Ventilatory and behavioural responses of the marbled sole Pseudopleuronectes yokohamae to progressive hypoxia.

This study identified ventilatory and behavioural responses in the marbled sole Pseudopleuronectes yokohamae under experimentally induced progressive decreases in dissolved oxygen (DO) levels. Ventilation frequency showed an increase with decreasing DO levels from normoxia to 2·75 mg O2 l-1 , followed by a decrease in ventilation frequency at decreased DO levels from 2·00 to 0·75 mg O2 l-1 . At DO levels below 2·00 mg l-1 , behaviours at the bottom were suppressed, whereas avoidance behaviours increased. A decrease in avoidance behaviours was observed from 1·00 to 0·75 mg O2 l-1 . Upside-down reversal and incapacitation at DO levels of 1·00-0·75 mg O2 l-1 suggested that sublethal effects on P. yokohamae were induced. The responses observed before the sublethal DO level could be interpreted as an effort to maintain oxygen uptake, reduce routine activities and facilitate avoidance. The observed DO level thresholds that induce behavioural responses, in addition to sublethal effects, indicate hypoxia-tolerance that is important for understanding the effects of hypoxia on coastal ecosystems.

A rare synaptonemal complex protein 3 gene variant in unexplained female infertility.

Synaptonemal complex protein 3 (SYCP3) plays a critical role in homologous chromosome pairing and recombination in meiosis, and mice deficient in this gene show infertility in males and subfertility in females. The aim of our current study was to determine whether genetic alterations in the SYCP3 gene are associated with female infertility in humans. We examined sequence variations of the SYCP3 gene in genomic DNA from 88 Japanese women with unexplained infertility and 165 samples obtained from a fertile control group. Case-control study using seven tagging single nucleotide polymorphisms revealed no significant association between common SYCP3 variants and unexplained infertility. However, only infertile women were homozygous for the minor allele of a novel rare variant in the coding region, c.666A>G (222Q>Q). The minor allele frequency was significantly higher in the infertile cohort (P< 0.05). This variant is predicted to create a cryptic splice site, although the expression of a mini-gene harboring the variant in HeLa cells or mouse testis did not demonstrate any effects on gene splicing. Our current findings therefore suggest that the c.666A>G variant in the SYCP3 gene might possibly contribute to female infertility in humans, although larger studies are needed to assess the possible effects of SYCP3 gene variation on human female infertility.

Lead-free MCP to improve coincidence time resolution and reduce MCP direct interactions.

Achieving direct imaging of the annihilation position of a positron on an event-by-event basis using an ultrafast detector would have a great impact on the field of nuclear medicine. Cherenkov emission is the most attractive physical phenomenon for realizing such an ultrafast timing performance. Moreover, a microchannel-plate photomultiplier tube (MCP-PMT) is one of the most promising photodetectors for fully exploiting the fast timing properties of Cherenkov emission owing to its excellent single photon time resolution of 25 ps full width at half maximum (FWHM). However, as the MCP structure generally contains a lead compound, the gamma rays frequently and directly interact with the MCP, resulting in the degradation of its timing performance and generation of undesirable side peaks in its coincidence timing histogram. To overcome this problem, we have developed a new MCP-PMT based on an MCP consisting of borosilicate glass, thus drastically reducing the probability of the photoelectric effect occurring in the MCP. To evaluate its insensitivity to gamma rays and its timing performance, a coincidence experiment was performed and showed that the probability of direct interactions was reduced by a factor of 3.4. Moreover, a coincidence time resolution of 35.4 ± 0.4 ps FWHM, which is equivalent to a position resolution of 5.31 mm, was obtained without any pulse height/area cut, improving to 28.7 ± 3.0 ps when selecting on the highest amplitude events by careful optimization of the voltage divider circuit of the new MCP-PMT. The timing performance of this new MCP-PMT presents an important step toward making direct imaging possible.

Insulin-mediated regulation of decidual protein induced by progesterone (DEPP) in adipose tissue and liver.

