Arthrogryposis multiplex congenita. Search for prenatal factors in 66 sporadic cases

In a family and epidemiological survey of 66 cases of arthrogryposis multiplex congenita all cases were found to be sporadic and no family association with clubfoot, congenital dislocation of the hip, or hereditary neuromuscular disease was found. The mothers were significantly older than average. Oligohydramnios was noted in only one-third of cases but many other complications of pregnancy, including probable attempts at abortion, had occurred. It is likely that most cases of arthrogryposis are nongenetic and result from a defective intrauterine environment, whether hormonal, vascular, mechanical, or possibly infective.     

Evaluation of Taenia solium and Taenia crassiceps cysticercal antigens for the serodiagnosis of neurocysticercosis

We evaluated the usefulness of seven cysticercal antigen extracts, four from Taenia solium cysticerci (whole parasite-TsoW, membrane-TsoMe, vesicular fluid-TsoVF and scolex-TsoSc) and three from T. crassiceps cysticerci (whole parasite-TcraW, membrane-TcraMe and vesicular fluid-TcraVF), for serodiagnosis of neurocysticercosis with an enzyme-linked immunosorbent assay (ELISA). Cysticercus-specific IgG were screened in serum samples from 23 patients with neurocysticercosis, 32 patients with other infections and 48 healthy persons. The best results were obtained with the TsoVF-ELISA (91.3% sensitivity; 96.2% specificity) and TcraVF-ELISA (91.3% sensitivity; 95% specificity). The ELISA done with whole parasite and membrane extracts from cysts of T. solium and T. crassiceps and the scolex extract from T. solium cysts showed a low performance in terms of sensitivity, ranging from 47.8% to 73.9%. None of the antigen preparations from T. solium and T. crassiceps cysticerci used in this study showed outstanding performance for the serodiagnosis of neurocysticercosis. However, considering the results obtained with the seven antigen preparations, vesicular fluid from T. solium and T. crassiceps cysticerci may be useful for detecting specific antibodies in sera from patients with neurocysticercosis.     

Cockroach allergens

Cockroaches produce several potent allergens associated with sensitization and the development of asthma. Many of these allergens have been cloned and produced as biologically active recombinant proteins. Three-dimensional structure and molecular modeling, in addition to studies on the biological functions of these proteins in the cockroach, have provided new insights into the ability of these allergens to cause immunoglobulin E antibody responses. Recent studies have pointed to a potential role of recombinant cockroach allergens for diagnosis and the development of novel therapeutic strategies that may benefit cockroachallergic patients.     

Influence of chemical and mechanical polishing on water sorption and solubility of denture base acrylic resins

Influence of polishing methods on water sorption and solubility of denture base acrylic resins was studied. Eighty samples were divided into groups: Classico (CL), and QC 20 (QC) - hot water bath cured; Acron MC (AC), and Onda Cryl (ON) - microwave cured; and submitted to mechanical polishing (MP) - pumice slurry, chalk powder, soft brush and felt cone in a bench vise; or chemical polishing (CP) - heated monomer fluid in a chemical polisher. The first desiccation process was followed by storage in distilled water at 37 +/- 1 masculineC for 1 h, 1 day, 1, 2, 3 and 4 weeks. Concluding each period, water sorption was measured. After the fourth week, a second desiccation process was done to calculate solubility. Data were submitted to analysis of variance, followed by Tukey test (p<0.05). Means of water sorption (%) and solubility (%), respectively, were: CL-MP: 1.92 and 0.02; CL-CP: 1.98 and 0.52; QC-MP: 2.31 and -0.05; QC-CP: 2.32 and 0.25; AC-MP: 2.45 and -0.07; AC-CP: 2.43 and 0.41; ON-MP: 2.32 and -0.06; ON-CP: 2.34 and 0.27. Mechanical polishing promoted significantly lower solubility of acrylic resins; initially, water sorption values were higher for chemically polished samples, however, after 4 weeks all groups were similar.     

