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At least 721 records · Page 40Linked to original sources
PubMed2005

[Intervention of maiwei dihuang oral liquid on hormonotherapy in treating active systemic lupus erythematosus].

OBJECTIVE: To observe the intervention of Maiwei Dihuang Oral Liquid (MDOL) on hormonotherapy in treating active systemic lupus erythematosus (SLE). METHODS: Sixty SLE patients in active stage were randomly and equally allocated into two groups, and administered with prednisone, which was medicated in initial dose of 0.5-1 mg/kg, and with the dose being reduced conditionally 6-8 weeks. To the 30 patients in the treated group 10 ml MDOL twice daily was given additionally. The therapeutic course was 3 months. RESULTS: The therapeutic effect in the treated group was better than that in the control group (P < 0.05). Systemic lupus erythematosus disease activity index (SLEDAI) was significantly improved in both groups (P < 0.01), but was superior in the treated group (P < 0.05). The dose of prednisone used was significantly reduced (P < 0.01), and the scores of Yin-deficiency fire-flourishing syndrome were obviously decreased (P < 0.01) in the treated group while in the control group, these indexes were unchanged (P > 0.05), the difference between the two groups was significant (P < 0.01). The occurrence of adverse reaction was significantly lower in the treated group than that in the control group (P < 0.05). CONCLUSION: MDOL can obviously improve the effect of hormonotherapy in SLE, it has advantages in reducing the dosage used and antagonizing the adverse reactions of glucocorticoid.

Adolescent↗
PubMed2004

[Association between subacute combined degeneration, vitamin B12 deficiency and megaloblastic anemia].

OBJECTIVE: To investigate the association between subacute combined degeneration (SCD) and vitamin B(12) (VB(12)) deficiency and megaloblastic anemia (MA). METHODS: The serum level of VB(12), severity of anemia and lesions in CNS were analysed in 36 cases diagnosed as SCD. In addition, MRI neuro-electrophysiologic examination and CSF myelin basic protein (MBP) concentration were monitored dynamically. The prognosis of SCD was evaluated in relation to the time of the initiation of therapy. RESULTS: Average ferrohemoglobin level in patients was (77.1 +/- 11.2) g/L and the average blood serum level of VB(12) was (87.0 +/- 21.4) ng/L before treatment with an abnormality rate of 47.2%. However, there was no linear correlation between the severity of lesions in CNS and ferrohemoglobin level or level of serum VB(12) (correlation coefficient: r = -0.1917, 0.0926, P > 0.5; r = 0.207, 0.101, P > 0.5, respectively). The comprehensive abnormal rate of evoked potential was 100%, which might occur prior to the clinical symptoms of SCD. The abnormal rate of MRI was 71.4%, and some lesions could diminish or disappear after treatment. The MBP levels in CSF were (3.96 +/- 1.66) ng/L, and (2.25 +/- 1.66) ng/L before and 3 months after the treatment. No significant improvement of symptoms and signs were seen when the treatment was initiated 6 months after the diagnosis. CONCLUSION: SCD is associated with VB(12) deficiency and often accompanied by MA, but there is no linear correlation. Lesions of SCD in spinal cord or brain can be demonstrated in MRI. Evoked potential is critical for early diagnose and identification of silent cases of SCD. The level of MBP in CSF can reflect the severity of the lesion and prosthetic state of myelin sheath. Early diagnosis and treatment play an important role in decreasing the degree of the permanent dysfunction of CNS in SCD.

Adolescent↗
PubMed2005

Phospholipid transfer protein deficiency impairs apolipoprotein-B secretion from hepatocytes by stimulating a proteolytic pathway through a relative deficiency of vitamin E and an increase in intracellular oxidants.

Genetic deficiency of the plasma phospholipid transfer protein (PLTP) in mice unexpectedly causes a substantial impairment in liver secretion of apolipoprotein-B (apoB), the major protein of atherogenic lipoproteins. To explore the mechanism, we examined the three known pathways for hepatic apoB secretory control, namely endoplasmic reticulum (ER)/proteasome-associated degradation (ERAD), post-ER pre-secretory proteolysis (PERPP), and receptor-mediated degradation, also known as re-uptake. First, we found that ERAD and cell surface re-uptake were not active in PLTP-null hepatocytes. Moreover, ER-to-Golgi blockade by brefeldin A, which enhances ERAD, equalized total apoB recovery from PLTP-null and wild-type cells, indicating that the relevant process occurs post-ER. Second, because PERPP can be stimulated by intracellular reactive oxygen species (ROS), we examined hepatic redox status. Although we found previously that PLTP-null mice exhibit elevated plasma concentrations of vitamin E, a lipid anti-oxidant, we now discovered that their livers contain significantly less vitamin E and significantly more lipid peroxides than do livers of wild-type mice. Third, to establish a causal connection, the addition of vitamin E or treatment with an inhibitor of intracellular iron-dependent peroxidation, desferrioxamine, abolished the elevation in cellular ROS as well as the defect in apoB secretion from PLTP-null hepatocytes. Overall, we conclude that PLTP deficiency decreases liver vitamin E content, increases hepatic oxidant tone, and substantially enhances ROS-dependent destruction of newly synthesized apoB via a post-ER process. These findings are likely to be broadly relevant to hepatic apoB secretory control in vivo.

