Concentration of metals, ceruloplasmin, metallothionein and the activity of N-acetyl-beta-D-glucosaminidase and gamma-glutamyltransferase in pregnant women who smoke and in those environmentally exposed to tobacco smoke and in their infants. Part I

Concentrations of metals (Zn, Cu, Se, Cd), metallotionein (MT) and ceruloplasmin (Cp), and the activity of N-acetyl-beta-D-glucosaminidase (NAG) and gamma-glutamyltransferase (gammaGT) in pregnant women who smoke and in passive smokers as well as in their newborns were measured. In smoking women a many-fold increase in cotinine concentrations in maternal and infant urine, amniotic fluid, placenta and milk was found as compared to passive smokers. Smoking lowered serum Se concentration in mothers and infants, increased serum ceruloplasmin in mothers and decreased serum Cu concentration in infants. Serum Zn level in infants was higher than in mothers, and smoking furthered its increase. Statistically significant increase in concentrations of Cd in placenta, amniotic fluid and milk, of Cu in placentae and amniotic fluid and of Zn in placenta and milk was revealed. Higher concentrations of metals were accompanied by an elevated MT level in placenta and amniotic fluid. In smoking women a significant increase in NAG activity in urine, amniotic fluid and milk, increase in gammaGT activity in urine and amniotic fluid and decrease in gammaGT activity in milk and placenta were observed. There was high, positive correlation between MT/NAG and MT/gammaGT in amniotic fluid of passive and active smokers, while similar correlation in milk was indicated only in the group of active smokers. The biochemical parameters analysed proved their usefulness in the evaluation of effects of exposure to cigarette smoke on pregnant woman and her fetus.     

Functional defects in lysosomal enzymes in autosomal dominant polycystic kidney disease (ADPKD): abnormalities in synthesis, molecular processing, polarity, and secretion

The phenotype of autosomal dominant polycystic kidney disease (ADPKD) is characterized by basement membrane abnormalities, hyperproliferation, and alterations in epithelial cell polarity. Since proteinases have been implicated in matrix degradation and growth factor activation, lysosomal enzymes were compared in normal and ADPKD tissues and cell cultures. Acidic proteolytic activity (azocasein) was reduced in ADPKD, and specific enzymatic assays detected disease-dependent decreases in the specific activities of beta-galactosidase, beta-hexosaminidase, and cathepsins, B, L, and H. Cathepsin D-specific activities were unchanged. Lucifer yellow fluorescence in ADPKD cells was consistent with an alteration in heterogeneity of lysosomal enzyme content in ADPKD rather than a decrease in total lysosomal number. Western analysis, metabolic labeling, and immunoprecipitation analysis confirmed decreases in the expression and synthesis of the major normal molecular immunoreactive species of beta-galactosidase and cathepsins B and H in ADPKD tissue and cells but no changes in cathepsin D. In addition, ADPKD-specific high-molecular-weight species of cathepsin H were seen and abnormal forms of cathepsin B and beta-galactosidase were common in ADPKD, suggesting abnormal molecular processing and posttranslational modifications. In addition, immunolocalization studies showed abnormal apical plasma-membrane localization of cathepsins B and H in ADPKD cyst epithelial cells, consistent with a protein sorting defect in ADPKD. Increased extracellular secretion of lysosomal enzymes was also measured in ADPKD cultured cells and in filter-grown epithelia shown to be predominantly directed to the basal compartment. These results demonstrate that lysosomal enzyme alterations in ADPKD may play a role in aberrant processing of the basement membrane. Alterations in the polarized secretion of lysosomal enzymes by ADPKD epithelia in vitro were also detected. Whereas all normal epithelia cells secreted lysosomal enzymes predominantly to the apical medium compartments, basally directed secretion was increased in all ADPKD epithelia and attained an overall reversal of polarity for cathepsins B + L. It is concluded that alterations in lysosomal enzyme function in ADPKD are the result of alterations in synthesis, molecular processing, and polarized secretion of specific enzymes and may have impact on proliferative and basement membrane abnormalities in this genetic disease. These results are consistent with a fundamental defect in protein processing sorting, and trafficking in ADPKD.     

