Portal Canals Research Articles

RECONSTRUCTION OF GASTROINTESTINES AND ADJACENT STRUCTURES IN THE EARLY PERIOD OF HUMAN ONTOGENESIS

The article describes the laying periods of: the stomach (embryos 4.5-5.0 mm long), the circular layer of the muscle membrane; gastric pits (embryos 14.7-15.0 mm long); gastric glands are formed in pre-fruits with a length of 66.0-68.0 mm. On the basis of graphic and computer reconstruction, the rotation of the stomach around the longitudinal axis of the embryo, the relationship of the stomach with neighboring structures – the liver, gall bladder, duodenum and pancreas – are studied. The fetal stomach undergoes heterogeneous and multifactorial rotation as a result of increased growth of the stomach wall on the left and increased gastric motility caused by the previous increase in the mesentery, and that the direction of rotation is determined by the forces exerted on the stomach and gastric mesentery by neighboring organs. The shape of the stomach is caused by a change in the dorsal-left sections of the tab, which leads to rapid growth compared to the ventroright sections. The cranial part of the stomach is wider than the caudal part. Uneven growth is observed not only in transverse, but also in cranial directions. The cranial part of the stomach is wider than the caudal part. A signifi cant change in the stomach occurs during 7.5 to 8.5 weeks. Due to the protrusion of the upper part of the large curvature, the bottom is formed. In an embryo of 4.5 weeks, the lumen of the loops of the proximal part of the intestinal tube has an oval shape and slightly exceeds that of the caudal part of the digestive tract. the topographical relationship of the stomach with the surrounding organs changes signifi cantly during the prenatal period of development. In embryos of 4.5-8.0 mm, the lining of the stomach is located deep behind the liver, which surrounds it on three sides. Dorsal to the stomach lining are the lining of the left adrenal gland, the left mesonephros, and the lining of the spleen. Cranially, the lining of the stomach abuts the lung to the left. At the end of the prenatal period, the diameters of the portal of the stomach, the portal canal, the bulb of the duodenum, the length of the portal canal along the lesser curvature and the portal canal along the greater curvature, and the size of the angle of the stomach were determined.

Cytological, histochemical, and ultrastructural study of human foetal liver of various gestation with future implications in segmental resection: an anatomical perspective.

The liver is the largest gland of the gastrointestinal tract having both exocrine and endocrine functions. Developmentally it arises as a ventral outgrowth from the gut endoderm during 3rd week of intrauterine life. The foetal liver is very important because of its synthetic and hemopoietic potential. The present work aimed to see the detailed histogenesis and development of the foetal liver by cytological, immunohistochemical and ultrastructural study. The liver tissue of nine aborted foetuses of various gestational age were studied. For cytology: special stains like Masson trichrome, periodic acid Schiff and reticulin were used, immunohistochemical staining was performed with triple antibodies (c-myc, Ki-67 and Ber-H2), and for ultrastructure: aluminium mounted specimens were coated with gold and argon gas and observed under scanning electron microscopy (EM). Cytology and immunohistochemistry showed the development of duct patterns and hemopoietic patterns in all stages of fetogenesis. The ductal plate was marked by the layer of dark brown staining cells at the edge of two portal tracts. The haemopoietic cells with sinusoids and aggregation of hepatocytes were observed in the early weeks of gestation. EM showed tree-like branching of a portal canal depicting hepatic segmentation of foetal liver. The organizational changes in lobular pattern, duct pattern, and microstructure of liver during fetogenesis are very crucial to achieve the adult morphology in feature. Histogenesis of the foetal liver follows a multistep process depending upon the gestational age, any deviation from normalcy may lead to structural and functional abnormality later in life.

Prognostic factors indicating survival with native liver after Kasai procedure for biliary atresia.

