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Biomedical subjects

R Favier

Publications and source records attributed to R Favier.

At least 19 recordsLinked to original sources
PubMed2006

High dietary sucrose triggers hyperinsulinemia, increases myocardial beta-oxidation, reduces glycolytic flux and delays post-ischemic contractile recovery.

Although the causal relationship between insulin resistance (IR) and hypertension is not fully resolved, the importance of IR in cardiovascular dysfunction is recognized. As IR may follow excess sucrose or fructose diet, the aim of this study was to test whether dietary starch substitution with sucrose results in myocardial dysfunction in energy substrate utilization and contractility during normoxic and post-ischemic conditions. Forty-eight male Wistar rats were randomly allocated to three diets, differing only in their starch to sucrose (S) ratio (13, 2 and 0 for the Low S, Middle S and High S groups, respectively), for 3 weeks. Developed pressure and rate x pressure product (RPP) were determined in Langendorff mode-perfused hearts. After 30 min stabilization, hearts were subjected to 25 min of total normothermic global ischemia, followed by 45-min reperfusion. Oxygen consumption, beta-oxidation rate (using 1-13C hexanoate and Isotopic Ratio Mass Spectrometry of CO2 produced in the coronary effluent) and flux of non-oxidative glycolysis were also evaluated. Although fasting plasma glucose levels were not affected by increased dietary sucrose, high sucrose intake resulted in increased plasma insulin levels, without significant rise in plasma triglyceride and free fatty acid concentrations. Sucrose-rich diet reduced pre-ischemic baseline measures of heart rate, RPP and non-oxidative glycolysis. During reperfusion, post-ischemic recovery of RPP was impaired in the Middle S and High S groups, as compared to Low S, mainly due to delayed recovery of developed pressure, which by 45 min of reperfusion eventually resumed levels matching Low S. At the start of reperfusion, delayed post-ischemic recovery of contractile function was accompanied by: (i) reduced lactate production; (ii) decreased lactate to pyruvate ratio; (iii) increased beta-oxidation; and (iv) depressed metabolic efficiency. In conclusion, sucrose rich-diet increased plasma insulin levels, in intact rat, and increased cardiac beta-oxidation and coronary flow-rate, but reduced glycolytic flux and contractility during normoxic baseline function of isolated perfused hearts. Sucrose rich-diet impaired early post-ischemic recovery of isolated heart cardiac mechanical function and further augmented cardiac beta-oxidation but reduced glycolytic and lactate flux.

Animals↗
PubMed2006

[The MYH9 syndrome: report of a new case with a new mutation of the MYH9 gene].

INTRODUCTION: Familial macrothrombocytopenias are a group of rare autosomal dominant platelet disorders including many syndromes in particular the May-Hegglin anomaly. They are characterized by thrombocytopenia with giant platelets and in some cases neutrophilic inclusions in peripheral blood granulocytes. Recently these different clinical entities have been demonstrated to be linked to mutations in the same gene, MYH9. CASE REPORT: We report in a young African woman presenting as a May-Hegglin anomaly a new mutation of the MYH9 gene. In regard of this case we present a brief review of the MYH9 syndrome. CONCLUSION: The MYH9 syndrome includes now several clinical entities who share some common clinical and biological characteristics such as a thrombocytopenia with giant platelets, presence or absence of other manifestations including Dohle like bodies, nephritis, sensorineural hearing loss, cataract. We report a new case in which a new mutation of the MYH9 gene was evidenced.

Adenine↗
PubMed2006

Chronic electrostimulation after nerve repair by self-anastomosis: effects on the size, the mechanical, histochemical and biochemical muscle properties.

This study tests the effects of chronic electrostimulation on denervated/reinnervated skeletal muscle in producing an optimal restoration of size and mechanical and histochemical properties. We compared tibialis anterior muscles in four groups of rats: in unoperated control (C) and 10 weeks following nerve lesion with suture (LS) in the absence of electrostimulation and in the presence of muscle stimulation with either a monophasic rectangular current (LSEm) or a biphasic modulated current (LSEb). The main results were (1) muscle atrophy was reduced in LSEm (-26%) while it was absent in LSEb groups (-8%); (2) the peak twitch amplitude decreased in LS and LSEm but not in LSEb groups, whereas the contraction time was shorter; (3) muscle reinnervation was associated with the emergence of type IIC fibers and proportions of types I, IIA and IIB fibers recovered in the superficial portion of LSEb muscles; (4) the ratio of oxidative to glycolytic activities decreased in the three groups with nerve injury and repair; however, this decrease was more accentuated in LSEm groups. We conclude that muscle electrostimulation following denervation and reinnervation tends to restore size and functional and histochemical properties during reinnervation better than is seen in unstimulated muscle.

