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Biomedical subjects

Luis Iglesias

Publications and source records attributed to Luis Iglesias.

12 recordsLinked to original sources
PubMed2005

CO(2)-fixing enzymes during moulting from third larval to fourth larval stage of Anisakis simplex and Hysterothylacium aduncum (Nematoda: Anisakidae).

The fixing of CO(2) is an important metabolic process for many organisms. In the anisakid nematodes, CO(2) has been shown to be necessary for their development, at least in vitro. The presence of CO(2) stimulates the moulting (M3) of the larvae from the third (L3) to the fourth (L4) stage and prolongs the survival, at least, in vitro. We determined the activity of CO(2)-fixing enzymes, common to many organisms, in two anisakids: Anisakis simplex, a parasite of cetaceans, and Hysterothylacium aduncum, a parasite of fish. Although no activity was detected for pyruvate carboxylase or carboxylating-malic enzyme, we detected phosphoenolpyruvate carboxykinase (PEPCK) and phosphoenolpyruvate carboxylase (PEPC) activity. In A. simplex, PEPCK was clearly higher than that of PEPC throughout the moulting process studied. In H. aduncum, although the activity of both enzymes was of similar magnitude, they showed different behaviour; PEPCK activity decreased after the moulting to L4, PEPC activity increased so that the ratio PEPCK/PEPC activity decreased from 1.90 before moulting to 0.59 after.

Animals↗
PubMed2004

Fusidic acid suspension twice daily: a new treatment schedule for skin and soft tissue infection in children, with improved tolerability.

OBJECTIVE: This multicentre, randomized, double-blind, parallel group study aimed to compare a new regimen of fusidic acid suspension against a standard regimen in children with skin and soft tissue infections. METHODS: Treatment groups were given either a new regimen of fusidic acid suspension (20 mg/kg divided b.i.d.) or a standard regimen (50 mg/kg divided t.i.d.), which were administered for 5 days in both groups and for a further 5 days if evidence of infection persisted. Assessment of those cured was carried out 14 days. RESULTS: Both regimens were effective. Cure was achieved in 194 (91.1%) of the 213 children given the new b.i.d. dosage and for 194 (89.4%) of the 217 children given the standard t.i.d. dosage (intention-to-treat population; p=0.72). Cure was maintained at the follow-up assessment for 94.8% (181 of 191) and 95.7% (180 of 188), respectively, of the children. Bacteriological cure of infections due to fusidic acid susceptible Staphylococcus aureus and/or group A beta-haemolytic streptococci, with elimination of pathogens, was achieved in all 121 (100%) children treated with the new b.i.d. regimen and in 123 (99.2%) of the 124 children treated with the standard TID regimen. CONCLUSION: The new twice-daily regimen had significantly better tolerance (p=0.025).

Administration, Oral↗
PubMed2003

[Tetracyclines, sulfonamides and metronidazole].

Tetracyclines form a group of natural and semisynthetic products that acts inhibiting the bacterial protein synthesis. They are bacteriostatic agents, exhibiting activity against a wide range of organisms, but they are at the present of limited use because of their acquired resistance. Doxycycline is currently the most frequently used tetracycline in human medicine and it is included in the List of Essential Medicines of the World Health Organization. Sulfonamides are synthetic, broad-spectrum bacteriostatic antibiotics. They were the first effective systemic antimicrobial agents. Their mode of action is based on the inhibition of DNA synthesis. Due to their toxicity and high adquired resistance their use is currently very low. Metronidazole is the main compound of 5-nitroimidazole family. It is a very active bactericidal antibiotic against anaerobic and some microaerophilic bacteria and it is still very useful in the treatment of bacterian and parasitic infections.

Anti-Infective Agents↗
PubMed2003

Molecular characterization of erythromycin-resistant clinical isolates of the four major antimicrobial-resistant Spanish clones of Streptococcus pneumoniae (Spain23F-1, Spain6B-2, Spain9V-3, and Spain14-5).

Erythromycin resistance and the characterization of the corresponding determinants of resistance were studied in clinical Streptococcus pneumoniae isolates belonging to the four major multiresistant pneumococcal Spanish clones (ermB and mefA genes for the Spain23F-1, Spain9V-3, serotype 14 variant of the Spain9V-3 and Spain14-5 clones and ermB gene for the Spain6B-2 clone). These isolates were confirmed as major clones by pulsed-field gel electrophoresis (PFGE), BOX-PCR, and multilocus sequence typing (MLST). The spread and prevalence of these erythromycin-resistant variants of the Spanish clones in an area of the north of Spain were dissimilar-low for the Spain9V-3 clone (5.8% among the isolates belonging to this clone, including isolates of the serotype 14 variant) and very frequent for the Spain14-5 clone (91.7%).

Anti-Bacterial Agents↗
PubMed2003

Spain14-5 international multiresistant Streptococcus pneumoniae clone resistant to fluoroquinolones and other families of antibiotics.