We analyzed the profile of the genes expressed in human adipose tissue and identified the fat-derived molecules, adiponectin and aquaporin 7, which modulate glucose and lipid metabolism. The same Bodymap analysis revealed abundant expression of the decidual protein induced by progesterone (DEPP) in the white adipose tissue. Northern blot analysis confirmed that human DEPP mRNA was highly expressed in white adipose tissue. Mouse DEPP mRNA was detected in heart, lung, skeletal muscle, and white adipose tissue under feeding state. In contrast, under fasting state, mouse DEPP mRNA was enhanced in lung, skeletal muscle, and white adipose tissue and it appeared also in the liver and kidney, suggesting up regulation of DEPP by fasting. Because fasting-induced DEPP expression was observed in insulin-sensitive organs, we investigated the regulation of DEPP in white adipose tissue and liver. During adipogenesis of mouse 3T3-L1 cells, DEPP mRNA increased in a differentiation-dependent manner similar to adiponectin and aquaporin 7. Treatment of cultured 3T3-L1 mature adipocytes, rat H4IIE, and human HepG2 hepatoma cells with insulin significantly decreased DEPP mRNA levels in dose- and time-dependent manners. IN VIVO experiments showed significant decrease of hepatic and adipose DEPP mRNA levels in refed mice, compared to fasted animals, and also showed significant increase in DEPP mRNA in streptozotocin-induced insulin-deficient diabetic mice. These results indicate that DEPP is a novel insulin-regulatory molecule expressed abundantly in insulin-sensitive tissues including white adipose tissue and liver.

Microarray analysis of differentially expressed fetal genes in placental tissue derived from early and late onset severe pre-eclampsia.

Although it has been well documented that pre-eclampsia is caused by a combination of maternal and fetal susceptibility genes, little is known about the precise etiology of this complicated disorder. To investigate how the expression of fetal genes contributes to the mechanisms underlying the progression of this disease, we have analyzed differentially expressed genes using placentas from 13 normal pregnancies and 14 pregnancies with severe pre-eclampsia. We performed genome-wide expression profiling using high-density oligonucleotide microarrays, followed by validation using real-time PCR. Among the 47,000 genes that were screened in the microarray, 137 genes were found to be differentially expressed between normal and pre-eclamptic tissues. Among these candidates, 70 were up-regulated and 67 were down-regulated. The up-regulated genes included leptin and inhibin A, which are well-known biological markers for pre-eclampsia, as well as FLT1, which was recently proved to be tightly linked with the etiology of this disease. Gene ontology analysis further revealed several biological processes that could be associated with the development of pre-eclampsia, including response to stress, host-pathogen interactions, lipid metabolism, and carbohydrate metabolism. Analyses of biological mechanisms highlighted some important pathways that may be involved in this disorder, such as the TGF-beta and CEBPA-related pathways. Furthermore, when our present subjects were classified as either severe cases of early onset or late onset pre-eclampsia, the expression of 11 genes could be correlated with the severity of this disorder. These genes may therefore prove to be novel biological markers by which the severity of this condition could be predicted. Our data are likely to be a useful future resource in the elucidation of the disease-process and in the identification of novel markers for pre-eclampsia.

Overproduction of the follistatin-related gene protein in the placenta and maternal serum of women with pre-eclampsia.