Animals↗
PubMed2001

Autosomal dominant glut-1 deficiency syndrome and familial epilepsy.

Glut-1 deficiency syndrome was first described in 1991 as a sporadic clinical condition, later shown to be the result of haploinsufficiency. We now report a family with Glut-1 deficiency syndrome affecting 5 members over 3 generations. The syndrome behaves as an autosomal dominant condition. Affected family members manifested mild to severe seizures, developmental delay, ataxia, hypoglycorrhachia, and decreased erythrocyte 3-O-methyl-D-glucose uptake. Seizure frequency and severity were aggravated by fasting, and responded to a carbohydrate load. Glut-1 immunoreactivity in erythrocyte membranes was normal. A heterozygous R126H missense mutation was identified in the 3 patients available for testing, 2 brothers (Generation 3) and their mother (Generation 2). The sister and her father were clinically and genotypically normal. In vitro mutagenesis studies in Xenopus laevis oocytes demonstrated significant decreases in the transport of 3-O-methyl-D-glucose and dehydroascorbic acid. Xenopus oocyte membranes expressed high amounts of the R126H mutant Glut-1. Kinetic analysis indicated that replacement of arginine-126 by histidine in the mutant Glut-1 resulted in a lower Vmax. These studies demonstrate the pathogenicity of the R126H missense mutation and transmission of Glut-1 deficiency syndrome as an autosomal dominant trait.

3-O-Methylglucose↗
PubMed1996

Clinical significance of the changes in serum fibronectin in severely burned patients.

The Agar gel single diffusion technique was used to investigate the changes in serum fibronectin (FN) in severely burned patients, and coupled with the study of simultaneous changes in the internal organ function, the development of MOF and severe systemic infection. The results suggested that the deficiency or decrease in serum FN made the host more prone to severe systemic infection, even to MOF.

Adolescent↗
PubMed2001

Genetic interactions between ATM and the nonhomologous end-joining factors in genomic stability and development.

DNA ligase IV (Lig4) and the DNA-dependent protein kinase (DNA-PK) function in nonhomologous end joining (NHEJ). However, although Lig4 deficiency causes late embryonic lethality, deficiency in DNA-PK subunits (Ku70, Ku80, and DNA-PKcs) does not. Here we demonstrate that, similar to p53 deficiency, ataxia-telangiectasia-mutated (ATM) gene deficiency rescues the embryonic lethality and neuronal apoptosis, but not impaired lymphocyte development, associated with Lig4 deficiency. However, in contrast to p53 deficiency, ATM deficiency enhances deleterious effects of Lig4 deficiency on growth potential of embryonic fibroblasts (MEFs) and genomic instability in both MEFs and cultured progenitor lymphocytes, demonstrating significant differences in the interplay of p53 vs. ATM with respect to NHEJ. Finally, in dramatic contrast to effects on Lig4 deficiency, ATM deficiency causes early embryonic lethality in Ku- or DNA-PKcs-deficient mice, providing evidence for an NHEJ-independent role for the DNA-PK holoenzyme.

Animals↗
PubMed1999

The plasminogen activator inhibitor-2 gene is not required for normal murine development or survival.

Plasminogen activator inhibitor-2 (PAI-2), a member of the serpin gene family, is thought to serve as a primary regulator of plasminogen activation in the extravascular compartment. High levels of PAI-2 are found in keratinocytes, monocytes, and the human trophoblast, the latter suggesting a role in placental maintenance or embryo development. The primarily intracellular distribution of PAI-2 also may indicate a unique regulatory role in a protease-dependent cellular process such as apoptosis. To examine the potential functions of PAI-2 in vivo, we generated PAI-2-deficient mice by gene targeting in embryonic stem cells. Homozygous PAI-2-deficient mice exhibited normal development, survival, and fertility and were also indistinguishable from normal controls in response to a bacterial infectious challenge or endotoxin infusion. No differences in monocyte recruitment into the peritoneum were observed after thioglycollate injection. Epidermal wound healing was equivalent among PAI-2 -/- null and control mice. Finally, crossing PAI-2 -/- with PAI-1 -/- mice to generate animals deficient in both plasminogen activator inhibitors failed to uncover an overlap in function between these two related proteins.

