Brain stem auditory evoked potentials in determining site of lesion of brain stem gliomas in children

Brain stem auditory evoked potential (BAEP) test results are reported on seven children (2 1/2-13 years) with brain stem neoplasms. In each case, the BAEP test results clearly indicated the site of lesion as determined by computerized tomography and observation during surgery. Seven criteria for the assessment of BAEP test results are also presented: 1. Peak latency, 2. Intra-peak latency, 3. Inter-peak latency, 4. Response stability, 5. Amplitude, 6. Waveshape, and 7. Peak presence. Six children had positive indications on at least four of the seven criteria described, while one child had two positive indications. However, dramatic abnormality on any single criterion warrants serious investigation.     

Analysis of test-retest variability in facial electroneurography

Facial electroneurography is an objective electrophysiologic measurement of a muscle compound action potential used to assess prognosis for recovery from facial paralysis. In the present study, test precision is accompanied by a test-retest variability of 6.2%. The primary source of this variability is trigeminal nerve artifact, but submaximal nerve stimulation, changing skin resistance, and inherent nerve properties may also influence results. An ideal stimulus intensity that avoids patient discomfort and trigeminal nerve artifact but attains maximal nerve response is not possible in every patient.     

Fading and tachyphylaxis to the contractile effects of substance P in the guinea-pig ileum

Substance P (SP) caused an immediate and vigorous contraction of the longitudinal smooth muscle layer of the guinea-pig ileum. The contractile response to SP, unlike that to acetylcholine or histamine was not maintained but faded to baseline levels in about 6 min. When 0.3-1.0 nM SP was added the fading time was shorter than 6 min and tachyphylaxis did not develop. Higher concentrations of SP produced fading times of about 6 min that could not be increased even by adding extremely high concentrations of the peptide, up to 1800 nM. Short fading times and the lack of development of tachyphylaxis are the result of the rapid adsorption and/or metabolism of SP. The addition of exogenous peptidases such as pronase, chymotrypsin and an extract of black widow spider venom gland dramatically increased the rate of degradation of SP, shortened the fading response and blocked the development of tachyphylaxis. Tetrodotoxin and atropine reduced the fading time by 25%, while eserine increased its duration several-fold; these findings are consistent with the existence of a cholinergic nerve component in the mediation of some of the effects of SP receptor and, in part, to adsorption and metabolism of the peptide. The magnitude of the tachyphylaxis to SP was proportional to the concentration of the desensitizing dose of the peptide and was specific to SP and to the related peptide physalaemin; no cross-tachyphylaxis towards other agents was found.     

The Mechanism of Vanadium-Mediated Developmental Hypomyelination Is Related to Destruction of Oligodendrocyte Progenitors Through a Relationship with Ferritin and Iron

The second post-natal week in rat is the period of the most intense oligodendrocyte development and myelination. This period coincides with peak iron import by oligodendrocytes. During that time oligodendrocyte progenitors (OPCs) are sensitive to agents that may disturb normal iron homeostasis and assimilation of iron into these cells. One mechanism by which iron homeostasis can be disrupted is by environmental exposure to other metals. Vanadium is a transition metal, and exposure to vanadium during early brain development produces hypomyelination with variety of related neuro-behavioral phenotypes. In the current study, we investigated mechanisms of hypomyelination induced by vanadium exposure in developing rat brain. We demonstrate that both in vivo and in vitro, OPCs are more sensitive to vanadium exposure than astrocytes or mature oligodendrocytes. Vanadium exposure in OPCs resulted in increased ROS generation and increased annexinV labeling suggestive of apoptosis. Because ferritin is a major iron delivery protein for oligodendrocytes, we exposed the cells to recombinant ferritin and iron both of which exacerbated vanadium cytotoxicity, while the iron chelator desferroxamine (DFO) prevented cytotoxic/apoptotic effects of vanadium. To illustrate relationship between ferritin and vanadium, we demonstrate that vanadium exacerbated DNA nicking produced by iron-rich spleen ferritin, but not iron-poor apoferritin, resulting in a single and double strand breaks in a DNA relaxation assay. We propose that developmental exposure to vanadium interferes with normal iron assimilation into oligodendrocytes resulting in oxidative stress and apoptosis. Therefore, depletion of OPCs due to vanadium exposure in early post-natal period may be an important mechanism of vanadium-induced hypomyelination.     

