Muscle volume is a major determinant of joint torque in humans

Muscle force (MF) is linearly related to physiological cross-sectional area (CSA), which is obtained from muscle volume (MV) divided by fibre length. Taking into account the fact that joint torque (TQ) is determined by MF multiplied by the moment arm, the maximal TQ would be a function of MV. This proposition was tested in the present study by investigating the relationship between MV and TQ for elbow flexor (EF) and extensor (EE) muscles of 26 males. The MVs of EF and EE were determined from a series of muscle CSA by magnetic resonance imaging (MRI), and pennation angle (theta) and FL by ultrasonography (US). Maximal isometric TQ was measured at right angle of elbow joint for EF and EE. There was a highly significant correlation between MV and TQ both for EF and EE (r=0.95 and 0.96 respectively) compared with that between muscle CSA and TQ, suggesting the dependence of TQ on MV. Furthermore, prediction equations for MV (MVULT) from muscle thickness (MT) measured by US was developed with reference to MVMRI by the MRI on 26 subjects, and the equations were applied to estimate MV of healthy university students (CON; 160 males) and sports athletes (ATH; 99 males). There were significant linear relationships between MVULT and TQ both for EF (r=0.783) and EE (r=0.695) for all subjects (n=259). The MVULT was significantly higher in ATH (by 32% for EF and 33% for EE, respectively) than in CON. Similarly, significantly greater TQ was observed in ATH (by 35% for EF, 37% for EE, respectively). The theta for EE showed no difference between both groups (17.8 degrees for CON and 17.5 degrees for ATH). On the other hand, the TQ to MV ratio were identical for CON and ATH. The results reveal that the muscle volume of the upper arm is a major determinant of joint torque (TQ), regardless of athletic training.     

Further development of a recombinant feline herpesvirus type 1 expressing the Gag protein of feline immunodeficiency virus

Summary.  We have previously reported the construction of a recombinant feline herpesvirus type 1 (FHV-1), designated C7301ddlTK-gag, expressing the Gag precursor protein of feline immunodeficiency virus (FIV). In this study, we report the construction of a further recombinant FHV-1 (ddlTK(gBp)-gag) which carries an FHV-1 gB promoter sequence upstream of the FIV gag gene of C7301ddlTK-gag. Strong expression of the FIV Gag protein by ddlTK(gBp)-gag was confirmed by immunoblot analyses and enzyme-linked immunosorbent assays. Although C7301ddlTK-gag and ddlTK(gBp)-gag failed to induce anti-FIV Gag antibodies in cats, we confirmed the infectivity and stability of these recombinants in cats. Received January 14, 2000 Accepted August 4, 2000     

Studies on plasma immunoreactive human brain natriuretic peptide (hBNP) levels in patients with congestive heart failure and present forms of hBNP in human cardiac ventricle

By using a specific radioimmunoassay (RIA) for human brain natriuretic peptide (hBNP), we measured immunoreactive hBNP (ir-hBNP) in plasma from patients with congestive heart failure (CHF). There appeared to be relationship between the enhanced ir-hBNP secretory activity and the severity of the failing heart as well as that of immunoreactive human atrial natriuretic peptide (ir-hANP). However, the secretion of ir-hBNP was augmented much more than that of ir-hANP in sever CHF patients. Gel permeation chromatography coupled with the RIA revealed that ir-hBNP in human ventricle is composed with gamma-hBNP and hBNP (1-32) as well as that of human atrium. However, we found differences of the gamma-hBNP/hBNP (1-32) ratio in atrial and ventricular tissues. These findings suggest that the hBNP secretion mechanism differ in the two areas of human heart.     

Dimerization and polymerization of butadiene with zero-valent nickel and protonic acids

The behavior of hydridonickel coordination compounds as catalysts for the oligomerization and polymerization of butadiene in various solvents was studied. In the presence of alcohol bis(tricyclohexylphosphine)chlorohydridonickel ( 4 , X = Cl) (HNiCl[P(C₆H₁₁)₃]₂) catalyzes the linear dimerization. With hydridotetrakis(phosphite)nickel(1+) ( 2 ) ([HNi{P(OR)₃}₄]⁺), which is prepared from tetrakis(phosphite)nickel ( 1 ) (Ni[P(OR)₃]₄) and trifluoroacetic acid, dimerization occurs in sec-alcohol but there is no reaction in tert-alcohol. The main product is 2-methylenevinylcyclopentane ( 8 ). The other products are 4-vinylcyclohexene ( 10 ), 1,5-cyclooctadiene ( 5 ), 1,3,7-octatriene ( 7 ) and 1,3,6-octatriene ( 9 ). The hydridonickel coordination compound, prepared with inorganic acids, does not afford the dimers but the 1,4-trans polymer.     

