The psychological support for women who underwent a stillbirth during their pregnancy: the quality of midwifery care.

PURPOSE: This review aims to investigate the role of midwifery care in perinatal death. Specifically, it aims to investigate the type and implications in the clinical practice of psychological and psychiatric support interventions for women/couples. METHODS: A scoping review was conducted following the PRISMA methodology. For this purpose, the following databases were queried: PubMed, APA PsycInfo, CINAHL Plus with Full Text, and ERIC, considering only studies published in the 2002-2022 time frame. RESULTS: 14 studies were found to be eligible by the literature review. These researches were divided into 3 macro-topics representing the most crucial factors in influencing the quality of care: the healthcare setting, the experience and training of caregivers, and the experience of parents. DISCUSSION: The healthcare figure who experiences such a tragic event most closely is the midwife. The health and geographic context in which care is provided - understood to be low-medium-high resources - have a fundamental impact on the quality of midwifery care and caregiver satisfaction. The training was found to be incomplete, and midwives' experiences revealed how they felt unprepared. Parents' experiences indicate the need for multidisciplinary care, better communicability, and follow-up including psychological/psychiatric support for mothers who are increasingly alone in coping with bereavement. To date, there are no guidelines for psychological support for this specific event in the literature. CONCLUSIONS: Birth-death management should be a structured part of professional courses so that new generations of midwives can improve the quality of care for affected families. Future research should focus on how to improve communication processes, and hospital centers should adopt protocols adapted to the needs of parents, including a midwifery-led model policy based on psychological support for the mothers/couples involved, as well as increase follow-ups.

Cancer screenings among sexual and gender minorities by midwives' point of view.

INTRODUCTION: Although women belonging to sexual and gender minorities are more at risk of gynecological and breast cancer, pieces of evidence have been provided that this population finds hardships getting involved in cancer screening programs. This happens because they tend to avoid clinical settings because of fear of discrimination, heteronormative assumptions, heterosexism, classism, and homophobic slurs by healthcare professionals. On the other hand, medical programs that allow healthcare providers to have experience with LGBTQ people are scarce and there are no specific tools to assess sexual cancer risks in this population. EVIDENCE ACQUISITION: Studies included were obtained searching MEDLINE with keywords "lesbians," "queer women," "trans women," "LGBTQ women," "cervical cancer screening," "pap test," "oncology screening," "mammogram" and "prevention." Furthermore, 1577 papers were found. After filtering for species, sex, language, and time range, 820 papers were left. The number of works included was 24 after title screening and 20 after abstract screening and full-text screening. EVIDENCE SYNTHESIS: More research will be needed to develop tools with an inclusive, non-judgmental, and open language capable of engaging the LGBTQ community. Cancer screening programs involve a large variety of healthcare providers including midwives. CONCLUSIONS: Midwives are multifaceted healthcare professionals whose large competence spectrum includes a variety of knowledge and skills going from antenatal care to education and research and they may efficiently provide cancer screenings. Midwives have been asking for more specialistic roles and calling for specific instruction to face the complex and ever-changing reality.

Doxorubicin induces an alarmin-like TLR4-dependent autocrine/paracrine action of Nucleophosmin in human cardiac mesenchymal progenitor cells.

