Research shows an overrepresentation of trans people in vulnerable socioeconomic situations, primarily due to experiences of discrimination. At the same time, rural or suburban living areas often ...lack specialized trans-related health care, which a majority of trans people rely on to some extent. Taken together, the lack of both socioeconomic resources and access to trans-related health care can exacerbate health-related distress and impairment for trans people. We illustrate this problem using case vignettes of trans people from rural and suburban areas in (Northern) Germany. They are currently participating in an e-health intervention and randomized controlled trial (RCT) called
, whose case vignettes provided the impetus for the scoping review. The scoping review analyzes the impact of place of residence and its intersection with barriers to accessing trans-related health care. PubMed and Web of Science Data bases were searched for relevant studies using a search strategy related to trans people and remote, rural, or suburban residences. 33 studies were selected after full-text screening and supplemented
reference list checks and study team expertise by 12 articles addressing the living conditions of remotely living trans people and describing requirements for trans-related health care. The literature on trans people living remotely reveals intersections of trans mental health with age, race, gender expression, geographic location, community size, socioeconomic status, discrimination experiences, and attitudes towards health care providers. Several structural health care barriers are identified. The role of health care professionals (HCPs) for remotely living trans people is discussed. There is no need assuming that rural life for trans people is inevitably worse for health and well-being than urban life. Nevertheless, some clear barriers and health disparities exist for trans people in remote settings. Empowering trans groups and diversity-sensitive education of remote communities in private and institutional settings are needed for respectful inclusion of trans people. Facilitating access to trans-related health care, such as through video-based e-health programs with HCPs, can improve both the health and socioeconomic situation of trans people.
Many transgender and gender diverse (TGD) people use the internet to find ways out of isolation, network, and share information on health-related topics. Thus, e-health services could reduce the ...health burden of TGD people and facilitate access to health care. Following the PRISMA guidelines, we conducted a systematic review on e-health approaches that could improve trans health care (i.e., services directly for TGD people or training programs for health care professionals, HCPs) and their effectiveness, acceptability, and feasibility. We searched PubMed, Web of Science, and PubPsych databases for publications from January 2000 to June 2021 with final updates before publication. The systematic review identified e-health services across 27 studies from 8 different countries. Few studies evaluated e-health services exclusively for TGD people. However, use of an e-health service was found to be effective and beneficial: TGD people improved in health-related outcomes, and HCPs improved in professional expertise. Service users find e-health services helpful and easy to integrate into their daily lives. Recommendations for further development of e-health services in trans health care are provided. In the future, given the rapidly evolving e-health research and care field, new treatment approaches for TGD people should be subject to ongoing evaluation and development.
Körpertechnologie, Körpernormierung, Körperausdruck - Körperlichkeit und der Umgang mit dem Körper haben sich zu starken Themen entwickelt, die in diesem Buch facettenreich vorgestellt werden. Die ...Beiträge aus Erziehungswissenschaft, Ethnologie, Medienwissenschaft, Medizin und Biotechnologie, Psychologie, Sport- und Tanzwissenschaft sowie Theologie beleuchten Körperumgangsweisen in ihren historischen Kontexten, in ihrer Bedeutung für den Aufbau von Identität sowie hinsichtlich ihrer gesellschaftlichen und geschlechterbezogenen Implikationen. Der multidisziplinäre Zugang ermöglicht einen faszinierenden Einblick in die vielgestaltigen Wechselwirkungen von gesellschaftlichen Rahmenbedingungen, individuellem Erleben des Körpers und körperbezogenem Handeln.
Korpertechnologie, Korpernormierung, Korperausdruck - Korperlichkeit und der Umgang mit dem Korper haben sich zu starken Themen entwickelt, die in diesem Buch facettenreich vorgestellt werden.Die ...Beitrage aus Erziehungswissenschaft, Ethnologie, Medienwissenschaft, Medizin und Biotechnologie, Psychologie, Sport- und Tanzwissenschaft sowie Theologie beleuchten Korperumgangsweisen in ihren historischen Kontexten, in ihrer Bedeutung fur den Aufbau von Identitat sowie hinsichtlich ihrer gesellschaftlichen und geschlechterbezogenen Implikationen.Der multidisziplinare Zugang ermoglicht einen faszinierenden Einblick in die vielgestaltigen Wechselwirkungen von gesellschaftlichen Rahmenbedingungen, individuellem Erleben des Korpers und korperbezogenem Handeln.
Abstract
Background
Bacterial meningitis is still a cause of severe neurological disability. The brain is protected from penetrating pathogens by the blood-brain barrier and the innate immune system. ...The invading pathogens are recognized by pattern recognition receptors including the G-protein-coupled formyl peptide receptors (FPRs), which are expressed by immune cells of the central nervous system. FPRs show a broad spectrum of ligands, including pro- and anti-inflammatory ones. Here, we investigated the effects of the annexin A1 mimetic peptide Ac2-26 in a mouse model of pneumococcal meningitis.
Methods
Wildtype (WT) and
Fpr1
- and
Fpr2
-deficient mice were intrathecally infected with
Streptococcus pneumoniae
D39 (type 2). Subsequently, the different mice groups were treated by intraperitoneal injections of Ac2-26 (1 mg/kg body weight) 2, 8, and 24 h post-infection. The extent of inflammation was analyzed in various brain regions by means of immunohistochemistry and real-time reverse transcription polymerase chain reaction (RT-PCR) 30 h post-infection.
