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Y Ohta

Publications and source records attributed to Y Ohta.

At least 307 records · Page 17Linked to original sources
PubMed1997

Reduction of disease causative T-cells in experimental autoimmune disease models by a new antirheumatic drug, TAK-603.

We investigated the mode of action of a new quinoline derivative, TAK-603 (ethyl 4-(3,4-dimethoxyphenyl)-6,7-dimethoxy-2-(1,2,4-triazol-1-ylmeth yl) quinoline-3-carboxylate), in adjuvant arthritis (AA), a model of rheumatoid arthritis. AA rat splenocytes transferred the arthritis to normal syngeneic rats upon inoculation, but the cells from AA rats treated with TAK-603 (6.25 mg/kg/day) caused only mild arthritis with significantly less foot pad swelling and a lower arthritis score. An effect of TAK-603 in the induction phase of AA was suggested. TAK-603 had little effect on CD4+ and CD8+ T-cell populations in the AA rat splenocytes. We therefore estimated the frequency of T-cells which are reactive to the so-called disease causative antigen using a limiting dilution assay (LDA). The ratio of T-cells responsive to PPD, which increased in AA rat splenocytes with the severity of the arthritis, was reduced in AA rats treated with TAK-603. Furthermore, the ratio of MBP (myelin basic protein)-reactive T-cells, which were generated in experimental allergic encephalomyelitis (EAE) rats, were also reduced by TAK-603 administration. These data suggest that TAK-603 acts on the immune system and reduces the number of cells reactive to the relevant antigen.

Animals↗
PubMed1997

Digital fluorescence imaging of elementary steps of neurosteroid synthesis in rat brain glial cells.

With fluorescence microscopic imaging, we have examined Ca2+ signaling, LDL uptake and distribution of cytochrome P450 scc on individual rat brain glial cells in order to investigate the molecular mechanisms of neurosteroid synthesis. Astrocytes and oligodendrocytes were cultured from newborn rat brain. Ca2+ signaling was observed in Calcium Green-1 loaded astrocytes upon neurotransmitter stimulations using video-enhanced microscopy. Upon stimulation of serotonin and glutamate, we observed typically three types of Ca2+ signaling which were Ca2+ oscillations, a transient increase in Ca2+ concentration and Ca2+ oscillations superimposed on a transient Ca2+ increase. On the other hand, histamine and ATP induced only a transient increase in Ca2+ without oscillatory response. Uptake of octadecyl rhodamine (R18) labeled LDL by astrocytes and oligodendrocytes was observed in the time scale of 30 min with confocal laser scanning microscopy. Some localization of LDL in the cytoplasm was observed for astrocytes. For oligodendrocytes, incorporated LDL was distributed over the entire cytoplasmic region of both cell body and multiple branched cell processes. The presence of a significant amount of cytochrome P450 scc was demonstrated with immunofluorescence staining in both astrocytes and oligodendrocytes. The density of P450 scc in both glial cells was suggested to be around 1% of that in bovine adrenocortical fasciculata cells. The results lead to an improved quantitative picture of neurosteroid synthesis in glial cells.

Adrenal Cortex↗
PubMed1997

Modulating role of endogenous reduced glutathione in tert-butyl hydroperoxide-induced cell injury in isolated rat hepatocytes.

