Cytogenetic analysis of chromosomal aberrations of peripheral lymphocytes in workers occupationally exposed to nickel.

The authors carried out a cytogenetic examination of chromosomal aberrations of peripheral lymphocytes (100 cells evaluated in each sample) with simultaneous monitoring of the level of exposure by means of determination of nickel in the urine, serum and hair. The series included 21 workers occupationally exposed to nickel at two workshops producing NiO (6 persons) and NiSO4 (15 persons) in a chemical plant. At the same time a comparable control group, i.e., 19 workers of the same chemical plant but without any direct occupational nickel exposure (clerks, service men, etc.), were examined in the same way. In the exposed group chromosomal aberrations of peripheral lymphocytes were detected with an average value of 6.41 +/- 1.9% (range 2-14%); in the group producing NiO it was, on the average, 9.5 +/- 3.2% (range 7-14%) whereas in the NiSO4 production workers it was only 5.2 +/- 1.9% (range 2-10%). There was a dependence of chromosomal aberrations of peripheral lymphocytes on the exposure time and on the nickel content of the biological material. Significantly increased values (in contrast to the normal value of chromosomal aberrations of peripheral lymphocytes, up to 2%) were detected in the control group as well (average value of 4.05 +/- 2.27%, range 1-10%). The authors explain this fact by the nickel-polluted environment of the whole observed chemical plant.     

A comprehensive study on neurobehavior, neurotransmitters and lymphocyte subsets alteration of Chinese manganese welding workers

The neurotoxicity of manganese has been demonstrated by many researches. But few reports have been found on its immunotoxicity in manganese-exposed workers. Here we selected welding workers (aged 34 years) as Mn-exposed subjects. They have been exposed to manganese for 16 years. The control group was from a flour plant. The average concentrations of Mn, Cd, Fe and Ni in work place were 138.40 +/- 11.60 microg/m3, 581.40 +/- 45.32 microg/m3, 3.84 +/- 0.53 microg/m3 and 12.64 +/- 2.80 ng/m3, respectively. Blood Mn (4.84 mug/dl) of welding workers was higher than that of the control group (1.92 microg/dl). Neurobehavioral core test battery (NCTB) recommended by WHO was conducted on the subjects and found that the scores of negative emotions, such as confusion-bewilderment, depression-dejection, fatigue-inertia, and tension-anxiety, were higher in welding workers. Visual simple reaction time and the fast simple reaction time were shorter than that of the control group. The numbers of digital span, forward digital span, backward digital span and digital symbol decreased in welding workers compared with control group. Monoamine neurotransmitters and their metabolism substances in urine were tested by HPLC-ultraviolet. NE, E, MHPG, HVA, DA, DOPAC and 5-HT in the urine of Mn-exposed group had no significant changes while 5-HIAA in Mn-exposed group had significantly decreased compared with that of the control group. Lymphocyte subsets of the subjects were determined by Flow Cytometer. CD3+ T cell, CD4+CD8- T cell, CD4-CD8+ T cell, CD4+CD45RO- "virgin" lymphocytes, CD4+CD45RO+ "memory" lymphocytes, and CD3-CD19+ B cell had no significant changes compared with the control group. The results showed that long-term exposure to manganese in welding might have adverse effects on mood state, neurobehavior, and peripheral neurotransmitters. However, they had no effects on lymphocyte subsets parameters.     

IL-3 augments adhesiveness for endothelium and CD11b expression in human basophils but not neutrophils.

