Three-stage total hepatectomy using a portocaval shunt tube in rats.
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Ammonia↗
Biomedical subjects
M Sasaki
Publications and source records attributed to M Sasaki.
Influence of donor condition on postoperative graft survival and function in human liver transplantation.
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Adult↗
Amplification and sequence analysis of partial bacterial 16S ribosomal RNA gene in gallbladder bile from patients with primary biliary cirrhosis.
BACKGROUND/AIMS: The etiopathogenesis of bile duct lesion in primary biliary cirrhosis is unknown, though the participation of bacteria and/or their components and products is suspected. In this study, we tried to detect and identify bacteria in the bile of patients with primary biliary cirrhosis by polymerase chain reaction using universal bacterial primers of the 16S ribosomal RNA gene. METHODS: Gallbladder bile samples from 15 patients with primary biliary cirrhosis, 5 with primary sclerosing cholangitis, 5 with hepatitis C virus-related liver cirrhosis, 11 with cholecystolithiasis, and from 12 normal adult gallbladders were used. In addition to the culture study, partial bacterial 16S ribosomal RNA gene was amplified by polymerase chain reaction (PCR) taking advantage of universal primers that can amplify the gene of almost all bacterial species, and the amplicons were cloned and sequenced. Sequence homology with specific bacterial species was analyzed by database research. Bacterial contamination at every step of the bile sampling, DNA extraction and PCR study was avoided. Furthermore, to confirm whether bacterial DNA is detectable in liver explants, the same analysis was performed using 10 liver explants of patients with primary biliary cirrhosis. RESULTS: In primary biliary cirrhosis, 75% (p<0.0001) of 100 clones were identified as so-called gram-positive cocci while these cocci were positive in only 5% in cholecystolithiasis (p<0.0001). In cholecystolithiasis gram-negative rods were predominant instead. One bacterial species detected in a normal adult was not related to those detected in primary biliary cirrhosis and cholecystolithiasis patients. No bacterial DNA was detected by PCR amplification in 10 liver explants of patients with primary biliary cirrhosis. CONCLUSIONS: The present results raise several possible roles of gram-positive bacteria in bile in the etiopathogenesis of primary biliary cirrhosis. However, these results could also reflect an epiphenomenon due to decreased bile flow in the patients with primary biliary cirrhosis at an advanced stage.
Adult↗
Otoacoustic emission in patients with neurological disorders who have auditory brainstem response abnormality.
Otoacoustic emissions (OAEs) were evaluated in 51 ears of 30 patients with a severe auditory brainstem response (ABR) waveform abnormality. Thirteen ears showed no ABR to click sound of higher intensity than 100 dBSPL (group 1). Fourteen ears exhibited only wave V or a decreased amplitude pattern of ABR (group 2). Twenty-four ears showed a predominant wave I or no wave III pattern (group 3). Almost all the ears with absent ABR showed no OAE, which strongly suggested hearing loss of cochlear origin, although one patient with alternating hemiplegia of childhood exhibited definite OAEs and auditory reactions without ABR. One patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) and her mother in group 2 had OAE abnormalities, which also suggested mild to severe hearing impairment. When OAEs are present, an accompanying ABR abnormality may be produced by brainstem dysfunction of the underlying disorder such as Pelizaeus-Merzbacher disease. There was a significant relationship (chi-square test P<0.001) between the positivity of the distortion product OAE response and the clinical auditory reactions in 24 patients, although their ABR abnormalities did not reflect hearing impairment directly. Careful examination of both audiometry and OAEs might be necessary for further assessment of the hearing function in pediatric patients with neurological disorders and specific auditory nerve disease.
Acoustic Stimulation↗
Siblings of Schwartz-Jampel syndrome with abnormal muscle computed tomographic findings.
Schwartz-Jampel syndrome (SJS) is a disorder characterized by myotonia, joint contractures, skeletal abnormalities, facial dysmorphism and growth retardation. We present two boys of ages 4 and 8 years with SJS. Their clinical, electromyographic and histopathological findings were similar to those described, except for computed tomography (CT) images that revealed diffuse high attenuation in sternocleidomastoid muscles and low attenuation in the paraspinal, quadriceps, sartorius, soleus and gastrocnemius muscles. This is the first report describing abnormal muscle CT findings associated with SJS. Additional studies of muscle CT might help to improve understanding of the pathogenesis of SJS.