The role of endogenous reduced glutathione (GSH) in tert-butyl hydroperoxide (TBHP)-induced cell injury was examined in isolated rat hepatocytes. When liver cell injury was estimated from release of transaminases from hepatocytes into the incubation medium, cell injury in hepatocytes (2 x 10(6) cells/ml) incubated in Hanks' balanced salt solution (pH 7.2) containing 1.0 mM TBHP at 37 degrees C was potentiated with enhanced lipid peroxidation by prior depletion of intracellular GSH which was induced by diethylmaleate, a GSH depletor. GSH-depleted hepatocytes were incubated with gamma-glutamylcysteinylethyl ester (gamma-ECOEt), which is known to be converted to GSH via glutathione synthetase after its hydrolysis by esterase, at concentrations of 1.0 to 10 mM in order to replenish intracellular GSH. Although TBHP-induced cell injury and lipid peroxidation were enhanced in GSH-depleted hepatocytes, these enhancements were prevented with the consumption of intracellular GSH in GSH-depleted hepatocytes pretreated with 5.0 mM gamma-ECOEt. These preventive effects were observed at any time point during the TBHP treatment over a 60 min period and depended on the concentration of gamma-ECOEt used. But, no preventive effect was found in GSH-depleted hepatocytes pretreated with 5.0 mM GSH. No prevention of the potentiation of TBHP-induced cell injury found in GSH-depleted hepatocytes occurred in GSH-depleted hepatocytes pretreated with both 5.0 mM gamma-ECOEt and 250 microM bis-(p-nitrophenyl)phosphate, a nonspecific esterase inhibitor. gamma-ECOEt treatment caused an increase in intracellular GSH content in GSH-depleted hepatocytes, while treatments of both gamma-ECOEt and the esterase inhibitor caused no increase in intracellular GSH content in the cells. These results indicate that endogenous GSH modulates TBHP-induced cell injury and lipid peroxidation in isolated rat hepatocytes. The present results suggest that endogenous GSH should play a critical role in TBHP-induced cell injury in isolated rat hepatocytes and that in rat hepatocytes treated with TBHP, enhanced lipid peroxidation with the consumption of intracellular GSH could be associated with the initiation of cell injury.

Alanine Transaminase↗
PubMed1997

Arthrobacter ureafaciens sialidase isoenzymes, L, M1 and M2, cleave fucosyl GM1.

Among bacterial, fungal and viral sialidases, the sialidase from Arthrobacter ureafaciens has the unique property of cleaving sialic acids linked to the internal galactose of gangliotetraose. In this study, we examined the ability to cleave the internal sialic acids of GM1 and fucosyl GM1 of sialidases from several bacterial and fungal origins, including Clostridium perfringens and Vibrio cholerae. We found that A. ureafaciens sialidase could liberate the sialic acid of GM1 at the highest rate, and was the only enzyme which could cleave fucosyl GM1 among the sialidases examined. The affinity-purified sialidase derived from the culture medium of A. ureafaciens was comprised of four isoenzymes with different molecular weights and isoelectric points, the isoenzymes that cleaved fucosyl GM1 being L (88 kDa, pl 5.0), M1 (66 kDa, pl 6.2) and M2 (66 kDa, pl 5.5), but not S (52 kDa, pl 6.2) which showed the highest specific activity toward colominic acid among the four isoenzymes.

Animals↗
PubMed1997

Relationship between changes of active oxygen metabolism and blood flow and formation, progression, and recovery of lesions is gastric mucosa of rats with a single treatment of compound 48/80, a mast cell degranulator.

The relationship between the changes of active oxygen metabolism and blood flow and the formation, progression, and recovery of lesions was examined in the gastric mucosa of rats treated once with compound 48/80, a mast cell degranulator. Gastric mucosal lesions appeared 0.5 hr after compound 48/80 treatment, became worst at 3 hr, and recovered fairly well at 12 hr. Increases in gastric mucosal lipid peroxide content and xanthine oxidase and myeloperoxidase activities and decreases in gastric mucosal vitamin E and hexosamine contents and Se-dependent glutathione peroxidase activity occurred with the formation and progression of gastric mucosal lesions. These changes were attenuated with the recovery of the lesion. Gastric mucosal nonprotein SH content decreased with the formation of gastric mucosal lesions, and this decreased SH content returned to near the original level with lesion progression. No changes in gastric mucosal superoxide dismutase and catalase activities occurred with the formation, progression, and recovery of gastric mucosal lesions. Gastric mucosal blood flow decreased with the formation of gastric mucosal lesions, and this decreased blood flow recovered with lesion progression. Serum serotonin concentration, an index of mast cell degranulation, increased with the formation of gastric mucosal lesions, and this increased serotonin level was attenuated with lesion progression and recovery. Pretreatment with ketotifen, a connective tissue mast cell stabilizer, prevented the formation of gastric mucosal lesions, the increases of gastric mucosal lipid peroxide content, xanthine oxidase and myeloperoxidase activities, and serum serotonin level; and the decreases of gastric mucosal nonprotein SH content, glutathione peroxidase activity, and blood flow found at 0.5 hr after compound 48/80 treatment. These results indicate that the changes of gastric mucosal active oxygen metabolism and blood flow are closely related to the formation, progression, and recovery of gastric mucosal lesions in rats with a single compound 48/80 treatment. The present results also suggest that this compound 48/80-induced gastric mucosal injury could be a kind of ischemia-reperfusion-induced injury occurring through degranulation of connective tissue mast cells.

