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PubMed1992

Forearm resistance vessel abnormalities and insulin resistance in obese adolescents.

To determine if structural changes in forearm resistance vessels are associated with insulin resistance, we evaluated the relation between minimum forearm vascular resistance and insulin resistance in 95 obese adolescents before and after weight loss. Insulin resistance was assessed by fasting insulin levels and sum of insulin values after an oral glucose tolerance test in all 95 subjects and whole body glucose uptake during euglycemic hyperinsulinemia in 35 of 95 subjects. Structural changes in forearm vessels were assessed by measurement of minimum forearm vascular resistance during 10 minutes of ischemic exercise. As compared with our normal values, obese adolescents had a significantly (p less than 0.01) decreased maximal forearm blood flow (41.6 +/- 1.4 versus 67.1 +/- 2.4 ml/min/100 ml) and increased minimum forearm vascular resistance (2.9 +/- 0.4 versus 1.6 +/- 0.7 mm Hg/ml/min/100 ml). There was a significant relation (p less than 0.01) between minimum forearm vascular resistance and fasting insulin, sum of insulins, and whole body glucose uptake. After a 20-week weight-loss program, minimum forearm vascular resistance decreased (3.0 +/- 0.3 versus 2.0 +/- 0.2, p less than 0.01), maximal forearm blood flow increased (41 +/- 2.3 versus 57.4 +/- 3.9, p less than 0.01), and forearm volume remained unchanged. We also observed a significant (p less than 0.01) relation between the decrease in minimum forearm vascular resistance and the decrease in fasting insulin (r = 0.29), decrease in sum of insulins (r = 0.42), and increase in whole body glucose uptake (r = 0.63).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

HIV resistance to antiretroviral drugs: mechanisms, genotypic and phenotypic resistance testing in clinical practice.

HIV resistance to antiretroviral agents is a major contributory cause of treatment failure. The dynamics of HIV replication, together with patient-, physician-, and drug-related factors, lead to emergence of HIV resistant strains in most of the patients. Phenotypic assays look for an increase in the antiretroviral drug (ARV) concentration that inhibits 50% of the growth of the tested HIV strain (IC50), comparatively with a reference strain cultivated in parallel. Genotypic tests detect resistance mutations in the reverse transcriptase and protease genes by comparing the gene sequences of a resistant virus to those of a wild-type strain that has previously been described. The efficacy of each ARV class and each individual ARV is threatened by specific mutations and resistance mechanisms. In retrospective studies of genotypic or phenotypic resistance testing, baseline resistance tests results were correlated with virological outcomes. There is some evidence from prospective studies that resistance testing may have some benefits when used to choose salvage regimens. However, problems in the areas of test interpretation, patient compliance, availability of active drugs, and technical test performance limit the usefulness of resistance testing in clinical practice. This article reviews the mechanisms underlying HIV resistance, the principles of phenotypic and genotypic tests, and the use of these tests in clinical practice.

Anti-HIV Agents↗
PubMed2003

In vitro efficacy of combined treatment depends on the underlying mechanism of resistance in imatinib-resistant Bcr-Abl-positive cell lines.

Imatinib mesylate (Gleevec, formerly STI571) is an effective therapy for all stages of chronic myelogenous leukemia (CML). While responses in chronic-phase CML are generally durable, resistance develops in many patients with advanced disease. We evaluated novel antileukemic agents for their potential to overcome resistance in various imatinib-resistant cell lines. Using cell proliferation assays, we investigated whether different mechanisms of resistance to imatinib would alter the efficacy of arsenic trioxide (As2O3) or 5-aza-2-deoxycytidine (decitabine) alone and in combination with imatinib. Our results indicate that resistance to imatinib induced by Bcr-Abl overexpression or by engineered expression of clinically relevant Bcr-Abl mutants does not induce cross-resistance to As2O3 or decitabine. Combined treatment with these agents and imatinib is beneficial in cell lines that have residual sensitivity to imatinib monotherapy, with synergistic growth inhibition achieved only at doses of imatinib that overcome resistance. In some imatinib-resistant cell lines, combination treatments that use low doses of imatinib lead to antagonism. Apoptosis studies suggest that this can be explained in part by the reduced proapoptotic activity of imatinib in resistant cell lines. These data underline the importance of resistance testing and provide a rational approach for dose-adjusted administration of imatinib when combined with other agents.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2001

