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R Waters

Publications and source records attributed to R Waters.

At least 37 records · Page 2Linked to original sources
PubMed1998

Escherichia coli strains lacking protein HU are UV sensitive due to a role for HU in homologous recombination.

hupA and hupB encode the alpha and beta subunits of the Escherichia coli histone-like protein HU. Here we show that E. coli hup mutants are sensitive to UV in the rec+ sbc+, recBC sbcA, recBC sbcBC, umuDC, recF, and recD backgrounds. However, hupAB mutations do not enhance the UV sensitivity of resolvase-deficient recG ruvA strains. hupAB uvrA and hupAB recG strains are supersensitive to UV. hup mutations enhance the UV sensitivity of ruvA strains to a much lesser extent but enhance that of rus-1 ruvA strains to the same extent as for rus+ ruv+ strains. Our results suggest that HU plays a role in recombinational DNA repair that is not specifically limited to double-strand break repair or daughter strand gap repair; the lack of HU affects the RecG RusA and RuvABC pathways for Holliday junction processing equally if the two pathways are equally active in recombinational repair; the function of HU is not in the substrate processing step or in the RecFOR-directed synapsis action during recombinational repair. Furthermore, the UV sensitivity of hup mutants cannot be suppressed by overexpression of wild-type or mutant gyrB, which confers novobiocin resistance, or by different concentrations of a gyrase inhibitor that can increase or decrease the supercoiling of chromosomal DNA.

Bacterial Outer Membrane Proteins↗
PubMed1997

Induction and repair of cyclobutane pyrimidine dimers in the Escherichia coli tRNA gene tyrT: Fis protein affects dimer induction in the control region and suppresses preferential repair in the coding region of the transcribed strand, except in a short region near the transcription start site.

We analysed induction and repair of UV induced pyrimidine dimers in the Escherichia coli tRNA gene tyrT. In wild-type (WT) log or stationary phase different patterns of induction occurred in the three Fis binding sites and the core promoter -35 sequence of the control region: this was absent in fis- cells. In stationary WT cells, slow, similar rates of repair occurred throughout the non-transcribed strand (NTS). Faster repair occurred in the NTS control region in WT log phase. NTS repair in fis- cells was similar, except the control region differed less between phases. Heterogeneous repair occurred along the transcribed strand (TS). In the control region repair was faster than in the NTS. Repair in the TS coding region changed between growth phases or if repair took place in different media. When irradiated log phase WT cells were in rich medium, two TS domains were evident: a fast-repaired domain within 31 nucleotides from the transcription start site; and a more slowly repaired domain composed of the rest of the TS. A sharp gradient existed in the small domain with very fast repair at the beginning and diminished repair towards the end. Fast transcription coupled repair (TCR) in the small domain was absent in the TS large domain, where repair was similar to the NTS and to the entire TS in mfd- cells. In similarly treated stationary phase WT cells, TCR occurred in the large domain. Depletion of Fis reinstates TCR to a lesser extent, whilst a substitution of five nucleotides at the Fis binding sites in the upstream activating sequence reinstates TCR. Reinstatement of TCR was also achieved by incubating irradiated WT cells in minimal salt medium without the required amino acid. Our results suggest that Fis indirectly suppresses preferential repair in the TS large domain by stimulating transcription.

Base Sequence↗
PubMed1997

Preferential incision of interstrand crosslinks induced by 8-methoxypsoralen plus UVA in yeast during the cell cycle.

Interstrand crosslink (ICL) induction by 8-methoxypsoralen plus UVA and the incision step of the repair have been investigated during the mitotic cell cycle of haploid Saccharomyces cerevisiae. Cells were synchronised by elutriation and events were examined at the level of the MAT alpha and the HML alpha loci in a SIR strain. The DNA sequence of these two loci is identical, but the MAT alpha locus may be replicated earlier in S phase and is transcriptionally active while the HML alpha locus may be replicated later in S phase and is transcriptionally inactive because of Sir repression that creates a heterochromatin-like structure at this locus. ICL were induced to similar extents in both loci during the stages of the cell cycle examined, and these levels were identical to those reported for asynchronous cultures. Preferential incisions occurred for ICL in the MAT alpha locus compared to those in the HML alpha locus, independently of the cell cycle phase studied. The levels of incision were comparable for events in the early G1 phase (eG1), late G1 phase (lG1), early S phase (eS), middle S phase (mS), late S phase (lS) or G2 phase (G2). Thus the preferential incision of ICL observed previously in asynchronous cell culture is maintained throughout the cell cycle and, surprisingly, occurs equally well in G1. Here the opportunities for recombination to further process the incised damaged are substantially limited compared to those in the S and G2 phases.

