Biomedical subjects

Na Liu

Publications and source records attributed to Na Liu.

At least 55 records · Page 3Linked to original sources

PubMed2004

Control of Atm-/- thymic lymphoma cell proliferation in vitro and in vivo by dexamethasone.

AIM: Ataxia telangiectasia (A-T) is an autosomal recessive disease in humans caused by mutations in the Atm (A-T mutated) gene. The disease involves multiple organ systems, and is associated with a high incidence of leukemias and lymphomas that develop in childhood. We have reported previously that thymic lymphoma development in Atm knockout (Atm-/-) mice is associated with elevated spontaneous DNA synthesis in thymocytes, and that dexamethasone (Dex) attenuates the elevated DNA synthesis and prevents thymic lymphoma development. The primary objectives of the present study were (1) to investigate possible mechanisms underlying the tumor-suppressing effect of Dex on Atm-/- thymic lymphoma cells, and (2) to determine whether Dex is an effective tumor-suppressing treatment in mice bearing transplanted Atm-/- thymic tumors. METHODS: Establishment of a number of Atm-/- thymic lymphoma (ATL) cell lines from Atm-/- mice, cell proliferation assays, cell cycle analyses, Western blotting and Hoechst nuclear staining were used to analyze the effects of Dex on Atm-/- thymic lymphoma cells. Atm-/- tumor cells were transplanted into the right flanks of Atm+/+ mice prior to the initiation of Dex treatment. RESULTS: Atm-/- tumor cells were highly sensitive to Dex, both in culture and in vivo as ectopic tumors in mice. In cultured ATL-1 cells, Dex induced apoptosis, arrested the cell cycle at the G1 phase and downregulated NF-kappaB and multiple cell cycle regulators, while upregulating the NF-kappaB inhibitor IkappaBalpha. In Atm+/+ mice transplanted subcutaneously with ATL-1 cells, tumor growth was either prevented completely or significantly suppressed by Dex treatment. CONCLUSIONS: Our findings identify potential mechanisms by which Dex affects the proliferation and survival of ATL-1 cells in culture, and provide evidence that Dex can suppress the proliferation of Atm-/- thymic lymphoma cells growing in the body. Together these results add to our earlier published data suggesting that the cellular pathways regulated by Dex may be promising therapeutic targets for prevention and treatment of thymic lymphomas in A-T individuals.

Animals↗

PubMed2004

Reversal of the malignant phenotype of gastric cancer cells by inhibition of RhoA expression and activity.

PURPOSE: The small GTPase RhoA has been implicated in the regulation of cell morphology, motility, and transformation, but the role of RhoA protein in the carcinogenesis of gastric cancer remains unclear. In the present study, we have analyzed the expression status of the RhoA protein in human gastric cancer cells and tissues and investigated the possible involvement of RhoA in regulating the malignant phenotype of gastric cancer cells. EXPERIMENTAL DESIGN: RhoA expression was analyzed by immunohistochemistry and Western blot in gastric cancer tissues and cell lines. The RhoA-specific small interfering RNA (siRNA) vector was designed and constructed. We examined the role of RhoA in the malignant phenotype of gastric cancer cells by using siRNA knockdown and dominant-negative RhoA mutant suppression of endogenous RhoA activity. RESULTS: RhoA was found frequently overexpressed in gastric cancer tissues and cells compared with normal tissues or gastric epithelial cells. RhoA-specific siRNA could specifically and stably reduce RhoA expression up to 90% in AGS cells. Both RhoA-specific siRNA and dominant-negative RhoA expressions could significantly inhibit the proliferation and tumorigenicity of AGS cells and enhance chemosensitivity of the cancer cells to Adriamycin and 5-fluorouracil. CONCLUSION: RhoA may play a critical role in the carcinogenesis of gastric cancer, and the interference of RhoA expression and/or activity could provide a novel avenue in reversing the malignant phenotype of gastric cancer cells.

Agar↗

PubMed2004

Suppression of the cell proliferation in stomach cancer cells by the ZNRD1 gene.

