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J Roa

Publications and source records attributed to J Roa.

At least 37 records · Page 2Linked to original sources
PubMed2000

Xanthine oxidase released from reperfused hind limbs mediate kupffer cell activation, neutrophil sequestration, and hepatic oxidative stress in rats subjected to tourniquet shock.

We have shown previously that rats subjected to tourniquet shock develop an acute form of remote organ injury of the liver that is both Kupffer cell (KC) and polymorphonuclear (PMN) leukocyte dependent. Circulating plasma xanthine oxidase (XO) has been shown to be responsible for the development of endothelial dysfunction and for remote organ injury of the lung and intestine after ischemia-reperfusion protocols. We now hypothesize that XO is released from rat hind limbs upon reperfusion and that it is responsible for KC and PMN leukocyte activation in this shock model. Our results show that about 30% of rat gastrocnemius muscle xanthine dehydrogenase (XD) is converted to XO during the 5-h tourniquet period and that it is released into the femoral vein within 10 min of reperfusion. Total muscle xanthine oxidoreductase activity (XO + XD) decreases within 30 min of reperfusion and is paralleled by a corresponding increase in femoral vein lactic dehydrogenase. In addition, liver tissue XO increases significantly within 30 min of reperfusion without a corresponding conversion of endogenous XD. Conversion of hepatic XD becomes evident 60 min after reperfusion is initiated, as does XO, and alanine aminotransferase (ALT) release into the hepatic vein, presumably from damaged hepatocytes as a consequence of oxidative stress. Tissue myeloperoxidase activity also increases significantly after the 60-min reperfusion period. That XO mediates KC and PMN activation is supported by the following observations: a) the close relationships between plasma XO and the time courses of tumor necrosis factor-alpha TNFalpha release into the hepatic vein and colloidal carbon clearance by KCs; b) that colloidal carbon clearance, TNFalpha and ALT release, loss of tissue free thiols, lipid peroxidation (TBARS), and liver infiltration by PMN neutrophils can also be induced by the administration of exogenous XO to normal rats; and c) pretreatment of rats with allopurinol inhibits KC activation and liver leukocyte infiltration. These results suggest that XO, released from the ischemic limb on reperfusion, is taken up by the liver were it mediates KC and PMN neutrophil activation and thus contributes to the development of multiple system organ failure after hind limb reperfusion.

Alanine Transaminase↗
PubMed2000

[P53 gene mutation in gallbladder cancer].

BACKGROUND: Gallbladder cancer frequency and mortality renders it one of the most important neoplastic diseases in Chile. P53 tumor suppressor gene has been studied in most types of cancer, but there is scarce information about it in gallbladder cancer. AIM: To study the frequency of P53 gene mutation in gallbladder cancer in the ninth region of Chile. MATERIAL AND METHODS: In 25 pathological samples of gallbladder cancer, the direct amplification and sequencing of p53 gene exons 5,6,7,8-8 was possible. RESULTS: Seventeen punctual mutations were observed in 13 cases (52%). There were 10 transitions, 5 transversions, one insertion (codon 194) and one deletion (codon 186). Eight cases had mutations in exon 5, six had mutations in exon 6, two had mutations in exon 7 and one had mutations in exons 8-9. In 14 of 25 cases, gene p53 protein was positive. When immunohistochemical expression of gene p53 protein was positive in more than 20% of cells, there was a high correlation between genetic alterations and immunohistochemical expression of the protein, with a specificity, sensitivity, positive and negative predictive values over 80%. CONCLUSIONS: P53 gene mutation is observed in a high proportion of gallbladder cancers at it can be accurately detected with conventional immunohistochemical techniques. The importance of this gene in the genesis of this carcinoma should be determined studying preneoplastic lesions and early carcinomas.

Adenocarcinoma↗
PubMed1999

Role of Küpffer cells and PMN leukocytes in hepatic and systemic oxidative stress in rats subjected to tourniquet shock.

