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PubMed2000

Expression of ERCC1 antisense RNA abrogates gemicitabine-mediated cytotoxic synergism with cisplatin in human colon tumor cells defective in mismatch repair but proficient in nucleotide excision repair.

Gemcitabine, or 2',2'-difluorodeoxycytidine (dFdC) is a new anticancer agent with significant activity against a broad spectrum of tumors either as a single agent or in combination with other active anticancer drugs. Studies in vitro and in vivo have demonstrated that dFdC produces cytotoxic synergism with cisplatin, or cis-diamminedi-choloroplatinum(II) (CDDP); however, the mechanism by which the synergism occurs has not been elucidated. We proposed that the nucleotide excision repair (NER) process, which is responsible for the cellular removal of CDDP-DNA adducts, may be a target for the mechanism of the cytotoxic synergism of dFdC and CDDP. Because the mismatch repair (MMR) pathway is involved in mediating CDDP cytotoxicity, making determination of the role of the NER in the cytotoxic synergism more complicated, and because tumors are often defective in MMR, we selected an NER-proficient, MMR-deficient, CP2.0 human colon carcinoma cell line as a model for this study. By an in vitro repair synthesis assay, we found that dFdC triphosphate (dFdCTP), the active metabolite of dFdC, inhibited the incorporation of [alpha-32P]dATP as well as the incorporation of [alpha-32P]dCTP, suggesting that the repair inhibition by dFdCTP does not result simply from competition for the incorporation site but rather is also due to prevention of chain elongation during the DNA resynthesis process. To determine whether the repair inhibition contributes to the cytotoxic synergism, we examined the effect of the constitutive expression of ERCC1 antisense RNA on the interaction of dFdC and CDDP. CP2.0 cells were transfected with pERCC1/AS, an ERCC1 antisense expression vector; eight hygromycine-resistant clones expressing various levels of the antisense RNA were selected for quantification of and correlation between the repair activity and cytotoxic synergism. The results show that stable expression of ERCC1 antisense RNA down-regulated the level of mRNA and repair activity; the down-regulation of the repair activity significantly correlated with the reduction of the cytotoxic synergism of the two agents. These data provide direct evidence to support the hypothesis that inhibition of the repair of CDDP-induced DNA lesions plays a critical role in dFdC-mediated cytotoxic synergism with CDDP in MMR-deficient tumor cells.

Antineoplastic Agents↗
PubMed2002

Pitfalls in the diagnosis of idiopathic pulmonary haemosiderosis.

Idiopathic pulmonary haemosiderosis is a very rare but devastating disorder. Diagnosis is sometimes difficult and the clinical course exceedingly variable, as illustrated by this report of a girl, aged 2 years 4 months, with severe iron deficiency anaemia. There was no response to iron therapy and transfusions. Sustained and striking reticulocytosis associated with low haptoglobin mimicked haemolytic anaemia. Positive faecal blood test was documented after repeated testing. There were no pulmonary symptoms. A chest radiograph showed bilateral diffuse alveolar infiltrates. Bronchoalveolar lavage fluid showed numerous siderophages. High resolution computed tomography of the thorax revealed early pulmonary fibrotic changes. Recurrent reticulocytosis appeared to be a very useful sign of recurrent bleeding episodes.

Anemia, Iron-Deficiency↗
PubMed2001

Quantitative (stereological) study of placental structures in women with pregnancy iron-deficiency anemia.

OBJECTIVE: To determine the compensatory morphometric changes of placental structures in cases of maternal iron-deficiency anemia. METHODS: Placentas were obtained from a random sample of 26 full-term pregnant women, and methacrylate-embedded vertical sections were utilized to estimate parameters of placental structures with stereological methods. Materials were divided into three groups based on maternal hemoglobin levels: anemic (hemoglobin<100g/l), intermediate and non-anemic (hemoglobin>or=110g/l). RESULTS: Placental volume and absolute volume of the intervillous space or the chorionic villi per placenta significantly increased in the anemic group. There was a significant negative correlation between maternal hemoglobin level and absolute volume or surface area of the intervillous space or the villi. No significant difference, however, was found between the groups in the volume fraction or surface density of placental structures. CONCLUSION: Placental hypertrophy was associated with mild and moderate degree of maternal iron-deficiency anemia and the enlargement of placenta appeared to be a uniform (proportional) physiological compensatory growth.