The number of the bile ducts in the portal canal/measured surface area of the portal canal (BDP ratio) indicates prognosis in biliary atresia (BA), as does an elevated cytokeratin 7 positivity percentage (PCK7). We compared these two markers. We reviewed 32 BA cases undergoing Kasai operation from 1976 to 2016 with >5 portal canals in biopsy samples. Group I required liver transplantation or died within a year of operation (n=8). Group II survived with their native liver (n=24). We determined the BDP ratio (102/mm2) and PCK7 (%), subdividing patients into three groups by their age at operation: Group A ≤60days (n=6, 1 Group I), 60< Group B ≤90days (n=16, 5 Group I), Group C >90days (n=10, 2 Group I). PCK7 (%) was 2.71±1.87 in Group I and 4.25±2.56 in Group II (p=0.13). BDP ratio (102/mm2) was 1.19±0.424 in Group I and 1.64±0.534 in Group II (p=0.04). Both markers were higher in Group C than in Group A or B (p<0.01). The BDP ratio is a better prognostic indicator than PCK7 in BA.

PORTACAVAL FIBROUS CONNECTIONS: LITTLE KNOWN ANATOMICAL STRUCTURES OF LIVER

Background &amp; Aims. Studies dealing with the architecture of the portal and caval canals of liver have overlooked the probability of the fibrous connections between the major portal complexes and hepatic veins when they touch each other. Such a probability is essential for both theoretical and practical medicine. Methods. We studied macro- and micro-morphological specimens from 104 normal adult and 18 normal embryonic and fetal livers. Results. We found that the fibrous sheathes of the portal complexes and hepatic veins fuse in certain areas where these structures cross each other. This anatomical relationship between the portal tracts and hepatic veins is a normal occurrence in human liver and originates at 11th-12th week of embryogenesis. Conclusions. The paper is an effort to demonstrate anatomical and clinical significance and embryogenesis of the portacaval fibrous connections.

Relation between amount of bile ducts in portal canal and outcomes in biliary atresia.

There is no good prognostic indicator for biliary atresia (BA). We reviewed liver biopsies taken during the initial procedure to find a prognostic marker. Thirty-two BA cases underwent Kasai operation from 1976 to 2009. We compared two groups at 1, 3, and 9years. Group A required liver transplantation or died. Group B survived with their native liver. Biopsies were analyzed for liver fibrosis, portal-central vein bridging (P-C bridging), ductal plate malformation (DPM) and the number of the bile ducts in portal canal/measured surface area of the portal canal (BDP ratio). Statistical comparisons of the multiple data were evaluated by Mann-Whitney U test, Student's t test and Pearson's Chi-square test. Regression analysis with P<0.05 was considered significant. BDP ratios (/mm(2)) were 2.4±1.5 in Group A1 (n=9) vs 4.6±2.4 in Group B1 (n=23) (P=0.01); 2.6±1.4 in Group A3 (n=14) vs 5.1±2.5 in Group B3 (n=18) (P<0.01), 3.0±2.2 in Group A9 (n=15) vs 4.9±2.5 in Group B9 (n=15) (P<0.05). There was no significant difference in any other finding. The BDP ratio is a sound prognostic indicator in BA.

Accessory liver lobe attached to the wall of the gallbladder: a cadaveric case report

Accessory liver lobe is found incidentally during laparoscopy, laparotomy or autopsy performed for unrelated reasons. The occurrence of accessory liver lobe attached to the gallbladder is reported rarely in the literature. During regular dissection classes, we came across an accessory liver lobe in the wall of the gallbladder in an adult male cadaver. On its left, it was connected to the quadrate lobe by a short fold of peritoneum. On the right, it was attached to the wall of the gallbladder. The fragment was triangular in shape, and was 20mm in length, 11mm in width and 6mm thick. The histology of the fragment revealed the unusual architecture of hepatic tissue with the absence of the classical hexagonal lobule pattern. Cords of hepatocytes surrounding the central vein, with an absence of portal canals, were observed. There were branches of hepatic artery, portal vein and hepatic duct in its peritoneal fold. Smooth muscle fibers were also observed along its attachment on the wall of the gallbladder. Awareness of the incidence of accessory liver lobe in the wall of the gallbladder is of clinical importance during the diagnosis and treatment of gallstones.

Distribution of rat hepatic steroid 5 alpha-reductase 1 as shown by immunohistochemistry.

