PubMed Health⌕ Search

Biomedical subjects

J Guzman

Publications and source records attributed to J Guzman.

At least 19 recordsLinked to original sources
PubMed2006

Thalidomide reduces IL-18, IL-8 and TNF-alpha release from alveolar macrophages in interstitial lung disease.

Thalidomide exhibits diverse actions of anti-inflammation, immunomodulation and anti-angiogenesis. The efficacy of thalidomide treatment in sarcoidosis with lupus pernio is thought to be due to inhibition of tumour necrosis factor (TNF)-alpha. The mechanisms that underlie the properties of thalidomide are still unclear in interstitial lung disease. The current authors investigated the potential inhibitory effects of thalidomide at concentrations of 0.1, 0.01 and 0.001 mM on the production of transforming growth factor-beta, TNF-alpha, interleukin (IL)-1beta, IL-6, IL-8, IL-10, IL-12p70, IL-12p40 and IL-18 by alveolar macrophages from bronchoalveolar lavage in patients with sarcoidosis (n = 8), hypersensitivity pneumonitis (HP; n = 8) and idiopathic pulmonary fibrosis (IPF; n = 12). In sarcoidosis and HP patients, thalidomide induced a dose-dependent, partial suppression of lipopolysacchride (LPS)-stimulated TNF-alpha, IL-12p40 and IL-18 release. At the highest thalidomide concentration (0.1 mM), LPS-stimulated IL-8 production was also suppressed. In IPF patients, although spontaneous production of TNF-alpha, IL-12p40, IL-18 and IL-8 was lower than in sarcoidosis and HP patients, with LPS stimulation the cytokines were significantly elevated and also partially inhibited by thalidomide. In conclusion, thalidomide has the potential to improve the therapeutic regimens for sarcoidosis, hypersensitivity pneumonitis and idiopathic pulmonary fibrosis by reducing tumour necrosis factor-alpha, interleukin-12p40, interleukin-18 and interleukin-8 production.

Aged↗
PubMed2006

Vanadium recovery from oil fly ash by leaching, precipitation and solvent extraction processes.

In order to reduce the environmental impact due to land disposal of oil fly ash from power plants and to valorize this waste material, the removal of vanadium was investigated using leaching processes (acidic and alkaline treatments), followed by a second step of metal recovery from leachates involving either solvent extraction or selective precipitation. Despite a lower leaching efficiency (compared to sulfuric acid), sodium hydroxide was selected for vanadium leaching since it is more selective for vanadium (versus other transition metals). Precipitation was preferred to solvent extraction for the second step in the treatment since: (a) it is more selective; enabling complete recovery of vanadate from the leachate in the form of pure ammonium vanadate; and (b) stripping of the loaded organic phase (in the solvent extraction process) was not efficient. Precipitation was performed in a two-step procedure: (a) aluminum was first precipitated at pH 8; (b) then ammonium chloride was added at pH 5 to bring about vanadium precipitation.

Aluminum↗
PubMed2005

Expression of tumour necrosis factor receptors by bronchoalveolar cells in hypersensitivity pneumonitis.

Tumour necrosis factor receptors (TNFR) and the Fas receptor (FasR) have been implicated in the pathogenesis of interstitial lung diseases. The current authors examined the expression of TNFR-1, TNFR-2 and FasR by bronchoalveolar cells in hypersensitivity pneumonitis (HP). Cell surface receptor expression on bronchoalveolar lavage cells was analysed by immunocytochemistry in 11 HP patients, 11 idiopathic pulmonary fibrosis (IPF) patients and 10 controls. TNFR-1, TNFR-2 and FasR were expressed on a higher percentage of alveolar macrophages (AM) in HP compared with controls and IPF patients. TNFR-2 and FasR expression on lymphocytes was also higher in HP than in controls and in IPF. TNFR-1, TNFR-2 and FasR expression correlated positively with the percentage of lymphocytes, and negatively with the percentage of AM in HP. Expression of TNFR-1 on AM and TNFR-2 on lymphocytes correlated with the percentage of neutrophils in HP. In conclusion, this study shows evidence of altered expression of tumour necrosis factor superfamily receptors in hypersensitivity pneumonitis.

