Total abdominal hysterectomy versus laparoscopically-assisted vaginal hysterectomy versus total vaginal hysterectomy.

INTRODUCTION: While total abdominal hysterectomy (TAH) and total vaginal hysterectomy (TVH) are conventional procedures, we have actively introduced laparoscopically-assisted vaginal hysterectomy (LAVH) since its advent. This study was the first attempt to retrospectively compare the surgical results, including invasiveness, among the three methods of performing a hysterectomy. METHODS: The subjects included 1181 patients who underwent total hysterectomies (TAH, n=465; LAVH, n=629; TVH, n=87) due to uterine fibroids or uterine adenomyosis at our hospital between January 1995 and December 2009. The mean age, parity, weight of the removed uterus, operative time, blood loss, rates of intra- and post-operative complications, length of post-operative hospital stay, leukocyte count, and CRP and hemoglobin levels were compared. RESULTS: The operative time was significantly longer in the LAVH group than the other two groups. Blood loss was significantly greater in the TAH group than the LAVH and TVA groups. The rates of intra- and post-operative complications were significantly higher in the TAH group than the LAVH group. The CRP level and leukocyte count were significantly lower in the LAVH group than the TAH and TVH groups. CONCLUSION: LAVH can be applied to nulligravidas or patients with relatively large uteri and it is proved less invasive than TAH and TVH in this study. We recommend active application of LAVH.

Advances in understanding sepsis.

Sepsis, a systemic inflammatory response to infection, is a leading cause of death in intensive care units. Recent investigations into the pathogenesis of sepsis reveal a biphasic inflammatory process. An early phase is characterized by pro-inflammatory cytokines (e.g. tumour necrosis factor-alpha), whereas a late phase is mediated by an inflammatory high-mobility group box 1 and an anti-inflammatory interleukin-10. Inflammation aberrantly activates coagulation cascades as sepsis progresses. This dual inflammatory response concomitant with dysregulated coagulation partially accounts for unsuccessful anti-cytokine therapies that have solely targeted early pro-inflammatory mediators (e.g. tumour necrosis factor-alpha). In contrast, activated protein C, which modifies both inflammatory and coagulatory pathways, has improved survival in patients in severe sepsis. Inhibition of the late mediator high-mobility group box 1 improves survival in established sepsis in pre-clinical studies. In addition, recent advances in molecular medicine have shed light on two novel experimental interventions against sepsis. Accelerated apoptosis of lymphocytes has been shown to play an important role in organ dysfunction in sepsis and techniques to suppress apoptosis have improved survival rate in sepsis models. The vagus nerve system has also been shown to suppress innate immune response through endogenous release and exogenous administration of cholinergic agonists, ameliorating inflammation and lethality in sepsis models.

Adenine deaminase activity of the yicP gene product of Escherichia coli.

During previous work on deriving inosine-producing mutants of Escherichia coli, we observed that an excess of adenine added to the culture medium was quickly converted to hypoxanthine. This phenomenon was still apparent after disruption of the known adenosine deaminase gene (add) on the E. coli chromosome, suggesting that, like Bacillus subtilis, E. coli has an adenine deaminase. As the yicP gene of E. coli shares about 35% identity with the B. subtilis adenine deaminase gene (ade), we cloned yicP from the E. coli genome and developed a strain that overexpressed its product. The enzyme was purified from a cell extract of E. coli harboring a plasmid containing the cloned yicP gene, and had significant adenine deaminase [EC 3.5.4.2] activity. It was deduced to be a homodimer, each subunit having a molecular mass of 60 kDa. The enzyme required manganese ions as a cofactor, and adenine was its only substrate. Its optimum pH was 6.5-7.0 and its optimum temperature was 60 degrees C. The apparent Km for adenine was 0.8 mM.

gsk disruption leads to guanosine accumulation in Escherichia coli.