Peptide fragments of rat liver 5 alpha-reductase were synthesized according to the published primary sequence data. The peptide were used (i) in free form and (ii) linked to keyhole limpet hemocyanin (KLH), respectively, for immunization of rabbits. Resulting antisera showed positive reaction with the respective peptide-antigen in an ELISA. In Western blot experiments the antisera specifically recognized a 26,000 mol wt protein in extracts from female and male rat liver. All antisera, as well as isolated immunoglobulins, showed inhibition of 5 alpha-reductase activity in microsomes prepared from rat liver. Positive immunohistochemical reactions were observed in the perinuclear cytoplasm of hepatocytes. No reaction was seen in Kupffer- and connective tissue cells. Acinar heterogeneity of the immunoreaction was seen in the male rat liver with a gradient from the portal canal to the central vein. After androgen-deprivation a considerable increase in immunoreactivity was seen in male rat liver cells, indicating androgen-dependent suppression of the enzyme in male liver.

Hepatic Circulation

Hepatic Circulation

Protective effect of N-acetylcysteine, caffeic acid and vitamin E on doxorubicin hepatotoxicity

The aim of this study was to compare the possible protective effects of N-acetylcysteine (NAC), caffeic acid (CAPE) and vitamin E (Vit-E) on doxorubicin-induced hepatotoxicity. Thirty-two male Wistar albino rats, weighing between 250 and 350 g were supplied and randomly divided into five groups. Animals in study groups were pretreated with a single dose of doxorubicin (Dox), which was administered intraperitoneally (i.p.). Control group (Group I) was treated with intraperitoneal saline injection. Group II did not received any antioxidant agent after the injection. Group III and Group IV were given CAPE and intraperitoneal vitamin E injection for eight days, respectively. Group V received NAC for eight days. The study was finished after 10 days. Tissue samples were collected from all animals and histopathological examination was performed. There was statistically significant difference between the experiment groups and controls by means of mononuclear cell infiltration and diameters of hepatic sinusoid, terminal hepatic venule (central vein) and portal area (portal canal). Changes related with hepatocellular damage were more prominent, whereas there was no significant difference between Dox and NAC given groups histopathologically. It was observed that structural changes were regressed after CAPE administration. However, this recovery was more prominent in vitamin E given group. These findings suggest that Dox induced liver damage could be efficiently reversed by vitamin E administration. It has been found that CAPE, but not NAC has protective effects on Dox-induced hepatocellular damage.

ZT glue immobilizes iodinated oil in vivo

Purpose ZT glue immobilizes iodinated oil to raise treatment efficiency. Materials and methods ZT glue and iodinated oil were mixed at a series of volume ratios on a level surface which be put vertically after 30 min. Five Sprague-Dawley rats (group 1) were subcutaneously injected in the groin with ZT glue and 131I-iodinated oil (volume ratio at 1:4, 0.1 ml per rat, 131I activity 13.6 × 37 × 10 3 Bq), at 1, 8, 12, and 27 days, a SPECT plain scan was performed to observe the 131I distribution in the body, and to calculate the γ counts at the site of injection. At 28 days, the rats were sacrificed and organs were collected. Iodinated oil states at the injection spot were recorded. Specimens from organs and the injection spot were used to detect γ counts. Another five Sprague-Dawley rats (group 2) were subcutaneously injected 131I-iodinated oil in the groin as control group. Through portal vein, five rabbits right liver lobe received 131I-iodinated oil (1 ml, 20 × 37 × 10 3 Bq) + ZT glue (0.25 ml). γ counts in the liver region were recorded on days 0, 1, 2, 3, 4, 5, 6, 7, 9, 12, 15, 21, 27, and 33 after surgery. Then, γ counting and pathological examination of the liver specimen and the lung specimen were performed. All γ counts data was processed by INDFIT1.0 software that was designed in our laboratory to establish nuclide metabolic equation. Result The mixed iodinated oil above the volume ratio of 1:12 stop at level surface local. At rat the injection site, the nuclide stagnation time of group 1 are longer than those of group 2, and the biological half-life of group 1 is four times that of group 2. Single agent analysis of variance comparing the biological half-life: F value is 81.999, p < 0.001. No visible damage was seen in the rat organs. All rat organs except the liver had no statistically significant γ counts difference. Tissue γ counts at the site of injection at day 28 had statistically difference between the two rat groups, F value is 5.608, p = 0.045. The iodinated oil metabolic patterns in rabbit liver revealed two portions, the rapid and the slow. ZT glue rabbit group had higher slow proportion than iodinated oil group. Pearson Goodness-of-Fit Chi-square test found the Chi-square value was 25.433, d.f. = 6, p < 0.0001. ZT glue rabbit group right liver lobe has iodinated oil and ZT glue depositing, some liver cells were degenerated and vacuolated in the cellular plasma. Fibrous tissue proliferated around hepatic portal canal regions. Conclusion ZT glue fixed iodinated oil is possible in vivo. This provides a new potentiality to delay iodinated oil metabolic in clinical liver cancer interventional treatment.

