Biomedical subjects

N Sato

Publications and source records attributed to N Sato.

At least 181 records · Page 10Linked to original sources

PubMed2001

Fulminant and relentless cutaneous necrosis with excruciating pain caused by calciphylaxis developing in a patient undergoing peritoneal dialysis.

A 50-year-old Japanese female with chronic renal failure who had been on continuous ambulatory peritoneal dialysis developed fulminant systemic cutaneous necrosis that began as painful livedo reticularis-like skin lesions on her thighs. Because of disseminated vascular calcification within the muscular layer of her lower limbs, we eventually diagnosed her with calciphylaxis. The skin necrosis progressed rapidly, and she died of sepsis and pneumonia on the 53rd hospital day. In addition to her long-lasting severe hyperparathyroidism and extremely elevated serum phosphorus and calcium levels, mechanical, frictional stimulation inflicted on the local skin and administration of corticosteroids were suspected to have precipitated the calciphylaxis. Our lack of awareness of this disease in its early stages resulted in our missing the chance to do a parathyroidectomy that might have changed the course. It is important to know the clinical features of this rare disease in order to make a diagnosis as early as possible.

Calciphylaxis↗

PubMed2001

A novel experimental mouse model of peritoneal dissemination of human gastric cancer cells: analysis of the mechanism of peritoneal dissemination using cDNA macroarrays.

We established a new cell line, NUGC-3P4T, with high peritoneal metastatic disseminating potential in nude mice. NUGC-3P4T cells were derived from the human gastric carcinoma line NUGC-3, which has low capacity for peritoneal dissemination. NUGC-3P4T cells developed peritoneal dissemination in 10 / 10 (100%) mice, whereas the parental NUGC-3 cells developed dissemination in 1 / 5 (20.0%) mice. The metastatic foci in the peritoneum showed essentially the same histological appearance as those induced by parental cells. The tumorigenicity, the motile activity and the adhesive activity to the laminin of NUGC-3P4T cells were stronger than those of NUGC-3 cells. Production of IL-8 was significantly higher in NUGC-3P4T than in NUGC-3. cDNA macroarrays analysis showed that a variety of cytokines, interleukins, and other immunomodulators and their receptors were up- or down-regulated at the mRNA level in NUGC-3P4T cells, compared with NUGC-3 cells. Thus, this unique cell line and in vivo model might be useful to study the biology of peritoneal dissemination of human gastric cancer.

Animals↗

PubMed2001

Quantitative analysis of hTERT mRNA expression in colorectal cancer.

OBJECTIVES: Telomerase is highly activated in a variety of malignant neoplasms including colon cancer. Among the major components of telomerase, human telomerase reverse transcriptase (hTERT) is thought to regulate telomerase activity. To assess the importance of telomerase for the diagnosis of colorectal cancer, we measured the expression of hTERT mRNA and telomerase activity in a large series of 140 colorectal cancers, 140 adjacent normal tissues, and 20 adenomas. METHODS: The expression level of hTERT was measured quantitatively by competitive reverse transcriptase-polymerase chain reaction (RT-PCR), and telomerase activity was examined by telomeric repeat amplification protocol (TRAP) assay in the same samples. RESULTS: The median expression level of hTERT mRNA in carcinomas was significantly higher than that in either adenomas or normal tissues. The median level of hTERT in adenomas was significantly higher than that in normal tissues. Telomerase activities in carcinomas were significantly higher than those in either adenomas or normal tissues. Telomerase activities in adenomas were also significantly higher than those in normal tissues. Furthermore, the relative expression levels of hTERT mRNA in adenomas and carcinomas were significantly correlated with the relative telomerase activities; the Spearman rank correlation was 0.53 (p = 0.021) and 0.18 (p = 0.031), respectively. CONCLUSIONS: Our data suggest that determination of hTERT mRNA by competitive RT-PCR is superior in quantitative accuracy and sensitivity and would support the importance of telomerase activity for the diagnosis of colorectal cancer.

Adenoma↗

PubMed2001

FDG PET of primary benign and malignant bone tumors: standardized uptake value in 52 lesions.