Aged↗
PubMed2004

Caspases, the enemy within, and their role in oxidative stress-induced apoptosis of inner ear sensory cells.

This review covers the general roles of members of the cysteine protease family of caspases in the process of apoptosis (programmed cell death) looking at their participation in both the "extrinsic" cell death receptor and the "intrinsic" mitochondrial cell death pathways. It defines the difference between initiator and effector caspases and shows the progression of caspase activations that ends up in the apoptotic cell death and elimination of a damaged cell. The review then presents what is currently know about the participation of caspases in the programmed cell death of inner ear sensory cells during the process of normal development and maturation of the inner ear and their importance in this process as illustrated by the results of caspase-3 gene knockout experiments. The participation of specific caspases and the sequence of their activation in the elimination (apoptosis) of damaged sensory cells from adult inner ears after an injury that generates oxidative stress are reviewed. Both the possibility and the potential efficacy of caspase inhibition with a broad-spectrum pancaspase inhibitor as an interventional therapy to treat and rescue oxidative stress-damaged inner ear sensory cells from apoptosis are presented and discussed.

Adult↗
PubMed2003

[Pulmonary fibrosis. Classification, diagnosis, therapy].

A new classification of the idiopathic interstitial pneumonia has recently been proposed, defining idiopathic pulmonary fibrosis (IPF) more rigorously and in contrast to further subentities. The new classification is of prognostic and clinical relevance. Diagnosis requires a combined clinical, radiological and pathological effort. In patients with characteristic clinical and HR-CT findings, the diagnosis of IPF can be made with sufficient confidence without surgical lung biopsy. Recent evidence suggests that the primary pathogenetic event in IPF involves epithelial injury and abnormal wound heeling. This explains the ineffectiveness of the usual anti-inflammatory therapy in the majority of patients. Since no antifibrotic drugs are available at present, the recommended standard therapy is a combination of prednisone with azathioprine or cyclophosphamide. New antifibrotic molecules are already tested in clinical trials.

Anti-Inflammatory Agents↗
PubMed2003

Copper sorption by chitosan in the presence of citrate ions: influence of metal speciation on sorption mechanism and uptake capacities.

The presence of organic ligands in a solution containing metal ions modifies metal speciation, which in turn changes the sorption mechanism, optimum pH range and maximum sorption capacity. The present work investigates the sorption of copper by chitosan in the presence of citrate at different metal/ligand ratios. Copper uptake in acidic solution takes place through electrostatic attraction between the protonated amine groups of chitosan and anionic copper-citrate complexes (mainly Cu(OH)L2- but also a small fraction of CuL-). Sorption was negligible below pH 3 due to competition from dissociated anionic ligand and counter ions brought about by dissociation of the acid used for pH control. Actually, copper sorption begins to be significant when the fraction of anionic copper-complexes exceeds that of anionic copper-free ligand. So sorption capacity strongly increases up to pH 4.5-5.5. Above pH 5.5, the progressive decrease of amine protonation leads to a linear decrease in sorption capacity. An excess of ligand leads to an increase in the fraction of free dissociated (anionic) ligand that may compete for electrostatic attraction on protonated amine groups and therefore leads to a decrease in sorption capacities.

Chelating Agents↗
PubMed2003

Idiopathic bronchiolitis mimicking diffuse panbronchiolitis.

Diffuse panbronchiolitis (DPB) is a distinct sinobronchial syndrome which has been almost exclusively reported in East Asia; only a few cases have been observed in non-Asians so far. Since 1990, when one of us described the first European case, we have screened all patients presenting with a clinical, physiopathological and radiological pattern compatible with DPB, in order to assess if the paucity of proven cases in Europe could reflect a lack of awareness of this disease among both pulmonologists and pathologists. Over a 10-years period we identified four additional DPBs, but also interestingly observed five cases of "idiopathic" bronchiolitis (IB) that had both clinical symptoms and high-resolution computed tomography (HRCT) findings indistinguishable from those of DPB, but did not show the typical histological changes. All these patients were Caucasians and presented with dyspnea, productive cough, an obstructive or mixed impairment on pulmonary function tests and chest HRCT features strongly suggesting a grade II to IV DPB. We suggest that diseases classified as IB in this study might be homogeneous entities which are clinically and radiologically similar to DPB.