Pyrethroid resistance and mechanisms of resistance in field strains of Helicoverpa armigera (Lepidoptera: Noctuidae).

Pyrethroid resistance was found in 54 field strains of Helicoverpa armigera collected between 1995 and 1999 from 23 districts in seven states of India. LD50 values of the field strains ranged from 0.06 to 72.2 microg/larva with slopes of 0.5-3.1. Resistance was highest in regions where pyrethroid use was frequent (four to eight applications per season). Resistance to deltamethrin was exceptionally high with resistance ratios of 13,570 and 27,160 in two strains collected during February 1998 in central India. Resistance to cypermethrin, fenvalerate and cyhalothrin also was high with resistance ratios of >1,000 in four strains collected from central and southern India. Resistance ratios were below 100 in >50% of the strains tested. Pyrethroid resistance was high in strains collected from the districts in Andhra Pradesh where a majority of the cotton farmer suicide cases in India were reported. Resistance to pyrethroids appeared to have increased over 1995-1998 in most of the areas surveyed. Studies carried out through estimation of detoxification enzyme activity and synergists indicated that enhanced cytochrome p450 and esterase activities were probably important mechanisms for pyrethroid resistance in field strains. Pyrethroid nerve insensitivity also was found to be a major mechanism in some parts of the country where the use of pyrethroids was high. The information presented illustrates the importance of proper insect management programs to avoid the consequences associated with improper insecticide use.

Animals↗
PubMed2002

Resistance and cross-resistance to four insecticides in populations of obliquebanded leafroller (Lepidoptera: Tortricidae).

Populations of obliquebanded leafroller, Choristoneura rosaceana (Harris), were collected from organic and conventionally managed orchards located in the Okanagan and Similkameen Valleys of British Columbia Neonate F1 progeny were assayed for resistance to azinphosmethyl, tebufenozide, methoxyfenozide, and indoxacarb using a leaf disk bioassay. Significant differences in resistance levels among populations were observed for all four insecticides. Insects collected from organic sites were more susceptible to all insecticides than were insects collected from conventional sites. Resistance to the benzoylhydrazine insect growth regulators tebufenozide and methoxyfenozide was highly correlated with resistance to azinphosmethyl across populations, indicating cross-resistance between these compounds. The highest levels of resistance were observed with indoxacarb, but resistance levels to indoxacarb did not correlate with those for azinphosmethyl. Dose-response regression lines for tebufenozide were parallel across populations, suggesting that the resistance mechanism(s) were quantitatively, but not qualitatively, different. Cross-resistance between azinphosmethyl and benzoylhydrazine insecticides indicates that a resistance management strategy for obliquebanded leafroller involving the rotation of these materials is not likely to be successful.

Animals↗
PubMed2006

Cadherin-based resistance to Bacillus thuringiensis cotton in hybrid strains of pink bollworm: fitness costs and incomplete resistance.

