NPF immunolocalization in cockroaches and locusts. Comparison of antisera to beetle, tapeworm, and pig NPY/NPF-type peptides.
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Animals↗
Biomedical subjects
W Zhu
Publications and source records attributed to W Zhu.
Identification of the low density lipoprotein receptor-binding site in apolipoprotein B100 and the modulation of its binding activity by the carboxyl terminus in familial defective apo-B100.
Familial defective apolipoprotein B100 (FDB) is caused by a mutation of apo-B100 (R3500Q) that disrupts the receptor binding of low density lipoproteins (LDL), which leads to hypercholesterolemia and premature atherosclerosis. In this study, mutant forms of human apo-B were expressed in transgenic mice, and the resulting human recombinant LDL were purified and tested for their receptor-binding activity. Site-directed mutagenesis and other evidence indicated that Site B (amino acids 3,359-3,369) binds to the LDL receptor and that arginine-3,500 is not directly involved in receptor binding. The carboxyl-terminal 20% of apo-B100 is necessary for the R3500Q mutation to disrupt receptor binding, since removal of the carboxyl terminus in FDB LDL results in normal receptor-binding activity. Similarly, removal of the carboxyl terminus of apo-B100 on receptor-inactive VLDL dramatically increases apo-B-mediated receptor-binding activity. We propose that the carboxyl terminus normally functions to inhibit the interaction of apo-B100 VLDL with the LDL receptor, but after the conversion of triglyceride-rich VLDL to smaller cholesterol-rich LDL, arginine-3,500 interacts with the carboxyl terminus, permitting normal interaction between LDL and its receptor. Moreover, the loss of arginine at this site destabilizes this interaction, resulting in receptor-binding defective LDL.
Animals↗
Frequency of HPRT gene mutations induced by N-methyl-N'-nitro-N-nitrosoguanidine corresponds to replication error phenotypes of cell lines.
We have examined whether cells with replication error-positive (RER+) and -negative phenotype (RER ) respond differently to the mutagen MNNG, employing three RER+ and two RER- human cell lines. Cells were treated with several concentrations of MNNG, and HPRT mutants were selected phenotypically by their growth in the presence of 6-thioguanine. While the variation of the mutation frequency within each group was about an order of magnitude, it was found that MNNG induced a level of mutations in the HPRT gene some 100- to 1000-fold higher in RER+ cells than in cells with RER-phenotype. MNNG, at a concentration of 30 microM, produced a mutation frequency 450-fold higher in HCT116 (RER+) cells than in SW480 (RER-) cells. Our findings suggest that the RER+ phenotype predisposes cells to MNNG-induced hypermutability.
Cell Line↗
Cell type-specific angiotensin II-evoked signal transduction pathways: critical roles of Gbetagamma subunit, Src family, and Ras in cardiac fibroblasts.
Angiotensin II (Ang II) induces hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts. To determine the molecular mechanism by which Ang II displayed different effects on cardiac myocytes and fibroblasts, we examined signal transduction pathways leading to activation of extracellular signal-regulated kinases (ERKs). Ang II-induced ERK activation was abolished by pretreatment with pertussis toxin and by overexpression of the Gbetagamma subunit-binding domain of the beta-adrenergic receptor kinase 1 in cardiac fibroblasts but not in cardiac myocytes. Inhibition of protein kinase C strongly inhibited activation of ERKs by Ang II in cardiac myocytes, whereas inhibitors of tyrosine kinases but not of protein kinase C abolished Ang II-induced ERK activation in cardiac fibroblasts. Overexpression of C-terminal Src kinase (Csk), which inactivates Src family tyrosine kinases, suppressed the activation of transfected ERK in cardiac fibroblasts. Ang II rapidly induced phosphorylation of Shc and association of Shc with Grb2. Cotransfection of the dominant-negative mutant of Ras or Raf-1 kinase abolished Ang II-induced ERK activation in cardiac fibroblasts. Overexpression of Csk or the dominant-negative mutant of Ras had no effects on Ang II-induced ERK activation in cardiac myocytes. These findings suggest that Ang II-evoked signal transduction pathways differ among cell types. In cardiac fibroblasts, Ang II activates ERKs through a pathway including the Gbetagamma subunit of Gi protein, tyrosine kinases including Src family tyrosine kinases, Shc, Grb2, Ras, and Raf-1 kinase, whereas Gq and protein kinase C are important in cardiac myocytes.
