Neurocysticercosis in Persons with Epilepsy in Medellín,Colombia

Summary: Purpose: A prospective series of 643 persons with epilepsy attending a reference neurologic center in Medellin, Colombia, was examined by computed tomography (CT scan) or serology or both with the enzyme-linked immunoelectrotransfer blot assay (EITB) to assess the prevalence of Taenia solium cysticercosis. Methods: All presenting patients were consecutively enrolled in the study. Five hundred forty-six persons underwent cerebral CT scans; 376 of them also had serum EITB performed. Results: Prevalence of neurocys@ercosis by CT scan was 13.92%. Overall prevalence of T. solium antibodies with EITB was 9.82%, but for those with late-onset epilepsy (onset after age 30 years), prevalence increased to 17.5% and 19% for those who originated from outside urban Medellin. Seroprevalence in individuals with mixed lesions (cysts and calcifications) was 88.2% and 64.10% in those with live cysts. Conversely, only 2.72% of persons with CT findings not related to neurocysticercosis had positive EITB tests. Conclusions: Our study shows that an important proportion of individuals with epilepsy have radiologic or serologic evidence of T. solium infection, suggesting that neurocysticercosis is an important etiology for epilepsy in Colombia.     

Pineal "synaptic" ribbons evolution over a 24 hour period during two different photoluminous seasons, a comparative and statistical analysis.

A comparative statistical analysis of "synaptic ribbons" evolution over a 24 hour period during two different photoluminous seasons (September, and winter) is carried out. Seventy male rats were used. Statistical analysis involved the Kolmogorov-Smirnov test, variance analysis, the Student t-test and Pearson's correlation test. The results show that "synaptic ribbons" evolve during the circadian phase and through two different seasons, with a clear and marked influence of point-time (p < 0.0001) and season (p < 0.0001).     

Hemorheological alterations in mild essential hypertension.

Blood rheological properties were studied in 21 patients suffering from essential hypertension (EHT), degree I-II according to WHO criteria. These patients were diagnosed "de novo". The whole blood filterability (WBF), blood viscosity (BV) at 230 s-1 and 23 s-1, red cell deformability (FI), erythrocyte aggregation in autologous (MEA) and normal plasma (MEAc), fibrinogen (Fbg) and hematocrit (Ht) have been evaluated. In the hypertensive patients we have found decreased WBF, greater BV and FI in comparison with the control group (p less than 0.001). Likewise, MEA and Fbg were increased, though the differences were less significant (p less than 0.01). The evaluation of Ht did not show any differences between the two groups. The results suggest that in the newly diagnosed EHT, clear hemorheological alterations occur, both in plasma and in the erythrocytes, which could play a role in the pathogenesis of the aforementioned disease.     

Free-floating left atrial thrombus in hypertrophic cardiomyopathy: echocardiographic findings

We report a free-floating left atrial thrombus detected by 2-dimensional echocardiography in a patient with hypertrophic cardiomyopathy. Two-dimensional echocardiography permitted definitive diagnosis, thereby indicating emergency cardiac surgery. To our knowledge, this is the first reported detection of a free-floating left atrial thrombus by 2-dimensional echocardiography in a patient with hypertrophic cardiomyopathy.     

Years of potential life lost: application of an indicator for assessing premature mortality in Spain and Portugal

In this article, the authors present an analysis of causes of death in Spain and Portugal in 1984 based on a calculation of the "years of potential life lost" (YPLL) between the first and the 70th birthdays, the latter age corresponding approximately to the average life expectancy in both countries. This analysis of the YPLL led to a substantially different ranking of the main causes of death, based on what might be termed "premature mortality" compared with that obtained from more conventional mortality indices. According to this criterion, which is especially appropriate for the planning and evaluation of health interventions, the main causes of premature death (1-69 years) in the two countries of the Iberian peninsula are malignant tumours and, particularly in Portugal, violent deaths (especially motor-vehicle accidents, but also suicides). This is in contrast to the predominance of cardiovascular diseases indicated by other weightings of age-specific mortality rates. Portugal shows significantly worse YPLL rates than Spain not only for general mortality (45% higher than in Spain), but also for several major groups of causes. In Spain only malignant neoplasms, diabetes and chronic rheumatic heart diseases show higher specific mortality rates than in Portugal, based on traditional mortality indicators.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of furosemide upon urinary kallikrein excretion

Having in mind the significant decrease of urinary kallikrein in rat with renal hypertension and in humans with essential hypertension, the effects of furosemide on kininogenase activity has been studied in urine of normal and hypertensive rats which received tap water or a 1% NaCl solution for drinking. Administration of 20 mg furosemide which produces maximal diuretic effect in normal rats, induced in these animals a 150–200% increase of the excretion of this enzyme after 8 hours, when compared to the activity measured before giving the drug. This increase which is observed in the normal rats drinking either water or a 1% NaCl solution shows a significant correlation with the excretion of sodium, potassium and water. In hypertensive rats, in 7 or 9 cases, an increase of kallikrein excretion (200–600%) is observed, which does not reach the levels of excretion in normal untreated rats. Furosemide did not produce increase of urinary kallikrein in hypertensive rats drinking 1% NaCl solution.     

Amyloidosis and the serum amyloid A protein response to muramyl dipeptide analogs and different mycobacterial species.