BACKGROUND: Doxorubicin (Dox) is an anti-cancer anthracycline drug that causes double-stranded DNA breaks. It is highly effective against several types of tumours; however, it also has adverse effects on regenerative populations of normal cells, such as human cardiac mesenchymal progenitor cells (hCmPCs), and its clinical use is limited by cardiotoxicity. Another known effect of Dox is nucleolar disruption, which triggers the ubiquitously expressed nucleolar phosphoprotein Nucleophosmin (NPM) to be released from the nucleolus into the cell, where it participates in the orchestration of cellular stress responses. NPM has also been observed in the extracellular space in response to different stress stimuli; however, the mechanism behind this and its functional implications are as yet largely unexplored. The aim of this study was to establish whether Dox could elicit NPM secretion in the extracellular space and to elucidate the mechanism of secretion and the effect of extracellular NPM on hCmPCs. RESULTS: We found that following the double-strand break formation in hCmPCs caused by Dox, NPM was rapidly secreted in the extracellular space by an active mechanism, in the absence of either apoptosis or necrosis. Extracellular release of NPM was similarly seen in response to ultraviolet radiation (UV). Furthermore, we observed an increase of NPM levels in the plasma of Dox-treated mice; thus, NPM release also occurred in vivo. The treatment of hCmPCs with extracellular recombinant NPM induced a decrease of cell proliferation and a response mediated through the Toll-like receptor (TLR)4. We demonstrated that NPM binds to TLR4, and via TLR4, and nuclear factor kappa B (NFkB) activation/nuclear translocation, exerts proinflammatory functions by inducing IL-6 and COX-2 gene expression. Finally, we found that in hCmPCs, NPM secretion could be driven by an autophagy-dependent unconventional mechanism that requires TLR4, since TLR4 inhibition dramatically reduced Dox-induced secretion. CONCLUSIONS: We hypothesise that the extracellular release of NPM could be a general response to DNA damage since it can be elicited by either a chemical agent such as Dox or a physical genotoxic stressor such as UV radiation. Following genotoxic stress, NPM acts similarly to an alarmin in hCmPCs, being rapidly secreted and promoting cell cycle arrest and a TLR4/NFκB-dependent inflammatory response.

Sex Differences in Health-related Quality of Life in Patients with Keratinocyte Carcinomas.

The difference between men and women in the impact of keratinocyte carcinomas on quality of life has not been widely studied. This study of 364 patients with keratinocyte carcinoma, measured quality of life using the self-administered 12-item Short Form Health Survey (SF-12) and Skindex-29. Results for both the physical and the mental components of SF-12 were worse in women than in men. For the mental component, women had significantly lower scores compared with men in almost all subgroups, based on demographic and clinical variables. The Skindex-29 emotions mean score was worse in women than in men. Women reported significantly higher level of worry that the disease could get worse and of developing scars, and more depression. On the other hand, men reported lower quality of sleep. The impact of keratinocyte carcinomas on quality of life is generally higher in women than in men. Such data may be important for tailored management of the disease in different categories of patients.

Correlation between Depression, Quality of Life and Clinical Severity in Patients with Hidradenitis Suppurativa.

Depression is frequent in patients with hidradenitis suppurativa. However, its relationship with quality of life and clinical severity needs further investigation. In this cross-sectional study, 341 adult, consecutive patients with hidradenitis suppurativa completed the 12-item General Health Questionnaire (GHQ-12), which has been shown to be able to identify cases of major depressive disorder in dermatological patients. The frequency of depression in hidradenitis suppurativa patients was 29.0%. In patients with depression, severity (International Hidradenitis Suppurativa Severity Score System (IHS4)), quality of life (Skindex-17; Dermatology Life Quality Index (DLQI)), and health status (36-item Short Form Health Survey (SF-36)) were significantly worse compared with patients with no depression. The highest linear correlation was observed between GHQ-12 and the psychosocial scale of the Skindex-17 and the SF-36 mental scale. In contrast, correlation between GHQ-12 and clinical severity was poor. Depression is an important comorbidity in hidradenitis suppurativa, which is strongly associated with impairment in quality of life, but not linearly correlated with clinical severity.

Intralesional ultrasound-guided combined treatment with triamcinolone plus lincomycin in hidradenitis suppurativa: A pilot study.

Hidradenitis suppurativa (HS) is a chronic, inflammatory, disease of the hair follicle. Intralesional corticosteroid treatment in HS patients has been reported, and while several data described this route of administration as an efficient delivery system, its efficacy is still debated. The aim of this study was to explore the clinical efficacy and the effect on quality of life (QoL) of an innovative intralesional treatment in HS patients. This was an interventional prospective study. The treatment consisted of two intralesional ultrasound-guided injections of triamcinolone plus lincomycin, at baseline and after 2 weeks. Lesions and QoL were evaluated at baseline and at 4 weeks following intralesional therapy. All clinical variables of 36 HS patients significantly improved after 4 weeks. Mean values of the visual analog scale (VAS) pain decreased from 4.6 to 1.5, P = .027. The Bodily Pain (BP) scale of the Short-Form Health Survey (SF-36) significantly improved from 36.2 at baseline to 53.9 at 4-week follow-up (P < .001). On a scale from 0 to 10, over 90% of the patients gave a satisfaction score of 8 or more. This combination of corticosteroids and antibiotics delivered intralesionally seems to be effective, as it improved both patient- and physician-reported outcomes.