Cell Cycle↗
PubMed1997

Excision repair at the level of the nucleotide in the Saccharomyces cerevisiae MFA2 gene: mapping of where enhanced repair in the transcribed strand begins or ends and identification of only a partial rad16 requisite for repairing upstream control sequences.

We wished to determine where transcription enhanced nucleotide excision repair begins and ends for a Saccharomyces cerevisiae gene transcribed by RNA polymerase II, and to examine the role of the RAD16 gene in repairing upstream, non-transcribed control sequences of such a gene. To do so, we developed a method to study the repair of UV induced cyclobutane pyrimidine dimers (CPDs) at the level of the nucleotide in the control and coding sequences of the MFA2 gene. This gene is active in haploid a mating type cells but inactive in alpha cells: its regulation is mediated by changes in chromatin structure. DNA from UV irradiated cells was cut with a CPD-specific endonuclease, restricted and selected strands of the MFA2 gene separated from genomic DNA prior to end-labelling and resolution on a sequencing gel. We confirmed repair trends seen using Southern blotting to examine kilobase size fragments, but were additionally able to elucidate subtle differences in repairing portions of the transcribed strand (TS) of MFA2. Enhanced repair of the TS when the gene is active, began well before the start of transcription. Clearly, enhanced repair in this region cannot be due to mRNA synthesis. The repair of CPDs is even further enhanced in the transcribed portion of the TS, and returns to a basal level after the termination of transcription. The approach also revealed that RAD16 has a role in the repair of the TS when MFA2 is active. Removal of CPDs from the TS control region was impaired but not totally defective in a rad16 a mutant. Repair from the TS coding sequence also has a Rad16 component, but a lesser one than for the upstream control sequences, and this was more marked for the sequences towards the end of the transcribed region. The system developed permits further dissection of the relationships between DNA repair, chromatin structure and transcription at the MFA2 locus.

Adenosine Triphosphatases↗
PubMed1997

Inducible nucleotide excision repair (NER) of UV-induced cyclobutane pyrimidine dimers in the cell cycle of the budding yeast Saccharomyces cerevisiae: evidence that inducible NER is confined to the G1 phase of the mitotic cell cycle.

We previously reported on an inducible component of nucleotide excision repair in Saccharomyces cerevisiae that is controlled by the RAD16 gene. Here we describe a study of this event at the MAT alpha and HML alpha mating-type loci and on the transcribed (TS) and nontranscribed (NTS) strands of the RAD16 gene. Events were examined at various stages of the mitotic cycle in cells synchronised by centrifugal elutriation. Repair of cyclobutane pyrimidine dimers (CPDs) following a single UV dose does not vary significantly in different stages of the mitotic cell cycle. CPDs are removed more rapidly from the transcriptionally active MAT alpha locus than from the silent HML alpha locus, and the TS of RAD16 is repaired faster than the NTS in all stages of the cycle following a single UV irradiation. Enhanced excision of CPDs at MAT alpha and HML alpha can be induced only in the G1 and early S stages of the cell cycle. Here prior irradiation of cells with 25 J/m2 enhances the removal of CPDs following a second UV dose of 70 J/m2. The level of enhancement of repair does not differ significantly between MAT alpha and HML alpha in G1. Enhanced removal of CPDs is absent when cells receive the inducing dose in late S or G2/M. Repair of CPDs in both strands of RAD16 is similarly enhanced only if cells receive the initial irradiation in G1 and early S. The level of enhanced removal of CPDs is not significantly different in the TS and NTS of RAD16 either in asynchronous cells or in cells preirradiated in G1 and early S. It has been shown by others that UV-induced expression of RAD16 remains at high levels if cells are held in G1 by treatment with alpha factor. Therefore the increase in RAD16 transcript levels in G1 may be responsible for the ability to enhance NER solely in this stage of the cell cycle.

Adenosine Triphosphatases↗
PubMed1997

The Saccharomyces cerevisiae RAD7 and RAD16 genes are required for inducible excision of endonuclease III sensitive-sites, yet are not needed for the repair of these lesions following a single UV dose.

