Exposure to inhaled particulate matter activates early markers of oxidative stress, inflammation and unfolded protein response in rat striatum.

To study central nervous system airborne PM related subchronic toxicity, SD male rats were exposed for eight weeks to either coarse (32 µg/m³), fine (178 µg/m³) or ultrafine (107 µg/m³) concentrated PM or filtered air. Different brain regions (olfactory bulb, frontal cortex, striatum and hippocampus), were harvested from the rats following exposure to airborne PM. Subsequently, prooxidant (HO-1 and SOD-2), and inflammatory markers (IL-1ß and TNFα), apoptotic (caspase 3), and unfolded protein response (UPR) markers (XBP-1S and BiP), were also measured using real-time PCR. Activation of nuclear transcription factors Nrf-2 and NF-κB, associated with antioxidant and inflammation processes, respectively, were also analyzed by GSMA. Ultrafine PM increased HO-1 and SOD-2 mRNA levels in the striatum and hippocampus, in the presence of Nrf-2 activation. Also, ultrafine PM activated NF-κB and increased IL-1ß and TNFα in the striatum. Activation of UPR was observed after exposure to coarse PM through the increment of XBP-1S and BiP in the striatum, accompanied by an increase in antioxidant response markers HO-1 and SOD-2. Our results indicate that exposure to different size fractions of PM may induce physiological changes (in a neuroanatomical manner) in the central nervous system (CNS), specifically within the striatum, where inflammation, oxidative stress and UPR signals were effectively activated.

Mortality due to lung cancer in Mexico.

The highest mortality due to cancer worldwide for both genders corresponds to lung cancer (1,179,000 deaths). In Mexico, the crude mortality rate due to lung cancer was of 5.01 per 10(5) inhabitants in 1979. The most important risk factor is smoking. The present study was aimed at analyzing the mortality due to lung cancer in Mexico, assessing data from each of the states constituting the Mexican Republic during the 1998-2004 period. Data were obtained from the National Institute of Statistics, Geography and Informatics (INEGI, for its initials in Spanish) corresponding to deaths due to lung cancer (1998-2004). We estimated the mean annual mortality rate (MAMR) for each of the 32 states of Mexico. We used the "World Population Standard". The MAMR was standardized according to age (ARS) direct method, and the standard error was determined by Poisson's approximation at a 95% confidence interval. To know the excess risk due to mortality, we calculated the standardized mortality ratios (SMRs) of ARS for each federal state, using the national rate as reference. In this period, 397,400 deaths due to malignant neoplasms were recorded, corresponding 45,578 (11.5%) to lung cancer; for men, 31,025 (68.1%) with MAMR of 8.9 and the respective ARS of 13.2 both x10(5) inhabitants. For women, results were 4553 (31.9%) deaths with MAMR of 4.1 and ARS of 5.4 both x10(5) inhabitants. The highest mortality rates due to lung cancer in both genders were observed in the north of Mexico, whereas for women this was observed in the central states. Although smoking is the main risk for lung cancer, there are other factors such as environmental pollution or exposure to toxicants that could be associated to this cancer. The years potentially lost due to lung cancer were 258,550 for men and 133,315 for women, with a total of 391,865 according to histopathology registry neoplasm malignant RHNM (1985-1995). Studies focused on the characterization and measurement of polluting agents would be a good start to determine the level of participation of air pollution in the development of lung cancer.

Priming of cytokine release and increased levels of bactericidal permeability-increasing protein in the blood of animal facility workers.

