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Biomedical subjects

G Jenkins

Publications and source records attributed to G Jenkins.

9 recordsLinked to original sources
PubMed1991

Cloning and characterization of two genes from Streptomyces lividans that confer inducible resistance to lincomycin and macrolide antibiotics.

Inducible resistance to lincomycin and macrolides in Streptomyces lividans TK21 results from expression of two linked genes: lrm, encoding a ribosomal RNA methyltransferase that confers high-level resistance to lincomycin with lower levels of resistance to macrolides, and mgt, encoding a glycosyl transferase that specifically inactivates macrolides using UDP-glucose as cofactor. The lrm and mgt genes have been cloned and sequenced. The deduced lrm product is a 26-kDa protein with much similarity to other ribosomal RNA methyltransferases, such as the carB, tlrA and ermE products, whereas the mgt product (predicted to be 42 kDa) resembles a eukaryotic glycosyl transferase. Macrolides that induce the lrm-mgt gene pair are substrates for inactivation by the mgt product, and the lrm product confers ribosomal resistance to such inducers.

Amino Acid Sequence↗
PubMed1991

In vivo and photophysical studies on photooxidative damage to lens proteins and their protection by radioprotectors.

Photooxidation, whether initiated by an endogenous or exogenous sensitizer, is an important mechanism in light induced damage to the lens. One of the substrates for this damage is lens protein. A porphyrin sensitizer which binds to lens proteins [mesotetra(p-sulfonatophenyl) porphyrin (TPPS)] was found to photooxidize Skh-2 pigmented mice lens protein in vivo. Uroporphyrin, a model for a non-binding photosensitizer, did not induce photooxidative damage to the mouse lens. The radioprotector 3-amino-2-hydroxypropyl phosphorothioate (WR-77913) was investigated as an agent to retard or negate in vivo photooxidative damage to the lens. Intraperitoneal injections of WR-77913 prior to irradiation reduced the TPPS induced photodestruction of lens protein in Skh-2 pigmented mice. The mechanism of protection was also investigated. Thiols were found to quench both the triplet state of porphyrins and the reactive intermediate singlet oxygen on the order of 10(5) and 10(6) M-1 s-1 respectively. These are probably not fast enough to explain most of the protection afforded by thiols. An additional mechanism may be the accelerated photobleaching of porphyrins by thiols which protects tissue by reducing the absorptions due to the porphyrins.

Amifostine↗
PubMed1990

An evaluation of triple-lumen catheter infections using a guidewire exchange technique.

One hundred fifty-six triple-lumen central venous catheters placed into 65 different sites in 52 surgical or trauma patients were prospectively evaluated to determine the frequency of catheter-related infection and the efficacy of multiple guidewire exchanges. Thirty-four anatomic sites in 33 patients without clinical signs of sepsis were compared to 31 anatomic sites in 19 patients with a clinical diagnosis of sepsis based on clinical, microbiologic, and radiologic evaluation. Anatomic sites were used indefinitely unless a positive semiquantitative catheter culture (greater than or equal to 15 cfu) or catheter-associated bacteremia developed. Seven catheter-related infections developed in five septic patients (26.3%) while no infections developed in the nonseptic group (p = 0.004). Three of 31 anatomic sites (9.6%) were associated with bacteremia. The number of hospital days to initial catheter insertion and the length of catheter site use were considerably higher in the septic patients compared to the nonseptic group. We conclude that triple-lumen catheter-related infections are uncommon in patients with no evidence of infection and can be safely guidewire-exchanged to prolong site use. Catheter-related infections in septic patients are much more frequent and unpredictable. Although guidewire exchange has a role in septic patients, multiple exchanges cannot routinely be recommended.

Adolescent↗