Living with alopecia areata: an online qualitative survey study.

BACKGROUND: Living with alopecia areata (AA) totalis and universalis (collectively referred to here as AA) involves unpredictable, sometimes rapid hair loss. There is currently no effective treatment and patients describe feelings of shock, loss, trauma and disrupted identity. Cultural meanings attached to hair and hair loss, including associations between hair and femininity, and hair loss and cancer may exacerbate distress. Consequently, wigs and make-up are frequently used as camouflage, but this can produce feelings of inauthenticity, shame and anxiety. OBJECTIVES: This article explores how meanings associated with hair and hair loss influence experiences of living with AA. We also aim to identify how this understanding might inform practice by healthcare professionals to best support patients to cope with the condition. METHODS: A total of 95 participants with AA completed an online qualitative survey about their experiences of living with the condition. Data were subjected to thematic analysis within a critical realist theoretical framework. RESULTS: The following four themes were identified: (i) It's (not) only hair; (ii) A restricted life; (iii) Abandon hope all ye who lose their hair and (iv) Seeking support in 'a highly personal journey'. CONCLUSIONS: Findings suggest that negative cultural meanings of hair and hair loss are pervasive and may drive social avoidance and camouflage behaviours in people with AA. Normalizing social interactions with healthcare practitioners, significant others and peers were cited as pivotal to positive adjustment. Support groups and online forums were highly valued particularly as few had been offered specialist psychological support. Future research should develop and evaluate psychological support in order to address the specific challenges of living with AA.

Second-hand smoke exposure levels and tobacco consumption patterns among a lesbian, gay, bisexual and transgender community in Ireland.

OBJECTIVES: To estimate and identify characteristics of tobacco use, including use of roll-your-own (RYO) cigarettes and second-hand smoke (SHS) exposure, among a self-identified lesbian, gay, bisexual and transgender (LGBT) community in Ireland. STUDY DESIGN: Web-based self-administered questionnaire survey using a cross-sectional study design. METHODS: A convenience sample of 661 self-identified LGBT respondents was recruited through a well-advertised web-based survey tool method between March and May 2012. Prevalence rates were adjusted for age, sexual orientation, social class and nationality. Multivariable logistic regression was performed to characterize tobacco use profile and SHS exposure levels for estimating adjusted odds ratios (AOR) with 95% confidence intervals (CI). RESULTS: Of the 661 respondents, 45.3% (95% CI 44.9-45.7) reported current use of tobacco and 15.6% reported current use of RYO cigarettes (results were significantly higher for lesbians in both categories). In addition, 40.3% (95% CI 39.9-40.6) of respondents reported SHS exposure at home (significantly higher in gays), and 50.1% (95% CI 49.3-50.8) reported SHS exposure in cars (significantly higher in lesbians); these two groups were not mutually exclusive. The oldest individuals and non-Irish nationals were more than twice as likely to report SHS exposure in cars compared with the youngest individuals and Irish nationals, and the least-educated individuals were more than twice as likely to report current use of RYO cigarettes compared with the most-educated individuals (AOR 2.26; 95% CI 1.06-4.79). Non-tobacco users were less likely to report SHS exposure at home compared with current tobacco users (AOR 0.31; 95% CI 0.21-0.46). DISCUSSION: Despite inherent methodological limitations associated with identification of such a study sample, the adjusted rates indicate that tobacco use is very high among the LGBT community in Ireland compared with the general Irish population (smoking rate 29%). High levels of SHS exposure at home and in cars further underscore the significance of smoke-free private vehicle and 100% smoke-free home policies. A targeted tobacco control strategy should be explored for this vulnerable population.

A shotgun optical map of the entire Plasmodium falciparum genome.

