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In-frame triplet deletions in RHD alter the D antigen phenotype.

BACKGROUND: The deletion of three adjacent nucleotides in an exon may cause the lack of a single amino acid, while the protein sequence remains otherwise unchanged. Only one such in-frame deletion is known in the two RH genes, represented by the RHCE allele ceBP expressing a "very weak e antigen." STUDY DESIGN AND METHODS: Blood donor samples were recognized because of discrepant results of D phenotyping. Six samples came from Switzerland and one from Northern Germany. The molecular structures were determined by genomic DNA nucleotide sequencing of RHD. RESULTS: Two different variant D antigens were explained by RHD alleles harboring one in-frame triplet deletion each. Both single-amino-acid deletions led to partial D phenotypes with weak D antigen expression. Because of their D category V-like phenotypes, the RHD(Arg229del) allele was dubbed DVL-1 and the RHD(Lys235del) allele DVL-2. These in-frame triplet deletions are located in GAGAA or GAAGA repeats of the RHD exon 5. CONCLUSION: Partial D may be caused by a single-amino-acid deletion in RhD. The altered RhD protein segments in DVL types are adjacent to the extracellular loop 4, which constitutes one of the most immunogenic parts of the D antigen. These RhD protein segments are also altered in all DV, which may explain the similarity in phenotype. At the nucleotide level, the triplet deletions may have resulted from replication slippage. A total of nine amino acid positions in an Rhesus protein may be affected by this mechanism.

Alleles↗

Critical importance of the triplet lifetime of photosensitizer in photodynamic therapy of tumor.

The relation between the lifetimes of the triplet states of various porphyrins and their photosensitizing effects on the photodynamic therapy (PDT) of tumor has been examined. Diethylene-triamine pentaacetic acid ester of 4-[1-(2-hydroxy-ethyloxy)ethyl]-2-vinyl deuteroporphyrin-IX gallium (III) complex (Ga-DP), zinc (II) complex (Zn-DP), and manganese (III) complex (Mn-DP) and Photofrin II (PII) are used as the photosensitizer. The triplet lifetimes have been measured for the samples adsorbed on filter paper (FP) and found to be 57 ms (Ga-DP), 26 ms (Zn-DP), less than or equal to 10 microseconds (Mn-DP) and 9 ms (PII). The phosphorescence of Ga-DP in tumor-bearing golden hamsters are measured both in tumor tissue and in liver. They show bi-exponential decay with the lifetimes of about 5 and 20 ms. From the values, the generation rate, kct[3O2], of singlet molecular oxygen in living animal tissue may be estimated to be an order of 10(2) s-1. The PDT effects have been quantitatively investigated for in vitro experiments; upon irradiation the growth inhibitions of mouse p388 leukemia cells are obtained as a function of concentration of Ga-DP, Zn-DP, Mn-DP and PII. The experimental results indicate that the PDT effects depend essentially on the triplet lifetimes of the photosensitizers.

Humans↗

Photointeraction of benzophenone triplet with lysozyme.

The quenching of the benzophenone triplet by lysozyme and its constituent amino acids in aqueous solutions have been studied. Native lysozyme quenches the benzophenone triplet with a high rate constant, 4 x 10(9) M-1 s-1. The quenching process takes place with production of significant amounts of free ketyl radicals, phi ketyl = 0.56, but with a very low benzophenone consumption yield (0.022). The consumption yield is considerably smaller than that observed for the free amino acids. This difference can be explained in terms of a dominant back hydrogen transfer to the protein in the disproportionation of the free radicals produced. Reduced and carboxymethylated lysozyme shows a higher quenching rate (7.8 x 10(9) M-1 s-1) and a larger benzophenone consumption yield (0.07). The deactivation of the benzophenone triplet by the native protein leads to its inactivation, with a quantum yield of 0.01. Tryptophan and arginine residues are destroyed with a quantum yield of 0.01. In the modified enzyme tyrosine and methionine groups are also consumed.