Recessive resistance to Bacillus thuringiensis (Bt) cotton, Gossypium hirsutum L., in laboratory-selected strains of pink bollworm, Pectinophora gossypiella (Saunders), is associated with three resistance alleles (r1, r2, and r3) of a cadherin gene. Previous experiments based on measurement of fitness components in Bt-resistant and Bt-susceptible strains revealed that fitness costs and incomplete resistance are associated with resistance. Here, we used two hybrid strains of pink bollworm, each containing a mixture of susceptible and resistant individuals, and polymerase chain reaction (PCR) amplifications to test the association between cadherin genotype and fitness components for individuals sharing a common genetic background. All survivors on Bt cotton had two r alleles, confirming that recessive cadherin alleles are tightly linked with resistance to Bt cotton. On non-Bt cotton, significantly greater developmental time for rr than ss larvae indicated a recessive fitness cost, but costs did not affect survival or pupal weight. Incomplete resistance was manifested as longer developmental time, lower survival, and smaller pupal weight in rr individuals developing on Bt cotton compared with non-Bt cotton. As in previous experiments, no significant variation in performance on Bt cotton was detected among rr genotypes. However, a meta-analysis of data from seven experiments revealed that survival on Bt cotton relative to non-Bt cotton was lower in r2r3 and higher in r1r2 compared with the other rr genotypes. Assessment of fitness components associated with cadherin genotypes in hybrid strains of pink bollworm confirms that recessive resistance to Bt cotton is associated with recessive fitness costs and incomplete resistance.

Animals↗
PubMed2003

Survey of resistance to permethrin and diazinon and the use of a multiplex polymerase chain reaction assay to detect resistance alleles in the horn fly, Haematobia irritans irritans (L.).

A field survey was conducted in 2001 to evaluate resistance to pyrethroid and organophosphate (OP) insecticides on horn flies, Hematobia irritans irritans (L.), from seven ranches in the state of Tamaulipas, Mexico, and from three locations in central Texas. Filter papers impregnated with either technical permethrin or diazinon were used to measure the levels of resistance to pyrethroids and OPs. A multiplex polymerase chain reaction (PCR) assay was used on individual horn flies from these field populations to detect the presence of the kdr and super-kdr alleles associated with pyrethroid resistance, and a mutated alphaE7 esterase allele associated with OP resistance. Relative to a susceptible laboratory (Kerrville) strain, horn flies from Mexico exhibited 5.1- to 28.3-fold resistance to permethrin at the LC50, and 23.8- to 136-fold resistance at the LC90. Horn flies from Texas ranches exhibited only two- to five-fold resistance. All field populations of the horn fly were highly susceptible to diazinon, and no mutant alphaE7 esterase alleles were detected. The super-kdr allele was found only in a single fly from a ranch in Mexico. Results of PCR assays showed that the kdr allele was present at various frequencies in field populations of horn flies. A gender-related bias in distribution of kdr genotypes was found in horn flies from Mexico, but not in horn flies from Texas. The overall kdr allelic frequencies in horn flies from Mexico were 23.2-37.8% higher in females than in males. Regression analysis revealed a significant correlation between kdr allelic frequencies and the levels of knockdown resistance to permethrin among the horn fly populations studied. The results validate the role of the PCR-based molecular assay as a diagnostic tool in monitoring resistance to pyrethroids and also provide useful information on population genetics of horn fly resistance to pyrethroids and OPs.

Alleles↗
PubMed2006

Multi-drug resistance in Salmonella enterica: efflux mechanisms and their relationships with the development of chromosomal resistance gene clusters.

Bacterial drug resistance represents one of the most crucial problems in present day antibacterial chemotherapy. Of particular concern to public health is the continuing worldwide epidemic spread of Salmonella enterica serovar Typhimurium phage type DT104 harbouring a genomic island called Salmonella genomic island I (SGI-1). This island contains an antibiotic gene cluster conferring resistance to ampicillin, chloramphenicol, florfenicol, streptomycin, sulfonamides and tetracyclines. These resistance genes are assembled in a mosaic pattern, indicative of several independent recombinational events. The mobility of SGI-1 coupled with the ability of various antibiotic resistance genes to be integrated and lost from the chromosomal resistance locus allows for the transfer of stable antibiotic resistance to most of the commonly used antibiotics and adaptation to new antibiotic challenges. This, coupled with the incidence of increasing fluoroquinolone resistance in these strains increases the risk of therapeutic failure in cases of life-threatening salmonellosis. Fluoroquinolone resistance has largely been attributed to mutations occurring in the genes coding for intracellular targets of these drugs. However, efflux by the AcrAB-TolC multi-drug efflux pump has recently been shown to directly contribute to fluoroquinolone resistance. Furthermore, the resistance to chloramphenicol-florfenicol and tetracyclines in DT104 isolates, is due to interaction between specific transporters for these antibiotics encoded by genes mapping to the SGI-1 and the AcrAB-TolC tripartite efflux pump. The potential for the use of efflux pump inhibitors to restore therapeutic efficacy to fluoroquinolones and other antibiotics offers an exciting developmental area for drug discovery.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed2026

