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

Publisher: Taylor & Francis

Description

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

  • Impact factor
    3.78
    Show impact factor history
     
    Impact factor
  • 5-year impact
    5.14
  • Cited half-life
    8.60
  • Immediacy index
    0.57
  • Eigenfactor
    0.00
  • Article influence
    1.49
  • Website
    Critical Reviews in Clinical Laboratory Sciences website
  • Other titles
    Critical reviews in clinical laboratory sciences, Chemical Rubber Company critical reviews in clinical laboratory sciences, CRC critical reviews in clinical laboratory sciences
  • ISSN
    1040-8363
  • OCLC
    1151594
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publisher details

Taylor & Francis

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 month embargo for STM, Behavioural Science and Public Health Journals
    • 18 month embargo for SSH journals
  • Conditions
    • Some individual journals may have policies prohibiting pre-print archiving
    • Pre-print on authors own website, Institutional or Subject Repository
    • Post-print on authors own website, Institutional or Subject Repository
    • Publisher's version/PDF cannot be used
    • On a non-profit server
    • Published source must be acknowledged
    • Must link to publisher version
    • Set statements to accompany deposits (see policy)
    • Publisher will deposit to PMC on behalf of NIH authors.
    • STM: Science, Technology and Medicine
    • SSH: Social Science and Humanities
    • 'Taylor & Francis (Psychology Press)' is an imprint of 'Taylor & Francis'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    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 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: 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: 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: 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: 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: 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: 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.
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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.
  • Critical Reviews in Clinical Laboratory Sciences 01/2007; 44(4):364.
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    ABSTRACT: One of the most effective ways to combat different types of cancer is through early diagnosis and administration of effective treatment, followed by efficient monitoring that will allow physicians to detect relapsing disease and treat it at the earliest possible time. Apoptosis, a normal physiological form of cell death, is critically involved in the regulation of cellular homeostasis. Dysregulation of programmed cell death mechanisms plays an important role in the pathogenesis and progression of cancer as well as in the responses of tumours to therapeutic interventions. Many members of the BCL2 (B-cell CLL/lymphoma 2; Bcl-2) family of apoptosis-related genes have been found to be differentially expressed in various malignancies, and some are useful prognostic cancer biomarkers. We have recently cloned a new member of this family, BCL2L12, which was found to be differentially expressed in many tumours. Most of the BCL2 family genes have been found to play a central regulatory role in apoptosis induction. Results have made it clear that a number of coordinating alterations in the BCL2 family of genes must occur to inhibit apoptosis and provoke carcinogenesis in a wide variety of cancers. However, more research is required to increase our understanding of the extent to which and the mechanisms by which they are involved in cancer development, providing the basis for earlier and more accurate cancer diagnosis, prognosis and therapeutic intervention that targets the apoptosis pathways. In the present review, we describe current knowledge of the function and molecular characteristics of a series of classic but also newly discovered genes of the BCL2 family as well as their implications in cancer development, prognosis and treatment.
    Critical Reviews in Clinical Laboratory Sciences 02/2006; 43(1):1-67.
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    ABSTRACT: The estrogen receptor (ER) exists in two forms known as ERalpha and ERbeta. Currently, a clinical role has only been established for ERalpha. The primary use of ERalpha in breast cancer is for predicting likely response to hormone treatment. Patients with breast cancers expressing ERalpha are approximately seven to eight times more likely to benefit from endocrine therapy than ERalpha-negative patients. For the initial three to five years after primary diagnosis, ERalpha-positive patients generally have a better outcome than ERalpha-negative patients. Overall, however, the prognostic value of ERalpha is relatively weak and only of limited value in the clinically important subgroup of patients with lymph node-negative disease. Further work is required to establish if ERbeta has a clinical role in breast cancer.
    Critical Reviews in Clinical Laboratory Sciences 02/2006; 43(4):325-47.
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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.

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