Child↗
Transient seizure disappearance due to bilateral striatal necrosis in a patient with intractable epilepsy.
An 8-year-old girl had suffered from intractable epilepsy due to cortical dysplasia. She developed mycoplasma pneumonia with massive pleural effusion. Fever continued for 3 weeks. Four weeks after the onset of this infection, she suddenly developed horizontal nystagmus, ataxia, choreoathetotic movements and confusion. CT disclosed swelling and low density of the heads of the caudate nuclei and putamina bilaterally. MRI revealed areas of symmetrical high intensity in the striatum on T2-weighted imaging. These lesions were thought to comprise bilateral striatal necrosis (BSN) mediated by the mycoplasma infection or Wernicke encephalopathy. Six months later, she had completely recovered clinically. During the 6 months after BSN, she did not have any epileptic seizures. Her epileptic seizures reappeared thereafter at a lower frequency. The striatum may be involved in the propagation pathway for epileptic seizure activity in this patient.
Cerebral Cortex↗
Correlation between proton magnetic resonance spectroscopic lactate measurements and vascular reactivity in chronic occlusive cerebrovascular disease: a comparison with positron emission tomography.
The purpose of this study is to investigate the correlation between lactate levels and cerebral vascular reactivity (VR) in regions outside an area of chronic cerebral infarction. Multivoxel proton magnetic resonance spectroscopy ((1)H-MRS) and positron emission tomography (PET) were performed in 11 patients who suffered chronic cerebral infarction. Of these 11 patients, 4 were examined before and after bypass surgery. Two regions-of-interests (ROIs) were placed outside the area of chronic infarction. One ROI was placed within a control region on the contralateral side. A lactate peak area was obtained in all ROIs. An N-acetyl aspartate (NAA) peak area was obtained in the ROI within the control region. The ratio of the lactate peak area and NAA peak area (Lct/NAA) was calculated for normalization of the lactate level, and was found to be 0.13 +/- 0. 10 (range, 0 to 0.43). The VR was recorded at 13.3 +/- 20.7% (range, - 44.3 to 68.9%), utilizing PET and administering acetazolamide. A significant negative correlation was observed between the Lct/NAA ratio and VR (r = - 0.709, p < 0.0001). These results suggest that lactate levels and VR are closely related in regions outside areas of chronic cerebral infarction.
Adolescent↗
Cerebral cortical dysplasia: assessment by MRI and SPECT.
The objective of this study was to establish correlations between image findings and pathologic deficits in patients with cerebral cortical malformations. The results of magnetic resonance imaging (MRI) and single-photon emission computed tomography (SPECT) in addition to clinical data for 15 patients with cerebral cortical malformations were reviewed retrospectively. MRI led to the diagnoses of bilateral perisylvian syndrome, hemimegalencephaly, focal polymicrogyria, band-heterotopia, and focal cortical dysplasia (FCD). Interictal SPECT did not reveal hypoperfusion in any case of polymicrogyria. Ictal SPECT images revealed hyperperfusion of the lesion in three patients with polymicrogyria, with accompanying hyperperfusion of the basal ganglia in two of the three patients. On the other hand, interictal SPECT images demonstrated hypoperfusion of the lesion in four patients with FCD. Ictal SPECT images revealed hypoperfusion of the lesion in two patients, hyperperfusion of the lesion in one patient, and hypoperfusion of the basal ganglia in two patients with FCD. This difference in perfusion between polymicrogyria and FCD observed in this study may reflect histologically different characteristics. This relative hyperperfusion of the cortex and the basal ganglia observed on ictal SPECT, which was found in two polymicrogyria patients with complex partial seizures and partial seizures evolving to secondary generalized seizures, respectively, suggests that the cortical-subcortical interaction is related to the mechanism of loss of consciousness or seizure generation.
Adolescent↗
Single-photon emission computed tomography of the brain in autism: effect of the developmental level.
