Progress, but at the Expense of Male Power? Institutional Resistance to Gender Equality in an Irish University.

Gender equality is a whole-organization endeavor. Building on Agócs (Journal of Business Ethics, 1997, 16 (9), 917-931) concept of institutionalized resistance this article undertakes a feminist critique of policy and practice around internal promotions to the equivalent of Associate Professor level in one Irish university (called the Case Study University). This university was selected because of its low proportion of women in senior academic positions. The methodology is a single case study design, employing documentary analysis, including secondary data. Since 2013 the proportion of women at Associate Professor in the Case Study University increased significantly (bringing them close to the national average): this being associated with increased transparency, with the cascade model in the background. However, men's "chances" have varied little over time and at 1:4 are the highest in Irish universities. This article uses Agócs (Journal of Business Ethics, 1997, 16 (9), 917-931) stages of institutional resistance to show that while some changes have been made, ongoing institutionalized resistance is reflected in its failure to accept responsibility for change as reflected in its refusal to challenge the "core mission" and restricting the focus to "fixing the women"; and its failure to implement change by focusing on "busy-ness" which does not challenge power and colluding with foot-dragging and slippage in key areas. It is suggested that such institutional resistance reflects the enactment of hidden or stealth power. The article implicitly raises questions about the intractability and the covertness of men's power and privilege and the conditions under which women's "chances" are allowed to improve, thus providing insights into the extent and nature of institutional resistance.

The value of lost productivity from workplace bullying in Ireland.

BACKGROUND: Workplace bullying is a pervasive problem with significant personal, social and economic costs. Estimates of the resulting lost productivity provide an important societal perspective on the impact of the problem. Understanding where these economic costs fall is relevant for policy. AIMS: We estimated the value of lost productivity to the economy from workplace bullying in the public and private sectors in Ireland. METHODS: We used nationally representative survey data and multivariable negative binomial regression to estimate the independent effect of workplace bullying on days absent from work. We applied the human capital approach to derive an estimate of the annual value of lost productivity due to bullying by sector and overall, in 2017. RESULTS: Bullying was independently associated with an extra 1.00 (95% CI: 0.38-1.62) days absent from work over a 4-week period. This differed for public and private sector employees: 0.69 (95% CI: -0.12 to 1.50) versus 1.45 (95% CI: 0.50-2.40) days respectively. Applying official data, we estimated the associated annual value of lost productivity to be €51.8 million in the public sector, €187.6 million in the private sector and €239.3 million overall. CONCLUSIONS: The economic value of lost productivity from workplace bullying in Ireland is significant. Although bullying is more prevalent in the public sector, it has a larger effect on absence in the private sector. Given this, along with the greater overall share of employees, productivity losses from bullying are considerably larger in the private sector in Ireland.

A study of workaholism in Irish academics.

BACKGROUND: Workaholism is recognized as a health risk for academics given the open-ended nature of academic work; however, current prevalence rates of workaholism in the academic setting are unknown. AIMS: To assess the prevalence of workaholism within academics and determine the impact of workaholism on psychological well-being, work-life conflict, work-life fit, job satisfaction and perceived work effort. METHODS: Academics in three Irish universities completed a survey including measures of workaholism, psychological well-being, work-life conflict and job satisfaction. Analysis of variance tests were used to compare workaholism types on the outcome measures. RESULTS: A total of 410 academics completed the survey and were categorized by workaholism type: workaholics (27%), enthusiastic workaholics (23%), relaxed workers (27%) and uninvolved workers (23%). Workaholics reported poorer functioning across all the outcome measures in comparison to the other three groups. CONCLUSIONS: This study demonstrates the high levels of workaholism within academia and highlights the negative impact of workaholism on work-related outcomes and psychological well-being. These findings are significant given the highly intensive nature of academic work today and reducing resources within this sector.

Expression of the sarco/endoplasmic reticulum calcium ATPase type 2 and 3 isoforms in normal skin and Darier's disease.