OBJECTIVE: To investigate cellular immune responses in laboratory animal workers who are exposed to high levels of animal allergens but also to other biologically active substances containing lipopolysaccharides (LPS), i.e., endotoxins. METHODS: A survey among 20 animal facility workers and 20 matched (gender, smoking) controls was conducted using exposure measurements (endotoxin, colony-forming units of bacteria and fungi) and a questionnaire on respiratory symptoms. Blood samples were taken to determine the ex vivo whole-blood release of tumor necrosis factor-alpha (TNF) and interleukin-8 (IL-8) as well as plasma levels of LPS-binding protein (LBP), bactericidal permeability-increasing protein (BPI), the 75-kDa soluble TNF receptor (sTNFR75), and total/specific IgE. RESULTS: Although exposure to endotoxin was low (range 0.05-2.8 ng/m(3)), a significant (P < 0.05) increase in plasma BPI (4-fold) and srTNF75 (1.2-fold) was found, suggesting a response to inhalation of LPS. Also, the capacity of blood leukocytes to release TNF and IL-8 in response to ex vivo exposure to workplace dust was increased. Data were not confounded by specific allergies, levels of IgE, smoking, or respiratory symptoms. CONCLUSIONS: A profound effect on the cellular immune response was seen in animal workers with low endotoxin exposure and a high antigenic load. It remains to be determined which other biologically active substance(s) are involved in this effect.

Human cervical cancer-associated nuclear matrix proteins.

The nuclear matrix is the nonchromatin protein structural component of the nucleus that governs nuclear shape and also exerts regulatory control over higher order gene organization. Recent studies have documented the presence of tumor-associated nuclear matrix proteins in several human cancers. We used high-resolution two-dimensional gel electrophoresis to compare nuclear matrix protein patterns in cervical carcinomas with those from normal cervical tissue. Tumors obtained from 20 patients undergoing hysterectomy for clinically localized cervical cancer were compared with normal cervical tissue. We have identified five polypeptides (CvC-1: Mr = 69,408 Da, pI = 5. 78; CvC-2: Mr = 53,752 Da, pI = 5.54; CvC-3: Mr = 47,887 Da, pI = 5. 60; CvC-4: Mr = 46,006 Da, pI = 5.07; and CvC-5: Mr = 44,864 Da, pI = 6.61) in the nuclear matrix from cervical carcinomas that were present in 20 of 20 cervical tumors but 0 of 10 normal tissues. These data extend similar findings of cancer-associated nuclear matrix proteins in other human cancers and suggest that nuclear matrix proteins may represent a new class of cancer markers that could aid the diagnosis or management of some types of cancer.

Induction of the lung myofibroblast PDGF receptor system by urban ambient particles from Mexico City.

Platelet-derived growth factor (PDGF) and its receptor system regulate mesenchymal cell proliferation. We recently reported that emission-source fly-ash particles and asbestos fibers induce the PDGF alpha-receptor through a macrophage-dependent pathway, and upregulation of this receptor greatly enhances the mitogenic response of lung myofibroblasts to PDGF (Lindroos and colleagues, Am. J. Respir. Cell Mol. Biol. 1997;16:283-292). In the present study we investigated the effect of particulate matter <= 10 micrometers in size (PM10) from the southern, central, and northern regions of Mexico City on PDGF receptor induction and compared these urban, ambient particles with Mt. St. Helen's volcanic ash particles as a negative control. All Mexico City PM10 samples, but not volcanic ash, stimulated rat alveolar macrophages to secrete a soluble, upregulatory factor(s) for the PDGF alpha-receptor on early passage rat lung myofibroblasts. The macrophage-derived upregulatory activity was blocked by the interleukin (IL)-1 receptor antagonist. The ability of PM10 to stimulate IL-1beta release was blocked in part by a recombinant endotoxin neutralizing protein (rENP). Lipopolysaccharide/endotoxin (LPS) and vanadium, both constituents that were present within these PM10 samples, also stimulated macrophages to secrete factor(s) that upregulated PDGF-Ralpha on lung myofibroblasts. Direct exposure of myofibroblasts to PM10 also elicited upregulation of the PDGF alpha-receptor, and this effect was blocked by rENP and mimicked by LPS, but not vanadium. These findings suggest that PM10 particles induce expression of the PDGF receptor system through macrophage-dependent and -independent mechanisms involving endotoxin and metals.

In vitro induction of abnormal anaphases by contaminating atmospheric dust from the City of Mexicali, Baja California, Mexico.

