Regression of plane warts following spontaneous inflammation

This paper describes the clinical and histopathological features in ten cases of spontaneously involuting plane warts. In all, rapid regression occurred after the sudden development of an inflammatory reaction. At an early stage a degenerative change appears in the upper epidermis and the typic features of the warts are masked. At the height of the reaction an intense mononuclear cell infiltrate in the dermis associated with epidermal spongiosis, exocytosis cell necrosis and focal parakeratosis is found. It is suggested that the development of cell mediated immunity may be responsible for spontaneous involution of warts.     

The effect of steroid sulphatase on stratum corneum shedding in patients with X-linked ichthyosis

After the application under occlusion of partially purified stratum corneum steroid sulphatase to the skin of patients with X-linked ichthyosis, the detachment ratio of stratum corneum fragments was significantly increased. There was no significant change in normal subjects or in patients with ichthyosis vulgaris.     

Ichthyosis linearis circumflexa: morphological and biochemical studies

Extensive morphological and biochemical studies were carried out on two sibling cases of ichthyosis linearis circumflexa. The condition was found to be similar to psoriasis in the following ways: effectiveness of PUVA therapy, psoriatic changes on light and electron microscopy, high urinary polyamine levels, elevation of several enzyme activities in the scales, and a remarkable change in keratin molecules. These results may reflect an increased epidermal proliferation with a reduced epidermal transit time, as occurs in psoriasis.     

Final Results of Cooperative Study of VEPA [Vincristine, Cyclophosphamide (Endoxan), Prednisolone and Adriamycin] Therapy in Advanced Adult Non-Hodgkin's Lymphoma: Relation Between T- or B-Cell Phenotype and Response

One hundred previously untreated adult patients with advancednon-Hodgkin's lymphomas were treated with VEPA (vincristine,cyclophosphamide, prednisolone and adriamycin in combination)therapy. The overall complete remission rate was 52%. The completeremission rate was markedly higher in the patients with lineage-undeterminedlymphomas (72.2%) as well as in the patients with B(non-T)-celllymphomas (58.5%) than in the patients with T-cell lymphomas(36.6%). The median duration of complete remission has not beenreached for lineage-undetermined lymphomas and most (77%) ofthe patients have been in remission for more than 2-yr, whilethe median duration of complete remission for B(non-T)-celltype was 16 mo with a 3-yr remission rate of 14%, and medianduration for the T-cell type was only 4 mo with a 2-yr remissionrate of 15% or less. Both complete remission and cell lineageof lymphomas markedly affected the survival period. Of the patientswho were not induced into complete remission, about 90% diedwithin 12 mo regardless of the cell lineage of the lymphoma,and their median survival was only 5–7 mo. On the otherhand, more than 90% of the patients with lineage-undeterminedlymphomas who were induced into complete remission are stillalive after 36 mo. Median survival was 37 mo and the 3-yr survivalrate was 56.1% in the case of B(non-T)-cell lymphoma with completeremission. Even in the T-cell lymphomas, significantly (a fewmonths) longer survival time will be expected in the patientsin complete remission. These facts indicate that complete remissioninduced by VEPA therapy contributes greatly to longer survivalof the patients, but its contribution is limited by the celllineage of the lymphoma. B(non-T)-cell lymphoma as well as lineage-undeterminedlymphoma responded well to VEPA therapy and some of the patientsmay be cured. On the other hand, T-cell lymphoma responded poorlyto VEPA therapy.     

Bile acid composition in primary hepatocellular carcinoma

Bile acid composition in human primary hepatocellular carcinoma (HCC) tissues from eight non-hyperbilirubinaemic patients was compared with that in the neighbouring liver tissues. Quantitation of bile acids was carried out using selected ion monitoring. Significant amounts (>14 pmol/mg liver) of bile acids were found to be present in HCC tissues of all patients. In four patients, the concentration of chenodeoxycholic acid was higher in HCC than the corresponding neighbouring liver tissues, whereas those of other bile acids were less. The ratio of cholic to chenodeoxycholic acid was lower in HCC than in adjacent liver tissues in seven out of eight patients. This may indicate predominant synthesis of chenodeoxycholic acid in HCC tissues. The large inter-individual variation in bile acid concentration and composition of HCC tissues may result from the grade of anaplasia of HCC cells. 3β-Hydroxy-5-cholenoic acid, thought to be excreted in increased amounts in the urine of HCC patients, was shown to be a minor constituent of HCC tissues and of the neighbouring liver tissues in most patients, indicating that the C26-hydroxylation pathway plays a minor role. Unusual bile acids, such as 23-nor-3α,7α,12α-trihydroxy-5β-cholanoic, 3β,7β-dihydroxy-5β-cholanoic, 7-oxo-3α,12α-dihydroxy-5β-cholanoic and 12-oxo-3α,7α-dihydroxy-5β-cholanoic acids, were found in trace amounts in HCC tissues but their significance is not clear at present.     

