To get through to survive: Exploring the symptom cluster management process during oncological treatment from the perspective of patients with lung cancer - A grounded theory study.

Purpose: To explore the symptom cluster management process from the perspective of patients with lung cancer within the oncological care context.

Methods: We used a constructivist grounded theory methodology to collect and analyze rich data from 15 patients with lung cancer via individual interviews and a two-dimensional symptom assessment scale.

Results: A situational theoretical model describes the symptom cluster management process through the main category 'To get through to survive', with the category 'Handling symptom clusters' together with six sub-categories concerning the patients' management strategies and the category 'Living with symptom clusters,' together with two sub-categories describing the outcome in their daily life.

Politically Contaminated Clothes, Chocolates, and Charities: Distancing From Neutral Products Liked by Out-Group or In-Group Partisans.

This research demonstrates that people distance themselves not just from out-group partisans or policies but also from completely neutral and apolitical consumer products that have been "contaminated" simply by being preferred by the political out-group. Using large representative samples of Swedish adults, we investigated how aesthetic judgments of clothes (Study 1), evaluations of chocolate bars (Study 2), and allocations to charitable organizations (Study 3) were influenced by a randomly assigned association between these products and the leader or supporters of the participant's least- or most-liked political party. Products liked by the least-liked party became less attractive in all studies; the results were mixed for products liked by the most-liked party.

Tau processing and tau-mediated inflammation differ in human and astrocytes.

Alzheimer's disease (AD) and progressive supra-nuclear palsy (PSP) are both proteinopathies, characterized by the accumulation of tau aggregates. is the greatest genetic risk factor for developing AD, while is a significant risk factor for developing PSP. In the brain, astrocytes are the predominant producer of ApoE, but they are also important for inflammation and overall brain homeostasis.

Mapping quality of life after balloon dilatation in subglottic stenosis using Dyspnea index and Short Form Health Survey-36.

Purpose: An accurate diagnosis and proper treatment plan are required to restore an adequate patent airway in fibrotic subglottic stenosis (SGS). Currently, the definitive treatment entails single-stage balloon dilatation with steroid injections. The primary aim was to evaluate successful airway restoration and general quality of life in cases with SGS in northern Sweden using robust patient reported outcomes.

Astrocytic accumulation of tau fibrils isolated from Alzheimer's disease brains induces inflammation, cell-to-cell propagation and neuronal impairment.

Accumulating evidence highlights the involvement of astrocytes in Alzheimer's disease (AD) progression. We have previously demonstrated that human iPSC-derived astrocytes ingest and modify synthetic tau fibrils in a way that enhances their seeding efficiency. However, synthetic tau fibrils differ significantly from in vivo formed fibrils.

Altered amyloid-β structure markedly reduces gliosis in the brain of mice harboring the Uppsala APP deletion.

Deposition of amyloid beta (Aβ) into plaques is a major hallmark of Alzheimer's disease (AD). Different amyloid precursor protein (APP) mutations cause early-onset AD by altering the production or aggregation properties of Aβ. We recently identified the Uppsala APP mutation (APPUpp), which causes Aβ pathology by a triple mechanism: increased β-secretase and altered α-secretase APP cleavage, leading to increased formation of a unique Aβ conformer that rapidly aggregates and deposits in the brain.

Amyloid-β deposits in human astrocytes contain truncated and highly resistant proteoforms.

Alzheimer's disease (AD) is a neurodegenerative disorder that develops over decades. Glial cells, including astrocytes are tightly connected to the AD pathogenesis, but their impact on disease progression is still unclear. Our previous data show that astrocytes take up large amounts of aggregated amyloid-beta (Aβ) but are unable to successfully degrade the material, which is instead stored intracellularly.

Exploring Symptom Clusters and Their Measurements in Patients With Lung Cancer: A Scoping Review for Practice and Research.

Problem Identification: This scoping review aimed to explore symptom clusters (SCs) in patients with lung cancer and how included symptoms and symptom dimensions are measured.

Literature Search: PubMed®, CINAHL®, Scopus®, and Cochrane Library were searched for studies published until December 31, 2021. Fifty-three articles were included.