A correlation analysis between arsenic and mercury resistance and the spread of antibiotic resistance genes in bacteria isolated from a highly contaminated brownfield.

Seventy-four bacterial strains from El Terronal (Asturias, Spain), a brownfield highly contaminated with mercury and arsenic but without anthropogenic antibiotic influx, were isolated and characterized in culture. No correlation was found between resistance to the aforementioned metal(loid)s and to antibiotics and biocides as tested by agar plates and disk diffusion method, as the number of strains deemed resistant to any of the analyzed antibiotics and biocides was not significantly higher among those with the highest resistance to arsenic and/or mercury. Genome sequencing of 17 of the isolated strains revealed a great number and diversity of antibiotic resistance genes (ARGs), as well as genes related to arsenic and mercury resistance, some of which were located in mobile genetic elements (MGEs). However, most of the detected ARGs were not located in MGEs, and no genes responsible for metal(loid) and antibiotic resistance were found to share an MGE. No evidence was found that resistance to arsenic and mercury influenced the dissemination of ARGs in the studied strains, although the abundance of antibiotic resistance mechanisms related to the presence of RND-type (Resistance-Nodulation-Division) efflux pumps could potentially contribute to cross-resistance.

antibiotics↗
PubMed2006

Chlorine resistance of Listeria monocytogenes biofilms and relationship to subtype, cell density, and planktonic cell chlorine resistance.

Strains of Listeria monocytogenes vary in their ability to produce biofilms. This research determined if cell density, planktonic chlorine resistance, or subtype are associated with the resistance of L. monocytogenes biofilms to chlorine. Thirteen strains of L. monocytogenes were selected for this research based on biofilm accumulation on stainless steel and rep-PCR subtyping. These strains were challenged with chlorine to determine the resistance of individual strains of L. monocytogenes. Planktonic cells were exposed to 20 to 80 ppm sodium hypochlorite in 20 ppm increments for 5 min in triplicate per replication, and the experiment was replicated three times. The number of tubes with surviving L. monocytogenes was recorded for each isolate at each level of chlorine. Biofilms of each strain were grown on stainless steel coupons. The biofilms were exposed 60 ppm of sodium hypochlorite. When in planktonic culture, four strains were able to survive exposure to 40 ppm of chlorine, whereas four strains were able to survive 80 ppm of chlorine in at least one of three tubes. The remaining five strains survived exposure to 60 ppm of chlorine. Biofilms of 11 strains survived exposure to 60 ppm of chlorine. No association of biofilm chlorine resistance and planktonic chlorine resistance was observed; however, biofilm chorine resistance was similar for strains of the same subtype. Biofilm cell density was not associated with chlorine resistance. In addition, biofilms that survived chlorine treatment exhibited different biofilm morphologies. These data suggest that chlorine resistance mechanisms of planktonic cells and biofilms differ, with planktonic chlorine resistance being more affected by inducible traits, and biofilm chlorine resistance being more affected by traits not determined in this study.

Biofilms↗
PubMed1980

In vivo and in vitro cross-resistance of kanamycin-resistant mutants of E. coli to other aminoglycoside antibiotics.

