FOLIA HISTOCHEMICA ET CYTOBIOLOGICA

Introduction

Insulin-like growth factor-I is encoded by IGF-I gene, composed of 6 exons. Its biological functions

are mediated by the activation of a specific receptor (IGF-IR). IGF-I exerts a series of significant effects,including remarkable proliferation and differentia-tion of target cells [27]. It also participates in the control of apoptosis, protecting both normal and tumor cells from this process. Its promoting role has been demonstrated in a number of human malignan-cies [25]. Increased serum IGF-I levels have been shown to be carcinogenesis predictor in some human

FOLIA HISTOCHEMICA ET CYTOBIOLOGICA V ol. 44, No. 4, 2006pp. 249-258

Expression of insulin-like growth factor-I (IGF-I) in alveolar macrophages and lymphocytes obtained by bronchoalveolar lavage (BAL) in interstitial lung diseases (ILD). Assessment of IGF-I as a potential local mitogen and antiapoptotic cytokine

Piotr Kopi?ski 1, Krzysztof S3adek 2, Jerzy Szczeklik 3, Jerzy Soja 2, Artur Szlubowski 2,Barbara Balicka-?lusarczyk 2, Bo?ena Lackowska 4, Marta Plato 1and Adam Szpechci?ski 1

1Chair of Gene Therapy, Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz

2Department of Occupational Medicine and Environmental Diseases, Jagiellonian University Medical College, Kraków

32nd Chair of Internal Medicine, Jagiellonian University Medical College, Kraków 4Department of Immunology, Center of Oncology, Kraków, Poland

Abstract:Little is known about IGF-I expression in the alveolar lymphocytes (AL), and about local role of IGF-I in phy-siological conditions and in interstitial lung diseases. Bronchoalveolar lavage was carried out in patients with silicosis,asbestosis, idiopathic pulmonary fibrosis (IPF) and sarcoidosis, as well as in control subjects (n=13, 9, 12, 56, 15, resp).Alveolar macrophages (AM) and lymphocytes (AL) were studied for (1) IGF-I, BCL-2, Fas and Fas Ligand expression and (2) cell cycle (incl. sub-G 1peak of late apoptosis) with propidium iodide (PI). Flow cytometry (FC) and immunocyto-chemistry were used. AL early apoptosis was detected by Annexin V FITC/PI staining. IGF-I was present in AL of all test-ed groups. The number of IGF-I positive AL was significantly higher in IPF (52 ± 6.7%) and in later (II and III) stages of sarcoidosis (39 ± 7.8 vs 16 ± 4.0% in controls, p<0.05). Increased BCL-2 expression in AL was detected in IPF and sar-coidosis. In all tested groups, AL were almost exclusively Fas+ T cells. Generally, a low number of AL entered apoptosis;no significant differences were found between patient groups, except decreased apoptosis rate in sarcoidosis (0.60 ± 0.17 vs 1.15 ± 0.33% in controls, p<0.05). Proportion of AL positive for IGF-I was significantly correlated with parameters reflect-ing AL and AM cell proliferation and BCL-2 expression (e.g.AL IGF-I+ vs AM in S phase of cell cycle: r s = +0.50,p=0.001), but not with apoptosis. The results show that human alveolar lymphocytes express IGF-I in normal conditions, as well as in ILD. The proportion of IGF-I+ lymphocytes was significantly increased in IPF and at later stages of sarcoidosis.In our material there was no evidence for profibrogenic or antiapoptotic activity of IGF-I. We suggest that IGF-I originat-ing from AL may be locally active as a mitogen for alveolar macrophages and lymphocytes in ILD.

Key words:Alveolar macrophages - Apoptosis - Asbestosis - Cell cycle - Insulin-like growth factor-I - Idiopathic pul-monary fibrosis - Lymphocytes - Sarcoidosis - Silicosis

Correspondence: Piotr Kopi?ski, Chair of Gene Therapy, Collegium Medicum, Nicolaus Copernicus University, M. Sk3odowskiej-Curie 9, 85-094 Bydgoszcz, Poland; e-mail: mpkopins@https://www.wendangku.net/doc/ed4412228.html,.pl

organs, such as brain, breast, ovary, prostate, colon and lung [30].

In the lower airways, IGF-I is permanently present.Its concentration in homogenized lung tissue of healthy subjects is about 234 mU/g [5]. Biological role of IGF-I in lungs includes tissue developmental growth, repair processes and compensatory growth of healthy lung,which appears after contralateral pneumonectomy [8,19]. Alveolar macrophages are usually considered to be the main local source of IGF-I: the commonly used for-mer name of insulin-like growth factor-I was alveolar macrophage derived growth factor, AMDGF [18].

IGF-I is regarded to participate in the pathogenesis of many interstitial lung diseases (ILD), including sar-coidosis, idiopathic pulmonary fibrosis (IPF) and pneu-moconioses (silicosis and asbestosis). It potentially acts as a mitogen for lung fibroblasts and, subsequently, as an activator of pulmonary fibrosis [10, 23].

In sarcoidosis, increased IGF-I level is considered to stimulate collagen synthesis by pulmonary fibroblasts [2]. In IPF, the enhanced local IGF-I expression seems to affect fibroblast growth and local collagen synthesis [31]. Increased IGF-I secretion was also observed in alveolar macrophages originating from silicosis and asbestosis patients [9, 21]. High surface expression of IGF-I receptor on AM could explain intensive macrophage proliferation observed in this subgroup of ILD [26]. It should be emphasized that all the mentioned disorders might be complicated by disseminated pul-monary fibrosis, resulting in severe respiratory failure and fatal outcome [24]. However, both in ILD patients and in normal conditions, little is known about IGF-I expression in cells other than alveolar macrophages.Apoptosis seems to be a powerful mechanism par-ticipating in the pathology of lower airways in ILD [1].The imbalance of prosurvival and proapoptotic signal-ing pathways in such cells as alveolar macrophages (AM) and lymphocytes (AL) may play an important role in the onset, progress and remission of ILD [22].For example, the reduced apoptosis of alveolar lympho-cytes was demonstrated in inflammatory diseases, char-acterized by high BAL lymphocytosis, such as extrinsic alveolitis and sarcoidosis [17, 28]. Recently, we report-ed similar findings in lung pneumoconioses [29].

In order to explain the dysregulation of pro-grammed cell death observed in ILD, many investiga-tors focused their attention on different components of antiapoptotic pathways, e.g.on interleukine-2 (AL in sarcoidosis), transforming growth factor-β(immune cells in pulmonary fibrosis), intracellular BCL-2 or BCL-X L expression (AL in sarcoidosis and extrinsic alveolitis), transcription factor NF-κB (AM in pneu-moconioses) or surfactant protein D (experiments on murine AM) [4, 6, 17]. It should be emphasized, how-ever, that the mechanisms responsible for normal immune cell apoptosis (the event that seems to be not

very common in physiological conditions), as well as for its extremely reduced rate in some lower airway dis-orders, are poorly understood. The role of IGF-I, which is probably active locally as a mitogen, profibrotic cytokine and antiapoptotic agent together, needs also more accurate explanation.

The purpose of the present study was to determine the expression of IGF-I in the alveolar immune cells both lymphocytes and macrophages in ILD, such as sar-coidosis, idiopathic pulmonary fibrosis, asbestosis and silicosis. The results of IGF-I expression, calculated separately for AL and AM, were referred to the clinical data and to the parameters characterizing the apoptosis and proliferation of immune cell. Especially, in the material coming from relatively large group of patients,we tested the statistical correlations between the per-centage of IGF-1-positive alveolar macrophages and lymphocytes and (1) the predicted value of vital capac-ity (VC), which decline in ILD serves as a clinical mark-er of lung fibrosis; (2) the percentage of apoptotic AM and AL (3) the rate of AM and AL proliferation (S and G 2M phases of the cells cycle). In this way we tried to assess the profibrotic, antiapoptotic and mitogenic role of IGF-I in interstitial lung diseases.

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Table 1.Anti-human monoclonal antibodies used for immunocy-tochemical staining (ICS) and flow cytometry (FC)

Materials and methods

Patients. The cytological material originating from bronchoalveo-lar lavage (BAL) was harvested from 90 patients with ILD, i.e.sar-coidosis (56 cases), asbestosis (9), silicosis (13) and idiopathic pul-monary fibrosis (12). A diagnosis of sarcoidosis was established in accordance with recently described criteria [12]. In all patients non-caseating granulomas were identified by transbronchial or endotransbronchial biopsy. None of patients included in the study had previously been treated with steroids. Patients were subdivid-ed according to conventional chest X-ray staging.