BACKGROUND: Darier's disease (DD) is caused by mutations in ATP2A2, which encodes the sarco/endoplasmic reticulum calcium ATPase type 2 (SERCA2), a member of a family of calcium pumps important in intracellular calcium signalling. SERCA2 has two isoforms. SERCA2a occurs mainly in cardiac and skeletal muscle, whereas SERCA2b occurs ubiquitously and is coexpressed with the related SERCA type 3 (SERCA3) in many tissues. It is not known why mutations in the widely expressed SERCA2 manifest as a focal skin disease. OBJECTIVES: To provide insight into the pathogenesis of DD by examining SERCA isoform expression in normal skin and DD skin. METHODS: Using immunohistochemistry we studied SERCA2a, SERCA2b and SERCA3 expression in nonlesional and lesional skin from seven patients with DD and normal skin from seven control subjects. We quantified SERCA2a and SERCA2b staining intensity by grey scale analysis of fluorescence intensity. RESULTS: In normal and DD epidermis both SERCA2a and SERCA2b staining was seen. SERCA2a staining in epidermis was less intense relative to pilar muscle whereas SERCA2b staining in epidermis was of marginally greater intensity than in pilar muscle. SERCA3 was not expressed in normal or DD epidermis, but was found in eccrine glands and blood vessels. No reduction was detected in SERCA2a or SERCA2b staining intensity in DD nonlesional epidermis compared with control epidermis. In within-patient comparisons, SERCA2a and SERCA2b staining in lesional epidermis was less intense than in nonlesional epidermis. CONCLUSIONS: Both SERCA2a and SERCA2b are present in epidermis, although the latter may predominate. The absence of coexpressed SERCA3 in epidermis may explain the localization of DD. Comparable SERCA2 staining intensity in nonlesional DD and control epidermis, even in patients predicted to be haploinsufficient, suggests partial compensation by upregulation of the normal allele. Unknown additional factors may trigger focal lesions by overcoming this compensation. Reduced staining intensity in lesional tissue may be secondary, or may reflect local downregulation of SERCA2 expression predisposing to development of focal lesions.

Feasibility of a men's health promotion programme in Irish primary care.

BACKGROUND: To assess the feasibility of offering health promotion and preventive medicine initiatives in primary care. AIMS: A pilot study aimed at men in general practice to establish the uptake, acceptability and effectiveness of interventions in health initiatives. METHODS: One thousand men aged 18-65 were selected at random from five general practices in the Western Health Board area. Practices were randomly allocated to one of four brief interventions: cardiovascular screening, cancer screening, stress management or general lifestyle advice. RESULTS: Fifty-five per cent of men responded, with 35.7% actually attending. There were minor but significant short-term changes in health status and behaviours. Participants expressed high levels of satisfaction, but tended to prefer interventions with an explicit clinical component. CONCLUSION: It is at least as feasible to offer health promotion for men in primary care as it is for other demographic groups, but adequate training and resources are required.

trans-dominant inhibition of connexin-43 by mutant connexin-26: implications for dominant connexin disorders affecting epidermal differentiation.

Dominant mutations of GJB2-encoding connexin-26 (Cx26) have pleiotropic effects, causing either hearing impairment (HI) alone or in association with palmoplantar keratoderma (PPK/HI). We examined a British family with the latter phenotype and identified a new dominant GJB2 mutation predicted to eliminate the amino acid residue E42 (DeltaE42) in Cx26. To dissect the pathomechanisms that result in diverse phenotypes of dominant GJB2 mutations, we studied the effect of three Cx26 mutants (DeltaE42, D66H and R75W) identified in individuals with PPK/HI, and another (W44C) present in individuals with non-syndromic HI on gap junctional intercellular communication. We expressed mutant Cx26 alone and together with the epidermal connexins Cx26, Cx37 and Cx43 in paired Xenopus oocytes, and measured the intercellular coupling by dual voltage clamping. Homotypic expression of each connexin as well as co-expression of wild-type (wt) Cx26/wtCx43 and wtCx26/wtCx37 yielded variable, yet robust, levels of channel activity. However, all four Cx26 mutants were functionally impaired and failed to induce intercellular coupling. When co-expressed with wtCx26, all four mutants suppressed the wtCx26 channel activity consistent with a dominant inhibitory effect. However, only those Cx26 mutants associated with a skin phenotype also significantly (P<0.05) inhibited intercellular conductance of co-expressed wtCx43, indicating a direct interaction of mutant Cx26 units with wtCx43. These results demonstrate, for the first time, a trans-dominant negative effect of Cx26 mutants in vitro. Furthermore, they support a novel concept suggesting that the principal mechanism for manifestation of dominant GJB2 mutations in the skin is their dominant interference with the function of wtCx43. This assumption is further corroborated by our finding that Cx26 and Cx43 focally colocalize at gap junctional plaques in affected skin tissue of two carriers of DeltaE42.