Use of the SF-12 questionnaire to assess physical and mental health status in patients with psoriasis.

Health-related quality of life (HRQoL) in psoriasis patients is generally measured using disease- or dermatology-specific questionnaires. Our objective was to use the generic 12-item Short Form Health Survey (SF-12) instrument to measure the physical and mental impact of psoriasis and to compare scores with those already published for different diseases. An observational study was conducted among mild-to-severe psoriasis outpatients. Health status was assessed by the SF-12, which includes a physical (PCS) and a mental (MCS) scale. The 12-item General Health Questionnaire (GHQ-12) was used to assess the possible presence of depression or anxiety, and the Skindex-17 to measure dermatology-specific HRQoL. Statistical analyses were performed to estimate the association between physical and mental health status and demographic and clinical characteristics. The study population included 1592 patients. Psoriasis PCS scores were similar to the general population and to non-severe diseases such as allergies, dermatitis, or back pain, while MCS mean scores were very similar to that of depression, and lower than those of all the other chronic conditions. Poor physical health was associated with female sex, older age, lower educational level, joint involvement, ≥2 comorbidities, moderate to very severe clinical status, GHQ-12 score ≥4, and moderate to severe Skindex-17 psychosocial scores. Poor mental health was associated with younger age (<30 years), GHQ ≥ 4, and severe Skindex-17 psychosocial scores. In conclusion, a general health measure, such as the SF-12, appears to be able to capture, in psoriasis patients, the burden of the disease both from a physical and a mental point of view.

The role of the 12(S)-HETE/GPR31/12-HETER axis in cancer and ischemia-reperfusion injury.

The G protein-coupled receptors (GPCRs) constitute a large superfamily of seven transmembrane-spanning receptors that are activated by several classes of ligands, including bioactive lipids. GPCRs are attractive therapeutic targets for the treatment of human diseases, as they finely regulate a wide array of cellular functions. In this minireview, we summarized what is currently known about the G protein-coupled receptor GPR31/12-HETER. We highlighted, in particular, its structural similarity with human homologs, the biological functions of its recognized ligand 12(S)-hydroxyeicosatetraenoic acid (HETE), an arachidonic acid metabolite, and the role that GPR31/12-HETER-mediated signals play in cancer cell growth, invasion and metastasis, and in liver ischemia-reperfusion (IR) injury. Recent studies shed light and interest on the 12(S)-HETE/GPR31/12-HETER-activated signaling pathways and functions. The full spectrum of GPR31/12-HETER-mediated biological functions has yet to be characterized. Further studies are needed to identify other potential ligands, i.e. other than 12(S)-HETE. Another important remaining question is whether the multiple 12(S)-HETE-induced biological activities, including its role in diabetes, neurodegeneration, neuroprotection, and platelet function, occur via GPR31/12-HETER and/or involve the activation of other receptor molecules and pathways.

Biologics for pityriasis rubra pilaris treatment: A review of the literature.

Pityriasis rubra pilaris (PRP) is a rare inflammatory papulosquamous skin disease that is often refractory to conventional therapies. The off-label use of biologics, such as anti-tumor necrosis factor, anti-interleukin (IL) 12/IL-23, and anti-IL-17 agents, has been proven successful in the past 2 decades for PRP treatment. Our aim was to analyse the literature for the use of biologics in PRP treatment. We conducted a review by performing PubMed and ClinicalTrials.gov searches. Sixty-eight articles met our selection criteria and are herein discussed. Out of 86 PRP patients, the vast majority were treated with anti-tumor necrosis factor, anti-IL-12/IL-23, or anti-IL-17 biologics, either alone or in combination therapy. A marked-to-complete response was observed in 50%-78%, a partial response in 11%-25%, and no or poor response in 11%-25%. This review has several limitations, including small sample sizes and the lack of shared study design criteria. In some instances, PRP might have resolved spontaneously. Further, the presence of concomitant therapy or the lack of detailed data on previous treatments, makes it difficult to strictly define a therapeutic role per se of specific biologics in PRP. This review shows that biologics may be regarded as a tool for PRP treatment alone or in combination therapy although clinical trials are needed to better assess their efficacy and safety.