Angiotensin II↗
[Analysis of expression of FMR-1 gene in male patients with fragile X syndrome using RT-PCR].
OBJECTIVE: To search the relationship between fragile X male patients and expression of FMR-1 gene and to establish a rapid and simple method for screening male patients in general population. METHODS: Two typical fragile X families demonstrated by cytogenetics method were analyzed by using RT-PCR. RESULTS: No expression of FMR-1 gene in all male patients in the two families was noted, but all normal individuals showed expression of FMR-1 gene. There was an expression of HPRT gene as internal control in each of the individuals detected. CONCLUSION: There is a strong relationship between loss of expression of FMR-1 gene and clinical phenotype of the fragile X male patients. Further research of this method will introduce a more simple and rapid method for detecting male patients with fragile X syndrome. This method may be used for general population screening.
Fragile X Messenger Ribonucleoprotein 1↗
Role of adenosine deaminase and dATP levels in thymocyte apoptosis.
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Adenosine Deaminase↗
Mechanism of high-density lipoprotein subfractions inhibiting copper-catalyzed oxidation of low-density lipoprotein.
OBJECTIVE: To investigate the role of HDL subfractions, HDL2 and HDL3, on the oxidation of LDL catalyzed by 5 microM Cu2+ ion, and to illustrate the mechanism of the generation of conjugated diene and thiobarbituric acid reactive substances (TBARS) during LDL oxidation. METHODS: LDL was incubated for 8 h with 5 microM Cu2+ ion in phosphate-buffered saline (PBS) alone, or in the presence of HDL2, HDL3, HSA, BSA, or transferrin. Meantime, LDL was incubated for 24 h with 10 microM Ni2+ ions in PBS. The amount of conjugated diene and TBARS in each sample of LDL were measured. RESULTS: (a) HDL2 and HDL3 could inhibit the generation of conjugated diene, but could not inhibit the generation of TBARS; (b) the transferrin containing HDL3 shows the ability of inhibiting the generation of both conjugated diene and TBARS; (c) the transferrin presented in blood exhibits the inhibitory effect on the generation of conjugated diene and TBARS, however, when the transferrin is saturated with Fe3+ ion, it could not inhibit the generation of TBARS; (d) HSA and BSA could prevent the generation of conjugated diene and TBARS; (e) Ni2+ ion could induce the generation of conjugated diene, but the amount of TBARS was much smaller than that induced by Cu2+ ion. CONCLUSION: HDL2 and HDL3 play important role in the copper-catalyzed oxidation of LDL; it is absolutely necessary to require chelation of Cu2+ ion for inhibiting generation of TBARS; whereas, inhibition of conjugated diene can be fulfilled either by chelating Cu2+ ion, or the free radicals scavenger.
Apoproteins↗
Pretreatment and biodegradability enhancement of DSD acid manufacturing wastewater.
Two advanced oxidation processes, Fenton's reagent oxidation and ozonation, were used for pretreatment of a 4,4'-diaminostilbene-2,2'-disulfonic acid (DSD-acid) manufacturing wastewater on a laboratory scale. The results showed that both methods are suitable for partial removal of chemical oxygen demand (COD) and color as well as the enhancement of biodegradability of DSD-acid manufacturing wastewater before the conventional biological treatment. Fenton's reagent oxidation by 9.0 g/L H2O2 and 150 mg/L Fe2+ and ozonation by 7.5 g/L O3 led to an improved biodegradability (BOD5/COD = 0.3). Fenton's reagent oxidation in combination with Fe3+ coagulation has shown to effectively remove COD and color. About 90% of COD and 95% of color removals were obtained at the optimum condition, oxidation by 150 mg/L Fe2+ and 2 g/L H2O2, followed by two-stage coagulation with 5 g/L and 2 g/L FeCl3, respectively.
