Case report. Cryptococcal cellulitis showing necrotizing vasculitis.

A 65-year-old woman with refractory anaemia who had been treated with systemic corticosteroids for several months developed cryptococcal cellulitis of the right cubital fossa. She was treated empirically for a presumed bacterial cellulitis with little response. Histological examination of debrided tissue revealed Cryptococcus as the causative organism. The tissue reaction involved suppurative inflammation with abscess formation in the dermis and subcutaneous adipose tissue. Necrotizing vasculitis, which has rarely been described in cryptococcosis, was seen in this case. Although the cellulitis was cured by local treatment in this patient, most previous reports recommended systemic antifungal therapy to treat cryptococcal cellulitis.

Malignant gastrointestinal stromal tumor showing remarkable whorl formations.

A case of malignant gastrointestinal stromal tumor (GIST) is reported. Histologically, spindle cell proliferation with remarkable whorl formations was predominant in the tumor. Immunohistochemically, the tumor cells were diffusely positive for CD117 (c-Kit) and vimentin and partially positive for CD34. Ultrastructurally, the desmosome-like structures and interdigitations occurred much more frequently in the areas with whorl formations. These organelles were considered to be closely associated with the whorl formations. Various kinds of cellular arrangements are revealed in GISTs, but remarkable whorl formations, such as in our case, are a rare variant pattern. Herein, we discuss the histopathologic differences between this and other tumors showing whorl formations and describe the meaning of this unique arrangement. GISTs are thought to be immature tumors, and, therefore, variations in histopathologic findings are recognized. Finally, the ultrastructural study of GISTs is useful for understanding the mechanisms forming whorl formations and the differentiation or pathogenesis of GISTs.

Ruthenium-catalyzed cyclic carbonylation of allenyl alcohols. Selective synthesis of gamma- and delta-lactones

[reaction: see text] Ruthenium complex-catalyzed carbonylation of allenyl alcohols quantitatively gave cyclic carbonyl compounds, gamma- and delta-lactones, in which the hydroxy group of allenyl alcohols participated in the cyclization. A wide variety of allenyl alcohols, such as mono-, di-, and trisubstituted alcohols, can be used in this reaction to produce 3- and 4-substituted gamma-lactones. Similarly, the cyclic carbonylation of 3,4-pentadien-1-ol 10a and 2-methyl-4,5-hexadien-2-ol 11a gave delta-lactones, 5,6-dihydro-3-methyl-2H-pyran-2-one 10b, and 5,6-dihydro-6,6-dimethyl-3-methyl-2H-pyran. 2-one 11b, respectively, in a quantitative yield.

[A Warthin's tumor showing extensive necrosis].

Warthin's tumors are one of the most easily recognizable tumors using light microscopy. However, histopathological diagnosis is difficult in a few cases when characteristic cystic cavities with papillary walling and underlying lymphoid stroma are obscured by reactive changes. We describe a case of an extirpated Warthin's tumor of the right parotid gland which demonstrated extensive necrosis, squamous metaplasia and xanthomatous inflammation. No characteristic structure for this tumor was noticed in a section of an initially sampled specimen. As a result, a destroyed fistula was suspected. An additional sampling was performed to confirm the diagnosis and the sampled specimen fortunately demonstrated the diagnostic structure of a Warthin's tumor excluding malignancy. An awareness of the morphological variation seen in this tumor should lead to additional sampling of specimens, thereby preventing erroneous interpretation.

[Subcutaneous phaeohyphomycosis of the right thumb].

