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PubMed2002

Hypermethylation of HPP1 is associated with hMLH1 hypermethylation in gastric adenocarcinomas.

The HPP1 gene was initially discovered because of its frequent hypermethylation in hyperplastic colon polyps, but it is also hypermethylated in colorectal adenomas and carcinomas. Expression of the DNA mismatch repair gene hMLH1 is diminished or absent in some hyperplastic polyps, and it has been suggested that HPP1 inactivation is associated with the progression of microsatellite-unstable colorectal tumors. We sought then to determine the prevalence of HPP1 silencing by DNA methylation in gastric adenocarcinomas and to define any association of this event with microsatellite instability (MSI) or hMLH1 hypermethylation. Thirty-two matched normal-gastric adenocarcinoma DNA pairs were studied for MSI status and hypermethylation of HPP1 and hMLH1. Five (100%) of 5 MSI-H tumors, 2 (50%) of 4 MSI-L tumors, and 8 (35%) of 23 MSS tumors demonstrated HPP1 hypermethylation. Eight (25%) of 32 tumors (5 of 5 MSI-H, 2 of 4 MSI-L, and 1 of 23 MSS) showed evidence of hMLH1 hypermethylation. All (8 of 8) of these hMLHI-methylated tumors demonstrated concomitant methylation at the HPP1 locus: there were no cases of hMLH1 methylation occurring in the absence of HPP1 methylation. In gastric adenocarcinoma, hypermethylation frequently targets HPP1. Moreover, hMLH1 hypermethylation occurs predominantly in the setting of HPP1 hypermethylation. HPP1 hypermethylation may represent an early event in mismatch repair-deficient gastric tumorigenesis.

Adaptor Proteins, Signal Transducing↗
PubMed2006

[On the direction reinforcing and reducing method in navel acupuncture therapy].

OBJECTIVE: To expound the principle of the direction reinforcing and reducing method in navel acupuncture therapy. METHODS: The relation between direction of navel acupuncture and reinforcing-reducing is analyzed from classification and characteristics of the navel acupuncture. CONCLUSION: The direction reinforcing and reducing method in navel acupuncture therapy originates from Yinyang-Shushu system of Chinese traditional culture, and it is established on relation of diseases and classification of directions. Skillfully grasping the direction reinforcing and reducing method in navel acupuncture therapy can produce obvious therapeutic effect on the diseases with coexistence of deficient and excessive syndromes.

Acupuncture Therapy↗
PubMed2005

Studies on the effectiveness of NaFeEDTA-fortified soy sauce in controlling iron deficiency: a population-based intervention trial.

The objective of this research was to study the effectiveness of NaFeEDTA-fortified soy sauce for controlling iron deficiency in a high-risk population. This was an 18-month, randomized, placebo-controlled intervention trial in 14,000 residents aged three years or older in Bijie City, Guizhou Province, China, using sodium-iron ethylene diamine tetraacetate (NaFeEDTA)-fortified soy sauce (29.6 mg Fe/100 ml). The study data included measurements of food consumption, hemoglobin, serum ferritin, and serum retinol. The results showed that the diet consisted primarily of cereals, fruits, and vegetables, with very little meat. Food consumption remained unchanged during the study period and was similar in the fortified and control groups. The average daily soy sauce consumption of the group consuming the fortified product was 16.4 ml per person, which provided 4.9 mg of iron from NaFeEDTA. At the end of the trial, all age and sex subgroups receiving NaFeEDTA had significantly higher hemoglobin levels, a lower prevalence of anemia, and higher plasma ferritin levels than the controls. The effects became statistically significant after six months of intervention and were maintained throughout the study period. We conclude that NaFeEDTA-fortified soy sauce was highly effective in controlling iron deficiency and reducing the prevalence of iron-deficiency anemia in men, women, and children. NaFeEDTA-fortified soy sauce is affordable and was well accepted by the study population.

Adolescent↗
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↗
PubMed2002

Thrombin-activatable fibrinolysis inhibitor (TAFI) deficiency is compatible with murine life.

