1)

(Kane and Trochim, 2007 and Trochim, 1989). We define key terms in Table 1. Prior to undertaking the concept mapping process, we developed a framework to identify stakeholders invested in the area of the built and social environments and older adults’ mobility (Schiller et al., 2013). We defined stakeholders as individuals and organizations with relevant interest or expertise, notably those who were either affected by or who could affect (Freeman, 1984) at least one component of the interaction between the built and social environments and older adults’ mobility. Relevant buy Lonafarnib expertise was conceptualized as employment at a relevant agency or organization, reputation within the research community as a content expert, the first-hand experience from older adults, or on recommendation as an appropriate stakeholder. We believed that all invited stakeholders would have insights into the needs of older adults so we did not restrict participation by age. Thus, based on our preliminary work developing a framework for identifying relevant individuals and organizations (Schiller et al., 2013), we recruited stakeholders from seven categories, including: policy/government; researchers; health practitioners/professionals; health and social service providers; not-for-profit organizations; private business, and older adults. Following the development of our framework, we invited two target groups: a broad group of stakeholders heavily targeting

older adults to gather their perspectives during the initial brainstorming task, and a smaller representative group of core stakeholders who participated buy CT99021 in both the initial brainstorming and the subsequent sorting and rating tasks (Kane and Trochim, 2007). For our older adult participants, we used an email-based recruitment strategy sent to

chapters of an organization for retired persons. To populate the other six categories of key stakeholders, we used email to invite stakeholders via known experts and Farnesyltransferase listservs for content area specializations and professional organization. As part of this recruitment strategy we targeted groups from the planning sector, health care sector as well as academia. We aimed for diverse perspectives to inform this project, and although responses were anonymized, we were able to capture some information on respondents (e.g., self-identified primary and secondary stakeholder group, location, occupation and age). We recruited a diverse group of stakeholders to participate; and seventy-five participants completed the brainstorming phase (including 49 participants from the broad group and 26 participants from the core group). Data from the brainstorming component were collected between May 23, 2012 and June 10, 2012. The mean age of participants was 65.1 (10.4) years (range 35–81 years); and they all resided in British Columbia, Canada, with N = 56 from Metro Vancouver, N = 10 from smaller urban centers outside of Metro Vancouver and N = 9 from rural communities.

report that GBS-positive breast milk is associated with heavy infant colonization [73]. To determine the effect of maternal immunization with GBS CPS-II and CPS-III antibody

on postnatal protection from disease a rodent model has been used, where increased survival in pups exposed postnatally to breast milk with high titers of antibody compared to low titers was shown, supporting the beneficial added effect of breast milk antibody following vaccination [74] and [75]. Oligosaccharides prevent cell adherence for S. pneumoniae [76] and Escherichia coli BMS-354825 mouse (E. coli) [77]. Additionally, E. coli and Campylobacter jejuni toxin can be neutralized by oligosaccharides [49] and [78] and milk glycoconjugates prevent cell adherence of Vibrio cholera and E. coli [79] and [80]. Taken together, these studies suggest that the transfer Selleckchem BTK inhibitor of human milk oligosaccharides delivers real protection to infants against many bacterial and viral infections. GBS type Ib and II polysaccharides are of interest as they are virtually identical to certain oligosaccharides present in human milk [75], [81] and [82] which raises the possibility of cross-reactivity with other human glycoconjugates [83]. The results from murine models suggest that these oligosaccharides may act as receptor analogues that anchor the bacteria in the mucosal layer and prevent cell adhesion in the epithelial layer, thus preventing

invasive disease. Most neonatal infections occur via mucosal membranes in the respiratory, gastrointestinal, and urinary tracts, yet there is only limited protection at these vast mucosal surfaces during the neonatal period. Breast milk provides considerable Bumetanide amounts of specific SIgA antibodies that are produced as a result of microbial and food antigens the mother has previously

encountered. Such SIgA antibodies from breast milk provide protection to the neonate at the mucosal surface. Breast milk additionally contains high concentrations of non-specific protective molecules, such as lactoferrin that has bactericidal, viricidal, and fungicidal properties. Milk oligosaccharides might block adherence of microorganism at the mucosal surface by functioning as receptor analogues. There is increasing data from recent publications that enhanced protection against diarrhea, respiratory tract infections, otitis media and H. influenzae infections, as well as wheezing illness may persist for years after breastfeeding. However, the role of breast milk antibody in protection from neonatal GBS disease remains poorly understood. Current research is evaluating transport, persistence and function of GBS antibodies and other immune-constituents in breast milk. These studies aim to identify protective factors involved in the passive transfer of immune components in breast milk and associated protection from colonization and infant disease. Additionally, research correlating neonatal colonization with antibody levels in breast milk would provide insight into possibly protective factors from disease.

