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PubMed2005

Myelodysplasic syndromes: a comprehensive review.

Myelodysplastic syndromes (MDS) are a set of oligoclonal disorders of hematopoietic stem cells characterized by ineffective hematopoiesis that manifest clinically as anemia, neutropenia, and/or thrombocytopenia of variable severity. The result often is transfusion-dependent anemia, an increased risk of infection or hemorrhage, and a potential to progress to acute myelogenous leukemia (AML). Although progression to acute leukemia can lead to death in patients with MDS, many deaths are consequences of cytopenias and marrow failure in the absence of transformation. Approximately 2/3 of patients succumb to the disease within 3-4 years after presentation, and individuals with high-risk MDS generally survive about 1 year. Given that the disease is more prevalent in the elderly who often have comorbid conditions, the current treatment of MDS consists mainly of supportive care. Curative treatments are restricted to younger, healthy individuals with histocompatible (HLA)-matched donors for allogenic transplant or those able to undergo intensive chemotherapeutic regimens. However, understanding of the pathophysiology of MDS and identification of potential cellular and molecular targets in recent years has led to novel therapeutic approaches. Encouraging results using these heterogeneous therapeutic approaches alone or in combination in Phase I and II trials, have, in turn, called into question previous classification systems and have confirmed the need for an all-encompassing molecular, diagnostic and prognostic staging system.

Anemia, Refractory↗
PubMed1994

[A progress in the diagnosis of malignant lymphoma].

Malignant lymphoma is usually divided into Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL) according to the biological characteristics. Although the exact nature of HD is still unclear, NHL is well known to be a neoplasm of monoclonal and malignant B- or T-lymphocytes. Nowadays, the classification of pathologic type in HD seems to be settled in the Rye classification. On the other hand, in NHL the LSG classification has been fixed routinely in Japan and the Working Formulation originating in the USA has been used internationally after some historical confusion. As a recent trend in lymphoma diagnosis, the introduction of immunological and molecular biological techniques has had an impact on the previous concept and classification of malignant lymphoma based mainly on morphological criteria. In this article, recent progress in the diagnosis of malignant lymphoma, mainly NHL, including the analysis of immunophenotype and immunogenotype (intragenic and intergenic gene rearrangement) is briefly described.

Female↗
PubMed2000

[Hodgkin lymphoma. Classification and pathogenesis].

In the last few years our understanding of Hodgkin's lymphoma (HL) has enormously progressed. Molecular analysis has revealed that almost all cases of this disease are clonal B cell neoplasms, therefore the term Hodgkin's lymphoma instead of Hodgkin's disease is being proposed in the new WHO classification. Lymphocyte predominance HL (LPHL) differs in respect to morphology, immunophenotype and clinical features from the other forms of HL and represents its own distinct entity. In addition to morphologic features (nodularity, presence of L&H cells) the immuno-phenotype of tumor cells is most important in establishing a diagnosis of LPHL, and particularly in differentiating LPHL from the other forms of HL. The remaining forms of HL (nodular sclerosis, mixed cellularity, lymphocyte depletion) display a mostly identical antigen profile and similar clinical characteristics, they are therefore grouped together in the REAL classification under the heading of classical HL. Recent immuno-histological analysis have revealed that one third of HL cases, which formerly were classified as LPHL, display the immuno-phenotype of classical HL. These cases are now considered to represent examples of classical HL and termed nodular lymphocyte rich classical HL. According to retrospective clinico-pathological analysis, the biological behaviour of this newly identified form of classical HL also differs from LPHL. Differences between classical HL and LPHL also occur on the molecular level. Thus LPHL often displays ongoing mutations of the immunoglobulin genes, and the tumor cells express immunoglobulin protein and transcripts, while these characteristics are absent in classical HL. Since peripheral B cells that do not express immunoglobulins die from apoptosis, these findings imply that the regulation of apoptosis is defective in Hodgkin and Sternberg Reed cells. Several laboratories are currently working intensely to clarify the defective apoptosis pathway in HL.

B-Lymphocytes↗
PubMed1980

Purification and characterization of Aleutian disease virus.