To investigate the consequence of deficiency in thrombin-activatable fibrinolysis inhibitor (TAFI), we generated homozygous TAFI-deficient mice by targeted gene disruption. Intercrossing of heterozygous TAFI mice produced offspring in the expected Mendelian ratio, indicating that transmission of the mutant TAFI allele did not lead to embryonic lethality. TAFI-deficient mice developed normally, reached adulthood, and were fertile. No gross physical abnormalities were observed up to 24 months of age. Hematological analysis of TAFI-deficient mice did not show any major differences including plasma fibrinogen level, prothrombin time, and activated partial thromboplastin time. TAFI-deficient mice did not suffer from excess bleeding as determined by blood loss following tail transection, although their plasma failed to prolong clot lysis time in vitro. In vivo, TAFI deficiency did not influence occlusion time in either an arterial or a venous injury model. TAFI deficiency did not improve survival rate compared with the wild-type in thrombin-induced thromboembolism, factor X coagulant protein-induced thrombosis, and endotoxin-induced disseminated intravascular coagulation. Furthermore, TAFI deficiency did not alter kaolin-induced writhing response, implying that TAFI does not play a major role in bradykinin catabolism. The current study demonstrates that TAFI deficiency does not change normal responses to acute challenges.

Animals↗
PubMed2000

[Therapeutic effect of weikangfu on gastric precancerous disorder with spleen deficiency syndrome and its effect of gastric mucosal zinc, copper, cyclic adenosine monophosphate, superoxide dismutase, lipid peroxide and 3H-TdR lymphocyte conversion test].

OBJECTIVE: To observe the clinical therapeutic effect of Weikangfu granule (WKF) on intestinal metaplasia (IM), atypical proliferation (ATP) and its therapeutic mechanism. METHODS: Sixty-one patients (treated group) were diagnosed by integrated TCM and western medicine (WM), and treated according to Syndrome Differentiation, the amount of WKF was adjusted according to various Syndromes. The control group consisted of 54 patients, took Weisu granule without considering their Syndromes. Besides, 15 healthy subjects comprised of the control group. Gastroscopy was conducted both before and after the treatment, mucosal sample was taken from antral region of stomach for pathological changes, for IM classification through histochemical staining and for determination of gastric mucosal Zn, Cu, cAMP, SOD, serum LPO and 3H-TdR lymphocyte conversion test (LCT). RESULTS: (1) The symptomatic and pathologic therapeutic effect of the treated group were markedly better than those of the control group (P < 0.05, P < 0.01). (2) The levels of gastric mucosal Zn, Cu, cAMP, SOD and 3H-TdR LCT of the treated group before treatment were all lower than that of the healthy control group, but they were markedly increased after treatment, while serum LPO, however, increased before treatment, significant difference existed between the above groups (P < 0.05, P < 0.01). CONCLUSION: WKF can reverse IM and ATP of Spleen Deficiency Syndrome through the mechanism of improving the level of gastric mucosal Zn, Cu, cAMP and SOD, promoting cytodifferentiation, improving cytoimmunity, reducing superoxide and LPO.

Adult↗
PubMed2003

[Analysis of an inherited FVII deficiency pedigree caused by homozygosity of Thr359Met].

OBJECTIVE: To explore the gene mutation type of an inherited coagulation factor VII deficiency pedigree. METHODS: FVII:Ag, FVII:C, FVIIa were detected to classify deficiency type. FVII gene mutations were analysed in the proband and her family members by DNA directly sequencing. Biostructural pathology of the identified mutation was analysed by molecular modeling. RESULTS: Homozygosity of C-->T transition at position 11514 in exon 8 resulting in Thr359Met was identified in the proband, and heterozygosity for Thr359Met was confirmed in her parents, her son and some other family members. Thr359Met induces CRM-deficiency. It is found by computer simulated molecular model that the replacement of Thr by Met which has a larger and longer side chain might cause steric hindrance, and change the number of H-bonds. CONCLUSIONS: Homozygous missense mutation Thr359Met was found in a pedigree of hereditary FVII deficiency. This mutation might change the configuration of protein molecule and result in severe FVII deficiency.

Adolescent↗
PubMed2005

Tumor necrosis factor alpha and glutathione interplay in chronic heart failure.

The pro-inflammatory cytokine, tumor necrosis factor alpha (TNF alpha), in concert with neurohormones, contributes to chronic heart failure (CHF) progression. This implies that TNF a antagonism may constitute an important target for CHF therapy. However, clinical trials in CHF patients using compounds that trap TNF alpha, comprising infliximab, an antibody directed to TNF alpha, and etanercept, a soluble recombinant receptor of TNF alpha, gave disappointing results bringing back to light the dual, short-term beneficial and long-term harmful effect of TNF alpha. This review focuses on the dual, concentration- and time-related effects of TNF alpha, the yin and yang action of TNF alpha in cardiac ischemia/reperfusion and contraction. Importantly, the harmful effects of TNF a are related to glutathione deficiency, a common hallmark to several other chronic inflammatory diseases. Recently, in rat models of CHF, oral administration of the glutathione precursor, N-acetylcysteine (NAC), was shown to hinder pathways of TNF alpha harmful signalling and to rescue cardiac structure and function. These results suggest that glutathione deficiency in association with TNF alpha activation may play a role in the pathophysiology of CHF and that NAC may represent a potential therapy in CHF.