Zinc ribbon domain-containing 1 (ZNRD1), a transcription-associated gene, was recently found to be downregulated in human gastric cancer tissues as compared to the matched adjacent nonneoplastic tissues. In this study, we constructed the siRNA eukaryotic expression vectors of ZNRD1 and transfected them into normal gastric epithelial cells (GES-1). We also introduced the ZNRD1 gene into gastric cancer cells that do (SGC7901) and do not (AGS) express ZNRD1 endogenously. GES-1 cells stably transfected with the ZNRD1-RNAi were found to exhibit significantly quicker proliferation than empty vector transfectants. AGS cells stably transfected with the ZNRD1 cDNA exhibited significantly decreased growth rate as compared to control vector transfectants, whereas SGC7901 cells did not. Furthermore, ZNRD1 suppresses growth of AGS cells in soft agar and tumor formation in athymic nude mice. This study clearly demonstrates that ZNRD1 may play an important role in the control of human gastric cancer development by regulating cell proliferation. These results provide new insights into the function of ZNRD1 and further validate ZNRD1 as a potential therapeutic target in gastric cancer.

Animals↗

PubMed2004

Inhibition of endothelial cell proliferation by targeting Rac1 GTPase with small interference RNA in tumor cells.

Hypoxia-induced angiogenesis plays an important role in the malignancy of solid tumors. A number of recent studies including our own have suggested that Rho family small GTPases are involved in this process, and Racl, a prominent member of the Rho family, may be critical in regulating hypoxia-induced gene activation of several angiogenesis factors and tumor suppressors. To fur-ther define Racl function in angiogenesis and to explore novel approaches to modulate angiogenesis, we employed the small interference RNA technique to knock down gene expression of Racl in gastric cancer cell line AGS that expresses a high level of Racl. Both the mRNA and protein levels of Racl in the AGS cells were decreased dramatically after transfection with a Racl-specific siRNA vector. When the conditioned medium derived from the Racl downregulated AGS cells was applied to the human endothelial cells. it could significantly inhibit the cell proliferation. Further study proved that, VEGF and HIF-la, two angiogenesis promoting factors, were found to be downregulated whereas p53 and VHL, which are tumor suppressors and angiogenesis inhibitors. were upregulated in the Racl siRNA transfected cells. Our results suggest that Racl may be involved in angiogenesis by controlling the expression of angiogenesis-related factors and provide a possible strategy for the treatment of tumor angiogenesis by targeting the Racl GTPase.

Cell Division↗

PubMed2004

Reversal of multidrug resistance of gastric cancer cells by downregulation of TSG101 with TSG101siRNA.

We have previously identified tumor susceptibility gene101 (TSG101), overexpressed in vincristine-resistant human gastric adenocarcinoma cell line SGC7901/VCR using a modified subtractive hybridization method and Western blot. In the present study, we constructed two siRNA eukaryotic expression vectors of TSG101 and transfected them into SGC7901/VCR cells to examine whether the down-regulation of TSG101 increased cell sensitivity towards chemotherapeutic drugs. After transfection, the expression of TSG101 was dramatically decreased in TSG101 siRNA transfectants compared with that in parental cells and empty vector control cells. The down-regulation of TSG101 could significantly enhance the sensitivity of SGC7901/VCR cells to vincristine and adriamycin. The capacity of cells to efflux adriamycin markedly decreased in TSG101 siRNA transfectants. These observations suggested that the siRNA constructs of TSG101 we made could effectively down-regulate the expression of TSG101 and reverse the resistant phenotype of gastric cancer cells. The preliminary study suggested that TSG101 might play an important role in multidrug resistance of gastric carcinoma.

Antineoplastic Agents↗

PubMed2004

Overexpression of ZNRD1 promotes multidrug-resistant phenotype of gastric cancer cells through upregulation of P-glycoprotein.

ZNRD1, a new zinc ribbon gene, has been previously identified as an upregulated gene in a multidrug-resistant gastric cancer cell line SGC7901/VCR comparing to its parental cell SGC7901 by subtractive hybridization and RT-PCR. The antisense nucleic acid for ZNRD1 could enhance adriamycin accumulation in SGC7901/VCR cells and sensitize SGC7901/VCR cells to vincristine. The present study aims to explore the role of ZNRD1 in multidrug resistance in gastric cancer cells. Upregulation of ZNRD1 protein in SGC7901/VCR cells was confirmed by Western blot and immunocytochmical staining. ZNRD1 was genetically overexpressed in SGC7901 cells by gene transfection. It was found that overexpression of ZNRD1 could sensitize SGC7901 cells to P-glycoprotein (P-gp)-related anticancer drugs (vincristine, adriamycin, etoposide) but not to P-gp-nonrelated drugs (5-fluorouracil and cisplatin), which was accompanied with significantly decreased adriamycin accumulation and retention and increased adriamycin releasing in SGC7901 cells. Verapamil, an inhibitor for P-gp, could reverse the effects of ZNRD1 on drug sensitivity and drug accumulation in SGC7901 cells to a great extent. Western blot and Northern blot revealed that overexpression of ZNRD1 could upregulate P-gp at both protein and mRNA levels. Together, these results suggest that overexpression of ZNRD1 could promote multidrug-resistant phenotype of gastric cancer cells through upregulation of P-gp.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2004