The Spain(14)-5 international multiresistant clone was initially described as resistant to penicillin, tetracycline, chloramphenicol and trimethoprim/sulfamethoxazole. In Gipuzkoa, Spain, Streptococcus pneumoniae isolated from 16 patients, and determined by PFGE and multilocus sequence typing to belong to the Spain(14)-5 clone, showed further resistance to fluoroquinolones (all strains had point mutations in the parC and gyrA genes). In addition, most strains showed resistance to amoxicillin (MIC > or = 8 mg/L), cefotaxime (MIC > or = 2 mg/L), macrolides and lincosamides. Two strains were resistant to rifampicin (MIC 8 mg/L). The multiresistance observed in these isolates converts the Spain(14)-5 clone into one of the most, if not the most, multiresistant of the international clones described.

Anti-Bacterial Agents↗
PubMed2003

Fluoroquinolone and macrolide treatment failure in pneumococcal pneumonia and selection of multidrug-resistant isolates.

Streptococcus pneumoniae serotype 3, isolated from a penicillin-allergic patient and initially susceptible to fluoroquinolones, macrolides, lincosamides, quinupristin-dalfopristin, and telithromycin, became resistant to all these drugs during treatment. Mutations in the parC and gyrA and in the 23S rRNA and the ribosomal protein L22 genes were detected in the resistant isolates.

Aged↗
PubMed2002

p16(INK4a) is selectively silenced in the tumoral progression of mycosis fungoides.

Knowledge about the molecular mechanisms involved in the pathogenesis of tumoral progression in mycosis fungoides (MF) is still scarce. Because the 9p21 locus seems to be a good target for a detailed study in MF, this prompted us to compare the mechanisms of inactivation of the p16(INK4a), p15(INK4b), and p14(ARF) genes in aggressive and stable forms of MF, performing microsatellite analysis, methylation-specific polymerase chain reaction, direct sequencing, and p16(INK4a) protein expression by immunohistochemistry. Additionally, the p53 gene was also sequenced in tumoral lesions. Thirty-nine patients with stable MF were studied. Alterations in p16(INK4a) and p15(INK4b) genes were detected in 18% and 5% of the cases, respectively. None of the cases analyzed showed alterations of the p14(ARF) gene. In contrast with these findings, in the 11 patients with aggressive MF, alterations of the p16(INK4a), p15(INK4b), or p14(ARF) genes were found in 8 (73%), 3 (27%), and 2 (18%) cases, respectively. A significant proportion (4/11) of these alterations were already present in the p16(INK4a) gene in the initial plaque lesions in these aggressive forms of MF. Alterations in the p16(INK4a) gene, either methylation or loss of heterozygosity, were clearly more frequent than those in the p15(INK4b) and p14(ARF) genes. These p16(INK4A) alterations were confirmed using immunohistochemistry. None of the nine tumoral lesions analyzed showed mutations in exons 1-2 of the p16(INK4a) gene or in exons 5-8 of the p53 gene. These results seem to suggest that 9p21 alterations, and selectively p16(INK4a) silencing, could be a characteristic phenomenon in MF progression.

Adolescent↗
PubMed2002

Lichenoid nail changes as sole external manifestation of graft vs. host disease.

A 56-year-old-man who had refractory anemia with an excess of blasts underwent an allogeneic peripheral blood stem cell transplantation (PBSCT) from his brother after preparation with melphalan and fludarabin. He received GvHD (graft-vs.-host disease) prophylaxis with cyclosporine from day -1 at a daily dose of 5 mg/kg of body weight. The daily dosage was tapered gradually from day +20. On post-PBSCT day 68 he developed acute cutaneous GvHD grade 3 and acute gastrointestinal GvHD grade 2-3, which was resolved with a daily dose of 1 mg/kg of body weight of prednisone. The patient was discharged in good clinical condition and without signs of GvHD, and he started tapering his immunosuppressive treatment. By day 160 he developed oral lichen planus-like changes, with several reticulate white lesions on the oral mucosa. A biopsy specimen was microscopically consistent with lichenoid GvHD (Fig. 1). By day 150 after PBSCT, when he was being treated with CsA 100 mg once daily and prednisone 10 mg once daily, his fingernails started to grow abnormally and gradually became dystrophic and painful. Two months later his toenails became similarly affected. Although affecting all finger and toe nails, the lesions were especially important in both thumbs. Physical examination revealed multiple findings on his nails (Fig. 2): thickening, fragility, onycholysis, longitudinal striations, and even pterygium. The micological cultures were negative. A biopsy specimen showed an sparse papillary dermis lymphoid infiltrate with focal exocytosis and presence of isolated multiple necrotic keratinocytes (Fig. 3). These findings were interpreted as a lichenoid GvHD with oral and nail involvement. The patient did not have other associated cutaneous lesions. He did not develop signs or symptoms consistent with hepatic GvHD. In May 2000 thalidomide was added to the immunosuppressive therapy, at a daily dose from 100 to 300 mg according to tolerance (constipation, sedation, ...). The lesions on the oral mucous showed a substantial improvement, but the nail changes remained more or less stable. Thalidomide was discontinued after 7 months because the patient displayed numbness and tingling in the hands and feet consistent with a peripheral neuropathy. Twenty days later he stopped taking thalidomide and the oral lichenoid lesions worsened, resulting in difficulty in eating. He also developed periungueal erythema, swelling and intense pain after minimal trauma. The daily dose of prednisone increased to 20-30 mg with moderate improvement. However, the dose could not be increased because of the secondary immunosuppressive effects. Twenty-three months post-PBSCT the patient remains with intense oral and nail lichenoid lesions.