Adenosine Triphosphatases↗
PubMed2005

Skeletal muscle HSP72 and norepinephrine response to static magnetic field in rat.

The present work was undertaken in order to investigate the noradrenergic system and skeletal muscle heat shock protein 72 (HSP72) response to static magnetic field (MF) in male rats. At thermoneutrality (25 degrees C), the exposition of rats 1 hour/day for 5 consecutive days to MF of 128 mT (m tesla) induced an increase in norepinephrine content in gastrocnemius muscle (+25%, p < 0.05) but had no effect at 67 mT (+1%, p > 0.05), indicating a stimulatory effect of sub-acute MF exposure on the noradrenergic system activity. Moreover, exposed rats to MF displayed a non-significant increase of HSP72 levels in gastrocnemius muscles (+29%, p > 0.05). The results indicate that noradrenergic systems in rat's gastrocnemius muscles are affected by MF exposure. Interestingly, sub-acute exposure insufficiency increased HSP72 levels in gastrocnemius muscles.

Animals↗
PubMed2005

Age-related sensitivity to lung oxidative stress during ozone exposure.

As immature and aged rats could be more sensitive to ozone (O(3))-linked lung oxidative stress we have attempted to shed more light on age-related susceptibility to O(3) with focusing our interest on lung mitochondrial respiration, reactive oxygen species (ROS) production and lung pro/antioxidant status. For this purpose, we exposed to fresh air or O(3) (500 ppb 12 h per day, for 7 days) 3 week- (immature), 6 month- (adult) and 20 month-old rats (aged). We determined, in lung, H(2)O(2) release by mitochondria, activities of major antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT)], heat shock protein (HSP(72)) content and 8-oxodG and dG-HNE nDNA contents, as DNA oxidative damage markers. In adult rats we did not observe alteration of pro/antioxidant status. In contrast to adults, immature rats exposed to O(3) higher nDNA 8-oxodG content and HSP(72) and without antioxidant enzymes modification. Aged rats displayed mild uncoupled lung mitochondria, increased SOD and GPx activities, and higher 8-oxodG content after O(3) exposure. Thus, in contrast to adults, immature and aged rats displayed lung oxidative stress after O(3) exposure. Higher sensitivity of immature to O(3) was partly related to ventilatory parameters and to the absence of antioxidant enzyme response. In aged rats, the increase in cytosolic SOD and GPx activities during O(3) exposure was not sufficient to prevent the impairment in mitochondrial function and accumulation in lung 8- oxodG. Finally, we showed that mitochondria seem not to be a major source of ROS under O(3) exposure.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2005

Adaptive changes in cardiac myosin heavy chain and creatine kinase isozymic profiles in rats native of altitude.

AIM: The developmental changes in the myosin heavy chain (MHC) profile, creatine kinase (CK) and lactate dehydrogenase (LDH) activities and isozyme expression occurring in heart were examined in rats born and living at altitude (La Paz, Bolivia, 3700 m, H(LP)) for 16 generations. We hypothesized that H(LP) rats respond differently to hypoxia than rats born and living at sea level, and secondarily exposed to altitude during 3 weeks (H(3W)). METHODS: The cardiac expression of MHC, CK and LDH was studied in left (LV) and right ventricle (RV) of H(LP) animals 1, 2, 3, 4 and 18 weeks after birth, and compared with control normoxic (C groups) and H(3W) animals. RESULTS: Rats secondarily exposed to hypoxia showed a lower alpha-MHC content than C or H(LP) rats in both LV and RV, 3 weeks after birth (P < 0.05), consistent with a delay in the maturation of the heart contractile phenotype. A global increase in the total CK activity was observed in the LV of H(3W) animals in comparison with C rats (P < 0.05), while no change was reported in H(LP) animals. In both ventricles, M-LDH activity was higher in H(3W) than in H(LP) and C rats (P < 0.05). The relative amount of alpha-MHC decreased by 20% in RV of 18-week-old H(LP) and H(3W) rats in comparison with C animals, consistent with the hypoxia-induced ventricular enlargement (P < 0.01). An increased activity of the foetal B-CK subunit was observed in both LV and RV of H(3W) rats in comparison with H(LP) and C animals (P < 0.05). CONCLUSION: This study demonstrates that rats native and living at altitude for several generations present some features relevant to genetic selection to altitude.

