Patients' preferences on information and involvement in decision-making for gastrointestinal surgery

Objective: The relationship between physicians and patients has undergone¦important changes, and the current emancipation of patients has led to¦a real partnership in medical decision-making. This study aimed to assess¦patients' preferences on different aspects of decision-making during treatment¦and potential complications, as well as the amount and type of preoperative¦information before visceral surgery.¦Methods: Prospective non-randomized study based on a questionnaire given¦to 253 consecutive patients scheduled for elective GI surgery.¦Results: Concerning surgical complications or treatment in the intensive care¦unit, 64% of patients wished to take actively part in any medical decisions.¦The respective figures for cardiac resuscitation and treatment limitations were¦89% and 60%. About information, 73%, 77% and 47% of patients wish¦detailed information, information on a potential ICUhospitalization and cardiac¦resuscitation, respectively. Elderly and low-educated patients were significantly¦less interested in shared medical decision-making (p = 0·003 and 0·015) and in¦information receiving (p = 0·03 and 0·05). Similarly, involvement of the family¦in decision-making was significantly less important in elderly and male patients¦(p = 0·05 and 0·03 respectively). Neither the type of operation (minor or major)¦nor the severity of disease (malignancies vs. non-malignancies) was a significant¦factor for shared decision-making, information or family involvement.¦Conclusion: The vast majority of surgical patients clearly want to get adequate¦preoperative information about their disease and the planned treatment. They¦also consider it as crucial to be involved in any kind of decision-making for¦treatment and complications. The family's role is limited to support the treating¦physicians if the patient is unable to participate in taking decisions.

Parent-child agreement and prevalence estimates of diagnoses in childhood: direct interview versus family history method.

Diagnostic information on children is typically elicited from both children and their parents. The aims of the present paper were to: (1) compare prevalence estimates according to maternal reports, paternal reports and direct interviews of children [major depressive disorder (MDD), anxiety and attention-deficit and disruptive behavioural disorders]; (2) assess mother-child, father-child and inter-parental agreement for these disorders; (3) determine the association between several child, parent and familial characteristics and the degree of diagnostic agreement or the likelihood of parental reporting; (4) determine the predictive validity of diagnostic information provided by parents and children. Analyses were based on 235 mother-offspring, 189 father-offspring and 128 mother-father pairs. Diagnostic assessment included the Kiddie-schedule for Affective Disorders and Schizophrenia (K-SADS) (offspring) and the Diagnostic Interview for Genetic Studies (DIGS) (parents and offspring at follow-up) interviews. Parental reports were collected using the Family History - Research Diagnostic Criteria (FH-RDC). Analyses revealed: (1) prevalence estimates for internalizing disorders were generally lower according to parental information than according to the K-SADS; (2) mother-child and father-child agreement was poor and within similar ranges; (3) parents with a history of MDD or attention deficit hyperactivity disorder (ADHD) reported these disorders in their children more frequently; (4) in a sub-sample followed-up into adulthood, diagnoses of MDD, separation anxiety and conduct disorder at baseline concurred with the corresponding lifetime diagnosis at age 19 according to the child rather than according to the parents. In conclusion, our findings support large discrepancies of diagnostic information provided by parents and children with generally lower reporting of internalizing disorders by parents, and differential reporting of depression and ADHD by parental disease status. Follow-up data also supports the validity of information provided by adolescent offspring.

Cybercafés de Bamako : les usages de l'Internet au prisme de la parenté et des classes d'âge

Au Mali, les technologies de l'information et de la communication ont suscité un vif engouement. Portés par l'ancien Président Alpha Oumar Konaré, de nombreux projets gouvernementaux ont vu le jour. Parallèlement, les cybercafés se sont multipliés : moins de dix en 1997, ils étaient presque plus de 120 en 2006. Si les possibilités de se connecter à domicile et sur son lieu de travail se sont développées, les cybercafés restent des espaces idéaux pour découvrir les pratiques numériques. Une façon d'étudier les usages de l'Internet est de s'intéresser aux liens qui se nouent autour de l'ordinateur. La situation est complexe à Bamako, car les personnes qui accompagnent les clients des cybercafés sont nombreuses. L'analyse de cette nébuleuse relationnelle est l'occasion de procéder à un double détour. Géographique tout d'abord, dans la mesure où l'anthropologue est conduit à quitter le cybercafé pour se rendre dans l'espace social plus vaste appelé Cyber. Disciplinaire ensuite puisque son regard se déplace progressivement du média vers l'étude des règles qui régissent la parenté et les classes d'âge.

