Transarterial chemoembolisation for palliative treatment of renal cell carcinoma in two dogs with pulmonary metastasis.

Two dogs with anorexia and rapid weight loss were referred to our hospital due to a right renal mass and several pulmonary nodules. Both dogs underwent needle core biopsy of the mass, followed by transarterial chemoembolisation of the renal mass. A catheter was inserted from the femoral artery and advanced into the right renal artery. A suspension of carboplatin (100 mg/m2 ) and equivalent lipiodol was administered via the inserted multipurpose catheter. Immediately after, under fluoroscopic guidance, pulse injections of small amounts of gelatin particles (diameter 1 mm) dissolved in iohexol were administered until complete embolisation of the renal artery. Histopathologic diagnosis was renal cell carcinoma in both dogs. Clinical signs improved for 134 and 358 days after transarterial chemoembolisation. In addition, postoperative radiographs demonstrated a decrease in the tumour size. The dogs died 215 and 525 days after the initial evaluation, respectively. As a palliative treatment, transarterial chemoembolisation might help reduce the tumour volume and improve the quality of life in dogs with renal cell carcinoma and distant metastases.

Congenital portopulmonary shunt in a cat.

A 9-year-old spayed female crossbreed cat with chief complaints of anorexia and hypersalivation had high serum concentrations of ammonia and fasting and postprandial total bile acid. Therefore, she was referred to our hospital. On the first evaluation, haematology, serum chemistry, radiography and ultrasonography findings suggested that she had a congenital portosystemic shunt. CT revealed a shunt vessel from the left gastric vein to the left pulmonary vein. During median celiotomy and sternotomy, gross findings and mesenteric portography revealed abnormal vessel shunting from the left gastric vein to the left pulmonary vein. Complete ligation of the shunt vessel was achieved. She recovered without any complications. Postoperative serum chemistry revealed that ammonia and total bile acid levels decreased to within the reference intervals. This report is the first to describe the clinical features and surgical outcome of a cat with a congenital portopulmonary shunt.

Development of a He- and He0 beam source for alpha particle measurement in a burning plasma.

Proof of principle experiments of neutral helium beam production for alpha particle diagnostics was carried out on a test stand. Negative helium ions were produced in the Li charge exchange cell, in which stable and long time operation was possible. He(-) beam was accelerated to 157 keV. Finally, He(0) beam was successfully produced after the flight in the drift-tube through the auto-electron-detachment process from He(-) to He(0). A neutral beam detector using a pyroelectric device was also developed to measure He(0) beam intensity. The metastable component in the neutral helium beam was found to be less than 2%.

An alpha particle measurement system using an energetic neutral helium beam in ITER (invited).

An energetic helium neutral beam is involved in the beam neutralization measurement system of alpha particles confined in a DT fusion plasma. A full size strong-focusing He(+) ion source (2 A, the beam radius of 11.3 mm, the beam energy less than 20 keV). Present strong-focusing He(+) ion source shows an emittance diagram separated for each beamlet of multiple apertures without phase space mixing, despite the space charge of a beamlet is asymmetric and the beam flow is non-laminar. The emittance of beamlets in the peripheral region was larger than that of center. The heat load to the plasma electrode was studied to estimate the duty factor for the ITER application.

Association of seminal plasma motility inhibitors/semenogelins with sperm in asthenozoospermia-infertile men.

Seminal plasma motility inhibitors (SPMIs) are proteinase-resistant fragments of semenogelin I and II (Sgs), which are the major proteins of semen coagulum. SPMIs inhibit the motility of spermatozoa, and Sgs are thought to be natural regulators of human sperm function. The mechanism underlying sperm motility regulation and its association with defective motility in infertile men remain unclear. The purpose of this study was to investigate the association between SPMIs and spermatozoa in infertile men with asthenozoospermia. Fifty-four semen samples from 37 asthenozoospermic patients and 17 samples from 9 normal healthy subjects were analyzed. Spermatozoa, washed by Percoll density gradients, were immunostained with anti-SPMI antibody and subjected to flow cytometric analysis. The proportion of spermatozoa labeled with the antibody and the average intensity of fluorescence labeling per spermatozoa were analyzed in relation to the parameters used for semen analysis. A significant negative correlation was found between sperm motility and the proportion (R = -0.68) and intensity (R = -0.38) of labeling. These results suggest that SPMIs remain on the sperm surface after liquefaction. This might account for some disorders of sperm motility observed in infertile men with asthenozoospermia.

