Pityriasis rotunda is an uncommon chronic dermatosis characterized by multiple, round or oval, hyperpigmented or hypopigmented patches that have a fine scale on the trunk and extremities. Most of the cases reported predominantly occurred in Oriental and black patients in association with internal disease. However, in Caucasians it has been documented in healthy persons usually as a familial tendency. We report a case of pityriasis rotunda which showed familial occurrence and had no underlying disease.
Extremities ; Humans ; Pityriasis* ; Skin Diseases

PURPOSE: To evaluate the radiological patterns of vascular invasion in peripheral cholangiocarcinomas. MATERIALS AND METHODS: Hepatic arteriography and portography in 20 cases with cholangiocarcinoma including 12 cases with anglographic CT were retrospectively analized. RESULTS: The arteriography showed no arterioportal shunt, hypertrophy of tumor vessel, or tumor staining extending to central portion of the mass in all cases. However, doughnut shaped peripheral tumor staining was seen until late hepatogram phase in 12 cases and compensatory hyperperfusion around the mass was seen in six cases(eight cases if include arterial CT). Encasement of tumor vessel was seen in 12 cases, and hypertrophy of feeding vessel in nine cases. On portogrphy, the filling defect on segmental portal branch could be demonstrated only in 11 cases. Shape of the portal defect was tapered narrowing in six cases, abrupt narrowing in two cases but intraluminal nodular filling defect was not seen. Remainning three cases were difficult to define the shape. On seven cases of CT during arterial portography, three cases showed mass shaped defect and four showed segmental defect but three of them could demonstrate the partially preserved portal flow in defective portal area. CONCLUSION: Hepatic arteriography in peripheral cholagiocarcinoma showed no evidence of hypertrophy of tumor vessels and tumor stain extending to central portion but peripheral staining on late hepatogram phase and compensatory hyperperfusion could be seen. Portal vein was more commonly involved through perivascular connective tissue invasion rather than by direct extension into the portal lumen.
Angiography* ; Cholangiocarcinoma* ; Connective Tissue ; Hypertrophy ; Portal Vein ; Portography ; Retrospective Studies

PURPOSE: To evaluate the radiological patterns of vascular invasion in peripheral cholangiocarcinomas. MATERIALS AND METHODS: Hepatic arteriography and portography in 20 cases with cholangiocarcinoma including 12 cases with anglographic CT were retrospectively analized. RESULTS: The arteriography showed no arterioportal shunt, hypertrophy of tumor vessel, or tumor staining extending to central portion of the mass in all cases. However, doughnut shaped peripheral tumor staining was seen until late hepatogram phase in 12 cases and compensatory hyperperfusion around the mass was seen in six cases(eight cases if include arterial CT). Encasement of tumor vessel was seen in 12 cases, and hypertrophy of feeding vessel in nine cases. On portogrphy, the filling defect on segmental portal branch could be demonstrated only in 11 cases. Shape of the portal defect was tapered narrowing in six cases, abrupt narrowing in two cases but intraluminal nodular filling defect was not seen. Remainning three cases were difficult to define the shape. On seven cases of CT during arterial portography, three cases showed mass shaped defect and four showed segmental defect but three of them could demonstrate the partially preserved portal flow in defective portal area. CONCLUSION: Hepatic arteriography in peripheral cholagiocarcinoma showed no evidence of hypertrophy of tumor vessels and tumor stain extending to central portion but peripheral staining on late hepatogram phase and compensatory hyperperfusion could be seen. Portal vein was more commonly involved through perivascular connective tissue invasion rather than by direct extension into the portal lumen.
Angiography* ; Cholangiocarcinoma* ; Connective Tissue ; Hypertrophy ; Portal Vein ; Portography ; Retrospective Studies

No abstract available.
Hypertrophy*

No abstract available.
Humans

OBJECTIVES: lschemic acute renal failure(ARF) is characterized by an abrupt and sustained decline in GFR within minutes to days after renal ischemia and not immediately reversed on restoration of renal blood flow. The typical delay of a few days to a few weeks suggests reversible parenchymal damage awaiting cell regeneration for functional recovery. Many potentially cell damaging factors, such as ATP depletion, plasma membrane phospholipid degradatian and superoxide-induced membrane damage, play a central part in ischemic injury. More recently, much attention has been focused on the role of calcium, especially ischemic cell injury and the possible therapeutic role of calcium channel blockers emerged from studies conducted several years ago. In the past, it was thought that activation of renin-angiotensin system plays a role in the pathogenesis of ARF. Now the role of angiotensin in human renal ischemia also appears to be controversial. The following study was done in order to investigate the effect of a calcium channel blocker, nifedipine, on gene expression of renin during acute ischemic renal injury. METHODS: The Sprague-Dawley rats were divided into 4 groups, group I(n=3) as the control, group II (n=3) as the sham operation group, group III(n=15) as the ischemic renal injury group without nifedipine pretreatment, and group IV(n=15) as the ischemic renal injury model by right nephrectomy and left renal artery clamping for 40 minutes with systemic nifedipine pretreatment(10mg/kg), 1n ischemic renal injury model(group III and IV), rats were further divided into three subgroups according to reperfusion time of 1,24,72 hours. The non-ischemic right kidney removed at the time of initial procedure served as paired control. Total renal RNA was extracted by Chomczynskis method and electrophoresis was done in a 1% agarose gel containing 2,2M formaldehyde. Northern was performed at 42degrees C with isotope labeled renin probe for 18 hours, Autoradiographs were obtained and quantitated by a densitometer measured at 530nm. RESULTS: 1) The expression of renin gene was markedly decreased after renal ischemia and slowly recovered to one half of the control level after 72 hours of reperfusion. 2) Renin gene expression pattern of ischemic renal injury with prior nifedipine treatment was similar to the ischemic group without nifedipine pretreatment. CONCLUSION: These findings suggest that the renin gene expression was markedly decreased after renal ischemia and slowly recovered. Systemic nifedipine pretreatment does not have a significant effect on gene expression pattern of renin in ischemic renal injury.
Adenosine Triphosphate ; Angiotensins ; Animals ; Calcium Channel Blockers ; Calcium Channels* ; Calcium* ; Cell Membrane ; Constriction ; Electrophoresis ; Formaldehyde ; Gene Expression* ; Humans ; Ischemia ; Kidney ; Membranes ; Nephrectomy ; Nifedipine ; Rats ; Rats, Sprague-Dawley ; Regeneration ; Renal Artery ; Renal Circulation ; Renin* ; Renin-Angiotensin System ; Reperfusion ; RNA ; Sepharose

No abstract available.
Amphotericin B* ; Hemoptysis*

No abstract available.
Acute Kidney Injury* ; Lymphoma*

No abstract available.
Glomerulonephritis, IGA* ; Immunity, Cellular* ; Immunoglobulin A*

No abstract available.
Glomerulonephritis, IGA* ; Immunity, Cellular* ; Immunoglobulin A*