bluuebunny/crossref_metadata_2025_split huggingface dataset:
High prevalence of occult hepatitis B in hepatitis C‐infected Egyptian children with haematological disorders and malignancies
Authors: Said Zeinab N.A. , El‐Sayed Manal H. , El‐Bishbishi Iman A. , El‐Fouhil Daad F. , Abdel‐Rheem Soad E. , El‐Abedin Maha Z. , Salama Iman I. 
Published: January 2009

AbstractObjective: This study investigates the prevalence of occult hepatitis B virus (HBV) in children and adolescents with haematological diseases with or without hepatitis C virus (HCV) infection.Methods: Forty‐nine children with haematological disorders (median age 11.4 years) and 51 with haematological malignancies (median age 8 years) were enrolled. Sera were tested for HCV antibodies, HCV‐RNA [nested reverse transcriptase polymerase chain reaction (PCR)], HBV markers (HBsAg, anti‐HBcAb IgM and total, HBeAg) and HBV‐DNA (nested PCR for s, c and x regions).Results: Anti‐HCV was detected among 40/49 (81.6%) children with haematological disorders (24/49; 49% HCV‐RNA positive) and 9/51 (17.6%) children with malignancies (12/51; 23.5% HCV‐RNA positive). HBV‐DNA was positive among 38%; positive c region in 33% (15/49 and 18/51 children with haematological disorders and malignancies respectively), s region in four leukaemics and x region in one leukaemic. Twenty‐one patients had occult HBV infection; one (2.6%) was HBeAg positive, four (19%) total HBcAb positive, 20 (95.2%) c region HBV‐DNA positive and one was s region positive (1/21; 4.8%). HCV‐RNA was the significant predictor for occult HBV (P<0.05), with an increased frequency of HBV‐DNA in the HBsAg negative (HCV‐RNA positive) (63.2%) compared with patients negative for HCV‐RNA (25%) (P=0.009).Conclusion: Occult HBV infection is not uncommon in transfused immunocompromised children with chronic HCV infection. Nucleic acid amplification should be considered in screening donors as post‐transfusion hepatitis B viraemia may be substantial.
Epilepsy after head injury: An overview
Authors: Lowenstein Daniel H. 
Published: January 2009

SummaryTraumatic brain injury (TBI) has been recognized as a cause of epilepsy since antiquity, and it remains one of the most common and important causes of acquired epilepsy today. Epidemiologic studies have demonstrated a clear relationship between the severity of injury and the likelihood of developing epilepsy, with the risk approaching 50% in TBI cases associated with direct injury to brain parenchyma. Importantly, many TBI victims develop epilepsy months or years following the initial injury, making this patient population a prime target for the development of antiepileptogenesis therapies. However, progress in this area of clinical research is hindered by the lack of reliable and valid biomarkers. Given current events in the Middle East and elsewhere, the importance of TBI and epilepsy deserves special attention due to the increase in severe head trauma associated with modern warfare.
From traumatic brain injury to posttraumatic epilepsy: What animal models tell us about the process and treatment options
Authors: Pitkänen Asla , Immonen Riikka J. , Gröhn Olli H.J. , Kharatishvili Irina 
Published: January 2009

SummaryA large number of animal models of traumatic brain injury (TBI) are already available for studies on mechanisms and experimental treatments of TBI. Immediate and early seizures have been described in many of these models with focal or mixed type (both gray and white matter damage) injury. Recent long‐term video‐electroencephalography (EEG) monitoring studies have demonstrated that TBI produced by lateral fluid‐percussion injury in rats results in the development of late seizures, that is, epilepsy. These animals develop hippocampal alterations that are well described in status epilepticus–induced spontaneous seizure models and human posttraumatic epilepsy (PTE). In addition, these rats have damage ipsilaterally in the cortical injury site and thalamus. Although studies in the trauma field provide a large amount of information about the molecular and cellular alterations corresponding to the immediate and early phases of PTE, chronic studies relevant to the epileptogenesis phase are sparse. Moreover, despite the multiple preclinical pharmacologic and cell therapy trials, there is no information available describing whether these therapeutic approaches aimed at improving posttraumatic recovery would also affect the development of lowered seizure threshold and epilepsy. To make progress, there is an obvious need for information exchange between the trauma and epilepsy fields. In addition, the inclusion of epilepsy as an outcome measure in preclinical trials aiming at improving somatomotor and cognitive recovery after TBI would provide valuable information about possible new avenues for antiepileptogenic interventions and disease modification after TBI.
Posttraumatic epilepsy: The challenge of translating discoveries in the laboratory to pathways to a cure
Authors: Dichter Marc A. 
Published: January 2009