Cross resistance of kanamycin-resistant mutants of E. coli Q13 to other aminoglycosides (streptomycin, neomycin, gentamicin and dibekacin) was demonstrated in vivo (growth) and in vitro (polyphenylalanine synthesis, codon misreading and translocation on the ribosomes). Kanamycin-resistant mutants, R1-4, R2-1, R2-2, R3-3 and R3-5 showed various degrees of cross-resistance to streptomycin, gentamicin, neomycin and dibekacin in vivo. In vitro, polyphenylalanine synthesis was more resistant to kanamycin, streptomycin, neomycin and gentamicin on the ribosomes of the kanamycin-resistant mutants than on those of the parental strain. In the presence of kanamycin, neomycin or gentamicin, less degrees of [14C]isoleucine uptake with poly[U] (codon misreading) were observed on the ribosomes obtained from the resistant mutants than on the sensitive cell ribosomes. The N-acetyl-[14C]phenylalanyl-puromycin synthesis enhanced by an elongation factor, EF-G and GTP (translocation) was more resistant to kanamycin and dibekacin on the mutant ribosomes than on the parental ribosomes. The results indicate that the cross-resistance to other aminoglycoside antibiotics, as well as the kanamycin resistance, are attributed to mutational alterations of the ribosomes in these mutants.

Aminoglycosides↗
PubMed1999

Myeloma cells selected for resistance to CD95-mediated apoptosis are not cross-resistant to cytotoxic drugs: evidence for independent mechanisms of caspase activation.

We have previously shown that selection for resistance to the anthracenes, doxorubicin or mitoxantrone, results in coselection for resistance to CD95-mediated apoptosis (Landowski et al: Blood 89:1854, 1997). In the present study, we were interested in determining if the converse is also true; that is, does selection for CD95 resistance coselect for resistance to chemotherapeutic drugs. To address this question, we used two isogenic models of CD95-resistant versus CD95-sensitive cell lines: 8226/S myeloma cells selected for resistance to CD95-mediated apoptosis; and K562 cells expressing ectopic CD95. Repeated exposure of the CD95-sensitive human myeloma cell line, 8226/S, to agonistic anti-CD95 antibody resulted in a cell line devoid of CD95 receptor surface expression and completely resistant to CD95-mediated apoptosis. Multiple clonal populations derived from the CD95-resistant cell line showed no difference in sensitivity to doxorubicin, mitoxantrone, Ara-C, or etoposide, demonstrating that cross-resistance between Fas-mediated apoptosis and drug-induced apoptosis occurs only when cytotoxic drugs are used as the selecting agent. Using the inverse approach, we transfected the CD95-negative cell line, K562, with a CD95 expression vector. Clones expressing variable levels of cell-surface CD95 were isolated by limiting dilution, and analyzed for sensitivity to CD95-mediated apoptosis and response to chemotherapeutic drugs. We show that CD95 surface expression confers sensitivity to CD95-mediated apoptosis; however, it does not alter response to chemotherapeutic drugs. Similarly, doxorubicin-induced activation of caspases 3 and 8 was identical in the CD95-sensitive and CD95-resistant cell lines in both isogenic cell systems. In addition, prior treatment with the CD95 receptor-blocking antibody, ZB4, inhibited CD95-activated apoptosis in 8226/S cells, but had no effect on doxorubicin cytotoxicity. These results show that CD95 and chemotherapeutic drugs use common apoptotic effectors, but the point of convergence in these two pathways is downstream of CD95 receptor/ligand interaction.

Anthracenes↗
PubMed2000

Co-transfection of MRP and bcl-2 antisense S-oligodeoxynucleotides reduces drug resistance in cisplatin-resistant lung cancer cells.

