Vote like your ETERNAL SOUL depends on it!

Brighteon Broadcast News, Oct 15, 2024

#MikeAdmas #Israel #Genocide #Trump #Kamala

Watch the full broadcast here https://www.brighteon.com/channels/hrreport/

Israel Ramps Up Use Of Suicide Drones Against Civilians https://madmaxworld.tv/watch?id=670ea22dcd7adb277e5a4ef8

A lot of civilians are dying in Gaza

https://newstarget.com/2024-10-14-israel-footage-shows-devastating-civilian-harm-gaza.html

56%.Despite recent advances in the treatment of colorectal cancer (CRC), patient's individual response and clinical follow-up vary considerably with tumor intrinsic factors to contribute to an enhanced malignancy and therapy resistance. Among these markers, upregulation of members of the inhibitor of apoptosis protein (IAP) family effects on tumorigenesis and radiation- and chemo-resistance by multiple pathways, covering a hampered induction of apoptosis/autophagy, regulation of cell cycle progression and DNA damage response. These mechanisms are tightly controlled by the tumor suppressor p53 and thus transcriptional and post-translational regulation of IAPs by p53 is expected to occur in malignant cells. By this, cellular IAP1/2, X-linked IAP, Survivin, BRUCE and LIVIN expression/activity, as well as their intracellular localization is controlled by p53 in a direct or indirect manner via modulating a multitude of mechanisms. These cover, among others, transcriptional repression and the signal transducer and activator of transcription (STAT)3 pathway. In addition, p53 mutations contribute to deregulated IAP expression and resistance to therapy. This review aims at highlighting the mechanistic and clinical importance of IAP regulation by p53 in CRC and describing potential therapeutic strategies based on this interrelationship.Introduction. Weather-related disasters, such as wildfires exacerbated by a rise in global temperatures, need to be better studied in terms of their mental health impacts. This study focuses on the mental health sequelae of the deadliest wildfire in California to date, the Camp Fire of 2018. Methods. We investigated a sample of 725 California residents with different degrees of disaster exposure and measured mental health using clinically validated scales for post-traumatic stress disorder (PTSD), major depressive disorder (MDD) and generalized anxiety disorder (GAD). Data were collected at a chronic time-point, six months post-wildfire. We used multiple regression analyses to predict the mental health outcomes based on self-reported fire exposure. Additionally, we included vulnerability and resilience factors in hierarchical regression analyses. Results. Our primary finding is that direct exposure to large scale fires significantly increased the risk for mental health disorders, particularly for PTSD and depression. Additionally, the inclusion of vulnerability and resilience factors in the hierarchical regression analyses led to the significantly improved prediction of all mental health outcomes. Childhood trauma and sleep disturbances exacerbated mental health symptoms. Notably, self-reported resilience had a positive effect on mental health, and mindfulness was associated with significantly lower depression and anxiety symptoms. Conclusion. Overall, our study demonstrated that climate-related extreme events, such as wildfires, can have severe mental illness sequelae. Moreover, we found that pre-existing stressful life events, resilient personality traits and lifestyle factors can play an important role in the prevalence of psychopathology after such disasters. Unchecked climate change projected for the latter half of this century may severely impact the mental wellbeing of the global population, and we must find ways to foster individual resiliency.HIV-1 infects T cells, but the most frequent AIDS-related lymphomas are of B-cell origin. Molecular mechanisms of HIV-1-induced oncogenic transformation of B cells remain largely unknown. https://www.selleckchem.com/products/vt103.html HIV-1 Tat protein may participate in this process by penetrating and regulating gene expression in B cells. Both immune and cancer cells can reprogram communications between extracellular signals and intracellular signaling pathways via the Akt/mTORC1 pathway, which plays a key role in the cellular response to various stimuli including viral infection. Here, we investigated the role of HIV-1 Tat on the modulation of the Akt/mTORC1 pathway in B cells. We found that HIV-1 Tat activated the Akt/mTORC1 signaling pathway; this leads to aberrant activation of activation-induced cytidine deaminase (AICDA) due to inhibition of the AICDA transcriptional repressors c-Myb and E2F8. These perturbations may ultimately lead to an increased genomic instability and proliferation that might cause B cell malignancies.Telerehabilitation offers a unique solution for continuity of care in pediatric rehabilitation under physical distancing. The major aims of this study were to (1) describe the development of telerehabilitation usage guidelines in a large hospital in Israel, and to (2) evaluate the implementation of telerehabilitation from the perspectives of healthcare practitioners and families. An expert focus group developed guidelines which were disseminated to multidisciplinary clinicians. Following sessions, clinicians filled The Clinician Evaluation of Telerehabilitation Service (CETS), a custom-built feedback questionnaire on telerehabilitation, and parents completed the client version of the Therapist Presence Inventory (TPI-C) and were asked to rate the effectiveness of sessions on an ordinal scale. Four goals of telerehabilitation sessions were defined (1) maintenance of therapeutic alliance, (2) provision of parental coping strategies, (3) assistance in maintaining routine, and (4) preventing functional deterioration. Principal Components Analysis was used for the CETS questionnaire and the relationships of CETS and TPI-C with child's age and the type of session were evaluated using Spearman's correlations and the Kruskal-Wallis H test. In total, sixty-seven telerehabilitation sessions, with clients aged 11.31 ± 4.8 years, were documented by clinicians. Three components (child, session, parent) explained 71.3% of the variance in CETS. According to therapists, their ability to maintain the therapeutic alliance was generally higher than their ability to achieve other predefined goals (p less then 0.01). With younger children, the ability to provide feedback to the child, grade treatment difficulty and provide coping strategies to the parents were diminished. Families perceived the therapist as being highly present in therapy regardless of treatment type. These results demonstrate a potential framework for the dissemination of telerehabilitation services in pediatric rehabilitation.