Adult↗
PubMed2001

Differential gene expression of adenosine A1, A2a, A2b, and A3 receptors in the human enteric nervous system.

Adenosine receptors (ADORs) in the enteric nervous system may be of importance in the control of motor and secretomotor functions. Gene expression and distribution of neural adenosine A1, A2a, A2b, or A3 receptors (Rs) in the human intestine was investigated using immunochemical, Western blotting, RT-PCR, and short-circuit current (I(sc)) studies. Adenosine A1R, A2aR, A2bR, or A3R mRNAs were differentially expressed in neural and nonneural layers of the jejunum, ileum, colon, and cecum and in HT-29, T-84, T98G, and Bon cell lines. A1R, A2aR, A2bR, and A3R immunoreactivities (IRs) were differentially expressed in PGP 9.5-immunoreactive neurons. A2bR IR occurs exclusively in 50% of submucosal vasoactive intestinal peptide (VIP) neurons (interneurons, secretomotor or motor neurons) in jejunum, but not colon; A2aR is also found in other neurons. A3R IR occurs in 57% of substance P-positive jejunal submucosal neurons (putative intrinsic primary afferent neurons) and less than 10% of VIP neurons. Western blots revealed bands for A3R at 44 kDa, 52 kDa, and 66 kDa. A2aR and A2bR are coexpressed in enteric neurons and epithelial cells. 5'-N-methylcarboxamidoadenosine or carbachol evoked an increase in I(sc). A2bR IR is more prominent than A2aR IR in myenteric neurons, nerve fibers, or glia. A1R is expressed in jejunal myenteric neurons and colonic submucosal neurons. Regional differences also exist in smooth muscle expression of ADOR IR(s). It is concluded that neural and nonneural A1, A2a, A2b, and A3Rs may participate in the regulation of neural reflexes in the human gut. Clear cell and regional differences exist in ADOR gene expression, distribution, localization, and coexpression.

Blotting, Western↗
PubMed2001

Bronchoalveolar lavage in interstitial lung disease.

Bronchoalveolar lavage (BAL) has become a standard diagnostic procedure for the majority of patients with interstitial disease. The technique is safe, minimally invasive, and reveals specific information in some disorders such as pulmonary alveolar proteinosis, Langerhans cell histiocytosis, alveolar hemorrhage, malignant infiltrates, or dust exposure. Here BAL can often replace lung biopsy. The results of BAL cell differentials with a lymphocytic, a neutrophilic, an eosinophilic, or a mixed cellular pattern can be used as an adjunct to diagnosis. If a BAL finding is compatible with the suspected diagnosis in the context of an appropriate disease history and clinical and radiologic findings, this can then be sufficient for disease confirmation. Recent research focused on the pathogenesis of various types of interstitial lung disorders. In this regard, BAL findings contributed to the characterization of idiopathic pulmonary fibrosis (IPF) as a condition with a predominant T-helper-2 (Th2) cytokine profile, whereas BAL findings in sarcoidosis and hypersensitivity pneumonitis are characterized by a Th1-dominant profile. The clinical value of BAL to assess the activity of disease processes and to provide prognostic information is still under debate. The routine performance of serial BAL is not recommended at present.

Alveolitis, Extrinsic Allergic↗
PubMed2001

Calprotectin expression and mononuclear phagocyte subpopulations in peripheral blood and bronchoalveolar lavage.

