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At least 487 records · Page 27Linked to original sources
PubMed2002

Cell lineage-specific effects associated with multiple deficiencies of tumor susceptibility genes in Msh2(-/-)Rb(+/-) mice.

Cooperative effects of genetic alterations are frequently observed during carcinogenesis. Mice carrying germ-line mutations in both Rb and p53 or Msh2 and p53 die earlier of tumors than mice with only one of these genes inactivated. Mice with a single wild-type Rb allele develop a syndrome of multiple neuroendocrine neoplasia, and inactivation of both alleles of Msh2 gene predisposes mice to gastrointestinal cancer, lymphomas and tumors of the skin that exhibit a mismatch repair defect. Here we showed that Msh2(-/-)Rb(+/-) mice developed lymphomas later than Msh2-deficient littermates, and the lymphomas observed in Msh2(-/-)Rb(+/-) mice have increased rates of apoptosis and rarely spread to other organs and tissues. In contrast to lymphomagenesis, courses of neuroendocrine, intestinal, and skin carcinogenesis were not significantly influenced by the Msh2(-/-)Rb(+/-) genetic combination. In these mice, neuroendocrine tumors displayed a loss of the remaining wild-type Rb allele but did not show microsatellite instability. On the other hand, the intestinal and skin tumors exhibited microsatellite instability but kept the remaining wild-type allele of Rb. Taken together, these data not only revealed a novel biological interaction between Rb and Msh2 but also cell lineage specificity effects associated with multiple deficiencies in these tumor susceptibility genes.

Animals↗
PubMed2001

[Effects of zinc deficiency on the distribution of elements in the tissue of pregnant rats and their fetuses].

The influence of zinc(Zn) deficiency on the distribution of elements in tissues of pregnant rats and their fetuses was investigated. Pregnant Wistar rats were divided into zinc deficiency (ZD), pair-fed(PF), zinc supplement (ZS) and control (C) groups. ZD rats were fed for 21 days a zinc deficient (0.7 mg/kg) diet and other rats were fed a similar diet supplemented with zinc (100 mg/kg). On the 21st day of gestation, blood was drawn from heart, laparotomy was performed, and liver, spleen, kidney, placentas, fetuses were removed for analysing on zinc, copper (Cu), iron (Fe), manganese (Mn) and calcium (Ca). The results showed that the element levels in blood, organs and fetuses from ZD rats were significantly lower than those from ZS and C rats. Furthermore, the levels of Cu, Fe, Mn in blood, liver, spleen, kidney of ZD rats were significantly lower than those of PF rats. It suggests that there are some coordination relationships in intestinal absorption and tissue distribution between Zn and other elements, and the decrease of elements in the body does not mainly result from the reduction of dietary intake caused by zinc deficiency. The Fe content in placentas and Fe, Ca content in fetuses of ZD rats showed a significant increase as compared with those of rats in other groups. There may be a competitive mechanism on the transportation of Zn and Fe in the placenta of rats. In brief, the distribution of minerals in maternal tissues induced by zinc deficiency might be different from those in fetuses.

Animals↗
PubMed2005

Reconstitution of caspase-3 sensitizes MCF-7 breast cancer cells to radiation therapy.

Caspase-3 plays an important role in apoptotic execution. Caspase-3 deficiency or down-regulation has been reported in breast and other kinds of cancers. Given the redundancy of caspase cascade, however, the impact of caspase-3 deficiency/down-regulation on radiation-induced apoptosis remains to be defined. In this report, the specific role of caspase-3 in radiotherapy-induced apoptosis was studied using MCF-7 control (MCF-7/pv, caspase-3 deficient) and caspase-3 reconstituted MCF-7 (MCF-7/c3) breast cancer cells. Caspase-3 reconstitution significantly enhanced radiation-induced apoptosis, with a decrease in the survival fraction, an increase in caspase activation, cleavage of cellular death substrates and mitochondrial depolarization. We also found that the activation of caspase-7 was caspase-3-dependent in radiation-induced apoptosis, which suggests a mini-cascade among the effector caspases and that caspase-3 is essential for signal amplification. In comparing the patterns of death substrates cleavage in radiation-induced apoptosis with that in doxorubicin and TNF-alpha-induced apoptosis, we found that cleavage of lamin B and beta-actin was relatively more susceptible to radiation, which is enhanced in the presence of caspase-3, suggesting cytoskeleton proteins might be preferred markers for radiation-induced apoptosis. These data indicate that caspase-3 plays a critical role in radiotherapy-induced apoptosis, and suggest that caspase-3 deficiency may contribute to the radioresistance of breast cancers.

