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At least 469 records · Page 26Linked to original sources
PubMed2001

The murine cysteinyl leukotriene 2 (CysLT2) receptor. cDNA and genomic cloning, alternative splicing, and in vitro characterization.

Two classes of cysteinyl leukotriene receptor, CysLT(1) and CysLT(2), have been identified and pharmacologically characterized in human tissues. Although the CysLT(1) receptor mediates the proinflammatory effects of leukotrienes in human asthma, the physiological roles of CysLT(2) receptor are not defined, and a suitable mouse model would be useful in delineating function. We report here the molecular cloning and characterization of the mouse CysLT(2) receptor (mCysLT(2)R) from heart tissue. mCysLT(2)R cDNA encodes a protein of 309 amino acids, truncated at both ends compared with the human ortholog (hCysLT(2)R). The gene resides on the central region of mouse chromosome 14 and is composed of 6 exons with the entire coding region located in the last exon. Two 5'-untranslated region splice variants were identified with the short form lacking exon 3 as the predominant transcript. Although the overall expression of mCysLT(2)R is very low, the highest expression was detected in spleen, thymus, and adrenal gland by ribonuclease protection assay, and discrete sites of expression in heart were observed by in situ hybridization. Intracellular calcium mobilization in response to cysteinyl leukotriene administration was detected in human embryonic kidney 293T cells transfected with recombinant mCysLT(2)R with a rank order of potency leukotriene C(4)(LTC(4) ) = LTD(4)>>LTE(4). [(3)H]LTD(4) binding to membranes expressing mCysLT(2)R could be effectively competed by LTC(4) and LTD(4) and only partially inhibited by LTE(4) and BAYu9773. The identification of mCysLT(2)R will be useful for establishing CysLT(2)R-deficient mice and determining novel leukotriene functions.

5' Untranslated Regions↗
PubMed2003

Leptin gene expression and serum leptin levels in zinc deficiency: implications for appetite regulation in rats.

Zinc deficiency in animals causes impaired growth and anorexia, and the mechanisms for these symptoms of zinc deficiency are not yet clear. We investigated whether circulating leptin levels and gene expression would be dysregulated under zinc deficiency and what would be the implications for appetite in rats. In study 1, 24 Sprague-Dawley rats were provided consecutively with three different dietary zinc intake levels: Zn-adequate (30 mg/kg of diet), Zn-depleted (1 mg/kg of diet), and Zn-replete (50 mg/kg of diet), for 1, 2, and 2 weeks, respectively. At the end of each dietary period, one-third of the rats were killed. In study 2, rats were assigned to one of the four Zn diet groups: Zn-adequate (30 mg/kg of diet), pair-fed (30 mg/kg of diet), Zn-deficient (1 mg/kg of diet), or Zn-sufficient (50 mg/kg of diet), and were fed for 4 weeks. Tissue Zn and serum leptin were measured, and leptin gene expression in adipose tissues (inguinal and abdominal) was determined by reverse transcription-polymerase chain reaction and northern blotting. Blood subfractions as plasma, red blood cells, and mononuclear cells and liver Zn level were decreased during the Zn-depletion period (P <.05). Serum leptin showed a tendency to increase during the Zn-depletion period and decreased back to the level of the Zn-repletion period. Leptin mRNA levels in inguinal adipocytes also increased during the Zn-depletion (P <.05) and Zn-deficient periods, which is consistent with the change in serum leptin. However, the decrease in leptin mRNA in abdominal adipocytes was not consistent with the increase in inguinal leptin levels and the change in serum leptin. Increased leptin levels in linguinal adipocytes is consistent with the expected physiological change of a decrease in appetite under Zn deficiency. However, before coming to any firm conclusion, further studies on adipose tissue-specific leptin expression, including the appetite-related neuropeptides, are necessary for clarifying the cause of lower appetite in zinc deficiency.

Adipocytes↗
PubMed1985

Selenium intake and metabolic balance of 10 men from a low selenium area of China.