Adaptation, Physiological↗
PubMed2005

Molecular study of the hematopoietic zinc finger gene in three unrelated families with gray platelet syndrome.

Hematopoietic zinc finger (HZF) null mice have features reminiscent of patients with gray platelet syndrome (GPS), a rare inherited bleeding disorder. This similarity has suggested that HZF deregulation might be involved in the human disease. The sequence of the eight exons of the HZF gene as well as the study of its expression in blood samples from five patients belonging to three different families did not reveal any modifications when compared with healthy donors. This study indicates that HZF is unlikely to be responsible for GPS.

Blood Platelet Disorders↗
PubMed2004

Effects of aging on the cardiac remodeling induced by chronic high-altitude hypoxia in rat.

Effects of chronic high-altitude hypoxia on the remodeling of right ventricle were examined in three age groups of rats: 2, 6, and 18 mo. The extent of right ventricular (RV) hypertrophy (RVH) showed an age-associated diminution. RV cell size and pericellular fibrosis showed a significant increase in the 2- and 6-mo-old exposed rats but not in the 18-mo-old exposed rats compared with control. A hyperplasic response was underscored in the three exposed age groups but appeared less pronounced in the 18-mo-old rats. A significant decrease in the transient outward potassium current (Ito) density was observed in RV cell only in the 2-mo-old exposed group compared with the control group. In the control group, there was a clear tendency for Ito density to decrease as a function of age. The sustained outward current density was modified neither by the hypoxia condition nor by the age. Neither the cytochrome c oxidase activity nor the heat shock protein 72 content in the RV was altered after hypoxic exposure regardless of age. The norepinephrine content in the RV was significantly decreased in each age group exposed to hypoxia when compared with their age-matched control group. Our findings indicate that the remodeling (at morphological and electrophysiological levels) induced by chronic hypoxia in the RV can be decreased by the natural aging process.

Aging↗
PubMed2004

A simple cryogenic holder for tensile testing of soft biological tissues.

To overcome the difficulty of gripping soft biological materials for tensile test, a simple inexpensive cryogenic holder was developed which allows rapid (3 min) preparation of samples. It is made of 6 parts, built in a bakelite cloth, which is an excellent thermal isolant, and is used with rectangular (8x10(-2)x10(-2)x10(-2)m) samples. The holder with the sample inside is completely immersed in liquid nitrogen for 50 s. This duration allows the freezing of the sample ends on a 10(-2)m length and gives a very flat freezing surface throughout the sample cross section. The 6x10(-2)m central part of the sample remained at ambient temperature. Two parts of the holder help maintain the sample until its ends are vertically gripped in the tensile machine thus avoiding any sample deformation during this step. No pressure was applied on the frozen part of the sample by grips of the tensile machine and this avoids breaks in this region. The sample is fixed by adhesion forces (>1 kN) between its frozen parts and 2 pieces of the holder. The procedure has been successfully tested with bovine and salmon muscle samples and results show tensile breaks randomly distributed in the unfrozen region of the samples. Particular attention has been paid to obtain a very flat freezing surface so that the axial strain is equal throughout the sample and therefore any strain-related mechanical parameters can be accurately determined. The dimensions of the holder can be easily modified to fit other sample geometries and can be used with other biological materials.

Animals↗
PubMed2004

Metabolic and hormonal responses to exercise in the anti-obese Lou/C rats.