Actins↗
PubMed1994

[Plasma endothelin level in patients with pregnancy induced hypertension and its correlation with atrial natriuretic peptide].

Plasma levels of endothelin (ET) and atrial natriuretic peptide (ANP) were measured in 32 normal pregnant women and 26 patients with pregnancy induced hypertension (PIH). The correlation between ET and ANP were examined. This study indicated that the levels of ET and ANP in hypertensive pregnancy were higher than those of the normal pregnancy (P < 0.01). There was no correlation between ET and ANP in normal pregnancy (r = 0.18, P > 0.05), but significant inverse correlation in the patient with PIH (r = -0.57, P < 0.05). There findings suggested that ET may play an important role in the pathogenesis of PIH. An imbalance of increased amount of ET relative to deficient ANP may lead to PIH.

Adult↗
PubMed1990

Induction of ovulation with pulsatile GnRH.

The use of pulsatile GnRH to treat infertile women who do not ovulate has been shown to be safe, simple, and effective and the preferred method of inducing ovulation in appropriately selected patients who are resistant to treatment with clomiphene citrate. Treatment with GnRH is particularly effective for restoring ovulation in patients with idiopathic hypogonadotrophic hypogonadism and partially recovered weight-related amenorrhoea, but less successful in patients with polycystic ovary syndrome and organic hypothalamic pituitary disease. Based on personal experience, we advocate routine use of the subcutaneous route, using 15 micrograms per pulse every 90 min, and we monitor the patient's progress by serial ultrasound scanning and measurement of serum gonadotrophin and oestradiol concentrations. If the patient does not respond we recommend adding treatment with clomiphene citrate (Homburg et al, 1988b). Treatment with intravenous GnRH is reserved for women who do not respond to the above combination of drugs. We do not treat patients with GnRH until their body mass index is in the normal range (between 20-25) and we avoid GnRH treatment in patients with hypersecretion of LH during the follicular phase. If LH concentrations are raised, an alternative method of treatment is recommended, such as ovarian diathermy (Armar et al, 1990). Finally, the question of whether GnRH deficiency in patients with hypogonadotrophic hypogonadism is caused by a specific genetic lesion is not yet fully resolved. Yang-Feng et al (1986) used a cDNA clone encoding the human GnRH precursor molecule in order to assign the GnRH gene to a particular human chromosome. They found a single site for GnRH sequences in the human genome and that the gene coding for GnRH is located on the short arm of chromosome 8. Experiments in the congenitally hypogonadal mouse have shown that it is possible to restore gonadal development and gametogenesis by gene transfer (Mason et al, 1987). Clearly an abnormality at the level of the genome may be responsible for the secretory defect in patients with hypogonadotrophic hypogonadism, but it has yet to be defined (Weiss et al, 1989). Presumably elucidation awaits the development of more refined methods because both the genetics and the clinical associations of GnRH deficiency are most persuasive. Meanwhile replacement treatment with GnRH provides a simple and safe form of treatment for managing the clinical syndromes of GnRH deficiency.

Anovulation↗
PubMed2001

[The genotype analysis of glucose-6-phosphate dehydrogenase deficiency in Yunnan province].

OBJECTIVE: To identify glucose-6-phosphate dehydrogenase (G6PD) gene mutations in 23 patients with G6PD deficiency and to gain further understanding of the molecular and genetic background of G6PD gene in Yunnan province, China. METHODS: The mutations located in exons 2-12 and in parts of introns of G6PD gene were analyzed by amplification refractory mutation system(ARMS), natural and mis-match primer PCR/restrict enzyme, polymerase chain reaction-single strand conformation polymorphism(PCR-SSCP ) analysis and automatic DNA sequencing. RESULTS: Among these 23 samples, 5 different point mutations in G6PD gene were identified, and they constituted 5 genotypes. There were 7 Han and 3 Dai patients with G487A mutation, 7 cases with both intron 11 T93C and C1311T mutations, 4 cases with intron 5 636 or 637 T-->del mutation, 1 case with G871A mutation, and 1 case with G487A/T93C/C1311T mutation. Two haplotypes, 93C/1311T and 93C/1311T/487A were identified in Yunnan. A strong association was observed between C1311T and the Nla III restriction site produced by intron 11 T93C. The findings of the investigators on IVS-5 636 or 637T-->del in Chinese, on G871A in mainland of China, and on G487A in the Han people of Yunnan have not been reported previously. CONCLUSION: G6PD deficiency is very heterogenous in Yunnan; G487A is one of the common mutations in that province and may be of different origins. Possibly IVS-11 T93C mutation is of non-African origin. IVS-11 T93C and C1311T might jointly result in G6PD deficiency. The above data on G6PD gene mutation types could be useful for clinical diagnosis, prevention of G6PD deficiency, and researches in the origin and migration of minorities in Yunnan or other regions.