Expression of seven main Rho family members in gastric carcinoma.

Rho GTPases were previously shown to have an important role in cancer development and progression, including cell transformation, proliferation, invasion, metastasis, and angiogenesis. However, there is still little information available on the clinical significance of Rho GTPases expression in human cancer specimens. In the present study, we systemically investigated the mRNA expression levels of seven main members RhoA, RhoB, RhoC, Rac1, Rac2, Rac3, and Cdc42 of Rho family using semi-quantitative reverse transcription-PCR in 53 patients with gastric carcinoma and 7 gastric cancer cell lines. The total and activities of RhoA, Rac1 and Cdc42 in 5 gastric cancer cell lines were also examined. The mean mRNA expression levels of RhoA and Rac1 in gastric cancer tissue specimens were significantly higher than those in the adjacent non-tumorous tissue specimens (p < 0.01). The higher expression of RhoA was significantly correlated with higher TNM stage (p < 0.05) as well as with pooly differentiated histological type (p < 0.05) of gastric carcinoma. The increased expression of Rac1 was related to higher TNM stages of gastric carcinoma (p < 0.05). The expression levels of mRNA, total protein and activities of RhoA and Rac1 in 7 gastric cancer cell lines were all higher than that in gastric mucosal epithelial cell line GES-1. These findings indicate that RhoA and Rac1 may play important roles in the carcinogenesis and progression of gastric carcinoma.

Adult↗

PubMed2004

Activation of endoplasmic reticulum stress signaling pathway is associated with neuronal degeneration in MoMuLV-ts1-induced spongiform encephalomyelopathy.

Temperature-sensitive mutant of Moloney murine leukemia virus-TB (MoMuLV-ts1)-mediated neuronal death in mice is likely due to both loss of glial support and release of cytokines and neurotoxins from ts1-infected glial cells. Cytotoxic mediators present in ts1-induced spongiform lesions may generate endoplasmic reticulum (ER) stress, which has been implicated in the pathogenesis of a variety of neurodegenerative diseases. We investigated whether ER stress signaling is involved in ts1-mediated neuronal loss in the brain of infected mice. ts1-infected brainstems were found to show significant increases in phosphorylation of the double-stranded RNA-dependent protein kinase-like ER kinase and eukaryotic initiation factor 2-alpha. In addition, increased expression of growth arrest DNA damage 153 (GADD153), glucose-regulated protein 78, and caspase-12 were accompanied by increases in processing of caspase-12 and its downstream target, caspase-3. All of these events are markers of ER stress. We observed that GADD153 and cleaved caspase-3 were present in degenerative neurons in the lesions of infected mice, but not in uninfected controls. Phosphorylated calmodulin-dependent protein kinase II-alpha was significantly increased, and was coexpressed with GADD153 in a large proportion of neurons undergoing early and advanced degenerative changes. Finally, neuronal degeneration in spongiform lesions was associated with increase in calcium (Ca(2+)) accumulation in mitochondria. Together, these results suggest that ts1 infection-mediated neuronal degeneration in mice may result from activation of ER stress signaling pathways, presumably initiated by perturbation of Ca(2+) homeostasis. Our findings highlight the importance of the ER stress signaling pathway in ts1 infection-induced neuronal degeneration and death.

Animals↗

PubMed2004

Possible involvement of both endoplasmic reticulum- and mitochondria-dependent pathways in MoMuLV-ts1-induced apoptosis in astrocytes.

