In vivo pre- and postoperative three-dimensional knee kinematics in unicompartmental knee arthroplasty

Background

Pre- and postoperative knee kinematics in unicompartmental knee arthroplasty (UKA) can be theoretically related to clinical outcome and longevity after UKA with regard to ligament function and the degree of arthritic changes. However, the preoperative knee kinematics of patients indicated for UKA remain to be elucidated, and it is also unclear whether the preoperative kinematics can be maintained by the UKA procedure. The objective of this study was to examine the in vivo pre- and postoperative three-dimensional knee kinematics in UKA while referencing the normal knee kinematics reported in our previous study.

Methods

We analyzed the knee kinematics in 17 knees (14 patients) undergoing UKA via a three-dimensional to two-dimensional registration technique employing femoral condylar translation and femoral axial rotation. The pre- and postoperative knee kinematics during squat motion were evaluated in the same subjects, employing consistent evaluation parameters.

Results

On average, both pre- and postoperative knee kinematics in the range 10–100° of knee flexion demonstrated near-consistent femoral external rotation and anterior translation of the medial condyle and posterior translation of the lateral condyle. However, the mean femoral external rotation angle and the posterior translation of the lateral condyle postoperatively were significantly smaller than the values observed preoperatively.

Discussion

Although the patterns of preoperative knee motion were similar to those seen in normal knees, the magnitude of this motion varied widely between patients, so it was not necessarily representative of normal knees. These variations may be due to the varying degrees of arthritic changes caused by osteoarthritis. Although the patterns of knee kinematics were largely maintained by the UKA procedure, the causes of the significant reductions in the magnitude of motion upon performing the UKA procedure should be investigated in subsequent studies with a larger number of patients.     

Is Memorial Sloan-Kettering Cancer Center risk classification appropriate for Japanese patients with metastatic renal cell carcinoma in the cytokine era?

ObjectivesWe investigated the prognosis of Japanese patients with metastatic renal cell carcinoma (RCC), and analyzed the validity of Memorial Sloan-Kettering Cancer Center (MSKCC) risk classification.Materials and methodsThe endpoint of the present study was overall survival. Relationships between overall survival and potential prognostic factors were assessed using the Cox proportional hazard model with a step-wise procedure. Prognostic assessment was also performed according to the MSKCC risk classification. The predictive accuracy of the MSKCC risk classification was measured employing the concordance index.ResultsThe median survival for all patients was 22 months (95% CI, 19–28 months). The eight factors were identified as independent prognostic factor; time from initial diagnosis to metastasis, low hemoglobin (Hb), lactate dehydrogenase (LDH), corrected serum calcium (cCa), C-reactive protein (CRP), and the presence or absence of liver metastasis, bone metastasis, and lymph node metastasis. When the MSKCC risk classification was applied to patients, the median overall survival was not reached and 26 and 10 months in the patients classified as favorable, intermediate, and poor risk, respectively. The c-index was 0.73.ConclusionsThe prognosis of Japanese metastatic renal cell carcinoma patients may be better than that of previous studies from North America or Europe. Although there are some differences in the rate of patients in the risk groups and survival time by risk group between these patients, the MSKCC risk classification may be applicable for Japanese patients with metastatic renal cell carcinoma.     

Immune response during interferon beta-1b treatment in patients with multiple sclerosis who experienced relapses and those who were relapse-free in the START study

We measured immune markers in subjects with multiple sclerosis (MS) treated with IFNβ-1b for 12 months. IL-17 levels were significantly higher at Month 6 (p = 0.036) in relapsing subjects while BDNF levels were significantly higher at Month 3 (p = 0.028) in relapse-free subjects. Change from baseline in IL-4 levels inversely correlated with disability score whereas change from baseline in IL-10/IFN-gamma ratio inversely correlated with occurrence of relapses. CXCR3 + CD8 + T-cells tended to be higher but declined with treatment in relapse-free compared with relapsing subjects. Findings show the potential of cytokine and neurotrophic factors as biomarkers of clinical response to IFNβ-1b.     

Hemodynamic factor evaluation using computational fluid dynamics analysis for de novo bleb formation in unruptured intracranial aneurysms

Neurological Sciences - Although bleb formation increases the risk of rupture of intracranial aneurysms, previous computational fluid dynamic (CFD) studies have been unable to identify robust...     

Chronic kidney disease and clinical outcomes in patients with COVID-19 in Japan

Clinical and Experimental Nephrology - Identifying predictive factors for coronavirus disease 2019 (COVID-19) is crucial for risk stratification and intervention. Kidney dysfunction contributes to...     

