Laryngomalacia: a cause for early near miss for SIDS

Six infants had recurrent apnea of infancy episodes (near miss sudden infant death syndrome) during their neonatal period. Physical examination and laboratory investigation were normal. Polygraphic sleep monitoring revealed recurrent obstructive sleep apnea. These infants underwent fiberoptic endoscopy which showed that airway obstruction occurred at the laryngeal orifice as a result of laryngomalacia. It is suggested that laryngomalacia may be a cause for early apnea of infancy.     

Changes in the African American female profile as depicted in fashion magazines during the 20th century.

This study evaluated changes in the profiles of African American women presented in fashion magazines during the 20th century. Twenty-six variables were measured on a total of 119 profile photographs collected from various fashion magazines published in the 1940s through the 1990s. The photographs were divided into 6 groups corresponding to the decade in which they were published. A 1-way analysis of variance was performed, and between-group differences were examined with a Tukey multiple comparison procedure. Significant between-group differences (P <.01) were found for anteroposterior lip position, nasolabial angle, and interlabial angle, with increased fullness and more anteriorly positioned lips in the more recent decades. No significant differences were found for the frontonasal angle, the nasal tip angle, and the relationship of the chin to the upper face (total facial angle). Esthetic standards for the African-American female profile changed during the 20th century and, similar to the standards for the white profile, show a trend toward fuller and more anteriorly positioned lips.     

Maturation of kainic acid seizure-brain damage syndrome in the rat. III. Postnatal development of kainic acid binding sites in the limbic system

The progressive appearance of [3H]kainic acid binding sites with age has been studied in membrane suspensions prepared from various regions of the rat limbic system, and by autoradiography. Binding sites with fast dissociation rate appeared earlier than binding sites with slow dissociation rate. Scatchard analysis demonstrated apparent receptor heterogeneity for both subclasses. High affinity components were detected in the hippocampus as early as 10 days after birth, but in the amygdala + piriform lobe were found only towards the end of the third week, when animals also respond to parenteral kainic acid, for the first time, with limbic seizures accompanied by metabolic activation of the amygdala. Slice autoradiography revealed distinct labelling of the hippocampal CA3 region by postnatal day 10. A comparison with the ontogenesis of the kainic acid-induced seizure-brain damage syndrome suggests a role of high affinity receptors as mediators of metabolic nerve cell activation by kainic acid. However, this receptor interaction per se does not result in neuronal damage to the vulnerable region of the Ammon's horn, which will only occur at an age when also the amygdala is activated by the neurotoxin.     

Mobilization of intracellular calcium stores participates in the rise of [Ca2+]i and the toxic actions of the HIV coat protein GP120

The HIV envelope glycoprotein, GP120, increases intracellular Ca2+ concentration and induces degeneration of human and animal neurons in culture. Using patch-clamp recordings and Ca2+ imaging techniques, we have now examined the contribution of intracellular stores of calcium in the effects of GP120. We report that in rat hippocampal neuronal cultures, GP120 induces a dramatic and persistent increase in [Ca2+]i which is prevented by drugs that either deplete (caffeine, carbachol, thapsigargin) or block (dantrolene) Ca2+ release from intracellular stores. In contrast, N-methyl-d-aspartate (NMDA) receptors or voltage-dependent calcium channels do not participate in these effects, as: (i) the increase in [Ca2+]i was not affected by NMDA receptor antagonists or calcium channel blockers; and (ii) and GP120 did not generate any current in whole-cell recording. Dantrolene, a ryanodine stores inhibitor, also prevented neuronal death induced by GP120. Our results show that the GP120-induced rise in [Ca2+]i originates from intracellular calcium stores, and suggest that intracellular stores of calcium may play a determinant role in the pathological actions of GP120.     