Balloon dilatation versus CO laser surgery in subglottic stenosis, a retrospective analysis of therapeutic approaches.

Background: Subglottic stenosis (SGS) is a narrowing of the airway just below the vocal folds. The cause of SGS and the optimal care for these patients, have remained elusive. Endoscopic surgery of SGS using either balloon or CO laser is associated with recurrence.

Astrocytic uptake of neuronal corpses promotes cell-to-cell spreading of tau pathology.

Tau deposits in astrocytes are frequently found in Alzheimer's disease (AD) and other tauopathies. Since astrocytes do not express tau, the inclusions have been suggested to be of neuronal origin. However, the mechanisms behind their appearance and their relevance for disease progression remain unknown.

Altered Distribution of SNARE Proteins in Primary Neurons Exposed to Different Alpha-Synuclein Proteoforms.

Growing evidence indicates that the pathological alpha-synuclein (α-syn) aggregation in Parkinson's disease (PD) and dementia with Lewy bodies (DLB) starts at the synapses. Physiologic α-syn is involved in regulating neurotransmitter release by binding to the SNARE complex protein VAMP-2 on synaptic vesicles. However, in which way the SNARE complex formation is affected by α-syn pathology remains unclear.

Long-term effects of amyloid-beta deposits in human iPSC-derived astrocytes.

Growing evidence indicates that astrocytes are tightly connected to Alzheimer's disease (AD) pathogenesis. However, the way in which astrocytes participate in AD initiation and progression remains to be clarified. Our previous data show that astrocytes engulf large amounts of aggregated amyloid-beta (Aβ) but are unable to successfully degrade the material.

Infiltrating immune cells in prostate cancer tissue after androgen deprivation and radiotherapy.

Objectives: Androgen deprivation therapy (ADT) has long been a cornerstone in treatment of advanced prostate cancer (PCa), and is known to improve the results of radiotherapy (RT) for high-risk disease. The purpose of our study was to use a multiplexed immunohistochemical (mIHC) approach to investigate the infiltration of immune cells in PCa tissue after eight weeks of ADT and/or RT with 10 Gy.

Methods: From a cohort of 48 patients divided into two treatment arms, we obtained biopsies before and after treatment and used a mIHC method with multispectral imaging to analyze the infiltration of immune cells in tumor stroma and tumor epithelium, focusing on areas with high infiltration.

Amyloid-β accumulation in human astrocytes induces mitochondrial disruption and changed energy metabolism.

Background: Astrocytes play a central role in maintaining brain energy metabolism, but are also tightly connected to the pathogenesis of Alzheimer's disease (AD). Our previous studies demonstrate that inflammatory astrocytes accumulate large amounts of aggregated amyloid-beta (Aβ). However, in which way these Aβ deposits influence their energy production remain unclear.

Intracellular deposits of amyloid-beta influence the ability of human iPSC-derived astrocytes to support neuronal function.

Background: Astrocytes are crucial for maintaining brain homeostasis and synaptic function, but are also tightly connected to the pathogenesis of Alzheimer's disease (AD). Our previous data demonstrate that astrocytes ingest large amounts of aggregated amyloid-beta (Aβ), but then store, rather than degrade the ingested material, which leads to severe cellular stress. However, the involvement of pathological astrocytes in AD-related synaptic dysfunction remains to be elucidated.

CRISPR-Cas9 treatment partially restores amyloid-β 42/40 in human fibroblasts with the Alzheimer's disease M146L mutation.

Presenilin 1 (PS1) is a central component of γ-secretase, an enzymatic complex involved in the generation of the amyloid-β (Aβ) peptide that deposits as plaques in the Alzheimer's disease (AD) brain. The M146L mutation in the PS1 gene () leads to an autosomal dominant form of early-onset AD by promoting a relative increase in the generation of the more aggregation-prone Aβ42. This change is evident not only in the brain but also in peripheral cells of mutation carriers.

Green, Black and Rooibos Tea Inhibit Prostaglandin E2 Formation in Human Monocytes by Inhibiting Expression of Enzymes in the Prostaglandin E2 Pathway.