Virus was isolated from infected mink organs by a combination of tissue homogenization, fluorocarbon extraction and ultracentrifugation. The final preparation was analysed by crossed immunoelectrophoresis and electronmicroscopy. Virions had a capsid diameter of 22 nm. Preparative agarose electrophoresis separated virions from contaminating ferritin. Crossed immunoelectrophoresis of virus gave a single precipitate with sera from infected mink. Crossed immunoelectrophoretic analysis with intermediate gels showed that a part of the virus preparation was complexed with antibody. Serum from a certain mink was found to contain precipitating antibody to (poly)nucleotid. Virus and virus-antibody complexes were found to focus at pH 4.0-4.4 in isoelectric focusing. In SDS-polyacrylamide gel-electrophoresis the main virus protein was found to have a molecular weight of 69000. This study gives further support to the classification of aleutian disease virus as a parvovirus.

Aleutian Mink Disease Virus↗
PubMed2003

Molecular analysis of transitional cell carcinoma using cDNA microarray.

The incidence of transitional cell carcinoma (TCC), the fourth most common neoplasm diagnosed in men, is rising. Despite the development of several noninvasive diagnostic tests, none have gained full recognition by the clinicians. Gene expression profiling of tumors can identify new molecular markers for early diagnosis and disease follow-up. It also allows the classification of tumors into subclasses assisting in disease diagnosis and prognosis, as well as in treatment selection. In this paper, we employed expression profiling for molecular analysis of TCC. A TCC-derived cDNA microarray was constructed and hybridized with 19 probes from normal urothelium and TCC tissues. Hierarchical clustering analysis identified all normal urothelium samples to be tightly clustered and separated from the TCC samples, with 29 of the genes significantly induced (t-test, P<10(-5)) in noninvasive TCC compared to normal urothelium. The identified genes are involved in epithelial cells' functions, tumorigenesis or apoptosis, and could become molecular tools for noninvasive TCC diagnosis. Principal components analysis of the noninvasive and invasive TCC expression profiles further revealed sets of genes that are specifically induced in different tumor subsets, thus providing molecular fingerprints that expand the information gained from classical staging and grading.

Adult↗
PubMed2004

[Current classification of gliomas].

The histologic classification of gliomas, which is based on oligodendroglial- or astrocytic-like morphology distinguishes gliomas in astrocytic tumors (grade 1- pilocytic astrocytoma to grade 4- glioblastoma), oligodendroglial and mixed tumors (grade 2 and 3) according to cell differenciation, cellularity, nuclear atypia, mitotic activity, necrosis and microvascular proliferation. Prognosis is correlated to grade. Based on interobserver variability, the histological diagnosis is often highly subjective and should be interpreted within the context of clinical and radiological data. Newly identified good prognostic markers (1p and 19q loss in oligodendrogliomas) and new molecular techniques such as microarray may further refine the existing classification.

Brain Neoplasms↗
PubMed2001

Histopathology (International Neuroblastoma Pathology Classification) and MYCN status in patients with peripheral neuroblastic tumors: a report from the Children's Cancer Group.

BACKGROUND: The International Neuroblastoma Pathology Classification (International Classification), which was established in 1999, is significant prognostically and is relevant biologically for the evaluation and analysis of patients with neuroblastic tumors (NTs). MYCN amplification is a known molecular marker for aggressive progression of NTs. These have been used together as important prognostic factors to define risk groups for patient stratification and protocol assignment. METHODS: A total of 628 NTs (535 neuroblastomas [NBs]); 21 ganglioneuroblastoma, intermixed [GNBi]; 9 ganglioneuromas [GN]; and 63 ganglioneuroblastoma, nodular [GNBn]) from the Children's Cancer Group studies were evaluated histologically (favorable histology [FH] tumors vs. unfavorable histology [UH] tumors) according to the International Classification and were tested molecularly for MYCN status (amplified vs. nonamplified). Four tumor subsets (FH-nonamplified, FH-amplified, UH-nonamplified, and UH-amplified) were defined by histopathology and MYCN status, and their prognostic effects were analyzed. Detailed analysis between morphologic indicators (grade of neuroblastic differentiation and mitosis-karyorrhexis index [MKI]) and MYCN status was done by using tumors in the NB category. RESULTS: There were 339 FH-nonamplified tumors (5-year event free survival [EFS], 92.1%); 8 FH-amplified tumors (EFS, 37.5%); 172 UH-nonamplified tumors (EFS, 40.9%); and 109 UH-amplified tumors (EFS, 15.0%). The prognostic effects on patients with tumors in the four subsets were independent from the factors of patient age and disease stage (P < 0.0001). MYCN amplification was seen almost exclusively in tumors of the NB category, and no patients with tumors in either the GNBi category or in the GN category and only two patients with tumors in the GNBn category had amplified MYCN. Among the patients with tumors in the NB category, patients with FH-nonamplified tumors (309 patients) had an excellent prognosis, and patients with UH-amplified tumors (107 patients) had the poorest clinical outcome in any age group. The prognosis for children with UH-nonamplified tumors (111 patients) was poor when they were diagnosed at age > 1.5 years. It was also noted that patients with UH-amplified tumors (median age, 2.14 years) were diagnosed at a significantly younger age compared with the patients with UH-nonamplified tumors (median age, 3.55 years). Histologically, MYCN-amplified tumors lacked neuroblastic differentiation regardless of the age of patients. MYCN amplification also was linked generally to increased mitotic and karyorrhectic activities. However, MKI classes in patients with MYCN-amplified tumors varied significantly, depending on the age at diagnosis, and younger patients had higher MKI classes. CONCLUSIONS: The combination of histopathologic evaluation and MYCN status distinguishes four clinical and biologic tumor subsets in patients with NTs. MYCN amplification seems to be the powerful driving force for preventing cellular differentiation regardless of patient age and for increasing mitotic and karyorrhectic activities in an age dependent manner.

