Prospective randomized comparison of 1-day versus 3-day application of topical levofloxacin in eliminating conjunctival flora.

PURPOSE: To compare efficacy of a 1-day versus 3-day application of topical levofloxacin in reducing ocular surface bacteria. METHODS: In this prospective randomized controlled trial, 100 volunteer patients (50 per group) were assigned to receive topical 0.5% levofloxacin four times daily for 1 day or 3 days. Conjunctival cultures were obtained prior to (T0) and after the application of antibiotics (T1). Additionally, all patients received topical levofloxacin at 5-minute intervals for three applications (T2), followed by two drops of topical 5% povidone-iodine (T3). Conjunctival cultures were obtained at timepoints T2 and T3. RESULTS: A 1-day application of topical levofloxacin significantly reduced (p = 0.0004) the number of eyes with positive conjunctival cultures from 41 eyes (82%) to 23 eyes (46%). Similarly, a 3-day application significantly reduced (p = 0.0001) the positive culture rate from 37 eyes (74%) to 17 eyes (34%). Two drops of povidone-iodine further reduced the positive culture rate for both groups to 20% (10 eyes for each group). There was no significant difference in positive culture rate between the 1-day and 3-day groups at T0 (p = 0.4689), T1 (p = 0.3074), T2 (p = 0.6706), or T3 (p = 1.000). CONCLUSIONS: The application of topical 0.5% levofloxacin for 1 or 3 days significantly reduced the number of eyes with positive conjunctival cultures. The addition of 5% povidone-iodine further eliminated bacteria from the conjunctiva. The application of levofloxacin for 1 day appears to be as effective as a 3-day application.

Diazepam promotes ATP recovery and prevents cytochrome c release in hippocampal slices after in vitro ischemia.

Benzodiazepines protect hippocampal neurons when administered within the first few hours after transient cerebral ischemia. Here, we examined the ability of diazepam to prevent early signals of cell injury (before cell death) after in vitro ischemia. Ischemia in vitro or in vivo causes a rapid depletion of ATP and the generation of cell death signals, such as the release of cytochrome c from mitochondria. Hippocampal slices from adult rats were subjected to 7 min of oxygen-glucose deprivation (OGD) and assessed histologically 3 h after reoxygenation. At this time, area CA1 neurons appeared viable, although slight abnormalities in structure were evident. Immediately following OGD, ATP levels in hippocampus were decreased by 70%, and they recovered partially over the next 3 h of reoxygenation. When diazepam was included in the reoxygenation buffer, ATP levels recovered completely by 3 h after OGD. The effects of diazepam were blocked by picrotoxin, indicating that the protection was mediated by an influx of Cl(-) through the GABA(A) receptor. It is interesting that the benzodiazepine antagonist flumazenil did not prevent the action of diazepam, as has been shown in other studies using the hippocampus. Two hours after OGD, the partial recovery of ATP levels occurred simultaneously with an increase of cytochrome c (approximately 400%) in the cytosol. When diazepam was included in the reoxygenation buffer, it completely prevented the increase in cytosolic cytochrome c. Thus, complete recovery of ATP and prevention of cytochrome c release from mitochondria can be achieved when diazepam is given after the loss of ATP induced by OGD.

The coexistence of myasthenia gravis and myotonic dystrophy in one family.

We are reporting the unique coexistence of two distinct neuromuscular diseases, myotonic dystrophy and the juvenile form of myasthenia gravis, occurring in one family. A 16-month-old previously healthy female presented with a two month history of bilateral varying drooping of both eyelids and bilateral external ophthalmoparesis. The acetylcholine receptor antibodies were elevated, and there was a dramatic response to edrophonium confirming the clinical impression of myasthenia gravis. Spontaneous remission of the ptosis was noted after six months with no specific treatment. Many other family members were examined; none of them had clinical or laboratory evidence of myasthenia gravis. The clinical examination of the mother and the maternal grandmother, neither of whom had any complaints, resulted in a definite diagnosis of myotonic dystrophy. The proband's father and a 3-year-old sister were examined and found to be normal. We studied the HLA antigens of all of the available family members; none were found to have the HLA antigens most commonly associated with myasthenia gravis. Secretor gene studies were not helpful in providing additional genetic identification. The question generated by the coexistence of these two uncommon disorders in one family is if there is a genetic or other relationship between them or if this was merely a coincidental occurrence. At this point in time the question remains unanswered and must await demonstration of additional similar circumstances.