OBJECTIVE: To characterise the follistatin-related gene (FLRG) in pre-eclampsia, one of the differentially expressed genes in pre-eclamptic placenta. DESIGN AND METHODS: We examined and compared the messenger RNA (mRNA) and protein levels of FLRG in placentas and maternal sera from women with uncomplicated pregnancy, and those with pre-eclampsia using real-time reverse transcription polymerase chain reaction, Western blot, immunohistochemistry, and enzyme-linked immunosorbent assay. SETTING: Antenatal clinics in a teaching hospital. POPULATION: Women with uncomplicated pregnancy (n = 21) and those with pre-eclampsia (n = 21). RESULTS: FLRG mRNA is overexpressed in pre-eclamptic placental tissues (P < 0.01). Upregulated FLRG protein consists of both an immature 28-kDa cellular product and a mature 33-kDa secretory form, which are differentially glycosylated. FLRG is normally produced at its highest levels in endothelial cells and at moderate amounts in syncytiotrophoblast cells, but in pre-eclampsia, the syncytiotrophoblast FLRG levels are dramatically increased. We also determined the maternal serum concentrations of FLRG in our uncomplicated pregnancy subjects and in our pre-eclamptic groups, and found that they are significantly elevated in pre-eclampsia in a similar manner to activin A and inhibin A. However, the increase in FLRG in these cases is independent of activin A or inhibin A, and is associated with low-birthweight outcomes. CONCLUSION: Our current data show the placental and secretory changes of FLRG protein in pre-eclampsia, and also indicate the potential usefulness of FLRG as an additional diagnostic marker for pre-eclampsia.

Structure of pressure-induced denatured state of human serum albumin: a comparison with the intermediate in urea-induced denaturation.

The structure of human serum albumin (HSA) in the pressure-induced denatured state was investigated by fluorescence spectroscopy. HSA undergoes a conformational change in the pressure range from 0.1 MPa to 400 MPa, at 25 degrees C. Several ligands bind to specific sites in HSA, and the fluorescence spectra of these ligands were used to study the conformational state of this protein. The warfarin-binding site (site I) and the dansylsarcosine-binding site (site II), are located in subdomains II and III, respectively. The fluorescence spectra of these probes reflected the structural changes in each of these subdomains. Dansylsarcosine completely dissociated from its binding site in domain III above 300 MPa, but substantial affinity of warfarin remained in this pressure range. Similar results were obtained for the urea-induced denaturation of HSA; although dansylsarcosine completely dissociated at urea concentration above 6 M, warfarin remained bound to site I in domain II at these concentrations. These results suggest that the structure of domain III is unfolded both in the initial stages of both pressure- and urea-induced denaturation of HSA. HSA possesses a single tryptophan residue (Trp-214) in domain II, and fluorescence from this residue reflects structural changes in this domain. In the urea-induced denatured state of HSA, a red-shift in the wavelength of maximum fluorescence occurred over urea concentrations ranging from 4 M to 6 M. This shift indicated that a structural change in domain II occurred simultaneously with the unfolding of domain III in this concentration range. On other hand, the shift in the wavelength of maximum fluorescence of Trp-214 was comparatively small in the pressure range from 0.1 MPa to 400 MPa indicating that the environment of Trp-214 was not affected. These results indicate that preferential unfolding of domain III occurs in the pressure-induced denatured state of HSA.

Enantioselective binding sites on bovine serum albumin to dansyl amino acids.

The enantioselective binding sites on bovine serum albumin were examined by HPLC using 19 racemic 5-N, N-dimethylamino-1-naphthalenesulfonyl derivatives of alpha-amino acids (dansyl amino acids) as chiral probes. On a bovine serum albumin bonded chiral stationary phase, seven L-forms eluted faster than their D-forms, while ten D-forms eluted before their L-forms. It was speculated that either two classes or two different binding sites exist on bovine serum albumin which can be distinguished by N-dansyl-L-proline and N-dansyl-D-norvaline. This was confirmed by fluorometric experiments where non-fluorescent 1-naphthalenesulfonyl derivatives were synthesized and competitive adsorption experiments were performed.

Adipocyte-derived plasma protein, adiponectin, suppresses lipid accumulation and class A scavenger receptor expression in human monocyte-derived macrophages.