Adolescent↗
PubMed2004

Phenotype-determining genes in inflammatory bowel disease.

Inflammatory bowel disease (IBD) has traditionally been categorized as either ulcerative colitis or Crohn's disease on the basis of clinical, radiological and histological criteria. Within these diseases however, significant heterogeneity is observed, suggesting the existence of phenotypic subtypes, based on features such as location and behaviour of disease. Evidence for a possible genetic basis for these subgroups emerged in the 1990s from epidemiological studies in multiply affected families. Recent advances in our understanding of the relationship between genotype and phenotype in IBD now challenge traditional clinical classifications, promising a taxonomy of disease based on precise molecular, rather than ambiguous clinical definitions. While many of the genes remain unidentified, the emerging data suggest that IBD comprises a heterogeneous family of oligogenic inflammatory disorders in which the specific clinical manifestations of disease in any individual are determined by the interaction of genetic and environmental factors. These data have highlighted both the importance and difficulties of classifying patients into accurately defined clinical subgroups, and suggest that a genetic basis for the observed disease heterogeneity may account for the discrepant findings from earlier genetic studies. Despite the considerable insights offered to investigators these advances have yet to impact on the clinical management of patients.

Genetic Predisposition to Disease↗
PubMed2005

High molecular mass proteome of androgen-independent prostate cancer.

We made a comprehensive study of protein expression of androgen-independent (AI) prostate cancer by means of agarose two-dimensional gel electrophoresis (agarose 2-DE) followed by liquid chromatography-tandem mass spectrometric analysis. The agarose 2-DE method being good at separating high molecular mass (HMM) proteins and alkaline ones, so we were able to successfully reveal differences between the proteomes of androgen-dependent (AD) tumors and those of AI tumors. During the creation of agarose 2-DE protein maps, we successfully identified 295 proteins (91.0%) out of 324 spots excised in total. Excluding redundant and mouse serum proteins, we considered the remaining 225 proteins to be related to the cancer. We divided the 225 cancer-related proteins into HMM and low molecular mass (LMM) groups by their molecular mass being above or below 80 kDa. Functional classification of the proteins in these two groups showed clear differences between the two: more than half (54.8%) of the HMM proteins, but less than one-third (29.1%) of the LMM ones were classified among transcription- or translation-related proteins. Eighteen proteins were regulated when the tumor progressed from an AD to an AI state. Five of these proteins, including antioxidant protein 2, superoxide dismutase 1, thioredoxin peroxidase, GTP-binding protein beta chain homolog, and the ha1225 gene product, had a function to protect cells against oxidant stress-induced apoptosis. We suggest that prevention against oxidative stress is one of the key points for prostate cancer to obtain androgen independency. We also found proteins that had not been previously reported in prostate cancer by use of genomic or conventional 2-DE based proteomic approaches. The proteomic approach, using agarose 2-DE focused on HMM proteins, has the capability to find novel biomarkers of prostate cancer.

Androgens↗
PubMed2006

Similarity networks of protein binding sites.