A diagnosis of pneumoconiosis (asbestosis or silicosis) was established according to chest X-ray standards of International Labor Organisation in subjects with proven professional or envi-ronmental (as happened in some cases of asbestosis) exposition to the respective inorganic dust. In these patients the exposition was additionally determined by BAL cytology, including the presence of ferrugineous bodies in asbestosis and silica dust light emission in polarized light in silicosis [15, 29].

Fifteen persons diagnosed for ILD, in which complete clinical investigation (incl. lung function tests, chest X-rays, DLCO and arterial blood gas analyses) finally excluded any lung pathology, served as the control group. They did not present any signs of infection or chronic lung disease and they were not treated with corticosteroids, immunosuppresive agents or any other drugs known as a potential ILD cause.

All involved subjects were nonsmokers. In this way we omit-ted the data interpretation problems concerned with distinct cytoimmunological pattern observed in the group of smokers [11]. Bronchoalveolar lavage (BAL). BAL was carried out according to criteria of European Respiratory Society [13]. In brief, the patients were premedicated with midazolam 2.5-5.0 mg i.v., fol-lowed by local anesthesia of upper airways with 2% lidocaine solu-tion. The Olympus Bf 20 bronchofiberoscope was inserted into the middle lobe or into the left lung lingula, alternatively. Lavage with 200 ml of 0.9% NaCl sterile solution (37°C) was carried out by sequential instillation of four 50 ml aliquots of saline. The BAL fluid fractions were retrieved carefully by gentle suction, then pooled and filtered. The fluid recovery was calculated as the per-centage of the instilled volume. The material was immediately sent to the laboratory.

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cells

Fig. 1.Examples of BAL immunocytochemistry are presented in the micrographs. A. In contrast to alveolar macrophages, alveolar lym-phocytes (AL) demonstrate moderate expression of IGF-I. Only some AL are intensely positive. Flow cytometry is more sensitive (see Fig. 2). Sarcoidosis, counterstained with Harris hematoxylin, × 200. B. BAL cytospin preparation with relatively high percentage of pos-itive lymphocytes. Asbestosis, counterstained with Harris hematoxylin, × 200. C. One of four AL is positive. It should be emphasized that positive alveolar lymphocytes frequently adhere to macrophages. Some AM present both cytoplasmic and superficial IGF-I expression (they absorb cytokine from microenvironment by IGF receptors?). Control group, counterstained with Harris hematoxylin, × 600.

D. Common superficial expression of Fas (CD95) on BAL immune cells. Control group, counterstained with Harris hematoxylin, × 200.

BAL routine cytology. The total cell count and cell viability (try-pan blue exclusion test) were calculated, as described before. BAL cytospin smears were stained simultaneously with hematoxylin-eosin (HE) and May-Grünwald-Giemsa (MGG). In each sample the differential count of BAL reactive cells was calculated as the mean result of both methods (at least 500 cells were counted) [14]. BAL immunocytochemistry. The immunocytochemical proce-dure was performed on samples obtained by BAL material cyto-centrifugation (100-300 μl of native BAL fluid, Shandon, Cytospin 3, 1000 rpm, 5 min followed by fixation in 70% ethanol, 10 min, stored at -80°C). The avidin-biotin-peroxidase method was used (LSAB 2 System, DAKO Cytomation, cat. no K0675). The immunostaining procedure was carried out using mouse anti-human monoclonal antibodies (MoAbs) directed against CD95, IGF-I and BCL-2 (details listed in Table 1), diluted in Antibody Diluent (Dako Cytomation, no S2022). As negative controls, we replaced primary antibodies with nonspecific mouse IgG1.

After rehydration, endogenous peroxidase activity was blocked by incubation with 3% hydrogen peroxide in PBS (5 min). Cytospin smears were then washed in TBS, blocked with 3% bovine serum albumin (BSA, POCh, 30 min, room temperature) to inhibit nonspecific immunoreactivity and incubated overnight at 4°C with the monoclonal antibodies (data in Table 1). Alternative-ly, the wet chamber incubation with diluted MoAbs at room tem-perature, 1 h, was carried out. Consecutive incubations were con-ducted with biotinylated anti-mouse secondary antibody (50 μl) and horseradish peroxidase solution linked with streptavidin (Streptavidin-HRP, 50 μl, LSAB 2 Systems, DAKO Cytomation, no K0675). Both incubations were carried out at room temperature for 15 min, and slides were rinsed 3× in TBS before each incuba-tion. Diaminobenzidine (DAB) was used as chromogen. The slides were rinsed with TBS buffer, pH 7.6 (Trismabase SIGMA, cat. no K5458) in NaCl solution, counterstained with Harris hematoxylin (2-5 min), rinsed in water, dehydrated with use of graded alcohols (50% 70% 90% and 99%, 5 min each), bathed in fresh xylene and covered with glycerol jelly. The cells were evaluated in light microscope. In each slide we counted at least 250 cells (500 on the average), calculating separately the percentage of positive macrophages and positive lymphocytes [14]. Intracellular expres-sion of IGF-I and surface staining for Fas (CD95) are presented in Figure 1.

BAL immune cell phenotyping. BAL material was centrifuged (300× g, 10 min) and a cell pellet was resuspended in PBS to 2-10× 106cells per ml. The samples containing 50 μl of cell suspension were incubated with mixture of saturating amounts of MoAbs for 30 min in the dark. Double- or three-colour typing was performed, according to the percentage of AL(more or less than 5% of BAL reactive cells, respectively). Mouse anti-human MoAbs directed against superficial CD3, CD 4, CD8, CD16+56, CD19, CD45, CD95 and CD178 antigens, fluorochrome-conjugated (FITC or

252P. Kopi?ski

et al. Fig. 2.FC analysis of IGF-I expression in AL and AM. Alveolar lymphocyte and macrophage gates are defined in flow cytometry due to cell CD45 expression and side scatter, SSC (upper left panel, gate R1 and R2 respect.) and then redefined, i.e.back-gated, acc. to FSC/SSC parameters (upper right panel, gate R3 and R4 respect.). Sample of AL(R3) gate analysis for IGF-I expression in left lower panel; parallel analysis of AM (R4) gate in right lower panel. About 30% of AL and > 95% of AM are positive. Markers set according to the negative isotype control. SSC presented in logarithmic scale in order to visualize dot plot of macrophages.

PE) were used in the study (Becton Dickinson Immunocytometry Systems, BDIS, Mountain View, CA, USA; R & D Systems, data in Table 1). Negative isotype control was used in sample series of every patient. After incubation, cells were washed in PBS (300× g, 10 min) and resuspended in 300 μl of PBS containing 1% formaldehyde [3, 14].

Flow cytometry was also applied to test BAL cell IGF-I and BCL-2 expression. The samples containing 50 μl of BAL cell sus-pension were preincubated with 0.3% saponin (200 μl, 10 min), washed in 0.1% saponin (1 ml, 300× g, 5 min) and incubated with saturating amounts of the respective MoAb (in 100 μl of 0.3% saponin, 30 min in the dark). Cells were washed and incubated with the secondary antibody (rabbit anti-mouse FITC conjugated serum, DAKO Cytomation, cat. no F031302) for 10 min in the dark. The same secondary antibody was used as negative control (primary MoAb was omitted). The cells were washed twice with PBS and resuspended in 300 μl of PBS with 2% formaldehyde for immediate flow cytometric analyses.

Early apoptosis detection with Annexin V FITC/PI staining. Detection of early apoptosis in BAL lymphocytes was performed according to the instruction of manufacturer (APOPTEST?-FITC, DAKO Cytomation, cat. no K2350). In brief, fresh BAL cells (105-106cells/ml) were washed, resuspended in 96 μl of ice-cold diluted binding buffer and incubated with 1 μl Annexin V-FITC and 2.5 μl propidium iodide for 10 min in the dark. The cell sample was diluted with 250 μl of binding buffer and then meas-ured immediately by flow cytometry. Negative control was carried out for each sample (incubation with binding buffer alone). For positive control, the cells were incubated on ice with 3% formalde-hyde in binding buffer for 30 min [29].

Late apoptosis detection with cell permeabilization and PI staining. BAL cells (1-2 × 106) were washed in PBS, resuspended in 0.03% Nonidet solution with 0.005% propidium iodide (PI), centrifuged (400 × g, 5 min) and incubated with 250 μl of the Nonidet/PI solution (room temperature, 15 min in the dark). The next incubation was carried out for 15 min with 250 μl of RNAse solution (88 Kunitz U per 100 ml PBS, room temperature, in the dark). The cells were finally suspended in 1 ml volume (adjusted with PBS) and acquired in FACSCalibur flow cytometer (BDIS) within 24 h from staining [29].

