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PubMed2005

Bone mass and mineral metabolism in HIV+ postmenopausal women.

The objective of this cross-sectional study was to estimate the prevalence of and risk factors for osteoporosis in HIV+ postmenopausal women. Bone mineral density (BMD) by dual energy X-ray absorptiometry (DXA) and biochemical indices of mineral metabolism were measured in 31 Hispanic and African American HIV+ postmenopausal women. BMD was compared with 186 historical controls, matched for age, ethnicity and postmenopausal status. Mean BMD was significantly lower at the lumbar spine and total hip in the HIV+ group, as compared with controls. Prevalence of osteoporosis was higher in the HIV+ group than controls at the lumbar spine (42% vs 23%, p =0.03) and total hip (10% vs 1%, p =0.003). Among HIV+ women, time since menopause and weight were significant predictors of BMD, while duration or class of antiretroviral therapy (ART), AIDS diagnosis, nadir CD4, steroid use, and vitamin D deficiency were not. Prevalence of osteoporosis is substantially higher in HIV+ Hispanic and African-American postmenopausal women than in controls. Established osteoporosis risk factors were more important in predicting BMD than factors associated with HIV infection and ART. Long-term management of the growing female HIV population should include the evaluation for and management of osteoporosis.

Absorptiometry, Photon↗
PubMed2006

In prostate cancer cells the interaction of C/EBPalpha with Ku70, Ku80, and poly(ADP-ribose) polymerase-1 increases sensitivity to DNA damage.

Prostate cancer cell lines were examined for proteins that partnered with the transcription factor C/EBPalpha by use of a pull-down assay with S-tagged C/EBPalpha combined with matrix-assisted laser desorption ionization time-of-flight mass spectroscopy analysis. Ku70, Ku80, and poly(ADP-ribose) polymerase-1 (PARP-1) were identified as proteins that associated with C/EBPalpha. The physical interaction of C/EBPalpha with these partner proteins was further demonstrated by glutathione S-transferase (GST) pull-downs using purified protein expressed in Escherichia coli. The strongest binding was between C/EBPalpha and PARP-1. Immunoprecipitation of C/EBPalpha expressed in prostate cancer cells co-precipitated Ku70, Ku80, and PARP-1. Deletion analysis of C/EBPalpha indicated that the C terminus of C/EBPalpha was essential for the interaction of C/EBPalpha with Ku70, Ku80, and PARP-1. Functional analysis of the interaction between C/EBPalpha and the Ku proteins as well as PARP-1 showed that cells exhibiting these interactions had increased radiation sensitivity and decreased ability to repair double strand DNA breaks. Deficient DNA repair was dependent on the prostate cancer cell line tested, suggesting a complex process. We conclude that the association of C/EBPalpha with Ku proteins and PARP-1 raises the likelihood that C/EBPalpha-expressing prostate cancer cells may be more sensitive to DNA-damaging agents and may be important in the design of new prostate cancer therapies.

Animals↗
PubMed1991

The necessity of dietary vitamin B6 to selenium biopotency for tissue selenium and glutathione peroxidase in rats.

Necessity of dietary vitamin B6 to the biopotency of selenium (Se) for the levels of Se and glutathione peroxidase (GSH-Px) in tissues was investigated. Male Wistar 12-week-old rats were fed a vitamin B6-Se-deficient basal diet for 3 weeks, and then the rats were divided into 6 groups. One group was fed the basal diet, the others were fed the diet supplemented with 250 micrograms vitamin B6/100 g as pyridoxine.HCl, or 0.25 mg Se/kg as Na2SeO3 (SeL) or DL-selenomethionine (Se-Met), or both (SeL+B6 or Se-Met+B6) for 10 week. The levels of Se and GSH-Px in erythrocytes and muscle were significantly higher in vitamin B6-supplemented groups than in vitamin B6-deficient groups. There was little effect of this vitamin deficiency on Se level in liver of rats fed SeL; however, a higher Se level in liver was observed in vitamin B6-deficient rats fed Se-Met than in the corresponding B6-supplemented rats. A significant decrease of GSH-Px activity in liver was found in vitamin B6-deficient animals fed Se-Met compared with vitamin B6-supplemented animals, whereas no significant decrease was observed in those fed SeL. These results suggest that this vitamin is involved in the transport and deliverance of Se in plasma to the other tissues and the incorporation of Se from Se-Met to GSH-Px in liver.

