849 in Brackley Point, PEI, son of JAMES ARTHUR and MARY BARR. He was born March 12, 1821 in Charlottetown, PEI, Canada, and died July 31, 1893 in Glasston, North Dakota, USA.
9. i. JANE EMILY3 ARTHUR, b. November 18, 1849, Charlottetown, PEI.
10. ii. WALLACE ARTHUR, b. May 4, 1851, Charlottetown, PEI; d. April 1, 1936, Edmonton, Alberta.
11. iii. JAMES BRUCE ARTHUR, b. April 14, 1853, Charlottetown, PEI; d. March 21, 1924, Vancouver, BC.
12. iv. EDWIN LEMUEL ARTHUR, b. January 8, 1855, Goderich, Ontario.
v. FREDERICK MARTIN ARTHUR, b. December 2, 1856.
13. vi. FRANCIS GEORGE ARTHUR, b. September 1, 1859, Goderich, Ontario.
vii. SARAH ADA ARTHUR, b. November 1, 1861.
14. viii. ALICE ARTHUR, b. March 14, 1864, Goderich, Ontario; d. Dominion city, Manitoba.
15. ix. JOSEPH WILLIAM ARTHUR, b. June 21, 1866, Goderich, Ontario; d. September 22, 1935, Manhattan Beach, LA Co. California.
5. EDMOND3 PROCTOR (JAMES WILLIAM2, GEORGE1) was born September 1848 in Hemlock Hills PEI, and died 1937 in Charlottetown, Mt Edward Road. He married MARY TRAINOR 1874 in St Anns PEI, daughter of EDWARD TRAINOR and CATHERINE MACELMEEL. She was born 1855 in St Patrick Road PEI, and died 1928 in Charlottetown PEI.
16. i. JAMES EDWIN4 PROCTOR, b. July 4, 1877, Hunter River PEI; d. August 28, 1964, Beachgrove Charlottetown PEI.
17. ii. CLARA PROCTOR, b. December 1875; d. October 10, 1947, At Home 68 Great George St Charlottetown PEI.
18. iii. ELLEN PROCTOR, b. 1879, Hunter River; d. 1967, Haverhill MASS USA.
19. iv. MINNIE PROCTOR, b. 1881; d. July 1963, Charlottetown PEI.
v. ROSE PROCTOR, b. 1885, Single; d. 1936, Haverhill MASS USA.
vi. JOHN LEAMING PROCTOR, b. 1883, Hunter River PEI; d. November 17, 1956, Charlottetown PEI; m. MARGARET SAMPLE, 1913; b. Peakes Station PEI.
vii. GEORGINA PROCTOR, b. 1888; d. 1968, Haverhill MASS USA.
6. SEMEON3 PROCTOR (JAMES WILLIAM2, GEORGE1) was born 1853, and died January 1938 in Crystal Maine USA. He married MINERVA MAIN 1887. She was born in Oxbow Maine.
i. JAMES CANTELO4 PROCTOR, b. 1893, Crystal Maine USA; d. 1965; m. ELLA GRANT.
20. ii. MARY MARIA PROCTOR, b. 1892; d. 1957.
iii. JOHN ROBERT PROCTOR, b. 1895, Crystal Maine USA; d. 1956.
iv. JOSEPH NOBLE PROCTOR, b. 1902.
7. JANE MARY E.3 PROCTOR (JAMES WILLIAM2, GEORGE1) was born 1851. She married JOHN MURPHY.
8. JOHN C.3 PROCTOR (JAMES WILLIAM2, GEORGE1) was born 1852, and died 1927 in New Glasgow PEI. He married MARGARET PARKS. She was born 1854, and died 1917.
9. JANE EMILY3 ARTHUR (SARA CANTELO2 PROCTOR, GEORGE1) was born November 18, 1849 in Charlottetown, PEI. She married JOHN ALEXANDER GIRVIN 1875 in Goderich, Ontario. He was born 1852.
21. i. ADA GLENN4 GIRVIN, b. 1876, Goderich, ONtario.
ii. ALICE MAY GIRVIN, b. September 22, 1879.
iii. DAVID ARTHUR CHESTER GIRVIN, b. May 12, 1882.
22. iv. FREDERICK HENRICKS GIRVIN, b. June 24, 1885, Goderich, Ontario; d. Simi, Los Angeles Co., USA.
v. HATTIE PEARSON GIRVIN, b. November 7, 1888.
vi. MAY GODFREY GIRVIN, b. November 7, 1888.
10. WALLACE3 ARTHUR (SARA CANTELO2 PROCTOR, GEORGE1) was born May 4, 1851 in Charlottetown, PEI, and died April 1, 1936 in Edmonton, Alberta. He married MARY-ANNE MILLION 1878 in Goderich, Ontario. She was born October 23, 1855 in Goderich, Ontario, and died March 12, 1918 in Winnipeg, Manitoba.
i. EDWIN4 ARTHUR, b. November 15, 1877, Goderich, Ontario; d. 1962, Letellier, Manitoba.
ii. MONA COMMA ARTHUR, b. 1879, Goderich, Ontario; d. 1881, Goderich, Ontario.
