Liver biopsy samples from 40 chronic alcoholic patients, including 9 with minimal changes of the liver, 6 with mild hepatic fibrosis, 14 with moderate fibrosis, and 11 with severe fibrosis (cirrhosis) were studied by electron microscopy to assess fibrogenesis in the Disse space and the role of fat-storing cells in this process. In the Disse space of normal liver, collagen fibers are few, and while lipid droplets containing fat-storing cells exist, their rough endoplasmic reticulum (RER) is inconspicuous. In the course of progressive hepatic fibrosis, collagen in the Disse space increased. This was significantly associated with gradual development of RER in fat-storing cells, confirmed by morphometric analysis. It is likely, therefore, that the development of RER in the fat-storing cells is a morphological correlative of their activated fibrogenesis and transformation into fibroblasts. To further clarify this, the rate of collagen synthesis was measured by the method of in vitro incorporation of [3H]proline into collagen in 17 liver biopsy samples from alcoholic patients and compared with the degree of morphological changes of RER in fat-storing cells. In liver samples with well-developed RER in fat-storing cells, a significantly higher rate of collagen synthesis was observed. These results suggest that in alcoholic liver injury, fat-storing cells may play an important role in Disse space fibrogenesis.

Adult↗

PubMedDate not supplied

Hypouricemia and hyperuricosuria as expressions of renal tubular damage in primary biliary cirrhosis.

Renal tubular damage, in particular, renal tubular acidosis is associated with primary biliary cirrhosis (PBC), but hypouricemia has not been described. We studied four patients with PBC whose serum uric acid levels were 1.4 to 1.8 mg per dl, and compared their renal and liver functions with those of 11 patients with PBC whose serum uric acid levels were normal. In the patients with PBC and hypouricemia, uric acid clearance (Cua) and the ratio of Cua and creatinine clearance (Cua/Ccr) were high enough to cause hypouricemia. Elevated Cua/Ccr was suppressed by administration of pyrazinamide, a blocker of tubular secretion of uric acid, but was not affected by probenecid; the effects of drugs on Cua/Ccr were similar to those reported in Wilson's disease. Elevation in Cua/Ccr was associated with increased serum bilirubin and urinary copper excretion. These observations indicate that hypouricemia and hyperuricosuria, which may be caused by defective postsecretory reabsorption of uric acid, are additional indicators of renal tubular damage in PBC.

Acidosis, Renal Tubular↗

PubMedDate not supplied

Myeloblastoma formation in acute myeloid leukemia.

The cell surface markers on the leukemic cells of 76 patients with adult acute myeloid leukemia (AML) have been analyzed by indirect immunofluorescence, and the presence of CD56+ leukemic cells was detected in ten of these patients. Four of these 10 CD56+ AML patients developed extramedullary myeloblastomas and in two of them an intracranial myeloblastoma. In contrast, in the remaining 66 CD56- AML patients, only one patient developed a myeloblastoma formation of the subcutaneous. It may be that the CD56 antigen which is an isoform of the neural cell adhesion molecule (NCAM), expressed on neurons, satellite cells of skeletal muscle cells, and on stromal cells, binds these tissues by a homophilic mechanism. CD56+ leukemic cells are capable of invading and of surviving in extramedullary tissues, where they proliferate and develop into a myeloblastoma. Because of this possibility, CD56+ AML patients should be carefully monitored for signs of myeloblastoma formation.

Adolescent↗

PubMedDate not supplied

Genetic dissection of the yeast 26S proteasome: cell cycle defects caused by the Deltarpn9 mutation.