Küpffer cells (KCs) have been implicated in leukocyte recruitment and microvascular dysfunction associated with liver inflammation. The overall objective of this study was to assess the role of KCs and polymorphonuclear (PMN) leukocytes on the oxidative stress elicited in the liver as a consequence of hind limb reperfusion in rats subjected to tourniquet shock, a shock model that differs from other models in that hepatic injury is a consequence of remote organ damage. Colloidal carbon clearance from blood and its incorporation into KCs demonstrate that these cells are activated after the 2 h hind limb reperfusion period and that they are responsible for the observed oxidative stress and for PMN leukocyte recruitment and activation. Liver oxidative stress in this model is evidenced by increased liver tissue GSSG/GSH ratio, thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation, myeloperoxidase (MPO) activity, an index of tissue-associated neutrophil accumulation, and a significant loss in total tissue superoxide dismutase (SOD) activity. Mean arterial blood pressure (MAP), as well as plasma levels of alanine aminotransferase (ALT), an index of hepatic tissue injury, total SOD activity, plasma levels of alpha-tocopherol and beta-carotene, and total plasma nitrite are also affected as a consequence of KC activation after the 2 h hind limb reperfusion period. Inhibition of KC activity by gadolinium chloride (GdCl3) reverted most of the above alterations to values that do no differ from those found in control animals. These results support the hypothesis that hepatic and systemic oxidative stress elicited by hind limb reperfusion in rats subjected to tourniquet shock is both KC and PMN leukocyte dependent.

Alanine Transaminase↗
PubMed1998

Inhibition of nitric oxide synthesis aggravates hepatic oxidative stress and enhances superoxide dismutase inactivation in rats subjected to tourniquet shock.

The role of nitric oxide (NO) on liver oxidative stress and tissue injury in rats subjected to tourniquet shock was investigated. This shock model differs from others in that injury is a consequence of remote organ damage. Liver oxidative stress becomes evident after hind limb reperfusion, as evidenced by the loss of total tissue thiols; by increases in tissue oxidized glutathione (GSSG), lipid peroxidation (LPO), plasma aminotransferases (alanine aminotransferase (ALT) and (aspartate aminotransferase (AST)), and plasma nitrites; and by a 36% loss in total superoxide dismutase (SOD) activity. Portal blood flow is reduced by 54.1% after 2 h of hind limb reperfusion. Inhibition of NO synthesis with Nomega-nitro-L-arginine methyl ester or L-arginine methyl ester increased mean arterial blood pressure; further reduced portal blood flow; and aggravated liver injury as assessed by further loss in total thiols, increased LPO and GSSG content, and further increases in plasma ALT and AST. Total plasma nitrites were lower than in control animals, and total tissue SOD activity decreased by more than 80%. Treatment with the NO donor sodium nitroprusside reverted the decrease in portal blood flow and also reverted tissue thiol loss, LPO, and GSSG increases, as well as the loss of ALT and AST to plasma and of SOD activity to levels comparable to untreated control shock animals. As expected, plasma nitrites were greater than in tourniquet control animals. These data support the hypothesis that endogenous NO formation protects the rat liver from the consequences of oxidative stress elicited by hind limb reperfusion in rats subjected to tourniquet shock.

Alanine Transaminase↗
PubMed1997

p53 tumour suppressor gene protein expression in early and advanced gallbladder carcinoma.

AIMS: Gallbladder carcinoma is one of the most frequent malignant tumours occurring in Chile and the mortality rate in both sexes ranks among one of the highest in the world. Mutation of p53 tumour suppressor gene has been demonstrated in many tumours. Our aim was to determine protein expression of p53 gene in early and advanced gallbladder carcinoma. METHODS AND RESULTS: Protein expression of gene p53 was studied by immunohistochemical means in 191 gallbladder carcinomas (157 primary tumours, 34 metastases) and 25 controls. In 86 out of 191 cases (45%), protein expression of gene p53 was observed. Differences related to sex, age, or race were not observed. All gallbladder controls were negative. Twenty-five per cent of well-differentiated tumours were p53 positive, while moderate or poorly differentiated carcinomas reached 50% (P = 0.04). p53 expression was observed in 23.5% of early carcinomas and in 48.2% of advanced carcinomas (P = 0.01). No differences between primary tumours and metastasis were demonstrated. CONCLUSIONS: Protein expression of p53 tumour suppressor gene is observed in 45% of gallbladder carcinomas. The absence of expression in controls and in normal mucosa adjacent to tumours suggests its utility in differentiating atypical gallbladder epithelia from neoplastic lesions.

Carcinoma↗
PubMed1997

DNA ploidy pattern and tumor suppressor gene p53 expression in gallbladder carcinoma.