An increasing attention has been dedicated to the characterization of complex networks within the protein world. This work is reporting how we uncovered networked structures that reflected the structural similarities among protein binding sites. First, a 211 binding sites dataset has been compiled by removing the redundant proteins in the Protein Ligand Database (PLD) (http://www-mitchell.ch.cam.ac.uk/pld/). Using a clique detection algorithm we have performed all-against-all binding site comparisons among the 211 available ones. Within the set of nodes representing each binding site an edge was added whenever a pair of binding sites had a similarity higher than a threshold value. The generated similarity networks revealed that many nodes had few links and only few were highly connected, but due to the limited data available it was not possible to definitively prove a scale-free architecture. Within the same dataset, the binding site similarity networks were compared with the networks of sequence and fold similarity networks. In the protein world, indications were found that structure is better conserved than sequence, but on its own, sequence was better conserved than the subset of functional residues forming the binding site. Because a binding site is strongly linked with protein function, the identification of protein binding site similarity networks could accelerate the functional annotation of newly identified genes. In view of this we have discussed several potential applications of binding site similarity networks, such as the construction of novel binding site classification databases, as well as the implications for protein molecular design in general and computational chemogenomics in particular.

Animals↗
PubMed2001

On the status of the Serranid fish genus Epinephelus: evidence for paraphyly based upon 16S rDNA sequence.

Historically, attempts to elucidate evolutionary relationships among members of the genus Epinephelus (Teleostei: Serranidae), commonly known as groupers, have been hindered by the overwhelming number of species (98, sensu stricto), a pan global distribution, and the lack of morphological specializations traditionally used in ichthyological classification. To date, no comprehensive phylogenetic study, morphological or molecular, to evaluate the monophyly of this genus has been presented. In this study, previous hypotheses regarding the relationships among the American grouper species and the allied genera were evaluated by examination of mitochondrial DNA sequences of the 16S ribosomal DNA region. A 590-bp region of the 16S rDNA gene was amplified using a universal primer pair for 42 serranid species, including members of the genera Epinephelus, Mycteroperca, and Paranthias from the New World and selected Indo-Pacific congeners. Maximum-parsimony criteria and neighbor-joining analysis dispute the monophyly of the American Epinephelus species as previously hypothesized. The data support the monophyly of Cephalopholis only with the inclusion of the morphologically distinct Paranthias and the monophyly of Mycteroperca with the inclusion of the Indo-Pacific Anyperodon leucogrammicus.

Animals↗
PubMed2001

Alpha-adrenoceptor subtypes.

Different studies have led to our present knowledge of the membrane receptors responsible for mediating the responses to the endogenous catecholamines. These receptors were initially differentiated into alpha - and beta-adrenoceptors. Alpha-adrenoceptors mediate most excitatory functions, and were in turn differentiated in the 1970s into alpha(1)- and alpha(2)-adrenoceptors. The alpha(1)-adrenoceptor type usually mediates responses in the effector organ. The alpha(2)-adrenoceptor type is located presynaptically and regulates the release of the neurotransmitter but it is also present in postsynaptical locations. Both alpha-adrenoceptors are important for the control of vascular tone, but we now know that neither alpha(1)- nor alpha(2)-adrenoceptors constitute homogeneous groups. Each alpha-adrenoceptor type can be subdivided into different subtypes and in this review we have turned our attention to these. The alpha(1)- and the alpha(2)-adrenoceptor subtypes were previously defined pharmacologically by functional and binding studies, and later they were also isolated and identified using cloning methods. In fact, the study of alpha-adrenoceptors was revolutionized by the techniques of molecular biology which permitted us to establish the present classification. The present classification of alpha(1)-adrenoceptors stands as follows: alpha(1A)-adrenoceptor subtype (cloned alpha(1c) and redesignated alpha(1a/c)), alpha(1B)-adrenoceptor subtype (cloned alpha(1b)) and alpha(1D)-adrenoceptor subtype (cloned alpha(1d) and redesignated alpha(1a/d)). It has not been easy to establish the distribution of these alpha(1)-adrenoceptor subtypes in the various organs and tissues, or to define the functional response mediated by each one in the different species studied. Nevertheless it seems that the alpha(1A)-adrenoceptor subtype is more implicated in the maintenance of vascular basal tone and of arterial blood pressure in conscious animals, and the alpha(1B)-adrenoceptor subtype participates more in responses to exogenous agonists. It has also been observed that the expression of the alpha(1B)-adrenoceptor subtype can be modified in pathological situations and particular attention has been paid to the regulation of expression of this receptor. The present classification of alpha(2)-adrenoceptors stands as follows: alpha(2A/D)-adrenoceptor subtype (today it is accepted that the alpha(2A)-adrenoceptor subtype and the alpha(2D)-adrenoceptor subtype are the same receptor but they were identified in different species: the alpha(2A) in human and the alpha(2D) in rat); alpha(2B)-adrenoceptor subtype (cloned alpha(2b)) and alpha(2C)-adrenoceptor subtype (cloned alpha(2c)). Today we know that the alpha(2A/D)- and alpha(2B)-adrenoceptor subtypes in particular control arterial contraction, and that the alpha(2C)-adrenoceptor subtype is responsible above all for venous vasoconstriction. We also know that the alpha(2 A/D)-adrenoceptor subtype fundamentally mediates the central effects of the alpha(2)-adrenoceptor agonists. Despite the validity of the above-mentioned classification of the alpha(1)- and alpha(2)-adrenoceptors, it seems clear that the contractions of a large number of tissues including smooth muscle are mediated by more than one alpha-adrenoceptor subtype. Moreover, few ligands recognise only one alpha-adrenoceptor subtype and the lack of specifity in the different drugs for each one limits their administration in vivo and their therapeutic use.