BACKGROUND AND AIM OF THE WORK: The phenotype of human alveolar macrophages (AM) can be affected by the process of maturation/differentiation and by multiple factors from the local environment. The aim of our study was to assess the expression of selected phenotypic markers characteristic for subsets of mononuclear phagocytes in bronchoalveolar lavage fluid (BAL) and peripheral blood with special attention to calprotectin (27E10), a marker of acute inflammatory macrophages. METHODS: The expression of calprotectin and 13 other phenotypic markers was evaluated by an immunoperoxidase slide assay and computer image analysis. RESULTS: We consider calprotectin (27E10 antigen) to be a marker of freshly recruited, monocyte-like, mononuclear phagocytes, being expressed in 84 +/- 13% PBM and only 10 +/- 11% of AM, p < 0.001. Computer image analysis confirmed that calprotectin-positive mononuclear cells in peripheral blood and BAL are morphologically very similar in contrast to the much larger calprotectin-negative AM. On the other hand, 25F9 antigen, the transferrin receptor (CD71), KiM8 (CD68), RFD1 (marker of dendritic cells), RFD7 (marker of mature macrophages), RFD9 (marker of epithelioid cells and macrophages of germinal centers), and RM3/1 (macrophages of late phase inflammation) were restricted preferentially to mature AM. CONCLUSIONS: Our study demonstrates phenotypic differences between mononuclear phagocytes derived from BAL and their peripheral blood precursors, and indicates markers useful for assessing the stages of maturation/differentiation of these cells. The percentage of calprotectin (27E10) positive AM might represent a parameter for assessing mononuclear phagocyte influx from peripheral blood to the lung in the very early stage of inflammatory reactions.

Adult↗
PubMed2000

Expression of oncogenic epidermal growth factor receptor family kinases induces paclitaxel resistance and alters beta-tubulin isotype expression.

Oncogenic transformation confers resistance to chemotherapy through a variety of mechanisms, including suppression of apoptosis, increased drug metabolism, and modification of target proteins. Oncogenic epidermal growth factor receptor family members, including EGFRvIII and HER2, are expressed in a broad spectrum of human malignancies. Cell lines transfected with EGFRvIII and HER2 are more resistant to paclitaxel-mediated cytotoxicity, and tubulin polymerization induced by paclitaxel is suppressed compared with cells expressing wild type epidermal growth factor receptor. Because differential expression of beta-tubulin isotypes has been proposed to modulate paclitaxel resistance, we analyzed beta-tubulin isotypes expressed in cell lines transfected with different oncogenes. EGFRvIII- and HER2-expressing cells demonstrated equivalent total beta-tubulin protein compared with cells transfected with wild type receptor or untransfected controls. EGFRvIII-expressing cells demonstrated increases in class IVa (2.5-fold) and IVb (3.1-fold) mRNA, and HER2-expressing cells showed increases in class IVa (2. 95-fold) mRNA. Expression of oncogenic Ha-Ras did not change class IV RNA levels significantly. Inhibition of EGFRvIII kinase activity using a mutant allele with an inactivating mutation in the kinase domain decreased expression of class IVa by 50% and partially reversed resistance to paclitaxel. Expression of oncogenic epidermal growth factor receptor family members is associated with modulation of both beta-tubulin isotype expression and paclitaxel resistance in cells transformed by expression of the receptor. This effect on tubulin expression may modulate drug resistance in human malignancies that express these oncogenes.

3T3 Cells↗
PubMed1999

[Diffuse panbronchiolitis. A rare differential diagnosis of chronic obstructive lung disease].

HISTORY AND ADMISSION FINDINGS: A 36-year-old Korean had since childhood suffered from a chronic progressive lung disease, marked by dyspnoea, productive cough and recurrent sinusitis. He was in a reduced general condition on admission. There were hyperresonant sounds on palpation over both lungs, a low diaphragm and slight vesicular breath sound as well as occasional rales and sibilant rhonchi. INVESTIGATIONS: Laboratory tests showed increased blood cell sedimentation of 52 mm at 1 h, leukocytosis of 24.3/nl, and a raised cold-agglutinin titre. Haemophilus influenza and Pseudomonas aerogenes were cultured from the bronchial secretion. Lung function tests revealed severe obstruction with hyperinflation and partial respiratory failure with a much reduced 1-sec forced expiratory volume (FEV1) of 0.71, 19% of normal; residual volume (RV) 6.61, 550% of normal; arterial oxygen partial pressure 61 mm Hg; arterial CO2 partial pressure 36 mm Hg. Chest X-ray showed emphysematous changes with diffuse small nodular shadows. Bronchoalveolar lavage revealed 96% neutrophils, indicating marked granulocytic inflammation. A video-assisted thoracoscopic biopsy was performed which showed diffuse panbronchiolitis. TREATMENT AND COURSE: The symptoms, radiological changes and lung functions clearly improved under long-term treatment with 500 mg erythromycin daily. CONCLUSION: Diffuse bronchiolitis is rarely seen outside of Asia, but it should be included in the differential diagnosis because, in contrast to other forms of chronic obstructive lung disease, it responds to long-term erythromycin medication.