BACKGROUND: Excessive lipid accumulation in macrophages plays an important role in the development of atherosclerosis. Recently, we discovered an adipocyte-specific plasma protein, adiponectin, that is decreased in patients with coronary artery disease. We previously demonstrated that adiponectin acts as a modulator for proinflammatory stimuli and inhibits monocyte adhesion to endothelial cells. The present study investigated the effects of adiponectin on lipid accumulation in human monocyte-derived macrophages. METHODS AND RESULTS: Human monocytes were differentiated into macrophages by incubation in human type AB serum for 7 days, and the effects of adiponectin were investigated at different time intervals. Treatment with physiological concentrations of adiponectin reduced intracellular cholesteryl ester content, as determined using the enzymatic, fluorometric method. The adiponectin-treated macrophages contained fewer lipid droplets stained by oil red O. Adiponectin suppressed the expression of the class A macrophage scavenger receptor (MSR) at both mRNA and protein levels by Northern and immunoblot analyses, respectively, without affecting the expression of CD36, which was quantified by flow cytometry. Adiponectin reduced the class A MSR promoter activity, as measured by luciferase reporter assay. Adiponectin treatment dose-dependently decreased class A MSR ligand binding and uptake activities. The mRNA level of lipoprotein lipase as a marker of macrophage differentiation was decreased by adiponectin treatment, but that of apolipoprotein E was not altered. Adiponectin was detected around macrophages in the human injured aorta by immunohistochemistry. CONCLUSIONS: The adipocyte-derived plasma protein adiponectin suppressed macrophage-to-foam cell transformation, suggesting that adiponectin may act as a modulator for macrophage-to-foam cell transformation.

Atherosclerosis in carotid artery of young IDDM patients monitored by ultrasound high-resolution B-mode imaging.

Ultrasound high-resolution B-mode imaging was used to assess the carotid arteries in 105 patients with insulin-dependent diabetes mellitus (IDDM), 4-25 years of age, with duration of diabetes ranging from 0.5-17 years, 529 patients with non-insulin-dependent diabetes (NIDDM), 31-86 years of age, with duration of diabetes ranging from 0.5-49 years, and 104 nondiabetic healthy subjects, 7-76 years of age, to determine the intimal plus medial thickness (IMT) of the arterial wall. The IMT values for IDDM patients 10-19 years of age (0.525 +/- 0.123 mm, n = 68) or 20-25 years of age (0.696 +/- 0.124 mm, n = 14) were significantly greater than those in age-matched nondiabetic subjects (0.444 +/- 0.057 mm, n = 12, P = 0.01169; 0.538 +/- 0.098 mm, n = 34, P < 0.00006). NIDDM patients showed IMT values equivalent to those in normal adults > or = 20 years of age. Multiple regression analysis showed that IMT in IDDM patients was positively related to the duration of diabetes (P = 0.00061) as well as to age (P = 0.00046). No other possible risk factors, such as serum total cholesterol level, serum high-density lipoprotein (HDL)-cholesterol level, serum low-density lipoprotein-cholesterol level, serum triglycerides, serum lipoprotein(a) level, or systolic or diastolic blood pressure, have shown significant correlations with IMT in IDDM patients. However, non-HDL-cholesterol, smoking, and systolic hypertension were independently responsible for increases in IMT values of NIDDM patients as well as age and duration of diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

PPARgamma ligands increase expression and plasma concentrations of adiponectin, an adipose-derived protein.

Insulin resistance and its dreaded consequence, type 2 diabetes, are major causes of atherosclerosis. Adiponectin is an adipose-specific plasma protein that possesses anti-atherogenic properties, such as the suppression of adhesion molecule expression in vascular endothelial cells and cytokine production from macrophages. Plasma adiponectin concentrations are decreased in obese and type 2 diabetic subjects with insulin resistance. A regimen that normalizes or increases the plasma adiponectin might prevent atherosclerosis in patients with insulin resistance. In this study, we demonstrate the inducing effects of thiazolidinediones (TZDs), which are synthetic PPARgamma ligands, on the expression and secretion of adiponectin in humans and rodents in vivo and in vitro. The administration of TZDs significantly increased the plasma adiponectin concentrations in insulin resistant humans and rodents without affecting their body weight. Adiponectin mRNA expression was normalized or increased by TZDs in the adipose tissues of obese mice. In cultured 3T3-L1 adipocytes, TZD derivatives enhanced the mRNA expression and secretion of adiponectin in a dose- and time-dependent manner. Furthermore, these effects were mediated through the activation of the promoter by the TZDs. On the other hand, TNF-alpha, which is produced more in an insulin-resistant condition, dose-dependently reduced the expression of adiponectin in adipocytes by suppressing its promoter activity. TZDs restored this inhibitory effect by TNF-alpha. TZDs might prevent atherosclerotic vascular disease in insulin-resistant patients by inducing the production of adiponectin through direct effect on its promoter and antagonizing the effect of TNF-alpha on the adiponectin promoter.