Animals↗
PubMed2006

Early growth response-1 is required for CD154 transcription.

CD154 (CD40 ligand) expression on CD4 T cells is normally tightly controlled, but abnormal or dysregulated expression of CD154 has been well documented in autoimmune diseases, such as systemic lupus erythematosus. Beyond regulation by NFAT proteins, little is known about the transcriptional activation of the CD154 promoter. We identified a species-conserved purine-rich sequence located adjacent to the CD154 transcriptional promoter proximal NFAT site, which binds early growth response (Egr) transcription factors. Gel shift assays and chromatin immunoprecipitation assays reveal that Egr-1, Egr-3, and NFAT1 present in primary human CD4 T cells are capable of binding this combinatorial site in vitro and in vivo, respectively. Multimerization of this NFAT/Egr sequence in the context of a reporter gene demonstrates this sequence is transcriptionally active upon T cell activation in primary human CD4 T cells. Overexpression of Egr-1, but not Egr-3, is capable of augmenting transcription of this reporter gene as well as that of an intact CD154 promoter. Conversely, overexpression of small interfering RNA specific for Egr-1 in primary human CD4 T cells inhibits CD154 expression. Similarly, upon activation, CD154 message is notably decreased in splenic CD4 T cells from Egr-1-deficient mice compared with wild-type controls. Our data demonstrate that Egr-1 is required for CD154 transcription in primary CD4 T cells. This has implications for selective targeting of Egr family members to control abnormal expression of CD154 in autoimmune diseases such as systemic lupus erythematosus.

Animals↗
PubMed2003

Apoptosis caused by cathepsins does not require Bid signaling in an in vivo model of progressive myoclonus epilepsy (EPM1).

Apoptosis can be mediated by mechanisms other than the traditional caspase-mediated cleavage cascade. There is growing recognition that alternative proteolytic enzymes such as the lysosomal cathepsin proteases can initiate or propagate proapoptotic signals, but it is currently unclear how cathepsins achieve these actions. Recent in vitro evidence suggests that cathepsins cleave the proapoptotic Bcl-2 family member Bid, thereby activating it and allowing it to induce the mitochondrial release of cytochrome c and subsequent apoptosis. We have tested this hypothesis in vivo by breeding mice that lack cathepsin inhibition (cystatin B-deficient mice) to Bid-deficient mice, to determine whether the apoptosis caused by cathepsins is dependent on Bid signaling. We found that cathepsins are still able to promote apoptosis even in the absence of Bid, indicating that these proteases mediate apoptosis via a different pathway, or that some other molecule can functionally substitute for Bid in this system.

Age Factors↗
PubMedDate not supplied

Peptidase allergen Der p 1 initiates apoptosis of epithelial cells independently of tight junction proteolysis.

Loss of epithelial cell polarity, which can arise following disruption of tight junctions (TJs), is a precursor to the care-fully orchestrated removal of moribund cells from epithelia in apoptosis. Ordinarily, this cycle of events has minimally disruptive effects on the function of the epithelial barrier, but some agents have been identified that induce apoptosis and promote epithelial leakiness. The allergen Der p 1 is a cysteine peptidase that cleaves TJ adhesion proteins and induces apoptosis in epithelial cells. This suggests the possibility that, at least for some inducers of apoptosis, these events might be causally linked. We report here that Der p 1 induces epithelial apoptosis before outright cell detachment and that apoptosis occurs within the same time span as increased paracellular permeability in polarized epithelial monolayers. Whilst TJ-deficient BEAS-2B cells were resistant to Der p 1-induced apoptosis, the cell line 1HAEo-, which was also TJ deficient, was sensitive to Der p 1, providing evidence against TJ proteolysis as a cause of apoptosis. To provide direct evidence, we propagated cells that normally express TJs in low calcium medium that prevented intercellular junction assembly. These cells retained full susceptibility to Der p 1, indicating that Der p 1-induced apoptosis is independent from TJ proteolysis.