La régression tumorale n'est pas un facteur de risque d'atteinte du ganglion sentinelle dans les mélanomes fins (indice de Breslow < or = 1 mm) [Tumour regression is not predictive for higher risk of sentinel node involvement in thin melanomas (Breslow thickness < or = 1 mm)]

Background: Thin melanomas (Breslow thickness <= 1 mm) are considered highly curable. The aim of this study was to evaluate the correlation between histological tumour regression and sentinel lymph node (SLN) involvement in thin melanomas. Patients and methods: This was a retrospective single-centre study of 34 patients with thin melanomas undergoing SLN biopsy between April 1998 and January 2005. Results: The study included 14 women and 20 men of mean age 56.3 years. Melanomas were located on the neck (n = 3), soles (n = 4), trunk (n = 13) and extremities (n = 14). Pathological examination showed 25 SSM, four acral lentiginous melanomas, three in situ melanomas, one nodular melanoma and one unclassified melanoma with a mean Breslow thickness of 0.57 mm. Histological tumour regression was observed in 26 over 34 cases and ulceration was found in one case. Clark levels were as follows: I (n = 3), II (n = 20), III (n = 9), IV (n = 2). Growth phase was available in 15 cases (seven radial and eight vertical). Mitotic rates, available in 24 cases, were: 0 (n = 9), 1 (n = 11), 2 (n = 2), 3 (n = 1), 6 (n = 1). One patient with histological tumour regression (2.9% of cases and 3.8% of cases with regressing tumours) had a metastatic SLN. One patient negative for SLN had a lung relapse and died of the disease. Mean follow-up was 26.2 months. Conclusion: The results of the present study and the analysis of the literature show that histological regression of the primary tumour does not seem predictive of higher risk of SLN involvement in thin melanomas. This suggests that screening for SLN is not indicated in thin melanomas, even those with histological regression.

Involvement of CD73, equilibrative nucleoside transporters and inosine in rhythm and conduction disturbances mediated by adenosine A1 and A2A receptors in the developing heart.

We previously established that exogenous adenosine (ADO) induces transient arrhythmias in the developing heart via the adenosine A1 receptor (A1AR) and downstream activation of NADPH oxidase/ERK and PLC/PKC pathways. Here, we investigated the mechanisms by which accumulation of endogenous ADO and its derived compound inosine (INO) in the interstitial compartment induce rhythm and conduction troubles. The validated model of the spontaneously beating heart obtained from 4-day-old chick embryos was used. Quantitative RT-PCR showed that enzymes involved in ADO and INO metabolism (CD39, CD73 and eADA) as well as equilibrative (ENT1, -3, -4) and concentrative (CNT3) nucleoside transporters were differentially expressed in atria, ventricle and outflow tract. Inactivation of ENTs by dipyridamole, 1) increased myocardial ADO level, 2) provoked atrial arrhythmias and atrio-ventricular blocks (AVB) in 70% of the hearts, 3) prolonged P wave and QT interval without altering contractility, and 4) increased ERK2 phosphorylation. Blockade of CD73-mediated phosphohydrolysis of AMP to ADO, MEK/ERK pathway inhibition or A1AR inhibition prevented these arrhythmias. Exposure to exogenous INO also caused atrial ectopy associated with AVB and ERK2 phosphorylation which were prevented by A1AR or A2AAR antagonists exclusively or by MEK/ERK inhibitor. Inhibition of ADA-mediated conversion of ADO to INO increased myocardial ADO and decreased INO as expected, but slightly augmented heart rate variability without provoking AVB. Thus, during cardiogenesis, disturbances of nucleosides metabolism and transport, can lead to interstitial accumulation of ADO and INO and provoke arrhythmias in an autocrine/paracrine manner through A1AR and A2AAR stimulation and ERK2 activation.

Ocular involvement in idiopathic hypereosinophilic syndrome: a rare finding [Augenbeteiligung beim idiopathischen Hypereosinophilen Syndrom: ein seltener Befund]

Hypereosinophilic syndrome (HES) is a myeloproliferative disorder characterised by persistent eosinophilia associated with multiple organ damage. The three criteria required for the diagnosis of the disease are: a sustained absolute eosinophilic count in the serum greater than 1500/μl present for longer than 6 months, no aetiology for secondary eosinophilia present and identification of signs and symptoms of end-organ involvement [1][2]. Despite significant progress in our understanding of the pathogenesis of some forms of hypereosinophilic syndrome, the current state of knowledge is still insufficient to formulate a new comprehensive etiologic definition of HES [3]. Very few reports can be retrieved describing ocular involvement in HES. Retinal arteriolar occlusions were observed in the pre-equatorial region and documented by angiography in one report [4], while the principal defects noted in a second report were occlusions of major retinal vessels, choroidal infarct, and patchy or delayed choroidal filling [5]. We present a case of extensive bilateral choroidal infiltrates in a patient suffering from idiopathic hypereosinophilia, potentially attributable to her disease.