PURPOSE: To evaluate the standardized uptake value (SUV) of 2-[fluorine-18]fluoro-2-deoxy-D-glucose (FDG) at positron emission tomography (PET) in the differentiation of benign from malignant bone lesions. MATERIALS AND METHODS: Fifty-two (19 malignant, 33 benign) primary bone lesions were examined with FDG PET prior to tissue diagnosis. The SUVs were calculated and compared between benign and malignant lesions and among histologic subgroups that included more than four cases. RESULTS: There was a statistically significant difference in SUV between benign (2.18 +/- 1.52 [SD]) and malignant (4.34 +/- 3.19) lesions in total (P =.002). However, giant cell tumors (n = 5; SUV, 4.64 +/- 1.05) showed significantly higher SUV than chondrosarcomas (n = 7; SUV, 2.23 +/- 0.74) (P =.036, adjusted for multiple comparisons) and had no statistically significant difference in SUV compared with osteosarcomas (n = 6; SUV, 3.07 +/- 0.96) (P =.171). There was no statistically significant difference in SUV between fibrous dysplasias (n = 6; SUV, 2.05 +/- 0.98) and osteosarcoma (P =.127) or chondrosarcomas (P =.667). Although the number of cases was small, three chondroblastomas, one sarcoidosis, and one Langerhans cell histiocytosis showed levels of FDG accumulation as high as that of osteosarcomas. CONCLUSION: Radiologists should be aware of the high accumulation of FDG in some benign bone lesions, especially histiocytic or giant cell-containing lesions. Consideration of histologic subtypes should be included in analysis of SUV at FDG PET of primary bone tumors.

Adult↗

PubMed2001

Cyclooxygenase-2 downregulates inducible nitric oxide synthase in rat intestinal epithelial cells.

Cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression has been demonstrated in inflamed intestinal mucosa. Although regulation of COX-2 and iNOS expression has been studied extensively, the interplay between these two enzymes remains unclear. Because they play crucial roles in inflammation and/or carcinogenesis, we investigated whether COX-2 regulates iNOS expression and evaluated the effects of COX-2 inhibitor and arachidonic acid (AA) on iNOS induction. The COX-2 gene coding region was stably transfected into rat intestinal epithelial cells (RIE sense cells). After interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS) administration, iNOS and COX-2 expression was evaluated by Western blotting. PGE(2) was measured by the enzyme immunoassay (EIA) method. Expression of IFN response factor-1, phosphorylated extracellular signal-related kinase-1 and -2, and Ikappa-Balpha was evaluated. Activator protein-1 and nuclear factor-kappaB (NF-kappaB) were examined by gel mobility shift assay; a supershift assay was performed to identify the NF-kappaB complex components. JTE-522 or AA was added before IFN-gamma and LPS administration, and effects on iNOS and PGE(2) induction were evaluated by Western blotting or EIA. iNOS protein and mRNA expression was inhibited in RIE sense cells. Although NF-kappaB activation was suppressed and Ikappa-Balpha protein was more stable, respectively, in RIE sense cells, no difference was noted in other transcription factors. JTE-522 increased iNOS protein expression in RIE cells. We conclude that COX-2 suppressed iNOS expression in RIE cells through suppression of NF-kappaB by stabilizing Ikappa-Balpha.

Animals↗

PubMed2001

Nitric oxide donors retard wound healing in cultured rabbit gastric epithelial cell monolayers.

Effects of nitric oxide (NO) on gastric wound healing were investigated in primary rabbit gastric epithelial cell cultures. We analyzed the speed of cell migration, proliferation, and apoptosis after creating a round wound on the cell cultures. The monolayers were incubated with or without the NO donor sodium nitroprusside, oxatriazolimine 1,2,3,4-oxatriazolium, 5amino-3-(3,4-dichlorophenylchloride), or the peroxynitrite generator 3-morpholinosydnomine-N-ethylcarbamide. The possible role of cGMP as a second messenger of NO was investigated with 8-bromo-cGMP. The role of O2(-*) was evaluated using diethyldithiocarbamate and pyrogallol. The effects of superoxide dismutase and allopurinol were also investigated. NO inhibited the speed of cell migration and proliferation and induced cell apoptosis in a dose- and time-dependent manner. The effects were augmented with O2(-*) generators and ameliorated by O2-(8) scavengers, whereas cGMP had no significant effect on wound healing. NO donors retard gastric wound healing by inhibiting migration and proliferation and inducing cell apoptosis. These effects do not seem to be mediated via cGMP, but O2(-*). or peroxynitrites may be involved.

