Lightning injuries in a pregnant woman: a case report and review of the literature.
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Adult↗
Biomedical subjects
J Meléndez
Publications and source records attributed to J Meléndez.
A phase II study of gemcitabine and cisplatin combination as induction chemotherapy for untreated locally advanced cervical carcinoma.
BACKGROUND: Cisplatin-based chemoradiation for locally advanced cervical carcinoma is now the standard of care for most patients with cervical carcinoma. However, induction chemotherapy followed by surgery, particularly with newer agents or combinations remains to be explored. This study was undertaken to evaluate the antitumor activity and toxicity of gemcitabine in combination with cisplatin for untreated locally advanced cervical carcinoma. PATIENTS AND METHODS: Open-label, single center, phase II, non-randomized study of neoadjuvant gemcitabine plus cisplatin. Forty-one patients with histologic diagnosis of cervical carcinoma, with no previous treatment and staged as IB2 to IIIB, were treated with three 21-day courses of cisplatin 100 mg/m2 day I and gemcitabine 1000 mg/m2 days 1 and 8, followed by locoregional treatment with either surgery or concomitant chemoradiation. Response and toxicity were evaluated before each course and at the end of chemotherapy. RESULTS: All patients were evaluated for toxicity and 40 for response. The overall objective response rate was 95% (95% confidence interval (CI): 88%-100%) being complete in 3 patients (7.5%) and partial in 35 (87.5%). A complete pathological response was found in 6 (26%) of the 23 patients that underwent surgery. Granulocytopenia grades 3-4 occurred in 13.8% and 3.4% of the courses, respectively, whereas non-hematological toxicity was mild. CONCLUSIONS: Induction chemotherapy with the combination of gemcitabine and cisplatin is highly active for untreated cervical cancer patients and has an acceptable toxicity profile.
Adenocarcinoma↗
Is decreased HIV-1 infectivity of placental macrophages caused by high levels of beta-chemokines?
The objective of this study was to determine the effect of beta-chemokine secretion on HIV infection of placental macrophages (HF) as compared to monocyte-derived macrophages (MDM). For this purpose, we measured chemokine production in supematants of LPS stimulated and unstimulated HF and MDM. LPS stimulated cultures produced 3 to 10 times higher levels of MIP-1alpha, MIP-1beta and RANTES than unstimulated cultures. The level of MIP-1beta was the highest of the three chemokines secreted upon stimulation of HF cells. Cell cultures were inoculated with HIV-BaL, a R5 virus, and tested for p24 antigen and chemokine production at days 5 and 10 post-infection (P.I.). We did not find significant differences in the level of chemokines produced by HIV-1-infected and uninfected MDM and HF cells. However, significant differences were found in p24 antigen released by unstimulated and LPS stimulated cells. In contrast to HF cells, MDM cultures showed a significant inhibition of p24 antigen production when cells were stimulated with LPS prior to infection. HF cells were less susceptible to HIV-1 infection than MDM, and chemokines produced by HF cells did not result in further inhibition of HIV-1 infection. We found that in contrast to MDM, decreased susceptibility HF cells to HIV infection is not due to increased levels of chemokines, but to decreased HIV-1 coreceptor expression.
CD4 Antigens↗
Extracellular regulated kinase, but not protein kinase C, is an antiapoptotic signal of insulin-like growth factor-1 on cultured cardiac myocytes.
This study aims to elucidate the signaling pathway for insulin-like growth factor-1 (IGF-1) in cultured neonatal rat cardiomyocytes and particularly the role of IGF-1 in cardiac apoptosis. IGF-1 stimulated polyphosphoinositide turnover, translocation of protein kinase C (PKC) isoforms (alpha, epsilon, and delta) from the soluble to the particulate fraction, activation of phospholipid-dependent and Ca(2+)-, phospholipid-dependent PKC, and activation of the extracellular-regulated kinase (ERK). IGF-1 attenuated sorbitol-induced cardiomyocyte viability and nuclear DNA fragmentation. These antiapoptotic effects of IGF-1 were blocked by PD-098059 (an MEK inhibitor) but not by bisindolylmaleimide I (BIM, a specific PKC inhibitor). The ERK pathway may therefore be an important component in the mechanism whereby IGF-1 exerts its antiapoptotic effect on the cardiomyocyte.
Animals↗
Cloning and expression of guinea pig TIMP-2. Expression in normal and hyperoxic lung injury.