Ustekinumab treatment of pityriasis rubra pilaris: A report of five cases.

Pityriasis rubra pilaris (PRP) is a rare, chronic, inflammatory skin disease of unknown etiology. Patients refractory to conventional therapies have been treated successfully with biologic drugs such as anti-tumor necrosis factor agents. Recently, a role of the interleukin-23/T-helper 17 axis in PRP has been described. Our objective was to assess the effectiveness of ustekinumab in five patients with adult-onset PRP refractory to conventional therapies. In the present study, four patients had type I and one patient type II adult-onset PRP. They were treated with three s.c. doses of ustekinumab at weeks 0, 4 and 16. Clinical response was evaluated monthly during treatment up to a 15-month follow-up period. All patients promptly showed a decrease in erythema, follicular hyperkeratosis and scaling. After three injections, complete remission of skin lesions was achieved in four out of five cases and a significant clinical improvement was shown in one case. To the best of our knowledge, this is the largest case series reported on ustekinumab treatment in PRP. Our results, in addition to previous studies from other groups, suggest that ustekinumab may be a possible first-line treatment for PRP patients refractory to conventional therapies.

Cyclophilin A modulates bone marrow-derived CD117(+) cells and enhances ischemia-induced angiogenesis via the SDF-1/CXCR4 axis.

BACKGROUND: Critical limb ischemia (CLI) is a major health problem with no adequate treatment. Since CLI is characterized by insufficient tissue vascularization, efforts have focused on the discovery of novel angiogenic factors. Cyclophilin A (CyPA) is an immunophilin that has been shown to promote angiogenesis in vitro and to enhance bone marrow (BM) cell mobilization in vivo. However, its potential as an angiogenic factor in CLI is still unknown. Thus, this study aimed to evaluate whether CyPA might induce neo-angiogenesis in ischemic tissues. METHODS AND RESULTS: Wild-type C57Bl/6j mice underwent acute hind-limb ischemia (HLI) and received a single intramuscular administration of recombinant CyPA or saline. Limb perfusion, capillary density and arteriole number in adductor muscles were significantly increased after CyPA treatment. Interestingly, BM-derived CD117(+) cell recruitment was significantly higher in ischemic adductor tissue of mice treated with CyPA versus saline. Therefore, the effect of CyPA on isolated BM-derived CD117(+) cells in vitro was evaluated. Low concentrations of CyPA stimulated CD117(+) cell proliferation while high concentrations promoted cell death. Moreover, CyPA enhanced CD117(+) cell adhesion and migration in a dose-dependent manner. Mechanistic studies revealed that CyPA up-regulated CXCR4 in CD117(+) cells and in adductor muscles after ischemia. Additionally, SDF-1/CXCR4 axis inhibition by the CXCR4 antagonist AMD3100 decreased CyPA-mediated CD117(+) cell recruitment in the ischemic limb. CONCLUSION: CyPA induces neo-angiogenesis by recruiting BM-derived CD117(+) cell into ischemic tissues, at least in part, through SDF-1/CXCR4 axis.

Transcriptional control of skin reepithelialization.

The wound healing process is characterized by a series of overlapping phases, such as coagulation, inflammation, reepithelialization/granulation tissue generation and remodeling. It is important to obtain a deeper insight into the cutaneous wound repair mechanisms, in order to develop novel pharmacological tools for the treatment of chronic non-healing ulcers which are a frequent and high morbidity complication of diabetes, ischaemia, venous insufficiency, and other local or systemic factors. Several transcription factors, many of which belong to gene families, are known to play a role in cutaneous wound repair through the orchestration of cellular responses which promote the reconstitution of skin integrity. The aim of this review is to provide an updated analysis of the transcription factor role in the reepithelialization process, in the context of skin wound repair.