Animals↗
PubMed2003

Identification of Shp-2 as a Stat5A phosphatase.

Stat5A, a member of the signal transducers and activators of transcription (Stat) family, is activated upon a single tyrosine phosphorylation. Although much is known about the activation process, the mechanism by which the tyrosine-phosphorylated Stat5A proteins are inactivated is largely unknown. In this report, we demonstrate that down-regulation of the tyrosine-phosphorylated Stat5A was via dephosphorylation. Using tyrosine-phosphorylated peptides derived from Stat5A, we were able to purify protein-tyrosine phosphatase Shp-2 from cell lysates. Shp-2, but not Shp-1, specifically interacted with Stat5A in vivo, and the interaction was tyrosine phosphorylation-dependent. Moreover, Shp-2 was able to accelerate Stat5A dephosphorylation, and dephosphorylation of Stat5A was dramatically delayed in Shp-2-deficient cells. Therefore, we conclude that Shp-2 is a Stat5A phosphatase, which down-regulates the active Stat5A in vivo.

Animals↗
PubMed2004

Influence of genetic background and gender on hypertension and renal failure in COX-2-deficient mice.

The present study was undertaken to determine whether the severity of renal failure or hypertension in homozygous cyclooxygenase (COX)-2-deficient (COX-2-/-) mice affected by genetic background or gender. COX-2 deletion was introduced into three congenic genetic backgrounds, 129/Sv (129/COX-2-/-), C57/BL6 (C57/COX-2-/-), and BALB/c (BALB/COX-2-/-), by backcrossing the original mixed-background knockout mice with the respective inbred strains for 9 or 10 generations. Evaluation of the severity of hypertension and renal failure was performed in knockout and wild-type mice at the age of 2.5-3.5 mo. Blood pressure measured by tail-cuff plethysmography was significantly elevated in the male 129/COX-2-/- mice (165.8 +/- 9.2 vs. 116 +/- 5.1 mmHg, P < 0.05), and to a much lesser extent in the female 129/COX-2-/- mice (127.4 +/- 3.3 vs. 102.4 +/- 3.3), whereas it was unchanged in the C57- or BALB/COX-2-/- mice regardless of gender. Urinary excretion of albumin, determined by EIA, was remarkably increased in the 129/COX-2-/- (16.4 +/- 4.1 vs. 0.16 +/- 0.043 mg albumin/mg creatinine, P < 0.001), and to a lesser extent in the male C57/COX-2-/- mice (0.595 +/- 0.416 vs. 0.068 +/- 0.019). Albumin excretion was not elevated in the male BALB/COX-2-/- or in female COX-2-/- mice on any of the three genetic backgrounds. Histological analysis showed abundant protein casts, dilated tubules, and infiltration of inflammatory cells in the male 129/COX-2-/- mice, but not in COX-2-/- mice in other strains or gender. However, the presence of small glomeruli in the nephrogenic zone was observed in all strains of COX-2 knockout mice, regardless of genetic background and gender. Therefore, we conclude that the severity of hypertension and renal failure in COX-2-deficient mice is influenced by genetic background and gender, whereas the incomplete maturation of outer cortical nephrons appears to be independent of genetic background effects.

Animals↗
PubMed2026

Disruption of the ubiquitin-mediated proteolysis pathway: a study of seed aging in Saposhnikovia divaricata caused by UBC1 gene family suppression.