Results
Ac2-26-treated WT mice showed less severe neutrophil infiltration, paralleled by a reduced induction of pro-inflammatory glial cell responses in the hippocampal formation and cortex. While meningitis was ameliorated in Ac2-26-treated
Fpr1
-deficient mice, this protective effect was not observed in
Fpr2
-deficient mice. Irrespective of Ac2-26 treatment, inflammation was more severe in
Fpr2
-deficient compared to
Fpr1
-deficient mice.
Conclusions
In summary, this study demonstrates anti-inflammatory properties of Ac2-26 in a model of bacterial meningitis, which are mediated via FPR2, but not FPR1. Ac2-26 and other FPR2 modulators might be promising targets for the development of novel therapies for
Streptococcus pneumoniae
-induced meningitis.
An important hallmark of Alzheimer's disease (AD) is the increase of Aβ1-42 burden and its accumulation to senile plaques, leading the reactive gliosis and neurodegeneration. The modulation of glia ...cell function represents an attractive therapeutic strategy, but is currently limited by an incomplete understanding of its relevance for AD. The chemotactic G-protein coupled formyl peptide receptor (FPR), which is known to modulate Aβ1-42 uptake and signal transduction, might be one candidate molecule regulating glia function in AD. Here, we investigate whether the modulation of FPR exerts beneficial effects in an AD preclinical model.
To address this question, APP/PS1 double-transgenic AD mice were treated for 20 weeks with either the pro-inflammatory FPR agonist fMLF, the FPR1/2 antagonist Boc2 or the anti-inflammatory FPR2 agonist Ac2-26. Spatial learning and memory were evaluated using a Morris water maze test. Immunohistological staining, gene expression studies, and flow cytometry analyses were performed to study neuronal loss, gliosis, and Aß-load in the hippocampus and cortex, respectively.
FPR antagonism by Boc2-treatment significantly improved spatial memory performance, reduced neuronal pathology, induced the expression of homeostatic growth factors, and ameliorated microglia, but not astrocyte, reactivity. Furthermore, the elevated levels of amyloid plaques in the hippocampus were reduced by Boc2-treatment, presumably by an induction of amyloid degradation.
We suggest that the modulation of FPR signaling cascades might be considered as a promising therapeutic approach for alleviating the cognitive deficits associated with early AD. Additional studies are now needed to address the downstream effectors as well as the safety profile of Boc2.
Summary
Bacterial meningitis is, despite progress in research and the development of new treatment strategies, still a cause of severe neuronal sequelae. The brain is protected from penetrating ...pathogens by both the blood–brain barrier and the innate immune system. The invading pathogens are recognized by pattern recognition receptors including the G‐protein coupled formyl peptide receptors (FPRs), which are expressed by immune cells of the central nervous system. The expression of FPRs is up‐regulated during bacterial meningitis, but the consequence on the progression of inflammation and impact on mortality are far from clear. Therefore, we used mFPR1 and mFPR2‐deficient mice to investigate the effects on inflammation, bacterial growth and mortality in a mouse model of pneumococcal meningitis. Our results revealed increased bacterial burden, increased neutrophil infiltration and higher mortality in mFPR1/2‐deficient mice in comparison to wild‐type mice. The mFPR1‐ or mFPR2‐deficient mice also showed significantly increased glial cell density, whereas the immune responses including the expression of anti‐inflammatory cytokines and antimicrobial peptides were decreased in bacterial meningitis. Taken together, the results suggest that FPR1 and FPR2 play an important role in the innate immune responses against Streptococcus pneumoniae within the central nervous system and the lack of the receptors leads to a dysregulation of the inflammatory response compared with wild‐type mice.
Large-scale clinical outcome studies demonstrated the efficacy of SGLT2 inhibitors in patients with type II diabetes. Besides their therapeutic efficacy in diabetes, significant renoprotection was ...observed in non-diabetic patients with chronic kidney disease (CKD), suggesting the existence of glucose-independent beneficial effects of SGLT2 inhibitors. However, the relevant mechanisms by which SGLT2 inhibition delays the progression of renal injury are still largely unknown and speculative. Previous studies showed that SGLT2 inhibitors reduce diabetic hyperfiltration, which is likely a key element in renoprotection. In line with this hypothesis, this study aimed to investigate the nephroprotective effects of the SGLT2 inhibitor empagliflozin (EMPA) in different mouse models with non-diabetic hyperfiltration and progressing CKD to identify the underlying diabetes-independent cellular mechanisms. Non-diabetic hyperfiltration was induced by unilateral nephrectomy (UNx). Since UNx alone does not result in renal damage, renal disease models with varying degrees of glomerular damage and albuminuria were generated by combining UNx with high NaCl diets ± deoxycorticosterone acetate (DOCA) in different mouse strains with and without genetic predisposition for glomerular injury. Renal parameters (GFR, albuminuria, urine volume) were monitored for 4-6 weeks. Application of EMPA via the drinking water resulted in sufficient EMPA plasma concentration and caused glucosuria, diuresis and in some models renal hypertrophy. EMPA had no effect on GFR in untreated wildtype animals, but significantly reduced hyperfiltration after UNx by 36%. In contrast, EMPA did not reduce UNx induced hyperfiltration in any of our kidney disease models, regardless of their degree of glomerular damage caused by DOCA/salt treatment. Consistent with the lack of reduction in glomerular hyperfiltration, EMPA-treated animals developed albuminuria and renal fibrosis to a similar extent as H
O control animals. Taken together, the data clearly indicate that blockade of SGLT2 has the potential to reduce non-diabetic hyperfiltration in otherwise untreated mice. However, no effects on hyperfiltration or progression of renal injury were observed in hypervolemic kidney disease models, suggesting that high salt intake and extracellular volume might attenuate the protective effects of SGLT2 blockers.
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