Black fungi are a group of fungi that are characterized by the development of a pale brown to black color in the cell walls of their vegetative cells, conidia, or both. A mycotic infection caused by a member of black fungi can be subdivided into three clinical entities: phaeohyphomycosis, chromoblastomycosis, and mycetoma. Phaeohyphomycosis is distinguished from mycetoma by the absence of grain (organized, interwoven mycelial aggregates) formation, and from chromoblastomycosis by the absence of sclerotic bodies (thick-walled muriform cells). Phaeohyphomycosis is a rare disease and has been sporadically reported. In the present report, phaeohyphomycosis of the right thumb of a 72-year-old man was presented. A precipitating trauma of two months earlier at the site was recalled. A solitary mass, 10 mm in diameter, was gradually formed in the palm side of the distal right thumb and finally resected. Histological examination disclosed a solitary granulomatous lesion surrounded by an incomplete fibrous capsule. The lesion mainly involved subcutaneous tissue and was composed of multiple pyogranulomas. Pigmented branched septate hyphae and yeast-like cells were sparsely found in the periphery of the abscess and within histiocytic cells of the granulomas. No sclerotic cells were detected. When pigmentation of black fungi in tissue is as faint as in the present case, Fontana-Masson staining is useful to accentuate the presence of melanin-like pigment of fungal cell walls.

Peripheral bombesin induces gastric vagal afferent activation in rats.

Bombesin's influence on gastric vagal afferent discharge (GVAD) was studied in urethan-anesthetized rats. Vehicle and peptides were injected intravenously at 30-min intervals. Cholecystokinin (CCK; 300 pmol) and bombesin (300 pmol) increased ongoing multiunit GVAD by 153 +/- 59 and 162 +/- 37%, respectively; similar increases were induced by a second injection of bombesin and CCK. The bombesin antagonist, ICI-216140, prevented bombesin-induced increase in GVAD, whereas the CCK response was not influenced. The CCK-A receptor antagonist devazepide reduced the activation of GVAD induced by bombesin from 107 +/- 11 to 63 +/- 6%, while abolishing the CCK response. Devazepide given alone or in combination with ICI-216140 did not modify gastric distension (3 ml)-induced increase in GVAD. Of 22 single units that were activated by gastric load (4 ml), 17 and 20 units responded also to bombesin (620 pmol) and CCK (870 pmol), respectively. Of the nine units that did not respond to gastric load, eight had an increase in GVAD induced by both bombesin and CCK. There was no specific binding of 125I-labeled [Tyr4]bombesin on cervical vagus, either intact or 24 h after ligation. These data suggest that intravenous bombesin-induced stimulation of GVAD is indirect and initially mediated through specific receptor activation influencing gastric smooth muscle and the release of CCK.

Peripheral bombesin decreases gastric vagal efferent activity in part through vagal pathways in rats.

The influence of intravenous (iv) bombesin on multiunit activities recorded from the ventral gastric branch of the vagus was investigated in urethan-anesthetized rats. Consecutive injections of bombesin (0.062, 0.62, 6.2, 62, and 620 pmol iv) decreased dose dependently gastric vagal efferent discharges to 79.8 +/- 4.9, 68.3 +/- 10.2, 47.0 +/- 6.7, 41.6 +/- 4.7, and 36.5 +/- 8.9%, respectively, from preinjection levels. Saline injection had no effect. Bombesin (62 pmol iv) reduced cervical vagal efferent discharges to 25 +/- 6% before and 67 +/- 5% after bilateral cervical vagotomy distal to the recording site. Bombesin (62 and 620 pmol iv) increased gastric vagal afferent discharges by 45 and 93%, respectively. These data show that systemic injection of bombesin potently decreases gastric and cervical vagal efferent activity in part through vagal-dependent mechanisms that may involve the increase in gastric vagal afferent activity.

Bombesin acts in the brain to decrease gastric vagal efferent discharge in rats.

The central nervous system action of bombesin to influence basal gastric vagal efferent discharge (GVED) was investigated in urethane-anesthetized rats. Bombesin (62, 620, and 6200 pmol) injected intracisternally (IC) decreased GVED to 78 +/- 10%, 50 +/- 4%, and 43 +/- 3% of preinjection levels, respectively. Bombesin (620 pmol) injected IV also reduced GVED to 36 +/- 6%. Pretreatment with bombesin monoclonal antibody 2A11 completely prevented the decrease in GVED induced by bombesin (620 pmol) given IV but not IC. These data indicate that both IC and IV injections of bombesin decrease basal GVED, and that the inhibitory effect of IC injection represents a central nervous system-mediated action.