Biomedical subjects

H Matsubara

Publications and source records attributed to H Matsubara.

At least 73 records · Page 4Linked to original sources

PubMed2000

Serum p53 antibody is a useful tumor marker in superficial esophageal squamous cell carcinoma.

BACKGROUND: Patients with superficial (mucosal or submucosal) esophageal carcinoma (SEC) have significantly better survival rates than patients with advanced carcinoma. Some patients with advanced esophageal carcinoma have been reported to test positive for serum p53 antibodies (Abs). Because very few patients with superficial carcinoma have been examined, the aim of this study was to evaluate the clinical significance of serum p53-Abs in patients with superficial esophageal squamous cell carcinoma (SESCC). METHODS: Thirty-five consecutive patients with SESCC were studied for serum p53-Abs by enzyme-linked immunoabsorbent assay before and after treatment. The clinicopathologic features of p53 seropositive and p53 negative patients were compared. The relation between the presence of serum p53-Abs and p53 immunoreactivity of the resected specimens was examined. Three tumor markers (squamous cell carcinoma antigen [SCC-Ag], CYFRA21-1, and carcinoembryonic antigen [CEA]) were assessed to compare their sensitivities with serum p53-Abs. RESULTS: Fourteen of 35 patients (40%) were p53 seropositive. Relatively few patients tested positive for the other tumor markers: CEA, 11.4%; SCC-Ag, 14.3%; CYFRA21-1, 5.7%. There were no significant correlations between clinicopathologic features and p53 seropositivity except for tumor location. A strong correlation between p53 immunostaining and the presence of serum p53-Abs was observed (P = 0.003). Of the 14 patients with seropositive results, 12 turned seronegative after resection, and the other 2 experienced disease recurrence. CONCLUSIONS: Surveillance of serum p53-Abs is superior to the three tumor markers for detecting SESCC. This serum marker is also useful for the detection of p53 protein overexpression and for the monitoring of residual tumor cells.

Aged↗

PubMed2000

Angiotensin II initiates tyrosine kinase Pyk2-dependent signalings leading to activation of Rac1-mediated c-Jun NH2-terminal kinase.

Ca(2+)-sensitive tyrosine kinase Pyk2 was shown to be involved in angiotensin (Ang) II-mediated activation of extracellular signal-regulated kinase (ERK) via transactivation of epidermal growth factor receptor (EGF-R). In this study, we tested the involvement of Pyk2 and EGF-R in Ang II-induced activation of JNK and c-Jun in cardiac fibroblasts. Ang II markedly stimulated JNK activities, which were abolished by genistein and intracellular Ca(2+) chelators but partially by protein kinase C depletion. Inhibition of EGF-R did not affect Pyk2 and JNK activation by Ang II. Stable transfection with a dominant negative (DN) mutant for Pyk2 (PKM) completely blocked JNK activation by Ang II. DN mutants of Rac1 (DN-Rac1) and MEK kinase (DN-MEKK1) also abolished it, whereas those of Cdc42, RhoA, and Ha-Ras had no effect. Induction of c-Jun gene transcription by Ang II was abolished in PKM, DN-Rac1, and DN-MEKK1, in which Ang II-induced binding of ATF2/c-Jun heterodimer to the activator protein-1 sequence at -190 played a key role. These results suggest that 1) in cardiac fibroblasts activation of JNK and c-Jun by Ang II is initiated by Pyk2-dependent signalings but not by downstream signals of EGF-R or Ras, 2) Rac1 but not Cdc42 is required for JNK activation by Ang II upstream of MEKK1, and 3) ATF-2/c-Jun binding to the activator protein-1 sequence at -190 plays a key role for induction of c-Jun gene by Ang II.

Angiotensin II↗

PubMed2000

Plasma endothelin-1 and thrombomodulin levels in coronary sinus during right atrial pacing and percutaneous transluminal coronary angioplasty.