The unicellular parasite Plasmodium falciparum is the cause of human malaria, resulting in 1.7-2.5 million deaths each year. To develop new means to treat or prevent malaria, the Malaria Genome Consortium was formed to sequence and annotate the entire 24.6-Mb genome. The plan, already underway, is to sequence libraries created from chromosomal DNA separated by pulsed-field gel electrophoresis (PFGE). The AT-rich genome of P. falciparum presents problems in terms of reliable library construction and the relative paucity of dense physical markers or extensive genetic resources. To deal with these problems, we reasoned that a high-resolution, ordered restriction map covering the entire genome could serve as a scaffold for the alignment and verification of sequence contigs developed by members of the consortium. Thus optical mapping was advanced to use simply extracted, unfractionated genomic DNA as its principal substrate. Ordered restriction maps (BamHI and NheI) derived from single molecules were assembled into 14 deep contigs corresponding to the molecular karyotype determined by PFGE (ref. 3).

Low birthweight and preterm birth rates 1 year before and after the Irish workplace smoking ban.

OBJECTIVE: It is well-established that maternal smoking has adverse birth outcomes (low birthweight, LBW, and preterm births). The comprehensive Irish workplace smoking ban was successfully introduced in March 2004. We examined LBW and preterm birth rates 1 year before and after the workplace smoking ban in Dublin. DESIGN: A cross-sectional observational study analysing routinely collected data using the Euroking K2 maternity system. SETTING: Coombe University Maternal Hospital. POPULATION: Only singleton live births were included for analyses (7593 and 7648, in 2003 and 2005, respectively). METHODS: Detailed gestational and clinical characteristics were collected and analysed using multivariable logistic regression analyses and subgroup analyses. MAIN OUTCOME MEASURES: Maternal smoking rates, mean birthweights, and adjusted odds ratios (ORs) of LBW and preterm births in 2005 versus 2003. RESULTS: There was a 25% decreased risk of preterm births (OR, 0.75; 95% CI, 0.59-0.96), a 43% increased risk of LBW (OR, 1.43; 95% CI, 1.10-1.85), and a 12% fall in maternal smoking rates (from 23.4 to 20.6%) in 2005 relative to 2003. Such patterns were significantly maintained when specific subgroups were also analysed. Mean birthweights decreased in 2005, but were not significant (P=0.99). There was a marginal increase in smoking cessation before pregnancy in 2005 (P=0.047). CONCLUSIONS: Significant declines in preterm births and in maternal smoking rates after the smoking ban are welcome signs. However, the increased LBW birth risks might reflect a secular trend, as observed in many industrialised nations, and merits further investigations.

Separate domains of the Ran GTPase interact with different factors to regulate nuclear protein import and RNA processing.

The small Ras-related GTP binding and hydrolyzing protein Ran has been implicated in a variety of processes, including cell cycle progression, DNA synthesis, RNA processing, and nuclear-cytosolic trafficking of both RNA and proteins. Like other small GTPases, Ran appears to function as a switch: Ran-GTP and Ran-GDP levels are regulated both by guanine nucleotide exchange factors and GTPase activating proteins, and Ran-GTP and Ran-GDP interact differentially with one or more effectors. One such putative effector, Ran-binding protein 1 (RanBP1), interacts selectively with Ran-GTP. Ran proteins contain a diagnostic short, acidic, carboxyl-terminal domain, DEDDDL, which, at least in the case of human Ran, is required for its role in cell cycle regulation. We show here that this domain is required for the interaction between Ran and RanBP1 but not for the interaction between Ran and a Ran guanine nucleotide exchange factor or between Ran and a Ran GTPase activating protein. In addition, Ran lacking this carboxyl-terminal domain functions normally in an in vitro nuclear protein import assay. We also show that RanBP1 interacts with the mammalian homolog of yeast protein RNA1, a protein involved in RNA transport and processing. These results are consistent with the hypothesis that Ran functions directly in at least two pathways, one, dependent on RanBP1, that affects cell cycle progression and RNA export, and another, independent of RanBP1, that affects nuclear protein import.

Increased seizure susceptibility in mice lacking metabotropic glutamate receptor 7.