23. iii. NINA WALLACE ARTHUR, b. October 27, 1881, Goderich, Ontario; d. February 7, 1951, Port Arthur, Ontario.
24. iv. FREDERICK ARTHUR, b. May 16, 1884, North Dakota, USA; d. 1945.
25. v. WILLIAM ROY ARTHUR, b. October 16, 1885, North Dakota, USA; d. 1961, North Battleford, SASK..
26. vi. MAY ELIZABETH ARTHUR, b. July 10, 1887, North Dakota; d. 1952, Winnipeg, Manitoba.
27. vii. SARA ALICE (ALLIE) ARTHUR, b. April 6, 1889, North Dakota; d. 1960, Letellier, Manitoba.
viii. JOSEPH PROCTOR ARTHUR, b. March 3, 1891, Hensel, North Dakota; d. 1946, Edmonton, Alberta; m. ANNIE FRY, 1946, Edmonton, Alberta.
28. ix. JANE VALENTINE ARTHUR, b. July 28, 1892, North Dakota; d. Edmonton, Alberta.
29. x. HERBERT CUSHMAN ARTHUR, b. September 21, 1894, North Dakota; d. Dominion City, Manitoba.
11. JAMES BRUCE3 ARTHUR (SARA CANTELO2 PROCTOR, GEORGE1) was born April 14, 1853 in Charlottetown, PEI, and died March 21, 1924 in Vancouver, BC. He married ELLEN 1878. She was born 1868.
i. GOULD R.4 ARTHUR, b. 1879.
ii. ORA M.ARTHUR, b. 1882.
iii. LILLIE D. ARTHUR, b. 1892.
iv. HAROLD E. ARTHUR, b. 1897.
v. LEONARD D. ARTHUR, b. 1899.
12. EDWIN LEMUEL3 ARTHUR (SARA CANTELO2 PROCTOR, GEORGE1) was born January 8, 1855 in Goderich, Ontario. He married MARY. She was born 1861.
i. FRANK4 ARTHUR, b. 1886.
ii. LEWIS ARTHUR, b. 1891.
13. FRANCIS GEORGE3 ARTHUR (SARA CANTELO2 PROCTOR, GEORGE1) was born September 1, 1859 in Goderich, Ontario.
14. ALICE3 ARTHUR (SARA CANTELO2 PROCTOR, GEORGE1) was born March 14, 1864 in Goderich, Ontario, and died in Dominion city, Manitoba. She married VALENTINE SCHOLTE 1884 in North Dakota, USA. He was born 1858 in Germany, and died in Dominion City, Manitoba.
30. i. MABEL4 SCHOLTE, b. 1885.
ii. ARTHUR SCHOLTE, b. 1889.
iii. PEARL SCHOLTE, b. 1891.
iv. EDGAR VALENTINE SCHOLTE, b. 1897.
15. JOSEPH WILLIAM3 ARTHUR (SARA CANTELO2 PROCTOR, GEORGE1) was born June 21, 1866 in Goderich, Ontario, and died September 22, 1935 in Manhattan Beach, LA Co. California. He married EDITH LEVINA STULL December 28, 1892 in Glasston, Pembina Co., North Dakota. She was born May 21, 1871 in Teeswater, Bruce Co. Ontario, and died December 31, 1938 in Hollywood, California.
31. i. WILLIAM STULL4 ARTHUR, b. February 6, 1894, St. Thomas Twp., North Dakota; d. March 24, 1953, Pasadena, California.
32. ii. EVELYN BESSIE ARTHUR, b. November 1895, Glasston, North Dakota; d. April 18, 1924, Pasadena, California.
iii. WALTER HALL ARTHUR, b. 1899.
33. iv. RUTH MARION ARTHUR, b. September 5, 1905, Glasston, North Dakota; d. November 30, 1965, San Gabriel, LA County, California.
34. v. JESSIE EDITH ARTHUR, b. December 27, 1908, Glasston, Pembina Co., North Dakota; d. January 5, 1984, Rosemead, LA County, California.
16. JAMES EDWIN4 PROCTOR (EDMOND3, JAMES WILLIAM2, GEORGE1) was born July 4, 1877 in Hunter River PEI, and died August 28, 1964 in Beachgrove Charlottetown PEI. He married CATHERINE GOODMAN November 18, 1913 in St Anns PEI, daughter of JOHN GOODMAN and MARGARET WYNN. She was born March 6, 1897 in St Patrick Road PEI, and died October 20, 1951 in St Patrick Road PEI.
17. CLARA4 PROCTOR (EDMOND3, JAMES WILLIAM2, GEORGE1) was born December 1875, and died October 10, 1947 in At Home 68 Great George St Charlottetown PEI. She married WILLIAM GRIMES 1918. He was born 1887 in Southport, and died September 18, 1959 in Charlottetown PEI.
18. ELLEN4 PROCTOR (EDMOND3, JAMES WILLIAM2, GEORGE1) was born 1879 in Hunter River, and died 1967 in Haverhill MASS USA. She married MARTIN COFFEY 1910 in Haverhill MASS USA.