Increases in the levels of plasma endothelins (ETs) have been reported after percutaneous transluminal coronary angioplasty (PTCA). To examine the mechanism of this increase, we measured plasma endothelin-1 (ET-1) and thrombomodulin (TM) levels in both the Valsalva sinus (VAL) and the great cardiac vein (GCV) together with oxygen saturation of the GCV (Sat.GCVO2) during right atrial pacing and PTCA. Thirty patients with stenoses in the left anterior descending coronary arteries were enrolled. A fiberoptic pulmonary artery catheter was placed in GCV for monitoring Sat.GCVO2, and blood sampling was repeated before and after each procedure. ET-1 did not increase during pacing, but after PTCA it significantly increased from basal levels to 24.4+/- 8.3 pg/ml in GCV (P<0.01) and 19.3 +/-7.4 in VAL (P<0.05). Basal TM levels in GCV and VAL were significantly higher in diabetic than in non-diabetic patients, but TM did not change during pacing and PTCA. Sat.GCVO2 significantly decreased from the basal level during pacing and PTCA. We speculate that direct endothelial cell damage is more responsible for the increase of ET-1 during PTCA than myocardial ischemia. Our data indicate that ET-1 may be a useful marker for acute endothelial damage, while TM reflects only chronic and general damage of endothelial cells.

Aged↗

PubMed2000

HTLV-I specific IFN-gamma+ CD8+ lymphocytes correlate with the proviral load in peripheral blood of infected individuals.

Human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is an inflammatory neurological disease caused by HTLV-I infection. It has been shown that HAM/TSP patients have high proviral loads and an extraordinarily high frequency of circulating CD8 + cytotoxic T lymphocytes specific for HTLV-I in their peripheral blood when compared to asymptomatic HTLV-I carriers (AC). We have previously described an intracellular cytokine detection assay, in which interferon-gamma (IFN-gamma) + CD8 + lymphocytes are specific for HTLV-I in infected individuals. Here, we have established a competitive polymerase chain reaction assay to measure the proviral load of patients and investigate a potential relationship between proviral load and virus-specific CD8 + lymphocytes. Genomic DNA was extracted from peripheral blood lymphocytes (PBL) from eight HAM/TSP patients and seven AC for the measurement of HTLV-I measuring proviral loads. The same PBL were analyzed for intracellular IFN-gamma expression by flow cytometry. In the HAM/TSP patients and AC, the average proviral loads were 34,482 and 9784 copy/microg DNA (P = 0.021), and the average of IFN-gamma + CD8 + lymphocytes in total PBL were 1.47 and 0.08% (P = 0.001), respectively. It was confirmed that HAM/TSP patients have both high proviral loads and increased HTLV-I-specific CD8 + lymphocytes. Furthermore, we found a positive correlation between both factors in the patients with HAM/TSP (P = 0.044) but not in the AC (P = 0.508). These findings suggest that the high number of HTLV-I-specific lymphocytes may result from the increased proviral load in HAM/TSP patients.

Aged↗

PubMed2000

A feasibility study of chemosensitivity assay by adhesive tumor cell culture system using biopsy specimens for gastric cancer.

BACKGROUND AND OBJECTIVES: The adhesive tumor cell culture system (ATCCS) is known to produce high colony-forming efficiency. We, therefore, studied the feasibility of ATCCS for gastric cancer by use of biopsy specimens and the relationship between the results of ATCCS and histological effects of anticancer drugs. METHODS: Tumor specimens extracted by gastroendoscopic biopsy were sufficient for obtaining the result of sensitivity to at least one drug in 24 out of 30 (80%) patients. Twenty patients were administered 5-fluorouracil (5-FU) for 14 days prior to surgery, and the results of ATCCS were compared with histological changes of the resected specimens. RESULTS: The histological response rate was found to be 100% (4/4) when the 90% inhibition concentration (IC90) of 5-FU was less than 0.24 microg/ml (sensitive) and was 0% (0/3) when IC90 was greater than 0.40 microg/ml (resistant). CONCLUSIONS: Although lacking in statistical significance, the results suggest that the drug to which the tumor revealed sensitivity in the ATCCS would produce histological effects and the drug to which the tumor was resistant would have no histological effect.

Aged↗

PubMed2000

Gene therapy for cancer.

The basic strategies for gene therapy that have been explored include immunogene therapy such as cytokine gene transfer, selective prodrug activation, so-called suicide genes, transfer of a tumor suppressor gene, and inhibition of activated oncogenes by antisense mechanisms. Many therapeutic protocols have so far been registered in the office of the Recombinant DNA Advisory Committee, NIH, as of June 1999. Regarding the basic research in gene therapy, we planned a clinical application of gene therapy for an esophageal cancer patient at our institution. We review herein the present status of gene therapy for cancer overseas, and describe a protocol of clinical trials for gene therapy for esophageal cancer at our institution.