We tried some improvement of inosine production using an inosine-producing mutant of Escherichia coli which is deficient in purF (phosphoribosylpyrophosphate (PRPP) amidotransferase gene), purA (succinyl-adenosine 5'-monophosphate (AMP) synthetase gene), deoD (purine nucleoside phosphorylase gene), purR (purine repressor gene) and add (adenosine deaminase gene), and harboring the desensitized PRPP amidotransferase gene as a plasmid. The guaB (inosine 5'-monophosphate (IMP) dehydrogenase gene) disruption brought about a slightly positive effect on the inosine productivity. Alternatively, the gsk (guanosine-inosine kinase gene) disruption caused a considerable amount of guanosine accumulation together with a slight increase in the inosine productivity. The further addition of guaC (guanosine 5'-monophosphate (GMP) reductase gene) disruption did not lead to an increased guanosine accumulation, but brought about the decrease of inosine accumulation.

NF-kappa B decoy suppresses cytokine expression and thermal hyperalgesia in a rat neuropathic pain model.

Pro-inflammatory cytokines have been shown to be involved in the genesis, persistence, and severity of neuropathic pain following nerve injury. The transcription factor, nuclear factor-kappa B (NF-kappaB), plays a pivotal role in regulating pro-inflammatory cytokine gene expression. To elucidate the role of NF-kappaB in the pathogenesis of neuropathic pain, using a gene-based approach of NF-kappaB decoy, we tested whether the activated NF-kappaB affected pain behavior via the expression of inflammatory mediators. Single endoneurial injections of NF-kappaB decoy, at the site of nerve lesion, significantly alleviated thermal hyperalgesia for up to 2 weeks and suppressed the expression of mRNA of the inflammatory cytokines, iNOS, and adhesion molecules at the site of nerve injury. This finding suggests that a perineural inflammatory cascade, that involves NF-kappaB, is involved in the pathogenesis of neuropathic pain.

Ultrastructure and function of dimeric, soluble intercellular adhesion molecule-1 (ICAM-1).

Previous studies have demonstrated dimerization of intercellular adhesion molecule-1 (ICAM-1) on the cell surface and suggested a role for immunoglobulin superfamily domain 5 and/or the transmembrane domain in mediating such dimerization. Crystallization studies suggest that domain 1 may also mediate dimerization. ICAM-1 binds through domain 1 to the I domain of the integrin alpha(L)beta(2) (lymphocyte function-associated antigen 1). Soluble C-terminally dimerized ICAM-1 was made by replacing the transmembrane and cytoplasmic domains with an alpha-helical coiled coil. Electron microscopy revealed C-terminal dimers that were straight, slightly bent, and sometimes U-shaped. A small number of apparently closed ring-like dimers and W-shaped tetramers were found. To capture ICAM-1 dimerized at the crystallographically defined dimer interface in domain 1, cysteines were introduced into this interface. Several of these mutations resulted in the formation of soluble disulfide-bonded ICAM-1 dimers (domain 1 dimers). Combining a domain 1 cysteine mutation with the C-terminal dimers (domain 1/C-terminal dimers) resulted in significant amounts of both closed ring-like dimers and W-shaped tetramers. Surface plasmon resonance studies showed that all of the dimeric forms of ICAM-1 (domain 1, C-terminal, and domain 1/C-terminal dimers) bound similarly to the integrin alpha(L)beta(2) I domain, with affinities approximately 1.5--3-fold greater than that of monomeric ICAM-1. These studies demonstrate that ICAM-1 can form at least three different topologies and that dimerization at domain 1 does not interfere with binding in domain 1 to alpha(L)beta(2).

Dimerization and the effectiveness of ICAM-1 in mediating LFA-1-dependent adhesion.