Adult↗
PubMed1999

Elevated levels of soluble TNF receptors in bronchoalveolar lavage fluid in extrinsic allergic alveolitis.

BACKGROUND: Soluble TNF receptors (sTNFR1 and sTNFR2) are inhibitors of TNF and can block TNF bioactivity. TNF plays an important role in the development of extrinsic allergic alveolitis (EAA). OBJECTIVE: To evaluate whether sTNFR1 and sTNFR2 are locally increased in EAA. METHODS: We measured sTNFR1 and sTNFR2 in bronchoalveolar lavage fluid (BALF) and serum from nine EAA patients and 11 control subjects using an ELISA method. RESULTS: BALF sTNFR1 and sTNFR2 levels were 0.24+/- 0.04 ng/mL and 0.59+/-0.16 ng/mL in EAA patients, and thus significantly elevated in comparison with the controls (0.13+/-0.02 ng/mL and 0.08+/-0.04 ng/mL, both P<0.05). Serum sTNFR levels were not significantly different between the two groups. Both sTNFR1 and sTNFR2 concentrations in BALF correlated significantly with the lymphocyte percentage of BALF (r = 0.57 and 0.81, respectively). CONCLUSION: The two alveolar sTNFRs, particularly sTNFR2, may be involved in the pathogenesis of EAA as counter-regulators of TNF.

Aged↗
PubMed1999

In vivo binding and antitumor activity of Ch14.18.

The melanoma reactive chimeric 14.18 (ch14.18) antibody can mediate enhanced in vitro lysis of human M-21 melanoma cells. This study analyzes the antitumor effects and the in vivo binding of ch14.18 antibody with M-21 melanoma cells in severe combined immunodeficiency (SCID) mice. Outgrowth of tumors was prevented in 6/6 animals by the simultaneous subcutaneous injection of peripheral blood mononuclear cells (PBMC) [3 x 10(6) cells (2 animals); 10 x 10(6) cells (2 animals); and 30 x 10(6) cells (2 animals)], with 0.5 mg ch14.18, 1,500 U interleukin 2 (IL-2), and 10(6) M-21 cells. In contrast, 7 of 7 control mice that received M-21 cells alone, 7 of 7 mice that received M-21 cells and ch14.18, and 5 of 6 mice that received M-21 cells plus PBMC plus IL-2, grew subcutaneous tumors. The in vivo localization of ch14.18 was then evaluated in an intraperitoneal (i.p.) tumor model, where 0.3 cm melanoma nodules develop within 3 weeks after the i.p. administration of M-21 cells. Flow cytometric and immunohistochemical analysis revealed the GD2 antigen present throughout the tumor nodule. Intraperitoneal administration of 0.01, 0.1, or 1.0 mg of ch14.18 to SCID mice previously engrafted i.p. with M-21 cells resulted in detectable ch14.18 binding to tumor cells in vivo within 10 hours of antibody administration. Ch14.18 penetration was limited to approximately 20 cell layers, demonstrating that ch14.18 has limited access to some cells in large tumor nodules. This study demonstrates that the addition of ch14.18 to IL-2 and human effector cells can result in significant antitumor activity by preventing the establishment of tumor nodules. These results suggest that clinical testing of IL-2 plus ch14.18 might be most effective if used in the setting of microscopic residual disease. Therapies that enhance ch14.18 penetration into tumor nodules should be evaluated with ch14.18 for patients with advanced melanoma.

Animals↗
PubMed1999

Pentoxifylline inhibits TNF-alpha production from human alveolar macrophages.

