An autopsy case of acquired immune deficiency syndrome (AIDS) with preceding aplastic anemia

A case of acquired immunodeficiency syndrome (AIDS) with preceding aplastic anemia is reported. The patient was a 36 year old female who had been diagnosed as having aplastic anemia 10 years before and thereafter had received multiple transfusions. Human immunodeficiency virus (HIV)-seropositivity was revealed 10 months prior to her death, but no particular clinical signs indicating HIV infection, pre-AIDS or onset of AIDS were recognized before serological diagnosis, although the slow progression of leukopenia was noted along with thrombocytopenia. Her general condition deteriorated during the last 10 months accompanied by an acute decrease In the CD4/CD8 ratio. Autopsy revealed full-blown AIDS: systemic aspergillosis, progressive multifocal leukoencephalopathy, Epstein-Barr virus-related B cell lymphoma arising in the diaphragm and severe lymphocyte depletion in the lymph nodes and spleen. Markedly hypo-plastic bone marrow was considered to be primarily attributable to the aplastic anemia but the affection of AIDS was not excluded. The possible transmission route of HIV and the effect of the preceding aplastic anemia on the infection and clinical course of AIDS are discussed.     

Magnesium restores high K-induced inactivation of the fast Na channel in guinea pig ventricular muscle

The effect of extracellular magnesium concentration (Mg_o) on the upstroke of the action potential was studied in guinea pig ventricular muscle under various K⁺ concentrations (2.7–19mM). Increased Mg_o shifted the steady state inactivation curve of the fast Na channel in the depolarizing direction and this effect was concentration-dependent (0–20mM). Such an effect could explain the Mg-induced increase in maximum rate of rise of the action potential which Späh and Fleckenstein (1979) proposed to be due to a Mg channel.     

Mouse Colon Carcinoma Cells Established for High Incidence of Experimental Hepatic Metastasis Exhibit Accelerated and Anchorage-Independent Growth

Highly metastatic variants of mouse colon 38 colon carcinoma cells were established by repeated selection in vivo for liver metastasis and designated as SL4 cells. The SL4 cells formed colonies in the liver of 100% of syngenic mice when injected intrasplenically, while the incidence of liver metastasis was 27% of mice injected with parental cells. The weight of livers, which is an indicator of experimental hepatic metastasis formation, was significantly higher after intrasplenic injection and subsequent splenoctomy with SL4 cells than colon 38 cells. The incidence of hepatic metastasis after intracecal injection of SL4 cells was significantly higher than that of colon 38 cells. The SL4 cells were tested in vitro for their properties. Differences were not detected in the motility and invasive behavior between colon 38 cells and SL4 cells. SL4 cells showed a higher proliferation rate than colon 38 cells under adherent conditions. SL4 cells maintained a capacity to proliferate under non-adherent conditions whereas parental cells did not. SL4 cells should be a useful tool to study the mechanism of hepatic metastasis of colon carcinoma cells and to develop methods to prevent hepatic metastasis.     

Identification of neural genes using Xenopus DNA microarrays.

To isolate novel genes regulating neural induction, we used a DNA microarray approach. As neural induction is thought to occur by means of the inhibition of bone morphogenetic protein (BMP) signaling, BMP signaling was inhibited in ectodermal cells by overexpression of a dominant-negative receptor. RNAs were isolated from control animal cap explants and from dominant-negative BMP receptor expressing animal caps and subjected to a microarray experiment using newly generated high-density Xenopus DNA microarray chips representing over 17,000 unigenes. We have identified 77 genes that are induced in animal caps after inhibition of BMP signaling, and all of these genes were subjected to whole-mount in situ hybridization analysis. Thirty-two genes showed specific expression in neural tissues. Of the 32, 14 genes have never been linked to neural induction. Two genes that are highly induced by BMP inhibition are inhibitors of Wnt signaling, suggesting that a key step in neural induction is to produce Wnt antagonists to promote anterior neural plate development. Our current analysis also proves that a microarray approach is useful in identifying novel candidate factors involved in neural induction and patterning.     

Effects of lysophosphatidylcholine on resting potassium conductance of isolated guinea pig ventricular cells

