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Biomedical subjects

E Martinez

Publications and source records attributed to E Martinez.

At least 127 records · Page 7Linked to original sources

Blood flow velocity waveforms of the abdominal arteries in appropriate- and small-for-gestational-age fetuses.

The aim of this study was to describe flow velocity waveforms of abdominal arteries in the appropriate- and small-for-gestational-age fetus. Splenic artery, superior mesenteric artery, hepatic artery and renal artery velocity waveforms were obtained from 57 appropriate-for-gestational-age and nine small-for-gestational-age fetuses with color flow Doppler ultrasonography. The pulsatility index was used to quantify the arterial waveforms. Repeated measure analysis of variance indicated significant differences in the pulsatility index values in both the appropriate-for-gestational-age and small-for-gestational-age fetuses. A multiple comparison test revealed a significantly lower value for the pulsatility index in the splenic artery when compared to that of the other vessels for both the appropriate- and small-for-gestational-age fetuses. In the small-for-gestational-age fetuses, a lower pulsatility index value was observed at the superior mesenteric artery level when compared to the renal artery. Because of its lower frequency of successful insonation, the hepatic artery was not considered for the analysis. In the normal fetus, the splenic artery had the lowest pulsatility index when compared to the other arteries we investigated. This difference remained in small-for-gestational-age fetuses, reflecting a lower vascular resistance at the fetal spleen in both normal and small-for-gestational-age fetuses. It appears that in small-for-gestational-age fetuses the renal artery has a higher pulsatility index than the superior mesenteric artery, suggesting a preferential distribution of blood flow to the bowel.

Abdomen↗

K-ras genotypes and prognosis in non-small-cell lung cancer.

BACKGROUND: Despite major advances in the treatment of many kinds of cancer over the past 25 years, the overall 5-year survival of non-small-cell lung cancer patients has scarcely improved. Even in stage I which has the best outcome long-term survival still falls below 70%. Since intriguing data suggest that the identification of genetic markers might allow prognosis to be assessed case by case. We were prompted to evaluate K-ras gene mutations as a putative prognostic marker in this neoplasm. MATERIALS AND METHODS: We used the polymerase chain reaction (PCR) followed by allele specific oligonucleotide (ASO) hybridization or single-strand conformation polymorphism (SSCP) assays, to detect K-ras mutations in DNA from formalin-fixed, paraffin-embedded tumor samples. K-ras mutations were examined in 192 stage I to IV non-small-cell lung cancer patients. RESULTS: K-ras mutations were detected in 51 of 192 of the cases studied (27%). All K-ras mutations detected by PCR/ASO hybridization were also identified by SSCP. In stage I disease, the median survival was 46 months in those patients whose tumors had no K-ras mutations and 21 months in those with aspartic acid and serine mutations at K-ras codon 12; in patients with stage IIIA disease, median survival time was 16 months in the K-ras negative group and 7 months in the aspartic acid and serine mutation group. No significant differences were observed for the remaining amino acid substitutions of K-ras, nor were they observed at all in more advanced disease. CONCLUSIONS: K-ras gene status has strong prognostic value in patients with stage IIIA non-small-cell lung cancer. The survival curve for patients with stage I and K-ras codon 12 aspartic or serine mutations is close to that of patients with stage IIIA without K-ras mutations. However, a non-small-cell lung cancer K-ras genotypic classification should be validated in larger studies.

Aged↗

Brain temperature modulations during global ischemia fail to influence extracellular lactate levels in rats.