Amino Acids↗

Formation of 7,8-dihydro-8-oxoguanine in the 1,2-dioxetane-induced oxidation of calf thymus DNA: evidence for photosensitized DNA damage by thermally generated triplet ketones in the dark.

Isolated calf thymus DNA was treated with the 1,2-dioxetanes 3-acetoxymethyl-3,4,4-tri-methyl-1,2-dioxetane, 2,3-dimethylbenzofuran dioxetane, 3-hydroxymethyl-3,4,4-trimethyl-1,2-dioxetane (HTMD), 3,3,4,4-tetramethyl-1,2-dioxetane and 3,4,4-trimethyl-1,2-dioxetane (TrMD), which on thermal decomposition generate triplet-excited carbonyl products. To monitor quantitatively the formation of the mutagenic oxidation product 7,8-dihydro-8-oxoguanine (8-oxoGua), a sensitive and selective HPLC electrochemical assay was used after acidic hydrolysis (HF/pyridine) of the dioxetane-treated DNA. High yields of 8-oxoGua (up to ca 4% of the available guanine) were obtained for HTMD and TrMD. Both were investigated in detail with respect to effects of concentration, time and temperature. The oxidative reactivity of 1,2-dioxetanes was compared with several type I (benzophenone and riboflavin) and type II (methylene blue and rose bengal) photooxidants and disodium 1,4-etheno-2,3-benzodioxin-1,4-dipropionate as a chemical source of singlet oxygen. The persistence of 8-oxoGua towards oxidation by HTMD was examined in the reaction with 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxodGuo) and with oxidized DNA. It was shown that, indeed, 8-oxoGua is consumed in the oxidized DNA on prolonged exposure to an excess of HTMD. The reaction of 8-oxodGuo with HTMD afforded the two 4R* and 4S* diastereomers of 9-(2-deoxy-beta-D-erythropentofuranosyl)-4, 8-dihydro-4-hydroxy-8-oxoguanine as main oxidation products. Trapping experiments with tert-butanol confirmed that hydroxyl radicals are not involved, whereas the use of the triplet quenchers sodium 9,10-dibromo-anthracene-2-sulfonate and 2,3-diazabicyclo[2.2.1]hept-2-ene established that triplet-excited states are mainly responsible for the observed DNA oxidation through type I action (electron transfer chemistry). The role of singlet oxygen was tested by means of deuterium isotope effects in D2O versus H2O, but no definitive conclusion could be reached in regard to the involvement of 1O2 in these oxidations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Control and detection of singlet-triplet mixing in a random nuclear field.

We observed mixing between two-electron singlet and triplet states in a double quantum dot, caused by interactions with nuclear spins in the host semiconductor. This mixing was suppressed when we applied a small magnetic field or increased the interdot tunnel coupling and thereby the singlet-triplet splitting. Electron transport involving transitions between triplets and singlets in turn polarized the nuclei, resulting in marked bistabilities. We extract from the fluctuating nuclear field a limitation on the time-averaged spin coherence time T2* of 25 nanoseconds. Control of the electron-nuclear interaction will therefore be crucial for the coherent manipulation of individual electron spins.

Journal Article↗

A CUC triplet confers leucine-dependent regulation of the Bacillus subtilis ilv-leu operon.

Regulation of the ilv-leu operon probably involves interaction of a tR NA(GAG) with leader region mRNA. Conversion of a CUC (Leu) triplet located within the leader region to UUC (Phe), CGC (Arg), or UAC (Tyr) converted reporter gene expression to control by corresponding amino acids. Conversion of the CUC triplet to CUU (Leu) decreased expression and disrupted regulation. The results suggested that other tRNAs can substitute for tRNA(Leu) but that interactions in addition to pairing of the anticodon with the CUC triplet are important for proper control.

Bacillus subtilis↗

Systematic use of the clinical-mammographic-cytologic triplet for the early diagnosis of mammary carcinoma.