A number of natural and recombinant human cytokines have been tested for their ability to activate basophil and neutrophil adhesiveness for human umbilical vein endothelial cells in vitro. Coincubation of basophils and endothelial cell monolayers for 10 min with biologically relevant concentrations of rIL-1, natural IL-2, rIL-4, rIL-5, rIL-6, rIL-8, rGM-CSF, and rIFN-gamma had no effect on basophil adhesiveness. In contrast, rIL-3 induced basophil adhesiveness for endothelial cells (optimal at 1 ng/ml: 144 +/- 18% of control adherence (mean +/- SEM); control basophil binding, 13 +/- 3%, n = 9, p less than or equal to 0.05). This increase in adhesiveness was similar in magnitude to that induced by an optimal concentration of a known potent inducer of basophil adhesiveness (1 microM FMLP, 164 +/- 15% of control adherence, n = 9). Under these experimental conditions, the effects of rIL-3 occurred at concentrations of 0.1 to 30 ng/ml, were partially dependent on calcium, and were not accompanied by histamine release. Fixation experiments demonstrated that the effect of rIL-3 was directed against the basophil rather than the endothelial cell. Neither rIL-3 nor the other cytokines tested had any effect on the adherence of 51Cr-labeled neutrophils, even when tested simultaneously on cells from the same donors. Under experimental conditions that permitted histamine release, no correlation was seen between the ability of rIL-3 (0.3 to 300 ng/ml) to induce histamine release or enhance adhesiveness (n = 8). mAb blocking experiments demonstrated a role for both CD11 and CD18 adherence glycoproteins in basophil adherence induced by rIL-3, and indirect immunofluorescence and flow cytometric analysis revealed that rIL-3 treatment led to rapid and sustained increases in cell surface expression of CD11b antigens on basophils but not neutrophils (e.g., after 10 min: 217 +/- 29 vs 91 +/- 11% of control mean fluorescence intensity, p less than 0.05). However, no correlation was seen between the magnitude of changes in CD11b expression and changes in adhesion when tested simultaneously. These results suggest that local production of IL-3 during allergic reactions in vivo may selectively promote basophil activation, adhesion to endothelium, and recruitment to extravascular sites of inflammation.     

Study of the cytogenetic effects of occupational exposure to pesticides on sanitation workers in Belo Horizonte, Brazil

Sanitation workers handling pesticides in the control of disease vectors constitute an occupationally exposed population to genotoxic substances. The aim of the present study was to investigate the relation between the occupational exposure to various pesticides and the presence of cytogenetic damage. Fifty-nine men were selected (29 sanitation workers and 30 control individuals) with ages varying between 18-57 years who lived and worked in the same area in Belo Horizonte (Brazil). The following parameters were determined for all individuals using the cytokinesis-block micronucleus (MN) assay in peripheral blood lymphocytes: MN/1000 binucleated cells (BC), BC with MN (BCMN)/1000 BC, nucleoplasmic bridges (NB)/1000 BC, apoptotic and necrotic cells/500 cells and nuclear division index. The analysis of covariance showed significantly higher (p < 0.05) mean frequencies of MN (15.81 +/- 1.31 vs 4.71 +/- 0.42), BCMN (15.10 +/- 1.22 vs 4.62 +/- 0.44), NB (4.59 +/- 0.76 vs 1.00 +/- 0.34), and necrotic cells (12.07 +/- 1.45 vs 5.17 +/- 0.70) in the exposed group when compared to the control group. There was no significant difference in the apoptotic cell frequency between the two groups, while the nuclear division index was significantly lower (1.49 +/- 0.02 vs 1.61 +/- 0.02) in the control group. Neither the time of exposure nor the smoking or alcohol drinking habit influenced the cytogenetic parameters examined. According to these results, occupational exposure to pesticides induced genotoxic and cytotoxic effects in sanitation workers.     

Calcium signaling capacity of the CD11b/CD18 integrin on human neutrophils.