OBJECTIVE: To detect the influence of antisense s-oligodeoxynucleotides (S-ODNs) of bd-2 and multidrug resistance-associated protein (MRP) genes multidrug resistance-associated protein gene and bcl-2 antisense S-oligodeoxynucleotides on cisplatin-resistant lung adenocarcinoma cell line A549DDP which overexpresses both bcl-2 and MRP. METHODS: A549DDP cells were treated with sense and antisense S-ODN mediated by lipofection. Expression of MRP and bcl-2 mRNA and protein in the treated cells was measured by RT-PCR and flow cytometry (FCM), respectively. Apoptosis was identified by DNA electrophoresis and terminal deoxynucleotidyl transferase (TdT)-mediated biotin dUTP nick end-labeling (TUNEL). The degree of drug resistance of the treated cells was detected by a cell viability 3'-[4,5-dimethylthiazol-2-yl]-2, 5-diphenyl-tefrazolium bromide thiazolylblue (MTT) assay. RESULTS: Expression of bcl-2 and MRP significantly decreased in the cells treated with bcl-2 or/and MRP antisense S-ODN for 48 h as compared to the cells untreated and sense-treated (P < 0.05). Resistance to cisplatin in the cells treated with bcl-2 or/and MRP antisense S-ODN decreased by 60.6% (6.5 times), 56.4% (7.2 times) and 71.0% (4.8 times), respectively, which paralleled the decrease of bcl-2 and MRP expression. Similarly, the resistance to etoposide and epirubicin in antisense-treated cells also reduced in parallel to decreases of the two gene expressions. The drug resistance in sense-treated cells was similar to that in untreated cells. Statistically significant dose- and concentration-dependent increases of apoptotic cells were observed in the groups exposed to 100 mumol/L cisplatin for 48 h after treatment by bcl-2 or/and MRP antisense. CONCLUSION: Bcl-2 and MRP were at least additive and possibly synergistic in conferring drug resistance in a cisplatin-resistant lung adenocarcinoma cell line. Antisense S-ODN could attenuate drug resistance by promoting cells apoptosis, which might lead to a new treatment for patients with non-small cell lung cancers (NSCLCs) who are refractory to conventional chemotherapy.

Adenocarcinoma↗
PubMed1959

Cross-resistance in insecticide-resistant strains of the German cockroach. Blattella germanica (L.

The authors describe a series of experiments designed to determine the extent to which cross-resistance exists in insecticide-resistant strains of the German cockroach. The tests were conducted by exposing females from a DDT-resistant strain, a chlordane-resistant strain, and a non-resistant strain to varying concentrations of several insecticides. From these tests mortality data were obtained and are presented in the form of regression lines.The insecticides used were DDT, methoxychlor, chlordane, dieldrin, Prolan, malathion, allethrin, and Lethane; these were chosen so that a wide variety of chemical types would be represented.The results indicate that the DDT-resistant strain is highly resistant to DDT and to its analogue, methoxychlor, but not to any of the other insecticides tested. Similarly, the chlordane-resistant strain is highly resistant to chlordane and to its analogue, dieldrin, but is susceptible to the other toxicants listed.From these results, as well as those obtained by others, it appears that the picture of cross-resistance in the German cockroach is in essential agreement with that which is emerging for other insects throughout the world.

Animals↗
PubMed1992

Resistance mechanisms in murine tumors with acquired multidrug resistance.

