Morphology of insertion sites on patellar side of medial patellofemoral ligament.

PURPOSE: The purpose of this study was to clarify the insertion sites on the patellar side of the medial patellofemoral ligament (MPFL). METHODS: A total of 35 nonpaired human cadaveric knees were used in this study. After identification of the MPFL, the insertion sites on the patellar side of the MPFL were marked. Three-dimensional images were created, and the location and morphology of these insertion sites were analysed. RESULTS: The morphology of the insertion sites on the patellar side of the MPFL was consistent. The proximal fibres of the MPFL were inserted to the deep fascia of the vastus medialis obliquus (VMO) and medial margin of the vastus intermedius (VI). The distal fibres of the MPFL were inserted to the medial margin of the patella directly. The insertion lengths of the VMO, VI, and patella were 26.7 ± 5.0, 28.5 ± 4.4, and 18.5 ± 4.4 mm, respectively. The rate of the vertical distance from the superior pole of the patella to the superior edge of the MPFL in relation to the total patellar height was 12 ± 4.4 %. At the distal edge, the rate was 58 ± 9.6 %. CONCLUSION: The insertion sites on the patellar side of the MPFL were consistent. The MPFL inserted into the VMO and VI was significantly longer than into the patella. The clinical relevance of this study is to improve understanding of the anatomy of the insertion sites on the patellar side of the MPFL and the pathophysiology of patellar dislocation.

Morphology of the femoral insertion site of the medial patellofemoral ligament.

PURPOSE: The purpose of this study was to identify the femoral insertion of the medial patellofemoral ligament (MPFL) and related osseous landmarks. METHODS: A total of 31 unpaired human cadaveric knees were studied. The MPFL was identified, and the site of its femoral insertion was marked. Three-dimensional images were created, and the location and morphology of the femoral insertion of the MPFL and related osseous structures were analyzed. RESULTS: The MPFL was identified in all knees. The femoral insertion of the MPFL was elliptical in shape, and the mean surface area was 56.5 ± 16.9 mm(2). The characteristic features of the femoral insertion of the MPFL could not be identified, but the adductor tubercle was clearly identified in all knees. The centre of the femoral insertion of the MPFL was 10.6 ± 2.5 mm distal to the apex of the adductor tubercle on the long axis of the femur, and the position of the insertion site was consistent in all knees. CONCLUSION: The adductor tubercle was clearly identified as an osseous landmark. The femoral insertion of the MPFL was approximately 10 mm distal to the adductor tubercle. These findings may improve understanding of the anatomy of the femoral insertion of the MPFL and may assist surgeons in performing anatomical reconstruction.

Morphology of the femoral insertion of the lateral collateral ligament and popliteus tendon.

PURPOSE: To clarify the femoral insertion of the lateral collateral ligament (LCL) and popliteus tendon (PT) and related osseous landmarks on three-dimensional images. METHODS: Twenty-six non-paired, formalin-fixed human cadaveric knees were evaluated in this study. Femoral insertion of the LCL and PT was identified and marked. Three-dimensional images were created, and the surface area, location, positional relationships, and morphology of the femoral insertion of the LCL, PT, and related osseous structures were analysed. RESULTS: The mean surface areas of the LCL and PT femoral insertions were 55.8 ± 25.0 and 52.5 ± 24.2 mm(2), respectively. Variations in the positional relationships between the LCL and PT insertions (PT inserted parallel and posterior to the LCL insertion to the long axis of the femur) were observed. The lateral epicondyle and popliteal sulcus could be clearly identified as osseous landmarks on three-dimensional images in all knees. Most of the LCL was inserted postero-distal to the apex of the lateral epicondyle, and the PT was inserted at the anterior end of the popliteal sulcus in all knees. CONCLUSION: We observed variation in the positional relationship between the femoral insertion of the LCL and PT. However, the relationships between their insertions and osseous landmarks were consistent. The findings of this study contribute to the understanding of the PLC osseous anatomy and should assist surgeons in performing PLC surgery with a more anatomic perspective.

The structure-activity relationship of aryloxyacetylthioureas for the inhibition of Orobanche minor radicle elongation.

Orobanchaceae root parasitic weeds cause significant damage to agriculture and become threats to global food security. Integrated pest management is a key concept in modern agriculture and requires chemicals with various modes of action. Planteose accumulates as a storage carbohydrate in the dry seeds of root parasitic weeds. In Orobanche minor seeds, planteose is hydrolyzed by an α-galactosidase, OmAGAL2, during germination. It was found that the OmAGAL2 inhibitor, PI-28, suppressed the radicle elongation of germinating O. minor seeds. This inhibitory activity against O. minor radicle elongation was evaluated for a series of aryloxyacetylthioureas synthesized based on the structure of PI-28. Compounds with a 3-Cl or 4-Cl substituent on the benzene ring in the phenoxy moiety in PI-28 exhibited more potent activity than the parent PI-28. This is the first report on the effect of aryloxyacetylthioureas on a root parasitic weed and will contribute to the development of control reagents for root parasitic weeds.

Subtoxic levels of hydrogen peroxide induce brain-derived neurotrophic factor expression to protect PC12 cells.

BACKGROUND: Oxidative stress is one of the mechanisms underlying pathogenesis in neurodegenerative diseases such as Alzheimer's disease. Generally, oxidative stress represents cell toxicity; however, we recently found that oxidative stress promotes the expression of growth factor progranulin (PGRN) in HT22 murine hippocampus cells, thereby protecting the HT22 cells. In this study, we attempted to clarify whether a similar system exists in the other neuronal cell model, rat pheochromocytoma (PC12) cells. RESULTS: After confirming that high concentrations of hydrogen peroxide (H2O2; 100-250 µM) initiate PC12 cell death, we analyzed growth factor expressional changes after H2O2 treatment. We found, intriguingly, that gene expression of brain-derived neurotrophic factor (BDNF), but not PGRN was significantly induced by H2O2. Although little expression of the high affinity BDNF receptor tropomyosin-related kinase TrkB was observed in PC12 cells, expression of low affinity neurotrophin receptor, p75NTR, was clearly observed. This BDNF signaling appeared to contribute to PC12 cell protection, since PC12 cell death was significantly attenuated by BDNF treatment. CONCLUSIONS: Based on our results, we conclude that the induction of BDNF by subtoxic levels of H2O2 and its signaling may have roles in PC12 cell protection.

Potential neuroprotective effects of SIRT1 induced by glucose deprivation in PC12 cells.

Nutrient availability is one of the most important signals regulating cellular fates including cell growth, differentiation, and death. Recent evidence suggests that the NAD(+)-dependent histone deacetylase sirtuin 1 (SIRT1) plays a prominent role in linking changes in nutritional availability with cellular fate regulation. SIRT1 expression is observed in neurons, yet the expressional and functional regulation of this protein is not fully understood. In the present study, we examined whether extracellular glucose concentration affects the expression and localization of SIRT1 in PC12 cells. Further, we examined levels of forkhead box O3a (FoxO3a), which is also controlled by changes in extracellular glucose concentration. We observed the total expression levels of SIRT1 and FoxO3a in PC12 cells were reduced when glucose availability increased via gene expressional control, at least in part. Nuclear localization of SIRT1 and FoxO3a was increased by glucose deprivation. Even though the changes in extracellular glucose concentration regulated SIRT1 and FoxO3a in a similar direction, the effects of nerve growth factor on these two proteins were completely different. Finally, we found the potent SIRT1 inhibitor enhanced glucose deprivation-induced cell death. Therefore, we propose that glucose deprivation-induced SIRT1 expression potentially plays a major role in protecting PC12 cells.