Carotid intima-media thickness in Japanese type 2 diabetic subjects: predictors of progression and relationship with incident coronary heart disease.

OBJECTIVE: To examine carotid intima-media thickness (IMT), predictors of its progression, and its relationship with incident coronary heart disease (CHD) in type 2 diabetic Japanese patients. RESEARCH DESIGN AND METHODS: Carotid IMT of 287 subjects with type 2 diabetes (mean age 61.6 years) without CHD or cerebrovascular disease was examined at baseline and after a mean follow-up of 3.1 years. RESULTS: The annual progression of IMT (means +/- SEM) was 0.04+/-0.004 mm/year. Stepwise multivariate analysis demonstrated that independent risk factors for progress of IMT were the initial IMT (P<0.001), the average HbA1c level (P<0.001), and age (P = 0.001). Both the initial IMT (odds ratio [OR] 4.9, 95% CI 1.7-14.1) and a low average HDL cholesterol (OR 0.2, 0.1-0.8) were identified as predictors of incident nonfatal CHD (angina pectoris or nonfatal myocardial infarction; 3-year incidence 10.1%) after adjusting for age, sex, average HbA1c, and other risk factors. CONCLUSIONS: The predictors of the progression of carotid IMT in Japanese type 2 diabetic subjects were its baseline thickness and the average HbA1c during the follow-up. Baseline carotid IMT and low HDL cholesterol predicted the incidence of nonfatal CHD.

Prevalence of carotid atherosclerosis in diabetic patients. Ultrasound high-resolution B-mode imaging on carotid arteries.

OBJECTIVE: To quantitatively assess atherosclerosis of the carotid artery in subjects with and without diabetes. RESEARCH DESIGN AND METHODS: Ultrasound high resolution B-mode imaging of carotid arteries was conducted on 71 nondiabetic subjects without hyperlipidemia or hypertension and 295 diabetic patients to determine IMT of the arterial wall. RESULTS: IMT was linearly related with age in nondiabetic (IMT = [0.0087 x age] + 0.3318) and diabetic subjects (IMT = [0.0155 x age] + 0.32450). The regression coefficient for age was significantly greater in diabetic than nondiabetic subjects. IMT (mean +/- SD) of diabetic subjects aged 20-29 was significantly greater than that of nondiabetic subjects aged 20-29 (0.73 +/- 0.27 vs. 0.52 +/- 0.07 mm, P less than 0.01). Multivariate regression analysis of 275 NIDDM patients indicated smoking, hyperlipidemia, duration of diabetes, hypertension, and age were factors determining thickness of the carotid arterial wall. CONCLUSIONS: Diabetes, along with age, hyperlipidemia, smoking, and hypertension, aggravates carotid atherosclerosis.

Visceral fat is a major contributor for multiple risk factor clustering in Japanese men with impaired glucose tolerance.

