Critical Reviews in Clinical Laboratory Sciences (CRIT REV CL LAB SCI )

Publisher: Taylor & Francis


Topics: Medical biochemistry; Microbiology and infectious disease; Laboratory hematology; Clinical hematology; Molecular biology; Cellular biology; Toxicology; Advances in pharmacology.

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  • Other titles
    Critical reviews in clinical laboratory sciences, Chemical Rubber Company critical reviews in clinical laboratory sciences, CRC critical reviews in clinical laboratory sciences
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    Periodical, Internet resource
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    Journal / Magazine / Newspaper, Internet Resource

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Taylor & Francis

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    • STM: Science, Technology and Medicine
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    • Publisher last contacted on 25/03/2014
    • 'Taylor & Francis (Psychology Press)' is an imprint of 'Taylor & Francis'
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Publications in this journal

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    [Show abstract] [Hide abstract]
    ABSTRACT: While iron is an essential trace element required by nearly all living organisms, deficiencies or excesses can lead to pathological conditions such as iron deficiency anemia or hemochromatosis, respectively. A decade has passed since the discovery of the hemochromatosis gene, HFE, and our understanding of hereditary hemochromatosis (HH) and iron metabolism in health and a variety of diseases has progressed considerably. Although HFE-related hemochromatosis is the most widespread, other forms of HH have subsequently been identified. These forms are not attributed to mutations in the HFE gene but rather to mutations in genes involved in the transport, storage, and regulation of iron. This review is an overview of cellular iron metabolism and regulation, describing the function of key proteins involved in these processes, with particular emphasis on the liver's role in iron homeostasis, as it is the main target of iron deposition in pathological iron overload. Current knowledge on their roles in maintaining iron homeostasis and how their dysregulation leads to the pathogenesis of HH are discussed.
    Critical Reviews in Clinical Laboratory Sciences 02/2007; 44(5-6):413-59.
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    ABSTRACT: Owing to their high turnover, the intestinal mucosal cells have a particularly high requirement for polyamines. Therefore, they are an excellent charcol for the study of polyamine function in rapid physiological growth and differentiation. After a cursory introduction to the major aspects of polyamine metabolism, regulation, and mode of action, we discuss the contribution of the polyamines to the maintenance of normal gut function, the maturation of the intestinal mucosa, and its repair after injuries. Repletion of cellular polyamine pools with (D,L)-2-(difluoromethyl)ornithine has considerably improved our understanding of how the polyamines are involved in the regulation of normal and neoplastic growth. Unfortunately, the attempts to exploit polyamine metabolism as a cancer therapeutic target have not yet been successful. However, the selective inactivation of ornithine decarboxylase appears to be a promising chemopreventive method in familial adenomatous polyposis. Presumably, it relies on the fact that ornithine decarboxylase is a critical regulator of the proliferative response of the protooncogene c-myc, but not of its apoptotic response.
    Critical Reviews in Clinical Laboratory Sciences 02/2007; 44(4):365-411.
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    ABSTRACT: Citrulline is a non-standard amino acid that can be incorporated into proteins only by post-translational modification of arginine by peptidylarginine deiminase (PAD) enzymes during a variety of biologic processes, including inflammation. Rheumatoid arthritis (RA) is an inflammatory autoimmune disease, with a prevalence of 0.3 to 1% worldwide, which leads to progressive joint erosion and substantial disability if not treated early. A reliable and specific test for a marker present early in the disease would be useful to identify RA patients prior to the occurrence of joint damage. A new group of autoantibodies, the anti-cyclic citrullinated peptide antibodies (anti-CCP), can be detected in up to 80% of patients with RA, are highly specific for the disease, and may be of value for both the diagnosis and the prognosis of RA. The fact that these antibodies may appear before the onset of the disease suggests a potential role in primary prevention. Interestingly, they may also play a role in the pathophysiology of this disabling disease. The process of citrullination, its physiologic role, and citrullination-related pathologies, as well as the use of anti-citrullinated protein antibody tests (ACPA) for the early diagnosis and prognosis of RA and their potential role in the pathophysiology of the disease, are discussed.
    Critical Reviews in Clinical Laboratory Sciences 02/2007; 44(4):339-63.