Flow cytometry. All BAL materials included in the study fulfilled the precise criteria of cytometric analyses, which were commented on elsewhere [14]. FC data were acquired within 24 h after stain-ing, using CellFit software and FACSCalibur cytometer (BDIS). An argon ion laser excitation 488 nm was used. The emitted light was detected by logarithmic amplification through barrier filters specific for the emission range of the different fluorophores: 530/22 nm for FITC (fluorescence channel FL1), 585/42 nm (FL2) for PE and >650 nm (FL3) for PE Cy5. In each sample 8000-12000 events (cells) were acquired.

Gates for AL and AM were determined due to the cell granu-larity (side scatter, SSC) and intensity of staining with CD45 FITC ("back gating"). The sample was presented in Figure 2. The results of lymphocyte typing and lymphocyte early apoptosis detection were yielded by quadrant analyses of FL1 vs FL2 channel dot plot and were presented as the percentage of gated lymphocytes [29].

For detection of late apoptosis, cells were acquired with the use of pulse processor. Cell cycle was assessed simultaneously. The conjunction of two gates was applied: forward scatter (characteriz-ing cell size) vs side scatter (FSC vs SSC), as well as pulse width vs pulse area in a fluorescence-2 standard channel (FL-2W vs FL-2A). Data on 15 000-20 000 BAL cells were collected and ana-lyzed with BDIS ModFit software. The sample was presented in Figure 3. Two distinct FSC/SSC gates were applied for separate AL and AM apoptosis/cell cycle FC analyses.

Statistical analysis. All BAL cytology and phenotype results were presented as medians ± SEM (due to nonparametric distribution of values) [20]. The Mann-Whitney U-test was used to compare the data obtained in analyzed groups (ILD patients vs controls). The Spearman's rank correlation coefficient r

s

was applied to test the correlation between two random variables. P-values < 0.05 were considered statistically significant.

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IGF-1 in BAL cells

Fig. https://www.wendangku.net/doc/ed4412228.html,te apoptosis and cell cycle

analysis of AL gate - samples of silico-

sis (the upper panel) and asbestosis (the

lower panel). Generally, AL late apop-

tosis (marker 1, M1) in the majority of

examined ILD patients is uncommon as

determined with the use of PI; the rela-

tively frequent AL apoptotic rate (>6%

in presented asbestosis sample) occurs

rarely. Another characteristic feature of

BAL material is a relatively low per-

centage of proliferating AL(G

2/S/M

phase, marker 2, M2).

Results

The basic information about groups included in the study, as well as their BAL cytological and immuno-logical data, are presented in Table 2. Increase in BAL total cell number was found in all tested groups, as compared with controls. Silicosis was characterized by higher percentage of alveolar macrophages and a rela-tive decline in BAL lymphocytes. In asbestosis,increased percentage of AM and neutrophils together with high CD4/CD8 ratio was found. IPF was charac-terized by increase in proportion of BAL lymphocytes,neutrophils and eosinophils; CD4/CD ratio was low.BAL distinct lymphocytosis together with mild eosinophilia and typical high CD4/CD8 ratio was characteristic for sarcoidosis patients.

AL population, in contrast to the respective periph-eral blood results, was dominated by T cells with only few NK and B cells, regardless of the tested group (data not shown). Additionally, in all groups, up to 100% of AM, Th (CD4) and Tc (CD8) cells expressed CD95 marker, suggesting high AM and AL suscepti-bility to proapoptotic stimuli. The results of Fas Ligand (CD178) expression on AL are presented in Figure 4. The percentage of CD178-positive AL was increased in asbestosis, and in IPF (for Tc cells only);it was decreased in total sarcoidosis, as compared with controls. However, we did not observe any association between Fas Ligand expression on AL and the number of apoptotic BAL immune cells.

Almost all AM, according to immunocytochemical staining, were positive for IGF-I: from 88 ± 4.9 (77-100)% in IPF to 93 ± 5.5 (44-100)% in sarcoidosis and 95 ± 3.8 (75-100)% in silicosis. The respective values for asbestosis and controls were 91 ± 3.7 (81-99)% and 94 ± 1.3 (91-97)%. There were no significant differ-ences in IGF-I and BCL-2 expression in AM between the tested groups.

Results of intracellular expression of IGF-I and BCL-2 in alveolar lymphocytes (data from flow cytometry) were presented in Figure 5. Sarcoidosis was subdivided according to the disease stages.

A noticeable number of alveolar lymphocytes expressed IGF-I. The percentage of IGF-I-positive

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et al.

Table 2.Patients' data and BAL cytoimmunology in interstitial lung diseases (ILD)

M - male, F - female; # Data presented as mean ± SD (range); other results presented as median ± SEM (range);*P < 0.05 as compared to controls; **P < 0.01 as compared to controls

lymphocytes was significantly higher in IPF (52 ± 6.7,range: 5-67%) and in later radiological sarcoidosis stages (39 ± 7.8, range: 6-88%) than in controls (16 ±4.0, range: 6-18%, p<0.05). Changes observed for stage I of sarcoidosis (25 ± 6.7, range: 2-65%), silico-sis (17 ± 7.8, range 5-38%) and asbestosis (34 ± 7.2,range 3-50%) were statistically insignificant. IGF-I expression was found in both major T cell subsets (Th and Tc, data not shown).

Significantly increased percentage of AL express-ing BCL-2 was detected in IPF and sarcoidosis.

The results of cell cycle and apoptosis examination are summarized in Table 3. Decreased apoptosis rate -both early and late one - was characteristic for AL in sarcoidosis, regardless of the stage of the disease (p<0.05). IPF was characterized by significantly high-er rate of proliferating AL (cells of G 2/S/M phase). The percentage of IGF-I-positive alveolar lympho-cytes was strongly and positively correlated with parameters reflecting proliferation of both AL and AM (Fig. 6). However, the percentage of alveolar

macrophages expressing IGF-I was correlated only with the respective data concerning AM alone and it was not related to any parameters of alveolar lympho-cyte proliferation. Surprisingly, despite the positive correlation between the percentage of IGF-I-positive AL and the proportion of BAL cells carrying BCL-2,no relation between immune cell IGF-I expression and any parameters characterizing their apoptosis was found.

The percentage of AL and AM expressing IGF-I was not correlated with any values of lung function tests, including VC and FEV 1/VC.

Discussion

It has been known for many years that almost all AM secrete IGF-I as so called alveolar macrophage-derived growth factor, AMDGF. In the present study we have proven that the expression of IGF-I is also present in alveolar lymphocytes. In opposite to alveo-lar macrophages, which are almost all IGF-I+ in every

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Fig. 4.Expression of Fas Ligand (CD178) - alveolar lymphocytes in ILD. Flow cytometry. Data presented as medians ± SEM of AL positive for CD178; *p < 0.05; **p <0.01 as com-pared to controls.

Fig. 5.Expression of IGF-I and BCL-2- alveolar lymphocytes in ILD. Flow cytometry. Data presented as medians ± SEM of AL positive for BCL-2; *p < 0.05 as compared to controls; **p < 0.01 as compared to controls.

tested individual, our results obtained in alveolar lym-phocytes were different in some groups of patients, i.e. percentage of IGF-I-positive AL was significantly higher in IPF and in the later stages of sarcoidosis as compared to the control group.

It should be established what is an actual impor-tance of IGF-I, including AL-derived IGF-I in the lower airways.

First of all, it has been considered for many years that IGF-I is active as a local fibroblast stimulator and profibrotic factor [8]. The secretion of IGF-I as well as expression of IGF-receptor were increased in BAL macrophages of patients with pneumoconioses and in AM of experimental animals exposed to silica [9, 26]. However, it should be emphasized that in large group of patients analyzed in the current study we did not observe any negative correlation between IGF-I expression and predicted value of VC. These results were in general consistent with some recent studies. In one of them, Krein et al.[16] suggested that IGF-I in lower airways, contrary to TGF-β, protects epithelial cell layer from injury and apoptosis. They questioned the link between IGF-I and interstitial fibrosis in ILD. The profibrotic role of IGF-I has not been confirmed in two other studies by Mustaers et al.[21] and V anhee et al.[32], who examined statistical correlations in BAL fluid of asbestosis and coal workers' pneumoconiosis patients. Furthermore, in BAL of IPF patients analyzed by Pala et al.[23], IGF-I level was positively correlated with the results of lung function tests. We conclude that IGF-I does not stimulate lung fibrosis in clinical condi-tions, despite findings from experimental studies.