Adult↗
PubMed2002

cDNA microarray analysis of gene expression during Fe-deficiency stress in barley suggests that polar transport of vesicles is implicated in phytosiderophore secretion in Fe-deficient barley roots.

To acquire Fe from soil, graminaceous plants secrete mugineic acid family phytosiderophores (MAs) from their roots. The secretion of MAs increases in response to Fe deficiency, and shows a distinct diurnal rhythm. We used a microarray that included 8987 cDNAs of rice EST clones to examine gene expression profiles in barley roots during Fe-deficiency stress. Approximately 200 clones were identified as Fe-deficiency-inducible genes, of which seven had been identified previously. In order to meet the increased demand for methionine to produce MAs, Fe-deficiency enhances the expression of genes that participate in methionine synthesis, as well as recycling methionine through the Yang cycle. Of these 200 genes, approximately 50 exhibited different transcription levels in Fe-deficient roots at noon and at night. Northern blot analysis of time course experiments confirmed that five of these genes exhibited a diurnal change in their level of expression. The diurnal changes in the expression of these genes suggest that polar vesicle transport is involved in the diurnal secretion of MAs.

Azetidinecarboxylic Acid↗
PubMed2000

[The preliminary study on the gene mutations of sixty patients with G6PD deficiency in Yunnan province].

OBJECTIVE: To analyze the types and distribution of glucose-6-phosphate dehydrogenase (G6PD) gene mutations in Yunnan province. METHODS: By using the natural primers or mis-matched primers mediated polymerase chain reaction (PCR) followed by endonuclease digestion methods, six types of G6PD gene mutations, G1388A, G1376T, C1024T, G392T, C592T and A95G were in sixty patients with G6PD deficiency. RESULT: Six types of mutation were revealed: 28.3% (17 of 60) were G1388A, 11.7% (7 of 60) G1376T, 6.7% (4 of 60) C1024T, 1.7% (1 of 60) G392T, 1.7% (1 of 60) C592T, 1.7% (1 of 60) A95G and 48.3% (29 of 60) unidentified. C592T mutation is the first report in Yunnan people. CONCLUSIONS: The G6PD gene in Yunnan people is heterogeneous. Research of G6PD gene mutation types may provide some useful data for clinical diagnosis and prevention of G6PD deficiency, and for human genetic study.

Amino Acid Substitution↗
PubMed2005

Pyrazolo[1,5-a]pyrimidin-7-yl phenyl amides as novel anti-proliferative agents: parallel synthesis for lead optimization of amide region.

A novel series of p21 chemoselective agents containing a pyrazolo[1,5-a]pyrimidin-7-yl phenyl amides were identified by high throughput screening. Optimization of the amide region by parallel synthesis and the iterative design toward understanding structure-activity relationship to improve potency are described. The isopropyl carbamate derivative 34 was identified as a highly chemoselective agent displaying a potency of 51 nM in the p21 deficient cell line.

Amides↗
PubMed2005

Characterization of lymphoblast mitochondria from patients with Barth syndrome.

Barth syndrome (BTHS) is a multisystem disorder of individuals who carry mutations in tafazzin, a putative phospholipid acyltransferase. We investigated the hypothesis that BTHS is caused by specific impairment of the mitochondrial lipid metabolism. The fatty acid composition of all major mitochondrial phospholipids, phosphatidylcholine (PC), phosphatidylethanolamine (PE), and cardiolipin (CL), changed in lymphoblasts from BTHS patients. These changes were most extensive in CL and least extensive in PE. The complementary nature of the fatty acid alterations in CL and PC suggested that fatty acid transfer between these two lipids was inhibited in BTHS. Fluorescence staining and electron microscopy showed abnormal proliferation of mitochondria in BTHS lymphoblasts. The mitochondrial membrane potential, monitored with the fluorescence probe JC-1, was reduced in BTHS lymphoblasts. However, mitochondrial ATP formation of permeabilized lymphoblasts remained unaffected in BTHS. The data suggest that phospholipid abnormalities of BTHS mitochondria led to partial uncoupling of oxidative phosphorylation and that lymphoblasts compensated for this deficiency by expanding the mitochondrial compartment.