Dimeric intercellular adhesion molecule-1 (ICAM-1) binds more efficiently to lymphocyte function-associated antigen-1 (LFA-1) than monomeric ICAM-1. However, it is unknown whether dimerization enhances binding simply by providing two ligand-binding sites and thereby increasing avidity, or whether it serves to generate a single "fully competent" LFA-1-binding surface. Domain 1 of ICAM-1 contains both the binding site for LFA-1, centered on residue E34, and a homodimerization interface. Whether the LFA-1-binding site extends across the homodimerization interface has not been tested. To address this question, we constructed four different heterodimeric soluble forms of ICAM-1 joined at the C terminus via an alpha-helical coiled coil (ACID-BASE). These heterodimeric ICAM-1 constructs include, (i) E34/E34 (two intact LFA-1-binding sites), (ii) E34/K34 (one disrupted LFA-1-binding site), (iii) E34/DeltaD1-2 (one deleted LFA-1-binding site), and (iv) K34/K34 (two disrupted LFA-1-binding sites). Cells bearing activated LFA-1 bound similarly to surfaces coated with either E34/K34 or E34/DeltaD1-2 and with an approximately 2-fold reduction in efficiency compared with E34/E34, suggesting that D1 dimerization, which is precluded in E34/DeltaD1-D2, is not necessary for optimal LFA-1 binding. Furthermore, BIAcore (BIAcore, Piscataway, NJ) affinity measurements revealed that soluble open LFA-1 I domain bound to immobilized soluble ICAM-1, E34/E34, E34/K34, and E34/DeltaD1-D2 with nearly identical affinities. These studies demonstrate that a single ICAM-1 monomer, not dimeric ICAM-1, represents the complete, "fully competent" LFA-1-binding surface.

Reversibly locking a protein fold in an active conformation with a disulfide bond: integrin alphaL I domains with high affinity and antagonist activity in vivo.

The integrin alphaLbeta2 has three different domains in its headpiece that have been suggested to either bind ligand or to regulate ligand binding. One of these, the inserted or I domain, has a fold similar to that of small G proteins. The I domain of the alphaM and alpha2 subunits has been crystallized in both open and closed conformations; however, the alphaL I domain has been crystallized in only the closed conformation. We hypothesized that the alphaL domain also would have an open conformation, and that this would be the ligand binding conformation. Therefore, we introduced pairs of cysteine residues to form disulfides that would lock the alphaL I domain in either the open or closed conformation. Locking the I domain open resulted in a 9,000-fold increase in affinity to intercellular adhesion molecule-1 (ICAM-1), which was reversed by disulfide reduction. By contrast, the affinity of the locked closed conformer was similar to wild type. Binding completely depended on Mg(2+). Orders of affinity were ICAM-1 > ICAM-2 > ICAM-3. The k(on), k(off), and K(D) values for the locked open I domain were within 1.5-fold of values previously determined for the alphaLbeta2 complex, showing that the I domain is sufficient for full affinity binding to ICAM-1. The locked open I domain antagonized alphaLbeta2-dependent adhesion in vitro, lymphocyte homing in vivo, and firm adhesion but not rolling on high endothelial venules. The ability to reversibly lock a protein fold in an active conformation with dramatically increased affinity opens vistas in therapeutics and proteomics.

Investigation of various genotype characteristics for inosine accumulation in Escherichia coli W3110.