We studied the effects of lysophosphatidylcholine (LPC), a toxic metabolite of ischemia, on the inward rectifier potassium channel current in isolated guinea pig ventricular cells. LPC (10-50 microM) added to the external solution decreased the resting membrane potential and occasionally induced repetitive action potential discharges, with or without loss of repolarization. In voltage clamp studies, LPC (20 microM) decreased the conductance at the levels of resting potentials (approximately equal to -80 mV) from 26 +/- 8 nS to 16 +/- 3 nS (mean and SD, n = 4) within 10 min. Prolonged application of LPC (greater than 12 min) produced transient inward currents after depolarizing clamp pulses, thereby suggesting that the LPC elevated intracellular Ca2+ concentrations. The effect of LPC on the single inward rectifier K channel current was examined using the patch clamp technique in a cell-attached mode. LPC decreased the single channel conductance, depending on the concentration (5-100 microM). The slope conductance in the presence of 150 mM K+ in the pipette decreased from 45 +/- 7 pS (control) to 32 +/- 17, 20 +/- 19, and 14 +/- 10 pS for 5, 20 and 100 microM LPC, respectively. LPC induced little change with regard to probability of the channel opening. These results suggest that LPC depolarizes membrane by decreasing single channel conductance of the inward rectifier K channel. This reduction partially contributes to the alleged LPC-induced abnormal automaticities and conduction disturbances in the heart.     

DETECTION OF HBsAg IN THE PANCREAS

Hepatitis B surface antigen (HBsAg) has been reported to be present in other organs than the liver.^3,9 So far as our knowledge is concerned, however, any report of cases dealing with pancreatic diseases induced by hepatitis B virus (HBV) has not been described in the English and Japanese literature. We report an autopsy case with a pancreatic lesion characterized by damage of both exocrine and endocrine epithelial cells with inflammatory response, which were immunohistochemically found to be positive for HBsAg, and electron-microscopically to possess core-like particles In the nucleus and cytoplasm.     

Epstein-Barr virus-related Hodgkin's disease showing B cell lineage in an immunosuppressive patient seropositive for HTLV-I

A case of Hodgkln's disease (HD), lymphocyte depression (LD) type In an Immunosuppressive patient is described. The patient was a 48-year-old male and his parents were born In the Kyushu area, which is an endemic area for adult T cell lymphomaheukemla (ATL). He was seropositive for ATL virus (ATLV, also referred to as HTLV-I) and showed a marked Immunosuppressive condition. He developed LD-HD and Pneumocystis carinii pneumonia, and died due to respiratory failure. The Immunohistochemical and in situ hybridization analyses revealed that the Reed-Sternberglike cells In the lymph node biopsy sample were positive for Ber-H2 (CD30), Leu-M1 (CD15), L-26 (CD20), Bcl-2, p53 and EBER, the viral genome of Epstein-Barr virus (EBV).     

Peripheral lung carcinomas associated with central fibrosis and mixed small cell and other histologic components

Three cases of peripheral small cell lung carcinoma (SCLC) with central fibrosis are presented. Central fibrosis is usually present in adenocarcinomas. Cases 1 and 2 are combined SCLCs with components of papillary adenocar-cinoma, and case 3 is a mixed SCLC with a large cell component. Small cell Components showed intermediate cell type in ail cases. In cases 1 and 2, there was a gradual transition between small cell carcinoma and papillary ade-nocarcinoma. Small cell components showed Grimelius argyrophilia, but other neuroendocrine markers such as neuronspecific enorase, chromogranin A, Leu-7 and syn-aptophysln were negative. The chest X-ray examination of case 1 demonstrated rapid enlargement of a tumor shadow, which was present two years before, for a recent year. Central fibrosis, coexistence of small cell carcinoma and papillary adenocarcinoma, and a change of growth rate in the chest x-ray may suggest that some SCLC derive from papillary adenocarcinomas.     

Masked excitatory action of noradrenaline on rat islet β-cells via activation of phospholipase C

The effect of noradrenaline (NE) on rat islet -cells was examined. NE reduced insulin secretion from rat islets exposed to extracellular solutions containing glucose at 5.5 or 16.6 mM. In islets treated with pertussis toxin (PTX), however, NE increased insulin secretion. The NE-induced augmentation of insulin secretion was inhibited by prazosin. In intact islets, NE increased phospholipase C (PLC) activity, an effect that was prevented by treatment of islets with U-73122. NE elevated intracellular [Ca²⁺] ([Ca²⁺]_i) in isolated -cells independently of PTX. Although this NE effect was inhibited by prazosin, phenylephrine did not mimic it. The [Ca²⁺]_i response to NE was also prevented by the treatment of cells with U-73122. NE produced depolarization of -cells followed by nifedipine-sensitive action potentials. NE reduced the whole-cell membrane currents through ATP-sensitive K⁺ channels (K_ATP), responsible for the depolarization. This NE effect was prevented by treatment of -cells with U-73122 or BAPTA/AM. Although at least some of our results imply the presence of ₁-adrenoceptors, -cells were not stained by a polyclonal IgG antibody recognizing all adrenergic ₁-receptor subtypes so far identified. These results suggest that an interaction of NE with an unknown type of receptor activates rat islet -cells via a PLC-dependent signal pathway. This effect is, however, masked by the inhibitory action via a PTX-sensitive pathway also activated by NE.