Blood outgrowth endothelial cell-based systemic delivery of antiangiogenic gene therapy for solid tumors.

Endothelial cells and endothelial cell precursors encoding a therapeutic gene have induced antitumor responses in preclinical models. Culture of peripheral blood provides a rich supply of autologous, highly proliferative endothelial cells, also referred to as blood outgrowth endothelial cells (BOECs). The aim of this study was to evaluate a novel antiangiogenic strategy using BOECs expressing fms-like tyrosine kinase-1 (sFlt1) and/or angiostatin-endostatin (AE) fusion protein. Conditioned medium from BOECs expressing sFlt1 or AE suppressed in vitro growth of pulmonary vein endothelial cells by 70% compared with conditioned medium from non-transduced BOEC controls. Reverse transcriptase-PCR analysis indicated that systemically administered BOECs proliferated in tumor tissue relative to other organs in C3(1)SV40 TAG transgenic (C3TAG) mice with spontaneous mammary tumors. Tumor volume was reduced by half in C3TAG mice and in mice bearing established lung or pancreatic tumors in response to the treatment with sFlt1-BOECs, AE-BOECs or their combination. Studies of tumor vascular density confirmed that angiogenic inhibition contributed to slowed tumor growth. In an orthotopic model of glioma, the median survival of mice treated with sFlt1-BOECs was double that of mice receiving no BOEC treatment (P=0.0130). These results indicate that further research is warranted to develop BOECs for clinical application.

Vascular calcification and secondary hyperparathyroidism of severe chronic kidney disease and its relation to serum phosphate and calcium levels.

BACKGROUND AND PURPOSE: Various complications consequent on disordered calcium and phosphate homeostasis occur frequently in chronic kidney disease (CKD) patients. Particularly, vascular calcification has high morbidity and mortality rates. There is a clear need for a better CKD model to examine various aspects of this disordered homeostasis. EXPERIMENTAL APPROACH: Oral dosing with adenine induced CKD in rats in only 10 days. Serum calcium, phosphate and parathyroid hormone were measured and calcification in aorta was assessed histologically. The effects of varying phosphorus content of diet or treatment with phosphate binders or active vitamin D(3) on these parameters were examined. KEY RESULTS: After adenine dosing, significant hyperphosphatemia, hypocalcemia and secondary hyperparathyroidism (2HPT) were observed during the experimental period of 15 weeks. Aortic calcification was detected in only some of the animals even at 15 weeks (approximately 40%). Treatment with vitamin D(3) for 18 days, even at a low dose (100 ng x kg(-1), 3-4 times week(-1), p.o), caused aortic calcification in all animals and increases in serum calcium levels up to the normal range. The vitamin D(3)-induced calcification was significantly inhibited by phosphate binders which lowered serum phosphate levels and the calcium x phosphate product, although serum calcium levels were elevated. CONCLUSIONS: These data suggest that rats dosed orally with adenine provide a more useful model for analysing calcium/phosphate homeostasis in severe CKD. Controlling serum calcium/phosphate levels with phosphate binders may be better than vitamin D(3) treatment in hyperphosphatemia and 2HPT, to avoid vascular calcification.

Greater development of 1,2-dimethylhydrazine-induced colon cancer in a rat model of type 2 diabetes mellitus.

Several clinical cohort and case-control studies have suggested a link between diabetes and colon cancer. Otsuka Long-Evans Tokushima Fat (OLETF) rats spontaneously develop type 2 diabetes mellitus and Long-Evans Tokushima Otsuka (LETO) rats are non-diabetic. The relationship between type 2 diabetes mellitus and colon cancer was examined in these rats. The carcinogen 1,2-dimethylhydrazine was administered subcutaneously once weekly for 10 weeks, and the animals were killed and necropsied in week 29. All OLETF rats and 80% of the LETO rats developed cancer. The number of colon cancers per rat was significantly greater in the diabetic than in the non-diabetic rats. Although the tumours tended to be larger in diabetic rats, the difference was not statistically significant. No significant differences were observed in the depth of invasion or histological type of cancer in the two groups. Type 2 diabetes mellitus may enhance the generation and growth of colon cancer.

A novel neuronal cell line derived from the ventrolateral region of the suprachiasmatic nucleus.