For the derivation of an inosine-overproducing strain from the wild type microorganism, it is known that the addition of an adenine requirement, removal of purine nucleoside hydrolyzing activity, removal of the feedback inhibition, and repression of key enzymes in the purine nucleotides biosynthetic pathway are essential. Thus, the disruption of purA (adenine requirement), deoD (removal of purine nucleosides phosphorylase activity), purR (derepression of the regulation of purine nucleotides biosynthetic pathway), and the insensitivity of the feedback inhibition of phosphoribosylpyrophosphate (PRPP) amidotransferase by adenosine 5'-monophosphate (AMP) and guanosine 5'-monophosphate (GMP) were done in the Escherichia coli strain W3110, and then the inosine productivity was estimated. In the case of using a plasmid harboring the PRPP amidotransferase gene (purF) that encoded a desensitized PRPP amidotransferase, purF disrupted mutants were used as the host strains. It was found that the innovation of the four genotypes brought about a small amount of inosine accumulation. Furthermore, an adenine auxotrophic mutant of E. coli showed inappropriate adenine use because its growth could not respond efficiently to the concentration of adenine added. As the presence of adenosine deaminase is well known in E. coli and it is thought to be involved in adenine use, a mutant disrupted adenosine deaminase gene (add) was constructed and tested. The mutant, which is deficient in purF, purA, deoD, purR, and add genes, and harboring the desensitized purF as a plasmid, accumulated about 1 g of inosine per liter. Although we investigated the effects of purR disruption and purF gene improvement, unexpectedly an increase in the inosine productivity could not be found with this mutant.

Glucocorticoid suppresses neutrophil activation in ventilator-induced lung injury.

OBJECTIVE: To investigate, in a rat model, the role of the Mac-1/ICAM-1 pathway and the anti-inflammatory activity of steroid in ventilator-induced lung injury. DESIGN: Prospective, randomized controlled study. SETTING: Animal investigation using Wistar rats. INTERVENTION: Rats in three randomly assigned groups of 18, a total of 54 animals, were subject to the following: Two groups received high peak inspiratory pressure (35 cm H2O) ventilation after pretreatment with methylprednisolone (high-methylprednisolone group) or pretreatment with methylprednisolone vehicle (high-vehicle group). The third group of animals received low peak inspiratory pressure (7 cm H2O) ventilation after pretreatment with methylprednisolone vehicle (low-vehicle group). Except for animals previously killed to establish baseline values, after 40 mins of mechanical ventilation, the animals in each group were killed. Some animals provided histological samples, and the rest received total lung lavage. MEASUREMENT: We measured flow cytometry of lavage fluid, cell counts of tissue samples, and pressure-volume curves before and after mechanical ventilation. RESULTS: In the groups that received high peak inspiratory pressure ventilation, both the number of neutrophils that infiltrated the lungs and the expression of Mac-1 and ICAM-1 on neutrophils and macrophages increased significantly more than in the low-vehicle group. Static lung compliance was reduced in the high peak inspiratory pressure groups. In the high peak inspiratory pressure groups, there were significantly fewer neutrophils in samples from the high-methylprednisolone group (0.412 +/- 0.1 x 10(5)) than from the high-vehicle group (1.10 +/- 0.1 x 10(5); p < .05). The high-vehicle group showed greater expression of CD11b on neutrophils, but this was significantly decreased by methylprednisolone (mean fluorescence intensity: high-vehicle, 118.4 +/- 34.3; high-methylprednisolone, 25.8 +/- 4.2; p < .05). The lung mechanics measured by pressure-volume curve analysis were deteriorated less in the high-methylprednisolone group. CONCLUSION: Our study suggests that a neutrophil-endothelium interaction via the Mac-1/ICAM-1 pathway is involved in the activation and recruitment of neutrophils in ventilator-induced lung injury. Activation and recruitment of neutrophils were lessened by pretreatment with methylprednisolone, which might have contributed to the improvement of lung dysfunction after mechanical ventilation.

An isolated, surface-expressed I domain of the integrin alphaLbeta2 is sufficient for strong adhesive function when locked in the open conformation with a disulfide bond.

We introduced disulfide bonds to lock the integrin alphaLbeta2 I domain in predicted open, ligand binding or closed, nonbinding conformations. Transfectants expressing alphaLbeta2 heterodimers containing locked-open but not locked-closed or wild-type I domains constitutively adhered to intercellular adhesion molecule-1 (ICAM-1) substrates. Locking the I domain closed abolished constitutive and activatable adhesion. The isolated locked-open I domain bound as well as the activated alphaLbeta2 heterodimer, and binding was abolished by reduction of the disulfide. Lovastatin, which binds under the conformationally mobile C-terminal alpha-helix of the I domain, inhibited binding to ICAM-1 by alphaLbeta2 with wild-type, but not locked-open I domains. These data establish the importance of conformational change in the alphaL I domain for adhesive function and show that this domain is sufficient for full adhesive activity.