The relationship between p53 gene expression and DNA content in advanced gallbladder carcinoma was studied. Fifty-three cases of advanced gallbladder carcinoma (45 primary tumors and 8 metastases) were analyzed, p53 protein expression was determined by immunohistochemistry, DNA content was measured by cytophotometric techniques. Study subjects included 45 (85%) female and 8 male patients, with an overall mean age of 58.6 years. Positive staining for p53 protein was observed in 27 (51%) cases. In subserosal tumors, the expression was significantly less than that in tumors that reached the serosa (P = 0.01). Twenty-nine (55%) cases were diploid and 24 were aneuploid. Sixty-seven % of primary tumors were diploid, whereas 87% of metastases showed an aneuploid DNA content. Both diploid and aneuploid tumors were positive for the p53 protein in the same proportion, and p53 was also expressed equally in both primary and secondary tumors. In advanced gallbladder carcinoma, the expression of the p53 gene was earlier than the accumulation of abnormal quantities of chromosomal DNA in the tumor cells. The determination of these events as markers in preneoplastic lesions is warranted in gallbladder carcinogenesis.

Adenocarcinoma↗
PubMed1996

Preneoplastic lesions and gallbladder cancer: an estimate of the period required for progression.

BACKGROUND & AIMS: Scarce biological information exists about the importance of preneoplastic lesions in gallbladder cancer. The aim of this study was to estimate the time required for the sequence of dysplasia (DY) to carcinoma of the gallbladder. METHODS: Eighty-four cases of DY, 60 cases of early carcinomas (ECs), 181 cases of advanced carcinomas (ACs), and 121 cases of metastatic (ME) gallbladder cancer were analyzed. Age was used as the main parameter. Statistical analysis was performed using analysis of variance and multiple regression analysis. RESULTS: Among all cases, the mean age of female patients was lower than the mean age of male patients (P = 0.001). A significant difference in mean age between sexes by specific type of lesion was also observed (P < 0.001). The mean age was 46.3 years (SD, 16) in the DY group, 57.5 years (SD, 16.7) in the EC group, 59 (SD, 13.7) in the AC group, and 61.1 (SD, 12.1) in the ME group. Multiple regression analysis showed statistically significant differences (r = 0.386; P < 0.001) in the mean age of patients with dysplastic lesions compared with the carcinoma group. CONCLUSIONS: According to these observations, the period required to progress from dysplasia to advanced gallbladder carcinoma would be around 15 years, observing a continuum in the progression of the lesions.

Adult↗
PubMed1995

Ventilatory response to arm elevation. Its determinants and use in patients with chronic obstructive pulmonary disease.

During arm elevation, normal individuals predominantly recruit the diaphragm, whereas chronic obstructive pulmonary disease (COPD) patients use more the accessory inspiratory and abdominal expiratory muscles. To test that arm elevation is useful to study the ventilatory muscle response in COPD, and to define the factors that determine this response, we studied 34 patients (FEV1 0.95 +/- 0.08 L) during 2 min of arm elevation. Transnasal balloons were used to determine end-inspiratory and end-expiratory gastric (Pg), pleural (Ppl) and transdiaphragmatic (Pdi) pressures. The slope of delta Pg/delta Ppl (= Pgi - Pge/Ppli - Pple) was used to infer respiratory muscle recruitment. With linear regression, the delta Pg/delta Ppl during arm elevation significantly correlated with resting delta Pg/delta Ppl (r = 0.68), hyperinflation (FRC/TLC, r = 0.52), and diaphragmatic tension time index (TTIdi) (r = 0.47). With multiple regression, resting delta Pg/delta Ppl, percentage predicted FRC (FRC %pred) and TTIdi influenced delta Pg/delta Ppl during arm elevation (r = 0.84). Over the 2 min of arm elevation, the dependency upon resting breathing pattern decreased, while hyperinflation and TTIdi became increasingly important. Higher resting TTIdi values were associated with a faster and shallower breathing pattern (f/VT > or = 38) during arm elevation. We conclude that the pattern of respiratory muscle recruitment during arm elevation depends primarily on the resting breathing pattern. Over 2 min, the degree of hyperinflation and the force reserve of the diaphragm increasingly impact on the ability to recruit the diaphragm. Measurement of f/VT during arm elevation is useful to determine functional reserve of the diaphragm in severe COPD.

Arm↗
PubMed1995

Ibuprofen protects rat livers from oxygen-derived free radical-mediated injury after tourniquet shock.