Expression of MUC1 and its significance in hepatocellular and cholangiocarcinoma tissue

To investigate the relation between MUC1 expression, distribution, and prognosis in hepatocellular and cholangiocarcinoma (HCC and CC) and cirrhotic liver tissues, and their significance in HCC and CC diagnosis. Expression and distribution of MUC1 were examined by immunohistochemical assay with anti-MUC1 mAb in 59 samples of HCC and 37 samples of CC, 20 samples of cirrhotic liver tissues, and 10 samples of normal liver tissues, seeking possible associations between MUC1 positive expression, distribution in HCC and CC (primary liver cancer, PLC) cases and the studied clinical data. Immunohistochemical analysis of MUC1 expression showed that in the 96 PLC samples, 68 (70.8%) were strong positive, and 6 (6.2%) were weak positive. Only 4 in the 20 cirrhotic liver tissues were found to be weak positive, while no expression of MUC1 was detected in normal liver tissues. Apparently, the high expression rate of MUC1 in PLC tissues was statistically significant in comparison to that in cirrhotic and normal liver tissues. The expressed MUC1 protein, stained in dark brownish or brownish-yellow particles, chiefly localized on the cancer cell membranes or in cytoplasm. In the 68 strong positive samples, 40 were detected on cell membrane and the other 28 were in cytoplasm. In addition, follow-up studies of those PLC cases demonstrated that MUC1 expression on cell membrane or in cytoplasm was closely associated with PLC prognosis. The expression of MUC1 in PLC had little statistical significance in respect of the pathological types and sizes of the tumors, but a strong relationship regarding histological differentiation, metastasis of lymph nodes, portal canal emboli, and post-operational recurrence of the carcinomas. After 3 years of tumor excision, the metastasis rate in MUC1 positive expression group (67.6%) was much higher than that in MUC1 weak expression group (33.3%) and negative expression group (31.8%), and thus the survival rate in MUC1-positive expression group was significantly different from that in weak and negative expression groups. Expression and localization of MUC1 proteins in primary liver carcinomas (PLCs) may act as prognostic markers, and MUC1 molecules might be helpful in differential diagnosis.

Distinguishing periportal fibrosis from portal fibrosis in hepatic schistosomiasis.