Adolescent↗
PubMed1991

TCM treatment of luteal phase defect--an analysis of 60 cases.

Sixty cases of infertility due to luteal phase defect were treated with herbs to tonify the kidney and regulate the menstrual cycle. After the treatment, the hyperthermal phase score of basal body temperature (BBT) was markedly increased (P less than 0.05), the hyperthermal phase 7-8 days after ovulation improved (P less than 0.001), the transitional period of BBT remarkably shortened, and the pregnancy rate in 32 uncomplicated cases of luteal phase defect was 56%. The close relationship between luteal phase defect and the kidney deficiency syndrome in TCM was discussed. The key points of the treatment included coordination of yin and yang, regulation of qi and blood, and combination of tonification with reduction.

Adult↗
PubMed2004

Comparison of a combination ferrous fumarate product and a polysaccharide iron complex as oral treatments of iron deficiency anemia: a Taiwanese study.

Despite efforts to improve iron supplements for iron deficiency anemia, there is no consensus on products that balance efficacy, safety and tolerability, and cost. Ferrous products are effective, but they are associated with more gastrointestinal side effects than ferric products. Ferric products tend to have lower absorption. We present results from a 12-week study that randomized 72 people with uncomplicated iron deficiency anemia to receive a ferrous iron supplement (Ferall, a combination of ferrous fumarate with ascorbic acid, folic acid, and cyanocobalamin) or a ferric iron polysaccharide complex (Niferex, ferro-glycine sulfate) plus ascorbic acid. The ferrous product was significantly more effective, the primary and secondary endpoints including changes in levels of hemoglobin and serum ferritin. There was a slightly higher frequency of gastrointestinal side effects in patients taking the ferrous product, but both supplements were well tolerated. No participant withdrew from the study because of side effects. We concluded that the ferrous product is safe and effective for use in uncomplicated iron deficiency anemia. The lack of direct comparison between single-agent ferrous fumarate and the combination ferrous product limited interpretation of results in terms of possible effects due to other components, such as ascorbic acid.

Administration, Oral↗
PubMed2005

Microcytosis in agnogenic myeloid metaplasia: prevalence and clinical correlates.

Microcytosis is a characteristic laboratory feature for both iron deficiency anemia and thalassemia. It is also infrequently seen in "anemia of chronic disease" that accompanies a spectrum of chronic conditions including rheumatoid arthritis, polymyalgia rheumatica, diabetes mellitus, connective tissue disease, and protracted infection. In addition, there is a well established but pathogenetically obscure association of microcytosis with Hodgkin's lymphoma, Castleman's disease, and renal cell carcinoma. In the current study, we show that microcytosis is a frequent laboratory feature in agnogenic myeloid metaplasia and investigate its clinical relevance in the particular setting.

Adolescent↗
PubMed2001

Chorea induced by thiamine deficiency in hemodialysis patients.

Thiamine deficiency is mainly encountered in alcoholics or food faddists, but it may complicate chronic dialysis because of low intake and accelerated loss of thiamine in dialysis patients. We report here 2 hemodialysis (HD) patients who developed chorea induced by thiamine deficiency. We propose that thiamine deficiency, with a consequent dysfunction of the basal ganglia, may induce chorea in HD patients.

Aged↗
PubMed2000

Rescue of fatal neonatal hemorrhage in factor V deficient mice by low level transgene expression.

Factor V (FV) is a critical component of the coagulation cascade. FV-deficient patients suffer moderate to severe bleeding, though residual FV activity is detectable in nearly all cases. In contrast, FV-deficient mice die either during mid-embryogenesis, or of massive perinatal hemorrhage. In order to examine the requirements for FV in murine embryogenesis and hemostasis, we generated transgenic mouse lines expressing a Fv minigene under control of either the tissue-specific albumin (Malb) or rat platelet factor 4 (Rpf4) promoter. A total of 12 Malb and 3 Rpf4 lines were analyzed. Though expression in the target tissue was detectable in most lines by RT-PCR, only low levels of transgene expression were achieved (<3% of endogenous Fv in all lines). Despite a low level of Fv transgene expression, rescue of the lethal Fv-/- phenotype was observed with one of the Malb transgenic (Tg+) lines. However, rescue appeared to be incomplete with continued loss of >1/2 of expected Tg+,Fv-/- mice in early embryogenesis. Rescued Tg+,Fv-/- mice have undetectable FV (<0.1%) in both plasma and platelet compartments, but survive the perinatal period and mature to adulthood without spontaneous hemorrhage. We conclude that FV present at <0.1% is sufficient to support postnatal survival. Failure of the Malb transgene to rescue the midembryonic block suggests that FV expression is required during mammalian development at higher levels or with a different tissue-specific or temporal pattern. Taken together, these data may explain the observation of residual FV activity in most human FV-deficient patients due to early embryonic lethality in those absolutely deficient, and suggest that minimal levels of FV expression, below the level of detection, also may be sufficient to support survival in humans.