Clinical Protocols↗

PubMed2000

TT virus infection among renal transplant recipients.

To clarify the prevalence of TT virus (TTV) infection in renal transplant recipients and to estimate the role of TTV in patients with post-transplant liver function abnormalities, TTV-DNA of 47 renal transplant recipients was screened by polymerase chain reaction (PCR) according to a method described by Okamoto et al. before and after the renal transplantation. One of them was positive for hepatitis B surface antigen (HBsAg), one was positive for anti-hepatitis C virus (HCV) and other 45 were negative for both HBsAg and anti-HCV. TTV-DNA was detected in 22 of 47 patients before renal transplantation, and nine became positive after transplantation. All 47 patients showed a normal level of ALT before transplantation. Three of nine (33%) who became positive for TTV-DNA after transplantation and three of 16 (19%) who were negative for TTV-DNA before and after transplantation showed transient elevation of ALT. These results indicate that TTV was highly prevalent among renal transplant recipients, but a clear association between TTV and post-transplant liver function abnormality was not found.

Journal Article↗

PubMed2000

Transactivation of EGF receptor induced by angiotensin II regulates fibronectin and TGF-beta gene expression via transcriptional and post-transcriptional mechanisms.

The signaling cascade elicited by angiotensin II (Ang II) resembles that characteristic of growth factor, and recent evidence indicates transactivation of epidermal growth factor receptor (EGF-R) by G protein-coupled receptors. Here, we report the involvement of EGF-R in Ang II-induced synthesis of fibronectin and TGF-beta in cardiac fibroblasts. Ang II stimulated fibronectin mRNA levels dose-dependently with a maximal increase (approximately 5-fold) observed after 12 h of incubation. Ang II-, or calcium ionophore-induced fibronectin synthesis was completely abolished by tyrosine kinase inhibitors and intracellular Ca2+ chelating agents. Ang II-induced fibronectin mRNA was not affected by PKC inhibitors or PKC depletion, whereas specific inhibition of EGF-R function by a dominant negative EGF-R mutant and tyrphostin AG1478 abolished induction of fibronectin mRNA. We isolated the rat fibronectin gene including the 5'-flanking region and found that the AP-1 binding site present in the promoter region was responsible for the Ang II responsiveness of this gene. Gel retardation assay revealed the binding of nuclear protein to the AP-1 site, which was supershifted with anti-c-fos and anti-c-jun but not anti-ATF-2 antibodies. Conditioned medium from Ang II-treated cells contained TGF-beta bioactivity and addition of neutralizing TGF-beta antibody modestly (46%) inhibited induction of fibronectin. Ang II-induced synthesis of TGF-beta was also abolished by inhibition of EGF-R function. The effect of TGF-beta was exerted by stabilizing fibronectin mRNA without affecting the promoter activity and required de novo protein synthesis. We concluded that Ang II-induced expression of fibronectin and TGF-beta is mediated by downstream signaling of EGF-R transactivated by Ca2+-dependent tyrosine kinase, and that Ang II-induced fibronectin mRNA expression is regulated by two different mechanisms; transcriptional control by binding of c-fos/c-jun complex to the AP-1 site, and post-transcriptional control by mRNA stabilization due to autocrine and/or paracrine effects of TGF-beta. Thus, this study suggested that the action of Ang II on extracellular matrix formation should be interpreted in association with the EGF-R signaling cascade.

Angiotensin II↗

PubMed2000

Vogt-Koyanagi-Harada syndrome in a pregnant patient treated with high-dose systemic corticosteroids.

PURPOSE: Vogt-Koyanagi-Harada (VKH) syndrome is usually treated with high-dose systemic corticosteroids. However, in a pregnant patient with VKH syndrome, the effects of high-dose corticosteroids on the fetus are controversial. We discuss treating VKH syndrome during pregnancy, systemic corticosteroids, and abnormalities in the delivered infant. METHODS: Case report and literature review. RESULTS: A 26-year-old Japanese woman in the 16th week of gestation was diagnosed with VKH syndrome and treated with high-dose systemic prednisolone after the 18th week of gestation. Although the patient's ocular findings gradually improved, a low-birth-weight infant was delivered with epibulbar dermoid, lipodermoids, and preauricular appendages. Although low birth weight might result from systemic prednisolone administration, the anomalies of the infant may have been inherited rather than caused by VKH syndrome and high-dose systemic corticosteroid administration. CONCLUSION: In this case and previously reported cases, VKH syndrome and systemic corticosteroids administered during pregnancy may not precipitate abortion and congenital malformation.