Lower expression of Th1-related cytokines and inducible nitric oxide synthase in mice with streptozotocin-induced diabetes mellitus infected with Mycobacterium tuberculosis

Diabetes mellitus is an important predisposing factor for tuberculosis. The aim of this study was to investigate the mechanism underlying this association using a murine model. Mice with streptozotocin-induced diabetes mellitus were prone to Mycobacterium tuberculosis infection, as indicated by increased numbers of live bacteria in lung, liver and spleen. In diabetic mice, the levels of IL-12 and IFN-gamma in the lung, liver and spleen were lower than those in control animals on day 14 postinfection, while the opposite was true for IL-4 levels in the lung and liver. The expression pattern of inducible nitric oxide synthase (iNOS), in the two mice types was as for IL-12 and IFN-gamma. In addition, peritoneal exudate cells obtained from diabetic mice produced lower amounts of IL-12 and NO than those from control mice, when stimulated in vitro with M. bovis BCG. Spleen cells from diabetic mice infected with M. tuberculosis produced a significantly lower amount of IFN-gamma upon restimulation with purified protein derivatives (PPD) than those from infected nondiabetic mice. Interestingly, addition of high glucose levels (33 mM) to the cultures of PPD-restimulated spleen cells reduced the synthesis of IFN-gamma only in diabetic mice, and not in nondiabetic mice. Finally, control of blood glucose levels by insulin therapy resulted in improvement of the impaired host protection and Th1-related cytokine synthesis. Our results suggest that the reduced production of Th1-related cytokines and NO account for the hampered host defense against M. tuberculosis infection under diabetic conditions.     

Suppressive effect of leflunomide metabolite (A77 1726) on metalloproteinase production in IL-1beta stimulated rheumatoid synovial fibroblasts

Leflunomide, an isoxazol derivative structurally unrelated to other immunomodulatory drugs, has proven to be efficacious in the treatment of rheumatoid arthritis (RA). This study was conducted to elucidate the mechanism by which leflunomide mediated antirheumatic effects. We investigated the effects of A77 1726, leflunomide's active metabolite, on mitogen-activated protein kinase (MAPK) activation in IL-1beta-stimulated rheumatoid synovial fibroblasts. The effects of A77 1726 on the secretion of matrix metalloproteinases (MMPs) from rheumatoid synovial fibroblasts were also examined. A77 1726 partially suppressed IL-1beta-induced ERK1/2 and p38 kinase activation. In contrast, A77 1726 efficiently suppressed IL-1beta-stimulated JNK1/2 kinase activation. Although no suppressive effect was demonstrated on MMP-2, A77 1726 markedly inhibited MMP-1, 3, and 13 secretions from IL-1beta-stimulated rheumatoid synovial fibroblasts. Tissue inhibitor of metalloproteinases-1 (TIMP-1) was constitutively produced from rheumatoid synovial fibroblasts and the suppressive effects of A77 1726 on TIMP-1 production were minimal. Our results suggest that the suppression of the MAPK signalling pathway and MMP synthesis in rheumatoid synovial fibroblasts is a possible mechanism for the inhibitory activity of leflunomide against rheumatoid arthritis.     

Stimulatory effect of CD5 antibody on B cells from patients with rheumatoid arthritis

In order to clarify the role of CD5 antigen on B cell in autoimmunity, we examined B cells from patients with rheumatoid arthritis (RA). The percentages of CD5 positive B cells were increased in peripheral blood from RA compared with normal. Normal and RA B cells were stimulated with two kinds of monoclonal antibodies to CD5 (Leu-1, SL-1) which recognize different epitopes. RA B cells proliferated and secreted IgM by CD5 antibody stimulation in combination with IL-1. Our observations imply that CD5 positive B cells in RA are in their differentiation stage and that CD5 antigen might be one of the triggers to activate CD5 positive B cells in vivo to produce autoantibody.