Allergens↗
PubMedDate not supplied

Treatment of longitudinal deficiency affecting the femur: comparing patient mobility and satisfaction outcomes of Syme amputation against extension prosthesis.

Patients with proximal focal femoral deficiency or longitudinal deficiency affecting the femur were selected from a large regional center. Twenty-eight such patients were identified and were divided into two groups depending on how their condition was managed. Group 1 had opted for the surgical approach of ankle disarticulation (Syme amputation) and the fitting of an above-the-knee prosthesis. The patients in group 2 had been managed in a nonsurgical fashion using an extension prosthesis. They were asked about their level of mobility using the recognized Locomotor Index and their overall satisfaction using self-designed questions. The two groups' scores were similar for mobility whether using their prosthesis or not, but group 1 had lower satisfaction scores than group 2. Current opinion advocates the use of surgery in the management of proximal focal femoral deficiency because it is believed to have better cosmetic and functional results, but in the authors' comparison similar scores for mobility were shown. The nonsurgical extension prosthesis was associated with fewer musculoskeletal and residual limb problems, fewer problems with public transport, and greater satisfaction than Syme amputation. Overall, this small study suggests that the nonsurgical approach is preferable.

Adolescent↗
PubMed2004

Periodic painful purpura: fact or factitious?

A 60-year-old woman with multiple psychosocial issues presented with a history of spontaneous painful bruising on her left upper arm. Extensive investigations did not reveal any abnormality apart from an elevated activated partial thromboplastin time as a result of factor XII deficiency. An autoerythrocyte sensitization test reproduced the tender bruises on her back. Our patient reported relief of pain with promethazine injections. She was subsequently referred to the psychiatric team for ongoing assessment and management. Having an awareness of this rare condition will assist in the prevention of unnecessary investigation of such cases and will allow the early referral of patients for appropriate psychological counselling.

Diagnosis, Differential↗
PubMed2006

[Production and identification of the monoclonal antibodies specific for MHC class I complexes bound with HPV16E7 CTL epitopic peptide.].

BACKGROUND: To produce specific monoclonal-antibodies (MAbs) for MHC class I complexes bound with HPV16E7 CTL epitopic peptide (49-57), and provide a foundation for the investigation of the present pathway of viral antigen protein after in vitro viral infection. METHODS: Highly purified HPV16E7CTL epitope (49-57) (RAHYNIVTF) was produced, and then TAP deficient RMA-S cells incubated with RAHYNIVTF were used to immunize the BALB/c mouse. The spleen cells of the mice were regularly harvested and fused with the SP2/0 cells. The growing fusion wells were screened and the abstracted Mabs were identified in terms of sensitivity, specificity and affinity. RESULTS: The screened hybriroma cells could steadily secrete the MAbs specific for MHC class I complexes bound with HPV16E7CTL epitopic peptide. The MAbs showed high reactivity with TAP-deficient RMA-S cells loaded with RAHYNIVTF and RMA-S cells which have the ability to process the endogenous MHC class I complexes, while minimally bound to class I molecules bearing other peptides, the results indicated excellent sensitivity, specificity and affinity of the MAbs. CONCLUSION: The experiments provide a method for producing MAbs for epitopic peptide bound MHC class I complexes.

Amino Acid Sequence↗
PubMed2005

IFN-gamma gene expression is controlled by the architectural transcription factor HMGA1.

We report for the first time that IFNG gene expression requires high mobility group (HMG)A1, the architectural transcription factor mediating enhanceosome formation. This finding is supported by our direct studies of T cells isolated from the HMGA1-transgenic mice displaying an up-regulation of IFN-gamma production and of HMGA1-deficient mice exhibited a decreased IFN-gamma induction. In parallel transfection studies in EL4 cells, we observed elevated IFNG gene promoter activity in cells stably over-expressing HMGA1 and a reduction of such activity in cells expressing dominant-negative HMGA1. In vitro binding assays further demonstrated a specific interaction of HMGA1 to defined regions of the IFNG gene proximal promoter.

