Fine structure of the mouse portal vein in relation to its peristaltic movement

The hepatic portal vein has been known to make a spontaneous peristaltic movement in some mammals, including the mouse and rat. To investigate the fine structure of the portal vein in relation to its physiological characteristics, we observed the mouse portal vein by using various histological techniques including conventional light microscopy, videomicroscopy, transmission and scanning electron microscopy, and real-time confocal laser scanning microscopy. The mouse hepatic portal vein was provided with a spiral fold which was produced by the inner layer, i.e. the endothelium and smooth muscles of the wall protruding into the lumen. Longitudinal smooth muscle cells spanned the interval of the fold, like a spirally arranged palisade around the vessel wall. The longitudinal muscle fibers ended at the spiral fold, being partly connected with a network of irregularly shaped smooth muscle cells. This network, hitherto unknown, was recognized to be restricted to the fold in distribution and characterized by numerous gap junctions connecting the muscle cells. Real-time confocal laser scanning microscopy using a Ca2+ sensitive fluorescent dye revealed that a transient and periodic increase in Ca2+ concentration occurred in the longitudinal smooth muscle cells and was transmitted spirally from the intestinal to the hepatic side. These findings indicate that, during the peristaltic movement, the contraction of smooth muscle cells is transmitted along the longitudinal smooth muscles of the portal vein wall toward the liver, presumably controlled by the network of the irregularly-shaped smooth muscle cells in the fold of the portal vein. Light microscopic observation in some specimens indicated an occurrence of cardiac muscle cells outside the smooth muscle layer. Restricted to the site of the porta hepatis in distribution, their involvement in the peristaltic contraction of the portal vein seemed unlikely.     

Acute hepatic failure in IFN-gamma-deficient BALB/c mice after murine coronavirus infection

We previously showed that an intraperitoneal infection with mouse hepatitis virus (MHV) persists in interferon-gamma (IFN-gamma)-deficient C57BL/6 (B6-GKO) mice and results in subacute fatal peritonitis, which bears a resemblance to feline infectious peritonitis. To examine the role of other host factors in MHV infection in mice, IFN-gamma-deficient mice with a BALB/c background (BALB-GKO) were infected intraperitoneally with MHV and compared with B6-GKO mice. In contrast to B6-GKO mice, BALB-GKO mice died within 1 week due to acute hepatic failure. The viral titer of the liver in BALB-GKO mice was significantly higher than that in B6-GKO mice. All hepatocytes in BALB-GKO mice were necrotic at 5 days post-infection, which was clearly distinct from large but limited lesion in the liver from infected B6-GKO mice. The serum alanine aminotransferase activity of infected BALB-GKO mice were higher than that of B6-GKO mice and was paralleled with the severity of the pathological changes and viral titers in infected mice. Administration of exogenous IFN-gamma to BALB-GKO partially inhibited the acute death. These results indicate that BALB-GKO and B6-GKO mice clearly show different diseases following MHV infection, although wild type counterparts of both mice apparently showed the same clinical course after MHV infection.     

Influence of Paternal 252Cf Neutron Exposure on Abnormal Sperm, Embryonal Lethality, and Liver Tumorigenesis in the F1 Offspring of Mice

Experiments were conducted to determine whether neutron-induced genetic damage in parental germline cells can lead to the development of cancer in the offspring. Seven-week-old C3H male mice were irradiated with ²⁵²Cf neutrons at a dose of 0, 50, 100, or 200 cGy. Two weeks or 3 months after irradiation, the male mice were mated with virgin 9-week-old C57BL females. Two weeks after irradiation, the irradiated male mice showed an increased incidence of sperm abnormalities, which led to embryo lethalities in a dose-dependent manner when they were mated with unirradiated female mice. Furthermore, liver tumors in male offspring of male mice in the 50 cGy group were significantly increased in 19 of 44 (43.2%) animals, in clear contrast to the unirradiated group (1 of 31; 3.2%) ( P < 0.01). In the 100 cGy group, 6 of 39 (15%) mice had lesions. At 3 months after irradiation abnormal sperm and embryonal lethality were not significantly increased. The incidences of liver tumors in male offspring from the 50 cGy, 100 cGy and 200 cGy groups were 6 of 20 (30%), 5 of 22 (23%) and 1 of 19 (5%), respectively, which are not significantly increased compared with the control. It is concluded that increased hepatic tumor risk in the F₁ generation may be caused by genetic transmission of hepatoma-associated trait(s) induced by ²⁵²Cf neutron irradiation.     

Suppression of cytotoxin-induced cell death in isolated hepatocytes by tea catechins

To elucidate the hepatoprotective effects of green tea catechins, the following experiments were conducted utilizing (−)-epigallocatechin-3-gallate (EGCG), the major component of green tea catechin, together with other catechins. The protective effects of catechins against hepatotoxins, bromobenzene or rubratoxin B, were examined in primary cultures of rat hepatocytes. Bromobenzene and rubratoxin B are known to induce necrosis and apoptosis of cells, respectively. After 24-h treatment with toxin, EGCG and (−)-epigallocatechin-3-(3″-O-methyl)gallate (EGCg-3″-OMe) suppressed the bromobenzene-induced morphological change and dose-dependently prevented bromobenzene-induced cell death. Both catechins also prevented apoptotic cell death caused by rubratoxin B. In rubratoxin B-treated cells, both catechins were found to suppress the activation of caspase-3 by rubratoxin B. The results in the present study suggest that EGCG and EGCg-3″-OMe are potent hepatoprotective agents. This report is the first to show that catechins suppress cytotoxin-induced cell death.     

Short-lasting impairment of tactile perception by 0.9Hz-rTMS of the sensorimotor cortex

To test whether low-frequency repetitive transcranial magnetic stimulation (rTMS) of sensorimotor cortex (SM1) has prolonged effects on somatosensory function, eight subjects were given 900 TMS pulses over the left hand SM1 (0.9Hz, 90% of the resting motor threshold) or at sites 3 cm anterior or posterior to it. Tactile threshold of the right hand was increased for a short duration after rTMS over SM1, but two-point discrimination and median nerve SEPs were unaffected after rTMS at any sites.     

Endotracheal tube electrodes to map and monitor activities of the vagus nerve intraoperatively. Technical note

Difficulty swallowing due to damage of the vagus nerve is one of the most devastating complications of surgery in and around the medulla oblongata; therefore, intraoperative anatomical and functional evaluation of this nerve is crucial. The authors applied endotracheal tube surface electrodes to record electromyography (EMG) activity from vocal cords innervated by the vagus nerve. The vagal nucleus or rootlet was electrically stimulated during surgery and vocalis muscle EMG activities were displayed by auditory and visual signals. This technique was used successfully to identify the vagus motor nerve and evaluate its integrity during surgery. The advantages of this method compared with the use of needle electrodes include safe simple electrode placement and stable recording during surgery. In cases involving a pontine cavernoma pressing the nucleus or a jugular foramen tumor encircling the rootlet, this method would be particularly valuable. Additional studies with a larger number of patients are needed to estimate the significance of this method as a means of functional monitoring to predict clinical function.