Animals↗

PubMed2001

Effects of hypercapnia and hypocapnia on [Ca2+]i mobilization in human pulmonary artery endothelial cells.

The hydrogen ion is an important factor in the alteration of vascular tone in pulmonary circulation. Endothelial cells modulate vascular tone by producing vasoactive substances such as prostacyclin (PGI2) through a process depending on intracellular Ca2+ concentration ([Ca2+]i). We studied the influence of CO2-related pH changes on [Ca2+]i and PGI2 production in human pulmonary artery endothelial cells (HPAECs). Hypercapnic acidosis appreciably increased [Ca2+]i from 112 +/- 24 to 157 +/- 38 nmol/l. Intracellular acidification at a normal extracellular pH increased [Ca2+]i comparable to that observed during hypercapnic acidosis. The hypercapnia-induced increase in [Ca2+]i was unchanged by the removal of Ca2+ from the extracellular medium or by the depletion of thapsigargin-sensitive intracellular Ca2+ stores. Hypercapnic acidosis may thus release Ca2+ from pH-sensitive but thapsigargin-insensitive intracellular Ca2+ stores. Hypocapnic alkalosis caused a fivefold increase in [Ca2+]i compared with hypercapnic acidosis. Intracellular alkalinization at a normal extracellular pH did not affect [Ca2+]i. The hypocapnia-evoked increase in [Ca2+]i was decreased from 242 +/- 56 to 50 +/- 32 nmol/l by the removal of extracellular Ca2+. The main mechanism affecting the hypocapnia-dependent [Ca2+]i increase was thought to be the augmented influx of extracellular Ca2+ mediated by extracellular alkalosis. Hypercapnic acidosis caused little change in PGI2 production, but hypocapnic alkalosis increased it markedly. In conclusion, both hypercapnic acidosis and hypocapnic alkalosis increase [Ca2+]i in HPAECs, but the mechanisms and pathophysiological significance of these increases may differ qualitatively.

Acidosis, Respiratory↗

PubMed2001

Mizoribine ameliorates the tubulointerstitial fibrosis of obstructive nephropathy.

Mizoribine has been shown to possess an immunosuppressive action that inhibits the proliferation of lymphocytes selectively by interfering with inosine monophosphate dehydrogenase. Recent studies have demonstrated that mizoribine improves renal tubulointerstitial fibrosis in the rat model of unilateral ureteral obstruction (UUO) by inhibiting the infiltration of macrophages. We, therefore, examined the dose dependency of the suppressive effect of mizoribine on the infiltration of interstitial macrophages and T lymphocytes and the interstitial volume in UUO-treated kidneys. Furthermore, we investigated the expression of osteopontin (OPN), known to be a chemoattractant protein for macrophages, in the renal cortex. In rats with UUO, the interstitial volume was markedly expanded, and macrophage and T lymphocyte infiltration in the interstitium and the expression of OPN in the cortical tubules were greatly increased. Treatment with mizoribine ameliorated the increase in interstitial volume induced by UUO. Interstitial infiltration of macrophages and T lymphocytes was dose dependently suppressed by mizoribine, and the decreased macrophage infiltration was correlated with inhibition of tubular OPN expression. These results suggest that mizoribine has a beneficial effect on several steps contributing to the progression of tubulointerstitial fibrosis caused by obstruction of the ureter.

Animals↗

PubMed2001

New compound heterozygous mutation in the CYP17 gene in a 46,XY girl with 17 alpha-hydroxylase/17,20-lyase deficiency.