The RAD7 and RAD16 genes of Saccharomyces cerevisiae have roles in the repair of UV induced CPDs in nontranscribed genes [1], and in the repair of CPDs in the nontranscribed strand of transcribed genes [2]. Previously, we identified an inducible component to nucleotide excision repair (NER), which is absent in a rad16 delta strain [3]. We have examined the repair of UV induced endonuclease III sensitive-sites (EIIISS), and have shown repair of these lesions to proceed by NER but their removal from nontranscribed regions is independent of RAD7 and RAD16. Furthermore, EIIISS are repaired with equal efficiency from both transcribed and nontranscribed genes [4]. In order to dissect the roles of RAD7 and RAD16 in the above processes we examined the repair of EIIISS in the MAT alpha and HML alpha loci, which are, respectively, transcriptionally active and inactive in alpha haploid cells. These loci have elevated levels of these lesions after UV (in genomic DNA EIIISS constitute about 10% of total lesions, whereas CPDs are about 70% of total lesions). We have shown that excision of UV induced EIIISS is enhanced following a prior UV irradiation. No enhancement of repair was detected in either the rad7 delta or the rad16 delta mutant. The fact that RAD7 and RAD16 are not required for the repair of EIIISS per se yet are required for the enhanced excision of these lesions from MAT alpha and HML alpha suggests two possibilities. These genes have two roles in NER, namely in the repair of CPDs from nontranscribed sequences, and in enhancing NER itself regardless of whether these genes' products are required for the excision of the specific lesion being repaired. In the latter case, the induction of RAD7 and RAD16 may increase the turnover of complexes stalled in nontranscribed DNA so as to increase the availability of NER proteins for the repair of CPDs and EIIISS in all regions of the genome.

DNA Repair↗
PubMed1997

Characterization of the rad14-2 mutant of Saccharomyces cerevisiae: implications for the recognition of UV photoproducts by the Rad14 protein.

The RAD14 gene of Saccharomyces cerevisiae is required for the incision step of the nucleotide excision repair process. The Rad14 protein can bind zinc, possesses a potential zinc finger DNA binding domain and has been shown to bind specifically to damaged DNA. Differences in UV sensitivity exist between a rad14 deletion strain and a putative rad14 point mutant, the point mutant being more resistant to UV than the deletion strain. Here, we confirm that the rad14 deletion strain repairs neither UV-induced cyclobutane pyrimidine dimers (CPDs) nor endonuclease III-sensitive damage sites, whereas the point mutant cannot repair the former but can repair the latter. From this it can be inferred that the point mutant produces an altered protein product allowing recognition of endonuclease III sensitive sites but not CPDs. To investigate this, the rad14 mutant allele was sequenced. It contained two GC-AT transition mutations when compared to the wild-type RAD14 gene sequence. When the rad14 point mutant sequence is translated, alterations within the putative zinc finger binding domain are observed, with one of the cysteine residues of the zinc binding motif being replaced by tyrosine. This suggests that alterations within the zinc finger binding domain of the Rad14 protein cause changes to the damage recognition properties of the protein. The use of the Rad14 protein from the point mutant should assist in experiments investigating the in vitro binding properties of the Rad14 protein to different types of DNA damage.

Alleles↗
PubMed1996

UV-induced endonuclease III-sensitive sites at the mating type loci in Saccharomyces cerevisiae are repaired by nucleotide excision repair: RAD7 and RAD16 are not required for their removal from HML alpha.

Ultraviolet irradiation of DNA induces cyclobutane pyrimidine dimers (CPDs) 6-4'-(pyrimidine 2'-one) pyrimidines and pyrimidine hydrates. The dimer is the major photoproduct, and is specifically recognized by endonuclease V of phage T4. Pyrimidine hydrates represent a small fraction of the total photoproducts, and are substrates for endonuclease III of Escherichia coli. We used these enzymes to follow the fate of their substrates in the mating type loci of Saccharomyces cerevisiae. In a RAD strain, CPSs in the transcriptionally active MAT alpha locus are preferentially repaired relative to the inactive HML alpha locus, whilst repair of endonuclease III-sensitive sites is not preferential. The rad1, 2, 3 and 4 mutants, which lack factors that are essential for the incision step of nucleotide excision repair (NER), repair neither CPDs nor endonuclease III-sensitive sites, clearly showing that these lesions are repaired by by NER pathway. Previously it had been shown that the products of the RAD7 and RAD16 genes are required for the NER of CPDs from the HML alpha locus. We show that, in the same locus, these gene products are not needed for removal of endonuclease III-sensitive sites by the same mechanism. This indicates that the components required for NER differ depending on either the type of lesion encountered or on the specific location of the lesion within the genome.