Polyamines regulate gap junction communication in connexin 43-expressing cells.

The control of cell-cell communication through gap junctions is thought to be crucial in normal tissue function and during various stages of tumorigenesis. However, few natural regulators of gap junctions have been found. We show here that increasing the activity of ornithine decarboxylase, or adding polyamines to the outside of cells, increases the level of gap junction communication between various epithelial cells. Conversely, reduction of ornithine decarboxylase activity decreases the level of gap junction communication. This regulation is dependent upon the expression of connexin 43 (Cx43 or Cxalpha1), which is a major connexin expressed in many different cell types, and involves an increase in Cx43 and its cellular re-distribution.

Human diseases: clues to cracking the connexin code?

The vertebrate gap junctions formed by the connexin family of transmembrane proteins came to the attention of geneticists in 1993 with the identification of mutations linked to a form of demyelinating neuropathy. Since then, several other genetic disorders have been linked to mutations in specific connexin genes. Also, different diseases can result from different mutations in the same connexin gene. In addition, specific connexin knockout mice have surprising phenotypes. This is leading cell biologists to look afresh at connexins and their involvement in intercellular communication through gap junctions, a process that seems central to coordinating cell function within tissues. Here, we comment on how genetic studies are giving a new impetus to the cell biology of gap junctions.

Critical care nurses' perceptions of DNR status.

PURPOSE: To describe the perceptions of nurses regarding do-not-resuscitate (DNR) decisions in critical care settings. DESIGN: A survey assessing knowledge, attitudes, and practices concerning DNR status was distributed to all critical care nurses who were registered with the provincial licensing body in Alberta, Canada, and held positions of staff nurse, educator, or manager. METHODS: Four hundred and five surveys were completed and returned. Descriptive analyses were conducted. FINDINGS: The term "DNR" was found to be ambiguous. The rationale for DNR orders were also not well articulated in practice. Although nurses believed that patients, families, and nurses should participate in DNR decisions, physicians were most often cited as being responsible for the decision. CONCLUSIONS: Documentation of a comprehensive patient treatment plan and awareness of the rationale for DNR designation are strategies suggested to help achieve desire patient care goals in critical care settings.

Upregulation of connexin 26 is a feature of keratinocyte differentiation in hyperproliferative epidermis, vaginal epithelium, and buccal epithelium.

In epidermis, it has been suggested, intercellular communication through gap junctions is important in coordinating cell behavior. The connexins, may facilitate selective assembly or permeability of gap junctions, influencing the distribution of metabolites between cells. Using immunohistochemistry, we have compared the distribution of connexins 26 and 43 with that of proliferating cells (Ki67 labeling) in normal epidermis, hyperplastic epidermis (tape-stripped epidermis, psoriatic lesions, and viral warts), and vaginal and buccal epithelia. Connexin 43 was abundant in spinous layers of all epidermal specimens and in vaginal and buccal epithelia. Connexin 26 was absent from the interfollicular and interductal epidermis of normal hair-bearing skin, and nonlesional psoriatic epidermis but present at very low levels in plantar epidermis. Connexin 26 was prominent in lesional psoriatic epidermis and viral warts and in vaginal and buccal epithelia. In three independent experiments connexin 26 appeared in a patchy intercellular distribution in the basal epidermis within 24 h of tape stripping, proceeding to more extensive distribution in basal and suprabasal layers by 48 h. The increase in connexin 26 preceded that in cell proliferation. In vaginal epithelium, buccal epithelium, and viral warts connexin 26 was restricted mainly to suprabasal, nonproliferating cells. In psoriatic lesional epidermis connexin 26 was also located mainly in suprabasal, nonproliferating cells. Connexin 26 was present in a patchy distribution in the basal layer of psoriatic lesional epidermis, but double labeling for connexin 26 and Ki67 showed that many connexin 26 positive basal cells were nonproliferative, suggesting that connexin 26 may be related to differentiation rather than to proliferation. These observations would be consistent with a role for connexin 26 containing gap junctions during both early and later stages of keratinocyte differentiation in hyperplastic epidermis and in vaginal and buccal epithelia.

Genetics of psoriasis: paternal inheritance and a locus on chromosome 6p.