This study aims to investigate the regulatory effect of hypoxia on human periodontal ligament stem cells (PDLSCs) through RNA sequencing (RNA SEQ). Human PDLSCs were cultured in normoxia (20% O
) or hypoxia (2% O
).

Total RNA was extracted and sequenced. The expression profiles of circRNAs, lncRNAs, and miRNAs were determined, and the lncRNA/circRNA-miRNA-mRNA networks were analyzed.

In total, 15miRNAs, 449lncRNAs, and 53 circRNAs were differentially expressed. Among them, 21 circRNAs, 262lncRNAs, 5miRNAs, and 5mRNAs were selected to construct competing endogenous RNA (ceRNA) networks. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were carried out to explore potential related pathways and regulatory functions. Several ceRNA axes (lncRNA-FTX/circRNA-FAT1-hsa-miR-4781-3p-SMAD5 and circRNA LPAR1-hsa-miR-342-3p-ADAR) may provide a theoretical basis on the study of osteogenic differentiation of PDLSCs under hypoxia.

This study revealed that the expression profiles of circRNAs, lncRNAs, and miRNAs had changed significantly in PDLSCs cultured in 2% O
; specific circRNAs/lncRNAs may play a competitive role in the differentiation of PDLSCs.
This study revealed that the expression profiles of circRNAs, lncRNAs, and miRNAs had changed significantly in PDLSCs cultured in 2% O2 ; specific circRNAs/lncRNAs may play a competitive role in the differentiation of PDLSCs.A kinetic model based on fundamentals of radical polymerization and literature known rate parameters for the polymerization of n-butyl acrylate is validated against molecular analysis and rheological data. The model is used to predict conversion, molar mass distribution, and branching densities in form of short and long chain branching. Rheological measurements of synthesized model polymers are evaluated along the Carreau-Yasuda and Van Gurp-Palmen presentations, allowing to detect small differences in the degree of long chain branching. Contributions of anharmonics to viscoelastic response in large amplitude oscillations are small and differences between the products are dominated by the differences in molar mass.Anti-bacterial autophagy, known as xenophagy, is a host innate immune response that targets invading pathogens for degradation. Some intracellular bacteria, such as the enteric pathogen Salmonella enterica serovar Typhimurium (S. Typhimurium), utilize effector proteins to interfere with autophagy. One such S. Typhimurium effector, SopF, inhibits recruitment of ATG16L1 to damaged Salmonella-containing vacuoles (SCVs), thereby inhibiting the host xenophagic response. SopF is also required to maintain the integrity of the SCV during the early stages of infection. Here we show disruption of the SopF-ATG16L1 interaction leads to an increased proportion of cytosolic S. Typhimurium. Furthermore, SopF was utilized as a molecular tool to examine the requirement for ATG16L1 in the intracellular lifestyle of Coxiella burnetii, a bacterium that requires a functional autophagy pathway to replicate efficiently and form a single, spacious vacuole called the Coxiella-containing vacuole (CCV). ATG16L1 is required for CCV expansion and fusion but does not influence C. burnetii replication. In contrast, SopF did not affect CCV formation or replication, demonstrating that the contribution of ATG16L1 to CCV biogenesis is via its role in autophagy, not xenophagy. This study highlights the diverse capabilities of bacterial effector proteins to dissect the molecular details of host-pathogen interactions.The oral microbiome is ecologically