Locking in alternate conformations of the integrin alphaLbeta2 I domain with disulfide bonds reveals functional relationships among integrin domains.

We used integrin alphaLbeta2 heterodimers containing I domains locked open (active) or closed (inactive) with disulfide bonds to investigate regulatory interactions among domains in integrins. mAbs to the alphaL I domain and beta2 I-like domain inhibit adhesion of wild-type alphaLbeta2 to intercellular adhesion molecule-1. However, with alphaLbeta2 containing a locked open I domain, mAbs to the I domain were subdivided into subsets (i) that did not inhibit, and thus appear to inhibit by favoring the closed conformation, and (ii) that did inhibit, and thus appear to bind to the ligand binding site. Furthermore, alphaLbeta2 containing a locked open I domain was completely resistant to inhibition by mAbs to the beta2 I-like domain, but became fully susceptible to inhibition after disulfide reduction with DTT. This finding suggests that the I-like domain indirectly contributes to ligand binding by regulating opening of the I domain in wild-type alphaLbeta2. Conversely, locking the I domain closed partially restrained conformational change of the I-like domain by Mn(2+), as measured with mAb m24, which we map here to the beta2 I-like domain. By contrast, locking the I domain closed or open did not affect constitutive or Mn(2+)-induced exposure of the KIM127 epitope in the beta2 stalk region. Furthermore, locked open I domains, in alphaLbeta2 complexes or expressed in isolation on the cell surface, bound to intercellular adhesion molecule-1 equivalently in Mg(2+) and Mn(2+). These results suggest that Mn(2+) activates alphaLbeta2 by binding to a site other than the I domain, most likely the I-like domain of beta2.

Ventilator-induced lung injury is associated with neutrophil infiltration, macrophage activation, and TGF-beta 1 mRNA upregulation in rat lungs.

Activated neutrophils contribute to the development of ventilator-induced lung injury (VILI) caused by high-pressure mechanical ventilation. However, exact cellular and molecular mechanisms have not been conclusively studied. Our investigation aimed to examine expression of adhesion molecules by both neutrophils and macrophages in lung lavage fluids of rats with VILI. Further, involvement of proinflammatory (tumor necrosis factor-alpha) and profibrogenetic (transforming growth factor-beta 1) mediators was analyzed at mRNA level in lung tissue. Wistar rats were ventilated by high pressure (45 cm H(2)O of peak inspiratory pressure, n = 23) or low pressure (7 cm H(2)O, n = 13) with 0 positive end-expiratory pressure. After 40 min of comparative ventilation, lung lavage was performed in 20 rats from the experimental group and 10 from the control for immunofluorescence analysis with anti-Mac-1 and anti-ICAM-1 monoclonal antibodies. The lung tissues from remaining rats were subjected to pathological and reverse transcription-polymerase chain reaction examinations. Although there was no significant change of PaO(2) in the low-pressure group, PaO(2) was decreased in the high-pressure group. The high-pressure group also had greater neutrophil infiltration into alveolar spaces, upregulation of CD54 and CD11b on alveolar macrophages, and more transforming growth factor-beta 1 mRNA in lung tissues. Tumor necrosis factor-alpha was not involved in the pathogenesis of the severe VILI observed. Histologic findings also demonstrated more infiltrating neutrophils, destructive change of the alveolar wall, and deposition of matrix in the high-pressure group. These results suggest that a series of proinflammatory reactions and profibrogenetic process may be involved in the course of VILI.