19. MINNIE4 PROCTOR (EDMOND3, JAMES WILLIAM2, GEORGE1) was born 1881, and died July 1963 in Charlottetown PEI. She married SAM ARBING 1914 in St Anns PEI. He was born in Bedford NS.
20. MARY MARIA4 PROCTOR (SEMEON3, JAMES WILLIAM2, GEORGE1) was born 1892, and died 1957. She married AUGUSSTUS WILLEY. He died 1957 in Crystal Maine USA.
21. ADA GLENN4 GIRVIN (JANE EMILY3 ARTHUR, SARA CANTELO2 PROCTOR, GEORGE1) was born 1876 in Goderich, ONtario. She married -----BARTRAM.
22. FREDERICK HENRICKS4 GIRVIN (JANE EMILY3 ARTHUR, SARA CANTELO2 PROCTOR, GEORGE1) was born June 24, 1885 in Goderich, Ontario, and died in Simi, Los Angeles Co., USA. He married (1) LILA. He married (2) ROSE in California.
23. NINA WALLACE4 ARTHUR (WALLACE3, SARA CANTELO2 PROCTOR, GEORGE1) was born October 27, 1881 in Goderich, Ontario, and died February 7, 1951 in Port Arthur, Ontario. She married THOMAS C. PREECE March 30, 1910 in Dominion City, Manitoba. He was born July 22, 1880 in Dorrington, England, and died July 17, 1945 in Dominion City, Manitoba.
24. FREDERICK4 ARTHUR (WALLACE3, SARA CANTELO2 PROCTOR, GEORGE1) was born May 16, 1884 in North Dakota, USA, and died 1945. He married LILA(ESTHER).
25. WILLIAM ROY4 ARTHUR (WALLACE3, SARA CANTELO2 PROCTOR, GEORGE1) was born October 16, 1885 in North Dakota, USA, and died 1961 in North Battleford, SASK.. He married NELLIE.
26. MAY ELIZABETH4 ARTHUR (WALLACE3, SARA CANTELO2 PROCTOR, GEORGE1) was born July 10, 1887 in North Dakota, and died 1952 in Winnipeg, Manitoba. She married JIM TRELEAVEN.
27. SARA ALICE (ALLIE)4 ARTHUR (WALLACE3, SARA CANTELO2 PROCTOR, GEORGE1) was born April 6, 1889 in North Dakota, and died 1960 in Letellier, Manitoba. She married WILLIAM CALDER. He was born 1876 in Letellier, Manitoba, and died 1947 in Winnipeg, Manitoba.
28. JANE VALENTINE4 ARTHUR (WALLACE3, SARA CANTELO2 PROCTOR, GEORGE1) was born July 28, 1892 in North Dakota, and died in Edmonton, Alberta. She married ROBERT BARBER in Dominion City, Manitoba.
29. HERBERT CUSHMAN4 ARTHUR (WALLACE3, SARA CANTELO2 PROCTOR, GEORGE1) was born September 21, 1894 in North Dakota, and died in Dominion City, Manitoba. He married ROSA WARRACK 1939 in Winnipeg, Manitoba. She died in Dominion City, Manitoba.
30. MABEL4 SCHOLTE (ALICE3 ARTHUR, SARA CANTELO2 PROCTOR, GEORGE1) was born 1885. She married ....FROOM in Dominion City, Manitoba.
31. WILLIAM STULL4 ARTHUR (JOSEPH WILLIAM3, SARA CANTELO2 PROCTOR, GEORGE1) was born February 6, 1894 in St. Thomas Twp., North Dakota, and died March 24, 1953 in Pasadena, California. He married MARIE DAPHNE MONTANEY December 17, 1919 in Pasadena, LA County, California. She was born June 17, 1896 in Pisgah, Butler Co., Ohio, and died May 5, 1983 in Arcadia, LA Co., California.
32. EVELYN BESSIE4 ARTHUR (JOSEPH WILLIAM3, SARA CANTELO2 PROCTOR, GEORGE1) was born November 1895 in Glasston, North Dakota, and died April 18, 1924 in Pasadena, California. She married HARVEL H. REEDER December 31, 1921 in 2123-2nd Ave, W. Vancouver, BC.
33. RUTH MARION4 ARTHUR (JOSEPH WILLIAM3, SARA CANTELO2 PROCTOR, GEORGE1) was born September 5, 1905 in Glasston, North Dakota, and died November 30, 1965 in San Gabriel, LA County, California. She married KENNETH WAYNE HARSHBARGER September 18, 1924 in Los Angeles, California, USA. He was born June 2, 1900 in Murdock, Illinois, USA, and died May 25, 1984 in San Gabriel, LA County, California.
34. JESSIE EDITH4 ARTHUR (JOSEPH WILLIAM3, SARA CANTELO2 PROCTOR, GEORGE1) was born December 27, 1908 in Glasston, Pembina Co., North Dakota, and died January 5, 1984 in Rosemead, LA County, California. She married MAXWELL HILL October 5, 1946 in Hollywood, California. He was born March 7, 1913 in San Francisco, California, and died January 15, 1973 in Los Angeles, California.

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