Animals↗
PubMed2004

Restoration of NK T cell development in fyn-mutant mice by a TCR reveals a requirement for Fyn during early NK T cell ontogeny.

NK T cells are a unique lymphocyte population that have developmental requirements distinct from conventional T cells. Mice lacking the tyrosine kinase Fyn have 5- to 10-fold fewer mature NK T cells. This study shows that Fyn-deficient mice have decreased numbers of NK1.1(-) NK T cell progenitors as well. 5-Bromo-2'-deoxyuridine-labeling studies indicate that the NK T cells remaining in fyn(-/-) mice exhibit a similar turnover rate as wild-type cells. The fyn(-/-) NK T cells respond to alpha-galactosylceramide, a ligand recognized by NK T cells, and produce cytokines, but have depressed proliferative capacity. Transgenic expression of the NK T cell-specific TCR alpha-chain Valpha14Jalpha18 leads to a complete restoration of NK T cell numbers in fyn(-/-) mice. Together, these results suggest that Fyn may have a role before alpha-chain rearrangement rather than for positive selection or the peripheral upkeep of cell number. NK T cells can activate other lymphoid lineages via cytokine secretion. These secondary responses are impaired in Fyn-deficient mice, but occur normally in fyn mutants expressing the Valpha14Jalpha18 transgene. Because this transgene restores NK T cell numbers, the lack of secondary lymphocyte activation in the fyn-mutant mice is due to the decreased numbers of NK T cells present in the mutant, rather than an intrinsic defect in the ability of the other fyn(-/-) lymphoid populations to respond.

Animals↗
PubMed2006

Biological functions of mammalian Nit1, the counterpart of the invertebrate NitFhit Rosetta stone protein, a possible tumor suppressor.

The "Rosetta Stone" hypothesis proposes that the existence of a fusion protein in some organisms predicts that the separate polypeptides function in the same biochemical pathway in other organisms and may physically interact. In Drosophila melanogaster and Caenorhabditis elegans, NitFhit protein is composed of two domains, a fragile histidine triad homolog and a bacterial and plant nitrilase homolog. We assessed the biological effects of mammalian Nit1 expression in comparison with Fhit and observed that: 1) Nit1 expression was observed in most normal tissues and overlapped partially with Fhit expression; 2) Nit1-deficient mouse kidney cells exhibited accelerated proliferation, resistance to DNA damage stress, and increased cyclin D1 expression; 3) cyclin D1 was up-regulated in Nit1 null mammary gland and skin; 4) Nit1 overexpression induced caspase-dependent apoptosis in vitro; and 5) Nit1 allele deficiency led to increased incidence of N-nitrosomethylbenzylamine-induced murine forestomach tumors. Thus, the biological effects of Nit1 expression are similar to Fhit effects. Adenoviruses carrying recombinant NIT1 and FHIT induced apoptosis in Fhit- and Nit1-deficient cells, respectively, suggesting that Nit1-Fhit interaction is not essential for function of either protein. The results suggest that Nit1 and Fhit share tumor suppressor signaling pathways, while localization of the NIT1 gene at a stable, rather than fragile, chromosome site explains the paucity of gene alterations and in frequent loss of expression of the NIT1 gene in human malignancies.

Acid Anhydride Hydrolases↗
PubMed2001

Neonatal jaundice--traditional Chinese medicine approach.

