Superficial Ulnar Artery and its Clinical Significance

We present a case with an atypical variation of the ulnar artery discovered while examining a cadaver in our routine Gross Anatomy lab dissection. A superficial ulnar artery was found in a 55-year-old male cadaver originating directly from the brachial artery. This is a rare variation where the route of the ulnar artery runs superficially to the flexor compartment in the forearm. Based on previous cadaver studies, the incidence of such variation in the adult population appears to be approximately 3.75%. Deviations in the ulnar artery can lead to a potential risk of injury to patients during surgery. The superficial ulnar artery can mistakenly result in the administration of medicines into the artery as opposed to the median cubital vein during the injection. Hemorrhaging as well as other potential traumas can occur. We will also discuss the potential complications that could arise from this variant and the clinical recommendations for treatment

Improving selection of documents for auditing by Fin Ware Quality Control Team

An inefficient process within a vital team causes workflow disruption between and among company departments, delay in product release, and inefficiency in the workplace thereby heightening the threat of potential loss of clients and stagnancy of the company. Thus, the need to improve the process within the Quality Control team to enable timely release of financial information to clients is imperative as this will facilitate and aid the clients with their business strategies and enhance their investment decisions. FinWare represents a Company engaged in providing clients with financial information and analytics. This action research paper aims to address the issue on inefficient selection of documents for audit as caused by the lack of an established selection process in the Quality Control team of FinWare Philippines Inc. The Action Research Cycle of Coghlan and Brannick was utilized as a guide through the course of this study. Methods of inquiry and collaboration with the Quality Control team and Operations team were conducted throughout the action research cycles to gather and analyze the data. The DMAIC framework was followed to deal with the change process and ensure sustainable results. After two action research cycles, I and my colleagues created an effective tracker to aid the Quality Control Associates in the proper selection of document. We also established a selection process guideline to remove non-value adding activities in the selection process within our Quality Control team. On a broader context, this action research paper contributes to the larger society through the synthesis of management theories and concepts, personal reflections and learnings, and social development principles, in order to create relevance to other organizations that are yet to undergo a similar process of change for quality management

Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology

Abstract Background The rare p.H157Y variant of TREM2 (Triggering Receptor Expressed on Myeloid Cells 2) was found to increase Alzheimer’s disease (AD) risk. This mutation is located at the cleavage site of TREM2 extracellular domain. Ectopic expression of TREM2-H157Y in HEK293 cells resulted in increased TREM2 shedding. However, the physiological outcomes of the TREM2 H157Y mutation remain unknown in the absence and presence of AD related pathologies. Methods We generated a novel Trem2 H157Y knock-in mouse model through CRISPR/Cas9 technology and investigated the effects of Trem2 H157Y on TREM2 proteolytic processing, synaptic function, and AD-related amyloid pathologies by conducting biochemical assays, targeted mass spectrometry analysis of TREM2, hippocampal electrophysiology, immunofluorescent staining, in vivo micro-dialysis, and cortical bulk RNA sequencing. Results Consistent with previous in vitro findings, Trem2 H157Y increases TREM2 shedding with elevated soluble TREM2 levels in the brain and serum. Moreover, Trem2 H157Y enhances synaptic plasticity without affecting microglial density and morphology, or TREM2 signaling. In the presence of amyloid pathology, Trem2 H157Y accelerates amyloid-β (Aβ) clearance and reduces amyloid burden, dystrophic neurites, and gliosis in two independent founder lines. Targeted mass spectrometry analysis of TREM2 revealed higher ratios of soluble to full-length TREM2-H157Y compared to wild-type TREM2, indicating that the H157Y mutation promotes TREM2 shedding in the presence of Aβ. TREM2 signaling was further found reduced in Trem2 H157Y homozygous mice. Transcriptomic profiling revealed that Trem2 H157Y downregulates neuroinflammation-related genes and an immune module correlated with the amyloid pathology. Conclusion Taken together, our findings suggest beneficial effects of the Trem2 H157Y mutation in synaptic function and in mitigating amyloid pathology. Considering the genetic association of TREM2 p.H157Y with AD risk, we speculate TREM2 H157Y in humans might increase AD risk through an amyloid-independent pathway, such as its effects on tauopathy and neurodegeneration which merit further investigation