Mycotic pseudoaneurysm caused by Mycobacterium tuberculosis

Mycobacterium tuberculosis can involve any organ of the body, including the arteries. Usually the mycobacteria infects the arterial wall spreading from a contiguous foci. We report a case of tuberculous pseudoaneurysm involving the iliac artery clinically manifested as fever of unknown origin. The diagnosis relied on abdominal CT-scanning. Tuberculous etiology was confirmed postoperatively by microbiologic and microscopic study. The antituberculous therapy was early started, but the patient died three months later as a consequence of a non-infectious abdominal aortic rupture. Clinicians should consider tuberculous etiology when the diagnosis of mycotic pseudoaneurysm is being entertained.     

Primary biliary cirrhosis-autoimmune hepatitis overlap syndrome. Contribution of two new cases

The autoimmune hepatitis (AIH)-primary biliary cirrhosis (PBC) overlap syndrome is characterized for clinical, biochemical, immunological, and histological features overlapping those of AIH and PBC, whose pathogenesis and more appropriate treatment are unknown at present. We describe two new patients of this entity, which made debut with cholestasic acute hepatitis accompanied of hypergammaglobulinemia. In the first patient was demonstrated the presence of AMA, ASMA, and anti-LKM1 autoantibodies; and ANA in the second one. The histological findings showed changes suggestive of AIH and PBC. After the start of immunosuppressive treatment, associated to ursodeoxycholic acid in one patient, a successful outcome was observed.     

YC-1, a novel activator of platelet guanylate cyclase

YC-1 [3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole] inhibited the aggregation of and ATP release from washed rabbit platelets induced by arachidonic acid (AA), collagen, U46619, platelet-activating factor (PAF), and thrombin in a concentration-dependent manner. YC-1 also disaggregated the clumped platelets caused by these inducers. The thromboxane B2 formation caused by collagen, PAF, and thrombin was inhibited by concentrations of YC-1 that did not affect formation of thromboxane B2 and prostaglandin D2 caused by AA. YC-1 suppressed the increase of intracellular Ca2+ concentration and generation of inositol 1,4,5-trisphosphate caused by these five aggregation inducers. Both the cAMP and cGMP contents of platelets were increased by YC-1 in a concentration- and time-dependent manner. Like sodium nitroprusside, YC- 1 potentiated formation of cAMP caused by prostaglandin E1 but not that by 3-isobutyl-1-methylxanthine. Adenylate cyclase and cAMP phosphodiesterase activities were not altered by YC-1. Activity of cGMP phosphodiesterase was unaffected by YC-1. Activities of guanylate cyclase in platelet homogenate and cytosolic fraction were activated by YC-1, whereas particulate guanylate cyclase activity was unaffected. The antiplatelet effect of sodium nitroprusside but not that of YC-1 was blocked by hemoglobin and potentiated by superoxide dismutase. After intraperitoneal administration for 30 minutes, YC-1 prolonged the tail bleeding time of conscious mice. These data indicate that YC-1 is a direct soluble guanylate cyclase activator in rabbit platelets. It may also possess antithrombotic potential in vivo.     

Intrasellar Tuberculoma – A Difficult Diagnosis

Tuberculosis is an exceptional cause of intrasellar mass lesion and diagnosis is usually established after histological examination following surgery. We report a 32-year-old women with headache and amenorrhea, analytical features of hypopituitarism and an intrasellar mass lesion in radiological studies. A transsphenoidal approach was performed and tissue examination revealed pituitary tuberculoma. Additionally, we review the previously reported cases. Received: March 21, 2001 · Accepted: October 26, 2001