An audit conducted in the UK63 found that out of 448 patients admitted to hospital with an AECOPD, less than two-thirds (n = 286) met the Selleckchem ABT 199 criteria for admission to an early pulmonary rehabilitation program. The most common reasons for exclusion were cognitive impairment or being unable to walk. Less than one-third of eligible patients were referred to early pulmonary rehabilitation (n = 90) and less than

half of those referred went on to complete the program (n = 43). This represents less than 10% of all hospital discharges with AECOPD. Little information is available to explain health professionals’ low rate of referral of eligible patients and further work is required to understand this failure of research translation. Patient-related barriers have received more attention. People with COPD who decline early pulmonary rehabilitation may experience feelings of low self-worth, be reluctant to seek help, feel they are doing enough exercise already and perceive pulmonary rehabilitation as of limited value.64

These factors suggest that supportive and flexible referral pathways will be required to facilitate access and uptake of early pulmonary rehabilitation for people recovering from AECOPD. Exacerbations of COPD have long-term consequences and high costs for individuals, communities and the health system. Whilst every exacerbation is important, a patient’s second exacerbation that is severe enough to require hospitalisation may be a sentinel event that marks an exponential HSP inhibitor increase in the rate of future severe

exacerbations and increased risk of mortality.65 This suggests that there may be a window of opportunity after the first hospitalisation for AECOPD in which health professionals can intervene to prevent or delay the second severe exacerbation and modify the disease course. This is an important opportunity for physiotherapists, who frequently have second contact with patients hospitalised for their first AECOPD and be able to positively influence future management. Vaccination and maintenance pharmacotherapy are the mainstays of exacerbation prevention in people with COPD. In community-dwelling older people, the influenza vaccine reduces the risk of hospitalisation for pneumonia and influenza by 27%, with an associated 48% reduction in the risk of death.66 The pneumococcal vaccine is also commonly given, although there is less evidence for its benefits. Large randomised controlled trials have shown convincing reductions in exacerbation risk and hospitalisation using the combination of inhaled corticosteroids and long-acting beta agonists67 or long-acting muscarinic antagonists.68 Current treatment protocols indicate that either regimen can be used to prevent exacerbations, or triple therapy can be given if necessary.

, 1997 and Chao et al., 2010), this correlation may embody a relevant pathophysiological response to seizures (Ueda et al., 2002). Previous study had already been conducted on the

expression of glutamate transporters following kainate treatment during brain development and no differences were found for hippocampal GLT-1 mRNA levels 4, 8 and 16 h after kainate-induced seizures in rats at 7 days old (Simantov et al., 1999). These differences between the studies could be due to the required time course for changes in the mRNA expression (measured in the Ref. Simantov et al., 1999) and in the detection on the translated protein (measured in our study). Interestingly, GLAST was the only glutamate transporter in newborn rats treated buy Crizotinib with kainate that remains up regulated and the OSI-906 solubility dmso same profile for GLAST mRNA levels was also observed in adult animals (Nonaka et al., 1998). Additionally, it is noteworthy that the glutamate uptake apparently follows the ontogeny of GLT-1 during brain development (Ullensvang et al., 1997). Although it remains to be determined if glutamate uptake in acutely isolated slices from rat pups could be related to nerve terminals, glial cells or both cellular compartments, a recent study reported that the uptake activity into acutely dissociated slices from adult animals was related to nerve terminals

rather than glial uptake (Furness et al., 2008). More investigations need to be performed helping to elucidate this topic. Our findings ruled out the participation of EAAC1 transporter in the kainate-induced seizures in newborns. Interestingly, the same could not be observed in adult animals submitted to kainate-induced Tolmetin seizures, since hippocampal EAAC1 mRNA expression remains increased up to 5 days after seizures (Nonaka et al., 1998). As the kainate toxicity depends on the release of endogenous excitatory amino acids (Ben-Ari, 1985, Coyle, 1983 and Sperk et al., 1983) and in vitro studies indicated