Phosphorylation of guanosine using guanosine-inosine kinase from Exiguobacterium acetylicum coupled with ATP regeneration.

Guanosine 5'-monophosphate (5'-GMP) and inosine 5'-monophosphate (5'-IMP) are widely used as flavor enhancers. Recently, a novel process for 5'-IMP production by phosphorylation of inosine using guanosine-inosine kinase coupled with ATP regeneration was reported. In this study, we demonstrated the practical possibility of producing 5'-GMP by phosphorylation of guanosine using a guanosine-inosine kinase from Exiguobacterium acetylicum coupled with ATP regeneration.

Computational design of an integrin I domain stabilized in the open high affinity conformation.

We have taken a computational approach to design mutations that stabilize a large protein domain of approximately 200 residues in two alternative conformations. Mutations in the hydrophobic core of the alphaMbeta2 integrin I domain were designed to stabilize the crystallographically defined open or closed conformers. When expressed on the cell surface as part of the intact heterodimeric receptor, binding of the designed open and closed I domains to the ligand iC3b, a form of the complement component C3, was either increased or decreased, respectively, compared to wild type. Moreover, when expressed in isolation from other integrin domains using an artificial transmembrane domain, designed open I domains were active in ligand binding, whereas designed closed and wild type I domains were inactive. Comparison to a human expert designed open mutant showed that the computationally designed mutants are far more active. Thus, computational design can be used to stabilize a molecule in a desired conformation, and conformational change in the I domain is physiologically relevant to regulation of ligand binding.

Does blood type B protect against haemolytic uraemic syndrome? An analysis of the 1996 Sakai outbreak of Escherichia coli O157:H7 (VTEC O157) infection. The Osaka HUS Critical Care Study Group.

OBJECTIVES: Expression of the P1 blood type antigen is suggested to have a protective effect against post-enteropathic haemolytic uraemic syndrome (HUS). The B blood type may also protect against HUS, since terminal trisaccharide sequences similar to those of the B blood type determinants are reported to have an affinity to Vero cytotoxin that is 23% as strong as that of the P1 determinants. Thus, we studied whether ABO blood types were related to the occurrence or severity of HUS. METHODS: We obtained clinical and laboratory data of 49 HUS patients treated in 14 critical care facilities during the 1996 Escherichia coli O157:H7 outbreak in Sakai, Japan. We retrospectively studied whether ABO blood types were related to the occurrence or severity of HUS. RESULTS: The numbers of patients with blood types A, B, O or AB were 29, 8, 12, and 0, respectively. For each blood type, the number of patients with severe renal complications was 16, 6, 9, and 0, respectively. The distribution of blood types among the HUS patients deviated from a population-based distribution of blood types (P<0.05, Chi-squared test); i.e., the frequency of the A blood phenotype was significantly higher among our HUS patients. However, there was no significant difference in the frequency of patients with the A antigen (A and AB blood groups) among our HUS patients, whereas the frequency of B antigen expression was significantly lower (P<0.05, Chi-squared test). The risk of severe renal complications did not appear to be related to ABO blood types. CONCLUSIONS: Our data suggest that expression of the B antigen has a protective effect against the onset of HUS, but that it does not affect the severity of the disease.

End-product regulation and kinetic mechanism of guanosine-inosine kinase from Escherichia coli.

Escherichia coli guanosine-inosine kinase was overproduced, purified, and characterized. The native and subunit molecular weights were 85,000 and 45,000, respectively, indicating that the enzyme was a dimer. A pI of 6.0 was obtained by isoelectric focusing. In addition to ATP, it was found that deoxyadenosine 5'-triphosphate, UTP, and CTP could serve as phosphate donors. The phosphate acceptors were guanosine, inosine, deoxyguanosine and xanthosine, but not adenosine, cytidine, uridine, or deoxythymidine. Maximum activity was attained at an ATP/Mg2+ concentration ratio of 0.5. In the presence of pyrimidine nucleotides, enzyme activity was slightly increased, while it was markedly inhibited by GDP and GTP. Initial velocity and product inhibition studies support an ordered Bi Bi mechanism in which guanosine was the first substrate to bind and GMP was the last product to be released. Guanosine kinase may be a regulatory enzyme that has a role in modulating nucleotide levels.

