Background: Numerous guidelines recommend pairing Semmes-Weinstein monofilament (SWM) testing with a secondary clinical test when screening for diabetic peripheral neuropathy, yet time is very limited in clinical practice. This study compared the time to complete and the diagnostic agreement of three vibratory sensation tests. Methods: Sixty-five individuals (42% male; aged: 61 ± 12 years) were recruited. A single investigator administered the following tests bilaterally: 10-site SWM, traditional tuning fork (TTF), electronic tuning fork (ETF), and vibration perception threshold (VPT) via biothesiometer. Times to physically administer the tests were compared with a one-way repeated measures ANOVA. Cochran’s Q test was used to compare the varied tests’ diagnostic agreement. Results: The ANOVA indicated there were significant ( P < .001, partial eta squared = .442) differences in time to complete the varied tests. Sidak post hoc comparisons indicated the VPT (21.2 ± 14.3) testing took an intermediate time to complete, while the ETF (9.7 ± 6.5) and TTF (10.1 ± 7.5) tests took the least amount of time, and the SWM (28.6 ± 8.4) test took the longest time. There were also numerous significant differences ( P ≤ .001) between the different tests in regards to neuropathy diagnoses. Conclusions: Tuning fork methods required 11 seconds less to administer than VPT testing. Although that may seem trivial, it is worth noting peripheral neuropathy screening often fails to occur in the precious few minutes clinicians are allotted per patient. Considering ETF’s intrinsic control of stimulus amplitude and its ease of use with an embedded timer, the ETF is recommended over the TTF. Clinicians should also be mindful that different tests yield different diagnostic conclusions.

Atherosclerosis involves interactions between inflammation system and dyslipidemia. MCPIP1 (Monocyte Chemotactic Protein induced Protein-1) is induced by proinflammatory molecules and serves as a negative feedback loop in regulating inflammatory responses. Our current study was designed to test the role of MCPIP1 in maintaining lipid homeostasis, the latter a pivotal factor that contributes to the pathogenesis of atherosclerosis. We found that MCPIP1 knockout mice displayed a decrease in levels of serum HDL-cholesterol and total triglycerides but an increase in serum LDL/VLDL-cholesterol levels when compared to wild-type mice. Additionally, ApoA-1 expression was reduced but LPL expression was upregulated in plasma from MCPIP1 knockout mice. The livers from the MCPIP1 knockout mice revealed a decrease in hepatocyte number and an increase in collagen deposition when compared to wild-type mice. These findings suggest that MCPIP1 deficiency can induce liver fibrosis, alter the expression of lipoproteins, and affect transportation and metabolism of lipids, indicating that MCPIP1 is involved in maintaining lipid homeostasis, possibly via negatively regulating inflammatory responses.