Oral cryptococcosis in a patient with AIDS. A case report

A 59-year-old Caucasian male patient with AIDS is described who presented with an oral lesion of cryptococcosis. The gingival ulceration was the only detectable lesion of cryptococcosis. Diagnosis was established by his-topathologic findings from biopsy and detection of serum cryptococcal antigen. The patient was treated with amphotericin B and flucytosine. After four weeks of therapy cryptococcal antigen turned negative. The oral ulceration diminished in size, but an inflammatory tissue reaction persisted.     

Radiologic approach to paragangliomas of the temporal bone

High-resolution computed tomography (HRCT) has become the primary radiologic method for evaluation of paragangliomas of the temporal bone. The HRCT evaluation of the integrity of certain bony landmarks has a profound effect on selection of surgical approach. The most important landmarks are the bony walls separating the carotid artery and the jugular bulb from the middle ear. Arteriography is not necessary if the lesion is confined to the middle ear. However, it is indicated in tumors that have eroded the above landmarks or in those patients with related neurologic symptoms.     

Galantamine protects against lipopolysaccharide-induced acute lung injury in rats

Lipopolysaccharide (LPS)-induced endotoxemia triggers the secretion of proinflammatory cytokines and can cause acute lung injury (ALI). The high mobility group box 1 (HMGB1) protein plays an important role as a late mediator of sepsis and ALI. Galantamine (GAL) is a central acetylcholinesterase inhibitor that inhibits the expression of HMGB1. This study evaluated the effects of GAL by measuring levels of inflammatory mediators and observing histopathological features associated with LPS-induced ALI. Sixty 8-10 week old male Sprague-Dawley rats (200-240 g) were randomized into three groups as follows: control group, LPS group (7.5 mg/kg LPS), and LPS+GAL group (5 mg/kg GAL before LPS administration). Histopathological examination of lung specimens obtained 12 h after LPS administration was performed to analyze changes in wet-to-dry (W/D) weight ratio, myeloperoxidase (MPO) activity, and HMGB1 expression level. Additionally, plasma concentrations of tumor necrosis factor-α, interleukin-6, and HMGB1 were measured using an enzyme-linked immunosorbent assay at 0 (baseline), 3, 6, 9, and 12 h after LPS administration. Mortality in the three groups was recorded at 72 h. LPS-induced ALI was characterized by distortion of pulmonary architecture and elevation of MPO activity, W/D weight ratio, and levels of pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin-6, and HMGB1. Pretreatment with GAL significantly reduced the LPS-induced lung pathological changes, W/D weight ratio, levels of pro-inflammatory cytokines and MPO activity (ANOVA). Moreover, GAL treatment significantly decreased the mortality rate (ANOVA). In conclusion, we demonstrated that GAL exerted a protective effect on LPS-induced ALI in rats.