Socialfobi och vårdarens möjlighet att stöda den drabbade

Syftet med detta arbete är att undersöka hur en individ med Social fobi upplever vardagen och hur kan vi i sjukvården hjälpa och stöda patienter med den sociala fobin. Denna studie är gjord utgående från en kvalitativ metod och dokumentforskning med ett Induktivt synsätt. Den valda forskningen utgår från litteratur och datainsamling från bloggar och studier gjorda på tidigare forskning, skribenten utgår från Antonovskys teoretiska modell KASAM. Som material har valts texter från bloggar med social fobi. Frågorna till analysen har valts från tidigare forskning och bloggar och studiens teoretiska bakgrund. Genom transkription har studiens bloggsvar gjorts från en analyseringsmall som användes för att analysera bloggtexten om Sociala fobin och ångest. Resultatet framkom från tidigare forskning, bloggar och den teoretiska bakgrunden de utgjorde en helhet och gav tillvisdel svar på syftet. I resultatet framkom det att många utvecklar sociala fobin under ungdomens tid på väg in i vuxenlivet och behöver stöd av sjukvårdare, vi behöver identifiera dessa människor som löper risk för att marginaliseras av samhället, identifiering av patientens behov, vi behöver kunna skapa ett band och utföra allvarliga diskussioner och vara en god lyssnare, kunskap behövs inom många områden från livsföring och framför allt KBTs - beteende exponeringar, Vibehöver hjälpa till med att stärka det sociala jaget och föra fram positiva tankegångar, dessutom behöver vi få patienten ut i samhället och neutralisera den negativa självbilden.Tämän työn tarkoituksena on selvittää, miten sosiaalista fobiaa sairastava henkilö kokee arjen ja miten voimme terveydenhuollossa auttaa ja tukea sosiaalifobiapotilaita. Tämä tutkimus perustuu kvalitatiiviseen menetelmään ja dokumenttitutkimukseen induktiivisella lähestymistavalla. Valittu tutkimus perustuu kirjallisuuteen ja blogeista kerättyyn tiedonkeruun sekä aikaisemmista tutkimuksista tehtyihin tutkimuksiin, tekijä perustuu Antonovskin teoreettiseen malliin KASAM. Aineistoksi on valittu tekstit sosiaalisia fobiaa sisältävistä blogeista. Analyysin kysymykset on valittu aikaisemmista tutkimuksista ja blogeista sekä tutkimuksen teoreettisesta taustasta. Transkription avulla tutkimuksen blogivastaus tehtiin analyysimallin avulla, jota käytettiin sosiaalisia fobiaa ja ahdistusta käsittelevän blogitekstin analysointiin. Tulokset nousivat aikaisemmista tutkimuksista, blogeista ja niiden muodostamasta teoreettisesta taustasta kokonaisuutena ja antoivat vastauksia tarkoitukseen. Tulokset osoittivat, että monille kehittyy sosiaalinen fobia murrosiässä matkalla aikuisuuteen ja he tarvitsevat sairaanhoitajien tukea, meidän on tunnistettava nämä ihmiset, jotka ovat vaarassa joutua yhteiskunnan syrjäytymiseen, tunnistaa potilaan tarpeet, meidän on kyettävä luoda side ja käydä vakavia keskusteluja ja olla hyvä kuuntelija, tietoa tarvitaan monilta aloilta elämäntavasta ja ennen kaikkea Kognitiivisestä käyttäytymisterapiasta (KKT), Meidän on autettava vahvistamaan sosiaalista minää ja edistämään positiivista ajattelua, lisäksi meidän on saatava potilas yhteiskuntaan ja neutralisoida sen negatiivinen minä kuva.The purpose of this work is to investigate how an individual with Social Phobia experiences everyday life and how can we in healthcare help and support patients with the social phobia. This study is based on a qualitative method and document research with an inductive approach. The selected research is based on literature and data collection from blogs and studies done on previous research, the author is based on Antonovsky's theoretical model KASAM. Texts from blogs with social phobia have been chosen as material. The questions for the analysis have been selected from previous research and blogs and the study's theoretical background. Through transcription, the study's blog response was made from analysis template that was used to analyze the blog text on Social Phobia and Anxiety. The results emerged from previous research, blogs, and the theoretical background they formed as a whole and gave some answers to the purpose. The results showed that many develop social phobia during adolescence on their way into adulthood and need the support of nurses, we need to identify these people who are at risk of being marginalized by society, identification of the patient's needs, we need to be able to create a bond and perform serious discussions and be a good listener, knowledge is needed in many areas from lifestyle and above all CBTs - behavioral exposures, We need to help strengthen the social self and promote positive thinking, in addition we need to get the patient out into society and neutralize it negative self-image

