Female residents experiencing medical errors in general internal medicine: a qualitative study.

BACKGROUND: Doctors, especially doctors-in-training such as residents, make errors. They have to face the consequences even though today's approach to errors emphasizes systemic factors. Doctors' individual characteristics play a role in how medical errors are experienced and dealt with. The role of gender has previously been examined in a few quantitative studies that have yielded conflicting results. In the present study, we sought to qualitatively explore the experience of female residents with respect to medical errors. In particular, we explored the coping mechanisms displayed after an error. This study took place in the internal medicine department of a Swiss university hospital. METHODS: Within a phenomenological framework, semi-structured interviews were conducted with eight female residents in general internal medicine. All interviews were audiotaped, fully transcribed, and thereafter analyzed. RESULTS: Seven main themes emerged from the interviews: (1) A perception that there is an insufficient culture of safety and error; (2) The perceived main causes of errors, which included fatigue, work overload, inadequate level of competences in relation to assigned tasks, and dysfunctional communication; (3) Negative feelings in response to errors, which included different forms of psychological distress; (4) Variable attitudes of the hierarchy toward residents involved in an error; (5) Talking about the error, as the core coping mechanism; (6) Defensive and constructive attitudes toward one's own errors; and (7) Gender-specific experiences in relation to errors. Such experiences consisted in (a) perceptions that male residents were more confident and therefore less affected by errors than their female counterparts and (b) perceptions that sexist attitudes among male supervisors can occur and worsen an already painful experience. CONCLUSIONS: This study offers an in-depth account of how female residents specifically experience and cope with medical errors. Our interviews with female residents convey the sense that gender possibly influences the experience with errors, including the kind of coping mechanisms displayed. However, we acknowledge that the lack of a direct comparison between female and male participants represents a limitation while aiming to explore the role of gender

Acoustic stimulation time-locked to the beginning of sleep apnea events reduces oxygen desaturations: a pilot-study.

We aimed to determine whether bone-conducted acoustic stimulation could prematurely terminate sleep apnea events, thereby decreasing amplitude and duration of subsequent oxygen desaturation. As oxygen desaturation has been linked to cardiovascular consequences, we postulate this could be a viable therapy in some cases. Eight patients with severe Obstructive Sleep Apnea (2 women, 45 [20-68] y.o. Apnea-Hypopnea Index: 77.7 ± 22.3/h) underwent polysomnography at the Lausanne University Sleep Center. Short acoustic stimulations were administered by bone conduction every second event of sleep apnea. Sounds were remotely administered using a Dreem® headband worn by patients while undergoing nocturnal polysomnography. Amplitude (%) and duration(s) of oxygen desaturations following terminated apneas were compared to that of non-stimulated previous and subsequent events. 549 stimulations (68.6 ± 38 sounds per patient) in N1 (16.2%), N2 (69.9%), N3 (4.2%), and REM(9.6%) were conducted. Compared to the previous and subsequent non-stimulated apnea, stimulations reduced event duration by 21.4% (-3.4 ± 7.2 s, p < 0.0001) while oxygen desaturation amplitude and duration were reduced by 30.4% (mean absolute difference ± SD: -1.9 ± 2.8%, p < 0.0001), and 39.6% (-5.7 ± 9.2 s, p < 0.0001) respectively. For these variables, each patient showed a significant improvement following acoustic stimulation. Sound-associated discomfort was rated 1.14 ± 1.53 on an 8 points scale (8 = worst) and only 6.8% of emitted sounds were perceived by the patients, suggesting a well-tolerated intervention. Bone-conducted sound stimuli decreased apnea events duration as well as duration and amplitude of associated oxygen desaturations. Stimulations were well tolerated and rarely perceived by patients. This therapeutic approach deserves further investigation, with monitoring of effects on sleep quality, daytime function/sleepiness and cardiovascular parameters

Elastic behaviour of the carotid artery in intact spontaneously hypertensive rats