Involvement of Parachlamydia in bovine abortions in Scotland.

Bovine abortion represents a major animal welfare issue and a cause of substantial economic loss yet the rate of successful diagnosis remains low. Chlamydia-related organisms including Parachlamydia have recently emerged as putative cattle abortifacients. Placental tissue samples and fetal lung from bovine abortion submissions across Scotland in Spring 2011 were investigated by histopathology for the presence of suspect Chlamydia-related organisms. Evidence of Chlamydia-related organisms was observed in 21/113 (18.6%) placenta samples. Thirteen of the suspect cases and 18 histopathology negative cases were analysed by molecular and immunohistochemical methods. All samples were PCR positive for Parachlamydia but sequencing revealed high homology between identified environmental 16S sequences in all but three cases. Parachlamydial antigen was detected in 10/31 placental samples (32.2%) with pathology consistent with chlamydial infection. This work supports the need for further surveillance investigations and experimental studies to determine the role of Parachlamydia in bovine abortion.

Involvement of nuclear factor-kappaB in macrophage migration inhibitory factor gene transcription up-regulation induced by interleukin- 1 beta in ectopic endometrial cells.

OBJECTIVE: To investigate the involvement of the nuclear factor (NF)-kappaB in the interleukin (IL)-1 beta-mediated macrophage migration inhibitory factor (MIF) gene activation. DESIGN: Prospective study. SETTING: Human reproduction research laboratory. PATIENT(S): Nine women with endometriotic lesions. INTERVENTION(S): Endometriotic lesions were obtained during laparoscopic surgery. MAIN OUTCOME MEASURE(S): The MIF protein secretion was analyzed by ELISA, MIF mRNA expression by quantitative real-time polymerase chain reaction (PCR), NF-kappaB translocation into the nucleus by electrophoresis mobility shift assay, I kappaB phosphorylation and degradation by Western blot, and human MIF promoter activity by transient cell transfection. RESULT(S): This study showed a significant dose-dependent increase of MIF protein secretion and mRNA expression, the NF-kappaB translocation into the nucleus, I kappaB phosphorylation, I kappaB degradation, and human MIF promoter activity in endometriotic stromal cells in response to IL-1 beta. Curcumin (NF-kappaB inhibitor) significantly inhibited all these IL-1 beta-mediated effects. Analysis of the activity of deletion constructs of the human MIF promoter and a computer search localized two putative regulatory elements corresponding to NF-kappaB binding sites at positions -2538/-2528 bp and -1389/-1380 bp. CONCLUSION(S): This study suggests the involvement of the nuclear transcription factor NF-kappaB in MIF gene activation in ectopic endometrial cells in response to IL-1 beta and identifies a possible pathway of endometriosis-associated inflammation and ectopic cell growth.

Anterior segment granuloma and optic nerve involvement as the presenting signs of systemic sarcoidosis.

PURPOSE: To report a case with anterior and posterior nodules associated with systemic sarcoidosis. METHODS: A patient with decreased vision underwent complete ophthalmologic examination, ultrasound biomicroscopy, fluorescein and indocyanine green (ICG) angiography. RESULTS: The patient presented a nodule of the iris of the OS and of the optic nerves of both eyes. Chest computed tomography and tissue biopsy established the diagnosis. CONCLUSIONS: Fluorescein and ICG angiography are the only objective exams to demonstrate the extent of ocular involvement in a patient with sarcoidosis.

Vasoactive intestinal peptide, pituitary adenylate cyclase-activating peptide, and noradrenaline induce the transcription factors CCAAT/enhancer binding protein (C/EBP)-beta and C/EBP delta in mouse cortical astrocytes: involvement in cAMP-regulated glycogen metabolism.