Selenium intake and urinary and fecal Se excretion of 10 healthy men from a low Se area in China were determined for three consecutive days, in summer, fall, and winter of 1983, and the spring of 1984 while self-selected diets were being consumed. Mean daily Se intake was 8.8 micrograms/day with a range of 2.3-35.5 micrograms/day, and was far below the recommended range of safe and adequate Se intake of 50-200 micrograms Se/day (National Academy of Sciences/National Research Council). Mean urinary and fecal Se outputs were 3.7 and 3.4 micrograms Se/day, respectively. Mean Se balance during this time was +1.8 micrograms Se/day. Apparent absorption of Se approximated 57%. The low Se intake in this area is a cause for concern since the residents of Molimo may be at risk for Se deficiency diseases.

Adult↗
PubMed1985

Bioavailability of selenium to residents in a low-selenium area of China.

For 8 wk 5 groups of 10 men each were given 0.5 g/day DL-methionine, 150 micrograms Se/day as sodium selenite with or without methionine or 150 micrograms Se/day as selenomethionine with or without methionine. Twenty subjects received placebo as controls. Initially plasma Se rose more rapidly than RBC Se. Increases in Se levels were significantly greater with selenomethionine than with the selenite supplement. In the placebo and methionine supplemented groups neither plasma nor RBC Se varied significantly over the course of the study. Supplementation with selenium resulted in marked increases in plasma and RBC GSH-Px within 2 and 4 wk, respectively. Plasma and RBC GSH-Px activity did not differ significantly between Se-supplemented groups. These studies suggest that selenomethionine-Se was more effective in raising plasma and RBC Se than was selenite-Se. Methionine supplements may increase the bioavailability of selenium in severely deficient subjects.

Adult↗
PubMed2006

Human interleukin-15 improves engraftment of human T cells in NOD-SCID mice.

Human nonobese diabetic-severe combined immune deficiency (NOD-SCID) mouse chimeras have been widely used as an in vivo model to assess human immune function. However, only a small fraction of transferred human T lymphocytes can be detected in human peripheral blood lymphocyte (huPBL)-NOD-SCID chimeras. To improve the reconstitution of human T lymphocytes in NOD-SCID mice, the use of recombinant human interleukin-15 (rhIL-15) as a stimulator of human lymphocytes was explored. Administration of rhIL-15 after transplantation of huPBLs into NOD-SCID mice increased reconstitution of human T lymphocytes in a dose-dependent manner, with an optimal dosage of 1 microg/mouse. The number of human T lymphocytes (HLA-ABC+ CD3+) in the lymphoid organs or tissue of rhIL-15-treated huPBL-NOD-SCID mice increased 11- to 80-fold, and phytohemagglutinin-induced T-lymphocyte proliferation and cytokine production were significantly enhanced. Additionally, although mature human cells have not been thought to enter the murine thymus, human T lymphocytes were detected in the huPBL-NOD-SCID thymus after rhIL-15 treatment. Thus, rhIL-15 can be used to optimize long-term peripheral T-cell engraftment in these human-mouse chimeras and may also be useful in clinical treatment of T-cell deficiencies.

Animals↗
PubMed2003

It takes two to tango: mast cell and Schwann cell interactions in neurofibromas.

Neurofibromas are benign tumors comprised primarily of Schwann cells and fibroblasts. Mast cell infiltration is a well-known phenomenon; however, their role in tumor pathogenesis has been enigmatic. In an elegant set of experiments using cells derived from a murine model of neurofibromatosis 1 (NF1), Yang et al. dissect the molecular pathways involved in mast cell migration to neurofibromin-deficient Schwann cells. These results set the stage for rational development of therapeutics that could influence the multicellular microenvironment of neurofibromas to inhibit the development and/or progression of these tumors in human NF1.

Alleles↗
PubMed1996

[Allotransplantation of fetal adrenal capsules for treating steroid deficiency].

A man suffering from bilateral adrenal carcinoma was treated by total adrenalectomy and steroids substitution. One and a half months later, two fetal adrenal capsules were grafted to his greater omentum. No immunosuppressive agent was given. From the fourth month exogenous steroid dose was gradually reduced. Five months after transplantation, substitution therapy was discontinued. The patient showed no signs of steroid deficiency and all laboratory studies were normal. Seven months later, the patient died of metastasis of the carcinoma. Pathological examination showed that much adrenal cortex had regenerated in the greater omentum. The findings suggest that this method for treating chronic steroid deficiency is simple and successful.

Adenocarcinoma↗
PubMedDate not supplied

Community-acquired Pseudomonas aeruginosa pneumonia complicated with loculated empyema in an infant with selective IgA deficiency.