Tissue inhibitors of metalloproteinases (TIMPs) play a key regulatory role in extracellular matrix remodeling. By screening a lung library with a human TIMP-2 cDNA probe, we have isolated the cDNA corresponding to guinea pig TIMP-2. The 3.5-kb cDNA presents an open reading frame that predicts a protein of 220 amino acids showing 97.2, 96.8, 97.2, and 77.3% overall identity with human, mouse, rat, and chicken TIMP-2, respectively. Guinea pig TIMP-2 cDNA was expressed in CHO-K1 cells, showing a protein with the expected molecular weight and activity. Northern blot analysis revealed TIMP-2 expression in brain, kidney, intestine, spleen, heart, and lung. Transforming growth factor-beta downregulated TIMP-2 mRNA in guinea pig lung fibroblasts, whereas a variety of other stimuli showed no effect. In normal and hyperoxia-exposed lungs, TIMP-2 mRNA was mainly localized in alveolar macrophages and epithelial cells. No quantitative differences were found by Northern blot. These results confirm that TIMP-2 is highly conserved in mammals and largely expressed in lungs.
Amino Acid Sequence↗
Surfactant components modulate fibroblast apoptosis and type I collagen and collagenase-1 expression.
During lung injury, fibroblasts migrate into the alveolar spaces where they can be exposed to pulmonary surfactant. We examined the effects of Survanta and surfactant protein A (SP-A) on fibroblast growth and apoptosis and on type I collagen, collagenase-1, and tissue inhibitor of metalloproteinase (TIMP)-1 expression. Lung fibroblasts were treated with 100, 500, and 1,000 microg/ml of Survanta; 10, 50, and 100 microg/ml of SP-A; and 500 microg/ml of Survanta plus 50 microg/ml of SP-A. Growth rate was evaluated by a formazan-based chromogenic assay, apoptosis was evaluated by DNA end labeling and ELISA, and collagen, collagenase-1, and TIMP-1 were evaluated by Northern blotting. Survanta provoked fibroblast apoptosis, induced collagenase-1 expression, and decreased type I collagen affecting mRNA stability approximately 10-fold as assessed with the use of actinomycin D. Collagen synthesis and collagenase activity paralleled the gene expression results. SP-A increased collagen expression approximately 2-fold and had no effect on collagenase-1, TIMP-1, or growth rate. When fibroblasts were exposed to a combination of Survanta plus SP-A, the effects of Survanta were partially reversed. These findings suggest that surfactant lipids may protect against intraluminal fibrogenesis by inducing fibroblast apoptosis and decreasing collagen accumulation.
Apoptosis↗
Effects of antihypertensive treatment on cardiac IGF-1 during prevention of ventricular hypertrophy in the rat.
There is some evidence that cardiac rather than circulating insulin-like growth factor-1 (IGF-1) levels contribute to the development of renovascular hypertensive left ventricular hypertrophy (LVH), remaining unknown the effects of antihypertensive drugs on IGF-1 levels. We have assessed here the preventive effects of enalapril, losartan, propanolol and alpha-methyldopa on left ventricle (LV) and circulating IGF-1 levels in a rat model of hypertension and LVH (Goldblatt, GB). Our results show that relative LV mass and the LV content of IGF-1 were significantly lower with all antihypertensive drugs in GB rats (p<0.001). Serum concentrations of IGF-1 were lower in GB rats treated with enalapril, alpha-methyldopa and propanolol (p<0.01), but not in those treated with losartan. These results support the hypothesis that local rather than seric IGF-1 contributes to the development of left ventricular hypertrophy induced by pressure overload in the rat.
Animals↗
Selective increase in cardiac IGF-1 in a rat model of ventricular hypertrophy.
There is evidence that insulin-like growth factor-1 (IGF-1) plays a role in the development of left ventricular hypertrophy, but it is uncertain whether cardiac IGF-1 changes before or after hypertension is established, and whether circulating IGF-1 are involved in cardiac hypertrophy. We have investigated changes in circulating and left ventricular IGF-1 and in the expression of the IGF-1 gene in the left ventricles of rats during the development of hypertensive left ventricular hypertrophy (Goldblatt model; 2 kidney-1 clamped). Our results show that the left ventricular contents of IGF-1 and its mRNA were increased at one and four weeks of hypertension and hypertrophy, and that both returned to control values after nine weeks. These changes were unrelated to the seric concentration of IGF-1 in the blood. These results show that local rather than circulating IGF-1 levels contributed to the development of renovascular hypertensive left ventricular hypertrophy.
Animals↗
Gelatinases A and B are up-regulated in rat lungs by subacute hyperoxia: pathogenetic implications.