Secondly, since IGF-I protects many cell types from apoptosis [27], we have tried to relate the results of IGF-I expression in BAL immune cells to data char-acterizing apoptosis of AL and AM. High proportion (up to 100%) of both T lymphocytes and alveolar macrophages expressed superficial Fas molecules. Additionally, many of these cells co-expressed Fas lig-and. Alveolar cells are susceptible then to apoptosis induced by membrane stimuli. Surprisingly, we found a relatively low apoptotic rate in both AM and AL, especially in BAL lymphocytes originating from sar-coidosis patients. In general, our results obtained in patients with sarcoidosis were consistent with the hypothesis on apoptosis resistance of alveolar lympho-cytes in this disorder [28]. However, account should be taken of the relatively low AL apoptosis rate obtained in the current study in other interstitial lung diseases, as IPF and asbestosis.

To our surprise, in our material there was no correla-tion between IGF-I expression in immune cells and the rate of AL and AM apoptosis. The only finding suggest-ing the influence of IGF-I on regulation of apoptosis in the lower airways was a significant positive correlation between the percentage of alveolar lymphocytes carry-ing IGF-I and expression of BCL-2 in both AL and AM. Finally, we have not proven the antiapoptotic activity of IGF-I in ILD immune cells. This lack of relation could be explained by the complex character of local interac-tions between prosurvival and proapoptotic factors [4, 6]. The mechanisms of this interaction have not been yet fully understood. For example, decreased BCL-2 expression can occur together with very low AL apop-totic rate in some lung disorders [17].

Thirdly, we expected that IGF-I expression in lower airways might affect cell proliferation in lower airways of ILD patients. Actually, the percentage of AL carry-

256P. Kopi?ski et al. Table 3.

Cell cycle and apoptosis in interstitial lung diseases (ILD)

All data concern alveolar lymphocytes, except the last two rows concerning alveolar macrophages (AM) Results are presented as median ± SEM (range), *P< 0.05 as compared to controls

ing IGF-I was positively correlated with proliferation rate of BAL immune cells. This relation was statisti-cally significant for both S and G2M phase of cell cycle in AL as well as AM. However, it should be emphasized that the immune cell proliferation rate observed in lung alveoli was in general low, if we take into consideration the active, extensive inflammation commonly present in sarcoidosis and other ILD. This infrequent proliferation may be explained by local activity of surfactant proteins and other potent mitosis inhibitors that appear in alveoli [7]. IGF-I seems to be unable to overcome them.

The cytological and immunological results obtained in the present study are in line with data reported by other authors and with our previous find-ings, described elsewhere [14, 15, 29].

Summing up, human lymphocytes in the lower air-ways express IGF-I both in normal conditions and in ILD. The proportion of IGF-I+ lymphocytes is signifi-cantly increased in IPF and in later (II and III) stages of sarcoidosis. The local role of IGF-I in normal con-ditions, as well as in ILD, needs further investigation. IGF-I seems to be a potent mitogen of alveolar lym-phocytes and macrophages, but in our material no evi-dence for its antiapoptotic or profibrotic function in ILD has been found.Acknowledgements:The work presented in the paper was per-formed in Krakow, Bydgoszcz and Bia3ystok, Poland. The study was supported by the grant of State Committee for Scientific Research no. 3P05D 15322 and by NATO grant no. LST.CLG 980617.

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[14]Kopi?ski P(1997) Flow cytometry applied in cytological

changes assessment in interstitial lung diseases (in Polish).

Folia Med Cracov 38: 69-115

[15]Kopi?ski P, Soja J, Czunko P, Jedynak U, Lackowska B,

Szczeklik J, S3adek K, Ch3ap Z (2000) Cytoimmunological alterations in bronchoalveolar lavage (BAL) obtained in non-symptomatic individuals chronically exposed to silica dust (in Polish). Pneumonol Alergol Pol 68: 109-119

[16]Krein P, Winston B (2002) Roles of insulin-like growth fac-

tor-I and transforming growth factor-βin fibrotic lung dis-ease. Chest 122: 289-293

[17]Laflamme C, Isra?l-Assayag E, Cormier Y(2003) Apoptosis

of bronchoalveolar lavage lymphocytes in hypersensitivity pneumonitis. Eur Respir J 21: 225-231

[18]Lohman-Matthes ML, Steinmüller C, Franke-Ullman G

(1994) Pulmonary macrophages. Eur Respir J 7: 1678-1689 [19]McAnulty RJ, Guerreiro D, Cambrey AD, Laurent GJ (1992)

Growth factor activity in the lung during compensatory growth after pneumonectomy: evidence of a role for IGF-1.

Eur Respir J 5: 739-747

[20]Merchant RK, Schwartz DA, Helmers RA, Dayton ChS, Hun-

ninghake GW(1992): Bronchoalveolar lavage cellularity. The distribution in normal volunteers. Am Rev Respir Dis 146: 448-453[21]Mustaers SE, Harrison NK, McAnulty RJ, Liao JY, Laurent

GJ, Musk AW(1998) Fibroblast mitogens in bronchoalveolar lavage (BAL) fluid from asbestos-exposed subjects with and without clinical evidence of asbestosis: no evidence for the role of PDGF, TNF-alpha, IGF-1, or IL-1 beta. J Pathol 185: 199-203

[22]Pabst R, Binns RM (1996) Lymphocytes migrate from the

bronchoalveolar lavage space to regional bronchial lymph nodes. Am J Respir Crit Care Med 151: 495-499

[23]Pala L, Giannini S, Rosi E, Cresci B, Scano G, Mohan S,

Duranti R, Rotella CM (2001) Direct measurement of IGF-I and IGFBP-3 in bronchoalveolar lavage fluid from idiopathic pulmonary fibrosis. J Endocrinol Invest 24: 856-864

[24]Piro?y?ski M, Piro?y?ska E (1999) Bronchoalveolar lavage

(in Polish). In: Bronchofiberoskopia, Piro?y?ski M [Ed], α-Medica Press, Bielsko-Bia3a, pp 118-127

[25]Pollak M (2000) Insulin-like growth factor physiology and

cancer risk. Eur J Cancer 36: 1224-1228

[26]Rom WN, Paakko P(1991) Activated alveolar macrophages

express the insulin-like growth factor-I receptor Am J Respir Cell Mol Biol 4: 432-439

[27]Rubin R, Baserga R (1995) Insulin-like growth factor-I recep-

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Increased production of platelet-derived growth factor, insulin-like growth factor type I, and transforming growth factor beta and relationship to disease severity. Am J Respir Crit Care Med 150: 1049-1055

Received: March 23, 2005

Accepted after revision: April 28, 2006

258P. Kopi?ski et al.

万和热水器e4解决方法

热水器在我们生活中起到了非常大的作用，给我们的生活带来了很大的优越感。特别是到了冬季北方天气寒冷，平时生活时刻离不开热水器，不管是洗脸刷牙洗菜做饭还是洗澡都要用热水。所以我们最怕的就是冬季家里的热水器出现故障，。因为热水器使用久了出现一些小的故障是避免不了的。为了让万和用户能更好的了解热水器一些常见故障，今天就给大家讲讲万和热水器显示E4故障代码怎么解决？ 万和恒温热水器出现故障的时候，在显示屏上面都会出现一个故障代码，一个故障代码代表一种含义。万和E4故障在冬季发生的很多，E4代码的意思是风机霍尔传感器故障，当我们开启热水器龙头后，热水器风机开始运转，可以风机霍尔传感器出现故障后，检测不到风机运转的型号，当电脑板接收不到风机工作的信号时就会报警显示E4故障代码。

这时我们可以把风机拆卸下来，去热水器配件市场购买一个风机霍尔传感器更换上就可以了，万和热水器售后每年维修大量的万和E4故障，可以说百分九十九都是风机霍尔故障，但是也有主板出现故障的，但是这种几率非常小。 1.E4是因为热水器水箱内部管温出现故障。 2.故障代码意义 接口故障（E0）：温度传感器开路或短路；点火系统故障（E1）：点火结束后，还未检测到火焰；燃气不足或意外熄火（E2）：正常燃烧后，检测不到火焰。出水温度过高（E3）：出水温度超过80℃或干烧。应更换电池（E4）：电池电压低于2V。 3.原因分析及解决方法： A、热水器的水温过高造成的。可以适当调低水温。 B、热水器风压力开关发生故障，需要进行更换。 C、热水器的感温探头损坏，需要进行更换。 D、水流出现异常，应该是堵塞造成的，需要把异物清除。 E、热水器主板故障，需要找专业人员进行检测或者更换热水器主板。 F、热水器主要元件故障，需要进行检测，这种故障只能进行元件的更换。 以上就是一些主要的解决方法，希望能够帮到大家！