The suprachiasmatic nucleus of the anterior hypothalamus is the center of an internal biological clock in mammals. Glutamate is the neurotransmitter of retino-hypothalamic tract responsible for mediating the circadian actions of light in rodents. N-methyl-d-aspartate receptors, particularly NR2B subunit are reported to be principally involved in photic resetting of the biological clock in vivo and in slice culture. But, the precise cellular mechanisms of the resetting are not elucidated, because no adequate neuronal cell lines derived from the suprachiasmatic nucleus have been established. We established a neuronal cell line, N14.5, derived from the suprachiasmatic nucleus of a transgenic rat harboring the temperature-sensitive simian virus 40 large T-antigen gene. When the cells were cultured at 39 degrees C, the morphological features were turned fibroblastic into neuronal round cell body with neurite extensions. These cells showed immunoreactivities for neuronal markers (betaIII-tubulin, microtubule-associated protein 2 and TAU2) and as well as for vasoactive intestinal peptide which is expressed in the ventrolateral region of the suprachiasmatic nucleus. The cells expressed N-methyl-d-aspartate receptors, particularly NR1 and NR2B subunits as revealed by quantitative PCR. N-methyl-d-aspartate activated phosphorylation of p44/42 mitogen-activated protein kinase and increased expression level of Per1 and Per2 mRNA. These results suggest that the N14.5 is a novel neuronal cell line derived from the ventrolateral region of the suprachiasmatic nucleus, and that N-methyl-d-aspartate receptors expressed in the cells are a functional receptor. The N14.5 cells may be a useful tool to elucidate numerous chronobiological processes, especially resetting mechanism induced by an external light signal.

Quantitative analysis of amyloid plaques in a mouse model of Alzheimer's disease by phase-contrast X-ray computed tomography.

Densely aggregated beta-amyloid peptides are believed to play a key role in the pathogenesis of Alzheimer's disease. Amyloid plaques are a potential target for molecular imaging to determine the clinical status of Alzheimer's disease. Phase-contrast X-ray imaging combined with computed tomography is a promising technique that can be used to visualize the physical density of structures in biological tissues non-invasively, and without the use of imaging agents. Using brain tissue isolated from a mouse model of Alzheimer's disease, we show that beta-amyloid 40-positive/beta-amyloid 42-positive amyloid plaques, but not beta-amyloid 40-negative/beta-amyloid 42-positive amyloid plaques, exist as high-density aggregates that can be specifically detected by phase-contrast X-ray computed tomography. The phase-contrast X-ray computed tomography detected beta-amyloid 40-positive/beta-amyloid 42-positive amyloid plaques in three-dimensions with an extremely high sensitivity comparable to that of histological analysis, and also enabled the load of amyloid plaques to be quantified. Furthermore, the use of phase-contrast X-ray computed tomography reveals that the physical density of beta-amyloid 40-positive/beta-amyloid 42-positive amyloid plaques increases with age, and that the large volume, high-density, amyloid plaques that are specifically observed in aged Alzheimer's disease mice are closely associated with neuritic dystrophy. These results demonstrate that phase-contrast X-ray computed tomography is a highly sensitive imaging technique for analyzing dense-cored amyloid plaques in postmortem samples, and is beneficial in elucidating amyloid pathophysiology in Alzheimer's disease.

A novel oligodendrocyte cell line OLP6 shows the successive stages of oligodendrocyte development: late progenitor, immature and mature stages.

The successive stages of development from oligodendrocyte progenitor to mature oligodendrocyte have been investigated in detail by using stage-specific antibodies. However, no cell lines are available that show stepwise differentiation from oligodendrocyte progenitors to mature oligodendrocytes. Here we show the establishment of an immortalized oligodendrocyte cell line, OLP6, from adult transgenic rats harboring the temperature-sensitive simian virus 40 large T-antigen gene. The OLP6 cells had a fibroblastic morphology and continuously proliferated at 33 degrees C. They displayed growth arrest and multipolar morphology when they were cultured at 39 degrees C. They express the oligodendrocytic markers O4, 2'-3'-cyclic-nucleotide 3'-phosphodiesterase, galactocerebroside and second endothelial differentiation gene receptor-2 at 39 degrees C. The OLP6 cells underwent apoptosis upon serum withdrawal at 39 degrees C. Lysophosphatidic acid inhibited this apoptosis and promoted the expression of myelin basic protein. These results demonstrate that the activation of endothelial differentiation gene receptor-2 exerts anti-apoptosis and myelinogenesis effects on the OLP6 cells. Taken together, the OLP6 cells in the late oligodendrocyte progenitor stage can progress to the immature oligodendrocyte stage by shifting culture temperature. Furthermore, lysophosphatidic acid promoted the maturation of OLP6 cells in the immature oligodendrocyte stage. Such OLP6 cells should provide a potent model system for studying the precise mechanism involved in stepwise differentiation of oligodendrocytes.