Schistosomiasis is an important disease in humans and various domestic animals in many parts of the world. The main clinical symptoms of schistosomiasis include serious hepatic lesions induced by the ova of schistosomes. Although the majority of ova deposited in the mesenteric veins are supposed to reach the intestinal lumen, a considerable number of ova are carried by the portal blood flow to the liver, where they are lodged in the small blood vessels of the portal tracts. Indeed, many investigators have tried to elucidate the characteristics of hepatic fibrosis induced by these ova. The pioneering work of Symmers in 1904 [1] described the hepatic lesions in humans caused by ova of Bilharzia haematobia. Symmers reported that the liver surface displayed a pronounced increase in the perivascular connective tissue, and the cross-sections were dominated by an enormous increase of fibrous tissue (Glisson’s capsule) which normally surrounds the portal canals, forming a pattern reminiscent of white clay-pipe-stems. Symmers’ work remains as a kind of creed or paradigm for investigators of hepatic schistosomiasis, but it has also initiated a persisting confusion as to the correct terminology of fibrosis in relation to the portal tracts. Symmers described the liver changes as a new form of liver cirrhosis and this description might have contributed to the terminological confusion because these changes do not meet the qualifications for cirrhosis according to current pathology textbooks. The confusion is centred on the crucial question: should fibrosis of the portal tracts, and particularly around branches of the portal vein, be called periportal fibrosis or portal fibrosis? There is a general agreement among anatomists, histologists and pathologists to use the terminology portal area, portal tract, portal canal or portal triad to describe the accumulation of connective tissue, which normally supports branches of the hepatic artery and portal vein, the bile ducts and lymphatic vessels. In addition, changes within these areas are described as portal and changes in the adjacent parenchyma outside these areas are described as periportal (see, for example, Refs [2–4]). Unfortunately, this terminology does not seem to have communicated itself to researchers of hepatic schistosomiasis among whom a difference of opinion has prevailed (Table 1). The difference, however, appears to be limited to the choice of terminology and is not based on a difference of opinion among the authors as to the nature of the fibrosis, which is generally described as an increase of connective tissue in the portal tracts. It is correct that fibrosis around a bile duct in a portal area is sometimes designated peribiliary fibrosis (or biliary fibrosis), but this does not warrant the designation of fibrosis around a portal vein in a portal area as periportal fibrosis. The consequence of this is that fibrosis around a branch of the hepatic artery would be designated perihepatic fibrosis. To avoid misunderstandings and misinterpretations in the future, we encourage researchers to coordinate their terminology in accordance with the terms generally applied by anatomists, histologists and pathologists. Fibrosis within a portal tract should be called portal fibrosis, and fibrosis of the parenchyma adjacent to a portal tract should be called periportal fibrosis. These are the logical and correct terms to apply to fibrosis in relation to the portal tracts and their immediate surroundings.

A case of inflammatory pseudotumor of the liver causing elevated serum CA19-9 levels

Inflammatory pseudotumor of the liver is a rare lesion characterized by proliferating fibrovascular tissue admixed with inflammatory cells. A 50-yr-old Japanese man was hospitalized because of upper abdominal pain and high fever. Computed tomography revealed a poorly demarcated, low density mass in the left lobe of the liver, and abnormal laboratory findings included WBC 9340/mm 3, CRP 10.5 mg/dl, and marked elevation of CA19-9 to 1167.9 U/ml. Endoscopic retrograde cholangiography showed irregularity of the intrahepatic bile duct of the left lateral segment, and the lateral segmental branches of the portal vein were not visualized on the venous phase of abdominal angiography. Ultrasound-guided liver biopsy was performed, but malignant disease, including intrahepatic cholangiocarcinoma, could not be completely ruled out. The patient underwent left hepatic lobectomy with lymph node dissection. Histopathological examination yielded a definitive diagnosis of inflammatory pseudotumor. The lesion was immunohistochemically stained for CA19-9 by the ABC method, and the biliary epithelium in severely inflamed portal canals was found to be positive. The markedly elevated preoperative level of CA 19-9 decreased to almost within the normal range and the patient remains well 2 yr 9 months after surgery, without any complications.

Monoclonal antibody-based immunohistochemical demonstration of Entamoeba histolytica in liver tissues of experimentally infected hamster ( Mesocricetus auratus)

Histopathological changes and the presence of Entamoeba histolytica trophozoites was sequentially followed after intrahepatic inoculation of the parasites in 42 hamsters, 35 of which received no treatment whereas the remaining seven were treated with metronidazole. The liver tissues were examined for amoebic trophozoites by a monoclonal antibody (mAb)-based immunonuorescence assay (IFA), a mAb-based immunoperoxidase (IPx) and H & E staining. The number of hamsters developing abscesses was increased with time and was highest on day 30. Cellular infiltration with inflammatory cells and glycogen depletion were observed as early as day 5, followed thereafter by more intense inflammation of portal canals, periportal fibrosis, bile duct proliferation and hepatocyte degeneration. In 7 metronidazole-treated hamsters, no obvious pathological damage was seen. In a group of seven hamsters each, both IPx and IFA were positive in 3, 3, 4, 5 and 4 hamsters and in 3, 4, 3, 3 and 5 hamsters on days 5, 10, 15, 20 and 30, respectively. In 18 control hamsters, IPx, IFA and H & E were all negative. If the result from H & E was used as a gold standard, agreement between H & E and IFA and H & E and IPx were 91.4%, and 88.6%, respectively. Sensitivity and specificity were 93.8% and 89.5%, respectively for IFA, and 93.8% and 84.2%, respectively for IPx.