diverse, complex, dynamic, and little understood. We describe the microbiota of four oral habitats in a birth cohort at age 32 and examine differences by sex, oral hygiene, and current smoking status, dental caries, and periodontal health. Oral biofilm samples collected from anterior labial supragingival, posterior lingual supragingival, subgingival, and tongue sites of 841 Dunedin Multidisciplinary Health and Development Study members were analysed using checkerboard DNA-DNA hybridization; focusing on 30 ecologically important bacterial species. The four habitats exhibited distinct microbial profiles that differed by sex. Streptococcus gordonii was more dominant in supragingival and tongue biofilms of males; Porphyromonas gingivalis exhibited higher relative abundance in subgingival biofilm of females. Males had higher scores than females for periodontal pathogens at supragingival sites. The relative abundance of several putative caries and periodontal pathogens differed in smokers and non-smokers. With poor oral hygiene significantly higher proportions of Gram-negative facultative anaerobes were present in subgingival biofilm and there were higher scores for the principal components characterised by putative cariogenic and periodontal pathogens at each site. Distinctive microenvironments shape oral biofilms and systematic differences exist by sex, oral hygiene, and smoking status.
Blastomycosis is an endemic fungal infection that causes pulmonary and systemic disease. It can occur irrespective of the patient's immune status. The risk factors associated with the severity of the disease are not well studied.

This is a retrospective study of patients admitted with blastomycosis at the University of Kentucky Hospital from 2004 to 2019. Logistic regression was used to identify variables associated with severe blastomycosis.

A total of 76 patients were identified; 22 (28.9%) had at least one immunosuppressive condition. Pulmonary blastomycosis was reported in 49/76 (65%) of the patients and disseminated infection in 27/76 (35.5%). All diagnostic tests were not significantly different in diagnostic results in immunocompromised vs immunocompetent patients. Cultures and histopathology were positive in 56/61 (91.8%) and 54/63 (85.7%) respectively. Blastomyces or Histoplasma antigen test was positive in 13/17 (76.4%) in immunocompromised patients compared to 26/42 (61.9%) in immunocompetent patients. Immunocompromised patients were more likely to be admitted to the hospital and ICU compared to immunocompetent patients. In the multivariate analysis, pulmonary multilobar disease (RR 5.68; 95% CI 2.13-15.15), obesity (RR 2.39; 95% CI 1.26-4.51), diabetes mellitus (RR 3.50; 95% CI 1.38-8.90) and immunosuppression (RR 2.28; 95% CI 1.14-4.56) were significant independent risk factors for severe blastomycosis. Inpatient mortality proportion was higher in immunocompromised patients but not statistically significant.

Pulmonary multilobar disease, obesity, diabetes mellitus and immunosuppression were risk factors associated with severe blastomycosis. Immunocompromised patients required more frequent hospitalisations compared to immunocompetent patients.
Pulmonary multilobar disease, obesity, diabetes mellitus and immunosuppression were risk factors associated with severe blastomycosis. Immunocompromised patients required more frequent hospitalisations compared to immunocompetent patients.
To examine and compare the medical burden of measles, influenza and COVID-19 outbreaks in the city of Bnei Brak, Israel.