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    ABSTRACT: The prevalence of secondary hypertension can be underestimated if appropriate tests are not performed. The importance of selecting patients with a high pre-test probability of secondary forms of hypertension is first discussed. The laboratory tests currently used for seeking a cause of hypertension are critically reviewed, with emphasis on their operative features and limitations. Strategies to identify primary aldosteronism, the most frequent form of secondary hypertension, and to determine its unilateral or bilateral causes are described. Treatment entails adrenalectomy in unilateral forms, and mineralocorticoid receptor blockade in bilateral forms. Renovascular hypertension is also a common, curable form of hypertension, that should be identified as early as possible to avoid the onset of cardiovascular target organ damage. The tests for its confirmation or exclusion are discussed. The various tests available for the diagnosis of pheochromocytoma, which is much rarer than the above but extremely important to identify, are also described, with emphasis on recent developments in genetic testing. Finally, the tests for diagnosing some rarer monogenic forms and other renal and endocrine causes of arterial hypertension are explored.
    Critical Reviews in Clinical Laboratory Sciences 02/2007; 44(1):1-85.
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    ABSTRACT: Leukemia is the most common childhood cancer and a major source of morbidity and mortality. The etiology of childhood leukemia remains largely unknown. Cytogenetic abnormalities determine disease subtypes, prognosis, clinical presentation, and course and may help in discovering etiological factors. Epidemiologic investigations of leukemia are complicated by many factors, including the rarity of the disease, necessitating careful study design. Two emerging areas of interest in leukemia etiology are birth weight and diet. High birth weight has been associated with increased risk of childhood leukemia. The biological mechanism behind this association may involve insulin-like growth factor I (IGF-I), which is associated with high birth weight. IGF-I may act by increasing the absolute number of stem cells available for transformation, stimulating the growth of cells that are already transformed, or a combination of effects. Diet has been linked with leukemia. Maternal dietary DNA topoisomerase II (DNAt2) inhibitor intake is associated with infant acute myeloid leukemia (AML) with the MLL gene translocation. Increased intake of fruits and vegetables has been associated with decreased leukemia risk and, relatedly, lack of maternal folate supplementation has been associated with increased childhood leukemia risk, possibly by causing DNA hypomethylation and increased DNA strand breaks. Methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms modify this risk.
    Critical Reviews in Clinical Laboratory Sciences 02/2007; 44(3):203-42.
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    ABSTRACT: von Willebrand factor (VWF) is a multimeric plasma protein that mediates platelet adhesion as well as platelet aggregation at sites of vascular injury and acts as a carrier of factor VIII. Although acquired or inherited VWF deficiency is associated with a bleeding tendency, there is increasing evidence that VWF has a pivotal role in thrombogenesis. In fact, while the presence in the plasma of unusually large VWF multimers, due to a congenital or acquired deficiency of a VWF-cleaving metalloprotease, has been implicated in the pathogenesis of thrombotic thrombocytopenic purpura, high plasma levels of VWF have been associated with an increased risk of both arterial and venous thrombosis. The role of VWF in normal and pathological hemostasis is discussed in this review, and important advances in the pathophysiology, diagnosis, and treatment of VWF-associated disorders are also described.
    Critical Reviews in Clinical Laboratory Sciences 02/2007; 44(2):115-49.
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    ABSTRACT: This review considers the past, present, and projected future clinical relevance of the serine protease urokinase-type plasminogen activator (uPA), and its inhibitor, plasminogen activator inhibitor-type 1 (PAI-1), in breast cancer. These factors play a key role in tumor invasion and metastasis in many cancers. In primary breast cancer, their prognostic and predictive impact has been validated at the highest level of evidence by a multicenter therapy trial (Chemo N0) and a large European Organisation for Research and Treatment Cancer-Receptor and Biomarker Group EORTC RBG pooled analysis (n = 8377). The greatest clinical use is in node-negative breast cancer, where the test can avoid over-treatment by adjuvant chemotherapy in patients with non-aggressive disease. In intermediate-risk patients as defined by the international St. Gallen consensus, it can be used to identify patients who should receive chemotherapy because their tumor is more aggressive than classical pathological factors would suggest. Gene expression signatures are already being used in clinical trials to define the population of patients with breast cancer who should receive chemotherapy. The decision for treatment ignores the highly validated information that could be provided by uPA/PAI-1. A current and future challenge is to integrate the information provided by tumor biological factors, particularly uPA/PAI-1, into refined risk assessment and decision support algorithms incorporating gene expression signatures. This article describes a paradigm ("marker fusion") for doing so and a bioinformatics approach based on this paradigm. This concept could be useful in assessing and maximizing the performance of risk assessment and the quality of therapeutic indications.