Animals↗
PubMed1997

Vascular endothelial growth factor and lymph node metastasis in primary lung cancer.

The relationship between vascular endothelial growth factor (VEGF) and lymph node metastasis was studied in 90 cases of primary lung cancer without distant metastasis. As a result of quantitative reverse transcription polymerase chain reaction (RT-PCR) analysis, the VEGF121 mRNA expression levels in lung cancer tissues with nodal metastasis (n = 35) were higher than in those without nodal metastasis (n = 55). However, no significant difference could be found in VEGF121 mRNA expression levels as stratified by tumour size (T1N0M0 vs T2N0M0). Simultaneously, ten lymph nodes (four node positive and six node negative) together with the corresponding primary lung tumours and adjacent normal lung tissue, were studied for VEGF expression. The VEGF mRNA expression in metastatic lymph nodes was intense in three out of the four cases examined. Further, while VEGF expression levels in metastatic lymph nodes were conspicuously higher than those for the primary site, all its expression levels in non-metastatic nodes were inferior to those of the primary tumours. Except for macrophages, the VEGF antigen was identified mainly in the cytoplasm of metastatic cancer cells and the endothelial cells of blood or lymphatic vessels in lymph nodes. Although the detailed mechanisms and the significance of strong VEGF expressions in metastatic lymph nodes are still unknown, these data are consistent with a model whereby VEGF increases the opportunity for nodal metastasis through neoblood and lymphatic vessels.

Aged↗
PubMed1997

Inhibition of lymph node metastasis by an anti-angiogenic agent, TNP-470.

We assessed the inhibitory action of TNP-470 on lymph node metastasis in a metastatic model system using athymic nude mice. Mice were injected subcutaneously with 5 x 10(6) HT-1080 cells in the right groin. TNP-470 (10, 30 and 100 mg kg-1) was injected subcutaneously nine times in total every other day from the 7th day after tumour inoculation. Axillar and inguinal lymph nodes were dissected, and DNA was extracted 5 weeks after tumour inoculation. Specific detection of a human beta-globin-related sequence in metastasized human tumour cells in nude mice was done by the polymerase chain reaction (PCR) technique and analysed by Southern blotting. Anti-tumour effects on primary sites were seen only in the 100 mg kg-1 treatment group. Lymph node metastasis of transplanted HT-1080 cells was seen in all mice of the no treatment group (5/5). On the other hand, incidences of lymph node metastasis in treated mice were 2/4 mice (100 mg kg-1, 2/5 mice (30 mg kg-1) and 4/5 mice (10 mg kg-1). The inhibition ratios of lymph node metastasis were 82.3% at 10 mg kg-1, 97.2% at 30 mg kg-1 and 97.5% at 100 mg kg-1 respectively. This agent may be useful to inhibit lymph node metastasis.

Animals↗
PubMed1997

TAK-603 selectively suppresses Th1-type cytokine production and inhibits the progression of adjuvant arthritis.

We have shown that TAK-603, a new anti-rheumatic drug, is more effective in animal models in which cellular immunity plays a central role. Here, we studied the effect of the drug on Th1 cytokines, which are dominantly produced in this type of immune reaction, in an in vitro system and an in vivo model. We established Th1- and Th2-dominant T-cell lines, and studied the effect of TAK-603 on their cytokine production. Th1 cell lines were BALB/c mouse allo-reactive T cells and C57BL mouse mite antigen-reactive T cells, and the Th2 cell line was BALB/c mouse ovalbumin-reactive T cells. TAK-603 suppressed the production of Th1 cytokines [interferon-gamma (IFN-gamma) and interleukin-2 (IL-2)] and not that of Th2 cytokines (IL-4, IL-5) in these cell lines. Furthermore, selective suppression of Th1 cytokine production was also observed in the T-cell clones obtained from the ovalbumin-reactive T-cell line. To investigate the effect on cytokine production in animal models of arthritis, we analysed the expression of cytokine messenger RNA using reverse transcription-polymerase chain reaction. In adjuvant arthritis rats, Th1-dominant cytokine production was observed both in the arthritic joint and the spleen, and the time-course paralleled the progression of arthritis. On the other hand, in type-II collagen-induced arthritis, in which TAK-603 has little effect, Th1-dominant cytokine production was not observed and Th2 cytokines were shown to be more important. The adjuvant arthritis rats treated with TAK-603 (6.25 mg/kg/day, per os) showed significantly lower cytokine mRNA expression both locally and systemically. These data suggest that TAK-603 selectively suppresses Th1 cytokine production, which is consistent with its effect on cellular immunity in animal models.