We have described previously a transcription-dependent induction of glycogen resynthesis by the vasoactive intestinal peptide (VIP) or noradrenaline (NA) in astrocytes, which is mediated by cAMP. Because it has been postulated that the cAMP-mediated regulation of energy balance in hepatocytes and adipocytes is channeled at least in part through the CCAAT/enhancer binding protein (C/EBP) family of transcription factors, we tested the hypothesis that C/EBP isoforms could be expressed in mouse cortical astrocytes and that their level of expression could be regulated by VIP, by the VIP-related neuropeptide pituitary adenylate cyclase-activating peptide (PACAP), or by NA. We report in this study that in these cells, C/EBP beta and C/EBP delta are induced by VIP, PACAP, or NA via the cAMP second-messenger pathway. Induction of C/EBP beta and -delta mRNA by VIP occurs in the presence of a protein synthesis inhibitor. Thus, c/ebp beta and c/ebp delta behave as cAMP-inducible immediate-early genes in astrocytes. Moreover, transfection of astrocytes with expression vectors selectively producing the transcriptionally active form of C/EBP beta, termed liver-enriched transcriptional activator protein, or C/EBP delta enhance the glycogen resynthesis elicited by NA, whereas an expression vector producing the transcriptionally inactive form of C/EBP beta, termed liver-enriched transcriptional inhibitory protein, reduces this resynthesis. These results support the idea that C/EBP beta and -delta regulate gene expression of energy metabolism-related enzymes in astrocytes.

Involvement of environmental mercury and lead in the etiology of neurodegenerative diseases.

The incidence of neurodegenerative disease like Parkinson's disease and Alzheimer's disease (AD) increases dramatically with age; only a small percentage is directly related to familial forms. The etiology of the most abundant, sporadic forms is complex and multifactorial, involving both genetic and environmental factors. Several environmental pollutants have been associated with neurodegenerative disorders. The present article focuses on results obtained in experimental neurotoxicology studies that indicate a potential pathogenic role of lead and mercury in the development of neurodegenerative diseases. Both heavy metals have been shown to interfere with a multitude of intracellular targets, thereby contributing to several pathogenic processes typical of neurodegenerative disorders, including mitochondrial dysfunction, oxidative stress, deregulation of protein turnover, and brain inflammation. Exposure to heavy metals early in development can precondition the brain for developing a neurodegenerative disease later in life. Alternatively, heavy metals can exert their adverse effects through acute neurotoxicity or through slow accumulation during prolonged periods of life. The pro-oxidant effects of heavy metals can exacerbate the age-related increase in oxidative stress that is related to the decline of the antioxidant defense systems. Brain inflammatory reactions also generate oxidative stress. Chronic inflammation can contribute to the formation of the senile plaques that are typical for AD. In accord with this view, nonsteroidal anti-inflammatory drugs and antioxidants suppress early pathogenic processes leading to Alzheimer's disease, thus decreasing the risk of developing the disease. The effects of lead and mercury were also tested in aggregating brain-cell cultures of fetal rat telencephalon, a three-dimensional brain-cell culture system. The continuous application for 10 to 50 days of non-cytotoxic concentrations of heavy metals resulted in their accumulation in brain cells and the occurrence of delayed toxic effects. When applied at non-toxic concentrations, methylmercury, the most common environmental form of mercury, becomes neurotoxic under pro-oxidant conditions. Furthermore, lead and mercury induce glial cell reactivity, a hallmark of brain inflammation. Both mercury and lead increase the expression of the amyloid precursor protein; mercury also stimulates the formation of insoluble beta-amyloid, which plays a crucial role in the pathogenesis of AD and causes oxidative stress and neurotoxicity in vitro. Taken together, a considerable body of evidence suggests that the heavy metals lead and mercury contribute to the etiology of neurodegenerative diseases and emphasizes the importance of taking preventive measures in this regard.

Involvement of PPAR nuclear receptors in tissue injury and wound repair.

Tissue damage resulting from chemical, mechanical, and biological injury, or from interrupted blood flow and reperfusion, is often life threatening. The subsequent tissue response involves an intricate series of events including inflammation, oxidative stress, immune cell recruitment, and cell survival, proliferation, migration, and differentiation. In addition, fibrotic repair characterized by myofibroblast transdifferentiation and the deposition of ECM proteins is activated. Failure to initiate, maintain, or stop this repair program has dramatic consequences, such as cell death and associated tissue necrosis or carcinogenesis. In this sense, inflammation and oxidative stress, which are beneficial defense processes, can become harmful if they do not resolve in time. This repair program is largely based on rapid and specific changes in gene expression controlled by transcription factors that sense injury. PPARs are such factors and are activated by lipid mediators produced after wounding. Here we highlight advances in our understanding of PPAR action during tissue repair and discuss the potential for these nuclear receptors as therapeutic targets for tissue injury.