To study the role of mGlu7 receptors (mGluR7), we used homologous recombination to generate mice lacking this metabotropic receptor subtype (mGluR7(-/-)). After the serendipitous discovery of a sensory stimulus-evoked epileptic phenotype, we tested two convulsant drugs, pentylenetetrazole (PTZ) and bicuculline. In animals aged 12 weeks and older, subthreshold doses of these drugs induced seizures in mGluR7(-/-), but not in mGluR7(+/-), mice. PTZ-induced seizures were inhibited by three standard anticonvulsant drugs, but not by the group III selective mGluR agonist (R,S)-4-phosphonophenylglycine (PPG). Consistent with the lack of signs of epileptic activity in the absence of specific stimuli, mGluR7(-/-) mice showed no major changes in synaptic properties in two slice preparations. However, slightly increased excitability was evident in hippocampal slices. In addition, there was slower recovery from frequency facilitation in cortical slices, suggesting a role for mGluR7 as a frequency-dependent regulator in presynaptic terminals. Our findings suggest that mGluR7 receptors have a unique role in regulating neuronal excitability and that these receptors may be a novel target for the development of anticonvulsant drugs.

Kainate receptors: subunits, synaptic localization and function.

Although it is well established that kainate receptors constitute an entirely separate group of proteins from AMPA receptors, their physiological functions remain unclear. The molecular cloning of subunits that form kainate receptors and the ability to study recombinant receptors is leading to an increased understanding of their functional properties. Furthermore, the development of kainate receptor-selective agonists and antagonists over the past few years is now allowing the physiological roles of these receptors and, in some cases, specific subunits to be investigated. As a consequence, the synaptic activation of postsynaptic kainate receptors and the presence of presynaptic kainate receptors that serve to regulate excitatory and inhibitory synaptic transmission have been described, and will be discussed in this article by Ramesh Chittajallu, Steven Braithwaite, Vernon Clarke and Jeremy Henley.

Characterisation of the effects of ATPA, a GLU(K5) kainate receptor agonist, on GABAergic synaptic transmission in the CA1 region of rat hippocampal slices.

Kainate receptors are implicated in a variety of physiological and pathological processes in the CNS. Previously we demonstrated that (RS)-2-amino-3-(3-hydroxy-5-tert-butylisoxazol-4-yl)propanoic acid (ATPA), a selective agonist for the GLU(K5) subtype of kainate receptor, depresses monosynaptically evoked inhibitory postsynaptic potentials (IPSPs) in the CA1 region of the rat hippocampus. In the current study, we provide a more detailed characterisation of this effect. Firstly, our data demonstrate a rank order of potency of domoate>kainate>ATPA>alpha-amino-3-(3-hydroxy-5-methyl-4-isoxalolyl)propionic acid Secondly, we confirm that the effects of ATPA are not mediated indirectly via the activation of gamma-aminobutyric acid receptors (i.e. either GABA(A) or GABA(B)). Thirdly, we show that the small increase in conductance induced by ATPA is insufficient to account for the depression of monosynaptic inhibition. Fourthly, we show that the effects of ATPA on IPSPs are antagonised by the GLU(K5)-selective antagonist (3S, 4aR, 6S, 8aR)-6-(4-carboxyphenyl)methyl-1,2,3,4,4a,5,6,7,8,8a-decahydroisoquinoline-3-carboxylic acid (LY382884). However, LY382884 is less potent as an antagonist of the effects of ATPA on IPSPs compared to its depressant effect on EPSPs.

Characterisation of the effects of ATPA, a GLU(K5) receptor selective agonist, on excitatory synaptic transmission in area CA1 of rat hippocampal slices.

Kainate receptors are involved in a variety of synaptic functions in the CNS including the regulation of excitatory synaptic transmission. Previously we described the depressant action of the GLU(K5) selective agonist (RS)-2-amino-3-(3-hydroxy-5-tert-butylisoxazol-4-yl)propanoic acid (ATPA) on synaptic transmission in the Schaffer collateral-commissural pathway of rat hippocampal slices. In the present study we report several new features of the actions of ATPA at this synapse. Firstly, the effectiveness of ATPA is developmentally regulated. Secondly, the effects of ATPA decline during prolonged or repeated applications. Thirdly, the effects of ATPA are not mediated indirectly via activation of GABA(A), GABA(B), muscarinic or adenosine A(1) receptors. Fourthly, elevating extracellular Ca(2+) from 2 to 4 mM antagonises the effects of ATPA. Some differences between the actions of ATPA and kainate on synaptic transmission in the Schaffer collateral-commissural pathway are also noted.

