Maximum Palmar Abduction Angle of the Trapeziometacarpal Joint in Healthy Subjects Can Be Evaluated Accurately Using a Radiograph-Based Measurement Technique.

In carpal tunnel syndrome, the abductor pollicis brevis, which is the primary muscle for the palmar abduction of the thumb, is almost inevitably impaired. The active palmar abduction of the thumb may be a better indicator of thumb disability. The authors aimed to establish a simple and accurate method to measure the angle of active palmar abduction of the thumb and to determine the maximum angle values in healthy women. Twenty-five women 20 to 21 years old with no disorder of the hand participated in this study voluntarily. Three measurement methods were tested. The first method was designed according to the Japanese Orthopaedic Association and the second method was designed according to the American Society of Hand Therapists; both use photographs to perform measurement calculations. In the third method, 2 orthopedic surgeons measured the same angle as that described in the second method on hand radiographs. Intra- and interobserver reliability were assessed for each method and described as interclass correlation coefficients. The first and third methods had strong inter- and intraobserver reliability. The second method had strong intraobserver reliability but medium interobserver reliability. The measurement obtained with the first method was significantly different from the values obtained by the second and third methods (almost double). Therefore, the authors regarded the third method as the most appropriate approach for measuring active palmar abduction of the thumb, which, in healthy individuals, yielded maximum values of 45.3°±6.4° and 44°±7° for the left hand and the right hand, respectively. [Orthopedics. 2020; 43(2):e95-e101.].

Occurrence of tumor antigen pRL1a specific CD8 T cells in spleen cells from syngeneic BALB/c, semiallogeneic (BALB/c x C57BL/6)F1 and allogeneic C57BL/6 mice.

We investigated the generation of CD8 cytotoxic T-lymphocytes (CTL) that recognized a dominant pRL1a peptide bound to H-2L(d) molecule on RL male 1 leukemia in spleen cells from RL male 1-bearing syngeneic BALB/c, semiallogeneic CB6F1 and allogeneic B6 mice by repetitive in vitro stimulation with RL male 1 tumor. CD8 T cells in cultures were also analyzed by H-2L(d)/pRL1a tetramer staining. We showed that pRL1a-specific CTL were more efficiently generated in spleen cells from RL male 1-bearing high responder CB6F1 mice than in low responder BALB/c mice, and this correlated well with the occurrence of H-2L(d)/pRL1a tetramer binding CD8 T cells. Furthermore, we showed that in spleen cells from RL male 1-bearing allogeneic B6 mice, H-2L(d)/pRL1a complex specific CD8 T cells were present at a significant frequency. H-2L(d)/pRL1a recognizing B6 CTL but not BALB/c or CB6F1 CTL gradually lost CD8 expression on their surface by multiplication of in vitro stimulation.

Analysis of CD8 T-cell response by IFNgamma ELISPOT and H-2L(d)/pRL1a tetramer assays in pRL1a multiple antigen peptide-immunized and RL male 1-bearing BALB/c and (BALB/c x C57BL/6) F(1) mice.

We previously identified an H-2L(d)-binding peptide pRL1a (IPGLPLSL) on RL male 1 that is predominantly recognized by cytotoxic T-lymphocytes (CTLs). MAP is a multibranched lysine core with antigenic peptides. Immunization of BALB/c mice with pRL1a MAP effectively induced pRL1a CTLs. Here, we demonstrate the presence of pRL1a-recognizing CD8(+) T-cells in pRL1a MAP-immunized and RL male 1-bearing BALB/c and (BALB/c x C57BL/6)F(1) mice by using IFNgamma ELISPOT and H-2L(d)/pRL1a tetramer assays. A few IFNgamma ELISPOTs and no tetramer-positive cells were detected ex vivo in spleen cells from BALB/c mice immunized with pRL1a MAP. After a single in vitro stimulation with RL male 1, 432 and 741 IFNgamma ELISPOTs/10(5) cells were detected and tetramer-positive CD8(+) T-cells occurred at relative frequencies of 5.7% and 30.8% in splenic CD8(+) T-cells from mice that had been doubly and triply immunized, respectively, against pRL1a MAP. Tetramer-positive cells displayed two distinct cell populations, CD62L(low) and CD62L(high). Secondary in vitro stimulation expanded CD62L(high) cells more efficiently than CD62L(low) cells. Furthermore, a higher frequency of IFNgamma-producing and tetramer-positive CD8(+) T-cells was detected ex vivo in RL male 1-bearing semi-allogeneic (BALB/c x C57BL/6)F(1) than in BALB/c mice on day 14 after tumor inoculation.

Effect of NOS2 gene deficiency on the development of autoantibody mediated arthritis and subsequent articular cartilage degeneration.

OBJECTIVE: To determine the effect of NOS2 gene deletion on articular cartilage degradation in autoantibody mediated arthritis (AMA). METHODS: Female C57BL/6Ai-[ko] NOS2 N5 (NOS2-/-) mice (7-8 weeks old) and the counterpart C57/Bl6 Crj mice (wild-type, WT) were studied. Arthritis was induced by intraperitoneal injection of 4 mg of an arthritogenic cocktail of 4 monoclonal antibodies raised against type II collagen twice on Day 0 and Day 1 followed by intraperitoneal injection of 50 micro g of lipopolysaccharide on Day 2. Individual limbs were scored for arthritis in 4 grades; the total maximum score per mouse was 16. Femoral condyles and tibial plateaus of both knee joints were collected on Day 15 for immunohistological studies on nitrotyrosine and matrix metalloproteinase (MMP)-3 and -9. DNA fragmentation in chondrocytes was detected by the nick-end labeling (TUNEL) method. Blood was also collected on Day 15 to determine serum levels of nitrite/nitrate and interleukin 1 beta (IL-1 beta). RESULTS: Both NOS2-/- and WT mice with AMA developed clinically apparent arthritis. In WT mice, the arthritis progressed rapidly and reached the peak score 11.4 +/- 2.9 on Day 12, whereas the arthritis in NOS2-/- mice was milder and the peak score was 7.7 +/- 2.8 on Day 13 (p < 0.05). The serum nitrite/nitrate levels, histological grades of articular cartilage degradation, and numbers of apoptotic chondrocytes and nitrotyrosine positive chondrocytes were significantly lower in NOS2-/- mice with AMA than in WT mice with AMA. Conversely, significant differences were not observed in MMP-3 or -9 expression in chondrocytes, or in serum IL-1 beta levels between these 2 groups of mice. CONCLUSION: NOS2 gene deletion did not affect the inflammatory responses, but reduced the cartilage degradation.