BACKGROUND: 17alpha-Hydroxylase/17,20-lyase deficiency is caused by a defect of P450c17 which catalyzes both 17alpha-hydroxylase and 17,20-lyase reactions in adrenal glands and gonads. RESULTS: In the present study, we analyzed the CYP17 gene in a Japanese patient with 17alpha-hydroxylase/17,20-lyase deficiency. The patient was a phenotypic girl and referred to us for right-sided inguinal hernia at the age of 4 years. Biopsy of the herniated gonad showed testicular tissue. The karyotype was 46,XY. At 6 years of age, hypertension was clearly recognized and the patient was diagnosed as having 17alpha-hydroxylase/17,20-lyase deficiency based on the clinical and laboratory findings. Analysis of the CYP17 gene revealed a compound heterozygous mutation. One mutation was an undescribed single nucleotide deletion at codon 247 in exon 4 (CTT to CT: 247delT) and the other was a missense mutation resulting in a substitution of His to Leu at codon 373 in exon 6 (CAC to CTC: H373L), which has been previously shown to abolish both 17alpha-hydroxylase and 17,20-lyase activities. The functional expression study of the 247delT mutant showed that this 247delT mutation completely eliminates both 17alpha-hydroxylase and 17,20-lyase activities. CONCLUSIONS: Together, these results indicate that the patient is a compound heterozygote for the mutation of the CYP17 gene (247delT and H373L) and that these mutations inactivate both 17alpha-hydroxylase and 17,20-lyase activities and give rise to clinically manifest 17alpha-hydroxylase/17,20-lyase deficiency.

Adrenal Hyperplasia, Congenital↗

PubMed2001

Short-term oral administration of L-arginine improves hemodynamics and exercise capacity in patients with precapillary pulmonary hypertension.

We sought to assess the effects of oral supplementation of L-arginine, the precursor of nitric oxide (NO), on hemodynamics and exercise capacity in patients with pulmonary hypertension. Acute hemodynamic responses to oral L-arginine (0.5 g/10 kg body weight) or placebo were examined in 19 patients with primary or precapillary secondary pulmonary hypertension. Cardiopulmonary exercise tests were performed to measure peak oxygen consumption (peak V O(2)) and the ventilatory response to carbon dioxide production (V E-V CO(2) slope) before and 1 wk after treatment with L-arginine (1.5 g/10 kg body weight/d) or placebo. Oral supplementation of L-arginine significantly increased plasma L-citrulline, which indicated enhancement of NO production. Supplemental L-arginine produced a 9% decrease in mean pulmonary arterial pressure (53 +/- 4 to 48 +/- 4 mm Hg, p < 0.05) and a 16% decrease in pulmonary vascular resistance (14.8 +/- 1.5 to 12.4 +/- 1.4 Wood units, p < 0.05). L-arginine modestly decreased mean systemic arterial pressure (92 +/- 4 to 87 +/- 3 mm Hg, p < 0.05). A 1-wk supplementation of L-arginine resulted in a slight increase in peak V O(2) (831 +/- 88 to 896 +/- 92 ml/min, p < 0.05) and a significant decrease in the V E- V CO(2) slope (43 +/- 4 to 37 +/- 3, p < 0.05) without significant systemic hypotension. Hemodynamics and exercise capacity remained unchanged during placebo administration. These results suggest that oral supplementation of L-arginine may have beneficial effects on hemodynamics and exercise capacity in patients with precapillary pulmonary hypertension.

Administration, Oral↗

PubMed2001

Testosterone 5alpha-reductase inhibitory active constituents from Anemarrhenae Rhizoma.

The diethyl ether extract of Anemarrhenae Rhizoma (rhizomes of Anemarrhena asphodeloides Bunge) showed testosterone 5alpha-reductase inhibitory activity. Two major constituents, cis-hinokiresinol (1) and 2,6,4'-trihydroxy-4-methoxybenzophenone (2) were identified as the active principles. The inhibitory activity of 1 was superior to that of ethinylestradiol, but that of 2 was weak.

5-alpha Reductase Inhibitors↗

PubMed2001

Roles of caspases in the programmed cell death of motoneurons in vivo.

Cysteine proteases comprising the caspase family have been considered one of the major executioners of programmed cell death. However, detailed analyses of the programmed cell death of developing motoneurons in mice following the genetic deletion of two key caspases, casp-3 and casp-9, and in the chick embryo following treatment with caspase inhibitors, indicate that normal amounts of cell loss occur although the death process is delayed. Motoneurons undergoing programmed cell death without caspase activities exhibit a nonapoptotic morphology in which nuclear changes such as chromatin condensation are absent or reduced and which exhibit extensive cytoplasmic vacuolization such as is rarely observed in degenerating control neurons. These results suggest that caspases are involved in, but are not indispensable for, the developmental death of motoneurons, and that one function of caspases may be to facilitate the removal of cells that are destined to die. Possible alternative caspase-independent pathways for the programmed death of motoneurons are discussed.