Mexicali dust (MD) is a mixture of particles of potassium aluminum silicates (98%) and sodium dioxide (2%) that induces pulmonary damage under experimental conditions, and is capable of inducing in vitro chromosomal alterations in exposed lymphocytes. It has been proposed as an atmospheric contaminant with pathogenic potential. Among the chromosomal alterations observed, numeric alterations were predominant. The present study was designed to evaluate the capacity of MD to induce anaphasic changes in the Balb c 3T3 cell line. Chrysotile asbestos was used as a positive control. MD was found to induce abnormal anaphases, and the percentage of abnormalities increased as the dose increased (27.41% with 20 mg/mL, 29.60% with 40 mg/mL and 37.10% with 80 mg/mL). Multipolar anaphases constituted the most frequent alteration (69.1-78.8%), followed by lagging chromosomes (18.2-29.5%) and anaphasic bridges (1.51-5.9%). The anaphasic alterations induced by MD showed differences in comparison to those observed with asbestos, especially for anaphasic bridges (10.4% vs. 1.51%, p<0.05). The capacity of MD to induce alterations reported in the process of chromosomal disjunction could explain the numeric aberrations reported previously by the authors of this paper. Therefore, these data support that MD could act as a clastogenic agent.

Pulmonary fibrogenesis after three consecutive inhalation exposures to chrysotile asbestos.

Previously, this laboratory developed a model of asbestos-induced pulmonary fibrogenesis in rats and mice after a brief (1 to 3-h) inhalation exposure. However, typical human environmental exposures would be repeated, although at lower concentrations than those used in our animal model. Here we have extended this model to encompass repeated exposures and consequent long-term effects. Groups of rats were exposed to chrysotile aerosol (10 mg/m3) for 3- to 5-h periods over 3 consecutive days. Lung fiber burden and pathologic features were studied for as long as 6 mo after exposure. We found that many of the longest (> or = 8 microm) fibers were retained in the lung for at least 6 mo, whereas shorter fibers were cleared more rapidly. The three exposures to chrysotile caused a large increase in DNA synthesis in the epithelium of terminal bronchioles and more proximal airways. When compared with a single exposure, the triple exposure caused an enhanced inflammatory response as well as a prolonged period of increased DNA synthesis in the proximal alveolar region. Hyperplastic, fibrotic lesions subsequently developed in the same region and persisted for at least 6 mo after exposure. These findings will be valuable in directing future studies of the mechanisms of pulmonary fibrosis in this model.

Maximal PDGF-induced lung fibroblast chemotaxis requires PDGF receptor-alpha.

Alteration of the platelet-derived growth factor (PDGF) receptor system could be important in enhancing the mitogenic and chemotactic potential of lung fibroblasts during pulmonary fibrogenesis. We previously reported that interleukin-1 beta (IL-1 beta) upregulates the PDGF receptor-alpha (PDGFR-alpha) gene, and in this study we sought to establish the importance of the PDGFR-alpha relative to the PDGFR-beta in mediating a chemotactic response to PDGF-AA, -AB, and -BB. Pretreatment of fibroblasts for 24 h with IL-1 beta increased chemotaxis to all three PDGF isoforms. IL-1 beta pretreatment markedly increased the maximal number of 125I-labeled PDGF-AA binding sites but did not change the number of 125I-PDGF-AB or PDGF-BB sites. However, IL-1 beta increased 125I-PDGFR-AB affinity twofold. Neomycin (5 mM) was used as a PDGFR-alpha antagonist and completely blocked 125I-PDGF-AA binding and PDGF-AA-induced chemotaxis. The binding affinity of 125I-PDGF-AB and 125I-PDGF-BB was increased two-to threefold by neomycin, and chemotaxis to PDGF-AB and PDGF-BB was enhanced. These results define a role for the PDGFR-alpha as a regulatory receptor subtype that is necessary for PDGF isoforms to exert maximal chemotaxis.

Lipopolysaccharide up-regulates platelet-derived growth factor (PDGF) alpha-receptor expression in rat lung myofibroblasts and enhances response to all PDGF isoforms.