某铀矿区水稻土—地表水铀含量对稻米铀含量的影响

以水稻土—地表水铀含量为视角,从水稻土剖面铀含量分布规律、水稻土与下伏岩体稀土元素特征、不同河流不同河段水稻土—地表水—稻米铀含量特征、水稻土与稻米铀含量关系4个方面研究721铀矿区稻米铀含量成因。结果表明,水稻土剖面铀含量从表层至半风化花岗质基岩层呈明显降低的特征,说明水稻土铀含量高的原因不是土壤母质铀含量高;岩石与水稻土稀土元素标准化模式均表现为向右倾斜型,均属轻稀土富集型,轻稀土分馏明显,表明水稻土为还原环境,吸附作用较强;不同河流不同河段水稻土—地表水—稻米铀含量平均值的特性均为上游最低、中游最高、下游次之。铀矿区地表水环境符合铀元素在水稻土中被平衡吸附的动力学条件,有利于铀元素在矿区内河流中游地区的水稻土中沉淀富集;正在采矿区水稻土与稻米铀含量具有高度的空间耦合性,呈指数正相关关系,相关系数0.749。矿区内河流沿岸稻米铀含量的分布特征是由铀元素的迁移途径决定的"采矿活动(铀尾矿露天堆放)→地表水→水稻土"。     

Morphological study of laryngeal ganglions and associated nerve cells in humans and five mammals

The arrangement and numbers of intralaryngeal ganglia and associated neurons in humans and four mammals (dogs, rabbits, guinea pigs and rats) were investigated morphologically and compared with the results obtained in the cat which have been reported previously. Intralaryngeal ganglia were mostly distributed in branches of the internal branch of superior laryngeal nerve in all species, dorsal and/or dorsolateral to the posterior cricoarytenoid muscle in humans, dogs and cats and around the inferior laryngeal nerve in humans, dogs, cats, guinea pigs and rats. The total number of laryngeal ganglionic neurons was 2,000 to 2,400 in humans, 300-450 in dogs, 600-800 in cats, 250-320 in rats, and 100-150 in rabbits and guinea pigs. More than 80 percent of ganglionic neurons were present in the supraglottis in all species, except the rat, in which about 60 percent were in the subglottis. Each ganglion in all species existed within the nerve bundle, and was chiefly encapsulated with fibrous tissue, many ganglionic cells, glial cells, Schwann cells, vessels and connective tissue. The present morphological study of intralaryngeal ganglia in humans and four mammals suggests that the laryngeal ganglionic neurons have the same arrangement as in cats.     

Rapid detection cytomegalovirus pneumonia in recipients of bone marrow transplant: evaluation and comparison of five survey methods for bronchoalveolar lavage fluid

To detect cytomegalovirus-associated interstitial pneumonia (CMV-IP) in recipients of BMT in its earliest stage, five CMV methods were assessed for their usefulness using bronchoalveolar lavage fluid as the test specimen. Of the 43 cases enrolled in the study, PCR was positive in 12 cases, shell vial in eight, culture in eight and cytology in three. There were no positive cases in in situ hybridization. Based on this result, the 43 cases were classified into four groups: Group 1, three cases: positive in PCR, shell vial and cytology; Group 2, five cases: positive in PCR and shell vial; Group 3, four cases: positive only in PCR; and Group 4, 31 cases: negative in all CMV tests. Cases in Group 1 were judged as having the highest risk of overt CMV-IP. They were successfully treated with a combination of ganciclovir and immunoglobulin. Group 2 was diagnosed as having active CMV infection and ganciclovir monotherapy was effective for these patients. Groups 3 and 4 were not given anti-CMV therapy, but they were free from CMV-related manifestations throughout the study. The sensitivity and specificity of each survey method for the detection of Groups 1 and 2 were 1.0 and 0.89 in PCR, 1.0 and 1.0 in shell vial, 0.88 and 1.0 in culture, and 0.38 and 1.0 in cytology. Similarly, the positive and negative predictive values were 0.67 and 1.0 in PCR, 1.0 and 1.0 in shell vial, 1.0 and 0.97 in culture, and 1.0 and 0.88 in cytology. Thus, CMV survey on bronchoalveolar fluid was thought to be useful in detecting post BMT CMV-IP in its earliest stage.     