Mechanisms of multidrug resistance were studied in murine leukemia (L 1210) and sarcoma (Sa 180) tumors after pretreatment with anthracyclines in vivo. Despite identical pretreatment protocols, a considerable difference in the level of resistance between L 1210 and Sa 180 tumors was noted (for doxorubicin: 45-fold versus 340-fold; for daunorubicin: 51-fold versus 275-fold). However, no difference in mdr 1 gene-amplification and the overexpression of mdr 1-RNA or P-glycoprotein was demonstrated. None of these parameters did increase by further treatment with a higher concentration of anthracyclines. Resistant sublines of Sa 180 revealed an overexpression of glutathione S-transferase-pi (GST-pi) in comparison to the parental line, whereas in sensitive and resistant sublines of L 1210 tumors the expression of GST-pi was similar. In order to study whether trifluoperazine can reverse the P-glycoprotein mediated component of multidrug resistance, trifluoperazine and doxorubicin were tested in vitro in L 1210 and Sa 180 cells. In contrast to the complete reversal of resistance in L 1210 tumors, resistance in Sa 180 was only partly circumvented. However, by buthionine sulfoximine treatment, the toxicity of multidrug resistant Sa 180 tumors could be increased. It was possible to reverse the resistance of Sa 180 tumors completely by trifluoperazine plus buthionine sulfoximine. Thus, multidrug-resistant Sa 180 tumors express different defense mechanisms whereas L 1210 tumors express only one defense mechanism (P-glycoprotein).

Animals↗
PubMedDate not supplied

Different roles for K+ channels in cisplatin-resistant cell lines argue against a critical role for these channels in cisplatin resistance.

Cisplatin resistance has been associated with altered K+ fluxes. Here, we focused our investigations on the detection of K+ channels in a series of cisplatin-resistant (CP-r) cells with increasing resistance and on the functional relationship of these K+ channels to resistance. Microarray analysis and confocal microscopy indicated that there was overexpression of the ether-a-gogo gene (HERG) and the inwardly rectifying potassium channel gene (TWIK) in a human epidermal KB and human liver BEL-7404 carcinoma cell line series selected for cisplatin resistance. With increased resistance, the plasma membrane potential, but not the mitochondrial membrane potential, also increases in these two series. For these reasons, we conducted cell proliferation studies in the presence of either antibodies directed against the detected K+ channels, omeprazole (a H+ pump inhibitor) or a specific inhibitor of the HERG channel (WAY-123398-A-5). The antibodies and omeprazole influenced cell growth only very slightly. The specific K+ channel blocker did not alter cisplatin resistance. We also observed that manipulation of K+ fluxes with antibodies and the H+ pump with omeprazole resulted in opposite effects on cisplatin resistance in these two cell lines. We conclude that K+ and H+ homeostasis are not critical factors in cisplatin resistance since they affect cisplatin resistance differently in KB and BEL-7404 cells.

Antineoplastic Agents↗
PubMed1990

Cross resistance studies with L1210 leukemia subline single and double resistant to cisplatin and iproplatin (CHIP).

Resistance to cisplatin (DDP) and/or iproplatin (CHIP) was induced in vitro in murine L1210 leukemia cells. Double-resistant sublines with combined resistance to both drugs were also developed. Cross resistance investigations with DDP, CHIP, oxoplatinum (OXO), carboplatin (CBDCA) and its quadrivalent derivative OXOCBDCA were performed in these resistant sublines. Lack of cross resistance between DDP and CHIP was found. A higher resistance to CHIP in the double-resistant sublines was observed. A multistep process in the development of resistance to this compound is supposed. The importance of the aminoligand and the role of different pharmacokinetics in the cross resistance are discussed.

Animals↗
PubMed1990

[Does exogenous airflow resistance reduce endogenous airway resistance in healthy persons?].

The aim of our investigation was to assess whether a preinserted model resistance of a certain magnitude will expand the airways during inspiration and thus reduce the resistance of the airways conceived as the sum of the value of the endogenous airway resistance without obstruction and the value of the exogenous pre-inserted model resistance. The model resistance and resistance of the airways were assessed by means of a whole-body plethysmograph. The airway resistance was evaluated in 10 healthy men during inspiration and expiration, using a dictated breathing pattern. When a model resistance of 0.75 kPa.l-1.s-1 was preinserted during dictated minute ventilation of 30 l.min-1 and an air current of 1 l.s-1 the value of the airway resistance increased markedly, as compared with the same breathing pattern without obstruction. The resistance increment was, however, by 30% lower than the expected value. At the same time the functional residual lung capacity increased.

Adult↗