BACKGROUND: Saposhnikovia divaricata (Turcz.) Schischk. is a perennial herb whose seed aging during storage significantly reduces germination rates, limiting industrial-scale production. Reactive oxygen species (ROS)-induced oxidative damage is a key driver of seed aging, but the underlying mechanisms in Saposhnikovia divaricata remain unclear. RESULTS: Suppression of the UBC1 gene family reduces the activity of ubiquitin-conjugating enzymes, leading to dysfunction of the ubiquitin-mediated proteolysis pathway, which in turn decreases protein degradation efficiency and causes the accumulation of damaged proteins. Transcriptome analysis revealed predominant downregulation of genes crucial for seed physiological maintenance. By the fourth year of storage, germination dropped sharply to 30.67%, accompanied by embryo cavitation. Downregulation of ribosome pathway genes hindered ribosome assembly and protein synthesis, while suppression of endoplasmic reticulum protein processing genes led to unfolded/misfolded protein accumulation and intensified cellular stress, accelerating aging. Proteomic analysis showed increased total differential and antioxidant-related proteins. ROS content fluctuated with storage time: peroxyl radicals peaked in year two (5.68 RFU/mg), whereas hydroxyl radicals and hydrogen peroxide were highest in year four (0.0655 pg/mL and 0.0946 pg/mL, respectively), with significant differences across periods. Elevated membrane-related proteins, increased electrical conductivity, and malondialdehyde content (maximum 54.30 nmol/g at year four) confirmed oxidative membrane damage. ROS-induced stress promotes protein misfolding, and reduced UBC1 expression is associated with impaired clearance of misfolded proteins by the ubiquitin-mediated proteolysis pathway. CONCLUSIONS: This study provides the first integrated transcriptomic and proteomic insight into UBC1 deficiency-mediated seed aging in Saposhnikovia divaricata. The findings enhance molecular understanding of seed aging and offer new directions for improving seed storage and viability.

Ubiquitin-Conjugating Enzymes↗
PubMed1999

Disruption of a retinal guanylyl cyclase gene leads to cone-specific dystrophy and paradoxical rod behavior.

One of two orphan photoreceptor guanylyl cyclases that are highly conserved from fish to mammals, GC-E (or retGC1) was eliminated by gene disruption. Expression of the second retinal cyclase (GC-F) as well as the numbers and morphology of rods remained unchanged in GC-E null mice. However, rods isolated from such mice, despite having a normal dark current, recovered from a light flash markedly faster. Unexpectedly, the a- and b-waves of electroretinograms (ERG) from dark-adapted null mice were suppressed markedly. Cones, initially present in normal numbers in the retina, disappeared by 5 weeks, based on ERG and histology. Thus, the GC-E-deficient mouse defines a model for cone dystrophy, but it also demonstrates that morphologically normal rods display paradoxical behavior in their responses to light.

Adaptation, Ocular↗
PubMed2006

[In vitro cytokines-induced differentiation in mononuclear cell derived dendritic cells from chronic myeloid leukemia].

The purpose of this study was to investigate the mechanism of effects of interferon-alpha (IFN-alpha) on chronic myeloid leukemia (CML). Bone marrow mononuclear cells (BMMNC) were obtained from heparinized blood of CML patients by Ficoll-Paque density gradient centrifugation. The expressions of CD1a, CD83, CD86, HLA-ABC, HLA-DR and CD54 on DC induced by IFN-alpha + GM-CSF, IFN-alpha + GM-CSF+IL-4 and IL-4 + GM-CSF for 7 days in vitro were assayed by flow cytometry. The morphologic features were observed by transmission and optical microscopy. The mixed lymphocyte reactions (MLR) with DC were evaluated by MTT assay. The results showed that the DC cultured in different cytokine combinations expressed significantly higher levels of CD1a, HLA-ABC, HLA-DR, CD86, CD54, and CD83 than those in the precultured. The DC growing with IFN-alpha + GM-CSF expressed significantly higher levels of HLA-ABC, HLA-DR than those in GM-CSF + IL-4. The CD86 expression and MLR levels in IFN-alpha + GM-CSF + IL-4 increased significantly. The expression rate of DC antigens and MLR in the IFN resistant group significantly lower than those in the newly diagnosed and the effectively treated groups after at least 6 months of IFN-alpha treatment (P < 0.05). The DC from the IFN resistant group did not express significantly CD86 and MLR in IFN-alpha + GM-CSF + IL-4 groups compared to those in the newly diagnosed and IFN effective treated groups. It is concluded that the BMMNC from CML cultured in combination with IFN-alpha and other cytokines can be induced into DC with typical morphologic and immunophenotypic characteristics. Addition of IFN-alpha + GM-CSF + IL-4 to DC cultures can significantly up-regulate the expression of major histocompatibility complex molecules, co-stimulatory molecules and various adhesion molecules. The deficiency of DC differentiation and function may play a role in the development of clinical resistance to IFN-alpha.

Bone Marrow Cells↗
PubMed1995

The NCI's AIDS antiviral drug screening program.