Disposition and metabolism of [3H]cocaine in acutely and chronically treated dogs

1. Beagle dogs were chronically treated with cocaine, 5 mg/kg subcutaneously twice daily for 6 weeks, followed by same dose of [3H]cocaine given intravenously. 2. The t1/2 values of cocaine in plasma, liver, spleen and heart, in acutely and chronically treated dogs, were: 1-2, 1-1; 2-2, 1-8; 1-8, 1-3; 2-0, 1-2 h, respectively. In both groups, cocaine disappeared from all areas of the central nervous system 12-24 h after injection but significant amounts of radioactivity due to benzoylnorecgonine and benzoylecgonine persisted in the CNS even 1 week after administration of cocaine. Brain-to-plasma ratios of cocaine were lower in chronically-treated than in acutely-treated dogs 2 and 4 h after injection. 3. Norcocaine, benzoylnorecgonine, benzoylecgonine and ecgonine were metabolites of cocaine in dog brain in both groups. Norcocaine and benzoylnorecgonine were present in higher amounts in brains of chronically treated dogs. Rate of disappearance of norcocaine was similar to cocaine in both groups. 4. The amounts of cocaine excreted in urine and faeces as percentage of dose were 0-9-5-0, 1-1-6 in the acute and 2-2-3-3 and 0-2-0-3 in the chronically treated dogs. Major excretion of radiactivity occurred in urine within 24 h in both groups. Total radioactivity (65% of dose) in urine plus faeces was similar in both groups. 5. Norcocaine, benzoylnorecgonine, benzoylecgonine, ecgonine, norecgonine, ecgonine methyl ester and unidentified compounds were urinary metabolites of cocaine in both groups. Benzoylnorecgonine and ecgonine were excreted in higher amounts and benzoylecgonine and norecgonine in lower amounts in the acute than in the chronically treated dogs. 6. The possible role of persistence of benzoylnorecgonine and benzoylecgonine (which possessed potent stimulant activity intracisternally) in the CNS is discussed.     

Distribution of six transplasma membrane NADH-dehydrogenases in rat brain tissue

Transplasma membrane redox plays a significant role in cellular activation and growth. Six isoenzymes could be prepared from purified rat brain synaptic plasma membrane. Polyclonal antibodies have been prepared against six transplasma membrane oxydoreductases (PMO-I to PMO-VI) and the tissue distribution of the various iso-enzymes have been investigated in adult rat brains by means of immunohistochemistry. PMO-I is densely observed in layers I, IV and V of the parietal cortex, in CA1 of the hippocampus (except for the molecular layer), in the caudate putamen, in the dorsal, granular and ventral parts of the auditory nuclei, in some loci of the vestibular nuclei as well as in the deep cerebellar nucleus and in the granular layer of the cerebellar cortex. PMO-II is mainly located in the polymorphic layer of the dentate gyrus and in the deep cerebellar nucleus and in the granular layer of the cerebellar cortex. PMO-III is abundant in the piriform cortex, in the pyramidal layers of both CA1 and CA2, in the diagonal band of the basal ganglia, in the supraoptic nucleus and in various loci of the magnetocellular paraventricular nucleus of the hippothalamus as well as in the vestibular nuclei from the brain stem. In addition PMO-III is also densely present in motor nuclei (oculomotor, facial, hypoglossal and ambiguus nuclei), in the reticular formation and in the deep cerebellar nucleus as well as in the Purkinje layer of the cerebellar cortex. PMO-IV has a similar location but is less abundant in the vestibular nuclei of the sensory brain stem and in the motor nucleus. PMO-V in contrast is poorly present in most brain areas compared to the other iso-enzymes, apart of the Purkinje layer of the cerebellar cortex. Finally PMO-VI is mainly present in the oriens layer and in the stratum radiatum of the hippocampus formation, in the supraoptic and lateral magnocellular nucleus of the hypothalamus, in the mesencephalic trigeminal nucleus, in the ventral auditory nucleus and in the facial nucleus of the brain stem as well as in red nucleus of the reticular formation and in the Purkinje layer of the cerebellar cortex. These data show that the iso-enzymes are located in specific brain nuclei. The significance of the results in respect to the yet very poorly defined function of PMO's is discussed.     