Pseudomonas aeruginosa is widely prevalent in the hospital environment, especially in intensive care units. Selective IgA deficiency is characterized by a serum IgA level less than 5 mg/dl with no deficiency of other immunoglobulins. The occurrence of community-acquired P. aeruginosa pneumonia with empyema is rare in pediatric patients. We present a 10-month-old male infant who was referred due to persistent fever and progressive respiratory distress for 1 week. A chest radiograph revealed a right lobar pneumonia with pleural effusion. P. aeruginosa that was subsequently isolated from both blood and pleural effusion cultures. The patient received treatment with ceftazidime and intrapleural instillation of urokinase to promote drainage of empyema. Subsequent immunological screening revealed a very low serum IgA level (<5 mg/dl). We present our experience in successfully treating a loculated empyema with intrapleural instillation of urokinase in an infant. It is also important for pediatricians to be aware that they should be alert for the patient who present with respiratory infections due to unusual organisms. An advanced immunological study to investigate the underlying disorders in these patients is mandatory.

Community-Acquired Infections↗
PubMed1991

Immunoglobulin G subclass deficiency in children with recurrent respiratory tract infections.

With monoclonal antibodies serum immunoglobulin G(IgG) subclasses were measured in seventy children aged 2 to 13 years with recurrent respiratory tract infections including upper respiratory tract infections, otitis media, sinusitis, asthmatic bronchitis and pneumonia. 211 healthy, aged-matched children served as control. IgG subclass deficiency was found in 19 out of the 70 patients (27.1%, single IgG1 deficiency in 7, IgG2 deficiency in 4, combined IgG1-IgG3 deficiency in 5, IgG1-IgG2-IgG3-IgG4 deficiency, IgG1-IgG2-IgG4 deficiency and IgG2-IgG4 deficiency each in 1). The incidence of IgG subclass deficiencies was in the sequence as follows: IgG1, 20%; IgG2, 10%; IgG3, 8.6% and IgG4, 4.3%. The results suggest that IgG subclass deficiency indicate a common disorder in children with recurrent respiratory tract infections.

Adolescent↗
PubMed1997

[Localization of ferritin in placental villous tissue and its role in the maternal-fetal iron transport].

OBJECTIVE: To investigate the localization and quantity of ferritin in placental villous tissue and its implications. METHODS: The localization of ferritin in placental villous tissue at different gestation period was assayed by immunocytochemistry. The quantity of ferritin in placental villous tissue was determined with radioimmunoassay. RESULTS: Ferritin was localized in all layers of the trophoblast, especially in the surface of the syncytiotrophoblast and basal membrane. The quantity of ferritin in placental villous tissue was increased with gestation progress and decreased in pregnant women with IDA. CONCLUSIONS: Ferritin may be the important carrier of transplacental iron transport, and its receptor plays a crucial role in the course. The placental iron transport varied with gestation progress and iron nutritional status of the mother.

Anemia, Iron-Deficiency↗
PubMed2001

Biochemical and biological characterization of a human Rac2 GTPase mutant associated with phagocytic immunodeficiency.

The Rho GTPase, Rac2, is expressed only in hematopoietic cell lineages, suggesting a specific cellular function in these cells. Genetic targeting studies in mice showed that Rac2 is an essential regulator of neutrophil chemotaxis, L-selectin capture and rolling, and superoxide production. Recently, a dominant negative mutation of Rac2, D57N, has been reported to be associated with a human phagocytic immunodeficiency. To understand further the cellular phenotypes associated with this D57N Rac2 mutant we examined its biochemical characteristics and functional effects when expressed in primary murine bone marrow cells. When compared with wild type (WT) Rac2, D57N Rac2 displayed approximately 10% GTP binding ability resulting from a markedly enhanced rate of GTP dissociation and did not respond to the guanine nucleotide exchange factors. These results suggest that D57N Rac2 may act in a dominant negative fashion in cells by sequestering endogenous guanine nucleotide exchange factors. When expressed in hematopoietic cells, D57N Rac2 reduced endogenous activities of not only Rac2, but also Rac1 and decreased cell expansion in vitro in the presence of growth factors due to increased cell apoptosis. Unexpectedly, D57N expression had no effect on proliferation. In contrast, expansion of cells transduced with WT Rac2 and a dominant active mutant, Q61L, was associated with significantly increased proliferation. Transplantation of transduced bone marrow cells into lethally irradiated recipients showed that the percentage of D57N-containing peripheral blood cells decreased markedly from 40% at 1 month to <5% by 3 months postinjection. Neutrophils derived in vitro from the transduced progenitor cells containing D57N demonstrated markedly impaired migration and O(2)(-) responses to formyl-methionyl-leucyl-phenylalanine, reflecting the same cellular phenotype in these differentiated cells as those described previously in patient cells. These data suggest that the phenotypic abnormalities associated with D57N Rac2 may involve not only neutrophil cellular functions, but also abnormal cell survival in other hematopoietic cells and that overexpression of Rac leads to increased proliferation of normal cells in vitro, whereas deficiency of Rac leads to increased apoptosis.

