Application of the QFD as a design approach to ensure comfort in using hand tools: can the design team complete the House of Quality appropriately?

Quality Function Deployment is proposed as an effective design method to integrate ergonomics needs and comfort into hand tool design because it explicitly addresses the translation of customer needs into engineering characteristics. A crucial step during QFD concerns the linking of engineering characteristics to customer needs in the House of Quality by the design team. It is generally assumed (looking at all the QFD success stories) that design teams can accurately predict the correlations between customer needs and engineering characteristics (also referred to as "Whats"/"Hows" correlations). This paper explicitly tests this assumption by comparing the "Whats"/"Hows" correlations estimated by a design team with those observed in a systematic user evaluation study, which has not been done before. Testing the assumption is important, because inaccurate estimates may lead to ergonomically ineffective (re)design of hand tools and a waste of company resources. Results revealed that the design team's correlation estimates were not as accurate as is generally assumed. Twenty-five percent of the estimates differed significantly with those observed in the user evaluation study. Thus, QFD is a useful method to assist design teams in designing ergonomically more comfortable hand tools, but only on the condition that the correlations between customer needs and engineering characteristics are validated, preferably by means of a systematic user evaluation study.

Disseminated linear calcinosis cutis associated with the Koebner phenomenon in an infant with congenital acute monocytic leukaemia.

We present a unique case of an infant with acute monocytic leukaemia who presented at birth with multiple rubbery, erythematous to violaceous subcutaneous nodules secondary to leukaemia cutis. As these infiltrates regressed with chemotherapy, numerous white to yellow linear confluent papules appeared in a scratch-like pattern. These lesions were widely disseminated but were concentrated across her face, trunk and extremities with relative sparing of the napkin area and back. We propose that these lesions represent a form of dystrophic calcinosis cutis that occurred secondary to koebnerization in an infant with congenital leukaemia cutis.

Epidemiology and outcome of nosocomial and community-onset bloodstream infection.

We performed a prospective study of bloodstream infection to determine factors independently associated with mortality. Between February 1999 and July 2000, 929 consecutive episodes of bloodstream infection at two tertiary care centers were studied. An ICD-9-based Charlson Index was used to adjust for underlying illness. Crude mortality was 24% (14% for community-onset versus 34% for nosocomial bloodstream infections). Mortality attributed to the bloodstream infection was 17% overall (10% for community-onset versus 23% for nosocomial bloodstream infections). Multivariate logistic regression revealed the independent associations with in-hospital mortality to be as follows: nosocomial acquisition (odds ratio [OR] 2.6, P < 0.0001), hypotension (OR 2.6, P < 0.0001), absence of a febrile response (P = 0.003), tachypnea (OR 1.9, P = 0.001), leukopenia or leukocytosis (total white blood cell count of <4500 or >20000, P = 0.003), presence of a central venous catheter (OR 2.0, P = 0.0002), and presence of anaerobic organism (OR 2.5, P = 0.04). Even after adjustments were made for underlying illness and length of stay, nosocomial status of bloodstream infection was strongly associated with increased total hospital charges (P < 0.0001). Although accounting for about half of all bloodstream infections, nosocomial bloodstream infections account for most of the mortality and costs associated with bloodstream infection.

Ultraviolet B(UVB)-induced cox-2 expression in murine skin: an immunohistochemical study.

