[Localized Castleman's disease in the cervical region].
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Biomedical subjects
Publications and source records attributed to A López.
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Deficiency in DNA mismatch repair (MMR) confers instability of simple repeated sequences and increases susceptibility to cancer. Some of the MMR genes are also implicated in other repair and cellular processes related to DNA damage response. Supposedly, lack of their function can lead to a global genomic instability, besides microsatellite instability (MSI). To study the spontaneous and induced genomic instability in germ cells, related to the Msh2 status, DNA alterations in the progeny of individual crosses of Drosophila deficient in one or two copies of the Msh2 gene, were analysed by the arbitrarily primed polymerase chain reaction (AP-PCR). The results indicate that the progeny of homozygous parents for the normal Msh2 allele (+/+) presents a significantly lower frequency of genomic alterations than those from heterozygous (+/-) or mutant homozygous (-/-) parents. In addition, the DNA damage transmitted to the progeny, after the adult parental males were exposed to bleomycin, indicates that whereas the induction of mutations related to MSI depends on the lack of the Msh2 function, the induction of other mutational events may require at least one functional Msh2 allele. Thus, the results obtained with heterozygous individuals may have special relevance for cancer development since they show that a disrupted Msh2 allele is enough to generate genomic instability in germ cells, increasing the genomic damage in the progeny of heterozygous individuals. This effect is enhanced by mutagenic stress, such as occurs after bleomycin exposure.
Mismatch repair (MMR) process confers a type of genomic stability that maintains stable single repeated sequences, hence a failure of this process could deviate in cancer development. A characteristic phenotype of MMR-deficient cells is microsatellite instability (MSI) that could be modulated by mutagenic agents. The induction of MSI by the mutagens, bleomycin (BLM), hydrogen peroxide (H(2)O(2)), 2-acetylaminofluorene (2-AAF) and ethidium bromide (EB) was evaluated in vivo, by using a Drosophila melanogaster-null mutant of the msh2 mismatch repair gene (spel1). Whereas in the germ cells of the spel1 strain, we found microsatellite mutations in the five repeated sequences studied in untreated individuals, no alterations were found in the MMR-proficient strain. On the other hand, the data obtained from the treatment experiments show that BLM and 2-AAF induced a slight mutagenic effect in the MMR-deficient background but not in the normal one. These results indicate that the use of the Drosophila spel1 mutant (MMR-deficient) could be of relevant importance to identify environmental factors involved in carcinogenesis processes through genomic instability.
We report a patient with progressive external ophthalmoplegia (PEO), exercise intolerance, and deafness after aminoglycoside exposure, harboring two pathogenic mutations in her mtDNA: an A1555G in the 12S rRNA gene and a G4309A in the tRNA(Ile) gene. Muscle histochemistry showed abundant ragged-red fibers, and biochemistry revealed normal respiratory chain function. The A1555G mutation was homoplasmic in blood from the proband and from all maternal relatives. The G4309A mutation was abundant in the proband's muscle, less abundant in her blood, still less abundant in the mother's blood, and absent in blood from other maternal relatives. Family members were asymptomatic. Our data suggest that the former mutation resulted in aminoglycoside-induced deafness and the latter caused PEO plus exercise intolerance.
Some drinks containing natural products with stimulant properties are highly consumed among young adults. The market for these drinks has increased in past years around the globe, and, although they might be harmless, overdoses or combination of these with other drinks could be harmful to the health of some consumers in certain circumstances. Samples were obtained at food shops and different popular brands were chosen. Cytotoxicity tests used were neutral red uptake, total protein content, and tetrazolium assay on Chinese hamster ovary cells. Results revealed that tested samples were not cytotoxic; however, studies have demonstrated the toxicity of high concentrations of some of these products. For this reason, the authors considered it to be of critical importance to carryout an in vitro toxicity screening of stimulant soft drinks that are highly consumed.
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The aim of the study was to prospectively evaluate pre- and postoperative findings of cystodefecoperitoneography (CDP) and to correlate the findings to the clinical examination in patients with genital prolapse. Twenty-five female patients were investigated both pre- and postoperatively with a standardized questionnaire, clinical examination and CDP, including contrast medium in the rectum, vagina, bladder, small bowel and peritoneal cavity. At preoperative clinical examination a rectocele was diagnosed in 24 patients, a cystocele in 7 and an enterocele in 2. At the preoperative CDP a rectocele was diagnosed in 21 patients, a cystocele in 22 patients and a peritoneocele in 9, of which six contained small bowel (i.e. an enterocele). Surgery was performed according to the clinical findings. At the postoperative clinical examination no rectocele was diagnosed, a cystocele was diagnosed in 3 patients and an enterocele in 1. Postoperative CDP showed a rectocele in 4 patients, a cystocele in 24 and a peritoneocele in 7 patients, of which three contained small bowel (i.e. an enterocele). CDP may complement the clinical assessment of patients with genital prolapse, in particular to confirm or detect defects involving the posterior compartment. The radiologic definition of cystocele needs further evaluation.