Pranlukast inhibits NF-kappa B activation in human monocytes/macrophages and T cells.

BACKGROUND: Pranlukast is a leukotriene 1 (LT1) receptor antagonist and is effective against bronchial asthma. Pranlukast inhibits contraction of the tracheal muscle, and thereby antagonizes the binding of LTC4, LTD4 and LTE4. However, the action of pranlukast on monocytes/macrophages and T cells is unknown. OBJECTIVE: We examined whether or not pranlukast inhibits TNF-alpha-induced activation of nuclear transcription factor NF-kappa B, a factor that is essential for the expression of proinflammatory cytokines, on human monocytic 1.3% dimethylsulphoxide (DMSO)-differentiated U-937 cells, which have cysteinyl LT1 (CysLT1) receptors on their membranes, and T cells (Jurkat), which do not. METHODS: We examined whether or not LTC4, LTD4 or LTE4 induced NF-kappa B activation in 1.3% DMSO-differentiated U-937 cells by Western blotting. The inhibitory effects of pranlukast and MK-571, which is an LTD4 receptor-selective antagonist, on TNF-alpha-induced NF-kappa B activation was evaluated by Western blotting and flow cytometry, and those on lipopolysaccharide (LPS)-induced interleukin-6 (IL-6) production in peripheral blood mononuclear cells (PBMC) were evaluated by enzyme-linked immunosorbent assaying. RESULTS: LTC4, LTD4 or LTE4 did not induce NF-kappa B activation in 1.3% DMSO-differentiated U-937 cells. Western blotting demonstrated that 10-5 M pranlukast inhibits NF-kappa B activation in 1.3% DMSO-differentiated U-937 and Jurkat cells by about 40% & 30%, respectively. Flow cytometry demonstrated that pranlukast and MK-571 inhibit NF-kappa B activation in 1.3% DMSO-differentiated U-937 and Jurkat cells in a dose-related manner. Moreover, 10-5 M pranlukast and MK-571 inhibited LPS-induced IL-6 production in PBMC by about 65% and 15%, respectively. CONCLUSION: Pranlukast and MK-571 partially inhibited NF-kappa B activation in 1.3% DMSO-differentiated U-937 and Jurkat cells, and IL-6 release in PBMC. These findings are consistent with the idea that, independently of CysLT1 receptor antagonism, micromolar concentrations of pranlukast suppress the production of proinflammatory cytokines via inhibition of NF-kappa B activation in monocytes/macrophages and T cells, but the contribution of this effect to the anti-inflammatory activity of pranlukast at oral therapeutic doses in asthmatic patients is unclear.

Edg-8 receptors are preferentially expressed in oligodendrocyte lineage cells of the rat CNS.

The messenger RNA for endothelial differentiation gene 8 receptors is known to be expressed almost exclusively in the rat CNS, but the nature of the expressing cells has not been defined. Using an antibody specific for endothelial differentiation gene 8, we investigated the immunohistochemical localization of endothelial differentiation gene 8 receptors in the rat CNS. Immunopositive staining was detected in a subset of glial cells distributed throughout the brain and spinal cord, including both gray and white matter, but not in the dorsal root ganglion. The distribution and morphological similarity in comparative immunostaining for endothelial differentiation gene 8 and various glial markers suggested that endothelial differentiation gene 8 is preferentially expressed in NG2-positive oligodendrocyte progenitor cells in adult rat brains. Counts of endothelial differentiation gene 8-positive cells and NG2-positive cells in the forebrain revealed that a subset of NG2-positive cells was endothelial differentiation gene 8-positive, and that the ratio of endothelial differentiation gene 8-positive cells to NG2-positive cells varied from region to region. In 17-day-old embryonic brains, the endothelial differentiation gene 8 distribution was similar to that of an oligodendrocytic marker, 2',3'-cyclic nucleotide 3'-phosphodiesterase. These data suggest that endothelial differentiation gene 8 receptors are preferentially expressed in oligodendrocyte lineage cells including oligodendrocyte progenitor cells and immature/maturating oligodendrocytes in rat CNS, and that they might have important functions in oligodendrocytic maturation and myelination.

beta-amyloid deposits in transgenic mice expressing human beta-amyloid precursor protein have the same characteristics as those in Alzheimer's disease.