The Moloney murine leukemia virus (MoMuLV)-ts1 retrovirus, a naturally occurring mutant of MoMuLV-TB, causes a neuroimmunodegenerative syndrome in mice. The authors show here that ts1 triggers apoptosis in immortalized astrocytes, C1 cells, and primary cultured astrocytes, and that this apoptosis is caused by endoplasmic reticulum (ER) stress resulting from accumulation of the viral envelope preprotein gPr80(env). In ts1-infected C1 cells, an unfolded protein response was identified by activation of the ER-resident transmembrane protein kinase PERK, an event that leads to hyperphosphorylation of eIF2 alpha, up-regulation of GRP78, increased amounts of GADD153/CHOP, and cleavage of procaspase-12. Up-regulation of GRP78 and cleavage of procaspase-12 were also detected in primary cultured astrocytes infected with ts1. In ts1-infected C1 cells, ER stress was followed by mitochondrial stress, detected as mitochondrial transmembrane potential dissipation, cleavage of procaspase-9, and induction of activated caspase-3. In the brainstems of ts1-infected mice, activated caspase-3 and damaged mitochondria were identified in astrocytes within areas showing spongiform degeneration. Together the data imply that both ER stress- and mitochondrial stress-related apoptotic pathways are involved in ts1-induced astrocyte death.

Animals↗

PubMed2004

Preparation and characterization of a novel monoclonal antibody specific to human ZNRD1 protein.

We have efficiently generated the first monoclonal antibody (MAb) against the human ZNRD1 protein, a transcription-associated protein, consisting of two zinc ribbon domains. Hybridomas were screened by indirect enzyme-linked immunosorbent assay (ELISA) using either purified 6 x His-ZNRD1fusion protein or purified 6 x His-OS-9 fusion protein as a control. One MAb named H6 (IgG(1)), effective in detecting the recombinant and cellular protein, was characterized by ELISA and Western immunoblotting. Thus, it binds to native ZNRD1 protein and should be useful in studies of ZNRD1 protein function and expression. By Western immunoblotting analysis of 16 patients with gastric cancer using the MAb, we found ZNRD1 protein was more overexpressed in incision margin than in carcinoma tissue. The results showed that ZNRD1 might be a novel modifier in gastric carcinogenesis.

Animals↗

PubMed2004

Activation of transcription factor Nrf-2 and its downstream targets in response to moloney murine leukemia virus ts1-induced thiol depletion and oxidative stress in astrocytes.

The neuroimmunodegenerative syndrome that develops in mice infected with ts1, a mutant of Moloney murine leukemia virus, resembles human AIDS. Both ts1 and human immunodeficiency virus type 1 infect astrocytes, microglia, and oligodendrocytes but do not infect neurons. Oxidative stress has been implicated in the neuropathology of AIDS dementia and other neurodegenerative diseases. We report here that ts1 infection of astrocytes (both transformed C1 cells and primary cultures) also induces thiol (i.e., glutathione and cysteine) depletion and reactive oxygen species (ROS) accumulation, events occurring in parallel with viral envelope precursor gPr80(env) accumulation and upregulated expression of endoplasmic reticulum chaperones GRP78 and GRP94. Furthermore, ts1-infected astrocytes mobilize their thiol redox defenses by upregulating levels of the Nrf-2 transcription factor, as well its targets, the xCT cystine/glutamate antiporter, gamma-glutamylcysteine ligase, and glutathione peroxidase. Depleting intracellular thiols by treating uninfected astrocytes with buthionine sulfoximine (BSO), a glutathione synthesis inhibitor, or by culturing in cystine-deficient medium, also induces ROS accumulation, activates Nrf-2, and upregulates Nrf-2 target gene expression in these astrocytes. Overexpression of Nrf-2 in astrocytes specifically increases expression of the above thiol synthesis-related proteins. Further treatment with BSO or N-acetylcysteine in transfected cells modulates this expression. Thiol depletion also accelerates cell death, while thiol supplementation promotes survival of ts1-infected cells. Together, our results indicate that ts1 infection of astrocytes, along with ts1-induced gPr80(env) accumulation, endoplasmic reticulum stress, thiol depletion, and oxidative stress, accelerates cell death; in response to the thiol depletion and oxidative stress, astrocytes activate their Nrf-2-mediated thiol antioxidant defenses, promoting cell survival.

Amino Acid Transport System y+↗

PubMed2004

[The expression and possible function of RhoA in human gastric cancer cell lines].