Adult↗

PubMed2000

Effect of short duration morning bright light in elderly men: sleep structure.

Sleep structure was measured in five healthy elderly men in their homes. The subjects were exposed to bright light (6000 lx) for 30 min in the morning or instructed to sit in front of a desktop lighting device without light. Relative to the control conditions, bright light exposure significantly decreased time in bed and the number of awakenings. Rapid eye movement sleep was significantly fragmented by stage 1 sleep in the control condition compared with the bright light condition. These findings indicate that a short duration of morning bright light changes sleep structure and is effective in maintaining sleep.

Aged↗

PubMed2000

Clinical benefits of steroid therapy on surgical stress in patients with esophageal cancer.

BACKGROUND: Despite improvements in surgical techniques and perioperative care, severe complications lead to long hospital stays for some esophageal cancer patients. The purpose of this study was to evaluate the safety and effectiveness of perioperative steroid therapy on the postoperative clinical course. METHODS: Fifty-seven patients operated for esophageal cancer in 1997 and 1998 were treated with perioperative steroid therapy. Fifty consecutive patients operated in 1995 and 1996 served as a control group. In the steroid group, each patient was given 250 mg of methylprednisolone intravenously before operation followed by 125 mg on postoperative days 1 and 2. Serum interleukin-6, polymorphonuclear cell elastase, and C-reactive protein levels, and the postoperative clinical course were compared between the groups. RESULTS: Morbidity rates including hyperbilirubinemia, anastomotic leakage, and liver dysfunction were significantly lower in the steroid group than in the control group. Days until extubation and hospital stay were significantly shorter for the steroid group. Inflammatory mediators, body temperature, heart rate, and respiratory index after the surgical procedure were significantly lower in the steroid group. Adverse effects possibly caused by steroid therapy were not observed. CONCLUSIONS: Perioperative steroid therapy was safe and effective for the inhibition of inflammatory mediators and the improvement of the postoperative clinical course of patients with esophageal cancer.

Acute-Phase Proteins↗

PubMed2000

Tissue and intracellular localization of indican and the purification and characterization of indican synthase from indigo plants.

Indican (indoxyl beta-D-glucoside) was found to accumulate only in green leaves of the indigo plant, and not in any other tissues. Comparisons of the indican content of protoplasts and vacuoles showed that indican was stored only in the vacuole of the cell. Indican content appeared and increased with the appearance and growth of leaves. In mature plants, the younger leaves contained larger amounts of indican than the older ones. Cell extracts of young leaves of indigo plant catalyzed the synthesis of indican from UDP-glucose and indoxyl. Indican synthase was extracted and purified from young leaves. The enzyme was separated into two fractions by anion-exchange chromatography. The enzyme in the fraction which was eluted by 0.1 M NaCl had a molecular weight of 53,000 by SDS-PAGE. Optimum pH of the enzyme was at about 10.0, indicating that the enzyme is likely localized in a different intracellular compartment from that of indican storage. The enzyme showed normal Michaelis-Menten kinetics and a K(m) value of 0.13 mM for UDP-glucose.

Glucosyltransferases↗

PubMed2000

Computed tomographic diagnosis of chronic obstructive pulmonary disease.

Recently, two-dimensional high-resolution computed tomography (2D-HRCT) and volumetric high-resolution computed tomography (VHRCT) have allowed great progress to be made in estimating small regions of hypoattenuation in the lung. VHRCT allows minimum-intensity projection (MINIP) imaging, which seems to be much more suitable than conventional 2D-HRCT for detecting subtle hypoattenuating regions, although the reliability of MINIP imaging data has not been conclusively shown. Three-dimensional computed tomography (3D-CT) images reconstructed from helical computed tomography (CT) acquisition over the whole lung field have been increasingly used to determine the absolute volume occupied by emphysematous changes. However, depending on the threshold CT values used for image reconstruction, whole-lung 3D-CT images may be distorted by considerable differences between the x-ray beam thickness and the effective section thickness, resulting in erroneous quantitation of emphysematous lesions by helical 3D-CT.