that glutamate stimulates glutamate transport in primary astrocyte cultures ( Gegelashvili et al., 1996), it can be hypothesized that the transient up regulation of both transporters could reflect an attempt to remove the excess of extracellular glutamate that accumulate during seizure periods ( Ueda et al., 2002). As the GLAST immunocontent was more specifically involved in short ( Duan et al., 1999) and prolonged ( Gegelashvili et al., 1996) stimulatory effect triggered by glutamate on its own uptake by cultured astrocytes, the longer lasting increase in the GLAST immunocontent after KA-induced seizures here observed (up to 48 h) could be interpreted as a neuroprotective response to the increase of hippocampal glutamate extracellular levels. It is interesting to note that the increase in the immunoreactivity for GFAP-positive astrocytes, which was measured 24 h after the end of seizures, accomplished the increase in the GLAST immunocontent.

88 for measuring ankle inversion ( Diamond et al 1989). Inter-rater reliability of measurements of physiological range of motion of the first ray in nonsymptomatic participants by podiatric physicians using a goniometer was unacceptable ( Van Gheluwe et al

2002). Finally, the only study in this review investigating accessory range of motion showed fair (Kappa 0.35) to moderate (Kappa 0.48) inter-rater reliability for measurements of medio-lateral talar motion by physiotherapists in symptomatic participants ( Erichsen et al 2006). This systematic review included 17 studies investigating inter-rater reliability of passive movements in lower extremity joints. Five studies demonstrated acceptable reliability. In four of these, physiotherapists acted as raters. Reliability Selleck EPZ-6438 of measurements of physiological range of motion ranged from Kappa –0.02 for rheumatologists using a goniometer to measure knee extension in patients with knee osteoarthritis,

to ICC 0.97 for physiotherapists visually estimating knee flexion in symptomatic participants. Measuring physiological range of knee flexion consistently yielded acceptable reliability using either vision or instruments. Measurements of end-feel check details were unreliable for all hip and knee movements. Two high-quality studies (Cibere et al 2004, Watkins et al 1991) reported acceptable reliability for measuring physiological range of knee flexion and extension. Overall, however, methodological quality of the included studies was poor. Inter-rater reliability for measurement

of passive physiological range of motion in lower extremity joints was, overall, considerably less than that in upper extremity joints (Van de Pol et al 2010). In upper extremity joints, measuring large physiological ranges of motion like those in the shoulder, wrist, or fingers using instruments frequently yielded satisfactory reliability (Van de Pol et al 2010). This finding could PD184352 (CI-1040) only partly be confirmed for the lower extremity. For instance, measurement of physiological knee flexion using either vision or instruments indeed showed acceptable reliability, but measurements of relatively smaller ankle movements were unreliable in four out of five studies. However, inter-rater reliability for hip measurements varied widely across movements and methods of measurement. This heterogeneity in reliability could be explained by the large variation among studies in operational definitions of measurement procedures particularly with respect to participant positioning and instruction, and raters’ execution of movements and handling of instruments. New research investigating inter-rater reliability for measurement of passive physiological hip movements should incorporate measurement procedures that are in accordance with international standards such as described by Clarkson (2005).

176-178 °C; IR (KBr, cm−1): 3069 (Ar C–H stretch), 2841 (Aliphatic C–H stretch), 1581–1550 TSA HDAC in vivo (Amidine C N stretch), 1479–1455 (Aromatic C C stretch), 1170 (C–N stretch); 1H NMR (CDCl3, 400 MHz) δ: 3.63 (s, 2H), 2.29–2.5

(broad, 8H, pip), 7.18–7.23 (m, complex, Ar–H), 7.23–7.49 (m, complex, Ar–H). 190–192 °C: IR (KBr, cm−1): 3065(Ar C–H stretch), 2835 (Aliphatic C–H stretch), 1605–1560 (Amidine C N stretch), 1490–1465 (Aromatic C C stretch), 1189 (C–N stretch) 1H NMR (CDCl3, 400 MHz) δ: 4.26 (s, 2H), 2.38–2.74 (broad, 8H, pip), 7.22–7.49 and 7.49–7.6 (m, complex Ar–H). Yield: 72%, m.p. Decitabine ic50 178–179 °C: IR (KBr, cm−1): 3061 (Ar C–H stretch), 2856 (Aliphatic C–H stretch), 1578–1540 (Amidine C N stretch), 1487–1445 (Aromatic C C stretch), 1210 (C–N stretch) 1H NMR (CDCl3, 400 MHz) δ: 4.22 (s, 2H), 3.24–3.29 (8H, pip), 6.97–7.29 (m, complex, Ar–H). Yield: 80%, m.p. 167–169 °C: IR (KBr, cm−1): 3058 (Ar C–H stretch), 2867 (Aliphatic C–H stretch), 1587–1540