OBJECTIVE: Lou/C rats are a substrain of Wistar rats that exhibit a spontaneous low caloric intake and no development of obesity with age. Recently, we reported that Lou/C rats, compared to equally food-restricted Wistar counterparts, show lower resting levels of plasma glucose, epinephrine and liver glycogen. To further explore this metabolic particularity, we used exercise (swimming 60 min) as a situation of high-energy demand, to test the ability of Lou/C rats to maintain euglycemia. DESIGN: Male Lou/C rats (14-week-old) were compared to age-matched male Wistar rats fed either ad libitum (WAL) or Wistar rats whose food was chronically restricted (WFR) to the same caloric intake as the Lou/C rats. RESULTS: In spite of low liver glycogen stores ( approximately 50% of normal values), Lou/C rats were able to maintain euglycemia during exercise even though liver glycogen breakdown was blunted. The decreased use of glycogen during exercise in Lou/C rats was associated with a reduced epinephrine response compared to WFR animals. By contrast, WFR were also able to maintain euglycemia during exercise but at the expense of a significant (P<0.01) decrease in liver and muscle glycogen content. Plasma free fatty acid and glycerol concentrations were increased (P<0.01) similarly in all three groups during exercise. In a separate experiment conducted in isolated hepatocytes from 24 h fasted Lou/C and Wistar rats, it was found that gluconeogenic flux from glycerol was found to be significantly (P<0.01) higher in Lou/C than in Wistar rats (5.4+/-0.2 vs 3.7+/-0.1 micromol/min/g dry cells). Resting and exercising plasma leptin levels were also significantly (P<0.05) lower in Lou/C than in the two other groups. CONCLUSION: It is concluded that Lou/C rats have the particularity to rely spontaneously less on their liver glycogen stores to meet their energy demands during exercise while maintaining euglycemia.

3-Hydroxybutyric Acid↗
PubMed2004

Stimulation of HSP72 expression following ATP depletion and short-term exercise training in fast-twitch muscle.

AIM: Previous data have reported increases in HSP72 expression in skeletal muscles after endurance training but the physiological and biochemical signals that induce HSP72 accumulation remain largely unknown. In this study, we tested the hypothesis that energy status is a key regulatory event for HSP72 accumulation in skeletal muscles. METHODS: Reduction of high-energy phosphate levels was induced by supplementation with a creatine analogue, beta-guanidinopropionic acid (GPA) for 3 weeks while control rats received distilled water in the same conditions. Half of the animals were kept sedentary while the others were submitted to a short-term (2 weeks) training program on a treadmill (30 m min-1, 0% slope; 50-70 min day-1). RESULTS: GPA supplementation resulted in a large drop ( approximately 50%) in adenosine triphosphate (ATP) level in both fast and slow muscles whether the animals were trained or remained sedentary. HSP72 level did not change with GPA alone, but the training-induced increase in HSP72 level was strongly enhanced by superimposition of GPA diet in fast but not in slow skeletal muscles. The changes in HSP72 level were not linked to changes in fibre typology and/or mitochondrial capacities. CONCLUSIONS: The results of the present investigation indicate that levels of high-energy phosphate per se do not play a direct role in determining HSP72 level in skeletal muscles. However, during superimposition of training to GPA, then the adaptive strategy of fast-twitch muscle (e.g. plantaris) seems to be directed towards appearance of some properties of red, oxidative fibres (increase in oxidative capacities and HSP72 level).

Adenosine Triphosphate↗
PubMed2004

Skeletal muscle HSP72 response to mechanical unloading: influence of endurance training.

AIMS: It has been shown that increased contractile activity results in heat shock protein 72 (HSP72) accumulation in various skeletal muscles. By contrast, there is no consensus for muscle HSP72 response to muscle disuse for short duration (5-8 days). On the basis of a greater constitutive HSP72 expression in slow-twitch muscles we tested the hypothesis that mechanical unloading for a longer period (2 weeks) would affect this phenotype to a greater extent. Secondly, we evaluated the effects of a physiological muscle heat shock protein (HSP) enhancer (endurance training) on HSP response to unloading and muscle remodelling. METHODS: Adult male Wistar rats were assigned randomly to four groups: (1) sedentary weight-bearing; (2) hindlimb-unloaded (HU) via tail suspension for 2 week; (3) trained on a treadmill (6 week) and (4) trained 6 week and then HU for 2 week. RESULTS: Unloading resulted in a preferential atrophy of slow muscles [soleus (SOL), adductor longus (AL)] and a slow-to-fast fibre transition with no change in HSP72 level. HSP72 levels were significantly lower in fast muscles [extensor digitorum longus (EDL) and plantaris (PLA)], and did not change with mechanical unloading. Endurance training was accompanied by a small (SOL) or a large (EDL, PLA) increase in HSP72 level with no change in AL. Training-induced accumulation of HSP72 disappeared with subsequent unloading in the SOL and PLA whereas HSP72 content remained elevated in EDL. CONCLUSION: The results of this study indicate that (1) after 2 weeks of unloading no change occurred in HSP72 protein levels of slow-twitch muscles despite a slow-to-fast fibre transition; and (2) the training-induced increase of HSP72 content in skeletal muscles did not attenuate fibre transition.