Brain single-photon emission computed tomography was performed in 22 autistic and 10 nonautistic disabled patients. The regional cerebral blood flow in both laterotemporal and dorso-medio-lateral frontal areas decreased significantly in the autistic group compared with in nonautistic group. In the autistic group, the regional cerebral blood flow was significantly higher in the right temporal and right parietal lobes than that in the left ones. Inversely, the regional cerebral blood flow in the frontal and occipital lobes was significantly higher on the left side than on the right side. In the nonautistic group, except for in the dorso-medio-lateral frontal lobes (left > right), there was no difference in the regional cerebral blood flow in either cerebrum or cerebellum. A positive correlationship between regional cerebral flow and development quotient (intelligence quotient) was observed in the left laterotemporal and both dorso-medio-lateral frontal areas, and a negative one was observed in the cerebellar vermis area. These results suggest that the regional cerebral blood flow decrease in the temporal and frontal areas relates to not only the brain mechanism of autism reported previously but also intelligence levels.
Adolescent↗
Automatic synthesis of L-[beta-11C]amino acids using an immobilized enzyme column.
We have developed a system for the automatic synthesis of L-[beta-11C]amino acids for i.v. injection by means of enzyme-mediated reactions from 11CO2 via 11CH3I and D,L-[beta-11C]alanine as labeled intermediates. This system, which incorporates an ultrafilter cartridge sterilized by electron beam irradiation and a column packed with immobilized enzymes, was effective for eliminating enzymes and endotoxins that may contaminate the product. Using this system, 1.3 +/- 0.5 GBq of 5-hydroxy-L-[beta-11C]tryptophan with a radiochemical purity of 97.1 +/- 0.6% and a specific activity of 39.6 +/- 8 GBq/mumol a pH value of 4 could be obtained in about 32 min (n = 3, at EOS). No endotoxin, enzyme, or bacteria was detected in the product. L-[beta-11C]dihydroxyphenylalanine (L-[beta-11C]DOPA) was also synthesized using this system.
Alanine↗
Therapeutic effects of an oral adsorbent on acute dextran sulphate sodium-induced colitis and its recovery phase in rats, especially effects of elimination of bile acids in gut lumen.
BACKGROUND: The pathogenesis of inflammatory bowel disease is still unknown. However, it is possible that faecal bile acids influence the clinical course. AIMS: To evaluate the eliminating effects of faecal bile acids by the oral adsorbent on dextran sulphate sodium-induced rat colitis. METHODS: Rats were given 3% dextran sulphate sodium aqueous solution for 7 days, with or without concomitant administration of oral adsorbent, or the rats were given dextran sulphate sodium for 7 days, followed with or without oral adsorbent for 5 days. Macroscopic and microscopic examinations of the colons and measurement of faecal bile acids were performed. The cytotoxicity of bile salts on Caco-2 cells was also evaluated. RESULTS: Oral adsorbent tended to attenuate the dextran sulphate sodium-induced colitis. Oral adsorbent was fairly effective in reducing faecal hyodeoxycholic acid concentration. A positive correlation was found between the size of the ulcer area and the faecal hyodeoxycholic acid concentration. In a cell culture study, cytotoxicity of bile acid was parallel with increasing hydrophobicity of the bile acid. However, hyodeoxycholate exhibited severe cytotoxicity, despite its hydrophilic properties. CONCLUSIONS: Oral adsorbent tended to attenuate the dextran sulphate sodium-induced colitis and tended to promote the recovery process. It is possible that bile acids in the gut lumen influence the progression of dextran sulphate sodium-induced colitis and its repair process.
Acute Disease↗
Effect of dietary conjugated linoleic acid on lipid peroxidation and histological change in rat liver tissues.
The effect of dietary conjugated linoleic acid (CLA) on hepatic lipid parameters in Sprague-Dawley rats was examined. When rats were fed a diet containing CLA at 0 (control), 1, or 2% of the weight of the amount of food given for 3 weeks, the liver weight exhibited a slight increase in the CLA-fed groups, although the difference was not significant. Lipid accumulation in the hepatocytes of CLA-fed rats was also demonstrated by electron microscopic observation. In addition, the liver thiobarbituric acid reactive substances levels were significantly higher in the 2 wt % CLA group than in the other two dietary groups, and the levels of phosphatidylcholine hydroperoxide were higher in CLA-fed groups when compared to that of the control group. On the other hand, the serum lipid peroxide levels were comparable among all three dietary groups. Levels of triglycerides in the white adipose tissue (WAT) and serum nonesterified fatty acid (NEFA) were reduced in a CLA-dose-dependent manner. CLA was shown to accumulate in the WAT much more than in the serum or liver. These results suggest that CLA accelerates the decomposition of storage lipids in WAT and the clearance of serum NEFA levels, resulting in lipid peroxidation and a morphological change in the liver.