Adrenergic alpha-Agonists↗
PubMed1998

Taxonomy of African horse sickness viruses.

Nine distinct genera are currently recognised within the virus family Reoviridae, which include a total of 63 virus groups or species (species = virus group = electropherotype or serogroup), comprising 214 virus serotypes or subtypes, as well as 20 provisional types or subtypes, most of which (149 + 9 tentative) are assigned to the genus Orbivirus [5, 9, 16]. The 19 species of orbiviruses (serogroups), were established principally on antigenic (serologic) grounds but many of these placements have been supported by molecular analyses. This introductory paper defines the taxonomy and classification of these viruses and establishes guidelines for use in other paper to be presented at this symposium and elsewhere.

African Horse Sickness↗
PubMed1991

Biology of pediatric peripheral neuroectodermal tumors.

The pediatric peripheral neuroectodermal tumors which include neuroblastoma, peripheral neuroepithelioma and Ewing's sarcoma may correspond to distinct neural crest cell lineages or tumors arrested at different stages of neural crest development. Besides a brief commentary on the salient clinical features of these tumors, this review examines how cell and molecular biological studies have contributed to a re-classification of these tumors. The differentiation of these tumors is reviewed with a particular emphasis on retinoic acid induced differentiation of neuroblastoma as a model to identify genes important in controlling cell growth, suppression of tumorigenicity and induction of differentiation.

Adolescent↗
PubMed2003

Protein aggregation/folding: the role of deterministic singularities of sequence hydrophobicity as determined by nonlinear signal analysis of acylphosphatase and Abeta(1-40).

The problem of protein folding vs. aggregation was investigated in acylphosphatase and the amyloid protein Abeta(1-40) by means of nonlinear signal analysis of their chain hydrophobicity. Numerical descriptors of recurrence patterns provided the basis for statistical evaluation of folding/aggregation distinctive features. Static and dynamic approaches were used to elucidate conditions coincident with folding vs. aggregation using comparisons with known protein secondary structure classifications, site-directed mutagenesis studies of acylphosphatase, and molecular dynamics simulations of amyloid protein, Abeta(1-40). The results suggest that a feature derived from principal component space characterized by the smoothness of singular, deterministic hydrophobicity patches plays a significant role in the conditions governing protein aggregation.

Acid Anhydride Hydrolases↗
PubMed2003

Posttransplantation lymphoproliferative disorders.

Over the last decade, much has been learned about the nature of PTLD. The pivotal role of EBV infection in most cases has been established, and the pathologic description of lesions has been simplified in the current classification. It seems likely that further understanding of the molecular pathology may lead to greater ability to define optimal treatment regimens and prognosis. Quantitative PCR techniques for EBV have enhanced the capability for early diagnosis of EBV infection and PTLD and have proved useful tools for monitoring response to therapy. In particular, this technique seems to help predict when reintroduction of immunosuppression should be instituted. Several exciting new therapies are on the horizon, including use of monoclonal antibodies against B-cell surface antigens and the development of cellular therapies, such as the use of EBV-specific cytotoxic T-cell infusions. Such strategies offer the promise of controlling abnormal B-cell proliferation without the risk of allograft rejection, because the host alloresponse is not enhanced by these therapies. The role of chemotherapy and the optimal regimens required remain to be defined fully. Understanding of the cause, behavior, and optimal treatment for EBV-negative PTLD remains limited, partly because of the rarity of these lesions. There is an increasing level of interest in PTLD among clinical and basic investigators and recognition of the need for multicenter trials to define optimal prevention and treatment strategies. A degree of optimism seems warranted.