加密狗使用说明

Ikey使用说明 用户需要将ikey（加密狗）插入电脑的usb接口后才能使用云南省房地产估价管理系统。使用加密狗之前需要在电脑上先安装ikey的驱动程序。 用户可以在https://www.wendangku.net/doc/ed4412228.html,的登录页面下载到驱动程序，驱动程序根据用户使用的操作系统的不同，分为： 请用户根据自己的操作系统选择相应的驱动程序。 在安装驱动程序过程中，需要注意： a)下载下来的驱动程序，路径名请确保没有中文。 b)如果杀毒软件弹出安全警告，请点击放过或允许。 c)在安装驱动程序前，请确保加密狗没有插在电脑上。 下面介绍一下，驱动程序的安装： 1.在Windows2000或Windows2003或WindowsXP上安装加密狗驱动程序 1)驱动程序下载下来后，图标为 2)双击ikeyAll.exe，看到如下界面： 3)点击两个Next，进入如下界面:

4)点击“是“，就会看到如下界面（如果这过程中杀毒软件弹出安全警告，请点击允 许或放过）： 5)到这个界面，表示安装时成功的，如果这过程中杀毒软件弹出安全警告，请点击允 许或放过。 6)将加密狗插入电脑的usb接口，过一会，就会自动跳到以下的界面： 7)单击“Finish“，驱动程序就安装完成。 8)打开https://www.wendangku.net/doc/ed4412228.html,/Appraisal/index.jsp，如果浏览器出现下列提示： 9)则右键点击提示，如下图所示：

10)点击“运行加载项”，会出现下列提示： 11)点击“运行”，然后刷新网页（按F5），安装完成。 2.在WindowsVista系统上安装加密狗驱动程序 1)下载下来的是一个压缩包，图标为 2)将IKEYforVista.rar解压缩。 3)进入IKEYforVista\IKEYDRVR-32bit-4.0.0.1017，看到如下文件夹： 4)双击setup.exe安装，看到如下界面： 5)点击“Next”，看到如下界面：

电动机启动器

Description –Overload protection – trip class 10A –Phase loss sensitivity –Disconnect function –Temperature compensation from -25 … +55 °C –Adjustable current setting for overload protection –Suitable for three- and single-phase application –Trip-free mechanism –Clear switch position indication ON/OFF Order data MS116 screw terminal Setting range A Type Trip class Order code Pack- ing unit PCE Weight per PCE kg 0.10...0.16MS116-0.1610A1SAM250000R100110.225 0.16...0.25 MS116-0.2510A1SAM250000R100210.225 0.25...0.40MS116-0.410A1SAM250000R100310.225 0.40...0.63 MS116-0.6310A1SAM250000R100410.225 0.63...1.00 MS116-1.010A1SAM250000R100510.225 1.00...1.60 MS116-1.610A1SAM250000R100610.265 1.60... 2.50 MS116-2.510A1SAM250000R100710.265 2.50...4.00 MS116-4.010A1SAM250000R100810.265 4.00...6.30 MS116-6.310A1SAM250000R100910.265 6.30...10.0 MS116-1010A1SAM250000R101010.265 8.00...12.0 MS116-12 10A1SAM250000R1012 10.265 10.0...16.0 MS116-1610A1SAM250000R101110.265 16.0...20.0MS116-2010A1SAM250000R101310.310 20.0...25.0MS116-2510A1SAM250000R101410.310 25.0...32.0MS116-3210A1SAM250000R101510.310 Note: MS116 with pre-assembled auxiliary contact HKF1-11, please order as follow 1SAM250005Rxxxx Manual motor starters are electro-mechanical protection devices for the main circuit. They are used mainly to switch motors manually ON/OFF and protect them fuse less against short-circuit, overload and phase failures. Fuse less protection with a manual motor starter saves costs, space and ensures a quick reaction under short-circuit condition, by switching off the motor within milliseconds. Fuse less starter combinations are setup together with contactors.2 C D C 2 4 1 0 0 1 F 0 0 0 9 Approvals A cULus UL 508 K C B scheme E CCC* D GOST-R GOST-F ABS* P Lloyd’s Register* GL* DNV* L RMRS* Bureau Veritas* Marks a CE * Note: the marked approvals are still pending for MS116-20 (32)

雷诺尔JJR软起说明书

JJR系列软起动器用户手册

目录 安全注意事项………………………………………………………………………………………安装准备……………………………………………………………………………………………使用及环境条件……………………………………………………………………………………1．概述……………………………………………………………………………………………… 典型应用简介…………………………………………………………………………………… JJR系列软起动功能……………………………………………………………………………2．购入检查…………………………………………………………………………………………3．安装………………………………………………………………………………………………4．电路连接………………………………………………………………………………………… 4.1主回路……………………………………………………………………………………… 4.2控制端子…………………………………………………………………………………… 4.3控制电路端子连接………………………………………………………………………… 4.4主回路连接………………………………………………………………………………… 4.5基本电路框图和端子………………………………………………………………………5．键盘及显示说明…………………………………………………………………………………6．数据的设定………………………………………………………………………………………7．通电运行…………………………………………………………………………………………8．保护显示说明……………………………………………………………………………………9．软起动控制模式………………………………………………………………………………… 9.1限流型……………………………………………………………………………………… 9.2电压控制型………………………………………………………………………………… 9.3软停车曲线………………………………………………………………………………… 9.4不同起动方式的电流波形比较……………………………………………………………10．结构特点………………………………………………………………………………………附表一应用场合……………………………………………………………………………………JJR1000系列二次接线图……………………………………………………………………………JJR2000系列二次接线图……………………………………………………………………………

万和燃气热水器打不着火不打火点不着火的原因分析

万和燃气热水器打不着火不打火点不着火的原因分析 导读：万和热水器打不着火的原因一：燃气通路故障；燃气热水器不打火的原因二：水路故障；燃气热水器打不着火的原因三：电路系统故障；万和热水器打不着火的原因四：热水器机械故障。 万和燃气热水器打不着火的原因：燃气通路故障 燃气通路是首先要检查的第一步：万和热水器中电磁阀在不通电时是将燃气通路关闭的，它是靠热水器脉冲控制器将阀门打开通气后才能使热水器点着火，这个位置的故障率极高，但通常不是电磁阀本身故障造成的，多数是由于它未能得到供电而导致开不了阀，燃气不能到达燃烧器导致万和热水器打不着火； 万和燃气热水器打不着火的原因：水路故障 万和燃气热水器水路故障主要有进水口过滤网堵塞、水阀结垢、水箱铜管变形堵塞、水压低等。它们造成燃气热水器打不着火的共同点是热水器出水量很小（燃气热水器的正常启动水压是0.02MPa，如果水压过低热水器就无法启动）。老式强排热水器这个现象很明显，所以排除是否因为水路故障造成燃气热水器点不着火只需要观察出水量或水压是否过低。 万和燃气热水器打不着火的原因：电路系统故障 热水器电路部分涉及的配件较多,是燃气热水器打不着火故障原因查找的核心部分,包括漏电保插头、热水器电源控制盒、脉冲点火器、电磁阀、风机启动电容、风机、风压检测开关、微动开关或水流传感器开关、点火针、感应针、冷热水开关。 燃气热水器脉冲点火器发出工作信号传送至热水器电源控制盒,通过一条连接到风压检测开关的负压管,使风压检测开关工作,此返回到脉冲点火器开始连续放电和延时2秒吸开电磁阀通气即可点着火,感应针感应到火焰正常后即通过脉冲给出电磁阀持续的维持电压,使电磁阀保持在开启状态,燃烧器便可持续正常工作。任何一个环节出现故障都会导致燃气热水器点不着火。 万和燃气热水器打不着火的原因：热水器机械故障 水气联动装置主要由水阀内部水压提供动力,推动联动杆,同时打开电路部分和其中一级燃气密封通道,若水气联动装置出现故障整个电路部分都没办法工作,导致燃气热水器打不着火;风机部分若因风叶卡死或电机转速慢达不到风压检测开关的启动压力,脉冲点火器无法得风压检测开关的信号,也会导致燃气热水器点不着火。 检查总结：燃气热水器打不着火可以分为无点火声不点火和有点火声打不着火，常见原因就是电源问题、电磁阀故障、电点火器故障、点火针或感应瓷针故障等这几个方面。

万和热水器维修：不打火故障维修

万和热水器e3，一般是风压过大或者烟管堵塞，但是烟管一般不会堵塞，而是燃烧器的位置堵塞，造成风压过大，导致风压开关断开，从而引发e3代码故障。我刚好修好了家里热水器的e3故障，下面我就介绍一下方法吧。 第二个可能就是风压开关老化导致容易触发。于是我更换了风压开关，并把动作压力稍微调大一点，也就是风压开关上面的一个旋钮，往里面旋转就是增大压力。网上有些人说这个不能乱调，其实你自己可以把握，只要你调到不出现e3故障即可，然后往回调记录下出现e3故障的位置，然后再往顺时针调，直到不出现e3故障为止，不能太过，免得真正堵塞的时候也不能产生断开动作，调好后为了验证堵塞是否产生动作，关闭煤气，开水点火，然后马上堵住热水器的烟管排风口（先把烟管拆下来，然后直接用手捂住排风口也可以），如果马上显示e3，说明保护起作用。 至此，修好了e3故障。其实，一般热水器烟管是不会堵塞的，除非有老鼠爬进去在里面做窝了。一般都是燃烧器的换热片那里老化导致通风不畅，从而导