Acetylcysteine↗
PubMed1999

Green and yellow vegetables can maintain body stores of vitamin A in Chinese children.

BACKGROUND: Vitamin A activity of plant provitamin A carotenoids is uncertain. OBJECTIVE: The objective was to determine whether plant carotenoids can sustain or improve vitamin A nutrition during the fall season in kindergarten children in the Shandong province of China. DESIGN: The serum vitamin A concentration of 39% of the children was <1.05 micromol/L and of 61% of the children was > or = 1.05 micromol/L. For 5 d/wk for 10 wk, 22 children were provided approximately 238 g green-yellow vegetables/d and 34 g light-colored vegetables/d. Nineteen children maintained their customary dietary intake, which included 56 g green-yellow vegetables/d and 224 g light-colored vegetables/d. Octadeuterated and tetradeuterated vitamin A were given before and after the interventions, respectively, and their enrichments in the plasma were determined by gas chromatography-mass spectrometry. Serum retinol and carotenoid concentrations were measured by HPLC. RESULTS: Carotenoid nutrition improved after consumption of green-yellow vegetables. Serum concentrations of retinol were sustained in the group fed green-yellow vegetables but decreased in the group fed light-colored vegetables (P < 0.01). The isotope-dilution tests confirmed that total-body vitamin A stores were sustained in the group fed green-yellow vegetables, but decreased 27 micromol (7700 microg retinol) per child, on average, in the group fed light-colored vegetables (P < 0.06). CONCLUSION: Green-yellow vegetables can provide adequate vitamin A nutrition in the diet of kindergarten children and protect them from becoming vitamin A deficient during seasons when the provitamin A food source is limited.

Analysis of Variance↗
PubMed1995

[Effect of zhuchun pill on immunity and endocrine function of elderly with kidney-yang deficiency].

After randomly dividing 45 elderly males with Kidney-Yang Deficiency into Zhuchun Pill (ZCP) group and placebo (starch capsule) group by single blind method, and treating them for 3 months, we found that ZCP could greatly improve the main symptoms of Kidney-Yang Deficiency, P < 0.01 by comparison with control group: the 3H-TdR lymphocyte transformation (3H-TdR LCT) rate, level of serum C3, IgA, IgD, IgG & IgM went up (P < 0.01); contents of plasma adrenocortical hormone (ACTH), testosterone (T) and cyclic adenosine monophosphate (cAMP) increased (P < 0.01-0.001): the level of superoxide dismutase (SOD) in serum also increased while lipid peroxide (LPO) in plasma decreased (P < 0.01). But for control group, there were no remarkable changes after treatment, so it revealed that the improvement of Kidney-Yang Deficiency by ZCP is realized through regulating the organism's immunity and endocrine function as well as through scavenging the free radical agents.

Adjuvants, Immunologic↗
PubMedDate not supplied

In utero exposure to methylmercury and Se deficiency converge on the neurobehavioral outcome in mice.

Pregnant female ICR mice, maintained on torula-based diets containing various amounts of Se (0.02, 0.05, or 0.4 mg/kg diet), were given methyl-mercury (MeHg; 0, 5, or 9 mg Hg/kg in total) on the 12-14th days of gestation. The neurobehavioral function of the offspring born to these dams was evaluated with respect to reflex and motor development, thermal preference, and open-field activity. Se deficiency per se as well as exposure to MeHg exerted additive or synergistic effects on the neurobehavioral functions examined. The group of mice most affected was the group given the lowest amount of Se and the highest dose of MeHg. Thus, the neurobehavioral outcome of in utero MeHg exposure and Se deficiency converged. Although the dietary level of Se did not affect the Hg concentration in the fetal brain, the Se concentration and the activity of glutathione peroxidase, a selenoenzyme, were severely depressed by MeHg in the neural tissue. The possibility that functional Se deficiency by MeHg exposure partly accounts for the neurobehavioral toxicity of MeHg is discussed.