Changes in hepatic lymph vessels in endotoxaemia.

This study was undertaken into rats to investigate changes in the hepatic lymph vessels and the space of Disse in endotoxaemia and to examine their relationship with the development of endotoxin-induced hepatic injury. Lymph stasis, namely dilatation of the lymph vessels and oedema, developed rapidly in the medium-sized portal canals, the large portal canals, and the liver hilum after endotoxin injection, but not in the small portal canals. Such changes reached their maximum 4-8 h after endotoxin injection and had recovered markedly by 16 h after the injection. The space of Disse remained within normal limits during this period. These findings suggest that the intrahepatic lymph stasis in endotoxaemia may be caused by a reduction in the pumping activity of the extrahepatic and the intrahepatic large lymph vessels rather than by an increase of lymph formation in the liver lobules. There was no evidence suggesting a direct relationship between the disturbance of hepatic lymph flow and the development of hepatic injury in endotoxaemia.

Combined toxicity of ethanol and methylmercury in rat

The hepatotoxic and nephrotoxic effects of methylmercury (CH 3Hg) and ethanol (EtOH) are well known; however, their interaction in vivo is not clearly understood. In order to investigate the combined effects of these 2 substances, 4 groups of male Wistar rats with an initial weight of approximately 190 g were treated for 7 weeks. Each group consisting of 8 rats was gavaged as follows: Group 1 with 5.0 ml/kg body weight of double distilled water, Group 2 with 5.0 ml/kg body weight of 25% EtOH, Group 3 with 2.5 mg/kg of CH 3Hg in water, and Group 4 with 2.5 mg/kg of CH 3Hg in 25% EtOH. At the termination of the experiment the mean body weights of the rats in Group 3 (372.5 ± 10.8 S.E.) and Group 4 (383.4 ± 13.4) were significantly lower than that of Group 1 (433.0 ± 7.8). Linear regression showed a positive feed conversion efficiency for Groups 1 and 2 (1.07 and 0.83, respectively), and a negative score for this parameter for Groups 3 and 4 (−1.43, −1.53). At necropsy, rat livers from Group 3 exhibited random multifocal tan spots. The relative liver weights were similar to those of controls. Semithin sections of liver revealed an increase in lipid droplets in Groups 2 and 3 compared to those in the other 2 groups while vacuolization was more striking in CH 3Hg treated rats (Groups 3 and 4). Severe hepatolysis and portal canal edema were noted in the groups of rats exposed to either EtOH alone or in combination with mercury. The relative weight of left kidney in Group 3 (0.70 ± 0.03) and Group 4 (0.51 ± 0.04) rats was significantly greater than of the control (0.39 ± 0.03). In gross appearance the kidney was pale and the urine production was significantly higher ( P<0.05) in Group 3 compared to that of Group 1. Group 4 rats had significantly more ( P <0.50) Hg in the kidney than Group 3; however, the inorganic percentages in both groups were similar. Morphological examination of the kidney proximal tubules from CH 3Hg treated rats (Groups 3 and 4) revealed an increase in lipid droplets, vacuoles, cell sloughing and tubular degeneration compared to Groups 1 and 2. These histological changes in the proximal tubules of Groups 4 rats indicate an additive effect of EtOH on the kidney pathology caused by CH 3Hg. This present study seems to suggest that ethanol in combination with mercury enhances the retention of mercury in the kidney and increases the nephrotoxicity while it has no effect on the neurotoxicity of mercury. EtOH and CH 3Hg combination (Group 4) showed increased fibroblast infiltration and fibrosis in the kidney cortex, and larger and more numerous dense bodies and swollen mitochondria in the tubular cells. However, these alterations of nephrotoxicity by EtOH require further study.

Pattern and distribution of intrahepatic lymph vessels in the rat.