Spinal adrenal cortical adenoma with oncocytic features: report of the first intramedullary case and review of the literature

Ectopic adrenal cortical neoplasms are extremely rare, and only a few have involved the CNS. We report the first case of an intramedullary oncocytic adrenal cortical neoplasm of the spinal cord with immunohistochemical (IMHC) confirmation. A 27-year-old man presented with progressive lower extremity weakness, spastic paraparesis, decreased reflexes, and hypoesthesia below T10. A spinal myelogram showed cauda equina blockade and obliteration of sacral nerve roots. This prompted emergent surgical intervention. A well-circumscribed, approximately 3 x 2 cm, light brown to tan, intramedullary tumor was identified at the level of the conus medullaris. Histologically, the tumor showed sheets and nests of plump, cytologically bland polygonal cells with abundant eosinophilic cytoplasm. A single mitosis, but no necrosis, was identified. By IMHC, the cells were positive for inhibin, melan-A, and synaptophysin, and negative for GFAP, EMA, cytokeratins, S-100, HMB-45, and chromogranin. Electron microscopy study performed from paraffin-embedded tissues demonstrated abundant mitochondria, and lipid vacuoles. This case confirms the occurrence of adrenal cortical neoplasms in the CNS and is the first report of an intradural, intramedullary adrenal cortical adenoma of the spinal cord, and the first to occur in a male. This tumor should be considered in the differential diagnosis of tumors of the CNS.     

Ionotropic glutamate receptors regulating labeled acetylcholine release from rat striatal tissue in vitro: possible involvement of receptor modulation in magnesium sensitivity

This study evaluated the role of glutamate ionotropic receptors on the control of [3H]acetylcholine ([3H]ACh) release by the intrinsic striatal cholinergic cells. [3H]-choline previously taken up by chopped striatal tissue and converted to [3H]ACh, was released under stimulation by glutamate, N-methyl-d-aspartate (NMDA), kainate and a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA). Experiments were conducted in the absence of choline uptake inhibitors or acetylcholinesterase inhibitors. A paradigm of two stimulations was employed, the first in control conditions and the second after 9 min of perfusion with the test agents MK-801, 2-amino-5-phosphonopentanoic acid (AP-5), tetrodotoxin (TTX), 6,7-dinitroquinoxaline-2,3-dione (DNQX), 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo-[f]quinoxaline-7-sulfonamide (NBQX), glycine and magnesium. Our results support that (1) in the absence of Mg2+, NMDA is the most effective agonist to stimulate [3H]ACh release from striatal slices (2) magnesium effectively antagonized kainate and AMPA stimulation suggesting that at least part of the kainate and AMPA effects might be attributed to glutamate release (3) besides NMDA, kainate receptors showed a more direct involvement in [3H]ACh release control based on the smaller dependence on Mg2+ and less inhibition by TTX and (4) stimulation of ionotropic glutamate receptors may induce long lasting biochemical changes in receptor/ion channel function since the effects of TTX and/or Mg2+ ions on [3H]ACh release were modified by previous exposure of the tissue to agonists.     

Lung microvascular permeability and neutrophil recruitment are differently regulated by nitric oxide in a rat model of intestinal ischemia-reperfusion

We investigated the effect of two inhibitors of nitric oxide (NO) synthesis, N(w)-nitro-L-arginine methyl ester (L-NAME) and aminoguanidine, on lung inflammation caused by intestinal ischemia/reperfusion in rats. Relative to the sham-operated rats, intestinal ischemia/reperfusion (ischemia: 45 min; reperfusion: 30 min, 2 and 4 h) induced neutrophil recruitment (increased myeloperoxidase activity) and increased microvascular permeability (Evans blue dye extravasation) in the lungs and increased tumor necrosis factor (TNF) levels in the serum (L-929 cytotoxicity assay). L-NAME given before the ischemia exacerbated neutrophil accumulation, plasma extravasation, serum TNF and caused death of the animals, which was prevented by concomitant injection of L-arginine. Lung and systemic effects of intestinal ischemia/reperfusion were not modified when L-NAME was given just before reperfusion. Treatment with aminoguanidine inhibited plasma extravasation without affecting the other parameters evaluated. Dexamethasone reduced all the parameters. Our results indicate that during intestinal ischemia/reperfusion both constitutive and inducible NO synthases are called to exert a differential modulatory effect on lung inflammation and that maintenance of adequate levels of NO during ischemia is essential for the animals survival.     