OBJECTIVE: To study the expression and possible function of RhoA in human gastric cancer cell lines. METHODS: The expression of RhoA in human gastrointestinal cancer cell lines was detected by Western blot. Antisense plasmid of RhoA was constructed by pGEFL and transferred into gastric cancer cell line AGS by lipofectamine. Cell survival was examined by MTT assays, and cell cycle was detected by flow cytometry. RESULTS: The expression of RhoA protein in 10 different kinds of human cancer cell lines was much higher than that in immortalized human intestinal epithelial cell line. After being transfected with antisense RhoA, with the decrease in RhoA protein expression, the growth rate of AGS was inhibited, and the number of cells in S phase was increased by 14%. CONCLUSION: RhoA is overexpressed in many human cancer cell lines. Some of the malignant characteristics of a gastric cancer cell line can be partially reversed by inhibiting RhoA expression.

Antisense Elements (Genetics)↗

PubMed2004

[Expression of RhoC in gastric cancer cell lines and construction and identification of RhoC-specific siRNA expression vector].

AIM: To study the expression of RhoC in human gastric cancer cell lines and to construct and identify the RhoC-specific siRNA expressing vector. METHODS: The expression of RhoC in human gastric cancer cell lines was detected by Western blot. According to the computer aided design(CAD),RhoC-specific siRNA gene was synthesized and cloned into the expression vector mU6pro. The constructed RhoC-siRNA was transiently transfected into high-metastatic gastric cancer cell line AGS and the inhibition effect of RhoC-siRNA on expression of RhoC in AGS cells was detected using Western blot. RESULTS: The expression level of RhoC was up-regulated in high metastatic cells lines. Double enzyme digestion analysis and DNA sequencing confirmed that the RhoC-specific siRNA expression vector was constructed successfully. RhoC expression in AGS cells was specifically suppressed after transfection of RhoC-siRNA. CONCLUSION: The RhoC-specific siRNA expression vector has been successfully constructed, which may provide a novel applicable strategy for gene therapy of gastric cancer.

Cell Line, Tumor↗

PubMed2004

[Studies on the change of intercellular connection and the appearance and function of ectodesmata-like structure in garlic clove during the dormancy development].

The characteristics of intercellular connection have been observed during the dormancy development of garlic by the transmission electron microscope (TEM). The results indicated that the appearances of the different states of intercellular connection were physiological adaptation to the development of garlic clove during storage. Ectodesmata-like existed at the wall boundary between the declining tissue and the living cells in the garlic during germination period. By Confocal Laser Scanning Microscopy (CLSM) combined with fluorescence probe, 457Da Lucifer Yellow (LYCH) which was impermeable to the membrane, could enter the living parenchyma cell through symplastic route. The result proved that ectodesmata-like structure, which may be recognized as the modified plasmodesata, still retained physiological activity during a certain time and function as the channels of the symplastic transport of nutrient.

Garlic↗

PubMed2004

[Expression and significance of DARPP-32 in gastric carcinoma].

OBJECTIVE: To investigate the significance of DARPP-32 protein expression in gastric carcinoma tissue and cell lines. METHODS: The expression of DARPP-32 protein in normal gastric mucosa and gastric carcinoma tissue was evaluated by immunohistochemical staining using streptavidin-biotin complex technique. The expression in gastric carcinoma tissue and cell lines was evaluated by Western blotting. RESULTS: The expression rate of DARPP-32 protein in gastric adenocarcinoma tissue (92.7%) was significantly higher than that in normal gastric mucosa (52.6%, P < 0.05). There was no significant association between DARPP-32 protein expression and degree of tumor differentiation, local invasion and distant metastasis. As compared with adjacent non-carcinomatous gastric mucosa, both DARPP-32 and its truncated isoform t-DARPP were overexpressed in gastric adenocarcinoma tissue (t = 2.45, P = 0.015); and t-DARPP overexpression was more frequently seen. Expression of DARPP-32 and t-DARPP could also be detected in human gastric cancer cell lines. The expression of DARPP-32 protein was obviously reduced in SGC7901 drug-resistant cell strains. CONCLUSIONS: DARPP-32 is overexpressed in gastric carcinoma. It may play an important role in gastric carcinogenesis. The underlying signal pathways in neoplastic gastric epithelium may also be related to the multi-drug resistance property of gastric cancer cells.

Adenocarcinoma↗

PubMed2004

[Expressions and activities of Rho GTPases in hypoxia and its relationship with tumor angiogenesis].