Tumor necrosis factor-alpha (TNF-alpha) is an important proinflammatory cytokine. Recently, pentoxifylline (POF) has been shown to suppress the synthesis of TNF-alpha from lipopolysaccharide (LPS)-stimulated human monocytes in cell cultures and in vivo. The aim of this study was to investigate whether POF-induced suppression of TNF-alpha secretion affects peripheral blood monocytes (PBM) and alveolar macrophages (AM) equally, and whether POF is able to suppress the spontaneous TNF-alpha production from AM in pulmonary sarcoidosis in vitro. In seven patients without interstitial lung disease we studied the effect of POF on LPS-stimulated PBM and AM cultured for 24 h. In six patients with sarcoidosis we investigated the effect of POF on the enhanced spontaneous TNF-alpha production by AM in vitro. POF induced a dose-dependent suppression of the LPS-stimulated TNF-alpha production which was not different for PBM and AM, respectively. In sarcoidosis, POF inhibited the spontaneous TNF-alpha production of AM at 0.1 mM by 91% and at 1 mM by 98%. In conclusion, POF inhibits LPS-induced TNF-alpha production from PBM and AM to a similar extent and can also inhibit the exaggerated spontaneous TNF-alpha production from AM in sarcoidosis in vitro. This may be the basis for further clinical trials to evaluate POF as an immunotherapeutic agent in sarcoidosis.

Adult↗
PubMed1999

Increased expression of apoptosis signalling receptors by alveolar macrophages in sarcoidosis.

The Fas receptor (FasR) and the tumour necrosis factor (TNF) receptor 55/60 kDa (TNFR1) are recognized as apoptosis signalling receptors. They are known to be expressed by lymphocytes in association with immune regulation and immunological disorders. This study aimed to investigate the expression of FasR and TNFR1 by alveolar macrophages (AM) in patients with sarcoidosis. Bronchoalveolar lavage (BAL) was performed in 12 patients with active sarcoidosis and 11 control subjects. BAL cells were characterized by monoclonal antibodies using a peroxidase-antiperoxidase method. Both FasR and TNFR1 were expressed on a higher percentage of AM in sarcoidosis with respect to control subjects (mean +/-sem 40.8+/-3.1% versus 14.9+/-1.7%, p<0.001 and 61.9+/-3.3% versus 23.1+/-4.1%, p<0.001, respectively). There was a close relationship between the expression of FasR and TNFR1 on AM (r = 0.86, p<0.001). The percentages of FasR+ AM and TNFR1+ AM were in direct proportion to the percentage of BAL lymphocytes (r = 0.75 and 0.84), the CD4/CD8 ratio (r = 0.78 and 0.78), and the percentage of the CD14+ AM subset (r = 0.77 and 0.87), p<0.001 for all correlations. This study indicates that alveolar macrophages expressing apoptotic receptors are increased in patients with active sarcoidosis. Further studies are required to determine whether these alveolar macrophages from patients with sarcoidosis undergo apoptosis more readily than those from control subjects.

Adult↗
PubMed1999

Probable effect of photoperiod on seasonal variation in the nuclear volume of the adrenal cortex of viscacha (Lagostomus maximus maximus).

The neuroendocrine system regulates several organic functions such as reproduction, metabolism and adaptation to the environment. This system shows seasonal changes linked to the environment. The experimental model used in the present study was Lagostomus maximus maximus (viscacha). The reproduction of males of this species is photoperiod dependent. Twenty-four adult male viscachas were captured in their habitat at different times during one year. The adrenal glands were processed for light microscopy. Serial cuts were stained with hematoxylin-eosin for the morphometric study, and 100 nuclei of each zone of the adrenal cortex were counted per animal. Data were analyzed statistically by ANOVA and the Tukey test. The cells of the glomerulosa zone are arranged in a tube-shaped structure. The fasciculata zone has large cells with central nuclei and clearly visible nucleoli and with a vacuolar cytoplasm. In the reticularis zone there are two of types of cells, one with a nucleus of fine chromatin and a clearly visible nucleolus and the other with nuclear pycnosis. Morphometric analysis showed maximum nuclear volumes during the February-March period with values of 133 +/- 7.3 microm3 for the glomerulosa, 286.4 +/- 14.72 microm3 for the fasciculata, and 126.3 +/- 9.49 microm3 for the reticularis. Minimum nuclear volumes were observed in August with values of 88.24 +/- 9.9 microm3 for the glomerulosa, 163.7 +/- 7.78 microm3 for the fasciculata and 64.58 +/- 4.53 microm3 for the reticularis. The short winter photoperiod to which viscacha is subjected could inhibit the adrenal cortex through a melatonin increase which reduces the nuclear volume as well as the cellular activity.

Adrenal Cortex↗