Cyclooxygenase (COX) is the rate-limiting enzyme in the production of prostaglandins from arachidonic acid. This enzyme exists in at least two isoforms, COX-1 and COX-2. COX-1 is constitutively expressed in most tissues and plays various physiological roles. However, COX-2 expression is induced by a variety of agents, which include pro-inflammatory agents and mitogens. Evidence exists to indicate that increased expression of COX-2 occurs in several types of epithelial neoplasms. In this study, we show the effect of chronic exposure of murine skin to carcinogenic UVB on cutaneous COX-2 expression. SKH-1 mice were irradiated with 180 mJ/cm(2) UVB daily for five days a week for periods ranging from 1 to 20 weeks. Nontumor bearing skin areas of irradiated mice, skin of age-matched controls and benign papillomas and malignant tumors were assessed immunohistochemically for COX-2 expression in these mice. No epidermal staining occurred in any of the non-UVB-treated controls throughout the experiment. Epidermal COX-2 expression only occurred in UVB-irradiated mice. After 1 and 5 weeks of irradiation, patchy epidermal staining mostly confined to the granular layer and stratum corneum was observed. At week 9, staining intensity had increased, particularly in the granular layer. At week 13, staining was uniformly seen in all epidermal layers with particular prominence in the basal cell layer underlying areas of visible epidermal hyperplasia. It is of interest that the most intense staining was seen in the perinuclear region of keratinocytes and at the plasma membrane. At week 20, COX-2 staining was predominant in the granular layer, although in some tissue sections, the entire epidermis was positive. In benign papillomas, staining was confined to the superficial layers of the epidermis and in squamous cell carcinomas (SCCs), patchy staining in the granular and spinous layers predominated. In general, COX-2 expression was more intense in well-differentiated SCCs than in papillomas. In summary, our results indicate that COX-2 serves as an early marker of epidermal UVB exposure and its expression increases in benign papillomas and in SCCs. These results suggest that pharmacological intervention using specific COX-2 inhibitors could have anticarcinogenic effects in UVB-induced human skin cancer.

Development and preliminary validation of a forced-choice test of response bias for posttraumatic stress disorder.

This article describes the development and preliminary validation of the Morel Emotional Numbing Test for PTSD (MENT), a forced-choice test for detecting response bias in assessments for posttraumatic stress disorder (PTSD). The differences in MENT error rates among four groups of military veterans applying for monetary compensation for combat-related PTSD and two groups of hospitalized military veterans were investigated (N = 102): (a) disability claimants with veritable self-presentations, who were diagnosed with PTSD; (b) disability claimants with veritable self-presentations, who were not diagnosed with PTSD; (c) older disability claimants (age 63 or older) with veritable self-presentations; (d) disability claimants with suspect self-presentations; (e) chemical-dependent inpatients; and (f) schizophrenic inpatients. Veritable versus suspect grouping among disability claimants was determined by examining MMPI-2 F-K dissimulation index scores. The results indicated that the suspect group produced more errors on the MENT than the credible groups or the hospitalized patient groups (p < .0001). Clinical decision rules were used to evaluate the relative effectiveness of the MENT to identify malingering in the claimant groups. The overall efficiency or hit rate on the MENT was 95.6%.

Adult naris closure profoundly reduces tyrosine hydroxylase expression in mouse olfactory bulb.

Peripheral afferent innervation appears to be required for the expression of the dopamine phenotype in the rodent main olfactory bulb. Experiments utilizing neonatal naris closure as a means of sensory deprivation also suggest that odor-induced afferent activity is required for the expression of the phenotype. These experiments are confounded, however, by the significant postnatal maturation of the dopamine system. The current experiments utilized adult unilateral naris closure to address this issue. As with neonatal closure, adult deprivation produces a profound reduction in the expression of tyrosine hydroxylase (TH), the first enzyme in the dopamine biosynthetic pathway. By 4 days a small decrease is observed in TH activity and immunoreactivity. Activity reaches a nadir of 12% of control levels at about 1 month. TH mRNA is reduced similarly when analyzed at about 2 months post-closure. Glutamic acid decarboxylase protein and mRNA expression, which are co-localized with TH, remain at close to control levels indicating the continued presence of the dopamine neurons. The time-course of the loss of TH is identical to that for zinc sulphate-induced denervation of the olfactory bulb. These data support the hypothesis that odor modulated afferent activity is required for expression of the dopamine phenotype and that, if a trophic factor is involved, its release is also activity dependent.