Differential expression of PDGF receptor alpha and beta subunits controls the response of mesenchymal cells to the three PDGF isoforms (AA, AB, and BB). Cultured rat lung myofibroblasts (RLMF) possess abundant PDGF receptor-beta (PDGF-Rbeta) and little PDGF receptor-alpha (PDGF-Ralpha). Here we show that LPS up-regulates expression of PDGF-Ralpha and increases the sensitivity of RLMF to all three PDGF isoforms. Treatment of RLMF for 4 to 48 h with LPS enhanced PDGF-Ralpha surface expression and mRNA 5- to 10-fold but caused no change in expression of PDGF-Rbeta. Both RNA and protein synthesis were necessary for up-regulation of PDGF-Ralpha, and the increase in PDGF-Ralpha mRNA was most likely regulated at the transcriptional level. PDGF-Ralpha up-regulation was not mediated by the IL-1R system and was independent of LPS-binding proteins in serum. Highly confluent cultures of RLMF responded more strongly to LPS than did subconfluent cultures. LPS treatment enhanced the mitogenic and chemotactic responses of RLMF to all PDGF isoforms at least threefold. We postulate that signal transduction by PDGF-receptor alphabeta heterodimers was important in the enhanced responses to PDGF-AB and -BB. We propose that regulation of PDGF-Ralpha is a critical event in the genesis of pulmonary fibroproliferative diseases.

Interleukin 1 beta (IL-1 beta) and the IL-1 beta-alpha 2-macroglobulin complex upregulate the platelet-derived growth factor alpha-receptor on rat pulmonary fibroblasts.

Fibroblasts are the primary proliferating cell type in pulmonary fibrosis. We previously showed that inorganic, fibrogenic particles alter the platelet-derived growth factor (PDGF) receptor system on rat lung fibroblasts (Bonner, J. C., et al. 1993, J. Clin. Invest 92:425-430). In lung fibroblasts, PDGF is the most potent proliferative cytokine, and the responses to PDGF isoforms depend on the relative amounts of two PDGF receptors (PDGF-R alpha and PDGF-R beta). Interleukin 1 beta (IL-1 beta) production by lung macrophages is increased following exposure to fibrogenic particles. We have examined the role of IL-1 beta in regulating the lung fibroblast PDGF receptor system. IL-1 beta induced a 10-fold increase in the number of binding sites for [125I]PDGF-AA, caused a 2-fold increase in affinity of [125I]PDGF-AB, but it had no effect on [125I]PDGF-BB binding. PDGF-R alpha gene expression was increased 5-fold after 4 h of IL-1 beta treatment. IL-1 beta increased the proliferative and chemotactic response to PDGF isoforms in the following order of potency: AA > AB > BB. IL-1 beta was tested for its ability to cause increased [125I]PDGF-AA binding when complexed to its binding protein, alpha 2-macroglobulin (alpha 2M). IL-1 beta bound covalently to fast methyl-amine-activated alpha 2M (alpha 2M-MA). IL-1 beta-alpha 2M-MA or alpha 2M-MA alone possessed minimal activity for inducing an increase in [125I]PDGF-AA binding. However, treatment of the IL-1 beta-alpha 2M complex with thioredoxin, which released bioactive IL-1 beta that was covalently bound to alpha 2M, maximally increased [125I]PDGF-AA binding to the same extent as free IL-1 beta. These results indicate that the fibroblast response to PDGF isoforms is modulated by a complex interaction involving IL-1 beta, alpha 2M, and thioredoxin, all of which are produced in vivo by activated macrophages.

Transforming growth factor beta 1 downregulates the platelet-derived growth factor alpha-receptor subtype on human lung fibroblasts in vitro.