Acute Disease↗
PubMed1980

Persistent transfusion-associated infectious mononucleosis with transient acquired immunodeficiency.

Trauma and blood transfusion led to profound, persistent infectious mononucleosis in a 21 year old man. Splenectomy and trauma had apparently produced transient immune deficiency which was complicated by osteomyelitis of a fractured tibia. The transfused blood probably contained Epstein-Barr virus (EBV). Infectious mononucleosis had ensued 25 days after a blood transfusion was given, antibodies to EBV appeared in his serum, and the infectious mononucleosis persisted for nearly two years. His immunity returned gradually to normal, but because of nonunion of the fracture site, which was infected by Staphylococcus aureus, above-knee amputation was required. The acquired, transient immune deficiency to EBV and profound infectious mononucleosis seen in this patient is analogous to inherited, permanent immune deficiency to this virus in the X-linked lymphoproliferative syndrome.

Adult↗
PubMed2005

Detection of three common G6PD gene mutations in Chinese individuals by probe melting curves.

OBJECTIVE: In order to develop and validate an assay for rapid detection of three common G6PD gene mutations in Chinese individuals. METHODS: In this report we design two sets of primers and fluorescently labeled hybridization probes recognizing adjacent sequences in the amplicon; after annealing, the fluorophores were in resonance energy transfer, providing real-time monitoring of the amplication process. At the completion of PCR, fluorescence was monitored as the temperature increased through the Tm of the probe/product duplex, and a characteristic melting profile for each mutation was obtained. By using the fluorescence method and PCR/RE, a total of 57 samples obtained from two groups of G6PD-deficient individuals were studied. RESULT: A rapid method for detection of three common G6PD gene mutations in Chinese individuals by probe melting curves was developed. This method shows 100% accordance with the traditional method. CONCLUSION: This fluorescent melting curve analysis is a simple, rapid, and effective method for clinical diagnosis and screening of G6PD deficiency.

China↗
PubMed2001

Alternations in quantities and activities of erythrocyte cytosolic carbonic anhydrase isoenzymes in glucose-6-phosphate dehydrogenase-deficient individuals.

BACKGROUND: This study was designed to evaluate the quantitative and activity alterations of cytosolic carbonic anhydrase (CA) isoenzymes in the erythrocytes of glucose-6-phosphate dehydrogenase (G6PD)-deficient individuals. METHODS: Western Blot and CA esterase activity analysis were employed to measure cytosolic erythrocyte CA isoenzymes. RESULTS: The total CA activities were analyzed from erythrocytes of 30 healthy and 30 G6PD-deficient individuals. The mean values with standard error (SE) were 22.9+/-1.69 U/gHb and 27.2+/-2.1 U/gHb (P<0.01), respectively. The ratio of CAI/CAII of G6PD-deficient individuals (1.28+/-0.06) was significantly lower than that of the normal subjects (3.79+/-0.18) (P<0.001). Furthermore, the concentration of CAIII in G6PD-deficient individuals was significantly lower than that of the normal subjects (P<0.001) and there were significant correlations between the concentration of CAI, CAII, CAIII, and ratio of CAI/CAII, and the activity concentration of G6PD. CONCLUSIONS: Different carbonic anhydrase isoenzymes may serve different roles in the G6PD-deficient erythrocyte. CAI could be used as an indicator for hemolytic anemia. CAII is able to compensate for the functions of CAI and increased expression of CAII will promote oxidative damage. CAIII can provide the G6PD-deficient persons with some extent of protection against oxidative damage.

Adult↗
PubMed2006

A Drosophila model of Barth syndrome.