Adipose Tissue↗
The effect of ultraviolet B irradiation on nitric oxide synthase expression in murine keratinocytes.
Nitric oxide (NO), which has several physiological functions in skin, is generated by NO synthase (NOS). NOS has at least three isoforms; endothelial NOS (eNOS), brain NOS (bNOS), and inducible NOS (iNOS). Ultraviolet B (UVB) irradiation has been reported to stimulate NO production in skin via induction or activation of NOS, however, the exact mechanism of NOS induction by UVB irradiation remains obscure. In this study, we investigated the direct effect of UVB on the expression of NOS isoforms in murine keratinocytes, and found a significant increase in NO production within 48 h. mRNA and protein expressions of bNOS were both enhanced by UVB irradiation in murine keratinocytes, whereas iNOS mRNA expression was suppressed at 4 and 12 h after UVB irradiation. These results suggest that the enhancement of NO production observed after UVB irradiation in murine keratinocytes may be explained in part by the upregulation of bNOS expression, but not iNOS expression.
Animals↗
Up-regulation of tyrosinase gene by nitric oxide in human melanocytes.
Ultraviolet light (UV) radiation causes skin-tanning, which is thought to be mediated by stimulating the release of melanogenic factors from keratinocytes as well as other cells. Nitric oxide (NO) has been reported to be generated after UV radiation and to stimulate melanocytes as one of the melanogens. In a previous experiment by another group on melanogenesis induced by NO, increases in both tyrosinase activity and tyrosinase protein levels were observed after daily stimulation of NO for 4 days. In the present study, we investigated tyrosinase gene expression within the first 24 hr of NO-induced melanogenesis. Tyrosinase mRNA expression was found to be induced 2 hr after a single treatment with S-nitroso-N-acetyl-L-arginine. An increase of tyrosinase activity was also detected time-dependently within the 24-hr period, accompanied by an increase of tyrosinase protein levels. The induction of mRNA expression was suppressed by a cyclic guanosine 3',5'-monophosphate (cGMP)-dependent protein kinase (cGMP/PKG) inhibitor. These results suggest that the enhancement of tyrosinase gene expression via the cGMP pathway may be a primary mechanism for NO-induced melanogenesis.
Alkaloids↗
Involvement of nitric oxide in UVB-induced pigmentation in guinea pig skin.
Ultraviolet (UV) B irradiation evokes erythema and delayed pigmentation in skin, where a variety of toxic and modulating events are known to be involved. Nitric oxide (NO) is generated from L-arginine by NO synthases (NOS). Production of NO is enhanced in response to UVB-stimulation and has an important role in the development of erythema. NO has recently been demonstrated as a melanogen which stimulates melanocytes in vitro, however, no known in vivo data has been reported to support this finding. In this study, we investigated the contribution of NO with UV-induced pigmentation in an animal model using an NOS inhibitor. UVB-induced erythema in guinea pig skin was reduced when an NOS inhibitor, L-NAME (N-nitro-L-arginine methylester hydrochloride), was topically applied to the skin daily, beginning 3 days before UVB-irradiation. Delayed pigmentation and an increased number of DOPA-positive melanocytes in the skin were markedly suppressed by sequential daily treatment with L-NAME. Furthermore, melanin content 13 days after UVB-irradiation was significantly lower in skin treated with L-NAME than in the controls. In contrast, D-NAME (N-nitro-D-arginine methylester hydrochloride), an ineffective isomer of L-NAME, demonstrated no effect on these UV-induced skin responses. These results suggest that NO production may contribute to the regulation of UVB-induced pigmentation.
Animals↗
Evidence of the participation of peribiliary mast cells in regulation of the peribiliary vascular plexus along the intrahepatic biliary tree.