Role of circadian rhythm disorders on EMT and tumour–immune interactions in endocrine-related cancers

International audienceThe circadian rhythm is a major environmental regulator of plants and animal physiology. The alternation of days and nights is translated at the cell and tissue level thanks to a molecular machinery, called the circadian clock. This clock controls in particular numerous endocrine functions, and its imbalances can have serious consequences on homeostasis. This is particularly true for the development of endocrine-related cancers, like breast, ovarian and prostate cancer. Circadian rhythm disorder (CRD) not only affects key hormone levels (including oestrogen, melatonin, insulin, glucagon, cortisol) but also favours a pro-inflammatory and immunosuppressive phenotype in the tumour microenvironment. This particular aspect is conducive to epithelial-mesenchymal transition (EMT) of solid epithelial tumours and cancer cell dissemination. It also favours resistance to chemo- and immunotherapy. Here, we discuss the current knowledge on this crosstalk between CRD, EMT and the immune microenvironment in endocrine-related cancers and its consequences for the development of efficient therapies

Effets des altérations du rythme circadien sur l’évolution du cancer du sein

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Dosing time dependent in vitro pharmacodynamics of Everolimus despite a defective circadian clock

Everolimus (EV), a rapamycin analogue mTOR inhibitor, is used in the clinic to treat Estrogen positive (ER+) breast cancer in order to avoid the resistance to hormonotherapy. Here, we investigated whether EV efficacy varied according to administration timing by using the ER+ breast cancer cell line MCF-7 as model system. Our results showed that instead of apoptosis, EV induced a G0/G1 phase blockage of MCF-7 cells. Following serum shock, MCF-7 cells displayed a statistically significant 24h rhythm of mammalian target of Rapamycin (mTOR) activity, but perturbed circadian clock genes oscillations. Interestingly, the different delivery schedule of EV presented different efficacy in G0/G1 phase blockage in serum shocked MCF-7 cells. Moreover, serum shock induced also a circadian-like oscillation in expression or activity of several important G1 phase progression proteins, such as Cyclin D1 and phosphorylated Retinoblastoma protein (RB). Inhibition mTOR activity by EV reduced Cyclin D1 and Cyclin D3 protein level as well as RB phosphorylation level. Taken together, the results indicated that serum shock synchronization induced a circadian oscillation in mTOR activity in MCF-7 cells, which rhythmically regulated the synthesis or phosphorylation of key G1 progression proteins, such as Cyclin D1 and phosphorylated RB, ultimately resulting in different G0/G1 blockage efficiency according to different EV administration timing

Platelet indices and platelet-to-lymphocyte ratio predict coronary chronic total occlusion in patients with acute ST-elevation myocardial infarction

Coronary chronic total occlusion (CTO) is caused by organized thrombi or atherosclerotic plaque progression. The presence of a CTO is an independent predictor of mortality in patients presenting with ST-segment elevation myocardial infarction (STEMI). Platelets have a crucial role in the pathophysiology of atherosclerosis. The aim of this retrospective study was to investigate platelet indices as predictors of CTO in patients with STEMI treated with primary percutaneous coronary intervention (pPCI). A total number of 334 patients admitted for STEMI between January 2011 and December 2013 were included and divided in two groups based on the presence of CTO (48 patients in CTO+ group, 286 patients in CTO-group). Platelet count, mean platelet volume (MPV), platelet distribution width (PDW), platelet-large cell ratio (P-LCR), lymphocyte and neutrophil count determined on admission were analyzed. MPV was larger in patients with CTO compared with patients without CTO (p=0.02), as were PDW (p=0.03) and P-LCR (p=0.01). Platelet-to-lymphocyte ratio (PLT/LYM) was lower in patients with CTO: 105.2 (75.86-159.1) compared to 137 (97-188.1), p<0.01. Receiver-operator characteristic curve analysis identified an area under the curve of 0.61 (95%CI=0.57-0.67, p< 0.01) for PLT/LYM in predicting the presence of a CTO, with a cut-off value at 97.73. Lower values than this were independent predictors of a CTO in multivariate logistic regression analysis, with an Odds Ratio of 2.2 (95%CI=1.15-4.20, p=0.02). Our results support the use of platelet indices and PLT/LYM as predictors of CTO in patients presenting with STEMI