Of about 8500 women with a minimum age of 30 years who had a breast examination at our Outpatient Clinic from April 1982 to March 1983, we found in 286 cases a clinically evident carcinoma, and in 534 cases an apparently benign or suspect solid lump. All 534 of these cases were subjected to the triplet clinical, mammographic and cytologic diagnostic investigation by needle aspiration within 1 to 4 days. The clinical judgment was based on a method of scoring of the characters of 9 physical features (Clinical Diagnostic Index) in use at our Institute. The results of the examinations were grouped into 5 categories: 1) certain benignancy or negativity of the examination; 2) probable benignancy (excluding the cytologic examination); 3) probable malignancy; 4) certain malignancy; 5) nonevaluability of the examination (excluding the clinical examination). Except for 80 cases with collectively negative examinations which were clearly or completely regressed at the control within 2 months, all the others were subjected to surgery. On the basis of the histologic examination (or if regression occurred), 284 of the 534 lumps examined were found to be benign or nontumoral, whereas the other 250 (47%) were carcinomas. Of the latter, 57% were not more than 20 mm in size, whereas in 67.6% there was no microscopic evidence of axillary metastases. Sensitivity of the clinical, mammographic and cytologic examinations was 0.79, 0.76 and 0.72, respectively; specificity 0.71, 0.75 and 0.94, respectively, and the predictive value for malignancy of the positive response of the three examinations 0.71, 0.75 and 0.93, respectively. The use of the diagnostic triplet demonstrated an overall sensitivity of 0.95, specificity of 0.59, and a predictive value for malignancy of 0.98 and 0.93 for benignancy. These results confirm the usefulness of the systematic use of the diagnostic triplet in solid breast lumps of over thirty aged women for the early detection of cancer.

Adult↗

Lutein is needed for efficient chlorophyll triplet quenching in the major LHCII antenna complex of higher plants and effective photoprotection in vivo under strong light.

BACKGROUND: Lutein is the most abundant xanthophyll in the photosynthetic apparatus of higher plants. It binds to site L1 of all Lhc proteins, whose occupancy is indispensable for protein folding and quenching chlorophyll triplets. Thus, the lack of a visible phenotype in mutants lacking lutein has been surprising. RESULTS: We have re-assessed the lut2.1 phenotypes through biochemical and spectroscopic methods. Lhc proteins from the lut2.1 mutant compensate the lack of lutein by binding violaxanthin in sites L1 and L2. This substitution reduces the capacity for regulatory mechanisms such as NPQ, reduces antenna size, induces the compensatory synthesis of Antheraxanthin + Zeaxanthin, and prevents the trimerization of LHCII complexes. In vitro reconstitution shows that the lack of lutein per se is sufficient to prevent trimerization. lut2.1 showed a reduced capacity for state I-state II transitions, a selective degradation of Lhcb1 and 2, and a higher level of photodamage in high light and/or low temperature, suggesting that violaxanthin cannot fully restore chlorophyll triplet quenching. In vitro photobleaching experiments and time-resolved spectroscopy of carotenoid triplet formation confirmed this hypothesis. The npq1lut2.1 double mutant, lacking both zeaxanthin and lutein, is highly susceptible to light stress. CONCLUSION: Lutein has the specific property of quenching harmful 3Chl* by binding at site L1 of the major LHCII complex and of other Lhc proteins of plants, thus preventing ROS formation. Substitution of lutein by violaxanthin decreases the efficiency of 3Chl* quenching and causes higher ROS yield. The phenotype of lut2.1 mutant in low light is weak only because rescuing mechanisms of photoprotection, namely zeaxanthin synthesis, compensate for the ROS production. We conclude that zeaxanthin is effective in photoprotection of plants lacking lutein due to the multiple effects of zeaxanthin in photoprotection, including ROS scavenging and direct quenching of Chl fluorescence by binding to the L2 allosteric site of Lhc proteins.

Cold Temperature↗

Neurofilament triplet protein interactions: evidence for the preferred formation of NF-L-containing dimers and a putative function for the end domains.