Excretion and metabolism of tipredane, a novel glucocorticoid, in the rat, mouse, monkey, and human

The excretion and metabolism of [3H]tipredane, a novel glucocorticoid, has been studied in mice, rats, marmosets, rhesus and cynomolgus monkeys, and humans. After oral administration, [3H]tipredane was rapidly absorbed, metabolized, and excreted into urine and feces. In mice and male rats, radioactivity was excreted primarily into feces or bile, whereas in female rats, monkeys, and humans, excretion was mainly via the renal route. Some sex differences in the proportions excreted into urine and feces were noted in rodents, with females eliminating relatively more radioactivity in urine. Tipredane was shown to be extensively metabolized, but the routes were highly species-dependent and, in the rat, they were sex-dependent. Unchanged tipredane was not detected in any urine, bile, or blood extracts. Urinary and blood extract profiles indicated that there were between 10 and 30 metabolites in rats and mice, the majority of which constituted < 2% of the dose. In these species, the major pathways involved loss of the thioethyl moiety, S-oxidation of the thiomethyl group, and saturation of the adjacent saturated C16-17 bond. Hydroxylation of the steroid B-ring was seen in the 7 alpha-position in mice and female rats, and in the 6 beta-position in male rats. Metabolism of tipredane in rhesus and cynomolgus monkeys and humans was similar, but less extensive and different to that seen in rodents. The major products, the 6 beta-hydroxylated sulfoxide and sulfone metabolites of tipredane, accounted for 21-36% of the dose in human and monkey urine, and were also major components in blood. In contrast to mice and rats, S-oxidation and an unsaturated C16-17 bond were evident in primates. Metabolism of tipredane was rapid and complex, with significant species differences, although the disposition in rhesus and cynomolgus monkeys seemed to be similar to humans.     

Leiomyosarcoma of the esophagus: results of surgical treatment

BACKGROUND: This study examined the results of surgical treatment of leiomyosarcoma of the esophagus. METHODS: Between January 1920 and December 1996, 17 patients (9 men and 8 women) with leiomyosarcoma of the esophagus were treated surgically at the Mayo Clinic. Median age was 58 years and ranged from 26 to 76 years. Symptoms included dysphagia in 11 patients (64.7%) and odynophagia in 6 (35.3%). The tumor was located in the middle third of the esophagus in 10 patients (58.8%) and in the cervical esophagus in 7 (41.2%). Procedures performed included esophagogastrectomy in 9 patients (Ivor Lewis in 5, left thoracoabdominal in 3, and transhiatal in 1), enucleation in 3, transgastric excision in 1, and exploration without resection in 4. RESULTS: The procedure was considered curative in 11 patients (64.7%). There was one operative death (mortality, 5.9%). Complications occurred in 3 patients (17.6%) and included anastomotic leak in 2 and bleeding requiring reoperation in 1. Growth pattern was infiltrating in 7, polypoid in 5, and intramural in 5. Histologically, the tumor was grade 1 in 6 patients, grade 2 in 2, grade 3 in 7, and grade 4 in 2. The tumor was postsurgically classified as stage I in 2 patients, stage IIA in 7, stage IIB in 1, stage IIIA in 5, stage IV in 1, and unknown in 1. Six patients (35.3%) received adjuvant treatment. Follow-up was complete in 16 patients (94.1%) and ranged from 1 to 182 months (median, 48 months). Five- and 10-year actuarial survivals were 47.0% and 31.0%, respectively. Seven patients (41.2%) are currently alive (median survival, 72 months); all underwent curative resection. Factors affecting survival included completeness of resection, growth pattern, postsurgical stage, tumor grade, and tumor location (p < 0.05). CONCLUSIONS: We conclude that leiomyosarcoma of the esophagus is rare. Complete resection provides long-term survival.     