Rpn9 is one of the subunits of the regulatory particle of the yeast 26S proteasome and is needed for stability or efficient assembly of the 26S proteasome. As anticipated from the fact that the rpn9 disruptant grew at 25 degrees C but arrested in G2/M phase at 37 degrees C, the CDK inhibitor Sic1p was found to be degraded at the G1/S boundary in the Deltarpn9 cells. The degradation of the anaphase inhibitor Pds1p was delayed in the Deltarpn9 cells. Clb2p in M phase, as well as that ectopically expressed in G1 and S phases, was degraded more slowly in the Deltarpn9 cells than in the wild type cells, indicating that the 26S proteasome lacking Rpn9 uses Sic1p as a better substrate than Pds1p and Clb2p. These results, in addition to the fact that multiubiquitinated proteins were accumulated in the Deltarpn9 cells incubated at 37 degrees C, strongly suggest that Rpn9 is involved in the proteolysis of a subset of the substrates degraded by the 26S proteasome. The Deltarpn9 Deltapds1 double mutant was unable to elongate spindle at a restrictive temperature, suggesting that some protein(s) other than Scc1 (cohesin) should be degraded during progression of anaphase.

Anaphase↗

PubMedDate not supplied

Anterior and posterior lobes of the pituitary gland: assessment by 1.5 T MR imaging.

Pituitary glands of 60 normal volunteers (30 men 20-36 years old, and 30 women 18-42 years old) were studied by 1.5 T magnetic resonance (MR) imaging. The T1-weighted images (T1WI) [repetition time (TR) = 400 ms; echo time (TE) = 25 ms] were obtained in the coronal, sagittal, and axial planes. Proton density (PD)/T2-weighted images (PDWI/T2WI) (TR = 2,000 ms; TE = 25/100 ms) were obtained in the sagittal plane using 3 mm slice thickness. On T1WIs of all subjects the posterior part (PP) of the pituitary fossa showed the highest signal, which was indistinguishable from fatty tissue. This study reveals that this region of high signal intensity (PP) corresponds to the posterior lobe and not intrasellar fat because its shape, size, and position are compatible with the posterior lobe; its signal intensity differs from that of fatty tissue on PDWI and T2WI; the absence of an intrinsic chemical shift artifact (CSA) characteristic of fat; and due to CSA, a dorsum with fatty marrow is shifted relative to the PP (or may be made to merge with it). Regarding the differentiation of the two lobes of the pituitary gland on MR, the morphology of the anterior and posterior lobes was evaluated and great variation found. Appreciation of normal is particularly important in evaluating coronal images for small pituitary lesions.

Adolescent↗

PubMedDate not supplied

Alcoholic liver disease in Japanese patients: a comparison with Caucasians.

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Aldehyde Dehydrogenase↗

PubMedDate not supplied

Increased urinary kallikrein-like activity during ADH-induced hyponatremia in rats.

The urinary kallikrein system was studied during hyponatremia associated with water and vasopressin administration in rats. Two groups of animals were studied. In the experimental group (n = 5), vasopressin (0.4 U/day) was injected intramuscularly for 7 days, and water (15%-20% body weight per day) was given via a stomach tube. The control group (n = 6) received only vasopressin. In the experimental group, plasma sodium concentration (PNa) decreased from 143.2 +/- 0.5 to 130.8 +/- 1.8 (m +/- SEM) mmol/liter (5th day, p less than 0.01) along with plasma osmolality. Urinary kallikrein-like activities (UkaV) increased from 99.1 +/- 7.5 to 172.6 +/- 23.5 mumol X min/day (100 g body weight) (5th day, p less than 0.05; 6th day, p less than 0.05; and 7th day, p less than 0.05) after the administration of vasopressin. Uric acid clearance (Cua) increased from 0.153 +/- 0.014 to 0.275 +/- 0.041 ml/min (5th day, p less than 0.05; 7th day, p less than 0.05). No change was observed in urinary aldosterone excretion (UAldV), creatinine clearance, or blood pressure. UkaV correlated with Cua (r = 0.81, p less than 0.01) and with the degree of change of PNa (r = --0.79, p less than 0.01), respectively. In the control group, no change was observed in the above parameters. A significant relationship between UkaV and fractional Na clearance (r = 0.60, p less than 0.01) was observed. We conclude that the urinary kallikrein system in rats may be stimulated during hyponatremia when induced by water and vasopressin. This increased activity is probably the result of volume expansion associated with water and vasopressin and may have some relationship to fractional Na clearance in the kidney.

Aldosterone↗