Development of an improved assay for purine nucleoside kinase activity in cell extracts and detection of inosine kinase activity in Brevibacterium acetylicum ATCC 953, related species, and Corynebacterium flaccumfaciens ATCC 6887.

An improved assay was developed to detect direct purine nucleoside phosphorylating activity in cell-free extracts. Direct inosine phosphorylating activity was detected in 2 of 70 species tested. Both activities, which depended on magnesium ion and ATP, phosphorylated a hydroxyl group at the 5' position of inosine. The new assay was shown to be useful for screening of direct purine nucleoside phosphorylating activity and have the potential to detect inosine kinase in the presence of a background of nucleoside phosphorylase and purine phosphoribosyltransferase activities. Previously, the latter two activities made it difficult to correctly detect direct phosphorylation of inosine by inosine kinase.

Associations of self estimated workloads with musculoskeletal symptoms among hospital nurses.

OBJECTIVES: To investigate the prevalence of neck, shoulder, and arm pain (NSAP) as well as low back pain (LBP) among hospital nurses, and to examine the association of work tasks and self estimated risk factors with NSAP and LBP. METHODS: A cross sectional study was carried out in a national university hospital in Japan. Full time registered nurses in the wards (n = 314) were selected for analysis. The questionnaire was composed of items on demographic conditions, severity of workloads in actual tasks, self estimated risk factors for fatigue, and musculoskeletal pain in the previous month. Rate ratios (RRs) and 95% confidence intervals (95% CIs) were calculated by the Cox's proportional hazards model to study the association of pain with variables related to work and demographic conditions. RESULTS: The prevalences of low back, shoulder, neck, and arm pain in the previous month were 54.7%, 42.8%, 31.3%, and 18.6%, respectively. The prevalence of musculoskeletal symptoms among hospital nurses was higher than in previous studies. In the Cox's models for LBP and NSAP, there were no significant associations between musculoskeletal pain and the items related to work and demographic conditions. The RRs for LBP tended to be relatively higher for "accepting emergency patients" and some actual tasks. Some items of self estimated risk factors for fatigue tended to have relatively higher RRs for LBP and NSAP. CONCLUSIONS: It was suggested that musculoskeletal pain among hospital nurses may have associations with some actual tasks and items related to work postures, work control, and work organisation. Further studies, however, are necessary, as clear evidence of this potential association was not shown in the study.

Effects of box weight, vertical location and symmetry on lifting capacities and ratings on category scale in Japanese female workers.

The aim was to clarify the effects of box weight, vertical location and symmetry on the lifting capacities and subjective burden in Japanese female workers with manual material handling tasks. Sixteen healthy females were tested. They performed 12 different lifting tasks (three heights * two weights * two symmetries). It is difficult for Japanese women to exert dynamic force in lifting a 15-kg weight from the elbow to the shoulder level. A remarkable increase was observed in heart rate and category scale with ratio properties (CR-10) on large muscle group in lifting a 15-kg weight as compared with lifting a 10-kg one. Judging from calculation of the Recommended Weight Limit using the application manual by the National Institute for Occupational Safe and Health, it was also suggested that lifting the 15-kg weight from the elbow to the shoulder level was difficult for female workers. Not only peak force, but also the average upward acceleration and peak velocity were lower in asymmetric liftings than those in symmetric liftings. CR-10 for the left back and right thigh were also higher in 90 degrees right lateral plane lifting than in the mid-sagittal plane. Thus, asymmetric lifting was supposed to impose higher stress on the back contralaterally and thigh ipsilaterally to the location of the weight.