Subacute hyperoxia may cause basement membrane disruption and subsequent fibrosis. To test the role of extracellular matrix degradation in hyperoxic damage, we analyzed the expression of gelatinases A and B and tissue inhibitors of metalloproteinases (TIMP)-1 and TIMP-2 in rats exposed to 85% O2. Oxygen-exposed rats were studied at 1, 3, 5, and 7 days, and compared with air-breathing rats. Lung mRNAs assayed by Northern and in situ hybridization showed an up-regulation of lung gelatinases A and B from the 3rd day on. Gelatinase A was localized in alveolar macrophages and in interstitial and alveolar epithelial cells. Gelatinase B mRNA and protein were localized in macrophages and bronchiolar and alveolar epithelial cells. Increased gelatinase A and B activities were demonstrated in bronchoalveolar lavage. TIMP-1 and TIMP-2 were constitutively expressed, and only TIMP-1 displayed a moderate increase with hyperoxia. To elucidate transcriptional mechanisms for increased gelatinase B expression after hyperoxia, nuclear transcription factor-kappabeta activation was explored. Oxidative stress significantly increased the lung expression of nuclear transcription factor-kappabeta (p65) protein, and nuclear transcription factor-kappabeta activation and increased levels of gelatinases A and B were found in isolated type II alveolar cells obtained from hyperoxic rats. Conceivably, subacute hyperoxia induces excessive gelatinase activity, which may contribute to lung damage.
Acute Disease↗
Factors influencing the sequelae of high tension electrical injuries.
The purpose of this study was to conduct a retrospective analysis of the clinical spectrum, treatment and morbidity of the patients who have suffered high tension electrical injuries with current passage through their body (59 patients). Voltage, localization and surgical treatment seem to be the main factors influencing the lesion and the morbidity. The following points were considered: (1) Is there any relation between known factors such as voltage and the localization of the points of contact with the incidence and the type of complications and sequelae? (2) Do the observations show that wound management and the excision of dead tissues is the most adequate? From factors studied in our patients (voltage, point of entry and pathway of current, associated multiple trauma or flame burns, surgical treatment) we have found that the voltage does not have any influence on the severity of the wound nor on the percentage of sequelae (cataracts, limb amputation, neurologic complications). The current pathway, as well as its points of entry, does not show any relation with the presence of renal failure, cardiac arrhythmia and cataracts. A clear relationship between the point of entry of the current and the appearance of neurologic injury with presence of paralysis and permanent regional anaesthesia at the same level was observed. The presence of associated burns was not related to any other complications or sequelae. For those patients whose length of contact has been shorter we find a lower rate of amputations despite having associated limb fractures. Fasciotomy incisions appear to confer benefit as this series shows that this procedure decreases the rate of limb amputations.
Acute Kidney Injury↗
Profile of HIV patients with and without bacterial endocarditis.
Bacterial endocarditis (BE) is a serious medical condition seen in the injecting drug users (IDU) with or without HIV. Studies report a low prevalence of BE in HIV/AIDS patients and the clinical manifestations have been considered non-specific making early diagnosis difficult. The HIV Registry in our Center has recruited 1500 HIV/AIDS cases since May 1992. We decided to review and compare the clinical and epidemiological variables of patients admitted to the Registry with BE (23 pts) and without. Fever, sweats and weight loss were seen most frequent in BE patients as well as meningitis and pneumonia. The majority of the patients were IDU. Staphylococcus aureus was the most common pathogen. The tricuspid valve was the most affected valve. Mild insufficiency was the rule. The mortality in BE patients was higher than in the total group. The triad of IDU, the described constitutional signs and symptoms and coexisting meningitis and/or pneumonia, in the HIV/AIDS patient, should alert the physician to the presence of BE particularly in the outpatient setting were a more aggressive diagnostic approach should probably be attempted.
Adult↗
Cyclic AMP-dependent protein kinase and mechanical heart function in ventricular hypertrophy induced by pressure overload or secondary to myocardial infarction.