The clinical records of 70 patients seen at our hospital between 1976 and 1998 and diagnosed as suffering from chronic myelomonocytic leukaemia (CMML) were reviewed in order to confirm the validity of the classification into two forms of disease that the French-American-British Co-operative Leukaemia Group (FAB) proposed in 1994: myelodysplastic (MD) and myeloproliferative (MP), depending on the peripheral white blood cell count (WBC) (less or more than 13 x 10(9)/l, respectively). After the rejection of incomplete records and lost to follow up patients, our study population consisted of 49 records. Our results confirm that, even though this classification is useful in order to separate two classes of patients, it is not enough to predict the prognosis in an accurate manner. A lot of studies have tried to find some prognostic factors, but the results have been discordant. The multivariate analysis of our group of patients showed three prognostic factors: serum lactate dehydrogenase (LDH) >1.5 times normal level, blasts in bone marrow >5%, and peripheral blood leukocytes >10 x 10(9)/l. A second multivariate analysis led us to distinguish two groups: high risk (2-3 risk factors) and low risk (0-1 risk factors) (median survival 7 and 44 months, respectively) with a very high statistic significance (P<0.0001). This score should be applied to other series of CMML patients in order to confirm its validity.
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Meconium aspiration syndrome is a major contributor to neonatal respiratory distress in infants and it has been sporadically recognized in neonatal animals. This investigation was designed to study the short and long term effects of meconium and amniotic fluid in the lungs of neonatal rats. Seven-day-old rats (n = 123) divided in three groups were intratracheally inoculated with saline solution, amniotic fluid or meconium. Rats were euthanatized on 1, 3, 7, 14, 28, 56 and 112 postinoculation days (PID) and the lungs were examined by light microscopy. Saline solution did not induce any change while amniotic fluid elicited only a mild foreign body response which disappeared by PID 14. In contrast, meconium induced an exudative alveolitis characterized by recruitment of neutrophilsn in the bronchoalveolar spaces. Meconium also induced atelectasis, hyperinflation and thickening of alveolar septa all of which had disappeared by PID 14. Starting at PID 7, neutrophils were progressively replaced by macrophages, giant cells, and some fibroblasts. There were sporadic foci of mineralization starting at PID 14 and lasting up to PID 112. Some mineralized foci became lined with cuboidal epithelial cells at PID 28. Meconium was slowly degraded but still evident by PID 112. It was concluded that inoculation of meconium in neonatal rats induces acute microscopic changes typical of meconium aspiration syndrome. The long term lesions induced by meconium consisted of persistent multifocal histiocytic alveolitis and bronchiolitis reaction with occasional foci of calcification.
CD61 is a membrane glycoprotein that associates with CD41 (alphaIIb) to form the heterodimeric complex gpIIb/IIIa (CD41/CD61), predominantly expressed in platelets and megakariocytes. CD61 or beta3 integrin also associates with alpha v (CD51) to form the vitronectin receptor, which is expressed in many tissues. We have used a monoclonal antibody against the porcine gpIIIa or CD61 (JM2E5) to study the distribution of this molecule in different normal pig tissues. As in humans, CD61 was broadly expressed in all tissues examined. In the kidney, strong expression of CD61 was observed in epithelial cells from renal tubules. In the testis, CD61 expression was detected in the Leydig cells. However, in liver, CD61 was weak or not detected. Many integrins are particularly involved in tumogenicity and in tumor progression mediating cell-cell interaction. Immunofluorescence experiments using cultured human tumor HeLa cells showed nuclear and cytoplasmic staining of mAb JM2E5. Immunohistochemical analysis of human tumor sections from several organs showed a heterogeneus distribution in metastatic cases from colon and breast carcinoma. However, no staining was found in metastasis from melanoma.