Interaction between paraventricular nucleus and medial septal area on the renal effects induced by adrenaline

The aim of the present study was to analyze the role of alpha1, alpha2-adrenoceptors, and the effects of losartan and PD123319 (selective ligands of the AT1 and AT2 angiotensin receptors, respectively) injected into the paraventricular nucleus (PVN) on the diuresis, natriuresis, and kaliuresis induced by administration of adrenaline into the medial septal area (MSA). Male Holtzman rats with a stainless steel cannula implanted into the MSA and bilaterally into the PVN were used. The administration of adrenaline into the MSA increased in a dose-dependent manner the urine, sodium, and potassium excretions. The previous administration of prazosin (an alpha1-adrenoceptor antagonist) injected into the PVN abolished the above effects of adrenaline, whereas yohimbine (an alpha2-adrenoceptor antagonist) doesn't affect the diuresis, natriuresis, and kaliuresis induced by adrenaline. Pretreatment with losartan into the PVN decreased in a dose-dependent manner the urine, sodium, and potassium excretions induced by MSA administration of adrenaline (50 ng), while PVN PD123319 was without effect. These results indicate that urinary and electrolyte excretion effects induced by adrenaline into the MSA are mediated primarily by PVN AT1 receptors. However, the doses of losartan were more effective when combined with the doses of PD123319 than given alone, suggesting that the urinary, natriuretic, and kaliuretic effects of MSA adrenaline may involve activation of multiple angiotensin II receptors subtypes into the PVN.     

Moxonidine and rilmenidine injected into the medial septal area reduces the salivation induced by pilocarpine

We determined the effects of moxonidine and rilmenidine 20 nmol (alpha(2)-adrenergic and imidazoline receptor agonists) injected into the medial septal area (MSA) on the pilocarpine-induced salivation, when injected intraperitoneally (i.p.), of male Holtzman rats weighing 250-300 g, with stainless-steel cannula implanted into the MSA. The rats were anesthetized with zoletil 50 mg kg(-1) b.wt. (tiletamine chloridrate 125.0 mg and zolazepan chloridrate 125.0 mg) into quadriceps muscle intramuscularly (IM), saliva was collected using pre-weighed small cotton balls inserted in the animal's mouth. The pre-treatment with moxonidine injected into the MSA reduced the salivation induced by pilocarpine (1 mg kg(-1)) injected i.p. (12+/-3 mg min(-1)) vs. control (99+/-9 mg min(-1)). The pre-treatment with rilmenidine 40 nmol also reduced the salivation induce by pilocarpine injected i.p. (20+/-5 mg min(-1)) vs. control (94+/-7 mg min(-1)). Idazoxan 40 nmol (imidazoline receptor antagonist) injected into the MSA previous to moxonidine and rilmenidine partially blocked the effect of moxonidine and totally blocked the rilmenidine effect in pilocarpine-induced salivation injected i.p. (60+/-8 and 95+/-10 mg min(-1), respectively). Yohimbine 40 nmol (alpha(2)-adrenergic receptor antagonist) injected into the MSA previously to moxonidine and rilmenidine partially blocked the moxonidine effect but produced no change on the rilmenidine effect on i.p. pilocarpine-induced salivation (70+/-6 and 24+/-6 mg min(-1), respectively). Injection of these alpha(2)-adrenergic and imidazoline agonists and antagonists agents i.p. produced no change on i.p. pilocarpine-induced salivation. These results show that central, but not peripheral, injection of alpha(2)-adrenergic and imidazoline agonists' agents inhibit pilocarpine-induced salivation. Idazoxan, an imidazoline receptor antagonist, totally inhibits the rilmenidine effect and partially inhibits the moxonidine effect on pilocarpine-induced salivation. Yohimbine produced no change on rilmenidine effect but partially inhibited the moxonidine effect. Both of these antagonists when injected into the MSA previous to pilocarpine i.p. potentiated the sialogogue effect of pilocarpine. The results suggest that alpha(2)-adrenergic/imidazoline receptor of the MSA when stimulated blocked pilocarpine-induced salivation in rats when injected intraperitonially. These receptors of the medial septal area have an inhibitory mechanism on salivary secretion.