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C Cui

Publications and source records attributed to C Cui.

45 records · Page 3Linked to original sources

Reporter genes in transgenic mice.

Although in vivo models utilizing endogenous reporter genes have been exploited for many years, the use of reporter transgenes to dissect biological issues in transgenic animals has been a relatively recent development. These transgenes are often, but not always, of prokaryotic origin and encode products not normally associated with eukaryotic cells and tissues. Some encode enzymes whose activities are detected in cell and tissue homogenates, whereas others encode products that can be detected in situ at the single cell level. Reporter genes have been used to identify regulatory elements that are important for tissue-specific gene expression or for development; they have been used to produce in vivo models of cancer; they have been employed for the study of in vivo mutagenesis; and they have been used as a tool in lineage analysis and for marking cells in transplantation experiments. The most commonly used in situ reporter gene is lacZ, which encodes a bacterial beta-galactosidase, a sensitive histochemical marker. Although it has been used with striking success in cultured cells and in transgenic mouse embryos, its postnatal in vivo expression has been unreliable and disappointing. Nevertheless, the ability to express reporter genes in transgenic mice has been an invaluable resource, providing insights into in vivo biological mechanisms. The development of new in vivo models, such as those in which expression of transgenes can be activated or repressed, should produce transgenic animal systems that extend our capacity to address heretofore unresolved biological questions.

Animals↗

Identification of a single missense mutation in the adenine phosphoribosyltransferase (APRT) gene from five Icelandic patients and a British patient.

We have completely sequenced the adenine phosphoribosyltransferase (APRT) gene from each of six patients--five (I-V) from Iceland and one (VI) from Britain. Cases I and II shared a common ancestor six and seven generations ago, and cases I and V shared a common ancestor seven generations ago, but cases III and IV were unrelated to the above or to each other, over seven generations. Genomic DNA was amplified by PCR, subcloned into M13mp18, and sequenced. Genomic and PCR-amplified DNAs were also analyzed by restriction-enzyme digestion and Southern blotting. The same missense mutation was identified in all six patients. This mutation leads to the replacement of asp (GAC) by val (GTC), at amino acid position 65. The gene sequences from all patients were otherwise identical to our wild-type sequence. The homozygous nature of the mutation was confirmed by sequencing the PCR product directly. All six patients were homozygous for the 1.25-kb TaqI RFLP. The Icelandic patients were also homozygous for the 8-kb SphI RFLP, but the British patient was heterozygous at this site. These studies suggest that a founder effect is likely to be responsible for APRT deficiency in the Icelandic population. The finding of the same mutation in a patient from Britain suggests that this mutation may have originated in mainland Europe.

Adenine Phosphoribosyltransferase↗

[Clinical types of trifascicular block and a follow-up study of pacemaker application].

UNLABELLED: Thirty five patients (pts) with trifascicular block (TFB) were followed up for 5 years, and indication of pacemaker and clinical types of TFB were discussed. All of the 35 pts were diagnosed with clinical, ECG monitoring and His bundle electrogram (HBE) and classified into 4 groups: (1) acute transient TFB (3 cases) characterized by RBBB + LAHB + I or II AVB, caused by acute myocarditis or AMI, recovered with medicinal treatment; (2) 4 cases of acute advanced TFB characterized by RBBB + LAHB or LAPB + III AVB with severe symptoms such as syncope and Adams-Stokes syndrome; (3) 12 cases of chronic TFB characterized by RBBB + LAHB or LPHB + I, II or III AVB, with 40 beats/min lower heart rate and severe symptoms; (4) 18 cases of chronic advanced TFB characterized by RBBB + LAHB or LPHB + 1, 11 or III AVB, with severe symptoms. The 32 pts in groups 2, 3, and 4 were treated with implanted pacemakers and recovered very well. 29 pts are still well with pacemakers, and 5 cases with cardiomyopathy died due to chronic heart failure during the follow-up period of 5 years. CONCLUSION: all of the pts with TFB and severe symptoms treated with pacemakers were appropriate, and are living well except those with chronic heart failure.