Animals↗

PubMed2001

Importance of CCK-A receptor for gallbladder contraction and pancreatic secretion: a study in CCK-A receptor knockout mice.

Bile and pancreatic secretions were determined in a CCK-A receptor deficient mouse mutant generated by gene targeting in embryonic stem cells. The targeting vector contained lacZ and neo insertions in exon 2. Under the urethane anesthesia, the common bile duct was cannulated, and the mixture of bile-pancreatic juice was collected every 30 min. After the 1 h basal secretion, CCK-8 (0.5 and 1.0 nmol/kg), acetylcholine (500 nmol/kg), and neuromedin C (1.0 micromol/kg) were injected subcutaneously, and the secretions were collected following 1 h. Amylase and bile acid outputs were determined as parameters of pancreatic secretion and gallbladder contraction, respectively. In some CCK-A receptor (+/-) animals, LacZ staining was performed. CCK-8 significantly increased amylase and bile acid outputs in CCK-A receptor (+/+) and (+/-) mice, whereas no response was observed in (-/-) mice. Neuromedin C and acetylcholine increased amylase secretion in CCK-A receptor (-/-) mice similar to (+/-) and (+/+) mice. The same doses of neuromedin C and acetylcholine could not increase bile acid secretion. The gallbladder smooth muscles, pancreatic acinar cells, duct cells, and islets were stained by LacZ. CCK and CCK-A receptor are important for pancreatic secretion and gallbladder contraction. Neuromedin C and acetylcholine may compensate pancreatic function, but not gallbladder contraction.

Acetylcholine↗

PubMed2001

Usefulness of endoscopic ultrasonographic analysis of variceal hemodynamics for the treatment of esophageal varices.

The correlation of between the endoscopic findings of esophageal varices and endoscopic ultrasound findings of the collaterals outside the esophageal wall in patients with portal hypertension remains unclear. We investigated the relationship between esophageal varices and the collaterals by endoscopy and endoscopic ultrasound. Moreover, we investigated the correlation between the collaterals around the esophagus and recurrence of esophageal varices in patients with portal hypertension who had undergone endoscopic injection sclerotherapy. The collaterals were divided into two groups: 1; those with peri-esophageal collateral veins (peri-ECVs) adjacent to the muscularis externa of the esophagus, and 2; those with para-esophageal collateral veins (para-ECVs) distal to the esophageal wall without contact with the muscularis externa. Peri- and para-ECVs were scored as mild or severe according to the stage of development. According to endoscopy, the varix form was significantly larger in severe peri-ECVs group than in mild peri-ECVs group. In contrast, the varix form did not differ significantly between the mild and severe para-ECVs group. The prevalence of perforating veins increased according to the varix form. With regard to variceal recurrence, in patients with variceal recurrences, EUS findings included a significantly higher incidence of severe-type peri-ECVs, a significantly larger number of perforating veins, and a significantly larger diameter of perforating veins compared with patients without recurrence. Moreover, when EUS found the abnormalities when no endoscopic recurrence was found, the results were the almost same as the findings when EUS was performed at the same time when endoscopic recurrence was found. In conclusion, the presence of severe peri-ECVs and large perforating veins in the esophageal wall strongly correlates with occurrence and recurrence of esophageal varices in patients with portal hypertension. An understanding of these EUS abnormalities on the basis of hemodynamics around the esophagus is thought to be important for management of esophageal varices in patients with portal hypertension.

Collateral Circulation↗

PubMed2001

MR evaluation of the hippocampus in patients with congenital malformations of the brain.

BACKGROUND AND PURPOSE: Developmental changes in hippocampal formations (HFs) have been reported in association with agenesis of the corpus callosum, lissencephaly, and holoprosencephaly. The purpose of this study was to evaluate the developmental changes in HFs in patients with a variety of other congenital brain malformations. METHODS: MR images of 44 patients with congenital brain malformations associated with 11 different brain disorders were reviewed retrospectively. Five patients had more than two anomalies. Imaging and clinical findings were evaluated for the shape, size, degree of inversion, and side of abnormal HF. RESULTS: Vertically oriented or globular-shaped HFs were observed in 28 patients (64%) on coronal MR images. All patients with agenesis of the corpus callosum (n = 7), lissencephaly (n = 1), holoprosencephaly (n = 3), and Fukuyama muscular dystrophy (n = 3) had an abnormal HF. A high prevalence of abnormalities was observed in patients with polymicrogyria (11/12, 92%), heterotopia (4/5, 80%), tuberous sclerosis (2/3, 67%), and schizencephaly (2/4, 50%). Patients whose abnormalities were symmetrical had bilateral abnormal HFs, whereas those with polymicrogyria, schizencephaly, and heterotopia, whose abnormalities were localized, tended to have unilateral abnormal HFs. CONCLUSION: Hippocampal developmental abnormalities are found in a high percentage of patients with congenital malformations. Focusing on the morphologic abnormalities of the HF on coronal MR images may help in the detection of diseases associated with brain anomalies, especially subtle cortical disorders.

