Role of hepatic artery in haemodynamics in normal and cirrhotic livers in rats

To examine the degree of influence of the hepatic artery on microcirculation in the liver, microscopic observation of blood flow in the hepatic minute blood vessels and the sinusoids and pressure measurements at key points in hepatic vascular pathways in vivo were performed before and after hepatic artery ligation in normal and cirrhotic rats. In normal rats, portal vein pressure (109 mmH2O) fell 10 mmH2O after hepatic artery ligation, but the pressures of the terminal portal venule, the terminal hepatic venule and the inferior vena cava did not change. In cirrhotic rats, portal vein pressure (206 mmH2O) and terminal portal venule pressure (106 mmH2O) fell 23 and 10 mmH2O after hepatic artery ligation respectively: the pressures in the terminal hepatic venule and the inferior vena cava did not change. These results suggests that the pressure transmitted from the hepatic artery was mostly supplied to the intrahepatic portal vein in normal rats and both to the intrahepatic portal vein and to the sinusoids in cirrhotic rats. In both normal and cirrhotic rats, however, the pressure transmitted from the hepatic artery was about 10 per cent of the initial portal vein pressure, and the blood flow in minute vessels and sinusoids did not change after hepatic artery ligation. Accordingly, it is believed that the hepatic artery plays only a small role in the haemodynamics of the liver in both normal and cirrhotic rats, irrespective of the distribution and manner of the hepatic arterial termination.     

Analysis of Fibrinolysis by the Use of Epsilon-Aminocaproic Acid: Preliminary Report

From the foregoing analysis of the inhibitory action of -aminocaproic acidin the fibrinolytic process, it is evident that the process involves two reactionphases, fibrinolysis and metafibrinolysis.

Fibrinolysopeptide and metafibrin are split off from fibrin in fibrinolysis.The former is a peptide with N-terminal glycine, while the latter is a monochloracetic acid-soluble metaprotein having both aspartic acid and tyrosineas N-terminal amino acids.

     

A Case of Esophageal Carcinoma and Collision Tumor of the Stomach

A case of double primary cancer of the esophagus and stomachwith metastasis of the esophageal cancer to the stomach is reported.The entire stomach and the lower part of the esophagus weresurgically resected and intrathoracic esophagojejunostomy wasperformed. Macroscopically, two tumors were found to be present,both in the lower esophagus and the stomach. There were twoprimary cancers, one a squamous cell carcinoma of the esophagusand the other a collision tumor of the stomach which consistedof well-differentiated adenocarcinoma and signet ring cell carcinoma.Furthermore, this collision tumor was present together witha metastatic lesion from the esophageal carcinoma.     

Pathogenesis of centrilobular necrosis following congestion of the liver

The exact pathogenesis of centrilobular necrosis following congestion of the liver is still unknown. We reviewed the clinical data related to systemic circulatory disturbance and histopathology of the liver and the gut in 320 autopsy subjects. Congestion of the liver alone was associated only with atrophy and loss of hepatocytes in centrilobular areas, but not with hepatocellular coagulative necrosis. In many patients with coagulative necrosis of centrilobular hepatocytes and congestion of the liver, fibrin thrombi and neutrophil infiltration in the sinusoids, which are the characteristic histopathological features of the liver in endotoxaemia, were found in and around the necrotic area. Congestion, erosion or haemorrhage of the intestinal mucosa, which may allow entrance of endotoxin into the liver through the portal vein, was seen in such patients. Prolonged hypotension or shock, which may lead to portal endotoxaemia, was present in half the patients with centrilobular necrosis and congestion of the liver. These results suggest that not only congestion of the liver but also portal endotoxaemia may be involved in the pathogenesis of centrilobular necrosis in patients with congestion of the liver.     

Pull-Through Esophagectomy Without Thoracotomy

Twenty patients with carcinoma of the hypopharynx, esophagusand thyroid underwent pull-through esophagectomy. Seventeenof them received combined resection of the larynx and trachea.Dissection of the lymph nodes at the upper mediastinum was performedin 11 patients by sternotomy. Seven patients received mediastinaltracheostomy after combined resection of the trachea and thelarynx. Pull-through esophagectomy was followed by pharyngogastrostomywithout thoracotomy via the posterior mediastinum. This techniqueis described in detail. Because there is no thoracotomy andligation of the esophageal vessels is ensured, no pulmonarycomplications and no massive mediastinal hemorrhages occurred.There were no operative deaths. This operation offers excellentpalliation and little morbidity. Moreover, the use of sternotomyand mediastinal tracheostomy for pull-through esophagectomymade it possible to dissect the upper mediastinal lymph nodes,and we could resect the affected trachea with certainty.     

Esophageal Cancer Associated with Gastric Cancer

Among a total of 1,137 patients with esophageal cancer, therewere 44 cases of esophageal cancer associated with gastric cancer,an incidence of 3.9%. The majority of the patients were between60 and 70 yr old. Forty-two patients were male and two werefemale. Eleven of these patients had a third cancer. Six had multiplecancers in the esophagus and/or stomach. Eighteen patients hadearly gastric cancer. Thirty-two of the cancers were synchronousand 12 were metachronous. Of these 44 patients, 21 had familyhistories of cancer, 37 were smokers, and 36 were drinkers.Twenty-five patients received surgery for all of their cancers,and two patients received resection of only esophageal cancer.Of these 27 patients. five patients lived more than 5 yr. Themost frequent cause of death in our series was esophageal cancer(52.9%). Surgical treatment of all of the cancers is desirable. Whenthis is impossible, the surgery must be emphasized for the esophagealcancer in most cases.     