Serum amyloid A protein (SAA) elevation accompanies induction of secondary amyloidosis in mice given Mycobacterium butyricum in Freund adjuvant. The synthesis of SAA by cultured hepatocytes is induced by a macrophage-derived mediator, which has been identified as interleukin 1. In these studies, SAA synthesis has been used as an index of macrophage activation to examine the in vivo response of mice to challenge with seven different mycobacteria and with synthetic analogs of the immunoadjuvant N-acetylmuramyl-L-alanyl-D-isoglutamine [MDP(L-D)]. SAA synthesis was stimulated by administration (by the intraperitoneal route) of the mycobacteria dissolved in saline, with Mycobacterium vaccae being the most active and Mycobacterium leprae being the least stimulatory. MDP(L-D), which is the minimal structure (molecular weight, 492) able to substitute for mycobacteria in Freund adjuvant, stimulated SAA synthesis, whereas the MDP(D-D) isomer was inactive. The butyl ester of MDP, which induces no detectable pyrogenicity but retains adjuvanticity, required a 100-fold greater dosage than MDP(L-D) in stimulating SAA synthesis. Amyloidosis was detected histologically only when active SAA inducers MDP(L-D), M. vaccae, and M. butyricum, were administered in incomplete Freund adjuvant, with amyloid-enhancing factor. These studies demonstrated that SAA elevation was a sensitive in vivo marker of the capacity of antigens to stimulate macrophages to produce interleukin 1. A point of considerable relevance to the human use of MDP was the observation that repeated injections of the adjuvant MDP in saline did not induce secondary amyloidosis.     

Characterization of plasmid-borne afa-3 gene clusters encoding afimbrial adhesins expressed by Escherichia coli strains associated with intestinal or urinary tract infections.

The afa gene clusters encode afimbrial adhesins (AFA) that are expressed by uropathogenic and diarrhea-associated Escherichia coli strains and belong to a family of hemagglutinins recognizing the Dr blood group antigen as a receptor. This family so far includes AFA-I and AFA-III as well as the Dr and F1845 adhesins (B. Nowicki, A. Labigne, S. Moseley, R. Hull, S. Hull, and J. Moulds, Infect. Immun. 58:279-281, 1990). Reported in this work is the genetic organization of the afa-3 gene cluster cloned from a uropathogenic E. coli strain (A30) which expressed a subtype of AFA designated AFA-III. The amino acid sequence of AFA-III was deduced from the nucleotide sequence of the afaE3 gene and was found to be highly homologous to that of the Dr adhesin (98.1% identity). A polymerase chain reaction assay was developed to detect the presence of afa-3 gene clusters in E. coli strains. Study of the genetic support of the afa-3 gene clusters in the strains which showed positive amplification revealed that they were always located on large, 100-kb plasmids whether the strains originated from patients with cystitis or with diarrhea. Moreover, the cloned afa-3 gene clusters from A30 and from the diarrhea-associated strain AL845 appeared to be carried by 9-kb plasmid regions which displayed a similar genetic organization. Chloramphenicol was reported to be a potent inhibitor of receptor binding by the Dr adhesin (Nowicki et al., Infect. Immun. 58:279-281, 1990). AFA-III expressed by strains AL845 and AL847 appeared to mediate, like the Dr adhesin, chloramphenicol-sensitive hemagglutination, whereas AFA-III produced by A30 conferred chloramphenicol-resistant adherence. A comparison of the sequences of these four proteins indicated that the amino acid at position 52 of the processed AFA could be part of the receptor-binding domain.     

Transplant aspirative cytology: Analysis of morphological and immunocytochemical parameters in renal allograft dysfunction

We have analyzed 245 transplant aspirative cytologies (TACs) from 96 renal allograft patients. TACs were divided in two chronological groups: Early (TACs performed during the first 3-mo post-transplantation) and late (TACs performed after the third month post-transplantation), in order to assess the effect of allograft tolerance on TAC features. Both morphological and immunocytochemical aspects were evaluated, including CD4, CD8, IL2-R, and HLA-DR immunolabeling. A final diagnosis for each case of allograft dysfunction was achieved by other independent diagnostic means. Four diagnostic groups were considered in the present study: acute rejection (AR), chronic rejection (CR), acute tubular necrosis (ATN), and Cyclosporin A toxicity (CsA-T). In addition, a control group (C) was established from patients with stable allograft function. We found that immunocytochemical analysis of TACs is particularly helpful in the diagnosis of late allograft dysfunction, a time period when the simple cytological study of renal infiltrate is not informative enough to help take therapeutic decisions.     

Loss of cell polarity causes severe brain dysplasia in Lgl1 knockout mice

Disruption of cell polarity is seen in many cancers; however, it is generally considered a late event in tumor progression. Lethal giant larvae (Lgl) has been implicated in maintenance of cell polarity in Drosophila and cultured mammalian cells. We now show that loss of Lgl1 in mice results in formation of neuroepithelial rosette-like structures, similar to the neuroblastic rosettes in human primitive neuroectodermal tumors. The newborn Lgl1(-/-) pups develop severe hydrocephalus and die neonatally. A large proportion of Lgl1(-/-) neural progenitor cells fail to exit the cell cycle and differentiate, and, instead, continue to proliferate and die by apoptosis. Dividing Lgl1(-/-) cells are unable to asymmetrically localize the Notch inhibitor Numb, and the resulting failure of asymmetric cell divisions may be responsible for the hyperproliferation and the lack of differentiation. These results reveal a critical role for mammalian Lgl1 in regulating of proliferation, differentiation, and tissue organization and demonstrate a potential causative role of disruption of cell polarity in neoplastic transformation of neuroepithelial cells.