The CD11b/CD18 integrin is a major cell adhesion molecule of myelomonocytic cells. Exposure of human neutrophils in suspension to CD11b or CD18 monoclonal antibodies (mAbs)2 does not affect the resting level of cytosolic free Ca2+ in these cells; however, a subsequent cross-linking of either of these antibodies triggers a prompt and significant cytosolic-free Ca2+ transient lasting about 10 min. The rise in cytosolic-free Ca2+ (from 130 +/- 2 to 414 +/- 12 nM or 111 +/- 12 to 331 +/- 22 nM caused by cross-linking of CD11b or CD18 subunits, respectively) is due to both mobilization of Ca2+ from intracellular stores and influx of Ca2+ across the plasma membrane. Cross-linking of the common leukocyte antigen (CD45) did not alter the basal level of cytosolic free Ca2+. In accordance with other adherence-induced phenomena and with CD11/CD18-mediated phagocytosis, these Ca2+ signals were only modestly affected by pertussis toxin. Thus, the present data clearly indicate that the CD11b/CD18 integrin on human neutrophils is capable of inducing a prompt cytosolic-free Ca2+ signal. These findings directly support the recent suggestion that the CD11b/CD18 integrin is responsible for the "spontaneous oscillations" of cytosolic-free Ca2+ observed in adherent neutrophils and, at least partially, also explain how integrin-mediated adherence can modify the functional responsiveness of neutrophils to a subsequent agonist stimulation.     

Induction of sister chromatid exchanges in traffic policemen exposed to vehicular exhaust

In urban areas there is an explosive growth of population and the number of automobiles. The ever-increasing vehicular traffic density is posing continued threat to the ambient air quality. Traffic policemen as a group of workers are exposed occupationally to the pollutants from vehicular exhaust. Sister chromatid exchanges (SCEs) as a biomarker of the pollutant's effect, were analyzed in peripheral blood lymphocytes of 85 traffic policemen and 60 control subjects. There was a significant increase in the mean SCEs+/-S.D./cell in the exposed group (9.31+/-5.29) when compared to the controls (4.18+/-1.85). Thus the present study concludes that vehicular exhaust might induce cytogenetic damage in traffic police. Further, the more pronounced frequency of SCEs observed in the smoking traffic policemen than in the non-smoking group suggests the joint effect of smoking and vehicular exhaust.     

Subclinical Neuropathy in Lead Workers

Evidence is presented for a minimal defect of peripheral nerve function in a group of lead accumulator workers without clinical evidence of a neurological lesion. Of the 19 men examined, 13 had blood levels above 80 μg./100 ml. and seven had haemoglobin levels below 12 g./100 ml., showing that considerable exposure to lead was occurring.     

Neutrophils transiently infiltrate intra-abdominal fat early in the course of high-fat feeding

Chronic inflammation of adipose tissue in obesity is by now an established phenomenon, but the initiating event(s) of the inflammatory cascade are still unknown. We hypothesized that neutrophil infiltration into adipose tissue may precede macrophage infiltration as in classical immune responses. Here we demonstrate that early (3 and 7 days) after initiating high-fat feeding of C57BL/6J mice, neutrophils transiently infiltrate the parenchyma of intra-abdominal adipose tissue. Mean periepdidymal fat myeloperoxidase expression (representing neutrophils) was significantly increased 3.5-fold (P < 0.01) and 2.9-fold (P < 0.03), at days 3 and 7 compared with day 0. Immunohistochemistry analysis demonstrated a physical binding between neutrophils and adipocytes, which was supported by in vitro adherence assay: mouse peritoneal neutrophils adhered to a monolayer of 3T3-L1 mouse adipocytes, in a manner dependent on their activation state, 41.9 +/- 3.7% or 29.5 +/- 2%, by PMA or the IL-8 analog CXCL1 (KC), respectively, compared with 24.8 +/- 1.5% in unstimulated neutrophils, respectively. The degree of surface exposure of CD11b (Mac-1) corresponded to the percentage of adhered neutrophils. The adherence was prevented by preincubating neutrophils or adipocytes with anti-CD11b or anti-ICAM-1 antibodies. Furthermore, immunoprecipitation of CD11b from lysates of a mixed neutrophil-adipocyte cell population resulted in coimmunoprecipitation of ICAM-1, indicating that the interaction is mediated by neutrophil CD11b and adipocyte ICAM-1.     