Intact spontaneously hypertensive rats (SHR) were studied to assess the effect of prolonged antihypertensive treatment on the elastic behaviour of the external carotid artery. Thirty-week-old SHR received the ACE inhibitor captopril, the ateriolar dilator hydralazine or their vehicle for 6 weeks. These rats were compared to normotensive, vehicle treated WKY rats. The internal diameter of the carotid artery was measured continuously in halothane-anaesthetized rats using an echo-tracking device, and intra-arterial pressure was also monitored continuously, on the controlateral side. Captopril- and hydralazinetreated SHR as well as normotensive controls had similar blood pressure values. No significant shift in the distensibility-pressure curves was observed among vehicle-treated SHR and WKY rats or the SHR which had received captopril or hydralazine. Histological examination of the carotid artery fixed ex vivo with paraformaldehyde showed a significant increase in cross-sectional area in vehicle-treated SHR as compared to their normotensive counterparts. These results therefore suggest that the elastic behaviour of elastic arteries is not necessarily altered by the structural changes developing in response to hypertensio

Toponyms for centers of endemism in Madagascar

A biogeographical model was proposed in 2006 to explain the centers of endemism and the importance of riparian forest of some watersheds as refuges or dispersal corridors during paleoclimatic oscillations. Here, we consider these geographical features highlighting their biological and socio-cultural importance. We explain the etymology or eponymy of the major rivers of the retreat - dispersal watersheds, i.e., the drainage basins of Bemarivo, Antainambalana, Mangoro, Manampatrana, Mananara South, Mandrare, Onilahy, Mangoky, Tsiribihina, Betsiboka, Maevarano, Sambirano, and Mahavavy North. We propose a toponymy for each of the 15 centers of endemism and highlight their peculiarities. We named the centers of endemism of Vohimarina, Masoala, Analanjirofo, Tanala, Manombo, Anosy, Ranopiso, Karimbola, Mikea, Menabe, Melaky, Sofia, Ampasindava, Ankify, and Ankarana. We illustrate each center of endemism with a flagship species and report on its natural and cultural histories, and conservation.RÉSUMÉUn modèle biogéographique a été proposé en 2006 pour expliquer les centres d’endémisme de la biodiversité et l’importance des ripisylves de certains bassins versants en tant que refuges ou couloirs de dispersion au cours des oscillations paléoclimatiques. Ici, nous considérons ces dispositifs géographiques en soulignant leur importance biologique et socio-culturelle. Dans un premier temps, nous expliquons la toponymie ou l’éponymie des grands fleuves des bassins refuges et de dispersion, à savoir les bassins de la Bemarivo, de l’Antainambalana, du Mangoro, de la Manampatrana, de la Mananara du Sud, du Mandrare, de l’Onilahy, du Mangoky, de la Tsiribihina, de la Betsiboka, de la Maevarano, du Sambirano et de la Mahavavy du Nord. Puis nous proposons une toponymie pour chacun des 17 centres et sous-centres d’endémisme en justifiant leurs particularités. Nous retenons ainsi les centres d’endémisme de Vohimarina, de l’Atsinanana (dont Masoala et Analanjirofo), Tanala, de Manombo, de l’Anosy, d’Ala maika (dont Ranopiso, Karimbola et Mikea), du Menabe, du Melaky, de la Sofia, d’Ampasindava, d’Ankify et de l’Ankarana. Nous illustrons chacun des centres d’endémisme avec une espèce symbolique et rapportons des aspects de son histoire naturelle et culturelle ainsi que de sa conservation

The Benefit of Menopausal Hormone Therapy on Bone Density and Microarchitecture Persists After its Withdrawal.

Menopausal hormone therapy (MHT) favorably affects bone mineral density (BMD). Whether MHT also affects bone microarchitecture, as assessed by trabecular bone score (TBS), has never been evaluated. Our objective was to assess the effect of MHT on TBS and BMD before and after its withdrawal. This was a cross-sectional study. This study included the general community. Data were collected from the OsteoLaus cohort (1500 women aged 50-80 years). After exclusion of women with bone-modulating treatments, 1279 women were categorized according to MHT status into current (CU), past (PU), and never (NU) users. Spine TBS and BMD at lumbar spine, femoral neck, and total hip were assessed by dual X-ray absorptiometry. Age- and body mass index-adjusted analysis showed higher TBS values in CU vs PU or NU (1.31 ± 0.01, 1.29 ± 0.01, and 1.27 ± 0.01, respectively; P < .001). All BMD values were significantly higher in CU vs PU or NU. Compared to NU, PU exhibited higher lumbar spine (0.94 ± 0.01 vs 0.91 ± 0.01 g/cm(2); P = .017) and total hip (0.86 ± 0.01 vs 0.84 ± 0.01 g/cm(2); P = .026) BMD and a trend for higher TBS (P = .066). The 10-year loss of TBS and BMD at lumbar spine and total hip was significantly lower for both CU and PU vs NU. MHT duration had no effect on bone parameters. In PU, the residual effect on TBS and BMD was significantly more prominent in early discontinuers (<2 years). MHT is associated with bone microarchitecture preservation, as assessed by TBS. The effect of MHT on TBS and BMD persists at least 2 years after withdrawal

