Agminated fibroblastic connective tissue nevus in a 1‐year‐old boy

Fibroblastic connective tissue nevus (FCTN) is a benign cutaneous mesenchymal lesion characterized by proliferation of CD34‐positive fibroblastic/myofibroblastic spindle‐shaped cells. We report a case of agminated FCTN on the right lower abdomen of a 1‐year‐old boy.     

Stereotyped behaviors and compulsive complaints of pain improved by fluvoxamine in two cases of frontotemporal dementia]

There have been no systematic efforts to manage and treat patients with frontotemporal dementia (FTD), but Perry described pharmacologic interventions for some behavioral syndromes in 2001. In Perry's report, selective serotonin reuptake inhibitors (SSRI) were recommended as first choice drugs because they were well tolerated and might have an effect on some symptoms such as compulsive symptoms and eating abnormalities. Some reports were presented concerning Japanese FTD patients which showed the effect of SSRI on stereotyped behaviors and eating abnormalities by Nishikawa, et al. (2001), Ikeda, et al. (2004), and others. We describe two FTD patients with compulsive complaints of pain, one mainly on abdomen and the other on lumbar region. Fluvoxamine markedly improved their complaints of pain as well as stereotyped symptoms. Fluvoxamine might be effective for behavioral disturbances due to improvement of serotoninergic dysfunction in frontal medial and cingulated cortices, as previously described. Moreover, it has been reported that an altered response to pain stimuli, either via a loss of awareness of pain or exaggerated reaction to pain, is a specific feature of FTD, but there have been only a few reports on this feature. Fluvoxamine might be effective for compulsive complaints of pain due to improvements of compulsive symptoms and exaggerated reactions to pain in FTD, or due to the analgesic effect of SSRI. SSRI may improve compulsive complaints of pain in FTD patients.     

Excitatory mechanism of deflationary slowly adapting pulmonary stretch receptors in the rat lung.

The excitatory responses of deflationary slowly adapting pulmonary stretch receptor (SAR) activity to lung deflation ranging from approximately -15 to -25 cm of H(2)O for approximately 5 s were examined before and after administration of flecainide, a Na(+) channel blocker, and K(+) channel blockers, such as 4-aminopyridine (4-AP) and tetraethylammonium (TEA). The experiments were performed in anesthetized, artificially ventilated rats after unilateral vagotomy. The deflationary SARs increased their activity during lung deflation and its effect became more pronounced by increasing the degree of negative pressure. During lung deflation the average values for the deflationary SAR adaptation index (AI) were below 40%. Intravenous administration of veratridine (50 microg/kg), an Na(+) channel opener, stimulated deflationary SAR activity: one maintained excitatory activity mainly during deflation and the other receptors showed a tonic discharge during both deflation and inflation. Despite the difference in deflationary SAR firing patterns after veratridine administration, flecainide treatment (6.0 mg/kg) blocked veratridine-induced deflationary SAR stimulation and also caused strong inhibition of the excitatory responses of deflationary SARs to lung deflation. Under these conditions, the average values for deflationary SAR AI were over 90%. The responses of deflationary SARs and deflationary SAR AI to lung deflation were not significantly altered by pretreatment with either 4-AP (0.7 and 2.0 mg/kg) or TEA (2.0 and 6.0 mg/kg). These results suggest that the excitatory effect of lung deflation on deflationary SAR activity is mediated by the activation of flecainide-sensitive Na(+) channels on the nerve terminals of deflationary SARs.     

Accelerated Appearance of Skin Tumors in Hairless Mice by Repeated UV Irradiation with Initial Intense Exposure and Characterization of the Tumors

Skin tumors were produced on the back of hairless mice, HOS (HR/De), by exposure to ultraviolet B light (UVB, 290–320 nm) with 4 different protocols. The first tumors appeared earlier (in 10 weeks in group I and 7 weeks in group III) when initial intense exposure was given, followed by repeated lower-level exposures, than when the mice were exposed to the repeated UV only (in 16 weeks both in group II and group IV). All mice developed skin tumors earlier in the groups given the repeated UV exposures three times a week than in the groups given the exposures twice a week. Most of the skin tumors produced by the UVB exposure were histologically malignant, being transplantable to nude mice, and the cultured cells grown from the tumors were capable of producing tumors when injected into nude mice. The accelerated development of skin tumors by initial intense exposure and short intervals of repeated exposure observed in this study may have implications for humans who expose themselves to intense sunbathing and UV tanning (burning) by fluorescent sun lamps.     

Dissecting aneurysm of the vertebral artery as a cause of Wallenberg's syndrome

Although it is well known that Wallenberg's syndrome is caused by occlusion of the vertebral artery (VA) or the posterior inferior cerebellar artery (PICA), the etiology of the occlusion is rarely documented. During the course of Wallenberg's syndrome, patients often complain of headache. We thought that these headaches might be caused by dissecting aneurysm (DA) of the vertebral artery, and so we studied the incidence of DA in our cases with Wallenberg's syndrome. Although many variants exist, Wallenberg's syndrome encompasses several neurological symptoms due to a disorder of the nucleus and nerve tracts located in the lateral part of the medulla. We diagnosed our patients as having Wallenberg's syndrome on the basis of symptoms such as loss of pain and temperature sensation in the unilateral face and contralateral body, cerebellar ataxia, and dysphasia. We investigated 22 cases of Wallenberg's syndrome over a five-year period, and excluded patients who developed subarachnoid hemorrhage upon onset of the syndrome. Our cases can be divided into two groups; one with severe stenosis or occlusion of VA (n = 15) and the other with occlusion of PICA (n = 5). The angiograms of the two remaining patients showed no abnormal findings. The mean age of the VA group (42.5 yrs.) was younger than that of the PICA group (64.2 yrs.). The age distribution of the PICA group is similar to that of other occlusive cerebrovascular diseases. Seven cases of the VA group demonstrated aneurysmal dilatation and luminal stenosis, and so they were diagnosed as having dissecting aneurysm of VA.(ABSTRACT TRUNCATED AT 250 WORDS)     

A case of aortitis syndrome complicated with amyloidosis, type AA]

We recently saw a patient who had aortitis syndrome associated with secondary amyloidosis. To our knowledge, she is the fourth report of this complication occurring in aortitis syndrome. In November 1985, the patient, a 18 year-old woman, was admitted to our hospital because of a high fever, back pain, abdominal pain and general fatigue. On physical examination, bruit was audible on the abdomen, bilateral radial artery was weakly palpable. Angiography showed the stenosis of bilateral carotid artery, subclavian artery, renal artery and superior mesenteric artery. From the above findings, she was diagnosed aortitis syndrome, and treatment was begun with prednisolone. However, she developed recurrently a high fever, chest pain, abdominal pain and exertional dyspnea. Laboratory findings at the active stage revealed the marked elevation of leukocytes, erythrocyte sedimentation rate and C-reactive protein. On her clinical course, the number of circulating thrombocytes was paralleled with the activity of the disease. On June 1988, she developed suddenly a high fever and severe pain of abdomen. Pathological findings of her stomach showed the deposition of amyloid protein A. Laboratory findings depicted the marked increment of thrombocytes, beta-thromboglobulin and platelet factor 4. These results suggest that circulating thrombocytes may play a role in product ion of amyloid protein.