The Developmental Therapeutics Program (DTP) in the National Cancer Institute has an unique mission by serving as a resource for all academic and private research institutions, the National Institutes of Health in the USA, and the global scientific community in the quest for effective therapeutic agents for treating patients with Acquired Immune Deficiency Syndrome (AIDS) as well as for cancer patients. This communication will concentrate on the developmental therapeutic program on anti-AIDS drug discovery.

Acquired Immunodeficiency Syndrome↗
PubMed1997

[Effect of monoclonal antibody against human tissue factor pathway inhibitor on plasma coagulation time].

The purpose of this study was to evaluate the influences of the monoclonal antibody against human tissue factor pathway inhibitor (TFPI), McAb4F8, on prothrombin time (PT) and activated partial thromboplatin time (APTT). The results showed that PT and APTT were prolonged by exogenous TFPI. Dilute thromboplastin coagulation time was shortened with a dose-dependent manner by McAb4f8. Low molecular weight heparin (LMWH) prolonged significantly PT and APTT, and this effect ws weakened by an antibody against human AT III. McAb4F8 was also proved to shorten dilute thromboplastin coagulation time of factor IX deficient plasma. These results indicated that the tissue factor pathway plays an important role not only in physiological coagulation but also in hemorrhage of hemophilia.

Animals↗
PubMed2006

[Effects of ferrous sulfate supplementation on bone marrow hemopoiesis in rats].

OBJECTIVE: To explore the influences of different dosage ferrous sulfate supplements on bone marrow hemopoiesis in rats. METHODS: Female weaning Wistar rats were fed with an iron deficient diet (< 10 mg/kg diet) until the level of hemoglobin of rats was lower than 100 g/L. Rats (n = 50) were randomly divided into five groups according to the levels of hemoglobin and body weight, iron deficiency control (ID), daily low iron diet supplement (LDs), daily high iron diet supplement (HDs), weekly low iron supplement (LWs), and weekly high iron supplement (HWs). RESULTS: After 12 weeks, bone marrow stainable iron was seldom in ID group, and ample in supplement groups. The proportions of iron staining of bone marrow smear in supplement groups were more than 30%. Bone marrow cells in all rats were hyperplastic or active hyperplastic. CONCLUSIONS: Daily high iron supplement or once weekly high iron supplement were safe to bone marrow hemopoiesis in rats.

Anemia, Iron-Deficiency↗
PubMedDate not supplied

Functional consequences of ferroportin 1 mutations.

The cellular iron exporter ferroportin 1 is expressed in both the duodenum and in cells of the mononuclear phagocyte system. Expression of ferroportin 1 protein on the cell surface is regulated by the interaction of ferroportin 1 with hepcidin. Hepcidin treatment of cells results in internalization and lysosomal degradation of cell surface ferroportin 1. Recently, ferroportin 1 mutations leading to hemochromatosis (HFE4) have been identified. HFE4 differs from classical hemochromatosis in that there is a greater amount of macrophage iron sequestration. The data presented here demonstrate that HFE4 mutations are heterogeneous in their effects on protein function. Some mutations result in loss of function with partial protein sequestration in the ER. Others are indistinguishable from native ferroportin 1 and have a similar ability to deplete transfected cells of iron as evidenced by activation of the iron-response proteins and cellular ferritin depletion. Significantly, all mutants appear to be unresponsive to hepcidin and do not demonstrate the expected internalization on exposure to hepcidin. The clinical phenotypes observed in patients may be secondary to cell-type-specific defects in hepcidin-mediated inhibition of ferroportin 1 expression.

Animals↗
PubMed1992

Dietary effects on cytochromes P450, xenobiotic metabolism, and toxicity.

The levels and activities of cytochrome P450 enzymes are influenced by a variety of factors, including the diet. In this article, the effects of selected non-nutritive dietary chemicals, macronutrients, micronutrients, and ethanol on cytochromes P450 and xenobiotic metabolism are reviewed in the light of our current understanding of the multiplicity and substrate specificity of cytochrome P450 enzymes. Although the mechanisms of action of several dietary chemicals on specific cytochrome P450 isozymes have been established, those for macro- and micronutrients are largely unknown. It is known, however, that specific nutrients may have varied effects on different cytochrome P450 forms and thus may affect the metabolism of various drugs differently. Nutritional deficiencies generally cause lowered rates of xenobiotic metabolism. In certain cases, such as thiamin deficiency and mild riboflavin deficiency, however, enhanced rates of metabolism of xenobiotics were observed. The effects of dietary modulation of xenobiotic metabolism on chemical toxicity and carcinogenicity are discussed.

Animals↗