Herbal treatment of neonatal jaundice (NNJ) has been practiced in China for a long time. Even to-date, a variety of herbal items, including "Yin-chin" (Artemisia), "Huang-qin" (Scutellaria), "Da-huang" (Rheum officinale), "Gan-cao" (Glycyrrhiza), and "Huang-lin" (Coptis chinesis), are still being prescribed to jaundiced infants, often in combination with modern treatment such as phototherapy and exchange transfusion. Their efficacy has, however, not been tested by properly conducted randomised controlled trial. On the other hand, exposure to herbs either before or after birth has been suspected to be a cause of hemolysis and jaundice in the newborns. It is also widely believed in the Chinese community that a number of herbal items are hemolytic agents in infants deficient in the enzyme glucose-6-phosphate dehydrogenase (G6PD). The belief is so deep rooted that each infant detected to have G6PD deficiency by neonatal cord blood screening is given a G6PD deficiency alert card, which states that the child must avoid these herb items for life. In a cohort of 1008 mother-infant pairs, however, we have previously shown that there was no association between maternal herb consumption during pregnancy and the incidence or severity of neonatal hyperbilirubinemia in their offsprings, including those who were deficient in G6PD. A thorough search of medical literature also fails to detect any evidence that any of the herbs stated in the G6PD deficiency alert card causes hemolysis in G6PD-deficient subjects. Thus, there are many misunderstandings and unsubstantiated beliefs about the relationship between herbal medicine and NNJ. Given the potential usefulness of Chinese traditional medicine, which has been practiced for almost 3000 years and is still gaining momentum in the modern days, extensive scientific studies to determine the therapeutic efficacy and potential harmful effects of the various herbal items are warranted.

Drugs, Chinese Herbal↗
PubMed2005

Infections of cefotaxime-resistant and cefmetazole-susceptible Escherichia coli and Klebsiella pneumoniae in children.

A search of the computerized database at the National Taiwan University Hospital was made for cefotaxime-resistant and cefmetazole-susceptible isolates of Escherichia coli and Klebsiella pneumoniae (which may be extended-spectrum beta-lactamase-producing strains) in pediatric wards and intensive care units between 1999 and 2001. Fourteen infectious episodes attributed only to study bacteria were identified, including 7 episodes of bacteremia. Nine patients (64.3%) had underlying medical conditions: 3 were premature babies, 3 were immunodeficient, 2 had malignancy, and 2 had a congenital heart disease with active heart failure even after surgery. Among the 7 patients with bacteremias, 5 may be catheter-related; 6 were treated with carbapenems and 1 was treated with cefmetazole successfully, with or without the removal of the catheter. Before the acquisition of the infection, a history of stay in an intensive care unit within 4 weeks was noted in 10 cases (71.4%); a history of use of extended-spectrum cephalosporins within 4 weeks was also noted in 6 cases (42.9%). Cefmetazole, with or without an aminoglycoside, was clinically effective in 6 cases (42.8%). Except for 1 episode of pneumonia that ended in mortality, all of the infectious episodes were successfully treated. The mortality rate was 7.1%.

Adolescent↗
PubMed2006

NK and CD4 cells collaborate to protect against melanoma tumor formation in the brain.

NK cells represent a potent immune effector cell type that have the ability to recognize and lyse tumors. However, the existence and function of NK cells in the traditionally "immune-privileged" CNS is controversial. Furthermore, the cellular interactions involved in NK cell anti-CNS tumor immunity are even less well understood. We administered non-Ag-loaded, immature dendritic cells (DC) to CD8alpha knockout (KO) mice and studied their anti-CNS tumor immune responses. DC administration induced dramatic antitumor immune protection in CD8alpha KO mice that were challenged with B16 melanoma both s.c. and in the brain. The CNS antitumor immunity was dependent on both CD4+ T cells and NK cells. Administration of non-Ag-loaded, immature DC resulted in significant CD4+ T cell and NK cell expansion in the draining lymph nodes at 6 days postvaccination, which persisted for 2 wk. Finally, DC administration in CD8alpha KO mice was associated with robust infiltration of CD4+ T cells and NK cells into the brain tumor parenchyma. These results represent the first demonstration of a potent innate antitumor immune response against CNS tumors in the absence of toxicity. Thus, non-Ag-loaded, immature DC administration, in the setting of CD8 genetically deficient mice, can induce dramatic antitumor immune responses within the CNS that surpass the effects observed in wild-type mice. Our results suggest that a better understanding of the cross-talk between DC and innate immune cells may provide improved methods to vaccinate patients with tumors located both systemically and within the CNS.

Animals↗
PubMed2002

DNA-based diagnosis of isolated sulfite oxidase deficiency by denaturing high-performance liquid chromatography.