Efficacy of tolvaptan on advanced chronic kidney disease with heart failure: a randomized controlled trial

Clinical and Experimental Nephrology - Tolvaptan (TLV) is reported to improve diuretic effects in patients with chronic kidney disease (CKD) when furosemide (FUR) is not sufficiently effective....     

Motor discoordination of transgenic mice overexpressing a microtubule destabilizer, stathmin, specifically in Purkinje cells

The proper regulation of microtubule (MT) structure is important for dendritic and neural circuit development. However, the relationship between the regulation of the MTs in dendrites and the formation of neural function is still unclear. Stathmin is a MT destabilizer, and we have previously reported that the expression and the activity of stathmin is downregulated during cerebellar Purkinje cell (PC) development. In this study, we generated transgenic mice that specifically overexpress the constitutively active form of stathmin in the PCs. These mutant mice did not show any obvious morphological or excitatory transmission abnormalities in the cerebellum. In contrast, we observed a decline in the expression of MAP2 and KIF5 signal in the PC dendrites and a discoordination of motor function in the mutant mice, although they displayed normal general behavior. These data indicate that the overexpression of stathmin disrupts dendritic MT organization, motor protein distribution, and neural function in PCs.     

Complex translocations derived stepwise from standard t(15;17) in a patient with variant acute promyelocytic leukemia

We report the case of an elderly man with an acute promyelocytic leukemia variant carrying complex variant translocations. The Q-banded karyotype and spectral karyotyping method revealed a typical t(15;17), and two complex rearrangements caused by stepwise translocation derived from a typical t(15;17). Chromosomes 8 and 14 were related to these rearrangements. The patient received induction chemotherapy using all-trans retinoic acid and achieved complete remission. To our knowledge, a case with complex rearrangements, caused by apparent stepwise translocation, at diagnosis, has not been reported previously.     

Migration of Tumor Antigen-Pulsed Dendritic Cells After Mucosal Administration in the Human Upper Respiratory Tract

Tumor-specific peptide-pulsed dendritic cells (DC) were administered via different routes to a group of patients with head and neck cancers. The migration and homing patterns of such antigen-stimulated cells was carefully studied employing single photon emission computed tomography (SPECT). The DC administered directly into the nasal submucosa quickly migrated very rapidly to the regional neck lymph nodes in the neck. However, after inoculation of the cells into the palatine tonsils, the DCs remained close to the site of administration and did not migrate to the regional lymph nodes or to other mucosal regions. After nasal submucosal administration of the DC, tumor-antigen-specific cytotoxic T cells were detected in the ipsilaterals but not in the contra lateral lymph nodes. These results suggest that after antigen processing, the regional lymph nodes serve as inductive sites for development of mucosal immune responses and for induction of memory cells during the local immunological responses in the nasopharyngeal-associated lymphoid tissue in man.     

Requirement of apelin-apelin receptor system for oxidative stress-linked atherosclerosis

The recently identified endogenous peptide apelin and its specific apelin receptor (APJ) are currently being considered as potential regulators in vascular tissue. Previously, we reported apelin mediates phosphorylation of myosin light chain and elicits vasoconstriction in vascular smooth muscle. In this study, physiological roles of the apelin-APJ system were investigated on atherosclerosis. In APJ and apolipoprotein E double-knockout (APJ(-/-)ApoE(-/-)) mice fed a high-cholesterol diet, atherosclerotic lesions were dramatically reduced when compared with APJ(+/+) ApoE(-/-) mice, in the absence of an effect of cholesterol levels. Immunohistochemical detection of smooth muscle cells, using a smooth muscle alpha-actin antibody, showed greatly reduced staining for these cells in lesions of APJ(-/-)ApoE(-/-) mice fed a high-cholesterol diet. Vascular production of superoxide radicals and the expression of nicotinamide-adenine dinucleotide phosphate oxidase subunits were decreased in APJ(-/-)ApoE(-/-) mice compared with APJ(+/+)ApoE(-/-) mice fed a standard normal diet. In vascular smooth muscle cells, apelin induced nicotinamide-adenine dinucleotide phosphate oxidase subunit expression. Apelin also induced vascular smooth muscle cell proliferation, which was inhibited by superoxide dismutase or diphenylene iodonium. The apelin-APJ system is a mediator of oxidative stress in vascular tissue, and thus we propose it to be a critical factor in atherogenesis under high-cholesterol dietary conditions. APJ deficiency is preventative against oxidative stress-linked atherosclerosis.