Synaptic activation of a presynaptic kainate receptor facilitates AMPA receptor-mediated synaptic transmission at hippocampal mossy fibre synapses.

The development of GluR5-selective kainate receptor ligands is helping to elucidate the functions of kainate receptors in the CNS. Here we have further characterised the actions of a GluR5 selective agonist, ATPA, and a GluR5 selective antagonist, LY382884, in the CA3 region of rat hippocampal slices. In addition, we have used LY382884 to study a novel synaptic mechanism. This antagonist substantially reduces frequency facilitation of mossy fibre synaptic transmission, monitored as either AMPA or NMDA receptor-mediated EPSCs. This suggests that GluR5-containing kainate receptors on mossy fibres function as autoreceptors to facilitate the synaptic release of L-glutamate, in a frequency-dependent manner.

Pharmacological evidence for an involvement of group II and group III mGluRs in the presynaptic regulation of excitatory synaptic responses in the CA1 region of rat hippocampal slices.

The actions of four mGluR antagonists, (+)-MCPG, MAP4, MCCG and (S)-4CPG, were evaluated against agonist-induced depressions of synaptic transmission at the Schaffer collateral-commissural pathway in rat hippocampal slices. (+)-MCPG (1 mM) reversed very effectively depressions of field EPSPs induced by (1S,3R)-ACPD and (1S,3S)-ACPD but had weak and variable effects on depressions induced by L-AP4. It had no effect on depressions induced by either (-)-baclofen or carbachol. In contrast, MAP4 (500 microM) reversed very effectively depressions induced by L-AP4 without affecting depressions induced by (1S,3S)-ACPD. MCCG (1 mM) had the opposite activity; it antagonized depressions induced by (1S,3S)-ACPD but not those induced by L-AP4. Finally, (S)-4CPG (1 mM) reversed small depressions of field EPSPs induced by high concentrations (50-100 microM) of (1S,3R)- and (1S,3S)-ACPD, but not L-AP4, whilst having no effect on large depressions induced by 10 microM (1S,3S)-ACPD in voltage-clamped cells. These results confirm and extend the effectiveness and selectivity of (+)-MCPG as an mGluR antagonist. The divergent effects of the group I antagonist, (S)-4CPG, can be explained by an indirect action on postsynaptic receptors which is manifest when high agonist concentrations are used in non-voltage-clamp experiments. The action of MCCG and MAP4 indicates that two pharmacologically-distinct mGluRs, belonging to classes II and III, can regulate synaptic transmission in the CA1 region via presynaptic mechanisms.

The GluR5 subtype of kainate receptor regulates excitatory synaptic transmission in areas CA1 and CA3 of the rat hippocampus.

Activation of kainate receptors depresses excitatory synaptic transmission in the hippocampus. In the present study, we have utilised a GluR5 selective agonist, ATPA [(RS)-2-amino-3-(3-hydroxy-5-tert-butylisoxazol-4-yl)propanoic acid], and a GluR5 selective antagonist, LY294486 [(3SR,4aRS,6SR,8aRS)-6-([[(1H-tetrazol-5-y l)methyl]oxy]methyl)-1,2,3,4,4a,5,6,7,8,8a-decahydroisoquinoline-3 -carboxylic acid], to determine whether GluR5 subunits are involved in this effect. ATPA mimicked the presynaptic depressant effects of kainate in the CA1 region of the hippocampus. It depressed reversibly AMPA (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptor-mediated field excitatory postsynaptic potentials (field EPSPs) with an IC50 value of approximately 0.60 microM. The dual-component excitatory postsynaptic current (EPSC) and the pharmacologically isolated NMDA (N-methyl-D-aspartate) receptor-mediated EPSC were depressed to a similar extent by 2 microM ATPA (61 +/- 7% and 58 +/- 6%, respectively). Depressions were associated with an increase in the paired-pulse facilitation ratio suggesting a presynaptic locus of action. LY294486 (20 microM) blocked the effects of 2 microM ATPA on NMDA receptor-mediated EPSCs in a reversible manner. In area CA3, 1 microM ATPA depressed reversibly mossy fibre-evoked synaptic transmission (by 82 +/- 10%). The effects of ATPA were not accompanied by any changes in the passive properties of CA1 or CA3 neurones. However, in experiments where K+, rather than Cs+, containing electrodes were used, a small outward current was observed. These results show that GluR5 subunits comprise or contribute to a kainate receptor that regulates excitatory synaptic transmission in both the CA1 and CA3 regions of the hippocampus.