Adjuvant therapy after excision and radiation of isolated postmastectomy locoregional breast cancer recurrence: definitive results of a phase III randomized trial (SAKK 23/82) comparing tamoxifen with observation

Background: Adjuvant systemic treatment for patients with isolated locoregional recurrence (ILRR) of breast cancer is based on a single reported randomized trial. The trial, conducted by the Swiss Group for Clinical Cancer Research, compared tamoxifen (TAM) with observation after complete excision of the ILRR and proper radiotherapy. We performed a definitive analysis of treatment outcome at >11 years of follow-up, after the majority of the patients had a subsequent event of interest. Patient and methods One hundred and sixty-seven patients with ‘good-risk' characteristics of disease were randomized. ‘Good-risk' was defined as estrogen receptor expression in the ILRR, or having a disease-free interval of >12 months and a recurrence consisting of three or less tumor nodules, each ≤3 cm in diameter. Seventy-nine percent of the patients were postmenopausal at randomization. Results: The median follow-up time of the surviving patients was 11.6 years. The median post ILRR disease-free survival (DFS) was 6.5 years with TAM and 2.7 years with observation (P = 0.053). The difference was mainly due to reduction of further local relapses (P = 0.011). In postmenopausal patients, TAM led to an increase of DFS from 33% to 61% (P = 0.006). In premenopausal women, 5-year DFS was 60%, independent of TAM medication. For the whole study population, the median post-recurrence overall survival (OS) was 11.2 and 11.5 years in the observation and the TAM group, respectively; premenopausal patients experienced a 5-year OS of 90% for observation compared with 67% for TAM (P = 0.175), while the respective figures for postmenopausal patients were both 75%. Conclusions: These definitive results confirmed that TAM significantly improves the post-recurrence DFS of patients after local treatment for ILRR. This beneficial effect does not translate into a detectable OS advantag

The Metabolic Benefits of Menopausal Hormone Therapy Are Not Mediated by Improved Nutritional Habits. The OsteoLaus Cohort.

Menopause alters body composition by increasing fat mass. Menopausal hormone therapy (MHT) is associated with decreased total and visceral adiposity. It is unclear whether MHT favorably affects energy intake. We aimed to assess in the OsteoLaus cohort whether total energy intake (TEI) and/or diet quality (macro- and micronutrients, dietary patterns, dietary scores, dietary recommendations)-evaluated by a validated food frequency questionnaire-differ in 839 postmenopausal women classified as current, past or never MHT users. There was no difference between groups regarding TEI or consumption of macronutrients. After multivariable adjustment, MHT users were less likely to adhere to the unhealthy pattern 'fat and sugar: Current vs. never users [OR (95% CI): 0.48 (0.28-0.82)]; past vs. never users [OR (95% CI): 0.47 (0.27-0.78)]. Past users exhibited a better performance in the revised score for Mediterranean diet than never users (5.00 ± 0.12 vs. 4.63 ± 0.08, p < 0.04). Differences regarding compliance with dietary recommendations were no longer significant after adjustment for covariates. Overall, these results argue against a major role of TEI and diet quality as possible mediators of the MHT metabolic benefits. Future research on this relationship should focus on other potential targets of MHT, such as resting energy expenditure and physical activity

Role for inducible cAMP early repressor in promoting pancreatic beta cell dysfunction evoked by oxidative stress in human and rat islets