Fibroblasts are the central target cell in pulmonary fibrotic diseases, and their proliferation is mediated largely by platelet-derived growth factor (PDGF) isoforms secreted by activated lung macrophages. Several other macrophage-derived cytokines that are increased during fibrogenesis, including interleukin-1 beta and transforming growth factor-beta 1 (TGF-beta 1), could potentially modulate the mitogenic and chemotactic activity of PDGF by altering the expression of cell-surface PDGF receptors on fibroblasts. The PDGF receptor system on fibroblasts from a variety of tissues shows heterogeneous responses to TGF-beta 1. Lung fibroblasts have not been investigated in this regard. TGF-beta 1 downregulated the gene expression of the 6.5 kb PDGF-alpha receptor (PDGF-R alpha) transcript in normal human lung fibroblasts in a concentration-dependent fashion that was maximal at 3 ng/ml TGF-beta 1; this corresponded with a decrease in cell-surface PDGF-R alpha as measured by radioligand binding assays using [125I]PDGF-AA. The TGF-beta 1-induced down-regulation of the PDGF-R alpha gene was rapid (maximal suppression by 2 h post-treatment) and preceded the decrease in cell-surface alpha-receptor (maximal reduction by 6 h post-treatment). TGF-beta 1 treatment did not alter the rate of PDGF-R alpha mRNA degradation following the inhibition of transcription using actinomycin D, indicating that TGF-beta 1 increases PDGF-R alpha transcription. Scatchard analysis of saturation binding data showed that TGF-beta 1 decreased the number of [125I]PDGF-AA binding sites 5-fold without affecting receptor affinity. [125I]PDGF-AB binding sites were downregulated approximately 25%, and the number of [125I]PDGF-BB binding sites was not changed by TGF-beta 1 treatment, indicating that the PDGF-beta receptor was not affected. TGF-beta 1 reduced the mitogenic and chemotactic response to PDGF-AA by > 90%, whereas these biologic response to PDGF-AB and PDGF-BB were inhibited 50% to 80%. The proliferative and chemotactic responses of fibroblasts during tissue remodeling or during lung fibrosis are likely controlled by a complex network involving PDGF isoforms and cytokines that modify the PDGF receptor system.

Differential binding and regulation of platelet-derived growth factor A and B chain isoforms by alpha 2-macroglobulin.

Alpha 2-Macroglobulin (alpha 2M) is a multifunctional secreted glycoprotein that serves as a ubiquitous proteinase inhibitor and as a binding protein for platelet-derived growth factor (PDGF) BB and homologues of PDGF-BB secreted in culture by macrophages. The interaction of alpha 2M with PDGF-A chain molecules has not been addressed. This is a potentially important issue because fibroblasts and smooth muscle cells produce PDGF-AA, whereas macrophages produce mainly PDGF-BB. Recombinant human 125I-PDGF-B chain molecules (AB and BB) bound to plasma-derived, native human, or bovine alpha 2M and trypsin-activated alpha 2M on Superose 6 fast protein liquid chromatography gel filtration and on nondenaturing polyacrylamide gel electrophoresis, whereas 125I-PDGF-AA did not. Similar results were obtained with 125I-PDGF isoforms binding to immobilized bovine alpha 2M and alpha 2M-methylamine. The same differential pattern of unlabeled PDGF isoforms binding to alpha 2M was observed by Western blotting of PDGF. Human lung fibroblasts secreted alpha 2M as measured by Western blotting, and fibroblast-derived alpha 2M possessed the same differential binding pattern for PDGF isoforms as did plasma-derived alpha 2M. The specific binding of PDGF-AB and -BB to these fibroblasts was inhibited by native bovine alpha 2M, although PDGF-AA binding was not affected. Native alpha 2M preferentially blocked fibroblast chemotaxis to the PDGF-B chain dimers. These data suggest that only PDGF-B chain dimers, such as those produced by macrophages or released from platelets, are regulated by alpha 2M and that PDGF-AA produced by fibroblasts and smooth muscle cells is not controlled by this cytokine-binding protein.

Platelet-derived growth factor (PDGF)-AA, -AB, and -BB induce differential chemotaxis of early-passage rat lung fibroblasts in vitro.