Graft vs Host Disease↗
PubMed1999

Stereochemically Controlled Synthesis of Ruthenium(II) Complexes Containing Bis(oxazolin-2'-yl)pyridine Ligands. X-ray Crystal Structures of trans-[RuCl(2)(PPh(3)){kappa(3)-N,N,N-(S,S)-(i)Pr-pybox}] and [RuCl(=C=C=CPh(2))(PPh(3)){kappa(3)-N,N,N-(S,S)-(i)Pr-pybox}][PF(6)] ((S,S)-(i)Pr-pybox= 2,6-Bis[4'-(S)-isopropyloxazolin-2'-yl]pyridine).

The treatment of achiral and chiral bis(oxazolin-2'-yl)pyridine (pybox) complexes trans-[RuCl(2)(eta(2)-H(2)C=CH(2))(k(3)-N,N,N-pybox)] [pybox= 2,6-bis(dihydrooxazolin-2'-yl)pyridine] (1a) and [RuCl(2)(eta(2)-H(2)C=CH(2))(k(3)-N,N,N-(SS)-(i)Pr-pybox}] [(SS)-(i)Pr-pybox= 2,6-bis[4'-(S)-isopropyloxazolin-2'-yl]pyridine] (1b) with an excess of triphenylphosphine in dichloromethane at 50 degrees C leads to the formation of the first ruthenium(II) derivatives containing both bis(oxazolin-2'-yl)pyridine and phosphine ligands trans-[RuCl(2)(PPh(3))(kappa(3)-N,N,N-pybox)] (2a) and trans-[RuCl(2)(PPh(3)){kappa(3)-N,N,N-(SS)-(i)Pr-pybox}] (2b). Chiral complex 2b slowly isomerizes in acetone at 50 degrees C to generate cis-[RuCl(2)(PPh(3)){kappa(3)-N,N,N-(SS)-(i)Pr-pybox}] (3). Complex 3 can be also obtained from the reaction of 1b with PPh(3) in MeOH. The structure of 3 has been confirmed by X-ray crystallography [orthorhombic; space group P2(1)2(1)2(1); Z = 4; a = 12.772(6) Å, b = 15.208(5) Å, c = 19.601(7) Å; final R1= 0.0565 and wR2 = 0.0944 (both for I > 2sigma(I))]. The reaction of the achiral pybox complex 2a with 1,1-diphenyl-2-propyn-1-ol and AgBF(4) in CH(2)Cl(2) stereoselectively affords the cationic allenylidene derivative [RuCl(=C=C=CPh(2))(PPh(3))(kappa(3)-N,N,N-pybox)][BF(4)] (4a), while the methoxycarbene complex [RuCl{=C(OMe)CH=CPh(2)}(PPh(3))(kappa(3)-N,N,N-pybox)][PF(6)] (5) is obtained when the reaction is conducted in methanol and in the presence of NaPF(6), via the addition of MeOH to the initially formed allenylidene complex 4a. In contrast, the chiral pybox complex 2b reacts with 1,1-diphenyl-2-propyn-1-ol and NaPF(6) in MeOH to give the stable allenylidene complex [RuCl(=C=C=CPh(2))(PPh(3)){kappa(3)-N,N,N-(SS)-(i)Pr-pybox}][PF(6)] (4b). The X-ray crystal structure of 4b [orthorhombic; space group P2(1)2(1)2(1); Z = 4; a = 14.79(3) Å, b = 16.254(8) Å, c = 22.917(18) Å; final R1 = 0.0545 and wR2 = 0.1381 (both for I > 2sigma(I))] shows an octahedral coordination of the ligands around the ruthenium atom with the chloride and triphenylphosphine ligands in a trans arrangement and mutually cis with respect to the allenylidene moiety. The allenylidene complex 4b is also formed by the reaction of the cis dichloride complex 3 with 1,1-diphenyl-2-propyn-1-ol and NaPF(6) in MeOH. IR, (1)H, (31)P{(1)H}, and (13)C{(1)H} NMR data of all novel compounds are also reported.

Journal Article↗