Adenosine Triphosphatases↗
PubMed1996

The levels of repair of endonuclease III-sensitive sites, 6-4 photoproducts and cyclobutane pyrimidine dimers differ in a point mutant for RAD14, the Saccharomyces cerevisiae homologue of the human gene defective in XPA patients.

In the accompanying paper we demonstrated that endonuclease III-sensitive sites in the MAT alpha and HML alpha loci of Saccharomyces cerevisiae are repaired by the Nucleotide Excision Repair (NER) pathway. In the current report we investigated the repair of endonuclease III sites, 6-4 photoproducts and cyclobutane pyrimidine dimers (CPDs) in a rad14-2 point mutant and in a rad14 deletion mutant. The RAD14 gene is the yeast homologue of the human gene that complements the defect in cells from xeroderma pigmentosum (XP) patients belonging to complementation group A. In the point mutant we observed normal repair of endonuclease III site (i.e. as wild type), but no removal of CPDs at the MAT alpha and HML alpha loci. Similar experiments were undertaken using the recently created rad14 deletion mutant. Here, neither endonuclease III sites nor CPDs were repaired in MATa or HMRa. Thus the point mutant appears to produce a gene product that permits the repair of endonuclease III sites, but prevents the repair of CPDs. Previously it was found that in the genome overall, repair of 6-4 photoproducts was less impaired that repair of CPDs in the point mutant. The deletion mutant repairs neither CPDs nor 6-4 photoproducts in the genome overall. This finding is consistent with the RAD14 protein being involved in lesion recognition in yeast. A logical interpretation is that the rad14-2 point mutant produces a modified protein that enables the cell to repair endonuclease III sites and 6-4 photoproducts much more efficiently than CPDs. This modified protein may aid studies designed to elucidate the role of the RAD14 protein in lesion recognition.

DNA Repair↗
PubMed1996

Nucleotide level detection of cyclobutane pyrimidine dimers using oligonucleotides and magnetic beads to facilitate labelling of DNA fragments incised at the dimers and chemical sequencing reference ladders.

We present a method for detecting cyclobutane pyrimidine dimers (CPDs) at the nucleotide level and an adaptation of Maxam-Gilbert sequencing for generating sequence reference ladders. UV irradiated genomic DNA from Escherichia coli was digested with restriction enzyme(s) and incised at the CPDs with Micrococcus luteus UV endonuclease. The subsequent specific fragments were separated using a biotin labelled oligonucleotide containing a sequence complementary to the fragments of interest and streptavidin magnetic beads. These fragments were then radiolabelled on the beads just prior to the running of the sequencing gel. For generating sequence reference ladders, the unlabelled DNA fragments of interest were base-specifically modified and subsequently cleaved at the A+G or C+T sites using the rapid Maxam-Gilbert sequencing treatments. These chemically cleaved fragments can be stored almost indefinitely. Whenever the sequence reference ladders are required, the chemically cleaved fragments can be labelled alongside the CPD-specifically incised DNA fragments using the same procedure. The adaptation of the method to detect other types of DNA damage is also discussed.

Base Sequence↗
PubMed1996

The identification and repair of DNA adducts induced by waterborne benzo[a]pyrene in developing Xenopus laevis larvae.

We report on the formation and subsequent repair of benzo[a]pyrene-induced DNA adducts in Xenopus laevis larvae in vivo, as monitored by 32P-post labelling. In vivo benzo[a]pyrene is metabolized by the cytochrome P450 family of enzymes to metabolites, of which the 7,8-diol-9,10-epoxides have been implicated as causing potentially tumourigenic lesions. Larvae were exposed to waterborne benzo[a]pyrene (0.01, 0.05 and 0.1 mg/l) for 24 h at stages 38, 45 and 50 of development (24 h, 5 days and 2 weeks post-hatching, respectively) and allowed to recover for up to 6 days. A wide range of adduct lesions were observed at stage 50, three of which were observed at all stages investigated. Adduct repair was biphasic, with an initial rapid repair over the first 24 h post exposure, followed by a much slower decline, resulting in persistence of adducts for at least 6 days post exposure. The individual lesions were repaired at different rates, with some being almost completely repaired after 6 days recovery, whereas one of the main adducts showed restricted repair at stage 50 and another no repair at all. Identification of some adducts has been achieved, by the inclusion of isomeric standards of (+)- or (-)-anti-benzo[a]pyrene diol epoxide reacted with deoxyguanosine and adenosine 3'-monophosphates prepared in vitro. The non-repairable lesion at stage 50 has been shown to be the (+)-trans-anti-benzo[a]pyrene diol epoxide-N2-guanine adduct. This adduct was observed at all stages, but was only maximally repaired at stages 38 and 45.