Animals↗
PubMed1997

Occurrence of two missense mutations in Cu-ATPase of the macular mouse, a Menkes disease model.

We have investigated the genetic defect of the Cu-ATPase gene (Atp7a) in the macular mouse, a genetic model of classical Menkes disease. Northern blot analysis showed that its placenta and kidney possess a normal amount of the Cu-ATPase mRNA of the normal size; sequencing analysis revealed two missense mutations, His674Arg and Ser1381 Pro, in a PCR-amplified cDNA for mutant Cu-ATPase. The latter mutation was suspected to affect the function of the ATPase, because it lies in the transmembrane segment that is thought to form a channel for the transportation of copper ions.

Adenosine Triphosphatases↗
PubMed1997

Preventive action of vitamin E-containing liposomes on cataractogenesis in young adult rats fed a 25% galactose diet.

The preventive action of vitamin E (Vit. E)-containing liposomes on cataractogenesis was examined in male Wistar rats (five weeks old) fed a 25% galactose diet. Vit. E-containing liposomes prepared with dipalmitoylphosphatidylcholine were instilled into both eyes three times a day over a 45-day period. Cataract appeared at 18-day galactose feeding and developed gradually thereafter. Simultaneous Vit. E-containing liposome instillation delayed this cataractogenesis. Lenses of 18-day galactose-fed rats showed decreases in Vit. E and reduced glutathione (GSH) contents and Na+, K(+)-ATPase activity and increases in lipid peroxide (LPO), galactitol, and water contents. Lenses of 45-day galactose fed rats showed decreases in GSH content and Na+,K(+)-ATPase activity and increases in Vit. E, LPO, galactitol, and water contents. Serum Vit. E and cholesterol levels decreased in 18-day galactose-fed rats, while both levels increased in 45-day galactose-fed rats. Simultaneous Vit. E-containing liposome instillation prevented these changes except for the changes of lenticular galactitol and water contents and serum Vit. E and cholesterol levels. These results indicate that simultaneously instilled Vit. E-containing liposomes can delay cataractogenesis in young adult rats fed a 25% galactose diet mainly by the antioxidative action of Vit. E contained in the instilled liposomes.

Animals↗
PubMed1997

Increased production of B-cell growth factor by T lymphocytes in Graves' thyroid: possible role of CD4+ CD29+ cells.

The possible role of B-cell growth factor (BCGF) in the abnormal activation of B cells in Graves' disease was investigated by measuring the production of BCGF by, and analyzing lymphocyte subsets of, peripheral blood cells and thyroid infiltrates from 10 patients with Graves' disease and peripheral blood cells from 9 healthy controls. Medium from peripheral blood and intrathyroidal T cells cultured in the absence or presence of phytohemagglutinin (PHA) was subjected to a bioassay with a cell line, KS-3.F10, responsive only to BCGF. The percentages of activated (DR+CD4+ and DR+CD8+) T cells in the thyroid of Graves' patients were significantly higher than those in the peripheral blood of patients or controls, whereas the percentage of naive (CD4+CD45RA+) T cells was lower. The percentage of B (CD20+) cells in peripheral blood was increased in patients compared with controls. BCGF production by T cells from the thyroid or peripheral blood of Graves' patients, in the absence or presence of PHA, was significantly greater than that by peripheral T cells from healthy controls. PHA-stimulated BCGF production by peripheral T cells of Graves' patients showed a significant negative correlation with the percentage of DR+CD8+ cells in peripheral blood, whereas spontaneous and PHA-stimulated BCGF production by intrathyroidal T cells from Graves' patients showed a positive correlation with the serum concentrations of triiodothyronine (T3) or thyroxine (T4). The different distributions of CD4+ T-cell subsets between thyroid and peripheral blood suggest an important role for intrathyroidal helper/suppressor-inducer (CD4+CD29+) cells in the increased production of BCGF and consequent exacerbation of autoimmunity in Graves' disease.

Adult↗
PubMed1997

The effect of priming with vecuronium and rocuronium on young and elderly patients.