BACKGROUND AND PURPOSE: While brain tissue lactate increases during cerebral ischemia and is known to be important in the pathogenesis of ischemic brain injury, patterns of extracellular lactate accumulation have been less well characterized, and the influence of brain temperature has not been previously investigated. Mild brain temperature modulations are known to affect the outcome of ischemia dramatically. This study examined changes of extracellular lactate during and after global cerebral ischemia, in which intraischemic brain temperature was held at either 30 degrees C, 37 degrees C, or 39 degrees C. METHODS: Halothane-anesthetized fasted male Wistar rats underwent 20 minutes of global cerebral ischemia produced by bilateral carotid artery occlusions plus systemic hypotension (40 to 50 mm Hg). Rectal temperature was maintained at 37 degrees C throughout, and intraischemic brain temperature was held at either 30 degrees C (n = 6), 37 degrees C (n = 5), or 39 degrees C (n = 5). Before and after the ischemic insult, brain temperature was maintained at 37 degrees C in all groups. A microdialysis cannula was implanted in the right dorsolateral striatum and perfused with Ringer's solution. Dialysate samples were collected at 10-minute intervals before, during, and after ischemia and were analyzed for lactate by enzymatic-fluorometric techniques. RESULTS: In all groups, extracellular lactate rose during ischemia and peaked at 10 to 30 minutes of recirculation. Maximal extracellular lactate elevations were sevenfold, eightfold, and eightfold above control in the 30 degrees C, 37 degrees C, 39 degrees C groups, respectively. Significant elevations with respect to control were observed in all groups at 10 to 30 minutes of recirculation. In the 30 degrees C group, these elevations above control were also significant at the 10- and 20-minute ischemic time points (P = .001). At 30 minutes of recirculation, however, lactate levels were lower in the 30 degrees C rats than in the other groups. CONCLUSIONS: These data provide evidence that extracellular lactate accumulation is not a crucial determinant of ischemic brain injury. Our results suggest that the increased lactate release during ischemia and the accelerated clearance of lactate during recirculation might contribute in part to the neuroprotection of intraischemic hypothermia.

Animals↗

The heart in the primary antiphospholipid syndrome.

Twenty consecutive female patients (mean age 30.1 years) with Primary Antiphospholipid Syndrome (PAPS) were studied cardiologically through noninvasive methods and compared with 20 age-and sex-matched healthy subjects. On physical examination 13/20 patients (65%) with PAPS had a valvular abnormality. In 12/20 (60%) patients with PAPS the ECG was abnormal, mainly due to sinus tachycardia in 5 (25%) and acute myocardial infarction in 3 (15%). In 7/20 patients with PAPS (35%) abnormal pulmonary findings were detected by X-ray and in 6 (30%) they were related to dilated pulmonary arch and pulmonary hypertension. In 14/20 cases (70%) with PAPS, abnormal echocardiographic findings were present; 13/20 patients (65%) had valvular complications attributable to PAPS: mitral insufficiency in six cases; mitral valve prolapse in three and aortic insufficiency in three. Two had pulmonary artery hypertension and two, tricuspid regurgitation (one attributable to PAPS). All valve diseases were regurgitant with mild to moderate hemodynamic repercussion. No stenotic lesions were detected. The mean mitral thickness in patients with mitral valve involvement was 7.0 +/- 1.6 mm, compared to 2.8 +/- 0.7 mm in patients with normal valves and 3.1 +/- 0.9 mm in the control group (p < 0.001). The mean aortic valve thickness in patients with aortic valve involvement was 3.6 +/- 0.5 mm compared to 1.5 +/- 0.3 mm in patients with normal valves and 1.4 +/- 0.4 in the control group (p < 0.001). None of the patients from the control group had valve disease (p < 0.0001). Three cases (15%) had pericardial effusion diagnosed by echo. Two patients with PAPS died during the 4.7 +/- 1.2 years of cardiological follow up, due to acute myocardial infarction and embolic cerebrovascular accident, respectively. In conclusion, cardiologic complications are common in PAPS, including left side regurgitant lesions that might be hemodynamically significant, acute myocardial infarction, pericardial effusion and pulmonary hypertension.

Adult↗

Overlapping transcription by RNA polymerases II and III of the Xenopus TFIIIA gene in somatic cells.