Granulocyte metabolism in workers at a coke-processing plant]

Acid phosphatase activity examinations and nitrotetrazolium blue reduction test after latex stimulation in peripheral blood neutrophils were performed in the group of 32 coking plant workers. Reference group consisted of 150 men not exposed to any toxic substances. Neutrophils of coking plant workers, comparing with the reference group, revealed decreased activity of acid phosphatase and impaired reduction of nitrotetrazolium blue after latex stimulation. The results suggest the possibility of toxic influence of coking plant environment on the lysosomal enzymes and oxygen-dependent metabolism of neutrophils what subsequently may diminish bactericidal powers.     

Analysis of chromosome aberrations and sister-chromatid exchanges in peripheral blood lymphocytes of workers with occupational exposure to the mancozeb-containing fungicide Novozir Mn80

Chromosome aberrations and sister-chromatid exchanges (SCEs) were analyzed in short-term cultures of peripheral lymphocytes of 44 workers occupationally exposed to mancozeb during the production of the pesticide Novozir Mn80 and 30 control persons. The results suggest that mancozeb exposure was associated with a significant increase in the frequencies of cells with structural chromosome aberrations (2.07% vs. 1.10% in the controls), and the number of SCEs per cell (9.19 +/- 1.81 vs. 7.82 +/- 1.04 in the controls).     

Incidence of chromosome aberrations in hothouse workers and the in vitro sensitivity of their lymphocytes to the cytogenetic action of dimatif

The cytogenetical survey of eight persons working in greenhouse and occupationally contacting with a complex of pesticides has shown a significant increase of chromosomal aberration level in comparison with the control group. It is determined that the cytogenetic effect of the greenhouse's workers differed significantly from that of the control group when lymphocytes of the examined persons were treated by the potent mutagen dimatyph in vitro. The occupational group on the whole was more sensitive than control persons to the clastogenic action of dimatyph (43.0 +/- 2.2 and 28.7 +/- 2.4%, respectively). An assumption is advanced on the modifying influence of the pesticide complex on the frequency of induced chromosomal aberrations in vitro.     

Neutrophils induce apoptosis of lung epithelial cells via release of soluble Fas ligand

Neutrophils release soluble Fas ligand (sFasL), which can induce apoptosis in certain Fas-bearing cell types (Liles WC, Kiener PA, Ledbetter JA, Aruffo A, and Klebanoff SJ. J Exp Med 184: 429-440, 1996). We hypothesized that neutrophils could induce alveolar epithelial apoptosis via release of sFasL. A549 pulmonary adenocarcinoma cells expressed surface Fas and underwent cell death (10 +/- 7% viability) and DNA fragmentation (354 +/- 98% of control cells) when incubated with agonistic CD95/Fas monoclonal antibody (P < 0.05). Coincubation with human neutrophils induced significant A549 cell death at 48 (51 +/- 9% viability; P < 0.05) and 72 h (25 +/- 10%; P < 0.05) and increased DNA fragmentation (178 +/- 42% of control cells; P < 0.05), with morphological characteristics of apoptosis. The addition of antioxidants did not inhibit apoptosis. sFasL concentrations were maximally increased in coculture medium at 24 h (4.9 +/- 0.7 ng/ml; P < 0.05). Neutrophil-induced A549 cell apoptosis was blocked by inhibitory anti-Fas (42 +/- 6% of control cells; P < 0.05) and anti-FasL monoclonal antibodies (29 +/- 3%; P < 0.05). Human neutrophils and Fas similarly affected murine primary alveolar epithelial cell bilayers, and caspase activation occurred in response to Fas exposure. We conclude that neutrophils undergoing spontaneous apoptosis induce A549 cell death and DNA fragmentation, independent of the oxidative burst, that is mediated by sFasL.     