致风压增大。 如果你不知道风压开关是哪一个，建议你百度一下“风压开关”，有详细的原理和说明。至于你提到的距离远的出水温度高，说明你的热水器不是真正的恒温热水器，或者恒温不起作用了。我家的热水器刚好跟你相反，距离近的水温高，距离较远的另一个洗手间由于热水传输过程中降温了，所以水温感觉会比实际标示低一度左右。如果你的热水器出水量小反而温度高，而且是保持温度高，说明不是恒温热水器，这种现象只会发生在固定火力的热水器上面，因为火力是固定的，水量越小温度越高。 另外我还调节了下面图片中的蓝色电位器从电路板上标示的意思我估计是第二个电磁燃气比例阀的流量调节，适当调小一点，会降低一点风压。因为燃气空气比例是有程序控制的，把燃气轻微调小了，风压也有所改变。仅供参考，自

加密狗专业网络版安装说明

加密狗专业网络版安装说明 1．运行环境： 局域网必须连通完好。 操作系统：Windows XP 简体中文版；内存：1G以上； 硬盘空间：600 兆以上； CPU：Pentium IV 以上；发声设备：声卡、音箱等必备的发声设备。可接外设：盲文点显器、盲文刻印机、打印机 2．在局域网中指定一台电脑为服务器，服务器端程序和软件加密狗安装在这台电脑上。服务器加密狗应便于专人管理，一般人不易接近，以免加密狗丢失，造成阳光读屏软件不能运行。如果安装服务器的电脑，使用的是Windows XP2 操作系统，则应将系统自带的防火墙选择“例外”放行阳光软件或将防火墙关闭。关闭防火墙的操作如下：选择：开始—所有程序—控制面板—Windows 防火墙-

双击 Windows 防火墙： 关闭防火墙。点击“确定” 3．安装服务器端程序：将安装盘插入光驱，打开“专业网络版服务器”文件夹： 双击 Setup 。 4．. 显示安装画面：

若您的电脑上没有并口，系统会有如下提示，选择确定 5．插入加密狗。 6．显示完成画面：

7．在屏幕右下角检查网络狗服务程序： 8．用右键点击R。 10．打开服务管理器 11．若下图右边红圈内为红色，说明狗没有工作 12．刷新硬件狗。 点击文件，选择刷新硬件狗：

13．若下图右边红圈内为黄色，说明狗工作正常 若刷新后红圈内仍为红色，应将服务器卸载后重新安装 如果按照上述说明操作，客户端仍提示： 可能是局域网中服务器和客户端的IP 地址不在同一个段内，请先查看服

务器的 IP 地址，方法如下：用鼠标右键点击“网上邻居”的“属性”如下图： 在打开窗口的右边查看“本地联结”的“属性”如下图： 选中下图红框部分：

德力西新程序 CDJ1系列数字式电机软起动器说明书..

CDJ1系列数字式电机软起动器 用户手册 2013年6月（第三版）

安全注意事项： 使用前请仔细阅读CDJ1安装说明书。如果不认真阅读有关说明，违反有关安全规定，有可能影响软起动器的正常使用。 安装前的准备 安装CDJ1请准备以下工具：螺丝刀、剥线钳、板钳等。 1、安装之前，请务必阅读“安全注意事项”。 2、只有专业技术人员允许安装CDJ1。 3、必须保证电动机与CDJ1匹配合适，安装时，请务必按用户手册章程 操作。 4、不允许将输入端（L1、L2、L3）接到输出端（U、V、W）。 5、不允许软起动器输出端U、V、W线接电容器，否则会损坏起动器。 6、CDJ1安装后将输入和输出端的铜线鼻用绝缘胶带包好。 7、远程控制时必须锁定键盘控制。 8、软起动器外壳请牢固接地。 9、维修设备时，必须断开进线电源。 使用及环境条件 【进线电源】交流380V 50H z±10% 【适用电机】鼠笼式三相异步电动机 【起动频度】每小时不超过12次 【使用湿度】90%无霜结 【使用温度】-30℃～+55℃ 【使用场所】室内无腐蚀性气体无导电尘埃且通风良好 【振动标准】海拔在3000米以下，振动力装置0.5G以下 【使用类别】AC-53b 提醒用户 如长途运输软起动器，在使用前，请用户仔细检查主电路、控制电路接线螺丝有无松动须紧固。 CDJ1-S型75kW以下壁挂式，需用户自配断路器。

目录 一、概述 ..................................................................................................... - 1 - 二、购入检查 ............................................................................................. - 2 - 三、安装 ..................................................................................................... - 3 - 四、基本接线图 ......................................................................................... - 4 - 五、软起动器的工作原理 ......................................................................... - 8 - 六、键盘及显示说明 ................................................................................. - 8 - 七、结构尺寸 ........................................................................................... - 21 - 八、故障排除 ........................................................................................... - 24 - 九、二次接线图 ....................................................................................... - 25 - 十、附表 ................................................................................................... - 26 - 附录一：MODBUS通信协议 ................................................................. - 27 -

万和热水器常见故障及原因

不少人反馈，万和热水器使用一段时间后，会出现各种各种的故障，客户都认为是热水器买的不好，其实并不是。因为如果热水器没有正确安装或者使用不当时，是会出现故障的。本文主要针对万和热水器的常见故障原因及处理方法，给大家分析分析，以供参考。 原因1：燃气压力低：燃气管道堵塞、燃气管路压力低； 解决方法：自查燃气管道是否堵塞（可从燃气表具处接一根管道到热水器燃气进口处，直接与热水器相接，如热水器能正常工作即从表具到热水器进口处的管路有堵塞），请燃气公司检查燃气管路压力。 原因2：水流量过大：管道压力过大、管道口径太大； 解决方法：可关小进水管的阀门及提高热水器的设定温度。

原因3：设置不当，应调在高档或冬天，而现在调在中档或春秋档； 解决方法：按说明书上的使用方法正确设置。 现象二：水太烫 原因1：水压低、水流量小、水管堵塞； 解决方法：a.将水管调换到一定的口径；b.加装增压泵；c.清理热水器进水管过滤网；d.调整热水器上的水量调节到大；e.调换花洒，花洒眼应尽量大。 原因2：燃气压力过高主要体现在液化气（LPG）上； 解决方法：调换液化气的减压阀（必须是劳动牌），将燃气压力调至要求值。 原因3：设置不当，主要是将热水器设置在高温区造成。 解决方法：按说明书上的使用方法正确设置 现象三：热水器点燃后有一段冷水，重新开水后又有一段冷水; 原因：这主要是强排风热水器的特性，不是故障。强排风热水器是为了提高用户使用的安全性，在热水器点燃前设置了前清扫，在热水器熄火后进行后清扫，将热水器中原有的废气排出热水器内，所以造成重新开水后又有一段冷水出现，另外，由于用户的龙头到热水器出水管的距离长短，及热水器将冷水加热到热水需一定的时间，造成热水器点燃后有一段冷水的原因。用户可缩短该段时间，将热水器先设置在高温档，等水热后再将水温设置在需使用温度。 现象四：智能恒温系列热水器的常见故障代码 显示01不是故障代码，代表热水器已运行了30分钟，提醒用户注意使用安全。显示11、12、14、16、31、32、72、73、90等，以上数字显示都是热水器出现故障后的代码，都必须进行保修。 现象五：风机运转声音

如何使用U盘制作Windows系统开机加密狗图文教程

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黑龙江省投标企业加密锁使用方法

黑龙江省建设工程招投标监管系统 投标企业 用户手册 黑龙江省建设厅信息中心 二○一二年四月

目录 1登陆、退出系统 (2) 登陆 (2) 退出 (5) 2投标企业信息管理 (5) 3投标管理 (7) 投标 (7) 3.1.1公开招标工程投标 (7) 3.1.2 邀请招标工程投标 (10) 修改投标 (14) 取消投标 (18) 查看投标 (19) 查询投标 (20) 4项目成员信息管理 (22) 1登陆、退出系统 登陆 打开IE浏览器，在地址栏中输入“后回车，打开黑龙江工程招投标网站，如图所示：

图１.1-1 黑龙江工程招投标网首页 单击网站右侧“建设工程招投标监管系统”，打开黑龙江省建设工程招投标监管系统登陆界面，如图所示： 图１.1-２黑龙江工程招投标网首页