Rats subjected to tourniquet shock suffer a severe form of circulatory shock, tissue and organ oxidative stress, and final multiple system organ failure (MSOF) and death of the animals within 24 h of tourniquet release. The oxidative damage observed in hind-limb muscle tissue after reperfusion does not by itself account for the final systemic and lethal MSOF. We have postulated that organ failure has its genesis in a primary perfusion abnormality, e.g. the hind limbs, which is followed by secondary hypoperfusion of other organs, such as the liver, as has been shown to be the case in several septic shock models. It has also been shown that injured or necrotic tissue can activate neutrophils, Küpffer cells, platelets, and both the complement and coagulation cascades. In turn, complement activation also leads to neutrophil and Küpffer cell activation as assessed by their capacity to generate oxyradicals. Herein we have evaluated the potential protective effect of ibuprofen on hepatic oxygen-derived free radical production, as well as its effects on both polymorphonuclear leucocyte (PMN) activation and liver infiltration. The protective effect of ibuprofen on hepatic oxidative injury was assessed by determining total thiol groups (SH), thiobarbituric acid-reactive substances (TBARS), and by the release of aspartic acid (AsT) and alanine (AIT) aminotransferases in control animals, in animals subjected to 5 h of tourniquets, and in animals after 2 h of hind-limb reperfusion. Liver infiltration by PMNs was determined by histology after staining with eosin-hematoxylin, and PMN activation by their capacity to reduce nitro blue tetrazolium (NBT).(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine Transaminase↗
PubMed1993

Transtracheal delivery of gas decreases the oxygen cost of breathing.

Transtracheally administered gases decrease inspired minute ventilation in both dogs and humans. To test if this is associated with a decrease in the oxygen cost of breathing and to evaluate subsequent changes in the breathing pattern, we studied five patients with chronic respiratory diseases while they spontaneously breathed air and different flows of tracheally administered gases. In a blinded crossover design, the gas consisted of either oxygen or air at 2, 4, and 6 L/min. Oxygen cost of breathing was estimated by the calculation of pleural pressure-time index (PPTI). The pattern of breathing was evaluated utilizing the tension time index for the diaphragm (TTdi). There were significant decreases in PPTI when the patients received 2, 4, and 6 L/min of transtracheal oxygen or air. TTdi also decreased as gas flow increased. This drop was significant at 6 L/min flow for both gases. We conclude that transtracheally administered gas reduces the oxygen cost of breathing. It also changes the respiratory pattern of the diaphragm to a less demanding pattern. This may offer an alternative form of treatment to rest overworked respiratory muscles.

Aged↗
PubMed1993

Estimation of ventilatory reserve by stair climbing. A study in patients with chronic airflow obstruction.

Clinicians and surgeons have used the subjective response to the climb of "one or two flights of stairs" to assess the "reserve" of patients with chronic airflow obstruction (CAO). Very little objective data exist regarding the metabolic and ventilatory cost for any level of stair climbing in these patients. Therefore, this study was designed to evaluate the use of symptom-limited stair climbing as a simple method to estimate the peak oxygen uptake (VO2) and minute ventilation (VE) in patients with CAO. We studied 31 men with varying degrees of CAO, who climbed stairs until they stopped at their symptom-limited maximum. During this climb, timed expired gas was intermittently collected and analyzed, and oxygen saturation and heart and respiratory rates were recorded. The patients achieved 81 +/- 14 percent of their predicted maximal heart rate and 90 +/- 27 percent of their predicted maximal VE. The number of steps or flights climbed correlated linearly with peak VO2 (r = 0.72, p < 0.01) and with VE (r = 0.7, p < 0.01). Stair climbing peak VE, VO2, heart and respiratory rate correlated well with those achieved during standard leg cycle ergometry. The mean +/- SD number of flights climbed was 4.2 +/- 1.7 with most patients (87%) reaching at least 3 flights (54 steps). The group of eight patients with very severe CAO (FEV1 < 0.9 L) climbed 3.4 +/- 0.9 flights (61 +/- 16 steps). We conclude that a symptom-limited maximal stair climb helps estimate peak VO2 and VE in patients with CAO. The frequently advocated test to climb one to two flights to evaluate cardiopulmonary reserve is not adequate for most patients with CAO. Symptom-limited maximal stair climbing is a simple, inexpensive and readily available test that may be used to evaluate the cardiopulmonary reserve of stable patients with CAO.

Adult↗
PubMed1991

[Ultrasonographic evaluation of bladder volume].