In this report we examine the molecular interactions that lead to formation of neurofilaments, the intermediate filaments in neurons. Using the yeast two-hybrid system, we found that the rod domains of all three NF triplet proteins interacted strongly with one another and with rod domains of the Type III IF proteins, vimentin and desmin. A slight preference toward NF-L-containing dimers was observed over ones not containing NF-L. Interactions among the full length NF triplet proteins exhibited more specificity. Full length NF-L had only a relatively weak interaction with another full length NF-L molecule, but reacted more robustly with full length NF-M or NF-H lacking only part of the head domain. No homologous or heterologous dimerization of NF-M and NF-H was detectable. These results support the hypothesis that neurofilaments are obligate heteropolymers and that heterodimeric subunits are the preferred building blocks. They further suggest that the mechanism that specifies heterodimeric interaction among the NF triplet proteins resides in the end domains.

Base Sequence↗

Triplet repeat gene sequences in neuropsychiatric diseases.

The human genome has many nucleotide repeat sequences. These range from a single repeating base to entire duplicated genes. Expansion of repeating triplets of nucleotides in the genome has recently been associated with nine degenerative and developmental neuropsychiatric diseases: fragile X syndrome, fragile X-linked mental retardation, myotonic dystrophy, Friedreich's ataxia, spinal and bulbar muscular atrophy, Huntington's disease, spinocerebellar ataxia type 1, dentatorubral-pallidoluysian atrophy, and Machado-Joseph disease. These diseases are all conditions of the central nervous system; in all of them, the inheritance pattern usually exhibits the phenomenon of anticipation (defined as progressively earlier age of onset or a worsening disease severity over successive generations), and the severity of the phenotypic expression and penetrance appears to be related to the extent of the triplet expansion. Identification of this pathological genetic phenomenon solves several of the mysteries that surrounded these conditions but raises many important questions regarding pathogenic mechanisms that may be shared. There is some indication that triplet expansions may also underlie other neuropsychiatric conditions such as schizophrenia or bipolar disorder.

Brain Diseases↗

Word recognition of digit triplets and monosyllabic words in multitalker babble by listeners with sensorineural hearing loss.

In an initial experiment (Wilson and Weakley, 2004), word recognition was assessed with six digit triplets presented at 14 signal-to-babble ratios (S/B) in 2 dB steps. An abbreviated version of the protocol was developed for clinic use involving three digit triplets at 7 S/Bs in 4 dB steps. The purpose of this experiment was to examine the relationship between the two digit protocols with comparisons made with other variables including age, pure-tone thresholds, subjective measures of understanding speech in quiet and in noise, and word recognition of monosyllabic words in quiet and in babble. Ninety-six listeners with sensorineural hearing loss participated. For equivalent performance, the short version of the digit triplets required (1) a 2.6 dB more favorable S/B than the long version and (2) a 15.1 dB less favorable S/B than the words. Age, hearing loss, and subjective evaluation of the ability to understand speech in quiet and in noise were not related to performance on digits or words in multitalker babble.

Acoustic Stimulation↗

Detection of polymorphic triplet repeats in the genomes of patients suffering from bipolar affective disorder.

Evidence for the operation of expanded trinucleotide repeats in the pathogenesis of bipolar affected disorder has recently been found at the molecular genetic level. For the screening of these repeat motifs in genomes of patients with bipolar affective disorder, we established a modified PCR-based fingerprinting technique, called triplet repeat enhanced arbitrarily primed PCR (TREAP-PCR). Using this approach, 40 patients suffering from bipolar affective disorder (ICD10: F31) and 15 healthy controls were investigated. Interindividual polymorphisms generated by TREAP-PCR seemed to depend on the type of triplet. Using CCG triplet primers, polymorphisms could be observed more often in the genomes of patients compared with controls, whereas no significant differences could be found using primers of the CAG or AAT type. These data might indicate the existence of subgroups of manic-depressive patients based on molecular genetic differences.

Adult↗

MICA gene triplet repeat polymorphism in patients with HLA-B27 positive and negative ankylosing spondylitis from Sardinia.