Acyltransferases↗
PubMed2004

Role of zinc in subclinical hepatic encephalopathy: comparison with somatosensory-evoked potentials.

BACKGROUND AND AIM: The purpose of the present paper was to determine the role of zinc in subclinical portosystemic encephalopathy (SPSE). METHODS: The serum zinc levels were studied for 10 cirrhotic patients who did not suffer SPSE and for 10 patients who did, and the results compared with those deriving from 10 healthy volunteers. The nutritional evaluation included serum prealbumin, albumin, and transferrin levels, body mass index (BMI), mid-arm muscle circumference (MAMC), and tricep skin-fold (TSF). The occurrence of SPSE was defined as a situation when the N20-N65 interpeak latencies of median nerve-stimulated somatosensory-evoked potentials (SEP) exceeded 2.5 SD of the control mean value. RESULTS: Cirrhotic patients suffering SPSE (57.5 +/- 10.5 microg/dL) had lower serum zinc levels than those not experiencing SPSE (69.5 +/- 16.6 microg/dL, P = 0.03) and controls (77.7 +/- 6.8 microg/dL, P < 0.001). Four of the non-SPSE and nine SPSE patients had zinc levels less than the lower normal limit. Cirrhotic patients suffering SPSE had lower levels of albumin (2.8 +/- 0.4 g/dL vs 3.8 +/- 0.4 g/dL, P < 0.001), prealbumin (9.0 +/- 4.3 mg/dL vs 14.3 +/- 6.0 mg/dL, P = 0.02), and transferrin (158 +/- 56 g/L vs 218 +/- 50 g/L, P = 0.01), but a greater total bilirubin level (1.2 +/- 1.5 mg/dL vs 0.9 +/- 0.4 mg/dL, P = 0.005) than those not suffering SPSE. The serum zinc levels correlated with N20-N65 interpeak latencies (P = 0.03), serum albumin (P = 0.006), prealbumin (P < 0.001), and total bilirubin (P = 0.02) levels. CONCLUSIONS: The data show that zinc deficiency is common in cases of non-alcoholic cirrhosis with SPSE. The early assessment of malnutrition and zinc deficiency are important.

Bilirubin↗
PubMed2006

Implications of mechanism-based inhibition of CYP2D6 for the pharmacokinetics and toxicity of MDMA.

The aim of this study was to model the in vivo kinetic consequences of mechanism-based inhibition (MBI) of CYP2D6 by 3,4 methylenedioxymethamphetamine (MDMA, ecstasy). A model with physiologically-based components of drug metabolism was developed, taking account of change in the hepatic content of active CYP2D6 due to MBI by MDMA. Based on the in vitro information, plasma concentration time profiles of MDMA after various doses were computed and compared with reported observations. The analysis suggested that a typical recreational MDMA dose could inactivate most hepatic CYP2D6 within an hour, and the return to a basal level of CYP2D6 could take at least 10 days. Thus, the genetic polymorphism of CYP2D6 and coadministration of CYP2D6 inhibitors may have less impact on MDMA pharmacokinetics and the risk of acute toxicity than previously thought. This is consistent with clinical observations that indicate no obvious link between inherited CYP2D6 deficiency and acute MDMA intoxication.

Algorithms↗
PubMed2000

Fatal hyperammonemia after orthotopic lung transplantation.

