Postoperative clinical outcomes of unicompartmental knee arthroplasty in patients with isolated medial compartmental osteoarthritis following medial meniscus posterior root tear

Background: Cartilage degradation progresses rapidly following medial meniscus posterior root tear (MMPRT). Unicompartmental knee arthroplasty (UKA) has been performed for medial compartmental osteoarthritis following MMPRT. We evaluated the clinical and radiographic outcomes of UKA for medial compartmental osteoarthritis after an untreated MMPRT. Methods: Twenty-one patients who underwent UKA for isolated medial compartment osteoarthritis following MMPRT were retrospectively investigated. Clinical outcomes were assessed using the Knee Injury and Osteoarthritis Outcome Score and knee range of motion. The posterior tibial slope and tibial component inclination were evaluated using plain radiographs. Results: The mean follow-up periods were 25.5 +/- 13.8 months. Clinical outcomes improved significantly postoperatively. The mean postoperative knee extension angle was-1.1 degrees +/- 2.1 degrees, and the knee flexion angle was 134.3 degrees +/- 4.9 degrees. The posterior tibial slope angle decreased from 9.0 degrees +/- 2.0 degrees preoperatively to 5.4 degrees +/- 1.8 degrees postoperatively, and postoperative tibial component inclination at the final follow-up was 2.9 degrees +/- 1.1 degrees varus. No aseptic loosening or deep infections were observed. Conclusion: UKA significantly improved clinical outcomes and could be a viable surgical option for treating isolated medial compartmental osteoarthritis accompanied by untreated MMPRT

Hearing Loss Controlled by Optogenetic Stimulation of Nonexcitable Nonglial Cells in the Cochlea of the Inner Ear

Light-gated ion channels and transporters have been applied to a broad array of excitable cells including neurons, cardiac myocytes, skeletal muscle cells and pancreatic β-cells in an organism to clarify their physiological and pathological roles. Nonetheless, among nonexcitable cells, only glial cells have been studied in vivo by this approach. Here, by optogenetic stimulation of a different nonexcitable cell type in the cochlea of the inner ear, we induce and control hearing loss. To our knowledge, deafness animal models using optogenetics have not yet been established. Analysis of transgenic mice expressing channelrhodopsin-2 (ChR2) induced by an oligodendrocyte-specific promoter identified this channel in nonglial cells—melanocytes—of an epithelial-like tissue in the cochlea. The membrane potential of these cells underlies a highly positive potential in a K+-rich extracellular solution, endolymph; this electrical property is essential for hearing. Illumination of the cochlea to activate ChR2 and depolarize the melanocytes significantly impaired hearing within a few minutes, accompanied by a reduction in the endolymphatic potential. After cessation of the illumination, the hearing thresholds and potential returned to baseline during several minutes. These responses were replicable multiple times. ChR2 was also expressed in cochlear glial cells surrounding the neuronal components, but slight neural activation caused by the optical stimulation was unlikely to be involved in the hearing impairment. The acute-onset, reversible and repeatable phenotype, which is inaccessible to conventional gene-targeting and pharmacological approaches, seems to at least partially resemble the symptom in a population of patients with sensorineural hearing loss. Taken together, this mouse line may not only broaden applications of optogenetics but also contribute to the progress of translational research on deafness

Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method for mtDNA typing in Hokkaido brown bear (Ursus aretos yesoensis)

To develop an easy method of typing of mitochondrial DNA (mtDNA) in Hokkaido brown bears (Ursus arctos yesoensis), the PCR-RFLP technique was improved using four restriction enzymes: Mbo 1, Cfr 13 I, TspE 1, and Fok 1. This approach identified seven groups of mtDNA haplotypes, HB1/2/5-7, HB3, HB4, HB8/9, HB10/11, HB12 and HB13 from 102 brown bears of northern, central and eastern Hokkaido