NMDA receptor dependence of mGlu-mediated depression of synaptic transmission in the CA1 region of the rat hippocampus.

1. The depression of synaptic transmission by the specific metabotropic glutamate receptor (mGlu) agonist (1S, 3R)-1-aminocyclopentane-1,3-dicarboxylate ((1S,3R)-ACPD) was investigated in area CA1 of the hippocampus of 4-10 week old rats, by use of grease-gap and intracellular recording techniques. 2. In the presence of 1 mM Mg2+, (1S,3R)-ACPD was a weak synaptic depressant. In contrast, in the absence of added Mg2+, (1S,3R)-ACPD was much more effective in depressing both the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) and N-methyl-D-aspartate (NMDA) receptor-mediated components of synaptic transmission. At 100 microM, (1S,3R)-ACPD depressed the slope of the field excitatory postsynaptic potential (e.p.s.p.) by 96 +/- 1% (mean +/- s.e.mean; n = 7) compared with 23 +/- 4% in 1 mM Mg(2+)-containing medium (n = 17). 3. The depressant action of 100 microM (1S,3R)-ACPD in Mg(2+)-free medium was reduced from 96 +/- 1 to 46 +/- 6% (n = 7) by the specific NMDA receptor antagonist (R)-2-amino-5-phosphonopentanoate (AP5; 100 microM). 4. Blocking both components of GABA receptor-mediated synaptic transmission with picrotoxin (50 microM) and CGP 55845A (1 microM) in the presence of 1 mM Mg2+ also enhanced the depressant action of (1S,3R)-ACPD (100 microM) from 29 +/- 5 to 67 +/- 6% (n = 6). 5. The actions of (1S,3R)-ACPD, recorded in Mg(2+)-free medium, were antagonized by the mGlu antagonist (+)-alpha-methyl-4-carboxyphenylglycine ((+)-MCPG). Thus, depressions induced by 30 microM (1S,3R)-ACPD were reversed from 48 +/- 4 to 8 +/- 6% (n = 4) by 1 mM (+)-MCPG. 6. In Mg(2+)-free medium, a group I mGlu agonist, (RS)-3, 5-dihydroxyphenylglycine (DHPG; 100 microM) depressed synaptic responses by 74 +/- 2% (n = 18). In contrast, neither the group II agonists ((2S,1'S,2'S)-2-(2'-carboxycyclopropyl)glycine; L-CCG-1; 10 microM; n = 4) and ((2S,1'R,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)glycine; DCG-IV; 100 nM; n = 3) nor the group III agonist ((S)-2-amino-4-phosphonobutanoic acid; L-AP4; 10 microM; n = 4) had any effect. 7. The depolarizing action of (1S,3R)-ACPD, recorded intracellularly, was similar in the presence and absence of Mg(2+)-AP5 did not affect the (1S,3R)-ACPD-induced depolarization in Mg(2+)-free medium. Thus, 50 microM (1S,3R)-ACPD induced depolarizations of 9 +/- 3 mV (n = 5), 10 +/- 2 mV (n = 4) and 8 +/- 2 mV (n = 5) in the three respective conditions. 8. On resetting the membrane potential in the presence of 50 microM (1S,3R)-ACPD to its initial level, the e.p.s.p. amplitude was enhanced by 8 +/- 3% in 1 mM Mg2+ (n = 5) compared with a depression of 37 +/- 11% in the absence of Mg2+ (n = 4). Addition of AP5 prevented the (1S,3R)-ACPD-induced depression of the e.p.s.p. (depression of 4 +/- 5% (n = 5)). 9. It is concluded that activation by group 1 mGlu agonists results in a depression of excitatory synaptic transmission in an NMDA receptor-dependent manner.