Platelet-derived growth factor (PDGF) isoforms are chemoattractants and mitogens for cells of mesenchymal origin that could be important mediators of pulmonary fibrogenesis. We have previously reported that particle-activated alveolar macrophages secrete homologues of PDGF that are composed of all three PDGF isoforms (PDGF-AA, -AB, and -BB). This mixture of macrophage-derived PDGF, once dissociated from the PDGF-alpha-macroglobulin complex, induces chemotaxis of rat lung fibroblasts (RLF) in the nanomolar range. In addition, we have reported that PDGF isoforms induce differential proliferation of RLF (PDGF-BB > PDGF-AB > PDGF-AA). In the present study, we sought to determine the relative chemotactic potency of the three PDGF isoforms and correlate these responses to the relative abundance of the two types of PDGF cell-surface receptors: PDGF-alpha receptor (PDGF-R alpha) and PDGF-beta receptor (PDGF-R beta). We also investigated the chemotactic activity of combinations of two PDGF isoforms simultaneously. Isolates of early-passage RLF were assayed for chemotaxis in 48-microwell chambers. Swiss mouse 3T3 cells were assayed in parallel as a positive control cell line for PDGF-R alpha and PDGF-R beta expression. RLF responded differentially to the PDGF isoforms: PDGF-AB and PDGF-BB were potent chemoattractants and stimulated maximal chemotactic responses between 4 and 8 ng/ml PDGF, whereas PDGF-AA elicited a weak chemotactic response that was maximally 15% of that obtained with either B-chain isoform. PDGF-AB and PDGF-BB were also the most potent chemoattractants for Swiss 3T3 cells, and their response to these B-chain isoforms was approximately 40% greater than that obtained for RLF.(ABSTRACT TRUNCATED AT 250 WORDS)

Application of an autopsy report specifically designed for cardiovascular diseases.

After modifying the format and content of the autopsy report traditionally used at the Instituto Nacional de Cardiología of México, Tlalpan, we present the results of the new, revised autopsy protocol here. The new autopsy protocol (model report) was designed as a "fixed format" to describe the cardiovascular diseases observed at our institution, thus pretending to collect more and better data, providing useful information, and contributing to better clinicopathologic correlations. The comparison between the model and traditional reports demonstrated an improvement in the autopsy data collection system--achieving better clinicopathologic correlations of the main disease and the cause of death, and identifying morphologic alterations that would explain it in more cases. The model report was also considered more accessible and useful since it permitted the answering of more questions raised by clinicians.

Ferruginous bodies as markers of environmental exposure to inorganic particles: experience with 270 autopsy cases in Mexico.

Ferruginous bodies (FB) were quantified in lung digests from 270 autopsy cases over 20 years of age. The cases were autopsied in three different hospitals of the Secretaria de Salud, Mexico, DF. Two hundred seventy samples of peripheral lung tissue were digested in commercial bleach, and all morphologic types of ferruginous bodies were quantified. The results showed that numbers of ferruginous bodies per gram of dry tissue increased over the years: 4.2 FB/g in cases from 1975 to 42.5 FB/g in cases from 1988 (r = 0.86). Higher counts of ferruginous bodies were seen in males, smokers, and Mexico City dwellers. However, more than 70% of them presented less than 100 FB/g. Our study demonstrates that most of our cases had a nonoccupational exposure to fibers.

Early-passage rat lung fibroblasts do not migrate in vitro to transforming growth factor-beta.

Lung fibrosis has been postulated to be mediated by the production of macrophage-derived growth factors that are both mitogenic and chemotactic for fibroblasts. In vitro studies from our laboratory demonstrated that alveolar and interstitial macrophages treated with iron and asbestos release platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta) into the media. This conditioned media was capable of inducing proliferation and chemotaxis of primary rat lung fibroblasts (RLF). TGF-beta is known to be present in the media, and RLF have high-affinity receptors for TGF-beta. However, we found that > 95% of the chemotaxis was blocked by a polyclonal anti-PDGF antibody, whereas anti-TGF-beta did not change cell migration. TGF-beta has been described previously as a potent chemoattractant for fibroblasts. Thus, we tested the potential of purified TGF-beta to induce RLF chemotaxis in an attempt to address this apparent contradiction in results. Four separate preparations of RLFs from four different rats, Swiss 3T3 cells, human and rat fetal skin fibroblasts, and human foreskin fibroblasts were tested for chemotaxis using purified porcine TGF-beta 1 as well as human TGF-beta. None of these cells responded chemotactically to TGF-beta over a broad range of concentrations used (0.004 pg/ml to 50 ng/ml). RLF plated at different densities also did not respond to TGF-beta. On the other hand, all the fibroblast types migrated vigorously to PDGF (4 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Modification of the Smith and Naylor technique for the identification of ferruginous bodies.