Amino Acid Substitution↗
PubMed1999

[Molecular characterization of glucose-6-phosphate dehydrogenase variants in four ethnic groups in Yunnan province of China].

OBJECTIVE: In order to understand the molecular evolution, race origin and the relationship between the G6PD gene structure and clinical symptoms, the authors identified the molecular characterization of glucose-6-phosphate dehydrogenase and determined the G6PD gene frequency in four ethnic groups in Yunnan province of China. METHODS: The point mutations of G6PD were detected by Mismatch-PCR/RE, SSCP,ARMS,DNA sequence and so on. G6PD gene frequency was determined by Hardy-Weinberg Law. RESULTS: G6PD G1388A, G1376T,A95G mutations were determined in Bai and Dai people for the first time and G1388A also in Harni people by DNA sequence. G6PD C1024T were detected in Dai population by Mismatch-PCR/RE. The gene frequency of G6PD in Bai population in Dali city is 0.0113, and the incidence is 1.19% which are different from those in Dai population. CONCLUSION: G6PD G1388A,G1376T, A95G and C1024T are the mutations in national minorities as well as in the Han people. The results suggest that different national minorities of China may have the same ancestor. The incidence of G6PD deficiency and the G6PD gene frequency in Bai population are different from those in Dai population. The distribution of G6PD deficiency in Yunnan is associated with the distribution of malaria epidemic in that province.

China↗
PubMed1990

Temperature sensitivity as a general phenomenon in a collection of chlorophyll-deficient mutants of sweetclover (Melilotus alba).

A collection of chlorophyll (Chl)-deficient mutants of sweetclover (Melilotus alba) with defects in eight nuclear loci were grown at 17 or 26 degrees C. Plants grown at either temperature were examined for Chl content, Chl a/b ratio, expression of the light-harvesting complex II (LHC-II) apoproteins, and protochlorophyllide (Pchlide) biosynthetic capacity. Except for the ch4 mutant, the parental strain and all mutants accumulate more Chl when grown at 26 degrees C than at 17 degrees C. The ch5 mutants, lacking Chl b under any growth condition, and the ch12 mutant showed little temperature-dependent phenotypic plasticity, whereas this was a marked phenomenon in the other mutants. The ch10 and ch11 mutants demonstrated extreme temperature sensitivity with regard to the production of Chl b and the Chl b-binding LHC-II apoproteins. When excised trifoliolates were supplemented with exogenously supplied delta-aminolevulinic acid, only the ch4 mutant was markedly impaired in the ability to produce Pchlide. These data indicate that temperature-sensitive phenotypic plasticity is a common phenomenon of chlorphyll-deficient mutants and substantiate that only a minority of Chl-deficient mutants is impaired in the biosynthesis of Chl.

Animals↗
PubMed2006

Knocking down dickkopf-1 alleviates estrogen deficiency induction of bone loss. A histomorphological study in ovariectomized rats.