CT of appendicitis in children

PURPOSE: Our goal was to review the CT findings and to help define the role of CT in the evaluation of appendicitis in children. METHOD: Of 730 children with surgically proven appendicitis, 22 underwent preoperative CT evaluation. Their CT scans and operative and pathology records were retrospectively reviewed. The CT scans were evaluated for appendiceal wall thickness, diameter, and location, appendicoliths, pericecal inflammation, phlegmon, abscess, free fluid, small bowel dilatation, and bowel wall thickening. Criteria for diagnosing appendicitis were (a) appendiceal wall thickening (> 1 mm) or (b) presence of abscess, phlegmon, or pericecal inflammation associated with appendicolith(s). Prospective reports of ultrasound examinations performed within 2 days of the CT scans were available in 14 children and were correlated with the CT findings. RESULTS: An abnormally thickened appendix, with a diameter ranging from 9 to 18 mm, was seen in four children. Three appendices were retrocecal and one was near the cecal tip, anterior to the iliac vessels. Appendicoliths were present in 10 children, multiple in 1. Abscesses were seen in 13 of 22 children, multiple in 5. Phlegmon was seen in five children and pericecal inflammation in two. Bowel wall thickening was present in seven children and small bowel dilatation was noted in six. Other findings included free fluid, hydronephrosis, thickening of urinary bladder wall, air in the uterus and vagina, adenopathy, and thickening of the abdominal wall musculature. CT was diagnostic of appendicitis in 11 of 22 children (50%). In 14 children with both ultrasound and CT studies, CT was slightly better in diagnosing appendicitis and visualizing the abnormal appendix and was superior in defining the presence and extent of abscess and inflammation in 9 of 14 children. CONCLUSION: CT is a useful adjunct in diagnosing appendicitis in children, with a major role in cases of complicated appendicitis.     

Cloning, purification, and properties of a phosphotyrosine protein phosphatase from Streptomyces coelicolor A3(2)

We have investigated by restriction fragment analysis genomic abnormalities involving the c-myc gene in DNA isolated from adenomas and hepatocellular carcinomas (HCCs). Adenomas and HCCs were induced by the "resistant hepatocyte" protocol in diethylnitrosamine-initiated male F344 rats. Southern-blot analysis of EcoRI-restricted DNA from normal liver, early and late adenomas, 12 weeks (EAs) and 30 weeks (LAs) after initiation, and HCCs, showed 2 bands of 18 and 3.2 kb hybridizing with c-myc, in all tissues. c-myc amplification occurred in almost all HCCs, and in the majority of EAs and LAs. These results were confirmed by dilution analysis. c-myc amplification was also seen in adenomas and HCCs by Southern analysis with HindIII-restricted DNA, and in HCCs by differential PCR. c-myc mRNA increase occurred in all adenomas and HCCs, but it was higher in the lesions showing gene amplification. Moreover, a 13-kb DNA extraband, hybridizing with c-myc, was found in the HindIII-restricted DNA from HCCs, but not in normal liver and adenomas, and a 7.1-kb extra band was present in EcoRI-digested DNA from one LA. EcoRI-restricted DNA from some adenomas exhibited a decrease in intensity of the 18-kb fragment, and an increase in intensity of the 3.2-kb fragment. No alteration in banding pattern occurred in the beta-actin gene in adenomas. These results provide evidence of amplification and some other rearrangements involving the c-myc gene, in pre-malignant and malignant liver lesions, induced by the RH protocol, and suggest a role of c-myc rearrangement in the progression of adenomas to malignancy.     