Twelve women of gynecologic dispensary of Hospital del Salvador are studied, making measurements of several ultrasound parameters of urinary bladder (diameters and perimeters), with known volumes instilled through catheterization. The results are mathematically and statistically studied with computer getting a formula of easy management to obtain the vesical volume. This formula is advantageously compared with others of literature. Advantages of ultrasound measurement of vesical volume are stressed in patients with uro-gynecologic pathology.

Adult↗
PubMed1990

Hypothyroidism and pleural effusions.

Serous effusions have been thought to be an unusual complication of hypothyroidism and most commonly have been associated with ascites, pericardial fluid and heart failure. Pleural fluid as an isolated finding in hypothyroidism is apparently rare and complete analysis of these hypothyroid-associated pleural effusions has not been described. To determine the frequency, chemical characteristics and clinical associations of hypothyroidism and pleural effusions, the medical records of 128 patients with hypothyroidism (defined by an increased serum TSH concentration) were reviewed. The majority of effusions in patients with hypothyroidism were due to other diseases. Effusions solely due to hypothyroidism appeared to be a real entity. These effusions were borderline between exudates and transudates and showed little evidence of inflammation.

Aged↗
PubMed1989

Cocaine exposure among children seen at a pediatric hospital.

The results of 1,680 consecutive urine and serum toxicologic screens from 1,120 patients, performed in a children's hospital during a 19-month period were surveyed. Among this sample, 52 (4.6%) patients had specimens that contained cocaine and/or metabolite. Fifteen specimens contained ethanol, a benzodiazepine, or a narcotic in addition to cocaine. Four patients were neonates, whereas three were infants from 1 to 7 months of age. The remaining 45 patients were adolescents with a mean age of 19 years. Among the adolescents, 11 had a significant chronic illness. In 19 patients (37%), cocaine exposure was unsuspected until the results of testing for toxic substances were known. The reasons for hospital evaluation included depression/attempted suicide in 19 patients, seizure in five, chest pain in 5, motor vehicle accident in three, syncope in three, abdominal pain in two, pneumomediastinum in two, accidental self-immolation in one, and apnea in one. Twenty patients required medical hospitalization for a total of 268 patient-days. One patient, a neonate, died. There is a striking prevalence of cocaine exposure in the pediatric age group. Among adolescents, this exposure may occur despite the presence of chronic illness. Although the age distribution appears bimodal, infants and young children may also have unsuspected exposure to this toxin. Greater awareness of cocaine exposure in childhood will be needed by primary and tertiary care pediatricians to identify affected children and provide appropriate intervention.

Adolescent↗
PubMed1988

The actions of phenol and pentachlorophenol (PCP) on axonal conduction, ganglionic synaptic transmission, and the effect of pH changes.

1. A comparison of phenol, pentachlorophenol (PCP) and procaine effects on axonal conduction were studied in vitro in the sciatic nerves of toad. PCP and procaine were respectively 6.3 and 3.15 times more potent than phenol in blocking axonal conduction. 2. Effects of PCP on synaptic transmission were studied in vitro in the eighth sympathetic ganglion of toad. 3. Axonal conduction block and synaptic transmission block by phenol was reversible, but not that by PCP. 4. When the PCP ionization was increased, a lesser per cent reached the site of action, reducing its capacity to block the axonal conduction and ganglionic transmission. 5. PCP plus, 3,4-Diaminopyridine (3,4-DAP) decreased synaptic transmission block from post-ganglionic compound action potential (CAP) responses to supramaximal preganglionic stimulation.

4-Aminopyridine↗
PubMed1986

The effects of hemicholinium-3 (Hc-3) during tetanic (TP) and posttetanic potentiation (PTP) on sympathetic ganglion.

An electrophysiological analysis has been made of the synaptic plasticity in the eighth sympathetic ganglion of the toad. The mean amplitude of Compound Action Potential (CAP) recorded extracellularly was taken as a measure of the synaptic transmission. Repetitive stimulation of the preganglionic axonal fibers at 50 Hz for 40 seconds in the presence of Hc-3 led to facilitatory and depressant actions on ganglionic synaptic transmission. Hc-3 in the presence of elevated extracellular Ca2+ concentration (5.4 mM) increased Tetanic Potentiation (TP) and Posttetanic Potentiation (PTP) on eighth sympathetic ganglion. Hc-3 plus 3,4-diaminopyridine (3,4-DAP) increased synaptic transmission, TP, and PTP from postganglionic CAP responses to supramaximal preganglionic stimulation.

4-Aminopyridine↗