A transgenic mouse expressing the human beta-amyloid precursor protein with the "Swedish" mutation, Tg2576, was used to investigate the mechanism of amyloid-beta peptide (Abeta) deposition. We characterized Abeta deposits in the cerebral cortex biochemically and pathologically. A surface-enhanced laser desorption/ionization affinity mass spectrometric study using the 6E10 monoclonal antibody demonstrated that the major species of Abeta in a formic acid-extracted fraction of the cortex were Abeta(1-38), Abeta(1-40) and Abeta(1-42). Immunohistochemistry using antibodies to the carboxy-terminal epitopes of Abeta(1-40) and Abeta(1-42), as well as 6E10, showed that plaques containing Abeta(1-42) were more numerous than those containing Abeta(1-40) throughout the cortex. Laser confocal analysis of the immunoreactivities in the plaques demonstrated that Abeta(1-40) was preferentially located in the central part of the Abeta(1-42) positive plaques. Enzyme-linked immunosorbent assay measurements of Abeta(1-40) and Abeta(1-42) showed that Abeta(1-40) was several-fold more abundant than Abeta(1-42). From these data we suggest that Abeta(1-42) deposition may precede Abeta(1-40) deposition, while Abeta(1-40) begins to deposit in the central part of the plaques and accumulates there. Furthermore, localization of Abeta(1-40) corresponded almost exactly to congophilic structures, which were associated with aberrant swollen synapses detected with antibodies to synaptophysin and alpha-synuclein. Thus, Abeta deposits in Tg2576 mice have similar characteristics to those in Alzheimer's disease.

Apolipoprotein E deposition and astrogliosis are associated with maturation of beta-amyloid plaques in betaAPPswe transgenic mouse: Implications for the pathogenesis of Alzheimer's disease.

A transgenic mouse expressing the human beta-amyloid precursor protein with the 'Swedish' mutation, Tg2576, was used to investigate the mechanism of beta-amyloid (Abeta) deposition. Previously, we have reported that the major species of Abeta in the amyloid plaques of Tg2576 mice are Abeta1-40 and Abeta1-42. Moreover, Abeta1-42 deposition precedes Abeta1-40 deposition, while Abeta1-40 accumulates in the central part of the plaques later in the pathogenic process. Those data indicate that Abeta deposits in Tg2576 mice have similar characteristics to those in Alzheimer's disease. In the present study, to understand more fully the amyloid deposition mechanism implicating Alzheimer's disease pathogenesis, we examined immunohistochemically the distributions of apolipoprotein E (apoE) and Abeta in amyloid plaques of aged Tg2576 mouse brains. Our findings suggest that Abeta1-42 deposition precedes apoE deposition, and that Abeta1-40 deposition follows apoE deposition during plaque maturation. We next examined the relationship between apoE and astrogliosis associated with amyloid plaques using a double-immunofluorescence method. Extracellular apoE deposits were always associated with reactive astrocytes whose processes showed enhancement of apoE-immunoreactivity. Taken together, the characteristics of amyloid plaques in Tg2576 mice are similar to those in Alzheimer's disease with respect to apoE and astrogliosis. Furthermore, apoE deposition and astrogliosis may be necessary for amyloid plaque maturation.

Mechanism for bone invasion of oral cancer cells mediated by interleukin-6 in vitro and in vivo.