Pathophysiology of infection with Ostertagia ostertagi in cattle

Infection with the abomasal nematode, Ostertagia ostertagi, is an important cause of impaired productivity in young cattle in temperate parts of the world. Such losses have been associated with marked changes in feed intake, gastrointestinal function, protein, energy and mineral metabolism, and in body composition. The reduction in feed intake is an important factor in the pathogenesis of infection and may account for a large part of the difference in weight gain between ad libitum fed control and infected calves. Despite the obvious importance of inappetance, only recently has an association been made between reduced intake, altered gut motility and elevated levels of certain gastrointestinal hormones, such as gastrin. It has been suggested that the elevated gastrin levels accompanying abomasal parasitism may impair reticulo-ruminal motility and slow down abomasal emptying, leading to a stasis of ingesta and a reduction in feed intake. The rise in blood gastrin levels may also be partly responsible for the marked hyperplasia of the fundic mucosa seen in abomasal infections. Pronounced changes in protein metabolism have also been associated with Ostertagia infection. Radioisotopic studies have demonstrated increased losses of albumin into the gastrointestinal tract which are accompanied by an increase in the rate of synthesis in the liver. Dietary protein breakdown in the abomasum is also likely to be impaired, although there is evidence of a compensatory increase in protein digestion in the lower gut of parasitised calves. Increased losses of albumin are not always accompanied by increases in faecal nitrogen, suggesting that albumin is broken down and recycled as ammonia. Radioisotopic studies in animals with intestinal nematode infections have demonstrated a marked reduction in muscle protein synthesis and an increase in protein synthesis in gastrointestinal tissue. Such changes in the balance of protein synthesis are likely to be brought about by alterations in the balance of certain metabolic hormones. Marked changes in energy metabolism also accompany Ostertagia infection. Parasitised calves exhibit a marked increase in non-esterified fatty acid levels, resulting from the mobilisation of adipose tissue, and a reduction in digestive efficiency of energy, probably associated with the increase in cycling of protein through the gastrointestinal tract and the compensatory increases in protein synthesis. Mineral metabolism may also be affected although relatively little work has been conducted in cattle. Changes in body composition reflect a reduction in deposition of muscle protein and fat, and an increase in bone content and water retention.     

Sex hormones and metabolism of glycosaminoglycans. I. Effect of orchidectomy and administration of testosterone in rabbits

The effect of orchidectomy in male rabbits and administration of testosterone to orchidectomized animals on the metabolism of glycosaminoglycans (GAG) has been studied. The response of the different GAG fractions in the aorta varies with the nature of the GAG, and in some cases is different in different segments of the aorta. Orchidectomy produced an increase in hyaluronic acid fraction, decrease in heparin sulphate fraction, and no response in the chondroitin sulphate A fraction in the aortic arch, thoracic aorta, and abdominal aorta. Chondroitin sulphate C and chondroitin sulphate B fractions decreased only in the abdominal aorta and were not significantly altered in the other two segments, while heparin fraction decreased only in the thoracic aorta and was not affected in the other segments. Administration of testosterone to the orchidectomized animals counteracted these changes in the aortic GAG fractures. The enzymes concerned with the synthesis of precursors of GAG--L-glutamine:D-fructose-6-phosphate aminotransferase, UDPG dehydrogenase, and UDPG pyrophosphorylase-- all decreased in the orchidectomized animals; testosterone administration increased their activity in the orchidectomized animals. Enzymes concerned with degradation of GAG--beta-glucuronidase, beta-hexosaminidase, aryl sulphatase, cathepsin, and hyaluronidase--increased in the orchidectomized and decreased on administration of testosterone. Concentration of PAPS and activity of sulphate-activating system and sulphotransferase also decreased in the orchidectomized animals, and testosterone administration tended to restore this decrease to normal levels.     