Pharmacology of postsynaptic metabotropic glutamate receptors in rat hippocampal CA1 pyramidal neurones.

1. Activation of metabotropic glutamate receptors (mGluRs) in hippocampal CA1 pyramidal neurones leads to a depolarization, an increase in input resistance and a reduction in spike frequency adaptation (or accommodation). At least eight subtypes of mGluR have been identified which have been divided into three groups based on their biochemical, structural and pharmacological properties. It is unclear to which group the mGluRs which mediate these excitatory effects in hippocampal CA1 pyramidal neurones belong. We have attempted to address this question by using intracellular recording to test the effects of a range of mGluR agonists and antagonists, that exhibit different profiles of subtype specificity, on the excitability of CA1 pyramidal neurones in rat hippocampal slices. 2. (2S, 1'S,2'S)-2-(2'-carboxycyclopropyl)glycine (L-CCG1) caused a reduction in spike frequency adaptation and a depolarization (1-10 mV) associated with an increase in input resistance (10-30%) at concentrations (> or = 50 microM) that have been shown to activate mGluRs in groups I, II and III. Similar effects were observed with concentrations (50-100 microM) of (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid ((1S,3R)-ACPD) and (1S,3S)-ACPD that exhibit little or no activity at group III mGluRs but which activate groups I and II mGluRs. 3. Inhibition of the release of endogenous neurotransmitters through activation of GABAB receptors, by use of 200 microM (+/-)-baclofen, did not alter the effects of (1S,3R)-ACPD (50-100 microM), (1S,3S)-ACPD (100 microM) or L-CCG1 (100 microM). This suggests that mGluR agonists directly activate CA1 pyramidal neurones. 4. Like these broad spectrum mGluR agonists, the racemic mixture ((SR)-) or resolved (S)-isomer of the selective group I mGluR agonist 3,5-dihydroxyphenylglycine ((SR)-DHPG (50-100 microM) or (S)-DHPG (20-50 microM)) caused a reduction in spike frequency adaptation concomitant with postsynaptic depolarization and an increase in input resistance. In contrast, 2S,1'R,2'R,3'R-2-(2',3'-dicarboxycyclopropyl)glycine (DCG-IV; 100 microM) and (S)-2-amino-4-phosphonobutanoic acid (L-AP4; 100-500 microM), which selectively activate group II mGluRs and group III mGluRs, respectively, had no effect on the passive membrane properties or spike frequency adaptation of CA1 pyramidal neurones. 5. The mGluR antagonists (+)-alpha-methyl-4-carboxyphenylglycine ((+)-MCPG; 1000 microM) and (S)-4-carboxyphenylglycine ((S)-4CPG; 1000 microM), which block groups I and II mGluRs and group I mGluRs, respectively, had no effect on membrane potential, input resistance or spike frequency adaptation per se. Both of these antagonists inhibited the postsynaptic effects of (1S,3R)-ACPD (50-100 microM), (1S,3S)-ACPD (30-100 microM) and L-CCG1 (50-100 microM). (+)-MCPG also reversed the effects of (SR)-DHPG(75 gM). (The effect of (S)-4CPG was not tested.) Their action was selective in that both antagonists did not reverse the reduction in spike frequency adaptation induced by carbachol (1 microM) or noradrenaline(10 microM) whereas atropine (10 microM) and propranolol (100 microM) did.6 From these data it is concluded that the mGluRs in CAl pyramidal neurones responsible for these excitatory effects are similar to the mGluRs expressed by non-neuronal cells transfected with cDNA encoding group I mGluRs.