Animals↗
PubMed1999

Atm is dispensable for p53 apoptosis and tumor suppression triggered by cell cycle dysfunction.

Both p53 and ATM are checkpoint regulators with roles in genetic stabilization and cancer susceptibility. ATM appears to function in the same DNA damage checkpoint pathway as p53. However, ATM's role in p53-dependent apoptosis and tumor suppression in response to cell cycle dysregulation is unknown. In this study, we tested the role of murine ataxia telangiectasia protein (Atm) in a transgenic mouse brain tumor model in which p53-mediated apoptosis results in tumor suppression. These p53-mediated activities are induced by tissue-specific inactivation of pRb family proteins by a truncated simian virus 40 large T antigen in brain epithelium. We show that p53-dependent apoptosis, transactivation, and tumor suppression are unaffected by Atm deficiency, suggesting that signaling in the DNA damage pathway is distinct from that in the oncogene-induced pathway. In addition, we show that Atm deficiency has no overall effect on tumor growth and progression in this model.

Animals↗
PubMed1983

Interaction of serum lipoproteins with the intestine. Evidence for specific high density lipoprotein-binding sites on isolated rat intestinal mucosal cells.

To determine if plasma lipoproteins interact and therefore possibly regulate intestinal lipoprotein metabolism, we investigated the binding, internalization, and degradation of 125I-labeled low density lipoprotein (LDL) and high density lipoprotein (HDL) by enzyme-dispersed rat intestinal mucosal cells. Both human and rat LDL and HDL were bound, internalized, and degraded in a concentration-dependent manner with calculated half-saturation occurring at approximately 30, 35, 35, and 15 micrograms/ml for human LDL, rat LDL, human HDL, and rat HDL, respectively. Isolated brush border membranes had no saturable or specific binding sites for 125I-labeled HDL or LDL, suggesting that lipoproteins may be bound to receptors on lateral or basal membranes of mucosal cells. Compared with HDL, LDL binding was characterized by a large non-specific component. LDL of human and the rat were not only displaced by excess LDL but at least as effectively by excess HDL of their own species. Labeled HDL was displaced by corresponding unlabeled lipoproteins, but human LDL could produce only minor displacement of human HDL3. ApoE-deficient rat HDL, separated by heparin-Sepharose affinity chromatography also showed highly specific saturable binding to intestinal cells. Thus, apparently two different lipoprotein binding sites exist in intestinal plasma membranes, one recognizing B and/or E apoproteins present in human and rat LDL and rat HDL while another binds human HDL3 and apoE-deficient rat HDL which contain A apoproteins as major components.

Animals↗
PubMed2003

[Molecular mechanisms of two novel mutations of factor XIII gene resulting in hereditary coagulation deficiency].

OBJECTIVE: To investigate the mechanisms of two novel missense mutations of factor XIIIA subunit gene (Arg77-->Cys,Ser413-->Trp) in the pathogenesis of hereditary factor XIII deficiency. METHODS: Site-directed mutagenesis was conducted to obtain 2 mutant human XIII A recombinant plasmids, mut-PCI/FXIIIA. Normal wild type factor XIII A recombinant plasmid, wt-PCI/FXIIIA, and mut-PCI/FXIIIA, were transfected into cultured COS7 cells line, renal fibroid cell of African green monkey using Superfect reagent respectively, The expression levels of DNA, RNA and protein of human factor XIII, both wild type and mutant, were detected by PCR, RT-PCR and Western blotting. Pulse-chase experiment was used to look into the changing of factor XIII A in the cytoplasm. Factor XIIIA activity was assayed by Biotin-pentylamine incorporation technique. RESULTS: The mRNA levels of the two mutants in transfected cells were similar to that of the wild type factor XIIIA. But the amount of mutant factor XIIIA protein and its activity in cells decreased markedly, even disappeared. Pulse-chase experiment revealed that at the two mutants existed chase time 0.5 h and 1 h considerable amounts in cells and then disappeared rapidly later. CONCLUSION: The 2 mutations of the factor XIIIA cause the instability, degradation, and rapid disappearance of FXIIIA in cytoplasm, thus resulting in hereditary factor XIII deficiency.

Animals↗
PubMed1994

[Observation on 104 senile chronic renal insufficiency patients treated with integrated traditional Chinese and Western medicine].

