Lymphatic drainage of the gallbladder

Based upon detailed dissections of the lymphatic system in adult cadavers, the lymphatic drainage of the gallbladder was divided into three pathways: (1) The cholecystoretropancreatic pathway, which had two routes, one running spirally from the anterior surface of the common bile duct to the right rear, and the other running almost straight down from the posterior surface of the common bile duct. These routes converged at the principal retroportal node at the posterior surface of the head of the pancreas. (2) The cholecysto-celiac pathway; this was the route running to the left through the hepatoduodenal ligament to reach the celiac nodes. (3) The cholecysto-mesenteric pathway; this was the route running to the left in front of the portal vein to connect with the nodes at the superior mesenteric root. The cholecysto-retropancreatic pathway can be regarded as the main pathway, and the principal retroportal node appeared to be critical as the main terminal node in the visceral lymphatic system of the gallbladder. These three pathways converged with the abdomino-aortic lymph nodes near the left renal vein, and the nodes in the interaortico-caval space were considered to be of particular importance. Offprint requests to: M. Ito     

An Autopsy Case of Tracheal Agenesis with Broncho-esophageal Fistula

Abstract True incidence of this malformation is probably greater than that reported since the definitive diagnosis has been made at autopsy in most cases. Various hypotheses on the pathogenesis of tracheal agenesis have been proposed but they are still controversial.
In this report, we present a case of tracheal agenesis with a broncho-esophageal fistula and discuss the formal genesis.     

Presence of ghost cells and the Wnt signaling pathway in odontomas

BACKGROUND: Although it has been reported that ghost cells are present in odontomas, the generation mechanism of these cells is unclear. To evaluate the presence of ghost cells and involvement of the Wnt signaling pathway, we examined the expression of hard keratins, beta-catenin and Lef-1 in odontomas. METHODS: Sixty-nine cases of odontoma were examined immunohistochemically with the use of antibodies against human hair proteins, beta-catenin and Lef-1. RESULTS: Expression of hard keratins was found only in the cytoplasm of ghost cells in 46 (66.7%) of the 69 odontomas. Compound odontomas (78.8%) showed a higher incidence of ghost cells than complex odontomas (29.4%). Histopathologically, ghost cells were found within odontogenic epithelium adjacent to immature enamel and in the centre of Liesegang-ring-like calcified materials. Expression of beta-catenin and Lef-1 was observed in the cytoplasm and nucleus of odontogenic epithelial cells adjacent to the ghost cells in immature odontomas. CONCLUSION: These findings suggest that odontoma is a hard keratin-expressing tumor-like lesion, and that the Wnt signaling pathway may be involved in the formation of ghost cells in odontomas.     

Pancreatic tumor antigen in transplantable adenocarcinomas induced by N-bis(2-hydroxypropyl)nitrosamine in hamsters

An attempt was made to detect a pancreatic tumor antigen (PTA) in transplantable pancreatic adenocarcinomas induced by N-bis(2-hydroxypropyl)nitrosamine (DHPN) in hamsters. Antibody against antigenic protein was raised by immunizing rabbits with whole homogenate of the tumors transplanted into the back of hamsters. PTA was purified by affinity chromatography and shown to have the physicochemical properties of a glycoprotein with a molecular weight of 800,000, migrating in the beta regions upon agarose gel electrophoresis. Loss of immunological properties was observed after heating at 65 degrees C for 30 min. Enzyme immunoassay revealed that the levels of PTA in the serum and tissue showed a positive correlation with the induction of the presence of tumor, and size of the tumor. It is tentatively suggested that PTA values above 150 ng/ml serum are indicators of tumors, because in normal hamsters the PTA range is from 25 to 130 ng/ml serum. Immunohistochemically, PTA was demonstrated to be localized within the cytoplasm of epithelial tumor cells of well-differentiated tubular adenocarcinomas.     

Modulation of infection-induced inflammation and locomotive deficit and longevity in senescence-accelerated mice-prone (SAMP8) model by the oligomerized polyphenol Oligonol.

