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Galectins are beta-galactoside binding mammalian lectins and they share homologous carbohydrate recognition domains. To date, 11 members of galectin family have been cloned and identified. They have been shown to play roles in diverse biological events, such as embryogenesis, oncogenesis, adhesion and proliferation of the cells, receptor for advanced glycation end products, mRNA splicing, bacterial colonization, apoptosis, and in the modulation of the immune response. The mechanisms by which galectins exert these diverse effects remain largely unknown. However, the elucidation of multi-functional proteins belong to galectin family are going to open new fields in clinical science including diagnosis and therapy of autoimmune disorders, cancers, and vascular complications in diabetes and hypertension.</P>

The objective of this study was to evaluate fast and ultrafast T2-weighted images (T2WI), including echo planar imaging (EPI), using an AMI-25 agar phantom. Image quality for conventional spin echo (CSE) and turbo spin echo (TSE) was almost equivalent. In high-resolution TSE, image quality was highest due to the use of a 512 x 256 matrix. Half-Fourier single-shot turbo SE (HASTE) was associated with blurring of images, and turbo-gradient SE (TGSE) showed a deterioration of image quality. EPI also suffered from poor image quality because this method is very sensitive to magnetic field inhomogeneity. CSE showed good signal-to-noise ratio (S/N) and contrast ratio (CR), but also required the longest imaging times. Among the TSE sequences, TSE with a short echo train length (ETL) was superior in terms of S/N. The CR of EPI and fast low angle shot (FLASH) images were improved in proportion to the effective echo time (TE). At present, TSE is inferior to CSE in terms of S/N and CR. However, taking into consideration scanning time, TSE with a short ETL is thought to be suitable for routine examinations. Effective TE is an important factor in gradient echo (GRE) examinations.</P>

The immune status of thirteen living and related kidney transplant recipients with stable allografts were examined. The immunological assays consisted of a mixed lymphocyte reaction (MLR), cell-mediated lympholysis (CML) assay, interleukin-2 (IL-2) production in mixed lymphocytes culture (MLC) and IL-2 receptor (IL-2 R) expression on MLC cells. The suppression rates of the monoclonal antibodies (mAbs) against IL-2 R were tested on MLRs. The stimulation indices (SI) of the MLR against both donor and third-party cells increased compared with those of pretransplantation. The MLC responder cells stimulated by donor cells produced detectable amounts of IL-2, these amounts were lower than those by third-party cells. The MLC cells against donor cells expressed IL-2 R alpha and beta chains to the same degree as those against third-party cells. Anti-IL-2 R mAbs equally inhibited the MLRs between recipient and donor or third-party cells. Cytotoxic T lymphocytes (CTL) against donor cells were not generated, even with the addition of recombinant IL-2 in any of recipients except one, while anti-donor CTL had been detected prior to transplantation and the CTL against third-party cells were induced in posttranspalnt CML

assays. These results indicate that the clonal anergy phenomenon might mediate the specific CTL unresponsiveness observed in kidney transplant recipients and the anergy phenomenon might serve in the long-term acceptance of allograft.

Hepatitis C virus (HCV), discovered in 1989, is the major causative agent of parenteral non-A, non-B hepatitis worldwide. Following the development of a method of diagnosing HCV infection, it became apparent that HCV frequently causes chronic hepatitis. Persistent infection with HCV is implicated in liver cirrhosis and hepatocellular carcinoma. Current worldwide estimations suggest that more than 170 million people have been infected with HCV, an enveloped positive single-stranded RNA (9.6-kilobases) virus belonging to the Flaviviridae. The HCV genome shows remarkable sequence variation, especially in the hypervariable region 1 of the E2 protein-encoding region, and globally, HCV appears to be distributed with more than 30 genotypes. Complicated "quasispecies" and frequent mutations of viral genomes have also emerged. The HCV genome encodes a large polyprotein precursor of about 3,000 amino acid residues, and this precursor protein is cleaved by the host and viral proteinases to generate at least 10 proteins in the following order: NH2-core-envelope (E1)-E2-p7-nonstructural protein 2 (NS2)-NS3-NS4A-NS4B-NS5A-NS5B-COOH. These viral proteins not only function in viral replication but also affect a variety of cellular functions. Although several explanations have been proposed, the mechanisms of HCV infection and replication in targeted cells, the mechanism of persistent viral infection, and the pathogenesis of hepatic diseases (hepatitis or hepatocellular carcinoma) are all poorly understood. A major reason why these mechanisms remain unclear is the lack of a good experimental HCV replication system. Although several classical trials using cultured cells have been reported, several new, more promising experimental strategies (generations of infectious cDNA clone, replicon, animal models, etc.) are currently being designed and tested, in order to resolve these problems. In addition, new therapies for chronic hepatitis have also been developed. The enormous body of information collected thus far in the field of HCV research is summarized below, and an overview of the current status of HCV molecular virology of HCV is provided.</P>