Barth syndrome is an X-linked disease presenting with cardiomyopathy and skeletal muscle weakness. It is caused by mutations in tafazzin, a putative acyl transferase that has been associated with altered metabolism of the mitochondrial phospholipid cardiolipin. To investigate the molecular basis of Barth syndrome, we created Drosophila melanogaster mutants, resulting from imprecise excision of a P element inserted upstream of the coding region of the tafazzin gene. Homozygous flies for that mutation were unable to express the full-length isoform of tafazzin, as documented by RNA and Western blot analysis, but two shorter tafazzin transcripts were still present, although the expression levels of their encoded proteins were too low to be detectable by Western blotting. The tafazzin mutation caused an 80% reduction of cardiolipin and a diversification of its molecular composition, similar to the changes seen in Barth patients. Other phospholipids, like phosphatidylcholine and phosphatidylethanolamine, were not affected. Flies with the tafazzin mutation showed a reduced locomotor activity, measured in flying and climbing assays, and their indirect flight muscles displayed frequent mitochondrial abnormalities, mostly in the cristae membranes. Thus, tafazzin mutations in Drosophila generated a Barth-related phenotype, with the triad of abnormal cardiolipin, pathologic mitochondria, and motor weakness, suggesting causal links between these findings. We conclude that a lack of full-length tafazzin is responsible for the cardiolipin deficiency, which is integral to the disease mechanism, leading to mitochondrial myopathy.

1-Acylglycerophosphocholine O-Acyltransferase↗
PubMed1999

Mitochondrial intermediate peptidase and the yeast frataxin homolog together maintain mitochondrial iron homeostasis in Saccharomyces cerevisiae.

Friedreich's ataxia (FRDA) is a neurodegenerative disease typically caused by a deficiency of frataxin, a mitochondrial protein of unknown function. In Saccharomyces cerevisiae, lack of the yeast frataxin homolog ( YFH1 gene, Yfh1p polypeptide) results in mitochondrial iron accumulation, suggesting that frataxin is required for mitochondrial iron homeostasis and that FRDA results from oxidative damage secondary to mitochondrial iron overload. This hypothesis implies that the effects of frataxin deficiency could be influenced by other proteins involved in mitochondrial iron usage. We show that Yfh1p interacts functionally with yeast mitochondrial intermediate peptidase ( OCT1 gene, YMIP polypeptide), a metalloprotease required for maturation of ferrochelatase and other iron-utilizing proteins. YMIP is activated by ferrous iron in vitro and loss of YMIP activity leads to mitochondrial iron depletion, suggesting that YMIP is part of a feedback loop in which iron stimulates maturation of YMIP substrates and this in turn promotes mitochondrial iron uptake. Accordingly, YMIP is active and promotes mitochondrial iron accumulation in a mutant lacking Yfh1p ( yfh1 [Delta]), while genetic inactivation of YMIP in this mutant ( yfh1 [Delta] oct1 [Delta]) leads to a 2-fold reduction in mitochondrial iron levels. Moreover, overexpression of Yfh1p restores mitochondrial iron homeostasis and YMIP activity in a conditional oct1 ts mutant, but does not affect iron levels in a mutant completely lacking YMIP ( oct1 [Delta]). Thus, we propose that Yfh1p maintains mitochondrial iron homeostasis both directly, by promoting iron export, and indirectly, by regulating iron levels and therefore YMIP activity, which promotes mitochondrial iron uptake. This suggests that human MIP may contribute to the functional effects of frataxin deficiency and the clinical manifestations of FRDA.

Animals↗
PubMed2005

Combined buccal mucosa graft and local flap for urethral reconstruction in various forms of hyposapdias.

PURPOSE: Hypospadias is one of the most common congenital deformities in the male urogenital system. Although there are more than 250 techniques for treating hypospadias, it is often difficult to repair severe hypospadias using conventional methods. MATERIALS AND METHODS: We combined a buccal mucosa graft with a local onlay flap for urethral reconstruction in cases of severe hypospadias or a failed previous operation. A total of 162 patients with hypospadias (glandular 11, penile 40, penoscrotal 49, scrotal 34 and perineal 28) were treated between July 2000 and November 2003. For patients whose urethral meatus was perineal 2 treatment steps were taken. First, we used the aforementioned method to construct the penile urethra, and then we constructed the scrotal and perineal urethra with a local flap. RESULTS: Of the 134 nonperineal cases 127 were managed successfully in 1 stage, and 26 of 28 perineal cases were managed successfully in 2 stages. Most patients had a satisfactory penile appearance. A urethral fistula resulted in 8 cases, of which 4 closed spontaneously within 1 month postoperatively. Meatal stenosis occurred in 1 case. CONCLUSIONS: This technique is simple, safe and reliable, especially in cases of failed previous operation or for salvage hypospadias repair with deficient local tissue.

Adolescent↗