4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
Exochelin genes in Mycobacterium smegmatis: identification of an ABC transporter and two non-ribosomal peptide synthetase genes.
Many strains of mycobacteria produce two ferric chelating substances that are termed exochelin (an excreted product) and mycobactin (a cell-associated product). These agents may function as iron acquisition siderophores. To examine the genetics of the iron acquisition system in mycobacteria, ultraviolet (UV) and transposon (Tn611) mutagenesis techniques were used to generate exochelin-deficient mutants of Mycobacterium smegmatis strains ATCC 607 and LR222 respectively. Mutants were identified on CAS siderophore detection agar plates. Comparisons of the amounts of CAS-reactive material excreted by the possible mutant strains with that of the wild-type strains verified that seven UV mutant strains and two confirmed transposition mutant strains were deficient in exochelin production. Cell-associated mycobactin production in the mutants appeared to be normal. From the two transposon mutants, the mutated gene regions were cloned and identified by colony hybridization with an IS6100 probe, and the DNA regions flanking the transposon insertion sites were then used as probes to clone the wild-type loci from M. smegmatis LR222 genomic DNA. Complementation assays showed that an 8 kb PstI fragment and a 4.8 kb PstI/SacI subclone of this fragment complemented one transposon mutant (LUN2) and one UV mutant (R92). A 10.1 kb SacI fragment restored exochelin production to the other transposon mutant (LUN1). The nucleotide sequence of the 15.3 kb DNA region that spanned the two transposon insertion sites overlapped the 5' region of the previously reported exochelin biosynthetic gene fxbA and contained three open reading frames that were transcribed in the opposite orientation to fxbA. The corresponding genes were designated exiT, fxbB and fxbC. The deduced amino acid sequence of ExiT suggested that it was a member of the ABC transporter superfamily, while FxbB and FxbC displayed significant homology with many enzymes (including pristinamycin I synthetase) that catalyse non-ribosomal peptide synthesis. We propose that the peptide backbone of the siderophore exochelin is synthesized in part by enzymes resembling non-ribosomal peptide synthetases and that the ABC transporter ExiT is responsible for exochelin excretion.
ATP-Binding Cassette Transporters↗
Test equating: what, why, how?
The purpose of this paper is to introduce test equating, including its concept, needs, and methods, to the field of physical education and exercise science. Both traditional and item response theory (IRT) equating methods, along with data collection designs, were described in detail, and the advantages and disadvantages of these methods were also introduced. In addition, equating errors and evaluation criteria, sample size, and related computer programs were introduced. Using an existing data set of sit-up tests, a test-equating application was illustrated through a step-by-step example. As a result, two sit-up tests were equated onto a common scale, and equating accuracy was evaluated using both equating and cross-validation samples. Finally, benefits and potential applications of test equating in assessing motor functions and skills, as well as future research challenges, were described.
Data Collection↗
An empirical evaluation of the prediction of maximal heart rate.
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Adult↗
Comments on "development of a cadence curl-up test for college students" (Sparling, Millard-Stafford, & Snow, 1997): concerns about validity and practicality.
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Abdominal Muscles↗
AvrXa10 contains an acidic transcriptional activation domain in the functionally conserved C terminus.