    Critical Reviews in Clinical Laboratory Sciences 02/2007; 44(2):179-201.
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    ABSTRACT: This review focuses on the possible role in human health of the consumption of lignan-rich foods. Most of the plant lignans in human foods are converted by the intestinal microflora in the upper part of the large bowel to enterolactone and enterodiol, called mammalian or enterolignans. The protective role of these compounds, particularly in chronic Western diseases, is discussed. Evidence suggests that fiber- and lignan-rich whole-grain cereals, beans, berries, nuts, and various seeds are the main protective foods. Many factors, in addition to diet, such as intestinal microflora, smoking, antibiotics, and obesity affect circulating lignan levels in the body. Lignan-rich diets may be beneficial, particularly if consumed for life. Experimental evidence in animals has shown clear anticarcinogenic effects of flaxseed or pure lignans in many types of cancer. Many epidemiological results are controversial, partly because the determinants of plasma enterolactone are very different in different countries. The source of the lignans seems to play a role because other factors in the food obviously participate in the protective effects. The results are promising, but much work is still needed in this area of medicine.
    Critical Reviews in Clinical Laboratory Sciences 02/2007; 44(5-6):483-525.
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    ABSTRACT: The fundamental process of implantation involves a series of steps leading to effective cross-talk between invasive trophoblast cells and the maternal endometrium. The molecular interactions at the embryo-maternal interface during the time of blastocyst adhesion and subsequent invasion are not fully understood. Embryonic trophoblast and maternal decidual cells produce corticotropin-releasing hormone (CRH) and express Fas ligand (FasL), a proapoptotic cytokine. Fas and its ligand are pivotal in the regulation of immune tolerance. Trophoblast and decidual CRH play crucial roles in implantation, as well as in the anti-rejection process that protects the fetus from the maternal immune system, primarily by killing activated T cells through Fas-FasL interaction. The potential use of CRH antagonists is presently under intense investigation. CRH antagonists have been used experimentally to elucidate the role of CRH in blastocyst implantation and invasion, early fetal immunotolerance, and premature labor.
    Critical Reviews in Clinical Laboratory Sciences 02/2007; 44(5-6):461-81.
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    ABSTRACT: Antiphospholipid antibodies (aPL) constitute a heterogeneous group of autoantibodies that share the ability to bind phospholipids (PL) alone, protein-PL complexes, or PL-binding proteins. They have been detected in isolation, in association with autoimmune diseases such as systemic lupus erythematosus (SLE), and during the course of different infections. aPL have been associated with an array of clinical manifestations in virtually every organ, although deep vein and arterial thrombosis as well as pregnancy morbidity are predominant. The co-occurrence of these clinical findings with aPL constitutes the so-called antiphospholipid syndrome (APS). aPL can be detected by immunological methods [e.g., anticardiolipin antibodies (aCL)] or by functional methods that exploit the effect of aPL on blood coagulation [lupus anticoagulant (LA)]. Since aPL are heterogeneous, numerous immunological and coagulation assays have been developed. These assays have not been fully standardized, and, therefore, problems such as high interlaboratory variation are relatively frequent. Recently, recommendations have been published regarding LA and aCL testing. Not all aPL are pathogenic. However, when they are not associated with infections, they have a role in the pathogenesis of APS. Clinical and experimental data have shown that aPL exert their pathogenic activity by interfering with the function of coagulation factors, such as thrombin and factors X, XI and XII, and with the function of anticoagulant proteins of the protein C system. In addition, aPL interaction with platelets and endothelial cells induces a pro-adhesive activated phenotype.
    Critical Reviews in Clinical Laboratory Sciences 02/2007; 44(3):271-338.
  • Critical Reviews in Clinical Laboratory Sciences 01/2007; 44(4):364.
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    ABSTRACT: The use of biochemical markers in the diagnosis and management of patients with acute coronary syndrome has increased continually in recent decades. The development of highly sensitive and cardiac-specific troponin assays has changed the view on diagnosis of myocardial infarction and also extended the role of biochemical markers of necrosis into risk stratification and guidance for treatment. The consensus definition of myocardial infarction places increased emphasis on cardiac marker testing, with cardiac troponin replacing creatine kinase MB as the "gold standard" for diagnosis of myocardial infarction. Along with advances in the use of more cardiac-specific markers of myocardial necrosis, biochemical markers that are involved in the progression of atherosclerotic plaques to the vulnerable state or that signal the presence of vulnerable plaques have recently been identified. These markers have variable abilities to predict the risk of an individual for acute coronary syndrome. The aim of this review is to provide an overview of the well-established markers of myocardial necrosis, with a special focus on cardiac troponin I, together with a summary of some of the potential future markers of inflammation, plaque instability, and ischemia.