Alteration of protease levels in different brain areas of suicide victims

Numerous recent studies found that proteases play a major role in brain function. In addition to their role in protein turnover, they have modulatory functions and an important role in apoptosis, pathological changes, and other mechanisms. To explore possible differences in brain protein metabolism of suicide victims, we examined the activity of two proteases, cathepsin D and calpain (I and II combined), in eleven discrete areas of postmortem brain tissue of 21 victims of suicide and of 31 age- and sex-matched control subjects without a history of psychiatric or neurological disease. The levels of functionally important amino acids in five of these areas were also measured. Cathepsin D activity was found to be lower in two of eleven regions of brains of suicide victims, the parahippocampal cortex and the medial hypothalamus, by 26% and 27%, respectively. Calpain activity was lower in two different areas tested, 29% in the medulla oblongata and 26% in the lateral prefrontal cortex, and was 18% higher in the midbrain. There were no significant differences in the other areas (globus pallidus, hippocampus, amygdala, caudate nucleus, ventral tegmental area, and nucleus accumbens). Protease distribution was regionally heterogeneous--the levels in the globus pallidus were low, and in the hippocampus high, with about a two-fold difference. The length of the postmortem period for obtaining tissue, the storage time of the frozen tissue, and the age of the subject had no apparent influence on the results obtained. Although there was a tendency toward higher levels of aspartate and glycine in brain areas from suicide victims, the difference was not significant. The variations among individual brains were greater in amino acid levels than in protease levels. The findings indicate the possible role of protein metabolism in depressive or suicidal behavior.     

Effects of niacin deficiency on the levels of soluble proteins and enzyme activities in various tissues of Japanese quail

The effects of niacin deficiency on the levels of soluble proteins and enzyme activities of Japanese quail have been investigated. SDS-polyacrylamide gel electrophoresis revealed that in the pectoral muscle the soluble proteins with molecular masses corresponding to 181, 128, 93, 76, 72, 62, 56, 43, 41, 28 and 20 kDa were present in lower amounts but those of 60, 50 and 37 kDa were present in higher amounts. In the heart the soluble proteins with a molecular mass of 181 kDa were present in lower amounts and in the brain those of 43 kDa were present in lower amounts but those of 221 kDa were present in higher amounts. In the intestine the soluble proteins with molecular masses corresponding to 181, 102, 83, 74, 72, 44 and 40 kDa were present in lower amounts but those of 41 kDa and 18 kDa were present in higher amounts. There was a marked reduction in the level of NAD and NADPH in the pectoral muscle of niacin deficient quail but not in other tissues. The specific activity of glyceraldehyde-3-phosphate dehydrogenase decreased markedly both in the liver and pectoral muscle of niacin deficient quail whereas that of 6-phosphogluconate dehydrogenase and malic enzyme decreased markedly in the liver or pectoral muscle, respectively. In contrast, the specific activity of acetylcholinesterase and carboxypeptidase increased markedly in the liver or the pectoral muscle, respectively. The results suggest that a severe niacin deficiency exerted specific effects on levels of some soluble proteins particularly in the pectoral muscle and intestine and on activities of certain enzymes in the liver and the pectoral muscle.     