图１.1-３黑龙江省建设工程招投标监管系统登陆界面插入投标企业身份认证锁，单击“登录”按钮即可进入黑龙江省建设工程招投标监管系统完成登录，如图所示系统界面： 图１.1-４黑龙江省建设工程招投标监管系统界面

系统界面分为三个区域，上部记载有当前用户登陆信息，左侧为系统功能菜单，右侧为工作面版用于显示操作功能菜单后的相关信息，详见上图标注。 退出 单击系统界面右上角的“退出”按钮，即可退出系统。 图１.2-1 黑龙江省建设工程招投标监管系统界面 2投标企业信息管理 此功能模块用于投标企业信息维护操作。 单击“投标企业基本信息”功能菜单，打开企业基本信息编辑页面，如图所示：

图投标企业基本信息编辑页面 填写企业基本信息后,单击“保存”按钮，保存投标企业信息。 相应资质库中已有企业信息，单击“确定”按钮，将企业数据同步即可，如图所示： 图２投标企业基本信息编辑页面 注：添加的企业信息（非同步资质系统信息）、资质信息、项目成员信息须省级审核通过后才可进行投标。

万和热水器说明书

万和热水器说明书 Company number：【WTUT-WT88Y-W8BBGB-BWYTT-19998】

万和热水器怎么样 万和热水器怎么样现在市场上的热水器数不胜数，人们想要在众多热水器中选择自己心仪的一款，就必须的对热水器有所了解。万能热水器是许多人都会选择的一个大牌子，但许多人对万能热水器又不怎么了解，下面由我为大家解答万和热水器质量怎么样万和热水器品牌怎么样万和热水器的分类是怎样万和热水器价格怎么样等 一、万和热水器品牌怎么样 万和于93年，成立于广东顺德，经过十九年的发展耕耘，目前是国内生产规模最大的燃气具研发制作企业，也是国内首个提倡和推动中国五金制品协会燃气用具的分会理事长。公司在研发节能环保的技术上，曾受到国务院总理温家宝的肯定和赞扬。 万和以“燃气具专家”为品牌定位，生产万和燃气热水器、万和燃气灶具、万和燃气壁挂炉、万和燃气烧烤炉、万和燃气空调、万和燃气取暖器等燃气具产品并与之相配套的万和电热水器、万和消毒碗柜、万和吸油烟机等厨卫电器产品，以及太阳能、热泵热水器等新能源产品和空气能+燃气、太阳能+燃气、电能+燃气等能源集成热水系统。 二、万和热水器分类 1、万和燃气热水器 万和燃气热水器怎么样 万和燃气热水器为广东万和新电气股份有限公司亚丁旗下品牌，多年来专注燃气具的研究和专业打造。万和燃气热水器开创了全自动燃气热水器时代，获省科技进步三等奖，万和燃气热水器在2002年获得中国名牌产品称号，多年被评定为中国名牌，其产品技术处于国内领先水平。 万和燃气热水器的价格 万和燃气热水器的性价比。万和燃气热水器的价格在市场中应该算是知足的，从几百到几千都是为满足人们的不同需求而设计的，在质量上有保障，有良好的维修服务和售后服务，一直都是大众信赖的产品。 万和燃气热水器产品 万和户外式燃气热水器：w24a 、w16a 万和平衡式燃气热水器：g12v1凝炼冷凝恒温型、2c 超薄智能 万和强排式燃气热水器：q24bv107 万和烟道式燃气热水器：d8c 2、万和电热水器 万和电热水器怎么样 万和电热水器是万和集团主营业务的重要组成部分。万和96年开始进军电热水器领域，经过十余年稳健发展，万和在电热水器的研发、生产、质量管理、营销、服务等各方面均已十分成熟，产品安全技术、节能技术、内胆技术和智能控制技术已经达到了国际先进水平，是《家用贮水式电热水器节能产品认证技术要求》的起草单位之一。目前万和电热水器已经形

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图3 共享版界面 下面我们分别说明发布版模式和共享版模式的加密方法。 4 首先是发布版模式如图2。发布版模式下没有次数，天数，时间等的设置，只有密码设 置，主要应用于保护自己模式的设置，防止别人更改。点击“写入/Write In”按钮，进入密码写入界面。如图4。如果我们是第一次写入密码，那么就直接勾选修改密码选项，在新密码下面的前一个输入栏里输入4位数字，在后面的输入栏里输入4数字，这样完成了密码的初步设定，然后在确认密码下的输入栏内重复输入上面设定的密码，然后点击确认，完成密码的设定。如果我们是修改密码的话，那么我们首先要在密码写入界面上方的输入密码下的正确输入栏内输入以前设定的密码，然后在勾选修改密码，输入新的密码。否则修改密码就会失败，并出现“密码错误”提示信息。 图4 密码写入界面 5 共享版的密码设定，如图3是共享版的界面。在这里我们首先要设定好限制使用的次数， 天数，时间，直接在后面的输入栏内直接输入即可。这里注意：我们所设定的时间，天数是以软件运行所在电脑的内部时钟为准的，我们编写之前一定要注意，我们所使用的电脑的时间是否准确。设定好这些后点击“写入/Write In”按钮，进入密码写入界面。 共享版的密码写入界面与发布版是一样的，操作也相同，可参考步骤4进行操作。

电机软启动器的主接线种类及常见故障

电机软启动器的主接线方法： 1、在线型： 所有软启动器的控制器都有电动机过载保护，当软启动器在线运行时软启动器的控制器能对电机进行过载保护，不要加装热过载继电器。由于经过可控硅后的电流谐波电流非常大，所以不能加装电子式热过载继电器，否则热继的误动作使系统不能正常工作。由于可控硅比较昂贵而且更换困难，为了保护可控硅要用快速熔断器防止软启动器下口发生短路烧毁可控硅，软起动器的上口不加接触器，在停车后将软启动器的电源断开。 2、旁路型： 旁路运行软启动器，离开旁路接触器是无法运行的，所以在两种主接线方案里都有。对于软启动器上口的接触器的作用和在线运行方式下作用相同在此不再重复。着重说明的是热继电器，把它安方在旁路接触器的下口，不通过起动电流最好，尤其是电子热继电器，由于经过软启动器后电流谐波很大能干扰电子热继电器误动作而使电机停车。另外因为可控硅的短时工作没必要安装快速熔断器，所以在主结线方案里没有加装快速熔断器。 3、内置旁路型： 它的主接线和在线型的大致相同，唯一的优点是因为可控硅的短时工作没必要安装快速熔断器。 电动机的过载保护是有软启动器的控制器实现的，它不仅在功能和性能上超过电子热继电器，而且不会因主回路的谐波电流及外界的干扰而误动作。 电机软启动器的常见故障 目前国内的软起动器生产厂家很多，大都是旁路型的，产品的可靠性与世界知名品牌相比差距越来越小，市场份额已经超过国外品牌。 软启动器的故障大体分如下几种： 1、电动机起不来： 电动机起不来的原因大致分两种情况：

一是六只可控硅的其中一只触发不可靠或是不导通，此时一相电路通过的是半波直流，电动机的两相绕组通过的直流对电动机起到了制动作用，不仅电机起不来，严重的还会烧毁电机和可控硅。 二是启动参数或启动曲线不合适造成电机起不来，这是常见故障。前者在使用过程当中会发生，但几率低于接触器的故障率。后者多发生在第一次投运调试，调试好以后就不会出现。多数的厂家不会出现此现象，启动程序性能好，出厂值设定的适用性强。只有很少厂家的产品需要厂家自己去调试。 2、可控硅烧毁： 可控硅击穿或爆炸，此类故障不分国内外品牌，因厂家而易，但都比接触器的故障率低，而且主要问题出现在饼式可控硅的安装工艺上。 3、控制器烧损： 相对于软启动器来讲，控制器烧毁故障是最严重的。有的厂家此类故障造成的返修率已超过30%。进口的或合资的厂家此类问题不多见。主要是控制器的电源和触发电路以及输入电路三部分容易烧毁。 4、软启动器误动作： 电动机在运行的装态下因软起动器受干扰而停机在停止状态下因软起动器受干扰而起动是时有发生，前者较普遍，后者只有两个品牌发生过。究其原因，一是产品质量问题，二是和线路布局有关。 5、软启动器内部插接件接触不良： 软启动器内部插接件选用本来不是问题，这是国内厂家容易忽略的问题，经常出现故障。