Zymosan-activated plasma causes prolonged decreases in PMN superoxide release in sheep

It is well established that activation of neutrophils within the pulmonary circulation produces acute lung injury in which adherence of neutrophils to endothelial cells is an obligatory step in the mechanism of injury. The effects of in vivo activation of neutrophils on the in vitro responses of these cells to stimulation have not been determined, although such information may be important in understanding how different etiological factors may interact to produce infection or acute respiratory failure. By using an assay to sequentially measure superoxide anion (O2-) release from adherent neutrophils stimulated with phorbol myristate acetate (PMA), we measured the in vitro activation response of peripheral blood neutrophils isolated before and 24 h after infusion of zymosan-activated plasma (ZAP; or untreated plasma as a control), air bubbles, or PMA in awake, instrumented sheep. Each of the three inflammatory agents produced an increase in lung microvascular permeability characteristic of acute lung injury; control plasma did not. For the in vivo ZAP experiments, stimulated O2- release in vitro by using PMA was approximately 50% lower (P less than 0.05) for neutrophils isolated 24 h after the in vivo infusion (4.3 +/- 0.8 nmol/500,000 cells) than before (8.1 +/- 0.2 nmol/500,000 cells). For the air emboli or PMA in vivo experiments, there were no changes in neutrophil activation responses in vitro. Similarly, infusion of control plasma did not result in reduced neutrophil O2- release. These results show that alterations in the inflammatory potential of neutrophils may occur in vivo and that such alterations appear to be dependent on the mechanism and agent by which lung injury is produced.     

Effect of proper-myl on humoral interactions between activated lymphocytes and neutrophils in patients with myeloproliferative diseases

The lymphokine synthesizing function of peripheral blood lymphocytes (PBL) was studied in 22 patients with chronic myeloid leukemia (CML), 28 patients with subleukemic myelosis (SLM) and 15 healthy persons. The index of the neutrophil stimulation (INS) in CML (1.73 +/- 0.068) and SLM (1.458 +/- 0.004) was statistically significantly lower than that in the healthy persons (2.6 +/- 0.07). The use of proper-myl in the complex therapy markedly increased the ability of PBL to produce the factor stimulating phagocytic activity of neutrophils (INS 1.94 +/- 0.04 and 1.832 +/- 0.092). On the basis of the findings it was recommended to use proper-myl for prevention and treatment of infectious complications.     

Ability of human T lymphocytes to adhere to vascular endothelial cells and to augment endothelial permeability to macromolecules is linked to their state of post-thymic maturation

The accumulation of mononuclear cells at sites of chronic inflammation is dependent on a number of factors including localized adherence of lymphocytes to vascular endothelial cells (EC), cytokine-mediated increased adhesiveness of endothelium, chemotactic factors and endothelial permeability. The present study investigates two of the above attributes of lymphocyte-EC interaction: namely, the ability of maturationally distinct subpopulations of human T lymphocytes to adhere to vascular EC and to increase vascular endothelial permeability to macromolecules in an in vitro model. Thus, human T lymphocytes were separated into CD4+ CD8-helper/inducer, CD4- CD8+ cytotoxic/suppressor, CD29+ CD45RA- CD45RO+ memory, and CD29- CD45RA+ CD45RO- naive/virgin T subpopulations, were activated with PHA and PMA, and then examined for their adherence to EC and also for their effect on endothelial permeability. Upon activation, cells within each of the above four subpopulations exhibited increased adherence to EC. In contrast, resting CD29+ CD45RA- CD45RO+ memory T lymphocytes exhibited two to three times greater ability to adhere to EC than their CD29- CD45RA+ CD45RO- naive/virgin counterparts. Consistent with their increased adherence to EC, CD29+ CD45RO+ memory T lymphocytes, when activated, significantly increased endothelial permeability to albumin. Although activated CD45RA+ naive T lymphocytes exhibited increased adherence to EC, these cells failed to increase significantly endothelial permeability. Similar to their polyclonal counterparts, Ag-specific CD4+ CD29+ CD45RO+ T cell clones, but not their actively released mediators, also increased endothelial permeability via a noncytolytic mechanism(s). This ability of CD29+ CD45RO+ memory T lymphocytes to augment endothelial permeability may facilitate their transendothelial migration into extravascular space. These observations may provide additional insights into molecular mechanism(s) underlying pathophysiology of localized chronic inflammatory responses in general and more specifically selective accumulation of CD29+/CD45RO+ memory T lymphocytes at sites of chronic inflammation such as rheumatoid synovium.     