Cycloheximide Reduces the Effects of Anoxic Insult In Vivo and In Vitro

In vivo and in vitro techniques were utilized to examine the influence of a protein synthesis blocker, cycloheximide (CHX), on the damaging effects of anoxia in the rat. CHX administered 1 h before transient (30 min) forebrain ischaemia increased the survival of animals, decreased body weight loss and reduced the occurrence of delayed degeneration in the CA1 pyramidal region. The same dose of CHX injected 1 h after ischaemia induced status epilepticus, a decrease in survival rate, and did not reduce weight loss or CA1 damage in any of the surviving rats. Electrophysiological techniques were then used to determine the effects of various periods of anoxia and aglycaemia (AA) on CA1 field excitatory postsynaptic potentials (EPSPs) in hippocampal slices incubated in the presence or absence of CHX. In CHX-treated slices, recuperation of EPSP amplitude (45±16%) was significantly greater than in control slices (9±9%) following an AA episode of 3 min 45 s. No difference was seen in the percent recuperation of EPSPs in the control and CHX-treated slices after shorter or longer episodes of AA. From these studies, it appears that CHX protects against the damaging effect of ischaemia in vivo or AA in vitro.     

Generation and propagation of 4-AP-induced epileptiform activity in neonatal intact limbic structures in vitro

We examined the generation, propagation and pharmacology of 4-aminopyridine (4-AP)-induced epileptiform activity (EA) in the intact interconnected limbic structure of the newborn (P0-7) rat in vitro. Whole-cell recordings of CA3 pyramidal cells and multisite field potential recordings in CA3, CA1, dentate gyrus, and lateral and medial entorhinal cortex revealed 4-AP-induced EA as early as P0-1. At this age, EA was initiated in the CA3 region and propagated to CA1, but not to the entorhinal cortex. Starting from P3-4, EA propagated from CA3 to the entorhinal cortex. Along the CA3 septo-temporal axis, EA arose predominantly from the septal pole and spread towards the temporal site. Whereas the onset of 4-AP-induced EA decreased with age from 21.2 +/- 1.6 min at P0-1 to 4.7 +/- 0.63 min at P6-7, the seizure duration increased in the same age groups from 98 +/- 14 s to 269.4 +/- 85.9 s, respectively. The EA was blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) but not by DL-2-amino-5-phosphonovaleric acid (APV), (+)-MK-801 hydrogen maleate (MK-801) or (+/-)-alpha-methyl-4-carboxyphenylglycine (MCPG), suggesting that they were mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate receptor activation. We conclude that: (i) the septal pole of the hippocampal CA3 region plays a central role in the generation of EA in the neonatal limbic system; and (ii) AMPA/kainate receptor-mediated EA can be generated in CA3 already at birth. Therefore, the recurrent collateral synapses and circuits required for the generation of EA are developed earlier than previously suggested on the basis of studies on hippocampal slices.     

Extension of transplantation free time by lamivudine in patients with hepatitis B-induced decompensated cirrhosis

BACKGROUND: Liver transplantation for hepatitis B virus (HBV)-induced cirrhosis carries a high risk of graft reinfection and poor prognosis. Active viral replication is considered a contraindication for transplantation in most centers. Lamivudine, a new nucleoside analog, is a potent inhibitor of HBV replication that has been used safely for pretransplantation suppression of HBV replication. METHODS: We report the pattern of response to lamivudine treatment in three consecutive patients with decompensated cirrhosis due to the replicative phase of chronic HBV infection. RESULTS: In addition to virological and biochemical response, impressive clinical improvement was noted in all three patients, with disappearance of the ascites and marked improvement of synthetic liver function tests. One patient converted to anti-hepatitis B surface and is free of symptoms 20 months after initiation of treatment. The other two patients experienced significant clinical improvement for 8 to 9 months and were removed from the waiting list for transplantation. However, progressive liver disease recurred in both patients--one underwent liver transplantation and the other is a candidate for the procedure. CONCLUSION: The administration of lamivudine for pretransplantation HBV suppression was associated with impressive clinical and biochemical improvement. Lamivudine may extend the transplantation free time in such patients. The mechanism of this desirable effect should be explored.