The role of cyclic AMP-dependent protein kinase (PKA) and systolic function during the development of left ventricular hypertrophy (LVH) still remain uncertain. The aim of this work is to study PkA activity and mechanical heart function in two experimental heart hypertrophy models: specifically, one induced by pressure overload (Goldblatt model: two kidneys, one clamped, Gb); and another secondary to myocardial infarction (MI) generated by ligation of the left coronary artery. Hypertension in the Gb group becomes evident by the third and fourth week after surgery without any significant change in the corresponding sham group. The myocardial infarction group did not show any change in systolic pressure. Different degrees of LVH for the two experimental models were observed. Relative cardiac mass (RCM) and relative ventricular mass (RVM) increased 23 and 16%, respectively, above the sham-operated rats in MI group (P < 0.05). For the pressure overload model, the increase values were 42 and 44%, respectively (P < 0.05). Left ventricular hypertrophy was also evaluated through quantitative changes in cardiac beta-myosin heavy chain which agreed with morphometric studies in Goldblatt rats. Ventricular PKA activity did not show any significant difference with respect to the sham-operated group after induction of pressure overload. For the MI model, ventricular PKA activity changed only at day 7 post-infarction with a 289% increase above the sham-operated group (P < 0.05). The absence of activation of ventricular PKA after constriction of renal artery or myocardial infarction was also corroborated by the patterns of PKA-dependent phosphorylated proteins. While force-generating capacity was increased, there was no change in ventricular PKA activity, indicating that there is no relation between this enzyme and systolic stress-strain regression lines in either pressure overload or myocardial infarction conditions. Cyclic AMP-dependent protein kinase activity had no relation with development of cardiac hypertrophy in the two experimental models of LVH. These findings contribute to the hypothesis for a multifactorial interaction of different intracellular biochemical and molecular mechanisms in the genesis of cardiac hypertrophy.
Animals↗
Effect of melatonin on beta-tubulin and MAP2 expression in NIE-115 cells.
Physiological concentrations of the pineal hormone melatonin induce an increase of microtubules in neuroblastoma NIE-115 cells. This effect is due to an increase in the polymerization state of tubulin. Concomitantly, higher levels of soluble beta-tubulin are present in the treated cells. Unexpectedly, no significant changes in the levels of beta-tubulin or its mRNA occur in the presence of melatonin reflecting perhaps a strict control of its steady state in a physiological context. In contrast, higher amounts of microtubule-associated-protein 2 are found when the cells are exposed to melatonin. These findings support the idea that tubulin polymerization process is one of the targets of melatonin action. Furthermore, our results might explain the increase in the length and number of neurites present in these cells when they are treated with this hormone.
Biopolymers↗
Enhancement of the Pockels component in the electroreflectance spectra of quantum wells.
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Journal Article↗
Regulation of apo B mRNA expression in liver and intestine during liver regeneration induced by CCl4.
Acute liver damage in CCl4-treated rats is accompanied by a decrease of the lipoprotein particles HDL and VLDL. However, once the regenerative process has occurred both lipoproteins increase to values higher than control. In this study we have further analyzed the molecular mechanism involved in the induction of the hyperlipidemia during liver regeneration in rats treated with CCl4. The expression of apolipoprotein (apo) B gene at the apo B mRNA editing level has been analyzed during the regenerative process of the liver. The percent of apo B-48 and apo B-100 mRNA was determined and compared to the plasma levels of LDL and VLDL. These results confirm the existence of two different hyperlipidemic stages during liver regeneration. Total apo B mRNA is increased in liver and intestine during both hyperlipidemic stages. The ratio of apo B-100/apo B-48 mRNA remains constant during the first hyperlipidemic stage but the serum levels of VLDL are decreased. Then once the regenerative process has occurred, the steady-state levels of total apo B mRNA remaining, increased with higher amounts of apo B-100 than apo B-48. At this experimental time point the high levels of total apo B mRNA correlate with serum levels of VLDL that are significantly higher than control. These results indicate that apo B gene expression is induced at the mRNA level in liver and intestine during liver regeneration affecting the apo B mRNA editing mechanism in a complex manner and suggest further regulation at the translational or post-translational level.
Animals↗
Method for analysis of polymer-supported organic compounds using mass spectrometry direct insertion.
A new approach on the use of mass spectrometry direct-insertion and a quadrupole detector for analysis of organic compounds supported in solid phase has been developed. This is a simple and efficient method based on cleavage due to the thermal-instability of the benzylic group of most commercial resins. The cleavage of supported compounds takes place in the spectrometer as a consequence of the high temperature in the instrument's chamber. These compounds are detected using a similar fragmentation pattern and a molecular ion corresponding to the same compound obtained by traditional synthesis. Polymer degradation fragments do not interfere with the spectrum interpretation, because only a few peaks and low intensities are detected. We report here the identification of different types of compounds supported in Merrifield resin, such as bis-o-aminobenzamides and simple aromatic and aliphatic compounds, using this new approach.
Journal Article↗
[Ectopic liver located in the gallbladder (author's transl)].
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Child↗