The formation of prostaglandin E2 (PGE2) is associated with adverse inflammatory effects. However, long-term treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) comes with risk of severe side effects. Therefore, alternative ways to inhibit PGE2 are warranted.

Cutibacterium acnes Induces the Expression of Immunosuppressive Genes in Macrophages and is Associated with an Increase of Regulatory T-Cells in Prostate Cancer.

Tumors and infectious agents both benefit from an immunosuppressive environment. Cutibacterium acnes () is a bacterium in the normal skin microbiota, which has the ability to survive intracellularly in macrophages and is significantly more common in prostate cancer tissue compared with normal prostate tissue. This study investigated if prostate cancer tissue culture positive for has a higher infiltration of regulatory T-cells (Tregs) and if macrophages stimulated with induced the expression of immunosuppressive genes that could be linked to an increase of Tregs in prostate cancer.

Traumatic brain injury in the presence of Aβ pathology affects neuronal survival, glial activation and autophagy.

Traumatic brain injury (TBI) presents a widespread health problem in the elderly population. In addition to the acute injury, epidemiological studies have observed an increased probability and earlier onset of dementias in the elderly following TBI. However, the underlying mechanisms of the connection between TBI and Alzheimer's disease in the aged brain and potential exacerbating factors is still evolving.

The deletion causes early onset autosomal dominant Alzheimer's disease by altering APP processing and increasing amyloid β fibril formation.

Point mutations in the amyloid precursor protein gene () cause familial Alzheimer's disease (AD) by increasing generation or altering conformation of amyloid β (Aβ). Here, we describe the mutation (Δ690-695), the first reported deletion causing autosomal dominant AD. Affected individuals have an age at symptom onset in their early forties and suffer from a rapidly progressing disease course.

Infiltration of M2 Macrophages and Regulatory T Cells Plays a Role in Recurrence of Renal Cell Carcinoma.

Background: It has been hypothesized that M2 macrophages and regulatory T cells (Tregs) may contribute to tumor progression by suppression of antitumor immunity.

Objective: To investigate the association between infiltration of CD163 M2 macrophages and CD4FOXP3 Tregs with clinical outcomes in renal cell carcinoma patients.

Design Setting And Participants: A cohort of 346 patients diagnosed with renal cell carcinoma at Örebro University Hospital between 1986 and 2011 was evaluated for CD163 M2 macrophage and CD4FOXP3 Treg infiltration by immunohistochemistry.

Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates.

Background: Alzheimer's disease (AD) and Parkinson's disease (PD) are characterized by brain accumulation of aggregated amyloid-beta (Aβ) and alpha-synuclein (αSYN), respectively. In order to develop effective therapies, it is crucial to understand how the Aβ/αSYN aggregates can be cleared. Compelling data indicate that neuroinflammatory cells, including astrocytes and microglia, play a central role in the pathogenesis of AD and PD.

Age-related increase of alpha-synuclein oligomers is associated with motor disturbances in L61 transgenic mice.

The pathogenesis of Parkinson's disease involves fibrillization and deposition of alpha-synuclein (α-syn) into Lewy bodies. Accumulating evidence suggests that α-syn oligomers are particularly neurotoxic. Transgenic (tg) mice overexpressing wild-type human α-syn under the Thy-1 promoter (L61) reproduce many Parkinson's disease features, but the pathogenetic relevance of α-syn oligomers in this mouse model has not been studied in detail.

Parkinson's Disease-Associated LRRK2 Interferes with Astrocyte-Mediated Alpha-Synuclein Clearance.

Parkinson's disease (PD) is a neurodegenerative, progressive disease without a cure. To prevent PD onset or at least limit neurodegeneration, a better understanding of the underlying cellular and molecular disease mechanisms is crucial. Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene represent one of the most common causes of familial PD.

Enhanced neprilysin-mediated degradation of hippocampal Aβ42 with a somatostatin peptide that enters the brain.

Aggregation of the amyloid-beta (Aβ) peptide is one of the main neuropathological events in Alzheimer's disease (AD). Neprilysin is the major enzyme degrading Aβ, with its activity enhanced by the neuropeptide somatostatin (SST). SST levels are decreased in the brains of AD patients.