Aims/hypothesis: Pro-atherogenic and pro-oxidant, oxidised LDL trigger adverse effects on pancreatic beta cells, possibly contributing to diabetes progression. Because oxidised LDL diminish the expression of genes regulated by the inducible cAMP early repressor (ICER), we investigated the involvement of this transcription factor and of oxidative stress in beta cell failure elicited by oxidised LDL. Methods: Isolated human and rat islets, and insulin-secreting cells were cultured with human native or oxidised LDL or with hydrogen peroxide. The expression of genes was determined by quantitative real-time PCR and western blotting. Insulin secretion was monitored by EIA kit. Cell apoptosis was determined by scoring cells displaying pycnotic nuclei. Results: Exposure of beta cell lines and islets to oxidised LDL, but not to native LDL raised the abundance of ICER. Induction of this repressor by the modified LDL compromised the expression of important beta cell genes, including insulin and anti-apoptotic islet brain 1, as well as of genes coding for key components of the secretory machinery. This led to hampering of insulin production and secretion, and of cell survival. Silencing of this transcription factor by RNA interference restored the expression of its target genes and alleviated beta cell dysfunction and death triggered by oxidised LDL. Induction of ICER was stimulated by oxidative stress, whereas antioxidant treatment with N-acetylcysteine or HDL prevented the rise of ICER elicited by oxidised LDL and restored beta cell functions. Conclusions/interpretation: Induction of ICER links oxidative stress to beta cell failure caused by oxidised LDL and can be effectively abrogated by antioxidant treatmen

Human high-density lipoprotein particles prevent activation of the JNK pathway induced by human oxidised low-density lipoprotein particles in pancreatic beta cells

Aims/hypothesis: We explored the potential adverse effects of pro-atherogenic oxidised LDL-cholesterol particles on beta cell function. Materials and methods: Isolated human and rat islets and different insulin-secreting cell lines were incubated with human oxidised LDL with or without HDL particles. The insulin level was monitored by ELISA, real-time PCR and a rat insulin promoter construct linked to luciferase gene reporter. Cell apoptosis was determined by scoring cells displaying pycnotic nuclei. Results: Prolonged incubation with human oxidised LDL particles led to a reduction in preproinsulin expression levels, whereas the insulin level was preserved in the presence of native LDL-cholesterol. The loss of insulin production occurred at the transcriptional levels and was associated with an increase in activator protein-1 transcriptional activity. The rise in activator protein-1 activity resulted from activation of c-Jun N-terminal kinases (JNK, now known as mitogen-activated protein kinase 8 [MAPK8]) due to a subsequent decrease in islet-brain 1 (IB1; now known as MAPK8 interacting protein 1) levels. Consistent with the pro-apoptotic role of the JNK pathway, oxidised LDL also induced a twofold increase in the rate of beta cell apoptosis. Treatment of the cells with JNK inhibitor peptides or HDL countered the effects mediated by oxidised LDL. Conclusions/interpretation: These data provide strong evidence that oxidised LDL particles exert deleterious effects in the progression of beta cell failure in diabetes and that these effects can be countered by HDL particle

Functional significance of repressor element 1 silencing transcription factor (REST) target genes in pancreatic beta cells

Aims/hypothesis: The expression of several neuronal genes in pancreatic beta cells is due to the absence of the transcription factor repressor element 1 (RE-1) silencing transcription factor (REST). The identification of these traits and their functional significance in beta cells has only been partly elucidated. Herein, we investigated the biological consequences of a repression of REST target genes by expressing REST in beta cells. Methods: The effect of REST expression on glucose homeostasis, insulin content and release, and beta cell mass was analysed in transgenic mice selectively expressing REST in beta cells. Relevant target genes were identified in INS-1E and primary beta cells expressing REST. Results: Transgenic mice featuring a beta cell-targeted expression of REST exhibited glucose intolerance and reduced beta cell mass. In primary beta cells, REST repressed several proteins of the exocytotic machinery, including synaptosomal-associated protein (SNAP) 25, synaptotagmin (SYT) IV, SYT VII, SYT IX and complexin II; it impaired first and second phases of insulin secretion. Using RNA interference in INS-1E cells, we showed that SYT IV and SYT VII were implicated in the control of insulin release. Conclusions/interpretation: The data document the critical role of REST target genes in pancreatic beta cells. Specifically, we provide evidence that the downregulation of these genes is detrimental for the exocytosis of large dense core vesicles, thus contributing to beta cell dysfunction and impaired glucose homeostasi