(Amidine C N stretch), 1467–1450 (Aromatic C C stretch), 1205 (C–N stretch) 1H NMR (CDCl3, 400 MHz) δ: 3.77 (s, 2H), 2.37–2.73 (8H, pip), 3.5 (s, 3H), 6.98–7.40 (m, complex, Ar–H). Yield: 75%, m.p. 188–191 °C: IR (KBr, cm−1): 3064 (Ar C–H stretch), 2847(Aliphatic C–H stretch), 1597–1550 (Amidine C N stretch), 1479–1450 (Aromatic C C stretch), 1190 (C–N stretch) 1H NMR (CDCl3, 400 MHz) δ: 4.26 (s, 3H), 2.74–3.24 (8H, pip), 3.8 (s, 3H), 7.23–7.6 (m, complex, Ar–H). Yield: 69%, m.p. 156–158 °C: IR (KBr, cm−1): 3064 (Ar C–H stretch), 2847 (Aliphatic ever C–H stretch), 1597–1550 (Amidine C N stretch), 1479–1450 (Aromatic C C stretch), 1190 (C–N stretch); 1H NMR (CDCl3, 400 MHz) δ: 3.66 (s, 2H), 3.23–3.38 (8H, pip), 2.31 (s, 3H), 7.22–7.6 (m, complex, Ar–H). Yield: 78%, m.p. 160–162: IR (KBr, cm−1): 3060 (Ar C–H stretch), 2847 (Aliphatic C–H stretch), 1597–1550 (Amidine C N stretch), 1479–1450

(Aromatic C C stretch), 1190 (C–N stretch); 1H NMR (CDCl3, 400 MHz) δ: 2.21 (s, 2H), 3.24–3.39 (8H, pip), 4.26 (s, 2H), 7.28–7.6 (m, complex, Ar–H). Yield: 55%, m.p. 125–127; IR (KBr, cm−1): 3054 (Ar C–H stretch), 2845 (Aliphatic C–H stretch), 1595–1557 (Amidine C N stretch), 1470–1440 (Aromatic C C stretch), 1179 (C–N stretch); 1H NMR (CDCl3, 400 MHz) δ: 4.26 (s, 3H), 2.74–3.24 (8H, pip), 3.8 (s, 3H), 7.23–7.6 (m, complex, Ar–H). The mice (22–25 g) were divided into twelve groups, each group contain five animals. The control group was received only Haloperidol (1 mg/kg i.p).

“
“The Transition

Care Program was established in 2004-05 as a jointly funded initiative between the Commonwealth and states and territories of Australia. It is provided to older persons at the end of a hospital stay in the form of a package of services (Department of Health and Ageing 2008). Between October 2005 and February 2008 there were 12 573 discharges from the Transition Care Program nationally (Department of Health and Ageing 2008). A common component for all Transition Care Programs is the provision of allied health services to aid the assessment, treatment and discharge planning of patients. Across Australia current practice involves a broad range of models of care relating to the provision of Transition Care Program physiotherapy services and the use of allied health assistants. Also, a diverse range of outcome measures are applied. It is a current requirement selleck products that all Transition Care Programs apply Ibrutinib nmr the Modified Barthel Index at admission to and discharge from the program (Department of Health and Ageing 2008). However, there is evidence that the Modified Barthel Index has a ceiling effect in older populations in hospital (de Morton et al 2007) and community settings (Hill et al 2008) and that it measures domains that

are not relevant to physiotherapy interventions (de Morton et al 2008c). Systematic reviews have identified drawbacks in the use of other activity limitation measures in hospital (de Morton et al 2008a) and community settings (Davenport