OBJECTIVE: We investigated the distribution of MICA triplet repeat polymorphism in a random population and in patients with seronegative spondyloarthritis from Sardinia compared to continental Italy. METHODS: We analyzed the distribution of MICA triplet repeat polymorphism in HLA-B*2709 [not associated with ankylosing spondylitis (AS)] and B*2705 (associated with AS) haplotypes, to verify whether the strong association of MICA-A4 with HLA-B27 reported in other populations is maintained in Sardinia, and compared the distribution of MICA-A alleles in HLA-B27 negative versus HLA-B27+ patients with AS. RESULTS: We found that the frequency of MICA-A4 triplet repeat allele in a random Sardinia population is higher (53.2%) than in other Caucasian populations (around 20%); this allele is strongly associated with both HLA-B*2709 and B*2705. No significant difference between HLA-B27+ patients with AS and healthy controls was found: the MICA-A4 allele was present in more than 90% of subjects. MICA-A4 was found in 16 out of 20 HLA-B27 negative Sardinian patients with AS, with a frequency (80%) more similar to that of the HLA-B27+ group of patients than that of controls. CONCLUSION: The high frequency of MICA-A4 allele in HLA-B27 negative patients with AS from Sardinia, suggests the presence within the HLA region of a susceptibility factor other and certainly weaker than B27. This factor is likely to be more easily found by analyzing genetically homogeneous populations like the Sardinian, characterized by a small number of very frequent haplotypes.

HLA-B27 Antigen↗

The contribution of singletons, twins and triplets to low birth weight, infant mortality and handicap in the United States.

Among multiple gestations the magnitude of neonatal mortality, morbidity and postneonatal handicap is unknown. Although the proportion of multiple births has risen dramatically during the past decade, the proportion of total births in the United States is relatively small. The vast majority of multiples are low birth weight (LBW) or very low birth weight (VLBW), conditions that magnify both short-term and long-term risks. In this study, the risks for infant mortality and for postneonatal morbidity and handicap have been calculated from race-, plurality- and birth weight-specific mortality rates from the National Infant Mortality Surveillance (NIMS) Project and birth weight-specific postneonatal handicap rates from the Office of Technology Assessment report Healthy Children in proportion to the 1988 U.S. birth cohort. U.S. health objectives for the year 2000 for race-specific birth weight and infant mortality rates were used for comparison. Compared with that of singletons, twins' and triplets' relative risks for LBW are 10.3 and 18.8, respectively. Their relative risks for VLBW are 9.6 and 32.7. Compared with singletons, twins and triplets have relative risks for infant mortality of 6.6 and 19.4, respectively. For twins and triplets, postneonatal survivors' relative risks for severe handicap are 1.7 and 2.9 while those for overall handicap are 1.4 and 2.0, respectively. Recommendations for optimizing pregnancy outcomes in multiple gestations include liberalized weight gains, reduced physical effort and early, comprehensive prenatal care.

Persons with Disabilities↗

[Anesthesia for a woman with triplet pregnancy presenting with acute abdomen after the recent epidural blood patch].

We report a case of primipara with triplet pregnancy who underwent combined spinal and epidural anesthesia 10 weeks after epidural blood patch. At 15 weeks of gestation, a woman with triplet gestation underwent Shirodkar operation under spinal anesthesia and subsequent epidural blood patch as a treatment of post-dural puncture headache. At 26 weeks she presented with acute abdomen and laparotomy was scheduled. Spinal anesthesia was selected with an epidural catheter inserted in case of prolonged operation and for postoperative pain control. The placement of an epidural catheter was without problem. Laparotomy revealed right paraovarian cyst torsion and the right salpingo-paraoophocystectomy was performed. Patient-controlled analgesia with epidural bupivacaine and fentanyl was effectively continued for two days. Postoperative course was uneventful and the triplets were delivered by cesarean section at 35 weeks.

Abdomen, Acute↗

Seven clusters in genomic triplet distributions.