We developed a method for human identification of forensic biological materials by PCR-based detection of a human-specific sequence in exon 3 of the myoglobin gene. This human-specific DNA sequence was deduced from differences in the amino acid sequences of myoglobins between humans and other animal species. The new method enabled amplification of the target DNA fragment from 30 samples of human DNA, and the amplified sequences were identical with that already reported. Using this method, we were able to distinguish human samples from those of 21 kinds of animals: the crab-eating monkey, horse, cow, sheep, goat, pig, wild boar, dog, raccoon dog, cat, rabbit, guinea pig, hamster, rat, mouse, whale, chicken, pigeon, turtle, frog, and tuna. However, we were unable to distinguish between human and gorilla samples. This method enabled us to detect the target sequence from 25 pg of human DNA, and the target DNA fragment from blood stored at 37 degrees C for 6 months, and from bloodstains heated at 150 degrees C for 4 h or stored at room temperature for 26 years. Herein we also report a practical application of the method for human identification of a bone fragment.</P>

The prevalence of penicillin non-susceptible Streptococcus pneumoniae (PNSSP) is increasing among isolates from acute otitis media (AOM). Repeated episodes of antibiotic exposure are a well-known risk factor for the isolation of PNSSP although otitis-prone or recurrent AOM cases frequently require repeated courses of antibiotic treatment. In order to evaluate the chronological alteration of S. pneumoniae during recurrences of AOM, strains of S. pneumoniae were isolated from 11 patients, each of whom had experienced 2-4 episodes of AOM, were examined. Every bacterial specimen obtained from a single episode of recurrent AOM was examined by PCR-based penicillin-binding protein (PBP) assay, serotyping, and amplified fragment length polymorphism (AFLP), then compared to other samples from the same case. Two cases (18.2%) showed strain diversity during repeated antibiotic treatments by serotyping or PBP-assay. By AFLP analysis, 6 cases (54.5%) demonstrated heterogeneous strains during recurrent AOM. Clonal survivors of previous episodes of AOM were not always the cause of subsequent episodes of AOM, even in otitis-prone cases.

Nephrin, a gene product of the congenital nephrotic syndrome of the Finnish type (NPHS1), is a 1242-residue putative transmembrane protein of the immunoglobulin family of cell adhesion molecules. The expression of this gene is localized in rat and human glomerular epithelial cells. Here we report the expression of nephrin in various tissues other than the kidneys in mice. The expression of nephrin mRNA in various tissues of mice, including the kidneys, testes, spleen, thymus and brain, were first investigated by the RT-PCR method, and it was shown that a high level of nephrin mRNA could be detected in the testes of mice 1-6 weeks old. In situ hybridization revealed the expression of the nephrin gene in the Sertoli cells. Additionally, immunofluorescent staining studies indicated that nephrin was colocalized with anchoring protein ZO-1 in the mouse testis. From these results, it is inferred that nephrin is an important component of the barrier system in testes.

Eighty-eight cases of cutaneous melanoma (CM) were analyzed in order to elucidate the relationship between thickness, angiogenesis, and prognosis. The thickness of the tumor was measured according to the Breslow method, and the microvessels were identified by an immunohistochemical study using anti-factor VIII monoclonal antibody on specimens from 40 patients with superficial spreading melanoma (SSM), and 48 with nodular type (NM). Microvessels were counted in the area of highest density. The overall survival and disease-free period were analyzed retrospectively. The proportion of patients with thicker CMs (> 1.5 mm) increased with age in both sexes. Mean vascular count was statistically significant different only between thinner and thicker tumors in the SSM group (P < 0.05). Prognosis was correlated with the thickness of CM (P = 0.0002), mean vascular count alone (P = 0.004), mean vascular count in association with CM thickness less than 1.5 mm (P = 0.0005), and with mean vascular count in NM (P = 0.02). These findings suggest that increasing microvessel density indicates a worsening prognosis.