Pelvic Autonomic Dysfunction without Tetraparesis: A Sequel of Rubella‐related Acute Longitudinal Myelitis

Objectives: Pelvic autonomic dysfunction without tetraparesis can be a sequel of acute longitudinal myelitis. Methods: A 25‐year‐old woman had suffered from pelvic dysfunction (urinary retention and severe constipation) without tetraparesis for 5 months as a sequel of rubella‐related acute longitudinal myelitis at the spinal segments of C2 to T9. She still had brisk deep tendon reflexes and extensor plantar responses. We performed autonomic function tests in the patient. Results: Pelvic autonomic function tests revealed acontractile detrusor and unrelaxing sphincter, suggesting the shock phase of a suprasacral spinal cord lesion; as well as loss of voluntary sphincter contraction, prolonged colonic transit time, decreased spontaneous phasic contractions, and paradoxical sphincter contraction on defecation, suggesting a suprasacral cord lesion. Conclusion: These findings indicated that the lateral medullary reticulospinal tracts just inside the pyramidal tract, for example, the descending pathways to the bladder and bowel, and the adjacent corticospinal tract to the sphincter, were selectively affected in our case.     

Differential Role of Epicardial and Endocardial KATP Channels in Potassium Accumulation During Regional Ischemia Induced by Embolization of a Coronary Artery with Latex

Epicardial and and Endocardial [K⁺]₀ Rise and K_ATP Channels. Introduction: K_ATP channels are activated predominantly in the epicardium during regional ischemia. Therefore, the role of K_ATP channels in ischemia-induced rise of extracellular potassium concentration ([K⁺]_o) might he greater in the epicardium. Methods and Results: In 18 anesthetized dogs, the left anterior descending coronary artery (LAD) was ligated, followed by injection of 23-μm latex heads into the occluded artery to interrupt collateral flow, by which accumulated [K⁺]_o might wash out. Epicardial and endocardial [K⁺]_o were measured during a 20-minute period of ischemia using a valinomycin membrane. The dogs were divided into three groups: 6 control dogs (CTRL); 7 dogs pretreated with intravenous glibenclamide (0.3 mg/kg [GLIB]), a blocker of K_ATP channels: and 5 dogs pretreated with intravenous nicorandil (0.2 to 0.25 mg/kg [NCR]), a K_ATP channel opener. Before LAD occlusion, there was no difference in [K⁺]_o among the three groups. In the control group, epicardial and endocardial [K⁺]_o were increased to a similar level as a function of time after occlusion (CTRL) at both layers. Ischemia-induced epicardial [K⁺]_o rise was suppressed by GLIB (8.4 ± 0.4 vs 6.7 ± 0.5 mM, P < 0.05) but augmented by NCR (12.9 ± 2.0 mM, P < 0.05). In contrast, endocardial [K⁺]_o, rise remained unaffected (7.6 ± 0.2 mM CTRL, 7.6 ± 1.3 mM GLIB, and 9.4 ± 2.2 mM NCR, P = NS). Conclusion: Activation of K_ATP channels plays an important role in epicardial [K⁺]_o rise, but not in endocardial [K⁺]_o rise, during regional ischemia. Another mechanism(s) may he important for endocardial [K⁺]_o accumulation.     

Intracellular Calcium Dynamics,Shortened Action Potential Duration,and Late‐Phase 3 Early Afterdepolarization in Langendorff‐Perfused Rabbit Ventricles

Calcium Dynamics, APD Shortening, and Late‐Phase 3 EAD. Introduction: To elucidate the mechanism of late‐phase 3 early after depolarization (EAD) in ventricular arrhythmogenesis, we hypothesized that intracellular calcium (Ca_i) overloading and action potential duration (APD) shortening may promote late‐phase 3 EAD and triggered activity, leading to development of ventricular fibrillation (VF). Methods and Results: In isolated rabbit hearts, we performed microelectrode recording and simultaneous dual optical mapping of transmembrane potential (V_m) and Ca_i transient on left ventricular endocardium. An I_KATP channel opener, pinacidil, was used to abbreviate APD. Rapid pacing was then performed. Upon abrupt cessation of rapid pacing with cycle lengths of 60–200 milliseconds, there were APD₉₀ prolongation and the corresponding Ca_i overloading in the first postpacing beats. The duration of Ca_i transient recovered to 50% (DCaT₅₀) and 90% (DCaT₉₀) in the first postpacing beats was significantly longer than baseline. Abnormal Ca_i elevation coupled with shortened APD produced late‐phase 3 EAD induced triggered activity and VF. In additional 6 preparations, the heart tissues were treated with BAPTA‐AM, a calcium chelator. BAPTA‐AM significantly reduced the maximal Ca_i amplitude (26.4 ± 3.5% of the control; P < 0.001) and the duration of Ca_i transients in the mapped region, preventing the development of EAD and triggered activity that initiated VF. Conclusions: I _KATP channel activation along with Ca_i overloading are associated with the development of late‐phase 3 EAD and VF. Because acute myocardial ischemia activates the I_KATP channel, late‐phase 3 EADs may be a mechanism for VF initiation during acute myocardial ischemia. (J Cardiovasc Electrophysiol, Vol. 23, pp. 1364‐1371, December 2012)