Ex vivo acidic preconditioning enhances bone marrow ckit+ cell therapeutic potential via increased CXCR4 expression.

AIMS: The chemokine receptor CXCR4 modulates endothelial progenitor cell migration, homing, and differentiation, and plays a key role in cardiovascular regeneration. Here we examined the effect of ex vivo acidic preconditioning (AP) on CXCR4 expression and on the regenerative potential of mouse bone marrow (BM) ckit(+) cells. METHODS AND RESULTS: Acidic preconditioning was achieved by exposing BM ckit(+) cells to hypercarbic acidosis (pH 7.0) for 24 h; control cells were kept at pH 7.4. Acidic preconditioning enhanced CXCR4 and stromal cell-derived factor 1 (SDF-1) mRNA levels, as well as CXCR4 phosphorylation. Acidic preconditioning ability to modulate CXCR4 expression depended on cytosolic calcium [Ca(2+)]i mobilization and on nitric oxide (NO), as determined by [Ca(2+)]i buffering with BAPTA, and by treatment with the NO donor (DETA/NO) and the NO synthase inhibitor (L-NAME). Further, AP increased SDF-1-driven chemotaxis, transendothelial migration, and differentiation toward the endothelial lineage in vitro. In a mouse model of hindlimb ischaemia, control and AP ckit(+) cells were transplanted into the ischaemic muscle; AP cells accelerated blood flow recovery, increased capillary, and arteriole number as well as the number of regenerating muscle fibres vs. control. These effects were abolished by treating AP cells with L-NAME. CONCLUSION: Acidic preconditioning represents a novel strategy to enhance BM ckit(+) cell therapeutic potential via NO-dependent increase in CXCR4 expression.

The SDF-1/CXCR4 axis in stem cell preconditioning.

We review the pivotal role of the stromal derived factor (SDF)-1 chemokine in tissue ischaemia and how it orchestrates the rapid revascularization of injured, ischaemic, and regenerating tissues via the CXC chemokine receptors CXCR4 and CXCR7. Furthermore, we discuss the effects of preconditioning (PC), which is a well-known protective phenomenon for tissue ischaemia. The positive effect of both hypoxic and acidic PC on progenitor cell therapeutic potential is reviewed, while stressing the role of the SDF-1/CXCR4 axis in this process.

C/EBPγ regulates wound repair and EGF receptor signaling.

We aimed at identifying novel regulators of skin wound healing (WH), in an epidermal scratch WH assay, by a small interfering RNA (siRNA) silencing approach. Several transcription factors have been previously reported to affect wound repair. We here show that gene silencing of the transcription factor CAAT enhancer-binding protein γ (C/EBPγ), STAT3, REL, RELA, RELB, SP1, and NFkB impaired WH in vitro, in keratinocytes, whereas E2F and CREBBP silencing accelerated the WH process. We further characterized C/EBPγ, as its silencing yielded the maximal impairment (52.2 ± 12.5%) of scratch wounding (SW). We found that C/EBPγ silencing inhibited both EGF- and serum-induced keratinocyte migration, whereas C/EBPγ overexpression enhanced cell migration to EGF and to serum via the EGFR. Further, C/EBPγ silencing impaired scratch-induced Y1068 and Y1173 EGFR phosphorylation, as well as Y118 paxillin phosphorylation, key molecules regulating cell migration and epidermal WH. Moreover, C/EBPγ levels were induced in keratinocytes, following both SW and EGF stimulation. C/EBPγ siRNA silencing in vivo impaired WH at 3, 5, 7, and 14 days following excisional wounding in mice inhibited both re-epithelialization and granulation tissue formation, and induced a decrease of arteriole number. In conclusion, we here report that C/EBPγ positively regulates wound repair both in vitro and in vivo, at least in part, by affecting EGFR signaling.