et al 2008). There are currently no best practice guidelines regarding the optimal method for measuring activity limitation for patients making the transition from hospital to the community. Physiotherapy focuses on the assessment and management of problems with movement (Jensen et al 1999). To conduct a Oxalosuccinic acid rigorous evaluation of the efficacy of physiotherapy for patients making the transition from hospital to the community, a tool for measuring activity limitation that, in particular, measures the construct of mobility accurately is required. According to the World Health Organisation International Classification of Functioning ‘mobility’ is classified as one of nine domains of ‘activity and participation’ and is defined as ‘moving by changing body position or location or by transferring from one place to another, by carrying, moving or manipulating objects, by walking, running or climbing, and by using various forms of transportation’ (WHO 2001). An instrument that can be applied in a broad range of environments and that will accurately measure and monitor changes in mobility for all patients in Transition Care Programs without floor or ceiling effects would have many benefits. In 2008, the de Morton Mobility Index (DEMMI) was developed and validated in an older acute medical population (de Morton et al 2008b); it has since been validated in subacute hospital (de Morton and Lane, 2010) and community settings (Davenport and de Morton, 2010, de Morton et al 2010).

Dominant antigenic sites inducing serotype specific neutralizing EPZ-6438 solubility dmso antibodies (nAbs) are mainly located on VP2, however, other structural and non-structural proteins – VP3, VP5, VP7, NS1 and NS2 – also induce humoral and cellular immune responses [4], [5], [6], [7], [8] and [9]. Since there is no successful treatment for AHS, vaccination is the most important approach to protect horses against AHS. Live-attenuated vaccines (LAVs) obtained by serial passages of AHSV in cell culture are available commercially for most serotypes in South Africa [1]. Although LAVs have been extensively used in South Africa and

other African countries, there are still concerns as LAVs cause viremia and could be transmitted by midges. However, the biggest concern of using these vaccines is reassortment between LAVs or

with wild type AHSV, which could result in more pathogenic virus variants. Moreover, the recent outbreak of AHSV serotype 9 in Gambia is suspected to be derived from vaccine strains [10]. Currently, LAVs are not licensed in Europe. To overcome safety issues, alternative AHS vaccines are under Z-VAD-FMK research buy development including inactivated virus, recombinant VP2, DNA vaccine and vaccinia virus vectors expressing VP2 protein [11], [12], [13], [14], [15], [16], [17], [18] and [19]. Outer capsid protein VP2 of orbiviruses determines the serotype and is the main target of nAbs [20], [21], [22] and [23]. Vaccination with recombinant VP2 of AHSV serotype 4, 5 or 9 has been reported to induce nAbs and protect horses against homologous AHSV challenge infection [13], [14], [16], [18], [19], [22] and [24]. To date, there are no reports regarding the immunogenicity of VP2 proteins of other serotypes of AHSV. In this report, VP2 of all nine AHSV serotypes were produced individually using the baculovirus expression system and their immunogenic Tryptophan synthase activities were investigated by immunization of guinea pigs, singly or in cocktail mixtures. The results demonstrated that

recombinant VP2 proteins of all nine AHSV serotypes have the potential to be used as safe subunit vaccines for AHS either individually or in a multi-serotype cocktail. AHSV reference strains (obtained from ANSES, France) were passaged and amplified in BSR cells, a derivative of the BHK-21 cell line, in Dulbecco’s modified Eagle’s medium (DMEM) (Sigma) supplemented with 10% fetal bovine serum (Invitrogen). Virus titers were determined by a plaque-forming assay in BSR cells and defined as plaque forming units per ml (pfu/ml) as described [25]. Insect cell lines of Spodoptera frugiperda, Sf9 and Sf21, were cultured at 28 °C in Insect-Xpress (Lonza, Basel, Switzerland) and TC100 medium (Biochrom AG, Berlin, Germany), respectively. TC100 medium was supplemented with 10% fetal bovine serum.