Amphibians↗
PubMed1996

Biomonitoring human exposure to environmental carcinogenic chemicals.

A coordinated study was carried out on the development, evaluation and application of biomonitoring procedures for populations exposed to environmental genotoxic pollutants. The procedures used involved both direct measurement of DNA or protein damage (adducts) and assessment of second biological effects (mutation and cytogenetic damage). Adduct detection at the level of DNA or protein (haemoglobin) was carried out by 32P-postlabelling, immunochemical, HPLC or mass spectrometric methods. Urinary excretion products resulting from DNA damage were also estimated (immunochemical assay, mass spectrometry). The measurement of adducts was focused on those from genotoxicants that result from petrochemical combustion or processing, e.g. low-molecular-weight alkylating agents, PAHs and compounds that cause oxidative DNA damage. Cytogenetic analysis of lymphocytes was undertaken (micronuclei, chromosome aberrations and sister chromatid exchanges) and mutation frequency was estimated at a number of loci including the hprt gene and genes involving in cancer development. Blood and urine samples from individuals exposed to urban pollution were collected. Populations exposed through occupational or medical sources to larger amounts of some of the genotoxic compounds present in the environmental samples were used as positive controls for the environmentally exposed population. Samples from rural areas were used as negative controls. The project has led to new, more sensitive and more selective approaches for detecting carcinogen-induced damage to DNA and proteins, and subsequent biological effects. These methods were validated with the occupational exposures, which showed evidence of DNA and/or protein and/or chromosome damage in workers in a coke oven plant, garage workers exposed to diesel exhaust and workers exposed to ethylene oxide in a sterilization plant. Dose reponse and adduct repair were studied for methylated adducts in patients treated with methylating cytostatic drugs. The biomonitoring methods have also demonstrated their potential for detecting environmental exposure to genotoxic compounds in nine groups of non-smoking individuals, 32P-postlabelling of DNA adducts being shown to have the greatest sensitivity.

Antineoplastic Agents, Alkylating↗
PubMed1996

The safety and efficacy of oral transmucosal fentanyl citrate for preoperative sedation in young children.

Oral transmucosal fentanyl citrate (OTFC) is a labeled preoperative pediatric sedative. Doses greater than 15 micrograms/kg are associated with a high incidence of post-operative nausea and vomiting and occasional respiratory depression. We studied the safety and efficacy of OTFC in children 6 yr old and younger at a dose of 15 micrograms/kg. Nineteen patients undergoing surgery associated with postoperative pain were randomized to receive OTFC/intravenous (IV) saline or placebo lozenge/IV fentanyl. After 45 min, patients receiving OTFC became more sedated than the placebo group, but there were no differences in cooperation, apprehension, parental separation, or induction cooperation scores. Preoperatively, neither respiratory depression nor oxygen desaturation occurred. Nine of 10 OTFC patients developed mild pruritus, and three of 10 OTFC patients vomited preoperatively; neither complication occurred in the placebo group. (The high incidence of preoperative vomiting led to the termination of the protocol before the anticipated enrollment of 40 patients.) General anesthesia was induced via a mask, followed by a propofol infusion. Spo2 and respiratory rate were monitored, and sedation, apprehension, cooperation, ease of parental separation, and induction cooperation were scored. One OTFC patient developed rigidity during induction. Emergence and recovery were not delayed by OTFC despite a 50% incidence of postoperative vomiting. We do not recommend the use of OTFC in a 15 micrograms/kg dose as a routine preoperative sedative in children 6 yr old and younger.

Administration, Oral↗
PubMed1996

Effects of erythrocyte infusion on VO2max at high altitude.

This study investigated whether autologous erythrocyte infusion would ameliorate the decrement in maximal O2 uptake (VO2max) experienced by lowlanders when they ascend to high altitude. VO2max was measured in 16 men (treadmill running) at sea level (SL) and on the 1st (HA1) and 9th (HA9) days of high-altitude (4,300 m) residence. After VO2max was measured at SL, subjects were divided into two matched groups (n = 8). Twenty-four hours before ascent to high altitude, the experimental group received a 700-ml infusion of autologous erythrocytes and saline (42% hematocrit), whereas the control group received only saline. The VO2max of erythrocyte-infused [54 +/- 1 (SE) ml.kg-1.min-1] and control subjects (52 +/- 2 ml.kg-1.min-1) did not differ at SL before infusion. The decrement in VO2max on HA1 did not differ between groups, averaging 26% overall, despite higher (P < 0.01) arterial hematocrit, hemoglobin concentration, and arterial O2 content in the erythrocyte-infused subjects. By HA9, there were no longer any differences in hematocrit, hemoglobin concentration, or arterial O2 content between groups. No change in VO2max occurred between HA1 and HA9 for either group. Thus, despite increasing arterial O2-carrying capacity, autologous erythrocyte infusion did not ameliorate the decrement in VO2max at 4,300-m altitude.