Xenopus TFIIIA gene expression is developmentally regulated. The per cell level of steady-state TFIIIA mRNA present in oocytes is drastically reduced (10(6)-fold) in adult somatic cells, suggesting regulation at the transcriptional level. This is supported by the presence of TFIIIA mRNAs with different 5'-ends in oocytes and in somatic cells, which suggests the presence of distinct cell-/stage-specific promoters, i.e. a strong oocyte-specific and a weak somatic-specific promoter. Here, by mapping the 5'-ends of TFIIIA RNAs found in Xenopus somatic cells, we document the activity not only of an upstream somatic-specific promoter, but also of a down-stream "oocyte-specific" promoter that gives rise to a minor population of somatic TFIIIA mRNAs initiated from the same transcription start site utilized in oocytes. This result explains the presence of an oocyte-type form of TFIIIA protein in somatic cells. Furthermore, by characterizing transcription from the Xenopus TFIIIA promoter in somatic cell nuclear extracts and comparing the in vitro transcription start sites with the 5'-ends of endogenous somatic TFIIIA transcripts in poly(A)+ and poly(A)- RNA fractions, we show that RNA polymerase III initiates at position -70 of the "oocyte-specific" core promoter and transcribes through the promoter and into the TFIIIA coding sequences in somatic cells. These results suggest a possible polymerase III transcription-mediated down-regulation of the oocyte-specific TFIIIA promoter in Xenopus somatic cells.

Animals↗

TATA-binding protein-associated factor(s) in TFIID function through the initiator to direct basal transcription from a TATA-less class II promoter.

The RNA polymerase II (Pol II) basal transcription factor TFIID is composed of the TATA box-binding protein (TBP) and several TBP-associated factors (TAFs). TBP is required for Pol II transcription from TATA-containing and TATA-less promoters. TATA-less promoters of mRNA-encoding genes often contain an initiator element at the transcription start site that is sufficient to direct accurate Pol II transcription. Here we address the mechanisms of functional TBP recruitment to the TATA-less initiator-dependent promoter of the mouse terminal deoxynucleotidyl transferase (TdT) gene. We show that the natural TATA-less TdT initiator region is sufficient to promote low levels of specific transcription in vitro and to direct the assembly of a stable preinitiation complex. In contrast to what is observed for several other promoters lacking a consensus TATA element, the TATA-binding activity of TBP is not required for the functional recruitment of TFIID to the natural TATA-less TdT and beta-polymerase promoters. Moreover, a comparison of TBP and highly purified epitope-tagged TFIID reveals that one or several TAFs function independently of distal regulatory elements to mediate initiator-directed (basal) transcription from the natural TATA-less TdT core promoter in crude nuclear extracts. Furthermore, by using a transcription system reconstituted with purified components, we present the first evidence for a basal transcription function of TAFs through the TdT initiator element. Altogether, our results suggest an alternative pathway for TFIID recruitment to initiator-dependent TATA-less class II promoters in which TAF(s) recruit TBP by interacting either directly or indirectly with the initiator region.

Base Sequence↗

Using the Hilbert uniqueness method in a reconstruction algorithm for electrical impedance tomography.

This paper presents a new version of the layer stripping algorithm in the sense that it works essentially by repeatedly stripping away the outermost layer of the medium after having determined the conductivity value in this layer. In order to stabilize the ill posed boundary value problem related to each layer, we base our algorithm on the Hilbert uniqueness method (HUM) and implement it with the boundary element method (BEM).

Algorithms↗

Assessment of sociocultural influences on the aesthetic body shape model in anorexia nervosa.

The prevailing aesthetic body shape model in our culture-that of slenderness-plays a leading role in eating disorders. A questionnaire (CIMEC) was prepared in an attempt to measure the influence of the agents and situations that transmit this model. The CIMEC questionnaire was applied to 59 anorectics and 59 normal girls matched by age and social class. Highly significant differences were found between the scores obtained from both groups, showing the patients to have a much greater involvement with the sociocultural agents encouraging weight loss. Factorial analysis of the discriminating items gave rise to 5 factors, each of which also significantly differentiated between anorectics and the normal group. The questionnaire, in two versions, showed satisfactory internal consistency and appropriate sensitivity and specificity and would serve as a sound instrument for screening. It calls into question the causal relationship between anorexia nervosa and sociocultural influences.