Oligonol is produced from the oligomerization of polyphenols (typically proanthocyanidin from a variety of fruits such as lychees, grapes, apples, persimmons, etc.) and contains catechin-type monomers and oligomers of proanthocyanidins. The ability of Oligonol to affect infection-dependent eye inflammation, locomotion and longevity in senescence-accelerated prone mice (SAMP8) (a model of senescence acceleration and geriatric disorders with increased oxidative stress and neuronal deficit) was investigated. Oligonol (60mg/kg) significantly modulated the extent of inflammation scores in the eye of SAMP8 mice. Examination of the mice indicated infection with mouse hepatitis virus and pinworm (Syphacia obvelata) in both males and females and with the intestinal protozoa (trichomonad) in males. A comparison of the two groups (using log-rank test) and the difference in the mean life span between groups (using Student's t-test) indicated significant differences in survival (p=0.043) and the mean life span (p=0.033) in male SAMP8 mice. Oligonol increased the mean life span and this was statistically significant. In the open-field locomotive test, the 7-week-old SAMP8 mice crossed more than 40 partitioned lines in 1min. At 48-week-old control untreated male SAMP8 crossed 2 lines. The Oligonol-treated 48-week-old male SAMP8 mice crossed 17 lines however. The improved locomotive activity was statistically significant even after 36weeks in the Oligonol-treated male SAMP8 but this was not the case throughout the time course of the study in the Oligonol-treated female SAMP8. Thus Oligonol treatment to SAMP8 mice modulated the severity of infection-dependent inflammation, prolonged life-span and significantly improved locomotive activity indicating potential benefit to aging-associated diseases such as Alzheimer's or Parkinson's diseases. This presents potential for further research to define infection-dependent inflammation associated with degenerative conditions and the molecular mechanism of dietary antioxidant protection.     

Functional innervation patterns in the corpus spongiosum and glans in the dog

The neural control of smooth muscle cells in the corpus spongiosum, helicine artery and bulbus glandis of the dog was investigated in relation to the mechanism involved in erection, using isometric tension recording and micro-electrode methods. In the corpus spongiosum, field stimulation evoked twitch-like contractions followed by relaxations. These relaxations were enhanced and prolonged by neostigmine and partly suppressed by atropine. Guanethidine abolished the twitch-like contractions and increased muscle tone. The relaxations observed after pre-treatment with guanethidine were abolished by tetrodotoxin (TTX), thereby indicating that these muscles are innervated by adrenergic excitatory, cholinergic and non-adrenergic non-cholinergic inhibitory nerves. In the helicine artery and bulbus glandis, field stimulation evoked contractions and these contractions were abolished by guanethidine or TTX, indicating that these muscles are innervated by adrenergic excitatory nerve fibres. After pre-treatment with guanethidine and atropine, muscle relaxation appeared in response to field stimulation in the helicine artery but not in the bulbus glandis, indicating that the helicine artery in the corpus spongiosum is also innervated by non-adrenergic non-cholinergic inhibitory nerves in addition to the excitatory adrenergic nerves. In the smooth muscle cells of the corpus spongiosum, slow potential changes were correlated with spontaneous contractions and field stimulation evoked excitatory or inhibitory junction potentials. The neural mechanism involved in erection is discussed in relation to the topical difference in the autonomic innervation patterns in the corpus spongiosum, helicine artery and bulbus glandis.     

Preferential inhibitions of hepatic P450IA2 expression and induction by lead nitrate in the rat

Male F344 rats were treated with lead nitrate and changes inthe expression and induction of P450IA subfamily enzymes anda placental form of glutathione-S-transferase (GST-P) in theliver were assessed by means of a bacterial mutation test, immunoblottingwith a monoclonal antibody reactive to P450IA1/IA2 and anti-GST-Psera and Northern blotting with P450IA2 cDNA as a probe. Treatmentof rats with lead nitrate (20, 50 or 100 µmol/kg bodywt) decreased P450IA2 mRNA and protein in the liver in the dose-dependentfashion and also decreased the microsomal activity for P450IA2-dependentmutagenization of aromatic amines. Pretreatment of rats withlead nitrate suppressed the inductions of both P450IA2 mRNAand protein by an inducer of P450IA subfamily enzymes in theliver. In addition, amount of the induced P450IA2 was decreasedalong with increase in that of the induced GST-P.