The pathogenesis of psoriasis is not fully understood, but population and twin studies suggest a large heritable component to the etiology. Several large population studies have also suggested a parental sex effect. Since 1994, three main genetic loci (on chromosomes 17q, 4q, and 6p) have been reported in genome scans. With a view to elucidating the genetic basis of psoriasis, we have carried out linkage analysis in a large number of families with well-characterized psoriasis. From a cohort of 1250 probands with psoriasis, 395 individuals (301 affected, 94 unaffected) in 103 families were recruited. Each subject was carefully examined by an experienced dermatologist and stringent diagnostic criteria applied. Genotypes were generated at 11 polymorphic loci on chromosomes 17q, 4q, and 6p and the results were analyzed parametrically and nonparametrically. In the population from which the probands were drawn, there was evidence of a parental sex effect, more probands having an affected father than an affected mother. Genetic anticipation was also apparent and most marked if the disease was inherited from the father. The loci on chromosomes 17 and 4 were not replicated but there was strong evidence for linkage to chromosome 6p (maximum two point LOD score 4.63 at D6S291). The evidence for linkage in sibling pair analysis was greatest when the allele was of paternal origin and was most significant in those families without psoriatic arthritis. These studies confirm the presence of a susceptibility gene on chromosome 6p. The available evidence suggests that a different genetic susceptibility may underlie psoriasis and psoriatic arthritis.

An immunohistochemical study of androgen, oestrogen and progesterone receptors in the vulva and vagina.

OBJECTIVE: To map potential sites of sex steroid action in the human vulva. METHODS: Monoclonal antibodies to androgen, oestrogen and progesterone receptors were used to stain frozen sections of vulval skin, vagina and suprapubic skin. A scoring system was devised to compare receptor distribution in the epidermis and dermis of skin with vaginal epithelium and stroma. RESULTS: Androgen receptors were seen in epidermal keratinocytes, sebaceous glands, sweat glands, hair follicles and dermal fibroblasts of skin, and epithelial cells and stromal fibroblasts of the vagina. Androgen receptor scores were significantly higher in the epidermis of labia majora and minora than in vaginal epithelium. Oestrogen receptors were seen in basal and suprabasal cells of vaginal epithelium and epidermis of labia minora but were restricted to basal keratinocytes in true skin. They were seen in stromal fibroblasts and vaginal smooth muscle, and dermal fibroblasts of the skin. Oestrogen receptors were highest in vaginal epithelium and stroma, and lowest in suprapubic skin. Progesterone receptors were seen in vaginal epithelium, fibroblasts and smooth muscle but not in the vulva. There was no evidence of significant differences in androgen or oestrogen receptor staining in the vulva of pre- or postmenopausal women. CONCLUSION: The transition from vagina to vulva is marked by an increase in androgen and a decrease in oestrogen and progesterone receptors. This distribution of receptors would indicate a limited role for oestrogen creams on the vulva.

Characterization and chromosomal localization of human hair-specific keratin genes and comparative expression during the hair growth cycle.

During anagen, cell proliferation in the germinative matrix of the hair follicle gives rise to the fiber and inner root sheath. The hair fiber is constructed from structural proteins belonging to four multigene families: keratin intermediate filaments, high-sulfur matrix proteins, ultra high-sulfur matrix proteins, and high glycine-tyrosine proteins. Several hair-specific keratin intermediate filament proteins have been characterized, and all have relatively cysteine-rich N- and C-terminal domains, a specialization that allows extensive disulfide cross-linking to matrix proteins. We have cloned two complete type II hair-specific keratin genes (ghHb1 and ghHb6). Both genes have nine exons and eight introns spanning about 7 kb and lying about 10 kb apart. The structure of both genes is highly conserved in the regions that encode the central rod domain but differs considerably in the C-terminal coding and noncoding sequences, although some conservation of introns does exist. These genes have been localized to the type II keratin cluster on chromosome 12q13 by fluorescence in situ hybridization. They, and their type I partner ghHa1, are expressed in differentiating hair cortical cells during anagen. In cultured follicles, ghHa1 expression declined in cortical cells and was no longer visible after 6 d, whereas the basal epidermal keratin hK14 appeared in the regressing matrix. The transition from anagen to telogen is marked by downregulation of hair cortical specific keratins and the appearance of hK14 in the epithelial sac to which the telogen hair fiber is anchored. Further studies of the regulation of these genes will improve our understanding of the cyclical molecular changes that occur as the hair follicle grows, regresses, and rests.