Bronchiolitis Obliterans↗

PubMed2000

Effects of cardiac sympathetic innervation on regional wall motion abnormality in patients with long QT syndrome.

AIM: To assess the spatial relation between regional cardiac sympathetic innervation and regional ventricular repolarisation indicated by ventricular wall motion abnormality in patients with congenital long QT syndrome. DESIGN: Regional percentage uptake and washout rate of (123)I metaiodobenzylguanidine (MIBG) were measured to assess cardiac sympathetic innervation in septum, anterior wall, lateral wall, and posterior wall. Left ventricular short axis images on echocardiography were digitised to reconstruct digitised M mode echocardiograms, from which left ventricular wall thickness curves were obtained. The wall thickening time (ThT) was defined as the period in which the instantaneous wall thickness exceeded 90% of the maximum wall thickness. The ThT was measured from the ventricular wall thickness curve at the same segments where regional percentage uptake and washout rate of (123)I MIBG were measured. PATIENTS: Seven patients with long QT syndrome. RESULTS: The regional washout rate (mean (SD)) of (123)I MIBG in patients with long QT syndrome was greater in the segments with decreased percentage uptake of (123)I MIBG than in those without (17.4 (10.6)% v 9.7 (16.5)%, p < 0. 03). ThT in segments both with and without decreased percentage uptake of (123)I MIBG was longer than in control subjects (p < 0. 0001). ThT was longer in the segments with decreased percentage uptake of (123)I MIBG than in those without (199 (70) ms v 150 (66) ms, p = 0.0018). CONCLUSIONS: Activation of regional cardiac sympathetic terminals is likely to participate in additional regional prolongation of ventricular repolarisation in patients with long QT syndrome.

3-Iodobenzylguanidine↗

PubMed2000

Postextrasystolic contractile decay always contains exponential and alternans components in canine heart.

In isolated, blood-perfused canine hearts, postextrasystolic potentiation (PESP) decays monotonically after a noncompensatory pause following a spontaneous extrasystole (ES). The monotonic PESP decay yields myocardial internal Ca(2+) recirculation fraction (RF). We have found that after a compensatory pause (CP), PESP decays in alternans, consisting of an exponential and a sinusoidal decay component. We have proposed that this exponential component also yields RF. In the present study, we examined the reliability of this alternative method by widely changing the ES coupling interval (ESI), CP, and heart rate in the canine excised, cross-circulated left ventricle. We found that all PESP decays consisted of the sum of an exponential and a sinusoidal decay component of variable magnitudes whether a CP existed or not. Their decay constants as well as the calculated RF were independent of the ESI and CP. This confirmed the utility of our alternative RF determination method regardless of the ESI, CP, and heart rate. Direct experimental evidence of Ca(2+) dynamics supportive of this alternative method, however, remains to be obtained.

Animals↗

PubMed2000

Existence of TT virus DNA in extracellular body fluids from normal healthy Japanese subjects.

Although recent studies indicate a high prevalence (12-92%) of TT virus (TTV) DNA in sera of healthy Japanese individuals, there is a paucity of information regarding the route of transmission of this virus. Analyzing the nucleotide sequences of the existing polymerase chain reaction (PCR) primers of TTV DNA, we developed a set of noble primers (HM-1) and looked for the prevalence of TTV DNA in sera from 39 normal healthy Japanese individuals using PCR. The existence of TTV DNA was also checked in saliva, urine, sweat, stool, and tears from 11 and in semen from 10 serum TTV-positive normal subjects. TTV DNA was detected in sera from 23 of 39 (59.0%) normal subjects. TTV DNA was also detected in saliva, stool, semen and tears from all cases with TTV-DNA-positive serum, but not in body fluids from subjects with TTV-DNA-negative serum. TTV DNA remained undetected in urine and sweat from all cases. Data from these experiments showing the existence of TTV DNA in different body fluids suggest that the high rates of prevalence of TTV among normal healthy subjects might be due to a possible fecal-oral, droplet, or sexual route of transmission of TTV.

Adult↗

PubMed2000

Importance of interleukin-8 in the development of reexpansion lung injury in rabbits.