The pattern and distribution of intrahepatic lymph vessels were examined by light and electron microscopy in rat livers fixed by perfusion through the portal vein. Lymph vessels were found in the connective tissue of the larger portal canals, where they coursed in close association with branches of the hepatic artery. The smallest portal canals contained no lymphatics. Of the portal canals that lacked a lymphatic, over 50% also lacked an arterial component. Direct connections between the lymphatic lumen and the spaces of Disse or Mall were not observed but lymphatics were found close to Mall's space, separated by only a sparse connective tissue space containing a few collagen fibrils. Lymphatics were neither seen within the parenchyma, nor associated with intercalated (sublobular) veins. Cross-sectional area (223.2 +/- 48.7 micron2 SEM), maximum diameter (20.5 +/- 2.0 microns), volume density (0.00098 +/- 0.00046 micron3/micron3) and profile density (1.8 +/- 0.3 lymphatics per 1 mm2) of hepatic lymph vessels were determined by stereological measurement by a computer-based image analyzer. These data were used to estimate the rate of lymph formation in the liver. It was concluded that 1) initial lymphatics probably originate in the portal canals; 2) the concept that fluid in the space of Disse can be regarded as the principal source of fluid-forming hepatic lymph is questioned, since initial lymphatics appear to be separated from the space of Disse by hepatocytes and the space of Mall; and 3) the rate of lymph formation in the liver of the rat is approximately 0.06-0.08 microliter/min/cm2 of lymphatic endothelium.

Pathogenicity of an isolate ofaspergillus fla vusin chickens

Cockerels aged 8 days were each given intraperitoneally a 1 ml suspension of Aspergillus flavus grown on Sabouraud's dextrose agar containing 10(6) colony forming units per ml. No clinical signs were observed but mortality was 37.5%. Liver and kidney were enlarged at necropsy. Granulomatous nodules were found in the serosa and lung parenchyma up to day 16 post-infection but by day 30 post-infection tiny nodules persisted only at the site of inoculation. Periodic acid-Schiff stained sections of the serosa, lung, kidney, liver, spleen and bursa of Fabricius showed the fungus in only the serosa and lungs. There was fibrosis of the hepatic portal canal, congestion and hyperplasia of the bile ducts. In the kidney there was degeneration of mainly the epithelium of proximal convoluted tubules followed by generalised pyknosis. Bursa and spleen showed lymphocytic depletion. The fungus was reisolated from the nodules up to day 16 post-infection. The above observations appear to describe a condition of concurrent mycotoxicosis and aspergillosis due to Aspergillus flavus.

Immunocytochemistry of albumin in hepatocytes after overnight starvation and during a diurnal cycle in young rats.

The indirect immunoperoxidase method was used to identify albumin in hepatocytes of young rats before and after periods of starvation and during a normal diurnal cycle. All liver cells in fed rats contained an abundance of albumin, whereas hepatocytes from overnight fasted animals showed minimal amounts of the protein. Hepatocytes in rats on the diurnal cycle generally contained more albumin during the light phase than in darkness. At the beginning of the dark phase, certain hepatocytes were low in albumin and they were located primarily around portal canals. Halfway through the dark period, these cells had increased in number and were located closer to terminal hepatic venules. Overnight starvation of young rats profoundly lowers hepatocyte albumin and the time of highest liver cell albumin content in the diurnal cycle of fed, young rats is during the first half of the light period.

Distribution of Collagen Type I and Type III and of two Collagenous Components of Basement Membranes in the Human Liver

The distribution of collagen type I and III and of the basement membrane collagens type IV and alphaA (alphaB)2 in normal and fibrotic human livers has been studied by indirect immunofluorescence using type specific antibodies. Collagens type I as well as type III are present in normal livers in the blood vessel walls and the wall of biliary ducts of the portal tracts. In the parenchyma both types are visible along the sinusoids. Basement membrane collagens are only present in the connective tissue of portal canals and of central veins whereas in the parenchyma both type IV and alphaA (alphaB)2-collagen are nearly absent. In the tissue of fibrotic livers basement membrane collagens are also found in the parenchyma in similar distribution as type I and III.