The CHA2DS2-VASc Score Predicts New-Onset Atrial Fibrillation and Hemodynamic Complications in Patients with ST-Segment Elevation Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention

Arrhythmic and hemodynamic complications related to ST-segment elevation myocardial infarction (STEMI) represent a major clinical challenge. Several scores have been developed to predict mortality in STEMI. However, those scores almost exclusively include factors related to the acute phase of STEMI, and no score has been evaluated to date for its ability to specifically predict arrhythmic and hemodynamic complications. We, thus, aimed to assess the ability of chronic risk factors burden, as expressed by the CHA2DS2-VASc score, to predict STEMI-related arrhythmic and hemodynamic complications. Data were collected from 839 consecutive STEMI patients treated by primary percutaneous coronary interventions (pPCI). CHA2DS2-VASc and GRACE scores were calculated for all patients, and their ability to predict STEMI-related arrhythmic (i.e., new-onset atrial fibrillation (AF), ventricular tachycardia/fibrillation) and hemodynamic (i.e., cardiogenic shock, asystole) complications was assessed in univariate and multiple regression analysis. Arrhythmic and hemodynamic complications occurred in 14.8% and 10.2% of patients, respectively. Although the GRACE score outweighed the CHA2DS2-VASc score in the ability to predict STEMI-related hemodynamic complications (p &lt; 0.0001), both scores had a similar predictive value for STEMI-related new-onset AF (p = 0.20), and both remained independent predictors of new-onset AF and of hemodynamic complications in the multiple regression analyses. A CHA2DS2-VASc score &gt; 2 points independently predicted new-onset AF (p &lt; 0.01) and hemodynamic complications (p = 0.04). Alongside the GRACE score, the CHA2DS2-VASc score independently predicted new-onset AF and hemodynamic complications in STEMI patients treated by pPCI. These data suggest that a combination of acute and chronic risk factors could provide additional benefit in identifying patients at risk of STEMI-related complications, who could benefit from closer follow-up and more intensive prophylactic and therapeutic strategies

The pro-inflammatory phenotype of the human non-classical monocyte subset is attributed to senescence

Abstract Human primary monocytes comprise a heterogeneous population that can be classified into three subsets based on CD14 and CD16 expression: classical (CD14high/CD16−), intermediate (CD14high/CD16+), and non-classical (CD14low/CD16+). The non-classical monocytes are the most pro-inflammatory in response to TLR stimulation in vitro, yet they express a remarkably high basal level of miR-146a, a microRNA known to negatively regulate the TLR pathway. This concurrence of a pro-inflammatory status and a high miR-146a level has been associated with cellular senescence in other cell types. Hence, we assessed the three monocyte subsets for evidence of senescence, including proliferative status, telomere length, cellular ROS levels, and mitochondrial membrane potential. Indeed, the non-classical subset exhibited the clearest hallmarks of senescence, followed by the intermediate and then the classical subset. In addition, the non-classical subset secreted pro-inflammatory cytokines basally in vitro. The highly pro-inflammatory nature of the non-classical monocytes could be a manifestation of the senescence-associated secretory phenotype (SASP), likely induced by a high basal NF-κB activity and IL-1α production. Finally, we observed an accumulation of the non-classical monocytes, in conjunction with higher levels of plasma TNF-α and IL-8, in the elderly. These factors may contribute to inflamm-aging and age-related inflammatory conditions, such as atherosclerosis and osteoarthritis. With our new understanding that the non-classical monocyte subset is a senescent population, we can now re-examine the role of this subset in disease conditions where this subset expands

Chronic circadian disruption modulates breast cancer stemness and immune microenvironment to drive metastasis in mice

International audienceBreast cancer is the most common type of cancer worldwide and one of the major causes of cancer death in women. Epidemiological studies have established a link between night-shift work and increased cancer risk, suggesting that circadian disruption may play a role in carcinogenesis. Here, we aim to shed light on the effect of chronic jetlag (JL) on mammary tumour development. To do this, we use a mouse model of spontaneous mammary tumourigenesis and subject it to chronic circadian disruption. We observe that circadian disruption significantly increases cancer-cell dissemination and lung metastasis. It also enhances the stemness and tumour-initiating potential of tumour cells and creates an immunosuppressive shift in the tumour microenvironment. Finally, our results suggest that the use of a CXCR2 inhibitor could correct the effect of JL on cancer-cell dissemination and metastasis. Altogether, our data provide a conceptual framework to better understand and manage the effects of chronic circadian disruption on breast cancer progression