A community-academic nursing partnership formed to care for the urgent healthcare needs of individuals extracted from human trafficking during a multidisciplinary team operation. During past human trafficking extraction operations, law enforcement and the state sexual assault nurse examiner coordinator recognized the need to meet the patients' immediate physical and emotional needs while providing essential comfort to the newly extracted individuals. To meet the immediate holistic healthcare needs during the recovery operation, the nursing faculty partnered with a local nonprofit community clinic to provide onsite trauma-informed, patient-centered healthcare and comfort items. The healthcare team consisted of advanced practice nurses, mental health nurses who triaged the patient's immediate psychological needs, sexual assault nurses who collected forensic specimens, and nurses with expertise in substance use disorder who evaluated the patient's treatment needs. The patient's physical comfort was met by providing hygiene kits, blankets, socks, food, and drinks. Trauma-informed language was utilized to help the patient feel safe and to convey respect for the patient's autonomy in making decisions during the extraction process. The innovative community-academic nursing partnership laid the groundwork for providing healthcare to future human trafficking extraction operations with plans to incorporate nursing students and graduate nursing students to increase the number of patients served while providing a rich learning experience to the students.
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http://dx.doi.org/10.1111/phn.13352 | DOI Listing |
Alzheimers Dement
December 2024
Shenzhen Bay Laboratory, Shenzhen, Guandong, China.
Background: The classic mode of STING activation is through binding the cyclic dinucleotide 2'3'-cyclic GMP-AMP (cGAMP), produced by the DNA sensor cyclic GMP-AMP synthase (cGAS), which is important for the innate immune response to microbial infection and autoimmune disease. Modes of STING activation that are independent of cGAS are much less well understood. We wanted to explore the interactome of STING on the organelles during its trafficking route and to understand the regulatory network of STING signaling.
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December 2024
Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE, DISTALZ, Lille, France.
Background: BIN1 is a major susceptibility gene for AD and BIN1 protein interacts with Tau. However, the contribution of BIN1 and its isoforms to AD pathogenesis remains unclear. We recently described that human BIN1 isoform1 (BIN1iso1) induces an accumulation of early endosome vesicles leading to neurodegeneration in Drosophila retina and that the early endosome size regulation was conserved in human induced neurons.
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December 2024
Buck Institute for Research on Aging, Novato, CA, USA.
Background: Synapses can modify their strength in response to activity, and the unique properties of synapses that regulate their plasticity are essential for memory. Long-term potentiation (LTP) is considered the physiological basis for how neurons encode new memories. A complex series of postsynaptic signaling events in LTP is associated with memory deficits in tauopathy models, but the mechanism by which pathogenic tau inhibits plasticity at synapses is unknown.
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December 2024
John P. Hussman Institute for Human Genomics, Miller School of Medicine, Miami, FL, USA.
Background: We identified the missense variant Ser1038Cys (rs377155188) in the tetratricopeptide repeat domain 3 (TTC3) gene that segregate in a non-Hispanic white late onset Alzheimer disease (LOAD) family. This variant is predicted to be deleterious and extremely rare (MAF<0.01%).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Background: Despite recent FDA approvement of disease-modifying treatments that reduce Aβ, the identification of novel therapeutic strategies that could delay the Alzheimer's disease (AD) development are needed. We identified and developed novel small molecule compounds that mildly inhibit mitochondrial complex I (MCI). Chronic treatment with a tool compound CP2 in 4 mouse models of familial AD was efficacious protecting against synaptic dysfunction and memory impairment, improving brain energetics and cognitive performance, reducing levels of human pTau and Ab.
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