Animals↗
PubMed2004

Analysis of biological phenotypes from 42 patients with inherited factor VII deficiency: can biological tests predict the bleeding risk?

BACKGROUND AND OBJECTIVES: Inherited factor VII (FVII) deficiency is a rare bleeding disorder characterized by a poor relationship between reported FVII clotting activity (FVII:C) and bleeding tendency. Our study was aimed at defining biological parameters that are possibly predictive for bleeding risk in this condition. DESIGN AND METHODS: Forty-two FVII-deficient patients (FVII:C <30%) were classified into two opposite clinical groups defined as severe and non-or-mild bleeders. For each patient, plasma samples were collected and then investigated for FVII:C (using a sensitive method and human recombinant thromboplastin as the reagent), FVII antigen, activated FVII coagulant activity (FVIIa:C) and the free-form of tissue factor pathway inhibitor. RESULTS: None of these tests could be used as highly accurate predictors of bleeding. Nevertheless, both FVII:C and FVIIa:C differed significantly between the two clinical groups. Using ROC-curve analysis, two critical values of 8% and 3mIU/mL for FVII:C and FVIIa:C, respectively, could be proposed to discriminate between severe bleeders and non-or-mild bleeders. INTERPRETATION AND CONCLUSIONS: A highly accurate diagnostic test for predicting bleeding tendency in inherited FVII deficiency still eludes definition, highlighting the fact that factors other than FVII itself interfere with the expression of bleeding phenotypes in this condition. Nevertheless, potential critical values using sensitive FVII:C and FVIIa:C methods may be useful in clinical laboratories for FVII-deficient patients. Those patients with FVII:C levels higher than 8% FVII:C or FVIIa:C higher than 3 mIU/mL, with no other hemostatic defect, seem to have a minimal risk of severe bleeding. Extended clinical studies are needed to support these findings.

Adolescent↗
PubMed2003

A novel homozygous splice junction mutation in GPIIb associated with alternative splicing, nonsense-mediated decay of GPIIb-mRNA, and type II Glanzmann's thrombasthenia.

This work reports the study of a patient suffering a bleeding disorder clinically diagnosed as Glanzmann's thrombasthenia (GT). Immunoblotting and flow cytometric analysis showed a low (</= 10% of control) platelet content of GPIIb-IIIa, confirming it was indeed a type II GT. The molecular genetic analysis of the proband revealed the presence of a homozygous G188A transition in GPIIb. This mutation alters the consensus sequence of the splice donor site of intron 1 changing arginine 63 for lysine (R63K). No other mutation than [G188A]GPIIb was found in the proband and her parents after complete analysis of GPIIb and GPIIIa coding sequences, and the promoter, 3'-UTR, and intronic flanking regions of GPIIb. The GT phenotype of the proband is the result of a limited availability of GPIIb-mRNA. The etiopathogenic role of the [G188A]GPIIb mutation is supported by the following observations: (i) both parents, who are heterozygous for the [G188A]GPIIb mutation, show a marked decrease in the platelet content of GPIIb-mRNA; (ii) exontrap analysis demonstrated that the G188A mutation leads to a marked reduction in the steady-state level of GPIIb-mRNA. The reduced availability of platelet GPIIb-mRNA associated with the G188A mutation seems to be caused by either inefficient RNA splicing or a preferred utilization of alternative intronic donor sites that generate an in-frame STOP codon with the result of activation of nonsense-mediated mRNA decay, or both.

Alternative Splicing↗
PubMed2002

[Imported malaria in children in 1999. Study of the Armand-Trousseau Hospital in Paris].