Children's coping with venipuncture.

Children's strategies for coping with the pain and distress of venipuncture were examined in this descriptive study. Eighty-five children (aged 5-13 years) were interviewed prior to and following blood collection. Prior to the procedure, children reported pain expectations and coping strategies that might be used. Self-reports of the pain experienced and coping strategies used were obtained immediately after the procedure. Twenty-seven different strategies were identified from the children's responses. These strategies were subsequently grouped into 11 coping categories: Active Involvement in Procedure, Behavior-Regulating Cognitions, Cognitive Reappraisal, Direct Efforts to Maintain Control, Diversionary Thinking, Emotion-Regulating Cognitions, Information Seeking, Reality-Oriented Working Through, Reliance on Health-Care Interventions, Support Seeking, and Avoidance and Catastrophizing. Direct Efforts to Maintain Control was the most frequently used category. Age and gender differences were observed in both number and type of strategies reported by the children. Further research is needed to examine the observed relationship between the type of coping strategies generated and the children's pain experience.

Correlation of clinical, endocrine and molecular abnormalities with in vivo responses to high-dose testosterone in patients with partial androgen insensitivity syndrome.

OBJECTIVE: To investigate the responses of two patients previously diagnosed as Reifenstein's syndrome to graded high-dose testosterone in terms of hormone levels, nitrogen balance and sebum secretion and to attempt to correlate these parameters with the properties of their androgen receptors and mutations in the androgen receptor gene. DESIGN: Nitrogen balance was determined by comparing controlled nitrogen intake to the amount excreted. Sebum excretion was measured on the forehead. Patients were studied during control periods (no treatment) and during administration of testosterone propionate. Blood samples were used as a source of genomic DNA and to measure peripheral hormone levels; androgen receptor binding was determined using genital skin fibroblasts. PATIENTS: Two patients of XY karyotype, with ambiguous external genitalia and problems of testicular descent who had required mastectomy as teenagers. Normal male controls of proven fertility. MEASUREMENTS: Nitrogen balance, sebum excretion rate and peripheral hormone levels (testosterone, dihydrotestosterone, LH and FSH) were studied before and after testosterone therapy (1 or 5 mg/kg/day). Genomic DNA was extracted from peripheral blood leucocytes and regions of the androgen receptor gene amplified by polymerase chain reaction using pairs of specific primers. Mobility of amplified DNA from patients was analysed on denaturing gradient acrylamide gels and fragments differing in mobility from those of normal controls were sequenced. Fibroblasts were cultured from scrotal skin biopsies and androgen receptor binding parameters, subcellular localization and up-regulation were determined. RESULTS: Testosterone therapy resulted in raised plasma testosterone, dihydrotestosterone and oestradiol in both patients. In patient 1 (lesser genital abnormality), LH was suppressed by 5 mg/kg/day testosterone to the upper limit of the normal range but FSH remained low normal. Both LH and FSH were suppressed by testosterone treatment in patient 2 (greater genital abnormality). Nitrogen retention was increased in both patients (4.2 and 3.0 g/24 h respectively); sebum excretion rate increased to normal in patient 1 but showed no change in patient 2. Mutations in the androgen receptor gene were identified in both patients. In patient 1 a single nucleotide change from adenosine to guanosine resulted in the substitution of glycine for glutamic acid at position 772 within the hormone binding domain of the receptor. In patient 2 a single nucleotide mutation from guanosine to adenosine resulted in the substitution of lysine for arginine at position 608 (exon 3) situated in the second zinc finger of the DNA binding domain. Both patients had a normal number of androgen binding sites in genital skin fibroblasts but those in patient 1 showed reduced binding affinity and rapid dissociation of receptor/ligand complexes while those in patient 2 showed defective nuclear localization. CONCLUSION: In patients with partial androgen insensitivity syndrome the type of androgen receptor mutation and responses to short-term androgen treatment can be correlated with the individual's potential to virilize. If there is a mutation in the androgen receptor DNA binding domain the patient may show little ability to virilize either spontaneously at puberty or after androgen treatment. Sebum excretion appears to be more discriminating than nitrogen balance or gonadotrophin suppression as an index of tissue response to androgens.