Enhanced labeling of mitotic retinal cells with an intraocular [3H]thymidine injection.

Tritiated thymidine ([3H]Tdr) was injected either intraocularly (i.o.) or intraperitoneally (i.p.). Autoradiography showed that more retinal cells were labeled by i.o. than by i.p. injection. Controls showed that the increased number of labeled retinal cells was not related to glioblast proliferation produced by trauma from the i.o. injection. After injection of identical doses, the peak concentration of [3H]Tdr available for incorporation into DNA was about 100 times greater after an i.o. than after an i.p. injection. The effective duration of the labeling pulse in goldfish was 9 times longer for an i.o. than an i.p. injection. This study shows that i.o. delivery of [3H]Tdr is preferable to i.p. injection for efficient delivery of label to proliferating retinal cells.

Topographic disorganization of the optic tracts following long-term optic nerve regeneration: a quantitative image analysis study.

Experiments were designed to find the degree to which regenerated optic axons occupied their previous locations in the optic tracts. Following optic nerve crush and regeneration, either the dorsal, ventral, peripheral, temporal, or nasal part of the retina was ablated. The axons of the remaining retinal ganglion cells (RGCs) were labeled with cobalt. Density of the regenerated dorsal and ventral axons in the dorsal vs. ventral optic tracts was determined digitally. In addition, we determined the density of temporal and nasal axons in the temporal vs. nasal compartments of each optic tract and the density of central axons in the central vs. peripheral compartments of both optic tracts. Regenerated axons were not distributed randomly in the optic tracts. Instead, they were slightly but, significantly biased toward growing through the tract or compartment that they had occupied previously. Still, the pathway specificity exhibited by the regenerated axons was closer to random than it was to the pathway specificity seen in normal animals. Dorsal, ventral, and central RGC axons were significantly better localized to their correct tract or compartment than were temporal or nasal RGC axons. Also, over time, dorsal and ventral axons tended to disappear from incorrectly chosen optic tracts. The slight bias toward choosing the appropriate optic tract or optic tract compartment may be enough to account for the topographic specificity of the regenerated retinotectal projection. Near-randomness of the axonal positions in the tracts argues against the presence of any specific guidance cues in the optic tracts of adult animals. Axonal density was highest in the correct compartment and diminished progressively with increasing distance into the incorrect compartment. Such a gradient of axonal density suggests that regenerating axons "drift" away from their previous positions in the optic pathways.

Axonal redirection at the dorsoventral intraretinal boundary.

Cobaltous-lysine applied to the goldfish optic nerve backfilled retinal ganglion cells and their axons. Confined to the ventronasal and ventrotemporal retina was a small population of retinal ganglion cells whose axons traveled dorsally and parallel to the retinal margin. On reaching the boundary between dorsal and ventral retina, the axons arched, joined radially oriented bundles of axons, and traveled toward the optic disk. Control studies showed that the axons came from retinal ganglion cells rather than from retinopetal cells. The somatic area of retinal ganglion cells (RGCs) with circumferential axons was 30-50 microns, and was similar to that of average ganglion cells. The axons of these cells coursed between the optic fiber and ganglion cell layers or between the ganglion cell and inner plexiform layers. Many somata were displaced slightly toward the inner plexiform layer, but were not really displaced ganglion cells. The aberrant axonal trajectory may be related to the slightly displaced location of the cell. However, ganglion cells that are displaced to the edge of the inner nuclear layer usually have radially coursing axons. We digitized the coordinates of the bending points and the dorsoventral retinal boundary. On average, the bending points occurred within 100 microns of the dorsoventral retinal border. These findings suggest that some molecular, rather than mechanical, factor at the dorsoventral retinal boundary alters the course of the circumferential axons. Furthermore, because there are cells with circumferential axons throughout the ventral retina, the data imply that at least ventral RGC axons avoid mingling with the axons from dorsal RGCs.