The study was conducted during 2018-2021. The numbers of hospitalisations for these infections and their complications were recorded. Hospitalisation rates were determined by using the number of children residing in Bnei Brak and hospitalised with these infections during the study period as the numerators. The denominators were the estimated paediatric cases of measles, influenza and COVID-19 in Bnei Brak and were calculated under both pragmatic and conservative assumptions.

A total of 247, 65 and 32 children were hospitalised with influenza, COVID-19 and measles respectively. Complication rates were higher following measles than after influenza and SARS-CoV-2 infections. Hospitalisation rates were 10% for measles, 0.6%-1.2% for influenza and 0.15% - 0.25% for COVID-19 infections. Relative risks (RR) with 95% confidence intervals (CI) for hospitalisation following measles compared with COVID-19 ranged from 42 (26.3-67.3) to 70.1 (43.8-112.1), while the relative risks for influenza hospitalisation ranged from 2.5 (1.83-3.41) to 8.2 (6.0-11.2), compared with COVID-19 infection.

Hospitalisation rates and direct medical burdens of measles and influenza were significantly higher than those of COVID-19 infection in children.
Hospitalisation rates and direct medical burdens of measles and influenza were significantly higher than those of COVID-19 infection in children.
Although lung macrophages are directly exposed to external stimuli, their exact immunologic roles in asthma are still largely unknown. The aim of this study was to investigate the anti-asthmatic effect of Acinetobacter lwoffii in terms of lung macrophage modulation.

Six-week-old female BALB/c mice were sensitized and challenged with ovalbumin (OVA) with or without intranasal administration of A. lwoffii during the sensitization period. Airway hyperresponsiveness and inflammation were evaluated. Using flow cytometry, macrophages were subclassified according to their activation status. In the in vitro study, a murine alveolar macrophage cell line (MH-S) treated with or without A. lwoffii before IL-13 stimulation were analysed by quantitative RT-PCR.

In a murine asthma model, the number of inflammatory cells, including macrophages and eosinophils, decreased in mice treated with A. lwoffii (A. lwoffii/OVA group) compared with untreated mice (OVA group). The enhanced expression of MHCII in macrophages in the OVA group was decreased by A. lwoffii treatment. M2 macrophage subtypes were significantly altered. A. lwoffii treatment decreased CD11b
M2a and CD11b
M2c macrophages, which showed strong positive correlations with Th2 cells, ILC2 and eosinophils. In contrast, CD11b
M2b macrophages were significantly increased by A. lwoffii treatment and showed strong positive correlations with ILC1 and ILC3. In vitro, A. https://www.selleckchem.com/products/cx-5461.html lwoffii down-regulated the expression of M2 markers related but up-regulated those related to M2b macrophages.

Intranasal A. lwoffii exposure suppresses asthma development by suppressing the type 2 response via modulating lung macrophage activation, shifting M2a and M2c macrophages to M2b macrophages.
Intranasal A. lwoffii exposure suppresses asthma development by suppressing the type 2 response via modulating lung macrophage activation, shifting M2a and M2c macrophages to M2b macrophages.While the eye is considered an immune privileged site, its privilege is abrogated when immune cells are recruited from the surrounding vasculature in response to trauma, infection, aging, and autoimmune diseases like uveitis. Here, we investigate whether in uveitis immune cells become associated with the lens capsule and compromise its privilege in studies of C57BL/6J mice with experimental autoimmune uveitis. These studies show that at D14, the peak of uveitis in these mice, T cells, macrophages, and Ly6G/Ly6C+ immune cells associate with the lens basement membrane capsule, burrow into the capsule matrix, and remain integrated with the capsule as immune resolution is occurring at D26. 3D surface rendering image analytics of confocal z-stacks and scanning electron microscopy imaging of the lens surface show the degradation of the lens capsule as these lens-associated immune cells integrate with and invade the lens capsule, with a subset infiltrating both epithelial and fiber cell regions of lens tissue, abrogating its immune privilege.