万和热水器e3不打火解决办法

家里的万和热水器e3，一般是风压过大或者烟管堵塞，但是烟管一般不会堵塞，而是燃烧器的位置堵塞，造成风压过大，导致风压开关断开，从而引发e3代码故障。下面我们就一起来看看怎么解决。 第二个可能就是风压开关老化导致容易触发。于是我更换了风压开关，并把动作压力稍微调大一点，也就是风压开关上面的一个旋钮，往里面旋转就是增大压力。网上有些人说这个不能乱调，其实你自己可以把握，只要你调到不出现e3故障即可，然后往回调记录下出现e3故障的位置，然后再往顺时针调，直到不出现e3故障为止，不能太过，免得真正堵塞的时候也不能产生断开动作，调好后为了验证堵塞是否产生动作，关闭煤气，开水点火，然后马上堵住热水器的烟管排风口（先把烟管拆下来，然后直接用手捂住排风口也可以），如果马上显示e3，说明保护起作用。

至此，修好了e3故障。其实，一般热水器烟管是不会堵塞的，除非有老鼠爬进去在里面做窝了。一般都是燃烧器的换热片那里老化导致通风不畅，从而导致风压增大。 如果你不知道风压开关是哪一个，建议你百度一下“风压开关”，有详细的原理和说明。 至于你提到的距离远的出水温度高，说明你的热水器不是真正的恒温热水器，或者恒温不起作用了。我家的热水器刚好跟你相反，距离近的水温高，距离较远的另一个洗手间由于热水传输过程中降温了，所以水温感觉会比实际标示低一度左右。如果你的热水器出水量小反而温度高，而且是保持温度高，说明不是恒温热水器，这种现象只会发生在固定火力的热水器上面，因为火力是固定的，水量越小温度越高。 另外我还调节了下面图片中的蓝色电位器（min）从电路板

上标示的意思我估计是第二个电磁燃气比例阀的流量调节，适当调小一点，会降低一点风压。因为燃气空气比例是有程序控制的，把燃气轻微调小了，风压也有所改变。仅供参考，自己研究，个人理解，由于不清楚厂家具体设计原理，所以没有权威的科学根据，仅仅是推测。如果调节错误会导致e1意外熄火故障，请谨慎。 快益修以家电、家居生活为主营业务方向，提供小家电、热水器、空调、燃气灶、油烟机、冰箱、洗衣机、电视、开锁换锁、管道疏通、化粪池清理、家具维修、房屋维修、水电维修、家电拆装等保养维修服务。

加密狗安装说明(必看)

请不要使用360或者卡巴斯基杀毒软件，这两个对系统干扰比较大。如果在安装第6步的时候提示有病毒，大家请放心这个没有问题的，关闭杀毒软件安装就可以了，同时全部安装完整后，在杀毒软件中设置广联达安装目录为免杀目录或者加入白名单。 本驱动适用人群： 1.必须是B锁客户（购买价格为145一个地区，185元2个地区的客户的狗。） 2.必须是2010年5月25日后汇款购买的客户使用或者在2010年5月25日后按照我们的提示把狗给我们发回升级过的客户使用。 3.正常安装所有的广联达软件后，最后安装6驱动。注意正版驱动全部用154(去广联达服务新干线随便下载一个就行了，不用分地区。)，不推进使用156或者157版驱动.新版软件目前没必要用这个两个版本的驱动。 有了这个驱动，开始买狗提供的光盘上的第6步驱动就不用装了，完全用现在的替换,复制狗驱动我们会不定期更新，请注意关注。 安装新驱动后，或者平时使用时软件提示一堆英文错误或者提示找不到狗，请按照如下方式解决： 1.直接删除C:\Program Files\Common Files目录下的Grandsoft Shared目录. 2.直接删除C:\Program Files目录下的Grandsoft Installation Information 目录 3.直接删除广联达的安装目录. 4.重装软件。 如果上述方法还是不行，那就只能格式化C盘重装XP，不要使用覆盖安装XP,否则没用。 所谓问题，就是提示一堆英文的语句之类的话或者提示没有找到狗。至于提示什么没装定额库，没有规则之类的都是客户自己的安装问题，这个自己检查。 如果想知道您的这个狗都支持什么软件请进入“开始”-“程序”-“广联达加密锁程序”-“查看已够产品程序”，这里面的所有内容都是您的狗所支持的，内容相当丰富，会给你一个惊喜的。 需要说明的问题； (1)复制狗绝不是一次性购买，就不在需要服务的，复制狗也要同正版一样升级，其中包括2个含义，第一个是在狗不变的情况下，狗的驱动（也就是上面说的6

万和热水器说明书

万和热水器怎么样 万和热水器怎么样?现在市场上的热水器数不胜数，人们想要在众多热水器中选择自己心 仪的一款，就必须的对热水器有所了解。万能热水器是许多人都会选择的一个大牌子，但许 多人对万能热水器又不怎么了解，下面由我为大家解答万和热水器质量怎么样？万和热水器 品牌怎么样？万和热水器的分类是怎样？万和热水器价格怎么样等 一、万和热水器品牌怎么样 万和于93年，成立于广东顺德，经过十九年的发展耕耘，目前是国内生产规模最大的燃 气具研发制作企业，也是国内首个提倡和推动中国五金制品协会燃气用具的分会理事长。公 司在研发节能环保的技术上，曾受到国务院总理温家宝的肯定和赞扬。 万和以"燃气具专家"为品牌定位，生产万和燃气热水器、万和燃气灶具、万和燃气壁挂 炉、万和燃气烧烤炉、万和燃气空调、万和燃气取暖器等燃气具产品并与之相配套的万和电 热水器、万和消毒碗柜、万和吸油烟机等厨卫电器产品，以及太阳能、热泵热水器等新能源 产品和空气能+燃气、太阳能+燃气、电能+燃气等能源集成热水系统。 二、万和热水器分类 1、万和燃气热水器 ? 万和燃气热水器怎么样？ 万和燃气热水器为广东万和新电气股份有限公司亚丁旗下品牌，多年来专注燃气具的研 究和专业打造。万和燃气热水器开创了全自动燃气热水器时代，获省科技进步三等奖，万和 燃气热水器在2002年获得中国名牌产品称号，多年被评定为中国名牌，其产品技术处于国内 领先水平。 ? 万和燃气热水器的价格 万和燃气热水器的性价比。万和燃气热水器的价格在市场中应该算是知足的，从几百到 几千都是为满足人们的不同需求而设计的，在质量上有保障，有良好的维修服务和售后服务， 一直都是大众信赖的产品。 ? 万和燃气热水器产品 万和户外式燃气热水器：w24a 、w16a 万和平衡式燃气热水器：g12v1凝炼冷凝恒温型、2c 超薄智能 万和强排式燃气热水器：q24bv107 万和烟道式燃气热水器：d8c 2、万和电热水器 ? 万和电热水器怎么样？ 万和电热水器是万和集团主营业务的重要组成部分。万和96年开始进军电热水器领域， 经过十余年稳健发展，万和在电热水器的研发、生产、质量管理、营销、服务等各方面均已 十分成熟，产品安全技术、节能技术、内胆技术和智能控制技术已经达到了国际先进水平， 是《家用贮水式电热水器节能产品认证技术要求》的起草单位之一。目前万和电热水器已经 形成年产200多万台的规模，市场占有率从2001年开始跻身于电热水器的第一集团，销售规 模以50%以上速度逐年增长，在众多电热水器品牌中脱颖而出，成为电热水器行业仅有的几 个中国名牌之一。 ? 万和电热水器维修 ：水不热 原因1：燃气压力低：燃气管道堵塞、燃气管路压力低。 解决方法：自查燃气管道是否堵塞(可从燃气表具处接一根管道到热水器燃气进口处，直 接与热水器相接，如热水器能正常工作即从表具到热水器进口处的管路有堵塞)，请燃气公司 检查燃气管路压力。

可逆电动机启动器

南京工程学院 课程设计说明书（论文）题目综合实训实习 课程名称可逆电动机起动器 院(系、部、中心) 专业 班级 学生姓名 学号 设计地点 指导教师 工程基础实验与训练中心 设计起止时间：2011年11 月 8日至2011年11月 19日

1设计任务................................................................................................ ３2设计过程：............................................................................................ ３ 2.1 方案描述，需求分析.................................................. ３ 2.2 方案结构图.......................................................... ３ 2.3 PLC选型分析........................................................ ４ 2.4 电气原理图.......................................................... ５ 2.5 电器柜布局图........................................................ ６ 2.6 I/O地址分配表...................................................... ７ 2.7 程序流程图.......................................................... ７ 2.8 PLC程序............................................................ ９3安装、调试说明 ................................................................................... ９ 3.1设置临时IP .......................................................... ９ 3.2通讯测试.......................................................... １１4设计中的问题分析 ........................................................................... １２5设计总结............................................................................................ １２6主要参考资料 ................................................................................... １３ 教科书：.............................................................. １３参考书：.............................................................. １３