Antiviral Agents↗
PubMed1997

Relevance of cytogenetic and fluorescent in situ hybridization analyses in the clinical assessment of soft tissue sarcoma.

Soft tissue sarcomas are a heterogeneous group of malignant tumors displaying a wide range of clinical presentations, morphological features, and biological behaviors. These characteristics and the recent development of differentiated treatment regimens for the different types of soft tissue sarcomas call for refined histological classification using additional ancillary approaches such as cytogenetic and molecular genetic analyses. We coupled classical cytogenetics and fluorescent in situ hybridization (FISH) on both metaphases and interphase nuclei to show the feasibility of this approach to characterize tumor type-specific chromosome rearrangements in soft tissue sarcomas of different histotype. In 35 cases analyzed, we detected the presence of specific chromosome rearrangements such as t(X;18) in synovial sarcoma (SS), t(12;16) in myxoid liposarcoma (MLS), t(11;22) in peripheral primitive neuroectodermal tumors (pPNET), t(2;13) in alveolar rhabdomyosarcoma (ARMS) and ring chromosomes in dermatofibrosarcoma protuberans (DFSP). In several cases, the presence of these cytogenetic rearrangements was of help for a differential diagnosis. The FISH analysis using painting probes not only confirmed the cytogenetic results but also allowed the identification of tumor-specific chromosome changes in those cases presenting low mitotic index or with poor quality chromosomes. Moreover, in the absence of analysable metaphases, FISH was successfully performed on interphase nuclei. Taken together, these results indicate both the diagnostic and clinical relevance of a molecular cytogenetic analysis in the study of soft tissue sarcomas.

Biomarkers, Tumor↗
PubMed2002

Extractable organic matter in PM10 from LiWan district of Guangzhou City, PR China.

PM10 (particulate matter with aerodynamic diameter <10 microm) samples were collected at LiWan District of Guangzhou, PR China during April and July 2001 using a high volume air sampler to determine the distributions of homologous compounds and biomarkers. Polycyclic aromatic hydrocarbons (PAHs) including non-alkylated PAHs, methyl-alkylated PAHs, and some PAHs containing S/O atoms and n-alkanes were measured using gas chromatography/mass spectrometry analysis. The sigma(n)-alkane and sigmaPAHs ranged from 26.4 to 719.2 ng/m3 and 7.4 to 159.4 ng/m3, respectively. A seasonal fluctuation was clearly evident with higher concentrations occurring during the colder months (April). In addition, some compositional differences are observed for the organic compounds in samples collected from different heights above ground level. Higher sites had a significant contribution from vascular plant wax. The presence of petroleum products with no carbon number preference, pristane, phytane and a significant unresolved complex mixture (UCM) with unresolved to resolved components ratio (U/R) of 6.2-13.2 confirm the petroleum component. The relative distribution of n-alkanes and the values of molecular diagnostic ratio, such as carbon preference index (CPI) values ranging from 1.0 to 1.4 (for the whole range of n-alkanes), indicated the importance of petroleum and diesel residues and gasoline emissions, as well as the minor contribution of n-alkanes emitted directly from epicuticular waxes. Indeed, the percent contribution of leaf 'wax' n-alkanes (5.2-19.4%) indicated a low contribution of biogenic sources. The fossil fuel biomarkers, hopanes and steranes were observed in the PM10 samples, which indicate a petroleum origin. The distribution pattern of PAHs was characteristic of anthropogenic emissions. Coupling carbon number maximum (Cmax), CPI, U/R values, molecular marker and molecular diagnostic ratios for alkanes and PAHs revealed a classification of natural biogenic and anthropogenic components of atmospheric aerosols. These analyses support the conclusion that vehicular emission was the major source of organic compounds during the study period, while the contribution of epicuticular waxes emitted by terrestrial plants was minor.

Air Pollutants↗