The state of immunity in the liquidators of consequences of the Chernobyl accident with cardio-vascular diseases

The purpose of the work was research and functional reserves immunity in participants in the Chernobyl with cardiovascular disease. A Clinical Lab 49 men aged 44 to 52 years with diseases of the cardiovascular system, participated in the Chernobyl nuclear power plant in 1986 to 1988. As control used data 33 patients with similar pathology, and 16 healthy men. Researched the total number of white blood cells, lymphocytes and transfusions, the absolute number and relative CD4+ and CD8+, CD 16, CD20+, CD95+ lymphocytes peripheral blood, number mononuclear, synthesizing IL-1beta, TNF-alpha, INF-alpha, IL-4, the content of lipids and proteins, the activity of alkaline phosphatase and mieloperoksidazy in neutrophils. To assess the functional reserve immune system blood samples studied people subjected to radiation doses 0.25, 50, 1.0 Gy of in vitro and studied the reaction cytochemical indicators neutrophils before and after the radiative forcing. The liquidators not detected significant changes in the absolute number of leucocytes, but compared with control groups noted significant reduction in the absolute number of CD8+ and CD20+ lymphocytes, increased the number of cells, expression of FAS-antigen, change the number of mononuclear spontaneously synthesizing and produce cytokines, decreased maintenance of cation proteins in neutrophils. Radiation samples peripheral blood liquidators caused the same reaction cytochemical indicators of neutrophils and control groups, the compensatory and adaptive nature of the changes in the immune system, developed in response to complex factors radiation accident.     

Cytogenetic analysis of nasal mucosa cells and lymphocytes from high-level long-term formaldehyde exposed workers and low-level short-term exposed waiters

The evidence for genotoxic potential of formaldehyde (FA) in humans is insufficient and conflicting. We previously reported a higher frequency of micronuclei in nasal and oral exfoliative cells from students exposed to formaldehyde vapor for short-term. To further evaluate the genetic effects of long-term occupational exposure to FA and short-term exposure to FA of indoor sources, the frequencies of micronuclei (MN) in nasal mucosa cells, sister chromatid exchanges (SCEs) of peripheral lymphocytes, and the lymphocyte subsets were evaluated in 18 non-smoking workers (mean exposure duration was 8.6 years) in an FA factory and 16 non-smoking waiters exposed to FA for 12 weeks in a ballroom. A non-smoking student group without occupational exposure (n=23) to FA was used as control. The 8h time-weighted average (TWA) concentrations of formaldehyde was 0.985+/-0.286 mg/m3 with the ceiling exposure concentration of 1.694 mg/m3 in the workshop, and 0.107+/-0.067 mg/m3 in the ballroom (5 h TWA). Higher frequencies of micronuclei per thousand cells in nasal mucosa cells of workers versus control (2.70+/-1.50 versus 1.25+/-0.65, p<0.05) and higher frequency of SCEs in peripheral lymphocytes of workers group (8.24+/-0.89 versus 6.38+/-0.41, p<0.05) were observed. Increased frequency of micronuclei in nasal mucosa cells or SCE in peripheral lymphocytes was not found among waiters group. The results suggest that the genotoxic potential of high level FA exposure may have occupational risks in long-term exposure groups.     