Common clonal origin of lymphocytes and plasma cells in splenic lymphoma with villous lymphocytes

In two-thirds of patients with splenic lymphoma with villous lymphocytes (SLVL) a small amount of M-protein can be detected in association with the presence of plasma cells in the peripheral blood (PB) and/or bone marrow (BM). However, it is not known whether lymphoma cells and plasma cells originate from the same clone. In this report we describe a case of SLVL which was characterized by the presence of marked monoclonal gammopathy (IgG-κ 90 g/l) and increased plasma cells in the BM. In an attempt to elucidate the origin of lymphoma cells and plasma cells, we performed morphological, cytogenetic and molecular studies on PB mononuclear cells (PBMNC) without plasma cells and BMMNC containing 10% plasma cells from this patient.
Immunofluorescence showed that lymphoma cells and plasma cells were positive for cytoplasmic γ heavy and κ light chains. Well-developed endoplasmic reticulum was observed in the cytoplasmic organelles of PBMNC using an electron microscope. The mean IgG concentration in the 3 d supernatant cultures of PBMNC was 374±24μg/l. More than 50% PBMNC differentiated into plasmacytoid cells in 6 d of liquid culture with IL-3 and IL-6. Analysis by two-colour FISH revealed that karyotypic abnormalities of monosomy X and trisomy 17 existed simultaneously in both lymphoma cells and plasma cells. JH gene rearranged bands from PBMNC and BMMNC by Southern blot hybridization were identical, whereas DNAs from PBMNC failed to hybridize with the Cμ probe.
These observations strongly suggest that lymphoma cells and plasma cells originate from the same clone, and that plasma cells, as well as lymphoma cells, which have undergone class switch recombination, could produce IgG type M-protein in this case.     

Double Adenocarcinoma in Barrett's Esophagus: A Case Report

At the National Cancer Center Hospital in Tokyo, a patient withBarrett's esophagus developed double adenocarcinoma of the esophagus.One carcinoma was located in the midesophagus and the otherjust above the anatomic cardia. Esophagoscopic examination withbiopsy revealed two carcinomas surrounded with columnar epitheliumand ectopic islets of gastric mucosa situated in the postcricoidregion. There was no ulcer or stricture in the esophagus. Thepatient received subtotal esophagectomy and survived the operation.Microscopically, depth of invasion of the proximal cancer wasto the proper muscle, and that of the distal one was to thesubmucosal layer. There was metastasis to two lymph nodes. Therewas no sign of inflammation or ulcer in the esophagus.     

A quantitative study of neurofibrillary tangles, senile plaques and astrocytes in the hippocampal subdivisions and entorhinal cortex in Alzheimer's disease, normal controls and non-Alzheimer neuropsychiatric diseases

Abstract  The present quantitative study was performed in order to discriminate pathological substrates for dementia from Alzheimer changes in normal controls (NC) and non-Alzheimer neuropsychiatric diseases (NAND). Regional densities of senile plaques (SP), neurofibrillary tangles (NFT) and astrocytes in the cornu ammonis (CA), subiculum and entorhinal cortex were measured and differences in these densities among Alzheimer's disease (AD), NAND and NC were statistically compared. Densities of NFT in the CA and subiculum were significantly higher in AD than in NAND, and densities of SP in all regions were significantly higher in AD than in NAND. Similarly, NFT density in the subiculum and SP density in all regions were higher in AD than in NC. Regional densities of astrocytes in most regions were closely correlated with those of Alzheimer changes. In conclusion, the attribution of the Alzheimer changes, particularly of NFT, to dementia is neglected when they are confined to the entorhinal cortex. However, the attribution of the Alzheimer changes to dementia should be appreciated when they spread from the entorhinal cortex to the subiculum and/or CA.     

Evaluation of proximal tubular function in preterm infants by urinary α1-microglobulin

α₁-Microglobulin is a low molecular weight protein that is relatively stable in urine of low pH. There have been few reports on urinary α₁-microglobulin (U-A₁M) excretion in preterm infants. This study was designed to establish the ranges for U-A₁M in clinically stable preterm infants and to investigate changes observed in sick preterm infants. We measured U-A₁M and urinary β₂-microglobulin (U-B₂M) levels at 1, 4, 7, 14, 28 and 90 days after birth in stable preterm infants (Group 1) and sick preterm infants who were depressed at birth and required immediate resuscitation (Group 2). In Group 1 infants, both parameters were high during the first 28 days and appeared to decline thereafter. U-A₁M in Group 2 infants was only significantly increased compared with Group 1 on day 1, as was U-B₂M. On each day of the study, U-A₁M had significant positive correlations with U-B₂M for all the infants studied. The changes of the two parameters observed in Group 1 probably reflect postnatal evolution of proximal tubular function in stable preterm infants. A comparison of groups 1 and 2 shows a high prevalence of acute tubular injury at birth in sick infants and also suggests that U-A₁M as well as U-B₂M may be a sensitive index for detecting acute tubular damage and for following its course in preterm infants.