BACKGROUND: A case of fatal hyperammonemia complicating orthotopic lung transplantation was previously reported. OBJECTIVE: To describe the incidence, clinical features, and treatment of hyperammonemia associated with orthotopic lung transplantation. DESIGN: Retrospective cohort analysis. SETTING: Academic medical center and lung transplantation center in Philadelphia, Pennsylvania. PATIENTS: 145 sequential adult patients who underwent orthotopic lung transplantation. MEASUREMENTS: Plasma ammonium levels. RESULTS: Six of the 145 patients who had had orthotopic lung transplantation developed hyperammonemia, all within the first 26 days after transplantation. The 30-day post-transplantation mortality rate was 67% for patients with hyperammonemia compared with 17% for those without hyperammonemia (P = 0.01). Development of major gastrointestinal complications (P = 0.03), use of total parenteral nutrition (P < 0.001), and lung transplantation for primary pulmonary hypertension (P = 0.045) were associated with hyperammonemia. CONCLUSIONS: Hyperammonemia is a potentially fatal event occurring after orthotopic lung transplantation. It is associated with high nitrogen load, concurrent medical stressors, primary pulmonary hypertension, and hepatic glutamine synthetase deficiency.

Adult↗
PubMed1985

Improvement in hearing among otherwise normal schoolchildren in iodine-deficient areas of Guizhou, China, following use of iodized salt.

According to a survey in Guizhou province of China, the average hearing level of otherwise normal schoolchildren in an area of endemic iodine-deficient goitre and cretinism was significantly poorer than in a non-endemic control area. After iodine prophylaxis for three years, audiometric tests showed that the average hearing level had improved and approached that of the non-endemic controls. In addition, mean values for thyroid function tests were restored to within the normal range. It is suggested that the most likely cause of the poorer hearing level among the ostensibly normal schoolchildren in endemic areas is subclinical hypothyroidism due to prolonged severe iodine deficiency.

Audiometry↗
PubMed1991

[Epidemiological survey on liver diseases of traditional Chinese medicine].

This paper reports the results of epidemiological survey about liver diseases of traditional Chinese medicine (TCM). It surveyed 5606 patients at the general hospitals, and 1013 (18.07%) of them were patients with liver diseases (TCM), including 61 cases of liver Qi depression syndrome, 215 cases of liver depression and Spleen deficiency syndrome, 135 cases of liver and gallbladder damp-heat syndrome, 79 cases of liver Fire flaming syndrome, 145 cases of liver Yang rising syndrome, 209 cases of liver Wind agitation syndrome, 62 cases of liver blood deficiency syndrome, 86 cases of liver-kidney Yin deficiency syndrome and 21 cases of liver cold syndrome. The results showed that constitution ration of liver diseases (TCM). It supplies some scientific data for the clinic and research of liver diseases (TCM).

Adolescent↗
PubMed1999

Case report: portal vein thrombosis associated with hereditary protein C deficiency: a report of two cases.

Protein C deficiency is one of the causes of curable or preventable portal vein thrombosis. We report two patients of portal vein thrombosis associated with hereditary protein C deficiency. The first patient presented with continuous right upper quadrant pain and high fever. The abdominal sonography revealed normal liver parenchyma but portal vein and superior mesenteric vein thrombosis. Based on a 55% (normal 70-140%) plasma protein C level, he was diagnosed as having protein C deficiency. A trace of his family history showed that his elder brother also had protein C deficiency with a 50% plasma C level. Both patients received anticoagulant therapy. The younger brother showed good response. Unfortunately, the elder one suffered from recurrent episodes of variceal bleeding and received a life-saving splenectomy and devascularization. We herein remind clinicians that early screening and therapy are helpful in preventing late complications of protein C deficiency with portal vein thrombosis.

Abdomen, Acute↗
PubMed1997

[Effects of iron deficiency on expression of transferrin receptor in human lymphocytes].

Cell culture in vitro, ABC-ELISA,RNA dot blot and atom absorption spectrum analysis were used to study biological effects of low concentration of iron citrate (Fe-cit) on the expression of transferrin receptor (TfR) in healthy human peripheral lymphocytes. Results showed that TfR increased by 36%, 50%, and 67% in groups with 1.25 x 10(-5), 5 x 10(-6) Fe-cit and without it, respectively as compared with a control group with 2.5 x 10(-5) mol/L Fe-cit. Levels of TfR-mRNA also increased with decrease of iron in substrate. Iron concentration within cells correlated inversely to the change in the number of TfR. It indicated that iron deficiency could regulate the number of TfR in lymphocytes and its gene expression.

Gene Expression↗