    Critical Reviews in Clinical Laboratory Sciences 02/2006; 43(5-6):427-95.
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    ABSTRACT: Inherited thrombophilia can be defined as a genetically determined predisposition to the development of thromboembolic complications. Since the discovery of activated protein C resistance in 1993, several additional disorders have been described and, at present, it is possible to identify an inherited predisposition in about 60 to 70% of patients with such complications. These inherited prothrombotic risk factors include qualitative or quantitative defects of coagulation factor inhibitors, increased levels or function of coagulation factors, defects of the fibrinolytic system, altered platelet function, and hyperhomocysteinemia. In this review, the main inherited prothrombotic risk factors are analyzed from epidemiological, laboratory, clinical, and therapeutic points of view. Finally, we discuss the synergism between genetic and acquired prothrombotic risk factors in particular conditions such as childhood and pregnancy.
    Critical Reviews in Clinical Laboratory Sciences 02/2006; 43(3):249-90.
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    ABSTRACT: Hepatitis B virus (HBV) infection is the major cause of hepatocellular carcinoma (HCC) worldwide. The pathogenesis of HBV-associated HCC has been studied extensively, and molecular changes during malignant transformation have been identified. It has been proposed that the insertion of HBV DNA into the human genome results in chromosomal instability and inactivation of tumor suppressor genes. Transactivation of oncogenes, inactivation of tumor suppressor genes, and alteration of the cell cycle by HBV proteins are also involved in the progression of hepatocellular carcinogenesis. Traditional clinical examinations of HCC, such as biopsy, computer tomography, ultrasonic imaging, and detection of such biomarkers as a-fetoprotein, are currently the "gold standard" in diagnosis. These tests diagnose HCC only in the late stages of disease. This limitation has greatly reduced the chance of survival of HCC patients. To resolve this problem, new biomarkers that can diagnose HCC in earlier stages are necessary. Based on recent molecular studies of the effects of HBV on cellular transformation, differentially expressed biomarkers of HBV infection have been elucidated. With the analyses of the HBV replication profile, the viral load (HBV DNA levels) of patients, and the viral protein expression, the severity of hepatitis in the preneoplastic stages can be assessed. In the future, with the molecular profiles identified by genomic and proteomic approaches, stage-specific biomarkers should be identified to monitor the progression and prognosis of HCC.
    Critical Reviews in Clinical Laboratory Sciences 02/2006; 43(1):69-101.
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    ABSTRACT: Cancer is a major and increasing public health problem worldwide. Traditionally, the diagnosis and staging of cancer, as well as the evaluation of response to therapy have been primarily based on morphology, with relatively few cancer biomarkers currently in use. Conventional biomarker studies have been focused on single genes or discrete pathways, but this approach has had limited success because of the complex and heterogeneous nature of many cancers. The completion of the human genome project and the development of new technologies have greatly facilitated the identification of biomarkers for assessment of cancer risk, early detection of primary cancers, monitoring cancer treatment, and detection of recurrence. This article reviews the various approaches used for development of such markers and describes markers of potential clinical interest in major types of cancer. Finally, we discuss the reasons why so few cancer biomarkers are currently available for clinical use.
    Critical Reviews in Clinical Laboratory Sciences 02/2006; 43(5-6):497-560.
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    ABSTRACT: Trypsinogens and PSTI/TATI/SPINK1 are expressed, usually together, at high levels by the pancreas but also by many other normal and malignant tissues. The present review describes studies on the expression and putative functions of trypsinogens and PSTI/TATI/SPINK1 in the human body. The clinical aspects are discussed, including the correlations between expression of trypsinogens and PSTI/TATI/SPINK1 in tissues, serum, and urine of patients with pancreatitis or cancer and clinicopathological characteristics, i.e., the roles of trypsinogens and PSTI/TATI/SPINK1 in spontaneous and hereditary pancreatitis, tumor progression, and prognosis.
    Critical Reviews in Clinical Laboratory Sciences 02/2006; 43(2):103-42.