Suntanning and sun protection: a review of the psychological literature.

Excessive sun exposure has been linked to skin cancer and to premature aging, drying and wrinkling of the skin, predominantly among Caucasians. This review examines the psychological literature on suntanning and sun protection behaviours among Caucasians. The research is examined in relation to: methods of study; attitude and normative beliefs towards suntanning and sun protection; differences in suntanning and sun protection knowledge and behaviour as a function of age and sun protection; differences to change sun related behaviours. A consistent finding across studies is that many people show a high level of knowledge of the dangers of excessive sun exposure and the need for sun protection, however, this knowledge often does not transfer into behaviour, with many people, particularly adolescents, still desiring and actively seeking a suntan. The implications of these findings for intervention studies are discussed.

Causal attributions, coping strategies, and adjustment to breast cancer.

In this retrospective questionnaire study of a convenience sample of 244 Australian women, type of causal attributions and their impact on coping strategies adopted by women with breast cancer were studied in relation to women's adjustment to their illness. Although 70% of the women made attributions about their cancer's origins, these women were not significantly better adjusted than women who had not make an attribution. Of those women who had made a causal attribution, type of attribution, whether controllable or uncontrollable (based on perceptions as to the controllability/uncontrollability of the cause of the disease), determined the extent to which exhibited information-seeking behavior. In the present study, women who perceived the cause of their cancer as emanating from uncontrollable circumstances were more active in seeking information about breast cancer than women who perceived the cause of their cancer as emanating from controllable circumstances. Different types of coping strategies adopted by women were associated with adjustment. Women who rated their adjustment as excellent displayed lower levels of helplessness, made fewer changes to their social behavior, were more anxiously preoccupied with their illness, sought more alternatives to medical therapy, and exhibited more information-seeking behavior than did their less-well-adjusted counterparts. The theoretical and practical implications of these results are discussed.

Breast self-examination training: a brief review.

A review of the literature on breast self-examination training indicated that any training in breast self-examination improves compliance, confidence, and proficiency; the evidence is unclear about the relative effectiveness of group or individual training; practice on breast models and on the woman's own breasts should be included in breast self-examination training; additional training sessions improve compliance and proficiency; reminders increase compliance, but the effect ceases when the reminders cease; and it is particularly important for older women to search their breasts slowly and thoroughly. Several other new approaches to breast self-examination training are discussed.

Painful ophthalmoplegia secondary to a mucocele involving the sella turcica, superior orbital fissure, and sphenoid sinus.

A case of painful ophthalmoplegia associated with an extensive lesion involving the sella turcica, superior orbital fissure, and sphenoid sinus in a 57-year-old man is reported. Even though nasal and ocular symptoms and signs represent the usual features of sphenoidal mucoceles, extension to the intracranial cavity as seen in this lesion is rare. Surgical exploration via a sublabial, transseptal approach revealed a mucocele of the sphenoid sinus. This case exhibited extensive and aggressive behavior simulating a malignant neoplasm.

Proteinuria in an Otago diabetic population.

A prospective examination was conducted of a five man group practice in Mosgiel, Otago. The incidence of diabetes was ascertained, and the frequency of proteinuria in that diabetic population. Thirteen percent of those examined showed proteinuria. Proteinuria appeared best related to the presence of retinopathy, and the known duration of the diabetes.

The influence of mothers' health beliefs on use of preventive child health care services and mothers' perception of children's health status.

During the first three years of life, many health problems are preventable, and health maintenance visits present an excellent opportunity to prevent disease and disability. Unfortunately, preventive child health care services are underutilized. Children who do not adequately use preventive health care services are often seen late in the course of an illness. Thus, they do not receive the continuing care that could eliminate the onset of preventable health problems. In our research, we sought to determine whether mothers' health beliefs influence their use of preventive child health care services and whether their use of preventive child health care services influence their perceptions of the child's health status. The sample was composed of low-income mothers living in an urban environment. No significant relationships were found between the variables. These results indicate the need to develop more sensitive tools to measure these variables in a similar sample.