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Magnetic resonance imaging (MRI) has allowed us to establish a set of radiologic signs associated with intracranial hypotension syndrome. Findings are partly influenced by cerebral displacement. Intracranial hypotension syndrome is characterized by a decrease in cerebrospinal fluid (CSF) pressure to less than 60 mm H2O associated with occipital headache radiating to the frontal and temporal zones. For diagnostic purposes, the most common cause is anesthetic or therapeutic dural puncture, although spontaneous CSF leakage can occur. CSF protein and lymphocyte counts may be high, while the cranial meninges biopsy is normal. MRI images may show a descended brain, taking the start of the sylvian aqueduct and the location of the cerebellar amygdalae as points of reference; diminished size of the subarachnoidal cisterns and occasionally of the cerebral ventricles; meningeal enhancement from increased uptake of the contrast solution; subdural hygromas and hematomas; and pituitary enlargement. Paraspinal fluid and dilated epidural veins may be observed. Radiologic images and clinical signs are related. When CSF pressure is very low, there is greater meningeal enhancement, subdural collection and cerebral displacement. Findings gradually disappear as symptoms diminish. The signs and symptoms that might develop during intracranial hypotension syndrome vary according to the brain structure that might be affected during descent, repositioning and the traction of anchoring structures. MRI allows the degree of cerebral and spinal involvement to be ascertained, to predict whether resolution of the clinical picture will be early or late and to visualize the effect of approaches to reducing CSF leakage.
Histiocytic necrotizing lymphadenitis, Kikuchi Fujimoto's disease (KFD) is characterised by fever and lymphadenopathy, usually large cervical, unilateral lymph nodes. Such clinical presentation demands a work-up to exclude serious medical conditions like malignancy and infections. Foci of necrosis with lymphocytic Histiocytic predominance in association with scarce polymorphonuclear cells on lymph node examination, confirm the diagnosis of KFD. Many different patterns of computed tomographic (CT) appearance of KFD have been reported. We describe the CT scan finding in two patients with this disease. All our cases showed, after two and three weeks of evolution respectively, enlarged lymph nodes with hypodense centres and peripheral ring enhancement. These radiological alterations correlated with the central lymph node necrosis found in the anatomopathological studies. In conclusion, KFD should be considered in patients with fever, cervical lymph node enlargement and CT scan showing hypointense centres and peripheral ring enhancement.
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AIM: To describe the distribution of intraneural adipose cells in relation to nerve fascicles in a portion of peripheral nerve usually involved in accomplishing an anesthetic blockade of a lower extremity. METHOD: Using a scanning electron microscope, we studied sciatic nerve samples from the point of amputation of a lower limb of three patients. The samples were obtained at the upper angle of the popliteal fossa, 10-15 cm cephalad to the knee joint line. RESULTS: During dissection of the sciatic nerve samples, we observed a solitary trunk, but examination of the cross-sections under the microscope revealed the components of two clearly separated branches joined by supporting tissue. The sciatic nerve had an oval form in the portion under study, measuring 6.5 to 7.5 mm by 3.6 to 3.9 mm. Between the fascicles, the adipose tissue varied in thickness from 0.5 mm in the central zones to 0.2 mm in the peripheral zones. The adipocytes, which were all similar in the size with diameters of 40 microns, were empty, as a result of elimination of the lipid vacuoles during fixation. The adipose tissue was distributed inside the epineurium to surround isolated fascicles or groups of fascicles. CONCLUSIONS: The adipose tissue inside a nerve surrounded the fascicles to form adipose sheaths that separated the fascicles from one another. The thicknesses of these adipose sheaths varied from one fascicle to another. Cells join to make it possible to create a compact adipose sheet that can delay the diffusion of local anesthetic injected near a nerve and that can therefore interfere with the characteristics of an anesthetic blockade.
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Foot and mouth disease (FMD) was first recognised in South America in 1870, almost simultaneously in the province of Buenos Aires (Argentina), in the central region of Chile, in Uruguay, in southern Brazil and coincidentally, on the northeastern coast of the United States of America. The epidemiology of the disease was unknown and no government action was taken following the initial outbreaks. This resulted in the disease spreading to other areas of Chile, as well as to Peru, Bolivia and Paraguay, reaching Venezuela and Colombia in the 1950s, and Ecuador in 1961. The entire continent was affected in the 1960s when national FMD control programmes were initiated, with the exception of Guyana, Surinam, French Guiana and Patagonia. In the 1970s, steps were taken to implement a regional control and eradication strategy in view of the impact of production and trade on the persistence of the virus. The Plan Hemisférico de Erradicación de la Fiebre Aftosa (PHEFA: Hemispheric FMD Eradication Plan), public- and private-sector policies, new diagnostic tools, the oil-adjuvanted FMD vaccine and regional strategies played a part in improving the epidemiological situation during the 1990s. A setback was encountered in 2000 and 2001, with outbreaks due to virus types A and 0 recorded in Argentina, Uruguay and Brazil.