Initial exposure to the

bacteria is in the nasopharynx, where they establish colonisation. Usually, episodes of nasopharyngeal colonisation are essentially asymptomatic, and do not lead to disease [2]. In certain cases however, when the range of innate and adaptive immune mechanisms is insufficient to prevent disease, aspiration of bacteria can lead to pneumonia. This is most common at the extremes of life and amongst immunocompromised individuals. Vaccines have been directed to this specific need. At present, licensed vaccines elicit protection through induction of opsonophagocytic antibodies against capsular polysaccharide antigens [3]. Once conjugated to carrier proteins, a process necessary to induce protection in infants, these vaccines can lead to reduction in carriage as well as disease. These conjugate vaccines are very effective at reducing disease caused by the S. pneumoniae serotypes included in the vaccine find more directly in the vaccinees and indirectly in the wider community. However, serotypes not included in the vaccine can replace the eliminated strains within the nasopharynx, leading to replacement

disease [4]. Despite recent increases in the number of serotypes included in vaccine formulations, it is likely that alternative strategies will be required in the long-term to protect against S. pneumoniae [3]. Live vaccines can lead to both humoral and cellular immune responses. Inclusion of a large number of antigens buy Autophagy inhibitor and natural bacterial adjuvants can lead to strong immunity in the absence of an exogenous adjuvant. Nasopharyngeal colonisation with live bacterial strains represents one such route of mucosal immunisation. Using murine models, we [5] and others [6] and [7] have studied the mechanisms by which

prior colonisation can protect against subsequent lethal before invasive pneumonia. Antibody responses induced through colonisation with a live wild-type (WT) strain are both necessary and sufficient to protect against invasive disease [5]. Such protection does not necessarily require antibodies to capsular polysaccharide, since experimental colonisation with unencapsulated strains is also protective [6]. Unencapsulated mutants are an attractive option for live attenuated vaccines due to their lack of virulence [6] and [8], but no direct comparison of the immunogenicity and protective efficacy of colonisation with isogenic strains with and without capsule has been reported. Bacterial lipoproteins are an important class of pathogen-associated molecular pattern (PAMP), capable of adjuvanting immune responses [9] by acting as ligands for TLR2 [10], and are common targets for adaptive immune responses [11] and [12]. Deletion of lgt, which encodes the protein diacylglyceryl transferase required to anchor lipoproteins to the cell membrane, results in an S.

Secondly, because of the choice of PRCC analysis as the core method of sensitivity analysis, our current GSA implementation presumes monotonicity of relationship between model parameters and analysed network outputs. Therefore, prior to analysis, the tests should be made, whether such an assumption can be justified (e.g. via visual evaluation of relevant scatterplots). If the monotonicity of input–output relationship cannot be assumed, the GSA procedure would require further adjustments, including replacement of PRCC analysis with a more appropriate method of SA (e.g. MPSA). GL conceived the idea of the study,

contributed to GSA design and coordination of the study, ran simulations, analysed and interpreted GSA and LSA results and wrote the manuscript. AS contributed to design BIBW2992 of the study, implemented and ran GSA and LSA procedure, participated in interpretation of results and drafting the manuscript.

DF, SPL, DJH planned the experiments, analysed data, contributed to drafting the manuscript. PD0325901 cost AG contributed to ErbB2/3 model development. PM performed the RPPA and in cell Western studies. SPL, DJH and IG contributed to design and coordination of the study, gave valuable advice and critically revised the manuscript. All authors read and approved the final manuscript. The Centre for Systems Biology at Edinburgh is a Centre for Integrative Systems Biology (CISB) funded by BBSRC and EPSRC, reference BB/D019621/1.

We also acknowledge support from Breakthrough Breast Cancer and the Scottish Funding Council. This work has made use of the resources provided by the Edinburgh Compute and Data Facility (ECDF) (http://www.ecdf.ed.ac.uk/). The ECDF is partially supported by the eDIKT initiative (http://www.edikt.org.uk). AG acknowledges the financial support of SICSA (Scottish Informatics and Computer Science Alliance). Authors are also grateful to Jane Hillston for helpful comments on the manuscript. “
“The allotype of omalizumab was erroneously reported to be G1m(f). However, the allotype of omalizumab is G1m(z), as determined serologically in our laboratory. The confusion arises from the fact Cediranib (AZD2171) that genetically, a and z are linked in such a way that one normally does not encounter z without a. Probably, omalizumab was engineered to introduce the allotype non-a (corresponding to E356/M358, as opposed to allotype a: D356/L358). The conclusions of the paper are not affected in any way. Different (CH3)2 and pFc’ fragments were compared. Here, only the a and non-a allotypic differences play a role. Whether these fragments are derived from antibodies that are either f or z is not relevant, since these allotypic markers are present in the CH1 domain. Thus, in Fig. 4C, the pFc’ fragment indicated as IgG1 (f) pFc’ corresponds to E356/M358, and this fragment should be labelled IgG1 (non-a) pFc’.