BACKGROUND: Osteoclastic bone resorption is an important step in bone invasion in several malignancies. Although interleukin (IL)-6 accelerates osteoclastic bone resorption, it remains unclear whether IL-6 may be involved in bone invasion of oral cancer. METHODS: The pit formation assay with calf femur-derived bone slices was performed to examine the bone-resorbing activity of osteoclasts and cancer cells. The chemotaxis activity of the culture media was analyzed by the use of Boyden chamber technique. Nude mice, which were inoculated with IL-6-producing oral cancer cells into masseter, were treated with anti-IL-6 neutralizing antibody, and mandibular-bone invasion of the cells was assessed. RESULTS: BHY, a bone-invasive oral cancer cell line, but not HNT, a noninvasive cell line, produced large amounts of IL-6. In a pit formation assay, addition of conditioned medium (CM) derived from BHY but not HNT increased osteoclastic bone resorption, and the effects were inhibited by anti-IL-6 antibody. BHY-secreted IL-6 showed significant chemotaxis activity for osteoclasts. Of note, CM from the cocultivation of osteoclasts and BHY markedly enhanced the cancer cell migration, and the chemotaxis activity was significantly reduced when anti-IL-6 antibody was added into the coculture and then CM were collected, but not when the antibody was added into the CM after they were collected. Furthermore, treatment with anti-IL-6 antibody almost completely inhibited mandibular bone invasion of BHY in nude mice. CONCLUSIONS: These results strongly suggest that IL-6 secreted by oral cancer cells plays a significant role in bone invasion.

Expression of cathepsin K mRNA during experimental tooth movement in rat as revealed by in situ hybridization.

The expression of cathepsin K. a novel collagenolytic enzyme specifically expressed in osteoclasts, was investigated in the rat maxillary dentoalveolar unit during experimental tooth movement by in situ hybridization histochemistry with a non-radioisotopic cRNA probe for rat cathepsin K. Orthodontic elastics were inserted into the interproximal space between the maxillary first and second molars of 7-week-old male SD rats according to Waldo's method and sections prepared from tissues obtained at 12 hr, 1, 2, 3, 4, 7, and 12 days after orthodontic force application. Cathepsin K mRNA expression was detected in the mono- and multinuclear osteoclasts on the pressure side of the alveolar bone at 12 hr after force application, and the distribution and number of cathepsin K mRNA-positive osteoclasts increased time-dependently on the pressure side. At 3-4 days, a marked increase in cathepsin K mRNA-positive osteoclasts was found not only on the pressure side but also on the tension side of the alveolar bone in response to tooth movement. At 7-12 days, the cathepsin K mRNA-positive osteoclasts on both sides had disappeared. These findings suggest that the recruitment of osteoclasts on the pressure side begins during the initial stage of orthodontic tooth movement and the site-specific early induction of cathepsin K mRNA may cause an imbalance in the relative resorption activities on the pressure and tension side incident to such movement.

Histological changes in the rabbit condyle following posterolateral disk perforation.

PURPOSE: To examine changes in condylar cartilage following perforation in the posterolateral region of the articular disk of the craniomandibular joint of a rabbit. MATERIAL AND METHODS: The circular perforation in the left joint of 25 female Japanese white rabbits measured precisely one-sixteenth of a disk. Histological examination, including the immunohistochemical proliferating cell nuclear antigen (PCNA) procedure, was performed on separate sets of five rabbits each 2, 4, 8, 12, and 24 weeks postoperatively. RESULTS: Microscopic examination revealed hypertrophy of the condylar cartilage with osteophyte formation up to 8 weeks after perforation. Proliferative activity then decreased near the condylar surface as the perforation flattened. Twenty-four weeks postoperatively, the condylar surface was found to be fibrous and flattened. Positive PCNA results in cartilage cells indicated proliferation following disk perforation which peaked in the 4th week and then decreased. CONCLUSION: Disk perforation was followed initially by hypertrophy of condylar cartilage, and later by degeneration of the condylar surface. Although osteoarthritic cartilage was found 24 weeks after perforation, degeneration decreased over time. This suggests that remodelling took place after the perforation.

Bacteriological investigation of an outbreak of Clostridium perfringens food poisoning caused by Japanese food without animal protein.

An outbreak of Clostridium perfringens food poisoning occurred in a senior citizen's home in Japan. Japanese food, spinach boiled with fried bean curd, was considered to be the causative food as a result of the detection of the C. perfringens enterotoxin gene by nested PCR. The number of enterotoxin-positive C. perfringens was enumerated as 4.3 x 10(5)/g in the causative food by the MPN method combined with nested PCR. By cultivation, enterotoxin-positive C. perfringens was isolated from all the fecal specimens of patients tested and the causative food. The isolates from patients were serotypable, heat-resistant and the majority produced enterotoxin, however most isolates from the causative food were nonserotypable, enterotoxin-negative and heat-sensitive.