Isolated sulfite oxidase deficiency is a rare autosomal recessive disease, characterized by severe neurological abnormalities, seizures, mental retardation, and dislocation of the ocular lenses, that often leads to death in infancy. There is a special demand for prenatal diagnosis, since no effective treatment is available for isolated sulfite oxidase deficiency. Until now, the cDNA sequence of the sulfite oxidase (SUOX) gene has been available, but the genomic sequence of the SUOX gene has not been published. In this study, we have performed a DNA-based diagnosis of isolated sulfite oxidase deficiency in a Chinese patient. To do so, we designed oligonucleotide primers for amplification of the predicted exons and intron-exon boundaries of the SUOX gene obtained from the completed draft version of the human genome. Using overlapping PCR products, we confirmed the flanking intronic sequences of the coding exons and that the entire 466-residue mature peptide is encoded by the last exon of the gene. We then performed mutation detection using denaturing high-performance liquid chromatography (DHPLC). The DHPLC chromatogram of exon 2b showed the presence of heteroduplex peaks only after mixing of the mutant DNA with the wild-type DNA, indicating the presence of a homozygous mutation. Direct DNA sequencing showed a homozygous base substitution at codon 160, changing the codon from CGG to CAG, which changes the amino acid from arginine to glutamine, i.e., R160Q. The DNA-based diagnosis of isolated sulfite oxidase deficiency will enable us to make an accurate determination of carrier status and to perform prenatal diagnosis of this disease. The availability of the genomic sequences of human genes from the completed draft human genome sequence will simplify the development of molecular genetic diagnoses of human diseases from peripheral blood DNA.

Child, Preschool↗
PubMedDate not supplied

L-Arabinosuria: a new defect in human pentose metabolism.

A female patient, the first child of healthy non-consanguineous parents, presented at the age of 16 months with delayed motor development and facial dysmorphism. In addition she displayed a palatoschizis and multiple skeletal abnormalities as hypoplastic scapulae, hypoplastic os ilea, and an extreme cervical kyphosis. Biochemical investigation of urine revealed no abnormalities except for the presence of large amounts of reducing sugars. The sugar was identified as L-arabinose, which mainly originated from fruit formula in her diet. In addition highly elevated levels of L-arabitol were found in urine, plasma, and cerebrospinal fluid. Although little is known about human arabinose metabolism, we presume that L-arabitol dehydrogenase is deficient in our patient. As polyols are potentially toxic to the central nervous system there could be deleterious long-term effects of this disorder. Withdrawal of dietary fruit led to normalization of polyol levels. The above-mentioned clinical abnormalities are probably not related to this new inborn error of metabolism and should be considered as a separate entity.

Arabinose↗
PubMed2006

Abnormal CpG island methylation occurs during in vitro differentiation of human embryonic stem cells.

Directed differentiation of human embryonic stem cells (hESCs) into specific somatic cells holds great promise for cell replacement therapies. However, it is unclear if in vitro hESC differentiation causes any epigenetic abnormality such as hypermethylation of CpG islands. Using a differential methylation hybridization method, we identified 65 CpG islands (out of 4608 CpG islands or 1.4%) that exhibited increased DNA methylation during the conversion of hESCs into neural progenitor/stem cells (NPCs). These methylated CpG islands belong to genes in cell metabolism, signal transduction and cell differentiation, which are distinctively different from oncogenic CpG island hypermethylation observed in cancer-related genes during tumorigenesis. We further determined that methylation in these CpG islands, which is probably triggered by de novo DNA methyltransferase Dnmt3a, is abnormally higher in hESC-NPCs than in primary NPCs and astrocytes. Correlating with hypermethylation in promoter CpG islands of metabolic enzyme gene CPT1A and axoneme apparatus gene SPAG6, levels of CPT1A and SPAG6 mRNAs are significantly reduced in hESC-NPCs when compared with hESCs or primary neural cells. Because CPT1A is involved in lipid metabolism and CPT1A deficiency in human is associated with the hypoketotic hypoglycemia disorder, the reduced CPT1A expression in hESC-NPCs raises a potential concern for the suitability of these cells in cell transplantation. Collectively, our data show that abnormal CpG island methylation takes place in a subset of genes during the differentiation/expansion of hESC derivatives under current culture conditions, which may need to be monitored and corrected in future cell transplantation studies.

Astrocytes↗