Primary adenocarcinoma of the appendix is rare, especially the colonic type. We report a case of appendiceal adenocarcinoma of colonic type associated with perforating peritonitis after aorto-femoral artery bypass surgery. A 79-year-old woman presented with fever and pain in the right lower abdomen. She had undergone aorto-femoral artery bypass surgery due to arteriosclerosis obliterans 6 months earlier. Abdominal ultrasonography and computed tomography showed a suspected pool of fluid surrounding the artificial vessel and a mass lesion in the upper end of the fluid collection. These findings suggested localized peritonitis due to appendiceal perforation. Emergency laparotomy showed a pool of pus around the artificial vessel and inflamed appendix, which adhered to the surrounding tissue. The mass was excised in combination with an ileocaecal resection, followed by an ileocolic anastomosis. The histological diagnosis was moderately differentiated adenocarcinoma of the appendix, colonic type. The tumour had infiltrated and obstructed the lumen of the orifice of the appendix, which may have caused perforation of the appendix. She was examined at regular periodic follow-ups and no evidence of recurrence or metastasis was noted in the 12-month postoperative period. These findings indicate that, in cases of acute appendicitis, especially with perforation, the possibility of appendiceal adenocarcinoma should be considered.

A prospective study was performed to determine the accuracy of magnetic resonance imaging (MRI) compared with operative findings in the evaluation of patients associated with rotator cuff tears. Fifty-four of 60 shoulders (58 patients) examined by MRI were confirmed as full-thickness tears and 6 as partial-thickness tears at the time of surgery. The oblique coronal, oblique sagittal, and axial planes of T2-weighted images with the 0.5 tesla MRI system were obtained preoperatively and compared with operative findings. MRI correctly identified 46 of 54 full-thickness rotator cuff tears and 5 of 6 partial-thickness tears. A comparison of MRI and operative findings in full-thickness cuff tears showed a sensitivity of 85%, a specificity of 83%, and a positive prospective value (PPV) of 99%. A comparison of partial-thickness tears showed a sensitivity of 83%, a specificity of 85%, and PPV of 39%. Linear regression analysis showed an excellent correlation between the MRI assessment and measurement at the time of surgery (r = 0.90, P < 0.01). MRI was useful in evaluating large and medium-sized rotator cuff tears, but less useful in distinguishing small full-thickness tears from partial-thickness tears.

Continuous caudal anesthesia has been commonly used for intra- and post-operative analgesia in infants and children. However, it has a potential risk of bacterial infection, especially in infants in whom the catheter site is easily contaminated with loose stool. To avoid infection, the authors applied a new procedure using subcutaneous tunneling for continuous caudal anesthesia. In the 18 cases studied with subcutaneous tunneling, clinical signs of infection were absent and bacterial colonization was not found on the catheter tip after 3.9 +/- 1.4 days of catheterization. The incidence of catheter colonization after continuous caudal anesthesia without tunneling had been reported. In their reports, the incidence of catheter colonization ranged from 20% to 37%. Therefore, caudal catheterization with subcutaneous tunneling is a simple and safe method, and has proved very effective to reduce the risk of epidural infection.

It is recognized that sustained ischemia-induced hyperactivity is related to abnormalities in dopamine function. However, it is unclear that dopaminergic neurotransmission triggers such ischemia-induced hyperactivity. Therefore, the relationship between dopaminergic neurotransmission and ischemia-induced hyperactivity was investigated in an animal model using Mongolian gerbils. When haloperidol 2 mg/kg was administered i.p. 30 min after ischemia, the ischemia-induced hyperactivity at 24 h after ischemia was blocked. General behavior was similar to that of sham-operated animals. Haloperidol at doses of 0.1 and 0.2 mg/kg had no effect on locomotor activity in sham-operated animals and decreased ischemia-induced hyperactivity when the drug was administered 24 h after ischemia; these doses did not have any effect on ischemia-induced hyperactivity when the drug was administered 30 min after ischemia. On the other hand, when the animal was confined to a small, restrictive cage for the 24 h period immediately following ischemic injury, locomotor activity at 24 h after ischemia increased. Such behavior also increased in animals when they were returned to their original more permissive cages immediately after ischemia. It is conceivable that the decrease in the level of activity was not related to ischemia-induced hyperactivity. These data suggested that the inhibition of ischemia-induced hyperactivity can be induced by complete blockage of dopaminergic receptors immediately after ischemia.

An 83-year-old man with a large internal iliac artery aneurysm (IIAA) was treated with the use of stent-graft, suggesting successful results at 3, 6, and 12 months after treatment. However, 24-month follow-up computed tomography showed minor peripheral opacification of the IIAA. The patient underwent surgical endoaneurysmorrhaphy. No previous report of long-term recanalization of a satisfactorily thrombosed iliac artery aneurysm at 2 years or more after stent-grafting has been previously reported. Further follow-up studies need to be performed on the present procedure before anyone can confidently recommend it in regard to its long-term safety.