SummaryTranslating laboratory discoveries into successful therapies for preventing epilepsy is a difficult task, but preventing epilepsy in those who are known to be at high risk needs to be one of our highest priorities. At present, we need to approach this task as a parallel set of research endeavors—one concentrating on laboratory experiments designed to learn how to prevent epilepsy after brain trauma and the other focusing on how to perform the appropriate clinical research in humans to demonstrate that whatever is discovered in the laboratory can be appropriately tested. It is too important to let the second process await conclusion of the first. Initially, we need to create a consortium of groups in trauma centers that are dedicated to antiepileptogenic studies and develop funding sources for long‐term studies. We need to experiment with clinical protocols, making the studies as cost‐effective as possible, while performing continuous data mining of outcomes and surrogate markers. The limitations of current technology to assist in antiepileptogenesis trials must be acknowledged: There is no currently available method for continuously monitoring electroencephalography (EEG) over prolonged periods, and there are no validated biomarkers for the process of epileptogenesis. As we learn more about the process of epileptogenesis and its underlying mechanisms, it is hoped that we will be able to prevent the development of epilepsy after traumatic brain injury (TBI) and after many other known epileptogenic lesions.
Sequence Variations of the Human MPDZ Gene and Association With Alcoholism in Subjects With European Ancestry
Authors: Karpyak Victor M. , Kim Jeong‐Hyun , Biernacka Joanna M. , Wieben Eric D. , Mrazek David A. , Black John L. , Choi Doo‐Sup 
Published: January 2009

Background:  Mpdz gene variations are known contributors of acute alcohol withdrawal severity and seizures in mice.Methods:  To investigate the relevance of these findings for human alcoholism, we resequenced 46 exons, exon–intron boundaries, and 2 kilobases in the 5′ region of the human MPDZ gene in 61 subjects with a history of alcohol withdrawal seizures (AWS), 59 subjects with a history of alcohol withdrawal without AWS, and 64 Coriell samples from self‐reported nonalcoholic subjects [all European American (EA) ancestry] and compared with the Mpdz sequences of 3 mouse strains with different propensity to AWS. To explore potential associations of the human MPDZ gene with alcoholism and AWS, single SNP and haplotype analyses were performed using 13 common variants.Results:  Sixty‐seven new, mostly rare variants were discovered in the human MPDZ gene. Sequence comparison revealed that the human gene does not have variations identical to those comprising Mpdz gene haplotype associated with AWS in mice. We also found no significant association between MPDZ haplotypes and AWS in humans. However, a global test of haplotype association revealed a significant difference in haplotype frequencies between alcohol‐dependent subjects without AWS and Coriell controls (p = 0.015), suggesting a potential role of MPDZ in alcoholism and/or related phenotypes other than AWS. Haplotype‐specific tests for the most common haplotypes (frequency > 0.05), revealed a specific high‐risk haplotype (p = 0.006, maximum statistic p = 0.051), containing rs13297480G allele also found to be significantly more prevalent in alcoholics without AWS compared with nonalcoholic Coriell subjects (p = 0.019).Conclusions:  Sequencing of MPDZ gene in individuals with EA ancestry revealed no variations in the sites identical to those associated with AWS in mice. Exploratory haplotype and single SNP association analyses suggest a possible association between the MPDZ gene and alcohol dependence but not AWS. Further functional genomic analysis of MPDZ variants and investigation of their association with a broader array of alcoholism‐related phenotypes could reveal additional genetic markers of alcoholism.
Innovation Leaders: How Senior Executives Stimulate, Steer, and Sustain Innovation by Jean‐Philippe Deschamps
Authors: Nelson Beebe 
Published: January 2009