Smith and Naylor's technique has been successfully used by many authors around the world to recover inorganic particles from the lungs. In this short report we compare the results of counting inorganic particles recovered from human lung tissue by two different methods: Smith and Naylor's technique and a modification to it. We used ferruginous bodies (FB) as markers for inorganic particles and we compared the results of the FB counts in both methods. In the traditional technique the interface formed in the 1:1 ethanol-chloroform mixture is discharged and FB are counted only in the formed pellet. Our modification also quantified FB in the interface fraction. Post-mortem samples from each of the lung lobes were taken from 22 individuals, totalling 198 samples. Each sample was digested in liquid commercial bleach and processed by both techniques. Our results showed that the modified technique was more sensitive in the detection of FB than the traditional method, with 16 out of 22 individuals showing positive identification against 14 out of 22, respectively. Furthermore, the modified technique proved not only to be more sensitive, but also almost twice as accurate: 49 FB/g vs. 26.7 FB/g of dry tissue.

[Presence of ferruginous bodies in cancerous pulmonary tissue]. / Presencia de cuerpos ferruginosos en tejido pulmonar canceroso.

The correlation between high counts of ferruginous bodies (FB) and pulmonary cancer was investigated. Autopsy cases between 1982 and 1988 were chosen, and studied at Instituto Nacional de Enfermedades Respiratorias. Two grams of lung tissue were digested with sodium hypochlorite. We found no differences in the histologic types of cancer: 18.0 FB per gram (FB/g) for the adenocarcinoma group and 16.0 FB/g for both the epidermoid and anaplastic groups. The asbestos core was predominant in all FB analysed (greater than 85%). Males, Mexico city residents and smokers showed to higher amounts of FB. We concluded that there is an environmental exposure to particles in the cases studied.

[Rupture of the middle left ventricle after a mitral valve replacement. A report on 27 autopsy cases]. / Rotura de la porción media del ventrículo izquierdo después de reemplazo valvular mitral. Comunicación de 27 casos de autopsia.

Left ventricular rupture is a serious complication of mitral valve replacement. The prevalence ranged from 0.5 to 14%, and is the principal cause of early postoperative death following mitral valve replacement. In this report we described certain morphologic observations and some clinical and epidemiological data of a series of 27 necropsy patients with midventricular rupture (type III). This complication was predominantly present in females (88.9%) with an average age of 44 +/- 11.4 years. The predominant valvular lesion was stenosis (70.4%). In all cases we found small-sized left ventricles and the ventricular wall hypertrophied. Perforation was observed in the 18.5% of the cases. In 59.2% of the patients high profile prostheses were used. Seventy-eight percent of patients died before 24 hours with refractory ventricular failure and only in the 25.9% of cases the clinical diagnoses was suspected and rupture unsuccessfully repaired. Our results suggested that age, sex, type of mitral lesion, ventricular size and type of prostheses are not risk factors for this complication. The mortality is high and the diagnosis was not suspected frequently. Midventricular rupture of the left ventricle is a lethal complication and is necessary to know all its characteristics to implement better methods of prevention and management.

[Myocardial infarct and rupture of the left ventricular free wall. Some considerations on incidence, morphological characteristics and risk factors]. / Infarto del miocardio y ruptura de la pared libre del ventrículo izquierdo. Algunas consideraciones sobre la frecuencia, características morfológicas y factores de riesgo.

Rupture of the left ventricle free wall is a sudden and unexpected event in myocardial infarction. It is considered the third most common cause of death, following cardiogenic shock and arrhythmias. The frequency of rupture varies because many patients may survive the initial insult of myocardial infarction. Conflicting reports regarding risk factors have been published by several authors. With these considerations in mind, the present investigation was undertaken to evaluate ventricular rupture in an autopsy population from the Instituto Nacional de Cardiología. We analyzed the salient morphologic features and the risk factors. Our results indicated an incidence rate of 17.7% of cardiac rupture in patients who died of acute myocardial infarction and were autopsied. Ruptures are more common in elderly female patient during their first infarct, they were localized preferentially in the anterior wall and occurred within the first four days after infarction. Chance of rupture was greater in hypertensive patients, whereas a history of previous infarct protected against this contingency.