METHODS: Eighty children were treated at the hospital Armand-Trousseau (Paris, France) for a malaria attack from 1999-01-01 to 2000-02-01. RESULTS: The parasites were: Plasmodium falciparum: 87.5%, Plasmodium malariae: 12.6%, Plasmodium ovale: 10%, Plasmodium vivax: 6.3%. Mean age was 8.1 years (range: three months to 15 y). The origin of patients was: West Africa for 60 children, Central Africa for ten children and Comores for seven. Sixty-six patients suffered from common malaria attack and seven children were admitted with a presentation of severe malaria. The severe attacks were cerebral malaria for six cases, associated with severe anemia in five cases; the 7th child had a respiratory distress (ARDS) and died. The other six cases were cured without sequelae. Relapses were observed for eight patients: one after a severe cerebral malaria, six after a common P. falciparum attack, one after a P. ovale attack. Parasitemia was higher than in preceding years (mean 2.9%) and more than 5% in 11 cases, but without clear link with severity. Treatment by halofantrine with a single cure was followed by five relapses. None of those children received an effective prophylaxis during and after travel (55/80 without any prophylaxis). CONCLUSION: These data emphasize the importance of a good appraisal of criteria of severe malaria and lead to advice hospitalization of children with malaria in temperate zone.

Adolescent↗
PubMed2001

Newly recognized cellular abnormalities in the gray platelet syndrome.

The gray platelet syndrome (GPS) is a rare congenital bleeding disorder in which thrombocytopenia is associated with increased platelet size and decreased alpha-granule content. This report describes 3 new pediatric cases presenting with the classical platelet abnormalities of GPS within one family with normal parents. Examination of blood smears of the 3 patients demonstrated not only gray platelets, but also gray polymorphonuclear neutrophils (PMNs) with decreased or abnormally distributed components of secretory compartments (alkaline phosphatase, CD35, CD11b/CD18). Secondary granules were also decreased in number as assayed by immunoelectron microscopy. These data confirm that the secretory compartments in neutrophils were also deficient in this family. Megakaryocytes (MKs) were cultured from the peripheral blood CD34+ cells of the 3 patients for 14 days, in the presence of thrombopoietin and processed for immunoelectron microscopy. Although von Willebrand factor (vWF) was virtually undetectable in platelets, vWF immunolabeling was conspicuous in cultured maturing MKs, particularly within Golgi saccules, but instead of being packaged in alpha-granules, it was released into the demarcation membrane system. In contrast, P-selectin followed a more classical pathway. Double-labeling experiments confirmed that vWF was following an intracellular pathway distinct from the one of P-selectin. In these 3 new cases of GPS, the MKs appeared to abnormally process vWF, with secretion into the extracellular space instead of normal alpha-granule packaging. Furthermore, the secretory compartment of another blood cell line, the neutrophil, was also affected in this family of GPS.

Alkaline Phosphatase↗
PubMed2001

Determination of myeloid antigen expression on childhood acute lymphoblastic leukaemia cells: discrepancies using different monoclonal antibody clones.

Prospective clinical studies including large numbers of patients have led to the conclusion that co-expression of myeloid antigens in childhood acute lymphoblastic leukaemia (My+ ALL) does not have prognostic significance. However, reports of the frequency of My+ ALL in children vary widely across laboratories using different mAb clones and staining and analysing procedures. Taking two commonly accepted thresholds of positivity for myeloid antigens (20 and 30%), we analysed the immunoreactivity of the most widely employed mAb clones against CD13 (SJ1D1, L138 and My7) and CD33 (My9, P67.6 and D3HL60) and compared the proportions of My+ ALL detected by these clones in childhood ALL. The correlation between myeloid antigen expression and the presence of the t(12;21) translocation was analysed concomitantly in the same samples. The percentage of ALL cases positive for myeloid markers varied significantly depending on the mAb clone and the positive threshold. Among patients with B-ALL, the proportion of CD13+ ALL was significantly lower using SJ1D1 than using L138 or My7, while the proportion of CD33+ ALL was significantly higher for My9 than for P67.6 or D3HL60. Analysis of the co-expression of CD13 and CD33 on B-ALL cells using combinations of mAb clones showed that this frequency was either underestimated by the SJ1D1/D3HL60 or overestimated by the L138/P67.6 and My7/My9 combinations. A correlation between CD13/CD33 positivity and the t(12;21) translocation was uniformly observed in B-ALL patients for a positive threshold of 30%, whereas SJ1D1/D3HL60 detected no correlation between t(12;21) and CD13/CD33 positivity when the threshold was lowered to 20%. These data show that the mAb clones commonly used to detect the CD13 and CD33 surface antigens have variable immunoreactivity against childhood ALL cells, which may partly explain the conflicting reports concerning the prognostic significance of myeloid antigen expression in paediatric ALL and its association with different translocations. The present findings may also be of clinical importance for therapeutic choices.

Antibodies, Monoclonal↗