OBJECTIVE: The significance of abdominal visceral fat accumulation was evaluated in Japanese men with impaired glucose tolerance (IGT). RESEARCH DESIGN AND METHODS: The IGT subjects (n = 123) were aged 55 +/- 9 years with a BMI of 24 +/- 3 kg/m(2). The 148 control subjects with normal glucose tolerance (NGT) were matched for age and BMI. IGT and NGT were classified according to the 1985 World Health Organization criteria. Abdominal fat distribution was analyzed by computed tomography at umbilical level. Plasma lipid, glucose, and insulin concentrations and blood pressure (BP) were measured. RESULTS: In subjects with IGT, the average visceral fat area (VFA) was significantly greater than in subjects with NGT. Fasting insulin, the sum of insulin concentrations during an oral glucose tolerance test, insulin resistance according to a homeostasis model assessment for insulin resistance (HOMA-IR), systolic BP, and serum triglyceride were significantly higher, whereas the DeltaI(30-0)/DeltaG(30-0) was significantly lower, in subjects with IGT. Subjects with IGT and NGT were then divided into three subgroups according to the number of risk factors they possessed (dyslipidemia, hypertension, neither, or both). In both IGT and NGT subjects, BMI, VFA, subcutaneous fat area, fasting insulin, HOMA-IR, and insulin secretion of the homeostasis model assessment were significantly higher in the double-risk factor subgroup than in the no-risk factor subgroup, and VFA was a potent and independent variable in association with the presence of a double risk factor. CONCLUSIONS: Visceral fat accumulation is a major contributor for multiple risk factor clustering in Japanese men with IGT and NGT.

[Staged operation of off-pump coronary artery bypass grafting using aortic connector system, and concomitant surgery for abdominal aortic aneurysm and gastric cancer; report of a case].

Recently the patient of the atherosclerotic disease associated with malignant disease has been increased. A 75-year-old man was referred to our section with an infrarenal abdominal aortic aneurysm (AAA) and a gastric cancer (GC). Preoperative coronary angiogram revealed the significant stenoses of the right coronary and the left anterior descending coronary artery. We selected the staged operation of off-pump coronary artery bypass grafting (CABG) [OPCAB] and the concomitant surgery for the AAA and the GC. Operative invasion could decrease with the surgical procedure of the OPCAB and the concomitant surgery compared to the conventional CABG or the separate operation. We used the aortic connector system during OPCAB to prevent such the serious complications of the aortic dissection or the systemic embolism due to the calcified ascending aorta.

Somatotopic organization of the primary sensory trigeminal neurons in the hagfish, Eptatretus burgeri.

Primary sensory trigeminal projections were investigated in the hagfish following application of horseradish peroxidase (HRP) to the sensory branches. In our control preparations we were able to distinguish five sensory ganglia and their respective nerves. HRP application confirmed the almost exclusive relation of each of these nerves to their respective ganglia, with very little overlap. In normal frontal sections of the medulla oblongata, five columns of fibers surrounded by neuronal cell bodies could be clearly distinguished, but the number is probably fortuitous, for there was no one-on-one relationship with the five trigeminal ganglia. From their peripheral connections, we surmised that columns 1 and 3 handle general cutaneous sensation, columns 2, 4, and 5 handle taste sensation, and column 5 handles general mucous cutaneous sensation conveyed by utricular ganglion cells. Dorsally located columns received projections from nerves with dorsal peripheral connections, and more ventrally located columns received projections from nerves with ventral peripheral connections. This relation is the reverse of that seen in other vertebrates.

Primary neurons of the lateral line nerves and their central projections in hagfishes.

The hagfish lateral line system was studied by horseradish peroxidase transganglionic transport. The anterior lateral line nerve innervates the group of lateral line canals situated anteriorly to the eye, and the posterior lateral line nerve innervates the group of canals situated posteriorly to the eye. Although both nerves pass through the muscle fascia at the same point, each runs a different course to the brain. The anterior lateral line nerve runs near the trigeminal nerve and its ganglion is closely attached to the trigeminal ganglion, but both systems are completely independent. The posterior lateral line nerve runs independently of any other cranial nerve and makes a peculiar U-turn at the point of entry to the brain capsule. The anterior lateral line ganglion contains both cutaneous sensory cells (small to large cells) and lateral line sensory cells (small cells); from this ganglion projections run to both the trigeminal sensory nucleus (fine and thick fibers) and medial nucleus of the area acousticolateralis (fine fibers). The posterior lateral line ganglion contains only small lateral line cells that project fine fibers to the medial nucleus of the area acousticolateralis. There are no efferent components in this lateral line system, and its only afferent terminal field is the medial nucleus of the area acousticolateralis.