Our pilot study disclosed that tryptase-positive mast cells (MC) were densely distributed around the intrahepatic bile ducts (peribiliary MC). In this study, the pathophysiologic roles of these MC were examined with respect to the microcirculation around the bile duct in 71 cases of histologically normal liver, 24 cases of chronic hepatitis, and 45 cases of liver cirrhosis. The tryptase-positive MC were very close to the microvessels of the peribiliary vascular plexus (PVP), which supply the intrahepatic biliary tree. The tryptase-positive MC were frequently found adjacent to vascular smooth muscle cells, including pericytes. The location of the tryptase-positive MC was confirmed by ultrastructural analysis. In cirrhosis, the numbers of both microvessels of PVP and peribiliary MC increased in parallel. Peribiliary MC were immunoreactive for endothelin 1 (ET-1), and were variably immunoreactive for histamine, chymase, inducible nitric oxide synthase (iNOS), and endothelin A and B (ET(A) and ET(B)) receptors, particularly in cirrhotic livers. On vascular endothelial cells of PVP, endothelial nitric oxide synthase (eNOS) and ET-1 were consistently detectable, and ET(A) receptors, ET(B) receptors, and iNOS were variably detectable. Pericytes of PVP expressed ET(A) and ET(B) receptors in addition to ET-1 and iNOS. Biliary epithelial cells also focally expressed iNOS, ET-1, and ET(A) and ET(B) receptors. These vasoactive substances were strongly expressed on the cellular components in cirrhotic liver. By in situ hybridization, iNOS mRNA signals were observed on iNOS-immunoreactive cell components, including peribiliary MC. These morphologic and immunohistochemical findings suggest that the cellular components displaying vasoactive substances in the milieu of the intrahepatic biliary tree are very dynamic in the vasoregulation of PVP in normal livers, even more so in cirrhosis, and that peribiliary MC exert local effects on the microcirculation of PVP, directly and indirectly.
Bile Ducts, Intrahepatic↗
Generation of the NUP98-HOXD13 fusion transcript by a rare translocation, t(2;11)(q31;p15), in a case of infant leukaemia.
We report a case of de novo acute myelomonocytic leukaemia with the t(2;11)(q31;p15) translocation in a Japanese female infant. The NUP98-HOXD13 fusion transcript generated by the translocation was detected in the patient's bone marrow cells by reverse transcription-polymerase chain reaction (RT-PCR). Additionally, ectopic expression of the normal allele of the HOXD13 gene was observed in this patient, suggesting that it might be associated with leukaemogenic development. This case is the third report of t(2;11) leukaemia with NUP98-HOXD13 and the first report showing that NUP98 rearrangements are associated with infant leukaemia, as well as therapy-related acute myelogenous leukaemia or myelodysplastic syndrome.
Aged↗
Activation of an ataxia telangiectasia mutation-dependent intra-S-phase checkpoint by anti-tumour drugs in HL-60 and human lymphoblastoid cells.
In yeast cells, the intra-S-phase checkpoint slows down the rate of DNA replication in response to DNA damage. Here we showed that a similar checkpoint mechanism is present and activated by anti-tumour drugs in HL-60 and Epstein-Barr virus (EBV)-transformed human lymphoblastoid cells. Using bromodeoxyuridine (BrdU) pulse labelling combined with two-dimensional flow cytometric analysis, we clearly visualized the cell-cycle progression of the BrdU-positive population (cells originally belonging to the S phase) and detected even subtle changes in S-phase progression induced by mild drug treatment conditions free of apoptosis. The DNA topoisomerase II inhibitors, doxorubicin and etoposide (250 nmol/l and 400 nmol/l, respectively, for 8 h), retained the BrdU-positive HL-60 cells in the latter half of S and G2/M positions, and the pyrimidine analogue anti-metabolite, cytosine beta-D-arabinofuranose (Ara-C; 50 nmol/l), kept them in early-to-late S phase after 8 h of incubation. Because 10 micromol/l of caffeine added 2 h later attenuated the S-phase retardation by these drugs in HL-60 cells, slowing of the S-phase progression should be actively regulated. Furthermore, two ataxia telangiectasia (AT)-derived lymphoblastoid cell lines were impaired in the doxorubicin-induced S-phase retardation, which indicated that the process is at least partially dependent on ataxia telangiectasia mutated (ATM) gene product. The inhibitory mechanism on S-phase progression elicited by anti-tumour drugs in HL-60 and lymphoblastoid cells may therefore correspond to the intra-S-phase checkpoint of the yeast cells.
Antimetabolites↗