The avrXa10 gene of Xanthomonas oryzae pv. oryzae, the causal agent of bacterial blight of rice, is a member of the avrBs3 avirulence gene family and directs the elicitation of resistance in a gene-for-gene manner on rice lines carrying the resistance gene Xa10. The carboxyl (C) terminus of AvrXa10 has a previously undescribed domain that is structurally similar to the acidic activation domain of many eukaryotic transcription factors in addition to three nuclear localization signal (NLS) sequences. Removal of the C-terminal 38 codons containing the putative activation domain, but retaining the NLS sequences, was concomitant with the loss of avirulence activity. The C-terminal coding regions of avrBs3 and avrXa7 can be replaced by the corresponding region of avrXa10, and the genes retained specificity for the resistance genes Bs3 in pepper and Xa7 in rice, respectively. The avrBs3 and avrXa7 avirulence activities of the hybrid genes were also lost upon removal of the terminal 38 codons. When fused to the coding sequence of the Gal4 DNA binding domain, AvrXa10 activated transcription in yeast and Arabidopsis thaliana. Removal of the carboxyl region severely reduced transcriptional activation. AvrXa10 would have to be localized to the host cell nucleus to function autonomously in transcriptional activation. Consistent with this requirement, mutations in all three NLS sequences of avrXa10 caused a loss in avirulence activity. The findings demonstrate the requirement of the C terminus for AvrXa10 function and the potential for the members of this family of avirulence gene products to enter the host nucleus and alter host transcription.
Amino Acid Sequence↗
Tetramethylpyrazine, a Chinese drug, blocks coronary vasoconstriction by endothelin-1 and decreases plasma endothelin-1 levels in experimental animals.
The purpose of this study was to investigate effects of tetramethylpyrazine (TMP), a Chinese plant-derived medicine, on coronary vasoconstriction and related electrocardiographic and histologic changes caused by endothelin-1 (ET-1), and on plasma ET-1 levels. ET-1 (75 pmol) was administered into the left coronary artery (LCA) in anesthetized closed-chest dogs with and without prior infusion of TMP (80 mg/kg). Coronary arterial diameter (CAD) was determined by coronary arteriography (CAG). Blood pressure and electrocardiogram (ECG) were monitored continuously. Histologic damage in tissues was ascertained microscopically. Plasma ET-1 and 6-keto-PGF1 levels were determined by RIA 90 min after i.v. injection of TMP (25 mg/kg; n = 5) in rabbits. Intracoronary injection of ET-1 resulted in a significant vasoconstriction of the entire vascular bed of the LCA, with a decrease in CAD of 35.9 +/- 5.7% (n = 5; p < 0.01) and ischemic changes on ECG and in tissues of endocardium, myocardium, coronary endothelial cells, and capillary vessels. Pretreatment with TMP produced a significant increase in CAD by 38.5 +/- 7.8% (n = 5; p < 0.01) and greatly suppressed the vasoconstriction produced by ET-1. The myocardial tissue damage estimated from the ratio of ischemic area for the entire area after ET-1 injection (35.6%) was completely abolished by TMP (0.6%). In addition, TMP injection induced a significant decrease in plasma ET-1 levels and an increase in 6-keto-PGF1 levels in rabbits. The Chinese medicine TMP could be a useful therapeutic agent in ischemic heart disease by suppressing coronary vasoconstriction and ischemic changes in the tissues produced by ET-1.
6-Ketoprostaglandin F1 alpha↗
A case of seborrheic keratosis distributed along skin cleavage lines.
A 65-year-old woman with seborrheic keratosis following skin cleavage lines is reported. The mostly brownish-yellow lesions were located on the back. The round, oval, spindle, comet, and slightly raised papules varied from 1 mm to 2 cm in diameter. The distribution of lesions was unusual; they tended to follow skin cleavage lines on her lower back and waist. The arrangement of lesions was streamlined. The skin biopsy specimen revealed hyperkeratosis, acanthosis, and papillomatosis. The acanthosis was caused by proliferation of squamous and basaloid cells.
Aged↗
Identification of rCop-1, a new member of the CCN protein family, as a negative regulator for cell transformation.