I am honored to have been chosen as the Journal of Product Innovation Management's (JPIM's) new book review editor. First and foremost, I want to thank Preston Smith for making the transition an easy one. Preston's experience and insights have helped bring me up the learning curve. His patience was much appreciated.Second, managing the book review process is certainly more complicated than I had imagined but is fascinating nonetheless. As in the development of any product or service there are many people involved in the creation process, and considerable planning takes place prior to actual publication.Last but not least is my admiration for our JPIM book reviewers. The care and effort taken to create the quality book reviews that meet JPIM's high standards requires critical thought and experience in new product development. We will continue to make our book reviews insightful, critical, and practical for you, our readers.Books reviewed in this issue:

Innovation Leaders: How Senior Executives Stimulate, Steer, and Sustain Innovation
Understanding A3 Thinking: A Critical Component of Toyota's PDCA Management System
Value Merchants: Demonstrating and Documenting Superior Value in Business Markets
Presence of thyrotropin receptor in hepatocytes: not a case of illegitimate transcription
Authors: Zhang Wei , Tian Li‐min , Han Yong , Ma Hong‐yan , Wang Lai‐cheng , Guo Jun , Gao Ling , Zhao Jia‐jun 
Published: January 2009

AbstractThe function of thyrotropin (TSH) in the thyroid gland is mediated by thyrotropin receptor (TSHR). In addition to the thyroid, TSHR expression has been described in some non‐thyroidal tissues, although it is uncertain whether TSHR is present in hepatocytes. One study has reported hepatic expression of TSHR mRNA, but this was considered to be because of illegitimate transcription, and there has not been a study investigating its protein expression and function in hepatocytes. Here, we examined the expression of TSHR in human and rat liver tissues, as well as human normal hepatocyte cell line L‐02. Our results demonstrated that hepatic TSHR mRNA could be detected and had the same sequence as that of thyroid‐derived mRNA. TSHR protein was also expressed and mainly located in the hepatocyte cell membrane. Moreover, bovine TSH and immunoglobulin from sera of patients with Graves’ disease stimulated cAMP production in these cells. Taken together, these data show that TSHR is present and functional in hepatocytes, and this expression is not a case of illegitimate transcription. Given the pivotal role of the liver in body metabolism and many human diseases, our findings provide important implications for a potentially novel physiopathological role of TSH via acting on the TSHR in hepatocytes besides its classical role in regulating the thyroid function.
Calcium sensing receptor‐dependent and receptor‐independent activation of osteoblast replication and survival by strontium ranelate
Authors: Fromigué Olivia , Haÿ Eric , Barbara Alain , Petrel Christophe , Traiffort Elisabeth , Ruat Martial , Marie Pierre J. 
Published: January 2009

AbstractAge‐related osteopenia is characterized by a negative balance between bone resorption and formation. The anti‐osteoporotic drug strontium ranelate was found to reduce bone resorption and to promote bone formation. Here, we investigated the implication of the calcium‐sensing receptor (CaSR) in the response to strontium ranelate using osteoblasts from CaSR knockout [CaSR−/−] and wild‐type [CaSR+/+] mice. We showed that calcium and strontium ranelates increased cell replication in [CaSR−/−] and [CaSR+/+] osteoblasts. Strontium ranelate rapidly increased ERK1/2 phosphorylation in [CaSR+/+] but not in [CaSR−/−] osteoblasts, indicating that strontium ranelate can act independent of the CaSR/ERK1/2 cascade to promote osteoblast replication. We also showed that strontium ranelate prevented cell apoptosis induced by serum deprivation or the pro‐inflammatory cytokines IL‐1β and TNF‐α in [CaSR−/−] and [CaSR+/+] osteoblasts, indicating that CaSR is not the only receptor involved in the protective effect of strontium ranelate on osteoblast apoptosis. Strontium ranelate activated the Akt pro‐survival pathway in [CaSR−/−] and [CaSR+/+] osteoblasts, and pharmacological inhibition of Akt abrogated the anti‐apoptotic effect of strontium ranelate. Furthermore, both the proliferative and anti‐apoptotic effects of strontium ranelate in [CaSR−/−] and [CaSR+/+] osteoblasts were abrogated by selective inhibition of COX‐2. The results provide genetic and biochemical evidence that the effects of strontium ranelate on osteoblast replication and survival involve ERK1/2 and Akt signalling and PGE2 production, independent of CaSR expression. The finding that CaSR‐dependent and CaSR‐independent pathways mediate the beneficial effects of strontium ranelate on osteoblasts, provides novel insight into the mechanism of action of this anti‐osteoporotic agent on osteoblastogenesis.
Oestrogen modulates human macrophage apoptosis via differential signalling through oestrogen receptor‐α and β
Authors: Subramanian Manikandan , Shaha Chandrima 
Published: January 2009