Reexpansion of a collapsed lung induces increased microvascular permeability leading to reexpansion pulmonary edema (REPE). This study was designed to prove the hypothesis that local overproduction of interleukin-8 (IL-8) induces inflammatory cell accumulation which leads to the induction of REPE. Initially, we examined the detailed characteristics of a rabbit model of REPE in association with IL-8 production and its mRNA expression. The lung tissue to plasma ratio of radiolabeled albumin (T/P ratio), the lung wet to dry ratio, and bronchoalveolar lavage (BAL) neutrophil counts were significantly increased in the reexpanded lung. IL-8 concentrations and mRNA expression were significantly increased in the reexpanded lung homogenate. Immunohistochemically, alveolar macrophages (AMs) and epithelial cells in the reexpanded lung and AMs in the collapsed lung were positive for IL-8. Second, we examined the effect of pretreatment with a specific monoclonal anti-IL-8 antibody (Ab) or control IgG on the development of REPE. The T/P ratio and BAL neutrophil counts were conspicuously decreased by pretreatment with anti-IL-8 Ab, but not with control IgG. On a histopathological study, lung injury and leukocyte infiltration were attenuated by the pretreatment with anti-IL-8 Ab. In conclusion, IL-8 production is enhanced in the reexpanded lung, and contributes to the development of REPE. The pretreatment with anti-IL-8 antibody may be useful as a novel protective therapy for this disease.

Animals↗

PubMed2000

Gonadotropins and cytokines affect luteal function through control of apoptosis in human luteinized granulosa cells.

The luteal phase in the normal human menstrual cycle is known to be about 14 days. The physiological mechanisms that regulate the corpus luteum remain to be clarified, although apoptosis is reported to be involved. This study was undertaken to investigate the regulation of luteal function by gonadotropins, cytokines, and PGs, concentrating attention on the incidence of apoptosis and its molecular mechanisms in cultured human luteinized granulosa cells collected at oocyte pick-up from patients undergoing in vitro fertilization and embryo transfer. Clusters of granulosa cells were pipetted in 0.1% hyaluronidase in phosphate-buffered saline. After cell separation by centrifugation using Ficoll-Paque, 1 x 104 viable cells/mL in RPMI 1640 medium with 10% FCS were used for experimentation. Substances added were FSH (100 ng/mL), hCG (100 ng/mL), LH (100 ng/mL), interleukin-1beta (IL-1beta; 10 ng/mL), transforming growth factor-beta1 (TGFbeta1; 10 ng/mL), macrophage colony-stimulating factor (MCSF; 10 ng/mL), tumor necrosis factor-alpha (TNFalpha; 10 ng/mL), and PGF2alpha (10 ng/mL). After 24-h culture at 37 C under 5% CO2 and air, cells were fixed with 4% neutral buffered formalin and stained with Hoechst 33258. Apoptotic bodies were counted under a fluorescence microscope, and immunostaining was performed using anti-Fas, Fas ligand, Bcl-2, Bax, and p53 antibodies. Incidences of apoptotic bodies in the group without substance addition were 0.7 +/- 0.2% (0 h), 5.9 +/-0.6% (24 h), and 7.9 +/- 1.2% (48 h); spontaneous increase was significant at the latter time points. Defining the incidence at 24 h as 100%, values after treatment were: FSH, 57%; LH, 84%; hCG, 44%; IL-1beta, 76%; TGFbeta1, 52%; M-CSF, 50%; TNFalpha, 177%; and PGF2alpha, 147%. Significant suppression was observed with FSH, hCG, TGFbeta1, and M-CSF (P < 0.01). On the other hand, significant induction occurred with TNFalpha and PGF2alpha (P < 0.01). On immunostaining, the incidence of stained cells with anti-Fas, Fas ligand, Bax, and p53 antibody was increased after 24-h incubation without addition. This was reduced by hCG, TGFbeta1, and M-CSF. No stained cells were observed with anti-Bcl-2 antibody before or after incubation. In conclusion, our results suggest that both gonadotropins (FSH and hCG) and cytokines (TGFbeta1 and M-CSF) may be involved in the support of luteal function via suppression of apoptosis, and that TNFalpha and PGF2alpha may contribute to ovarian dysfunction and/or luteal regression via its induction in human luteinized granulosa cells. Our results also suggest that Fas, Fas ligand, p53, and Bax may play roles in this apoptosis controlled by hCG, TGFbeta1, and M-CSF.

Adult↗