UNLABELLED: The priming principle consists of administering a subparalyzing dose of nondepolarizing neuromuscular blocking drug 3-6 min before giving a second dose for tracheal intubation. This study was performed to observe the effects of priming doses of vecuronium and rocuronium on pulmonary function tests and muscular weaknesses in young (25-35 yr of age) and elderly (65-73 yr of age) patients. Ten young and 10 elderly patients were each placed in vecuronium and rocuronium groups. Oxygen saturation and train-of-four (TOF) ratio were determined, and pulmonary function tests were performed. Then 20% of the 95% effective dose (ED95) of the muscle relaxants was given intravenously. All tests were performed again 4 min after vecuronium and 3 min after rocuronium. Other signs of muscular weaknesses were also recorded. Elderly patients showed more signs of muscle weakness in both groups. The TOF ratio was 0.77 and 0.79 in the elderly rocuronium and vecuronium groups, respectively, and 0.89 and 0.90 in the young rocuronium and vecuronium groups, respectively. Dynamic spirometry revealed decreases in forced expiratory volume in 1 s and forced vital capacity in both groups, and no significant changes in peak expiratory flow rate. The expiratory reserve volume was reduced more in the elderly groups. Oxygen saturation decreased in both groups. We conclude that oxygen saturation, pulmonary function, and muscle strength decrease more in the elderly than in their younger counterparts from priming doses of vecuronium or rocuronium. IMPLICATIONS: The priming principle consists of giving a subparalyzing dose of muscle relaxant 3-6 min before giving a second dose for tracheal intubation. We found that priming doses of vecuronium and rocuronium produced greater decreases in oxygen saturation and pulmonary function in the elderly (aged 65-73 yr) than their younger (aged 25-35 yr) counterparts. Priming may not be a safe approach in elderly patients.

Adult↗
PubMed1997

Pressure support ventilation augments spontaneous breathing with improved thoracoabdominal synchrony in neonates with congenital heart disease.

UNLABELLED: In neonates, during spontaneous breathing with demand-type continuous positive airway pressure (CPAP), high airway resistance caused by small endotracheal tubes, time delay for triggering, and rapid respiratory frequency may result in patient-ventilator asynchrony. Such asynchrony may alter normal breathing patterns and thoracoabdominal synchrony. We, therefore, studied whether pressure support ventilation (PSV) could augment spontaneous breathing and improve synchrony between the rib cage (RC) and the abdominal (AB) motions in nine postoperative neonates with congenital heart disease. Three successive levels of PSV (0, 5, and 10 cm H2O) were used randomly. With increasing levels of PSV, the tidal volume (VT) increased and the respiratory frequency decreased, associated with an increase in minute ventilation. To assess thoracoabdominal synchrony, maximum compartment amplitude (MCA)/VT (MCA = AB + RC) and the phase delay of the RC-to-AB motion during inspiration (the ratio of the time delay to the inspiratory time) were measured using respiratory inductive plethysmography. When the motions of the RC and AB were out of phase, MCA/VT exceeded 1.0. MCA/VT decreased significantly from 1.3 +/- 0.3 without PSV to 1.0 +/- 0.0 with PSV of 10 cm H2O. The phase delay and paradoxical motion of the RC observed in seven of the nine cases without PSV also disappeared with PSV of 10 cm H2O. In conclusion, PSV can effectively augment spontaneous breathing with better thoracoabdominal synchrony in neonates. IMPLICATIONS: Assisting spontaneous ventilation in a neonate is often difficult. Because pressure support ventilation facilitates coordination between the patient and ventilator in adults and children, we thought it might be effective in neonates. Our study supports this conclusion.

Abdomen↗
PubMed1997

Characterization of adenosine receptors mediating spinal sensory transmission related to nociceptive information in the rat.