Acclimatization↗
PubMed1995

Development of a human biomonitoring assay using buccal mucosa: comparison of smoking-related DNA adducts in mucosa versus biopsies.

The aim of this study was to determine whether buccal mucosa would provide an alternate source of tissue for human biomonitoring. Samples of clinically normal oral biopsies were excised, and buccal mucosa were scraped or brushed from patients while they were undergoing surgery for the excision of intra-oral squamous cell carcinoma. Extracted DNA was 32P-postlabeled using the butanol enhancement method, and DNA adduct levels were quantified to compare the accuracy of adduct detection in buccal mucosa versus oral biopsies. For both tissues, tobacco smokers were found to have statistically significant higher levels of DNA damage than samples obtained from nonsmokers (P < 0.001). Mean relative adduct labeling in smokers was very similar for oral biopsies (6.16 x 10(-7)) and buccal mucosa (6.73 x 10(-7)). Likewise, mean relative adduct labeling values for nonsmokers were comparable in the two tissues (1.66 x 10(-7) for biopsies and 2.1 x 10(-7) for mucosa). Overall, an excellent correlation (r = 0.79; n = 32) was obtained between adduct levels in biopsies and mucosa for all classes of patient. These data indicate that buccal mucosa provides an additional tissue for monitoring human exposure to environmental genotoxins. The tissue is obtained rapidly in a noninvasive fashion when harvested by brushing. It can clearly be used to study components in cigarette smoke which cause DNA damage, and it is on the major route of exposure to many environmental genotoxins.

Autoradiography↗
PubMed1994

DNA damage induced by the environmental carcinogen butadiene: identification of a diepoxybutane-adenine adduct and its detection by 32P-postlabelling.

To date only a few studies have been undertaken on DNA adducts formed by epoxybutene (EB) and diepoxybutane (DEB), the two active metabolites of 1,3-butadiene. Our interests have focused on further investigating DNA alkylation by the two epoxides, especially in relation to the development of a method for human biomonitoring. Here, following the reaction of deoxyadenosine monophosphate and poly(dA-dT)(dA-dT) with DEB and subsequent HPLC, we have identified an adenine adduct. MS analyses indicate the structure of an adenine adducted by DEB at the N6 position. A HPLC/32P-postlabelling method was developed for its measurement in DNA samples and the adduct was detected in calf thymus DNA and DNA from Chinese hamster ovary cells exposed to DEB. The 100% labelling efficiency during postlabelling, the amount of the adduct and its elution before the normal nucleotides during HPLC suggest it could be a suitable indicator of BUT exposure.

Adamantane↗
PubMed1994

Single-stage reconstruction of key pinch and extension of the elbow in tetraplegic patients.

The results in ten arms of nine patients who had post-traumatic tetraplegia at the fifth or sixth cervical level were reviewed after combined transfer of the brachioradialis to the flexor pollicis longus and of the posterior part of the deltoid to the triceps tendon to restore key pinch and extension of the elbow. The average age of the patients was twenty-nine years, the average time from the injury to the operation was five years, and the average duration of follow-up was thirty-one months. Key pinch improved from essentially none preoperatively to an average of 2.0 pounds (0.9 kilogram) postoperatively: an average of 3.0 pounds (1.4 kilograms) for the patients who had tetraplegia at the sixth cervical level and an average of 0.9 pound (0.4 kilogram) for those who had tetraplegia at the fifth cervical level. Key pinch was favorably influenced by extension of the wrist, while the position of the elbow had no effect. Maximum active extension of the elbow against gravity was within 20 degrees of full extension in eight of the ten arms. There was an improvement in the performance of activities of daily living, including wheelchair use, and most of the patients discontinued use of special equipment for the upper extremity. The results of this study, when compared with those of each procedure performed separately, suggest that a combination of the operations improves function of the upper extremity and shortens the duration of dependence postoperatively.

Activities of Daily Living↗