AbstractHuman macrophages express oestrogen receptors and are therefore competent to respond to the hormone present in their microenvironment, which is implicated in sexual dimorphism observed in several immune and autoimmune phenomena. An earlier study from this laboratory demonstrated 17β‐oestradiol (E2) induced apoptosis in macrophages derived from human peripheral blood monocytes and THP‐1 acute monocytic leukaemia cell line when Bcl‐2 was down‐regulated; however, the involvement of E2 receptor subtypes in the modulation of death pathways in these cells remain unknown. Using macrophages derived from THP‐1 human acute monocytic leukaemia cells as a model, we demonstrate that plasma membrane associated oestrogen receptor (ER) ‐α participate in E2 induced Bcl‐2 increase, through activation of the mitogen activated protein kinase (MAPK) pathway whereas cytosolic ER‐β transmits signals for the pro‐apoptotic event of Bax translocation. The mechanistic basis of Bax translocation comprised of ER‐β mediated increase in intracellular pH, facilitated by activation of the Na+–H+ exchanger. Intracellular alkalinization accompanied by concomitant Bcl‐2 increase and Bax migration does not cause cellular apoptosis; however, siRNA mediated down‐regulation of ER‐α during E2 exposure leads to inhibition of Bcl‐2 increase and consequently apoptosis due to the unopposed action of mitochondrial Bax. In summary, this study underscores the importance of integrative signalling modality from multiple oestrogen receptor pools in modulating oestrogen effects on human monocyte‐derived macrophage apoptotic signalling pathway, which opens new vistas to explore the use of selective oestrogen receptor modulators in apoptosis‐based therapies.
Characterization of the S‐denitrosylating activity of bilirubin
Authors: Barone Eugenio , Trombino Sonia , Cassano Roberta , Sgambato Alessandro , de Paola Barbara , Stasio Enrico Di , Picci Nevio , Preziosi Paolo , Mancuso Cesare 
Published: January 2009

AbstractBilirubin‐IX‐α (BR) is an endogenous molecule with a strong antioxidant feature due to its ability to scavenge free radicals. In this paper, we demonstrated that BR, at concentrations close to those found within the cell (0.1–2.5 μM), acted as a denitrosylating agent and increased the release of nitric oxide from S‐nitrosoglutathione (GSNO) and S‐nitrosocysteine (SNOC) (2.5 μM). The complexation of BR with saturating concentrations of human serum albumin (HSA, 2.5 μM) did not further increase nitric oxide release from GSNO and SNOC. At concentrations similar to those reached in plasma (5–20 μM), BR denitrosylated S‐nitroso‐HSA (2.5 μM), the main circulating S‐nitrosothiol, and this effect was potentiated by the complexation of BR with saturating HSA (20 μM). Furthermore, the product(s) of the reaction between nitric oxide and BR were identified. Ultraviolet and mass spectrometry analysis revealed that nitric oxide binds to BR forming a N‐nitroso derivative (BR–nitric oxide) with extinction coefficients of 1.393 mM−1cm−1and 2.254 mM−1cm−1in methanol and NaOH, respectively. The formation of BR–nitric oxide did not occur only in a reconstituted system, but was confirmed in rat fibroblasts exposed to pro‐oxidant stimuli. These results provided novel insights on the antioxidant characteristic of BR through its interaction with nitric oxide, a gaseous neurotransmitter with a well‐known dual effect, namely neuroprotective under physiological conditions or neurotoxic if produced in excess, and proposed BR–nitric oxide as a new biomarker of oxidative/nitrosative stress.
Sensitizing capacity and cross‐reactivity of phenyl glycidyl ether studied in the guinea‐pig maximization test
Authors: Pontén Ann , Zimerson Erik , Bruze Magnus 
Published: January 2009