BACKGROUND: Adenosine analogs have been shown to produce antinociception after intrathecal administration. To determine the adenosine receptor subtype involved in spinal antinociception, the effects of selective agonists and an antagonist on the evoked potentials recorded from a neonatal rat spinal cord were studied. The measured potentials are a slow ventral root potential (slow VRP), which is the C-fiber-evoked excitatory response associated with nociceptive information; a monosynaptic reflex (MSR), which reflects a non-nociceptive transmission related to motor function; and a dorsal root potential (DRP), which reflects a gamma-aminobutyric acidA (GABA(A)) receptor-mediated presynaptic inhibition associated with analgesia. METHODS: The evoked potentials were recorded in response to electric stimulation of a lumbar dorsal root. Dose-response curves of agonists for these responses were obtained to determine their relative potency order. The antagonist dissociation constants (K(D) values) were estimated by Schild analysis. RESULTS: Adenosine agonists dose dependently inhibited the slow VRP and the MSR. However, the slow VRP was five to eight times more sensitive to them than was the MSR. The rank order of agonist potency was N6-cyclohexyladenosine (CHA) = N6-(R)-phenylisopropyladenosine (R-PIA) > 5'-N-ethylcarboxamidoadenosine (NECA) >> CGS 21680 in both responses. 8-Cyclopentyltheophylline produced dose-dependent parallel shifts to the right of NECA dose-response curves for these responses. Schild analysis gave linear plots with slopes near unity. The K(D) values of CPT for the MSR and the slow VRP were estimated to be 5.5 nM and 4.3 nM, respectively. The DRP was also depressed by adenosine agonists with potency order of CHA > NECA >> CGS 21680. 8-Cyclopentyltheophylline antagonized the inhibitory effects of CHA on the DRP. CONCLUSIONS: The results indicate that adenosine agonists inhibit spinal sensory transmission related to nociception by acting at the A1 receptors. The A1 receptor also seems to be involved in transmission related to the spinal motor system. Feedback inhibition mediated by GABA(A) receptors does not contribute to this antinociceptive action.

Adenosine↗
PubMed1997

Lichen planus and Sjögren-type sicca syndrome in a patient with chronic hepatitis C.

We report a 54-year-old Japanese male with lichen planus and Sjögren-type sicca syndrome, accompanied by the latent complication of chronic hepatitis C. The patient first showed erythematous and erosive lesions with white irregular striae in the buccal mucous membrane, and blepharitis and hyperemia of conjunctiva in his eyes. He later had two small erosions on the glans penis, and flat-topped violaceous papules on the dorsa manus and nape. A biopsy specimen of the lower lip lesion demonstrated a lichenoid tissue reaction at the basement membrane zone, and lymphocytic focal accumulations in the salivary glands. Immunohistochemical study of this specimen revealed CD45RO- (T) cells associated with the expression of HLA-DR antigens predominantly in both the lichenoid tissue reaction and the lymphocytic sialadenitis. Objective keratoconjunctivitis sicca was confirmed by the Schirmer and Rose-Bengal tests. Anti-DNA antibody was positive; however anti-SS-A, and anti-SS-B antibodies were negative. Increased levels of transaminase enzymes, TTT, ZTT, and IgG were observed in first laboratory examinations; thereafter, antihepatitis C virus (HCV) antibodies and HCV-RNA were detected. The high serum amylase level, in which salivary amylase predominated, was normalized by etretinate therapy in parallel with the clinical improvement of the oral LP lesions. Our case is considered to support the hypothesis that an etiologic association may be present among lichen planus, Sjögren's syndrome, and chronic hepatitis C.

Amylases↗
PubMed1997

A case report of twenty-nail dystrophy.

A case report of twenty-nail dystrophy in a 21-year-old woman is presented. All her finger nails were affected with numerous small superficial pits. The histological findings showed the focal spongiotic change in the nail matrix reflecting the clinical appearance of the nail plate surface.

Adult↗
PubMed1997

Two distinct human uterine cervical epithelial cell lines established after transfection with human papillomavirus 16 DNA.

We have established two distinct human cervical cell lines, NCC16 and NCE16, after transfecting human papillomavirus type 16 (HPV16) DNA into normal human ecto-cervical and endo-cervical epithelial cells, respectively. Both lines expressed HPV16 E6 and E7 as detected by reverse transcriptase-polymerase chain reaction and northern blot hybridization. These cells have been passaged for over 100 population doublings and express strong telomerase activity. Neither cell line was tumorigenic in athymic nu/nu mice. However, both NCC16 and NCE16 developed abnormally stratified architectures following implantation with a silicon membrane sheet in the back of athymic nude mice. The former cells were pathohistologically similar to carcinoma, while the latter produced Alcian-blue positive cells, suggesting the occurrence of metaplastic changes. These distinct cell lines offer a useful model system for the study of cervical carcinogenesis and of its regulatory mechanism after HPV infection in different regions of the uterine cervix.

Animals↗