OBJECTIVE: To study the expressions and activities of Rho GTPases in hypoxia and its relationship with tumor angiogenesis. METHODS: Three tumor cell lines were used in this study: gastric cancer cell lines AGS, SGC7901 and hepatocellular carcinoma cell line HepG2. Expression level of Rac1 mRNA was detected by semi-quantitative RT-PCR. Activity of Rac1 was determined by pull-down assay and expression of HIF-1alpha, VEGF, p53 and PTEN protein was detected by Westernblot. RESULTS: The expression level of Rac1 mRNA was significantly increased in hypoxia compared to normoxia. Pull-down assay showed that hypoxia-induced activity of Rac1 was elevated in a time-dependent manner and climaxed at 3 hours. The expressions of HIF-1alpha and VEGF protein were up-regulated, while those of PTEN and p53 protein were down-regulated. CONCLUSION: These results indicate that hypoxia enhances Rac1 expression which might be involved in tumor angiogenesis by reacting with hypoxia-responsive genes.

Cell Hypoxia↗

PubMed2004

[Effects of sperm and oocyte quality control on intracytoplasmic sperm injection (ICSI) in goats].

ABSTRACT Effects of sperm and oocyte quality control on the efficiency of ICSI of in vitro matured goat oocytes were studied in this paper. The results showed that when injected intracytoplasmically, spermatozoa from caput, corpus and cauda epididymidis resulted in similar rates of fertilization, cleavage and morulae/blastocysts, but when injected subzonally, spermatozoa from caput and corpus gave rise to significantly lower rates of fertilization and embryo development than spermatozoa from the cauda epididymidis and ejaculates. When dead spermatozoa collected from semen that had been preserved in different ways were used for ICSI, those dead from liquid storage at 20 degrees C for 24 h gave rise to the best, but those dead from liquid storage at 5 degrees C for 15 days produced the poorest fertilization and embryo development. When spermatozoa were treated with different concentrations of Triton X-100 before ICSI, significantly higher rates of fertilization, cleavage and morulae/blastocysts were obtained with 0.0005% Triton X-100 than with other concentrations and manual immobilization. Oocytes were classified as of good and poor qualities by treatment in hypertonic sucrose solution, and rates of fertilization and embryo development were significantly higher in the good than in the poor oocytes after ICSI. Post-injection activation of oocytes with either A23187 or ionomycin/6-DMAP significantly increased the rates of fertilization, cleavage and morulae/blastocysts after ICSI. It is therefore concluded that (i) epididymal maturation mainly endowed spermatozoa with the capacity to fuse with the egg plasma membrane; (ii) different methods of semen storage caused different impairment of sperm fertilizing capacity; (iii) pre-injection treatment of spermatozoa with proper concentrations of Triton X-100 might be used to replace manual immobilization for ICSI; (iv) oocyte quality was a major factor influencing the efficiency of ICSI; (v) post-injection activation treatment of oocytes improved fertilization and embryo development after ICSI.

Animals↗

PubMed2004

[Determination of soluble organic fraction in diesel exhaust particulates by gas chromatography/mass spectrometry].

The soluble organic fractions (SOF) in diesel exhaust particulates have been extracted with ultrasonic separator and analyzed by gas chromatography/mass spectrometry (GC/ MS). The GC/MS conditions were as follows: an HP SE-50 capillary column (30 m x 0.2 mm i. d. x 0.2 microm); temperature programming started at 100 degrees C, holding for 2.0 min, then increased to 160 degrees C at a rate of 4.0 degrees C /min, then to 250 degrees C at 8 degrees C/min, finally, kept at 250 degrees C for 31.75 min; boiling chamber temperature 260 degrees C; helium gas as carrier; chapiter pressure 45 kPa; sample size 1 microL; electron impact energy of mass spectrometer 70 eV; multiplier voltage 1 800 V; mass range 300 - 500 u. The results showed that under exhaust temperature, about 80% of SOF in particulates were normal or isomeric alkanes with carbon numbers from 9 to 28. The rest of the fractions of SOF were polycyclic aromatic hydrocarbons (homologs of indene, fluorene, phenanthrene, naphthalene etc.) and other organic substances. It is demonstrated that most of SOF were from unburned diesel and engine oils. The testing conclusion should be useful in designing and evaluating particulate filters.

Air Pollutants↗