Background:  Simultaneous contact allergies to the reactive diluent phenyl glycidyl ether (PGE) and epoxy resins based on diglycidyl ether of bisphenol A (DGEBA) or epoxy resins of the bisphenol F‐type have been reported. The latter epoxy resins contain three isomers of diglycidyl ether of bisphenol F (DGEBF). PGE, DGEBA, and DGEBF are chemically similar with respect to the reactive glycidyl group and an aromatic ring, making cross‐reactivity one of the possible explanations to simultaneous reactions.Aim:  To investigate the sensitizing capacity of PGE and the cross‐reactivity of PGE versus the epoxy resin monomers DGEBA and the three DGEBF monomers and vice versa.Method:  The guinea‐pig maximization test.Results:  PGE is a strong sensitizer. Induction with DGEBA resulted in a statistically significant number of animals reacting to PGE, but when induced with PGE, the animals did not react significantly to DGEBA.Conclusions:  When the results are applied to humans, it can be assumed that patients sensitized primarily to DGEBA react to PGE, but when sensitized exclusively to PGE, they do not react to DGEBA. Both reactive diluents and epoxy resins should be tested when contact allergy to epoxy resin systems are suspected.
Assessment of the sensitization potential of persulfate salts used for bleaching hair
Authors: Cruz María‐Jesús , De Vooght Vanessa , Muñoz Xavier , Hoet Peter H. M. , Morell Ferran , Nemery Benoit , Vanoirbeek J. A. J. 
Published: January 2009

Background:  Persulfate salts have been associated with both allergic contact dermatitis and bronchial asthma. Because there is currently no experimental data available on the sensitizing properties of persulfate salts (ammonium, sodium, and potassium persulfates), we determined their dermal sensitizing capacity, using the murine local lymph node assay (LLNA).Material and Methods:  For three consecutive days, BALB/c mice were dermally treated with ammonium, sodium, or potassium persulfate or with the vehicle alone (dimethyl sulfoxide) on each ear (2 × 25 μl). On D6, mice were injected intravenously with [3H]‐methyl thymidine. The draining auricular lymph nodes were removed, and the incorporation of [3H]‐methyl thymidine was compared with that of vehicle‐treated control mice. A stimulation index (SI) relative to the vehicle‐treated control value was derived. The sensitizing potency of the chemicals tested was determined by estimating the concentration of chemical required to induce a SI of 3 (EC3).Results:  All three chemicals provoked positive responses in the LLNA, with dose‐dependent increases in proliferation. Maximal SIs recorded were 6.8 ± 1.8, 6.5 ± 1.2, and 5 ± 1.0 at 5% for ammonium, sodium or potassium persulfate, respectively. The EC3 values were 1.9%, 0.9%, and 2.4% for ammonium, sodium, and potassium persulfates, respectively.Conclusions:  All three persulfate salts need to be considered strong‐to‐moderate sensitizers according to the murine LLNA.
Contamination versus preservation of cosmetics: a review on legislation, usage, infections, and contact allergy
Authors: Lundov Michael Dyrgaard , Moesby Lise , Zachariae Claus , Johansen Jeanne Duus 
Published: January 2009

Cosmetics with high water content are at a risk of being contaminated by micro‐organisms that can alter the composition of the product or pose a health risk to the consumer. Pathogenic micro‐organisms such as Staphylococcus aureus and Pseudomonas aeruginosa are frequently found in contaminated cosmetics. In order to avoid contamination of cosmetics, the manufacturers add preservatives to their products. In the EU and the USA, cosmetics are under legislation and all preservatives must be safety evaluated by committees. There are several different preservatives available but the cosmetic market is dominated by a few preservatives: parabens, formaldehyde, formaldehyde releasers, and methylchloroisothiazolinone/methylisothiazolinone.Allergy to preservatives is one of the main reasons for contact eczema caused by cosmetics. Concentration of the same preservative in similar products varies greatly, and this may indicate that some cosmetic products are over preserved. As development and elicitation of contact allergy is dose dependent, over preservation of cosmetics potentially leads to increased incidences of contact allergy. Very few studies have investigated the antimicrobial efficiency of preservatives in cosmetics, but the results indicate that efficient preservation is obtainable with concentrations well below the maximum allowed.