The authors analyzed the 5-year and 9-year survival in 134 of 165 patients who underwent total knee arthroplasties from 1989 to 1996 in our department. Patients were followed until December 31, 1998, or until the time of death. Diagnoses were rheumatoid arthritis in 81 patients (132 knees) and osteoarthritis in 53 patients (79 knees). The survival of the patients was compared to that of the age- and sex-adjusted general population. Kaplan-Meier survival curves were constructed. Twenty-two patients in the study died before the end of the follow-up. The cumulative 5-year patient survival was 88.7%, and 9-year patient survival was 64.4% for total knee arthroplasty patients. The standardized mortality ratio was 0.11 (95% confidence interval: 0.02-0.40) for the patients with osteoarthritis, and 0.81 (95% confidence interval: 0.52-1.25) for the patients with rheumatoid arthritis. The Cox proportional hazards model showed that the factors of male sex and rheumatoid arthritis were related to a higher mortality rate in the total knee arthroplasty group.

This study investigated the relation between asthma attacks and levels of plasma fibronectin (FN) and serum eosinophilic cationic protein (ECP) in patients with bronchial asthma in order to clarify the role of FN in the airway inflammation of bronchial asthma. Plasma levels of FN were significantly higher (P < 0.025) in patients with bronchial asthma than in healthy controls. They were also significantly higher (P < 0.05) in non-atopic asthmatics than in atopic asthmatics. Furthermore, plasma FN was lower during the attack than the non-attack stage (P < 0.025), and a significant increase of plasma FN was noted (P < 0.05) in asthmatics who had more severe and more frequent attacks. Serum levels of ECP were significantly higher during the attack than the non-attack stage (P < 0.005). An increase of plasma FN in the non-attack stage after attacks showed a significant correlation (P < 0.05) with a decrease of serum ECP. These observations clearly indicate that the decrease in plasma FN associated with attacks is closely related to aggravation of airway inflammation, and that the increase in plasma FN in the non-attack stage reflects chronic airway inflammation. These results suggest that the fluctuation in plasma levels of FN may be one of the factors affecting allergic inflammation and attacks in bronchial asthma.

Non-traumatic rhabdomyolysis associated with organophosphate intoxication has not been generally reported. We report here in a severe case of fenitrothion poisoning complicated by rhabdomyolysis. A 43-year-old woman ingested approximately 100 ml of fenitrothion emulsion (50%) in an attempt to commit suicide. On day 3 after admission, her creatine phosphokinase (CPK) peaked at 47,762 IU/L. She received supportive treatment included sodium bicarbonate and fluid resuscitation. However, muscarinic symptoms including excessive miosis and salivation developed on day 5 when her CPK levels decreased. The delay in cholinergic symptoms might have been due to the trihexyphenidyl she took with the antipsychotic drugs. Fortunately, the present patient recovered from the acute cholinergic crisis, and acute renal failure was prevented by early diagnosis. This is a case of organophosphate poisoning complicated by rhabdomyolysis in a psychiatric patient. The masking of acute cholinergic symptoms should be taken into consideration in such patients.

With the development of new treatments, there is an increasing need for early diagnosis of sporadic Alzheimer's disease. Therefore, biological markers allowing positive diagnosis early in the course of the disease are highly desirable. Cerebrospinal fluid levels of protein tau were shown to be significantly increased in patients with Alzheimer's disease. Although sensitivity is high, poor specificity limits the diagnostic value of this marker. The same is true for the 42 amino acid isoform of beta-amyloid protein that is significantly decreased in cerebrospinal fluid of Alzheimer's disease patients. However, combining both markers could improve specificity at least allowing differentiation between Alzheimer's disease, normal ageing and depressive pseudodementia. Other biological markers such as cerebrospinal fluid levels of neurotransmitters, cytokines or superoxide dismutase were shown to have even less diagnostic value. The apolipoprotein epsilon 4 allele is a risk factor for Alzheimer's disease but not a diagnostic marker as many individuals who inherit epsilon 4 do not develop the disease. Till now, a single diagnostic marker allowing

discrimination between Alzheimer's disease and other dementias does not exist. Combined cerebrospinal fluid levels of beta-amyloid protein and tau protein might be used as a marker that helps discriminating Alzheimer's disease from normal ageing and depression.