Adolescent↗

Effect of hyperthermia on glutamate release in ischemic penumbra after middle cerebral artery occlusion in rats.

Using microdialysis, we investigated the effect of hyperthermia on glutamate release in penumbral cortex of rats with 2 h of either normothermic (37 degrees C) or hyperthermic (39 degrees C) middle cerebral artery (MCA) occlusion. Penumbral blood flow (CBF) was measured by laser-Doppler flowmetry. CBF values (expressed as % preischemic values) in normothermic and hyperthermic groups were 24 +/- 11 (SD) and 24 +/- 16%, respectively, during ischemia and 102 +/- 81 and 147 +/- 79% during recirculation. Average extracellular glutamate in the hyperthermic group increased from a baseline of 7 +/- 2 microM to a peak of 217 +/- 184 microM at 10-20 min after onset of ischemia but returned to near baseline after 60 min. Glutamate in the normothermic group increased from 4 +/- 2 microM to a peak of 26 +/- 17 microM at 10-20 min after MCA occlusion but fell to near-baseline before recirculation. Thus reuptake systems appeared to remain functional in ischemic penumbra, even during hyperthermia. Ischemic glutamate release was significantly higher in hyperthermic than in normothermic rats: average values of individual rats' peak levels were 251 +/- 221 microM and 37 +/- 34 microM, respectively. The ischemic CBF threshold value for glutamate release was 33% of control in the normothermic group but 61% in the hyperthermic group.

Analysis of Variance↗

Psychophysiological reactions in humans during an open sea dive to 500 m with a hydrogen-helium-oxygen mixture.

Six commercial divers were investigated for neurological and psychosensorimotor responses during an open sea dive to 500 m with a hydrogen-helium-oxygen mixture containing 49% hydrogen. Results showed only moderate neurological symptoms of high-pressure nervous syndrome, whereas the narcotic effect of hydrogen was detectable, as investigated by psychosensorimotor tests. Nevertheless, the divers successfully carried out the main purpose of the operational dive, which was to prove the feasability of such diving methods by connecting specific elements of an offshore oil installation. Finally, these data support the hypothesis that hydrogen can alleviate some of the symptoms of the high-pressure nervous syndrome and can constitute a useful gas for commercial diving, as it decreases the density of the breathing mixture and therefore improves the living conditions, work, and comfort of the divers. Nevertheless, the present results underscore the relevance of research on individual susceptibility to pressure environment regardless of the composition of the breathing mixture.

Adult↗

Abnormalities of Doppler waveform of the hepatic veins in patients with chronic liver disease: correlation with histologic findings.

OBJECTIVE: Changes in the Doppler waveform of the hepatic veins are associated with chronic liver disease, particularly cirrhosis. We correlated abnormalities in Doppler waveforms of hepatic veins with histologic findings in the liver to determine the accuracy of Doppler imaging in the detection of cirrhosis. SUBJECTS AND METHODS: Fifty-two patients with chronic hepatitis C were examined prospectively and blindly by two sonographers. In the same session, a liver biopsy specimen was obtained from each patient and submitted to three independent pathologists for conventional interpretation and for grading of severity according to a predetermined scoring system. Duplex sonography of the hepatic veins was also performed in 50 control subjects. RESULTS: Abnormal hepatic vein waveforms were detected in 12 of 16 patients with cirrhosis and in eight of 36 patients without cirrhosis. However, histologic examination of the biopsy specimens showed that only two of the eight patients without cirrhosis had no significant abnormalities, other than mild portal inflammation. Abnormal waveforms were seen in no control subjects. We found a correlation between fibrosis and steatosis and abnormalities in the Doppler waveform of the hepatic veins (r = .50, p < .001). Portal inflammation, intralobular degeneration, and necrosis did not correlate with an abnormal waveform. CONCLUSION: Duplex sonography of the hepatic veins may be useful for studying liver disease associated with fibrosis and steatosis. In patients with well-compensated liver disease, flattening of the Doppler waveform of the hepatic vein suggests the presence of cirrhosis.

Female↗