Adolescent↗

PubMed2001

[Indication of H. pylori eradication therapy--who should be treated?].

With increased evidence of H. pylori infection being deeply related with various gastric diseases, its curative therapy will be approved by social security foundation soon also in Japan. Japanese Society of Helicobacter reported a guideline for H. pylori diagnosis and treatment in July 2000. In the guideline, only peptic ulcers and low grade MALT lymphomas are recommended as an indication of H. pylori eradication and other diseases such as atrophic gastritis, post EMR state for early gastric cancer and post-operated stomach due to gastric cancer, hyperplastic polyps and non-ulcer dyspepsia, were not included. It is speculated that while benefit of eradication therapy for peptic ulcers and low grade MALT lymphomas has been supported by much clinical evidence, that for other diseases was judged not to be enough. Especially as to atrophic gastritis, eradication therapy might be considered in aspect of decreasing gastric cancer risk in Japan. Since accumulated epidemiological and experimental data strongly support its positive correlation with cancer risk, patients in high risk group for gastric cancer could be included for a target eradication therapy. In present, indication of the therapy should be clinically and socially decided according to individual patient.

Clinical Trials as Topic↗

PubMed2001

Mechanisms of photoreceptor cell death in cancer-associated retinopathy.

PURPOSE: In a previous study, both recoverin and heat shock cognate protein (hsc) 70 were recognized as autoantigens by sera from patients with cancer-associated retinopathy (CAR), and retinal dysfunction similar to CAR was inducible by intravitreous injection of anti-recoverin and anti-hsc 70 antibodies to Lewis rat. The purpose of the present study was to elucidate the effects of these antibodies on retinal photoreceptor cell functions, the contribution of caspase during the photoreceptor degeneration, and the roles of aberrant expression of recoverin in tumor cells. METHODS: As photoreceptor functions, rhodopsin phosphorylation using freshly prepared rod outer segments (ROS) and electroretinogram (ERG) were studied. Expression of recoverin in several kinds of tumors was examined by reverse transcription-polymerase chain reaction and Western blot analysis. The effects of recoverin on calcium-dependent protein phosphorylation were studied using the A549 lung adenocarcinoma cell line, which does not express recoverin. RESULTS: Rhodopsin phosphorylation in bovine ROS was significantly promoted by the addition of anti-recoverin antibody. Similar effects on rhodopsin phosphorylation and ERG impairment were observed in rat eyes treated with anti-recoverin antibody. Co-injection of caspase inhibitors with anti-recoverin antibody inhibited ERG impairment and significantly suppressed the antibody-induced enhancement of rhodopsin phosphorylation. Aberrant expression of recoverin was found in 15 of 30 tumor tissues from patients with cancer without CAR. Profiles of calcium-dependent protein phosphorylation of cell lysate from A549 cells were modulated by the presence of purified recoverin. CONCLUSIONS: These observations suggest that anti-recoverin antibody is incorporated into rod photoreceptor cells and modulates rhodopsin phosphorylation, which in turn produces activation of caspase-dependent apoptotic pathways. Regarding antibody generation in CAR, a high incidence of aberrant expression of recoverin in cancer tissues is important, as suggested previously.

Animals↗

PubMed2001

[Hematopoietic stem cell transplantation].

Hematopoietic stem cell transplantation, which started as an experimental medicine more than four decades ago, has now become an indispensable and powerful tool to treat intractable hematologic disorders through the considerable efforts of D. Thomas and his colleagues. A short review of hematopoietic stem cell transplantation is reported with emphasis on cord blood transplantation and non-myeloablative stem cell transplantation.

Bone Marrow Transplantation↗