A clinical study on 104 cases of senile chronic renal insufficiency (SCRI) was conducted. In order to analyze the clinical features of SCRI and the efficacy of integrated TCM-WM treatment, all cases were treated by this combined therapy, except for the treatment of primary diseases and removing the aggravating factors. It was concluded that the effective rate reached 57% it had no significant difference with 61% of non-senile group, P > 0.05. The senile patients featured Kidney Yang Deficiency in TCM Syndrome Differentiation. It could guide the clinical treatment and thus the senile patient's Yang should be strengthened at usual time. When Kidney Qi was insufficient and frequent nocturia appeared, sufficient water supply as well as Warming Kidney Yang drugs should be given and that Yang Qi should be protected all the time. Also diuretics and purgatives should not be misused which might damage Yin and Yang.

Adult↗
PubMed2006

Interleukin-18 affects local cytokine expression but does not impact on the development of kidney allograft rejection.

Interleukin-18 is predominantly a macrophage-derived cytokine with a key role in inflammation and cell-mediated immunity. Having previously demonstrated IL-18 upregulation in a rat model of kidney rejection, here we examined IL-18 in a fully MHC-mismatched murine model of acute kidney rejection using IL-18-deficient recipients (IL-18-/-) and animals administered neutralizing IL-18 binding protein (IL-18BP). Gene expression of IL-18 and its receptor were significantly upregulated in allografts compared to isografts, as was the cellular infiltrate (T cells and macrophages) (p < 0.001). Allografts developed kidney dysfunction (p < 0.05) and tubulitis (p < 0.01) not observed in controls. There was a significant reduction in gene expression of IL-18 downstream pro-inflammatory molecules (iNOS, TNFalpha and IFNgamma) in IL-18-/- recipients (p < 0.01), and IL-18BP-treated animals. The CD4+ infiltrate and IL-4 mRNA expression was greater in the IL-18-/- recipients than wild-type (WT) allografts and IL-18BP-treated animals (p < 0.05), suggesting a Th2-bias which was supported by IFNgamma and IL-4 ELISPOT data and an increased eosinophil accumulation (p < 0.001). Neither IL-18 deficiency nor neutralization prevented renal dysfunction or tubulitis. This study demonstrates increased production of IL-18 in murine kidney allograft rejection and provides evidence that IL-18-induced pathways of inflammation are active. However, neither IL-18 deficiency nor neutralization was protective against the development of allograft rejection.

Animals↗
PubMed2026

KEAP1 loss-of-function suppresses immunogenic ferroptosis and limits PD-1 blockade efficacy through an NRF2-FSP1 pathway.

Loss-of-function mutations in Kelch-like ECH-associated protein 1 (KEAP1) frequently occur in lung adenocarcinoma and are associated with poor prognosis and limited benefit from immunotherapy. However, the mechanisms linking KEAP1 deficiency to immune evasion remain elusive. We combined clinical data analysis, in vivo tumor models, and in vitro co-culture systems to investigate how KEAP1 deficiency shapes dendritic cell (DC) biology and response to PD-1 blockade. Ferroptosis induction assays, damage-associated molecular patterns (DAMPs) quantification, cytokine profiling, and mechanistic interrogation of the FSP1-CoQ10 axis were performed to delineate pathways.KEAP1 mutations correlated with poor response to PD-1 blockade and reduced DC infiltration. In mice, KEAP1-deficient tumors exhibited accelerated growth and reduced DC and CD8+ T-cell infiltration, consistent with an immune-cold phenotype. Mechanistically, KEAP1 loss impaired DC function in vitro, as evidenced by reduced maturation, phagocytosis, and na&#xef;ve CD8+ T-cell priming capacity. This defect was linked to two mechanisms. First, KEAP1-deficient tumor cells resisted ferroptosis and failed to release immunogenic DAMPs, including extracellular ATP, HMGB1, and calreticulin. Second, KEAP1 deficiency reprogrammed the cytokine secretion profile, with downregulation of CCL2, IL-6, CXCL1, and CXCL2, thereby diminishing DC recruitment and inflammatory signaling. Notably, inhibition of the FSP1-CoQ10 antioxidant axis restored ferroptosis-associated immunogenic cell death. Our study identifies KEAP1 deficiency as a driver of immune-cold tumor microenvironments and resistance to PD-1 blockade, acting through impaired ferroptosis-induced immunogenic cell death and disrupted DC function. Genetic FSP1 deletion restored ferroptosis-associated immunogenicity and DC activation in KEAP1-deficient cells, supporting FSP1 as a potential therapeutic target for further in vivo evaluation.

DAMPs↗