CD177~+中性粒细胞在溃疡性结肠炎患者外周血中的表达及临床意义

目的:通过对比CD177~+中性粒细胞在溃疡性结肠炎(UC)患者与正常对照者外周血中的表达差异,分析CD177~+中性粒细胞在溃疡性结肠炎发生发展中的临床意义。方法:收集30例UC患者及20例正常对照者外周血,采用流式细胞术检测中性粒细胞CD177~+中性粒细胞表达情况,对比两组CD177表达差异。结果:UC患者外周血中CD177~+中性粒细胞表达明显高于正常对照组(P 0. 01),中度活动UC外周血CD177~+中性粒细胞表达较轻度者明显增高(P 0. 05),UC患者外周血CD177~+中性粒细胞%与Mayo评分呈显著正相关(r=0. 384,P=0. 036)。结论:CD177~+中性粒细胞在UC患者外周血表达明显增高,且与疾病活动程度密切相关,能够反映UC患者临床疾病活动程度。     

A quantitative method for determining polarization of neutrophil adhesion molecules associated with ischemia reperfusion

Ischemia-reperfusion-induced neutrophil adhesion to endothelium is CD18-dependent, but information regarding polarity of CD18 adhesion molecules remains speculative. This study evaluated neutrophil adhesion using an in vitro cell adhesion assay and introduces a quantitative method of measuring CD18 membrane distribution using confocal microscopy. Neutrophils from normal animals were isolated from whole blood and incubated with plasma from rat gracilis muscle flaps with no ischemia and reperfusion (nonischemic control, n = 10) or 4 hours of ischemia and 90 minutes of reperfusion (ischemia/reperfusion, n = 10), on coverslips pretreated with and without (phosphate-buffered saline) soluble intercellular adhesion molecules. Coverslips without intercellular adhesion molecules represented a negative control (intercellular adhesion molecules were required for adhesion). Percent adherence to intercellular adhesion molecules was expressed as a ratio of adherent cells/total cells. CD18 polarization was assessed by staining neutrophils with fluorescein isothiocyanate-labeled anti-CD11b, followed by confocal microscopy and Z-stack analysis. Membrane-associated CD18 was expressed as fluorescence intensity units in three equal areas of the cell membrane. Capping was defined as twice as much fluorescence in 33 percent of the cell membrane as in the remaining 67 percent. Neutrophils exposed to ischemia and reperfusion plasma showed a significant increase in adhesion (0.8 +/- 0.1 percent versus 16.7 +/- 2.2 percent, p < 0.001) and CD18 polarization (6.2 +/- 1.7 percent versus 43.9 +/- 12.2 percent, p = 0.0206) compared with controls. This article describes an in vitro assay that reliably reproduces the neutrophil adhesion phenomenon associated with ischemia-reperfusion injury. Results from confocal microscopy allowed for quantitative estimation of membrane-associated receptor polarization.     

Forefoot structural predictors of plantar pressures during walking in people with diabetes and peripheral neuropathy

Various foot structures are thought to influence forefoot plantar pressures during walking. High peak plantar pressures (PPP) during walking in people with diabetes mellitus (DM) and peripheral neuropathy (PN) can cause skin breakdown. The question addressed by this study is "What are the primary forefoot structural factors that predict regional PPP during walking in groups of people with and without DM and PN?" Twenty people with DM and PN (mean age 55+/-9 years, 6 female, 14 male, BMI=33+/-8) and 20 people without DM, matched for gender, age, and BMI were tested. Measures of foot structure were taken from three-dimensional images constructed from spiral X-ray computed tomography. Peak plantar pressure data were recorded during walking. Hierarchical multiple regression analysis was used to predict regional PPP at the great toe and five metatarsal heads from selected structural and walking variables. Metatarsal phalangeal joint angle (hammer toe deformity) was the most important variable predicting pressure, accounting for 19-45% of the PPP variance at five of the six locations in the DM group. Soft tissue thickness, hallux valgus, and forefoot arthropathy were the most important predictors of PPP in the control group. Combinations of structural and walking variables accounted for 47-71% of the variance in the DM group and 52-83% of the variance of PPP during walking in the control group. These structural variables, especially hammer toe deformity, should be considered in attempts to develop strategies to reduce excessive forefoot PPP that may contribute to skin breakdown or other injury.