Pathological findings in four cases of human angiostrongyliasis

Three adults and a 3 1/2-year-old child presented with eosinophilic meningitis. A history of consumption of raw snails was elicited in 2; evidence of a constant diet of raw food, in the form of opisthorchiasis and taeniasis, as well as angiostrongyliasis, was present in the third; no history of raw food ingestion was obtained in the fourth, the child. Pathologic changes were similar in all 4 cases. There was infiltration of the meninges and around intracerebral vessels by varying proportions of lymphocytes, plasma cells and eosinophils. Numerous tracks and microcavities were found in the brains, and in the spinal cords in 2 cases, varying in size from 0.1 to 2 mm, and in age, with older tracks containing debris and gitter cells, newer tracks showing disruption of brain tissue, with and without haemorrhage. Numerous 4th and 5th stage Angiostrongylus larvae, alive and dead, were found in the meninges and brain tissue, sometimes in blood vessels or perivascular spaces, in 3 cases; in the fourth case a 5th stage larva was found on the surface of the right frontal lobe. In one case a degenerating larva was found in a pulmonary vessel. Cellular reaction was more often associated with dead larvae.     

Ultrastructure, distribution, and density of lamellar bodies in human peritoneum

OBJECTIVE: To determine the ultrastructure, relative density, and location of lamellar bodies in the various regions, structures, cells, and intercellular matrix in normal human peritoneum; to carry out engineering analysis of the role of lamellar structures in serosal lubricancy and deduce what effect this system may have on the process of peritoneal dialysis. DESIGN: Five samples of normal human parietal peritoneum obtained at elective operation were fixed in a tannic acid-glutaraldehyde mixture and submitted to examination by transmission electron microscopy. Detailed analysis using reconstruction of serial electron micrographs and tracings of montages were employed in determining location, disposition, density, and geometric patterns of lamellar bodies in all levels of the peritoneal membrane. RESULTS: Lamellar profiles were found in greatest density enmeshed in surface microvilli and in mesothelial cytoplasm. Lamellar bodies were frequently observed capping the external portion of mesothelial junctional complexes, and within intercellular junctions. Lamellar bodies were also encountered in macrophages, both in the peritoneal cavity and submesothelial tissue, and also in fibroblasts. Lamellar bodies were present in low density in the matrix ground substance of submesothelial connective tissue, in blood vessel walls between smooth muscle, in endothelial cell cytoplasm, and in vascular lumina. CONCLUSION: Three-dimensional analysis of lamellae on mesothelial surfaces indicates that an arrangement of constantly changing microscopic spheres and cylinders would act as "ball and roller bearings" among the microvilli for the lubrication of opposing surfaces. The entrapment of fluid in lamellar bubbles, which in normal peritoneum fill the microvillous layer, would, if maintained in peritoneal dialysis, constitute a stagnant layer of considerable stability and inertia.     

Alterations of antioxidant enzymes and oxidative damage to macromolecules in different organs of rats during aging

Oxygen free radicals have been hypothesized to play an important role in the aging process. To investigate the correlation between the oxidative stress and aging, we have determined the levels of oxidative protein damage and lipid peroxidation in the brain and liver, and activities of antioxidant enzymes in the brain, liver, heart, kidney, and serum from the Fisher 344 rats at ages of 1, 6, 12, 18, and 24 months. The results showed that the level of oxidative protein damage (measured as carbonyl content) in the brain and liver was significantly higher in older animals than in young animals. No statistical difference was observed in the lipid peroxidation of the liver and brain between young and old animals. The activities of antioxidant enzymes in most tissues displayed an age-dependent decline. Superoxide dismutases in the heart, kidney, and serum, glutathione peroxidase activities in the serum and kidney, and catalase activities in the brain, liver, and kidney, significantly decreased during aging. Cytochrome c oxidase, an enzyme involved in electron transport in mitochondria, initially increased, but subsequently decreased in the aged brain, whereas no significant alteration was observed in the liver mitochondrial antioxidant enzymes. The present studies suggest that the accumulation of oxidized proteins during aging is most likely to be linked with an age-related decline of antioxidant enzyme activities, whereas lipid peroxidation is less sensitive to predict the aging process.