Auxiliary partial orthotopic liver transplantation from living donors: significance of portal blood flow.

BACKGROUND: Auxiliary liver transplantation has several advantages over standard orthotopic liver transplantation. However, functional competition has been reported even in auxiliary partial orthotopic liver transplantation (APOLT). We evaluated herein the interaction in APOLT between the native liver and the graft in terms of portal blood flow and regeneration. The need for diversion of the portal blood flow to the graft was also assessed. METHODS: A total of 15 patients received APOLT from living donors. Portal blood flow to the native liver was preserved in 6 patients, and the portal vein to the native liver was preemptively transected at the time of transplantation in 9 patients. RESULTS: Of the patients with preservation of the portal blood flow to the native liver, two showed inadequate graft portal blood flow just after operation, and in the other three patients the graft portal blood flow decreased or the graft atrophied after deterioration of the graft function. In the patients with preemptive transection of the portal vein to the native liver, optimal graft portal blood flow was obtained, and the native liver, supplied only by arterial inflow, supported a small-for-size graft until the graft regenerated. The damage to the native liver was minimal. CONCLUSIONS: Functional competition may occur in APOLT with preservation of the portal blood flow to the native liver, whereas preemptive transection of the native liver portal vein is a safe procedure and effectively prevents the portal steal phenomenon.

Coexistence of a graft with the preserved native liver in auxiliary partial orthotopic liver transplantation from a living donor for ornithine transcarbamylase deficiency.

BACKGROUND: Auxiliary partial orthotopic liver transplantation (APOLT) has recently been performed in patients with noncirrhotic metabolic liver diseases. However, long-term outcomes for the preserved native liver and the transplanted liver graft have not been clearly established yet. METHODS: The recipient was a 36-month-old girl with ornithine transcarbamylase deficiency. She underwent APOLT, using her father's left lateral segment. RESULTS: Liver function was normalized soon after APOLT and the patient was able to ingest a normal diet without medication. Coexistence of the well-functioning native liver and graft was demonstrated in a computed tomography scan, Doppler ultrasonography, scintigraphy, and histological examination, during a relatively long-term follow-up period. CONCLUSIONS: APOLT seems to be most useful for the treatment of noncirrhotic metabolic liver diseases.

Reduction by clofibric acid of serum arachidonic acid in rats. Effect on the acyl composition of renal phospholipids.

Alterations induced by p-chlorophenoxyisobutyric acid (clofibric acid) in the composition of phosphatidylcholine and cholesterol esters in serum and their influence on the composition of phosphatidylcholine in the kidney were studied. Rats of different ages responded differently to the drug in terms of the levels of arachidonic acid (20:4) and linoleic acid (18:2) in the phosphatidylcholine and cholesterol esters in the serum. Administration of clofibric acid to 26-week-old rats for 2 weeks caused a marked decreased in the relative level of 20:4 in phosphatidylcholine and cholesterol esters in serum, whereas similar treatment of 6-week-old rats resulted in a reduction of 18:2 and, to a lesser extent, of 20:4 in serum lipids. The decrease in phosphatidylcholine that contained 20:4 in the serum of old rats was mainly due to a decrease in the concentration of stearoyl-arachidonoyl (18:0-20:4) species. The decrease in cholesterol arachidonate in serum caused by the treatment of old rats with clofibric acid seemed to be due to a reduction in the relative level of serum phosphatidylcholine containing 20:4. The marked reduction in serum lipids that contained 20:4 caused a decrease in the relative level of 20:4 in renal phospholipids, in particular, a decrease in the proportion of palmitoyl-arachidonoyl (16:0-20:4) and 18:0-20:4 phosphatidylcholine.