Dickkopf-1 (DKK1) has been found to act as a potent Wnt signaling-inhibitory factor for regulating skeletal disorders. We investigated whether modulation of DKK1 expression by end-capped phosphorothioate DKK1 antisense oligonucleotide could alter estrogen loss-induced bone loss. Ovariectomized or sham-operated rats were given 20 microg/kg/day DKK1 sense or antisense oligonucleotide or vehicle for 28 days. Femurs and tibiae were dissected to assess bone mass, biomechanical strength, immunohistochemistry and ex vivo osteoclast formation. We found that DKK1 antisense oligonucleotide significantly abrogated the suppressing effect of ovariectomy on weight, mineral content, mineral density and peak load of femurs. DKK1 antisense oligonucleotide treatment reduced ovariectomy promotion of ex vivo osteoclast differentiation of primary M-CSF-dependent bone marrow macrophages. Histomorphometric observation demonstrated that DKK1 antisense oligonucleotide treatment increased osteoblast number and impaired ovariectomy-promoted trabecular bone loss and osteoclast number in bone tissue. Osteoblastic cells adjacent to endosteum of trabecular bone and chondrocytes at calcified cartilage expressed intensive DKK1 and RANKL and weak OPG immunostaining in ovariectomized rat bone microenvironments. Osteogenic cells and chondral cells displayed weak DKK1, RANKL and OPG expression of bone tissue after DKK1 antisense oligonucleotide treatment. Taken together, attenuation of DKK1 expression in ovariectomized rat bone tissue alleviated loss of bone mass and biomechanical property. The regulatory action of DKK1 antisense oligonucleotide treatment on bone tissue appeared to suppress the promoting effect of estrogen deficiency on osteoclastogenesis-stimulatory factor RANKL expression and osteoclast differentiation. Control of DKK1 signaling can be used in the future as an alternative strategy for protecting estrogen deficiency induction of bone loss.

Animals↗
PubMedDate not supplied

DNA damage and repair in lymphoblastoid cell lines from normal donors and fragile X syndrome patients.

BACKGROUND: Because lymphocytes from fragile X patients have been reported as hypersensitive to bleomycin-induced chromatid breaks and because the number of trinucleotide repeats in families with fragile X syndrome has a propensity to expand, we have investigated the possibility that fragile X cells may be hypersensitive to DNA damage and have a lower capacity for DNA repair. METHODS: Lymphocytes from normal and fragile X syndrome donors were immortalized by Epstein-Barr virus transformation. Characteristics of fragile X syndrome including the folate-sensitive fragile site on chromosome Xq27.3, length of CGG repeat expansion, and FMRP expression in Epstein-Barr virus-transformed lymphoblastoid cell lines were analyzed by standard cytogenetic methods, Southern blot, and Western blot, respectively. Analysis of DNA damage and repair induced by hydrogen peroxide, bleomycin, ethyl methanesulfonate, 4-nitroquinoline-N-oxide, etoposide, and mitomycin C was carried out by single-cell gel electrophoresis assay (known as comet assay). RESULTS: Lymphoblastoid cell lines from fragile X donors had a folate-sensitive fragile site on chromosome Xq27.3, no or low FMRP expression, and expansion of the CGG repeat. Results of comet assay showed that fragile X cells were not more sensitive to mutagen-induced DNA strand breaks and did not have lower DNA repair capacity in comparison with normal cells. Furthermore, one fragile X cell line showed hyposensitivity to DNA strand breaks induced by hydrogen peroxide, bleomycin, and ethyl methansulfonate. CONCLUSIONS: The results of this study do not support the notion that CGG trinucleotide expansion in fragile X syndrome is caused by permanent deficiency in DNA repair.

4-Nitroquinoline-1-oxide↗
PubMed2001

Reconstitution of caspase 3 sensitizes MCF-7 breast cancer cells to doxorubicin- and etoposide-induced apoptosis.

MCF-7, a breast cancer-derived cell line, is deficient of caspase 3 and relatively insensitive to many chemotherapeutic agents. To study the association of caspase 3 deficiency and chemotherapeutic resistance, we reconstituted caspase 3 in MCF-7 cells and characterized their apoptotic response to doxorubicin and etoposide. Western blots demonstrated that caspase 3 was constitutively expressed in the reconstituted MCF-7 cells. Both morphological observation and survival assays showed that caspase 3 reconstitution significantly sensitized MCF-7 cells to both drugs. Remarkably increased activation of caspases 3, 6, and 7, cleavage of cellular death substrates, and DNA fragmentation were detected in the reconstituted MCF-7 cells after drug treatment. Together, these data demonstrated a specific role for caspase 3 in chemotherapy-induced apoptosis and in activation of caspases 6 and 7. Our results also suggest that caspase 3 deficiency may contribute to chemotherapeutic resistance in breast cancer.

Antibiotics, Antineoplastic↗