Bundle-Branch Block↗

The role of hydrophobic interactions in binding of polyamines to non NMDA receptor ion channels.

Block of kainate subtype glutamate receptor channels by internal polyamines was analysed using outside out patches from HEK 293 cells transiently transfected with GluR6(Q). Tetramines with different numbers and spacing of methylene groups between NH2 groups produced biphasic rectification well fit by the Woodhull model for a weakly permeable ion channel blocker. Such analysis revealed an increase in binding energy of 611 cal M(-1) for each methylene group added over the range 6-12 (CH2), suggesting that a major component of block by polyamines involves hydrophobic binding. Isomers with the same number of CH2 groups but different spacing between NH2 groups showed similar affinity. Due to differences in pKa values for protonation of NH2 groups, the average charge on the tetramines studied would be expected to vary from 3.98 to 2.22 at physiological pH; despite this, the voltage dependence of block was similar for all tetramines tested, with a mean value for ztheta of 1.82, similar to values for polyamines with five or six NH2 groups. In contrast, for 1,3-propane diamine (DA3 ztheta 0.83), and the N-propyl- (ztheta 1.42) and N,N'-diethyl- (ztheta 1.37) analogues of DA3, there was an increase in the voltage dependence of block on addition of hydrophobic groups.

Cell Line↗

Syntheses and structures of the arylaluminum chalcogenides (ArAlE)2 (Ar = 2-(NEt2CH2)-6-MeC6H3, E = Se; Ar = 2,6-(NEt2CH2)2C6H3, E = Se, Te).

Two intramolecular stabilized arylaluminum dihydrides, (2-(NEt2CH2)-6-MeC6H3)AlH2 (1) and (2,6-(NEt2CH2)2C6H3)AlH2 (2), were prepared by reducing the corresponding dichlorides with an excess of LiAlH4 in diethyl ether. Reactions of 1 and 2 with elemental selenium afforded the dimeric arylaluminum selenides [(2-(NEt2CH2)-6-MeC6H3)AlSe]2 (3) and [(2,6-(NEt2CH2)2C6H3)AlSe]2 (4). Reaction of 2 with metallic tellurium gave the dimeric arylaluminum telluride [(2,6-(NEt2CH2)2C6H3)AlTe]2 (5). The possible reaction pathway is discussed, and molecular structures determined by single-crystal X-ray analyses are presented for 3 and 5.

Journal Article↗

Clinical applicability of bioelectric impedance to measure body composition in health and disease.

The applicability of bioelectric impedance analysis (BIA) as a measure of body composition in children and young adults in both health and disease was studied in 155 subjects (5 mo to 54 yr of age) who were healthy (n = 21), had cystic fibrosis (n = 16), or had end-stage liver disease with variable clinical ascites or edema (n = 62). BIA and phase angle measured at a frequency of 50 kHz between the wrist and contralateral ankle by use of a tetrapolar measuring technique was compared with fat-free mass (FFM) estimated from skin-fold (SK) thickness measurements (n = 57), and body cell mass (grams potassium) measured by total-body potassium (TBK) counting. In a subgroup of subjects with end-stage liver disease, BIA was compared with total-body water measured by deuterium dilution (n = 21). High levels of correlation were found in healthy subjects, cystic fibrosis patients, and patients with end-stage liver disease when impedance (height2/resistance) was used to predict TBK (r = 0.96, 0.96, 0.98, respectively), and SK was used to predict FFMs (r = 0.96, 0.99, 0.90, respectively), by linear regression analysis. However, less satisfactory relationships were found when the methods were more appropriately analyzed with an estimated limits of agreement procedure (1 SD = 8.5, 5.0, 27.7% [TBK] and 9.4, 6.7, 23.0% [FFMs], respectively). A poor level of technique agreement (1 SD = 14%) was found when this method was compared with total-body water measured by isotope dilution in patients with liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