In several recent papers new gene-detection algorithms were proposed for detecting protein-coding regions without requiring a learning dataset of already known genes. The fact that unsupervised gene-detection is possible is closely connected to the existence of a cluster structure in oligomer frequency distributions. In this paper we study the cluster structure of several genomes in the space of their triplet frequencies, using a pure data exploration strategy. Several complete genomic sequences were analyzed, using the visualization of tables of triplet frequencies in a sliding window. The distribution of 64-dimensional vectors of triplet frequencies displays a well-detectable cluster structure. The structure was found to consist of seven clusters, corresponding to protein-coding information in three possible phases in one of the two complementary strands and in the non-coding regions with high accuracy (higher than 90% on nucleotide level). Visualizing and understanding the structure allows to analyze effectively the performance of different gene-prediction tools. Since the method does not require extraction of ORFs, it can be applied even for unassembled genomes.

Algorithms↗

Mutagenesis of the Arg-Gly-Asp triplet in human complement component C3 does not abolish binding of iC3b to the leukocyte integrin complement receptor type III (CR3, CD11b/CD18).

The leukocyte integrin complement receptor type III (CR3, CD11b/CD18) binds the C3 cleavage product iC3b. Many other integrins bind their ligands via an Arg-Gly-Asp (RGD) triplet. Both the RGD-containing C3 peptide 1390TRYRGDQDATMS1401 (pro-C3 numbering) and the RGD-like fibrinogen peptide GGAKQAGDV, which binds to the platelet integrin glycoprotein IIb-IIIa, were shown to inhibit the iC3b-CR3 interaction, suggesting that this binding is also RGD-mediated (Wright, S.D., Weitz, J.I., Huang, A. J., Levin, S.M., Silverstein, S.C., and Loike, J.D. (1988) Proc. Natl. Acad. Sci. U.S.A. 85, 7734-7738). However, unlike other integrin-ligand interactions, that of CR3 and iC3b is unaffected by the hexapeptide GRGDSP, and substitutions in the RGD triplet of C3 from other species appear to be tolerated. It was, therefore, proposed (Grossberger, D., Marcuz, A., du Pasquier, L., and Lambris, J.D. (1989) Proc. Natl. Acad. Sci. U.S.A. 86, 1323-1327) that the highly conserved DATMS portion of the inhibitory C3 peptide may have been responsible for its binding. To address these inconsistencies and directly assess the role of the 1390-1401 segment within the complete iC3b molecule in mediating binding to CR3, a human C3 cDNA was altered by site-directed mutagenesis and the expressed recombinant proteins were examined in a CR3-specific assay. Replacement of RGD by AAA did not abolish rosetting of the corresponding iC3b-coated erythrocytes to human CR3-bearing leukocytes. In addition, mutant iC3b molecules in which the positively charged R1391 (corresponding to K in the fibrinogen peptide) and the highly conserved 1397DATMS sequence were replaced by Q and NAAMA respectively, were still bound by CR3. We conclude that the iC3b-CR3 interaction is not mediated by the RGD triplet or its neighboring residues.

Amino Acid Sequence↗

Quantum yields of triplet and O2(1 delta g) formation of 4-thiouridine in water and acetonitrile.

The quantum yield of triplet formation, phi T, and that of the photosensitized formation of singlet molecular oxygen, phi delta, were determined for a rare nucleoside, 4-thiouridine (4t-Urd), in water and in acetonitrile, using singlet molecular oxygen phosphorescence, laser-induced optoacoustics and time-resolved thermal lensing. These yields, phi T and phi delta, the latter in aerated solutions, were found to be, respectively, in water: 0.67 +/- 0.17 and 0.18 +/- 0.04 and in acetonitrile: 0.61 +/- 0.15 and 0.50 +/- 0.20. The fraction of the 4t-Urd triplet molecules quenched by oxygen leading to singlet molecular oxygen, S delta, was calculated to be between 0.7 and unity in both solvents, this value being indicative of a pi pi*character for the lowest triplet state of 4t-Urd.

Acetonitriles↗