By using a model system for cell transformation mediated by the cooperation of the activated H-ras oncogene and the inactivated p53 tumor suppressor gene, rCop-1 was identified by mRNA differential display as a gene whose expression became lost after cell transformation. Homology analysis indicates that rCop-1 belongs to an emerging cysteine-rich growth regulator family called CCN, which includes connective-tissue growth factor, CYR61, CEF10 (v-src inducible), and the product of the nov proto-oncogene. Unlike the other members of the CCN gene family, rCop-1 is not an immediate-early gene, it lacks the conserved C-terminal domain which was shown to confer both growth-stimulating and heparin-binding activities, and its expression is lost in cells transformed by a variety of mechanisms. Ectopic expression of rCop-1 by retroviral gene transfers led to cell death in a transformation-specific manner. These results suggest that rCop-1 represents a new class of CCN family proteins that have functions opposing those of the previously identified members.
Aging↗
Effects of low-impact, moderate-intensity exercise training with and without wrist weights on functional capacities and mood states in older adults.
This study examined the effects of low-impact, moderate-intensity exercise training with and without wrist weights (0.68 kg.wrist-1) on functional capacities and mood states in older adults (age 68.6 +/- 5.6, mean +/- SD). Twenty-three senior citizens residing in the community were randomly assigned to wrist weight (WW; n = 12) and no-wrist weight (NW; n = 11) exercise groups while 11 matched subjects served as non-exercise controls (NE). Exercise training was performed for 10 weeks, 3 days/week, for 60 min/session and consisted of low-impact aerobic dance (50-70% of maximal heart rate) combined with exercises to promote muscular fitness, flexibility, and balance. Before and after the intervention, each participant's aerobic fitness, muscular strength, flexibility, static and dynamic balance, skinfold thickness, and psychological mood states were assessed under standardized testing conditions. Exercise training resulted in significant improvements in peak oxygen uptake, lower extremity muscle strength, and psychological vigor (p < 0.05) but did not affect other fitness components (p > 0.05). There were no differences between the WW and NW exercise groups for any of the same variables studied (p > 0.05). No significant pre- to post-test changes were found for the NE control group (p > 0.05). It is concluded that 10 weeks of low-impact, moderate-intensity exercise training of the type that can be considered well-rounded in nature provides a sufficient stimulus to augment aerobic fitness, beneficially affects leg strength, and increases feelings of vigor in older adults. The present observations indicate that the use of light wrist weights has no beneficial or adverse effects on the measured training outcomes.
Activities of Daily Living↗
Expression of the human integrin beta6 subunit in alveolar type II cells and bronchiolar epithelial cells reverses lung inflammation in beta6 knockout mice.
Inactivation of the integrin beta6 subunit gene in mice resulted in an unexpected phenotype-functionally significant inflammation of the skin and lungs. These findings suggested a role for ligation of the alphav beta6 integrin on epithelial cells in downregulating epithelial inflammation. However, the results of gene inactivation could have been due to inactivation of adjacent genes and provided no information about the role of this integrin in specific populations of epithelial cells. In the current study, we used transgenic mice constitutively expressing the human beta6 subunit in alveolar type II cells and bronchiolar epithelial cells to examine directly the significance of alphav beta6 in these cells. Expression of this transgene largely inhibited the increases in airspace lymphocytes and macrophages and the lymphocyte and macrophage activation caused by inactivation of the beta6 subunit gene, and reduced the peribronchial and perivascular accumulations of lymphocytes. In the genetically mixed mice used for this study, we identified airway eosinophilia as an additional effect of beta6 inactivation. This effect was also partially inhibited by limited expression of the human transgene. These results definitively identify a role for distal lung epithelial alphav beta6 in downregulating pulmonary inflammation and suggest that interventions augmenting beta6 expression or function in these cells could influence the course of inflammatory lung diseases.
Animals↗