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H Mizoguchi

Publications and source records attributed to H Mizoguchi.

At least 73 records · Page 4Linked to original sources
PubMed2000

Disruption of the ABC transporter genes PDR5, YOR1, and SNQ2, and their participation in improved fermentative activity of a sake yeast mutant showing pleiotropic drug resistance.

Clotrimazole-resistant mutants from sake yeasts show improved fermentative activity in sake mash and pleiotropic drug resistance (PDR). The PDR mechanism is interpreted by overexpression of ATP-binding cassette (ABC) transporters, which extrude various kinds of drugs out of a cell. In a clotrimazole-resistant mutant, CTZ21, isolated from the haploid sake yeast HL69, the levels of mRNA for three major ABC transporter genes, PDR5, SNQ2, and YOR1, markedly increased. These three genes of CTZ21 were disrupted to investigate which participated in the improved fermentative activity of CTZ21. The fermentative activities of deltapdr5 and deltasnq2 strains of CTZ21 were reduced to that of HL69 in the initial and middle stages of fermentation. In the last stage, however, the sake meter [(1/gravity - 1) x 1443] of the deltapdr5 and deltasnq2 strains rose faster than that of HL69. On the other hand, a deltayor1 strain of CTZ21 fermented sake mash in a manner nearly identical to that of CTZ21 until the last stage of fermentation. But in the last stage, fermentation of the deltayor1 slowed down compared with that of CTZ21. A deltayor1 strain of HL69 also exhibited much reduced fermentative activity in the middle and last fermentation stages. The YOR1 gene seems necessary for sake fermentation to be completed efficiently. The ATP content in sake mash brewed with CTZ21 was drastically decreased throughout the whole fermentation period. This low ATP level was restored to a medium level in the cases of both the deltapdr5 and deltasnq2 strains of CTZ21. In contrast, the deltayor1 of CTZ21 exhibited a low ATP level in sake mash in the same manner as CTZ21. These results suggest that the low ATP level of CTZ21 contributes to a certain extent its improved fermentative activity in the initial and middle stages of sake fermentation.

Journal Article↗
PubMed2000

Shortening of telomeres in recipients of both autologous and allogeneic hematopoietic stem cell transplantation.

Telomere length of peripheral blood mononuclear cells (PBMCs) from 23 autologous HSCT patients ranging from 4 to 61 years old, and 46 allogeneic HSCT recipients from 6 to 52 years old were studied to confirm whether excessive shortening of telomeres is associated with HSCT. After autologous HSCT, telomere length of PBMCs ranged from 6.8 to 12.0 kb. The comparison between transplanted PBMCs and PBMCs after autologous HSCT showed shortening by up to 1.9 kb (mean +/- s.d.: 0.64 +/- 0.50 kb). There was a difference between autologous HSCT patients and normal volunteers in the slopes of regression lines. After allogeneic HSCT, telomere length of PBMCs ranged from 6.8 to 12.0 kb. Telomeres of recipients were up to 2.1 kb (0.60 +/- 0.468 kb) shorter than those of donors. The slope of regression lines for allogeneic HSCT patients and normal volunteers were parallel. Although all patients were transplanted with more than 2.0 x 10(8) cells/kg, telomere length did not correlate with the number of transplanted cells. There was no significant correlation between telomere length and recovery of hematological parameters. However, three patients with an average telomere length of 6.8 kb after HSCT took a longer period to reach the normal hematological state. Taken together, these data suggest that most HSCTs are performed within the biological safety range of telomeres, while the patients who have telomeres shorter than 7.0 kb after HSCT should be observed carefully for long-term hematopoiesis and the occurrence of hematopoietic disorders.

Adolescent↗
PubMed2000

Ectopic expression of c-myc fails to overcome downregulation of telomerase activity induced by herbimycin A, but ectopic hTERT expression overcomes it.

Telomerase plays a key role in the maintenance of chromosomal stability in tumors, but the mechanism regulating telomerase activity is still unclear. Recent studies have suggested that c-myc may be vital for regulation of hTERT mRNA expression and telomerase activity. In this study, we investigated the changes of telomerase activity and telomerase-related genes induced by herbimycin A in K562 human chronic myelogeous leukemic cells. Telomerase activity showed a biphasic pattern in herbimycin A-treated K562 cells. Initially, the telomerase activity decreased along with the decline of cells in S and G2/M phases, but it recovered slightly at the end of treatment. Expression of mRNA for the telomerase catalytic subunit (hTERT) was decreased before the decline of telomerase activity, and increased slightly before the reactivation of telomerase activity. During herbimycin A treatment, both c-myc and cyclin D1 mRNA showed transient downregulation before the increase of G1 cells. Herbimycin A treatment caused the downregulation of both telomerase activity and hTERT mRNA in cyclin D1-transfected K562 cells, while telomerase activity was partially restored in c-Myc-transfected cells. In contrast, hTERT-transfected K562 cells maintained a high level of telomerase activity during herbimycin A treatment. Neither the template RNA component of telomerase (hTERC) nor telomerase-associated protein (TEP-1) were altered in any of the transfected K562 cells. These results indicate that telomerase activity is mainly regulated by hTERT, and that c-Myc protein is one of the positive regulators of hTERT in leukemic cells but is not enough to counteract the downregulation of telomerase activity by herbimycin A completely.

Benzoquinones↗
PubMed2000

The roles of nitric oxide and prostaglandins in alterations of ulcerogenic and healing responses in adjuvant-induced arthritic rat stomachs.

AIM: To examine alterations of gastric ulcerogenic and healing responses in adjuvant-induced arthritic rats. METHODS: Arthritis was induced in male Dark Agouti rats by injection of Freund's complete adjuvant into the right hind paw. RESULTS: The gastric ulcerogenic response to indomethacin was markedly increased in AA rats, depending on the degree of arthritic change. By contrast, HCl/ethanol-induced gastric lesions were significantly suppressed in arthritic rats when compared with normal rats. The increased ulcerogenic response to indomethacin was significantly prevented by L-NAME and antineutrophil serum but not by FR167653, while the reduced ulcerogenic response to HCl/ethanol was significantly prevented by L-NAME and partly by indomethacin or NS-398. On the other hand, the healing of chronic gastric ulcers induced by thermal cauterization was also significantly delayed in arthritic rats when compared with normal rats. This delayed healing of gastric ulcers was affected by neither L-NAME, indomethacin nor FR167653. The gastric mucosa of arthritic rats showed a significant increase in both inducible nitric oxide synthase (iNOS) activity and prostaglandin (PG) E2 contents. CONCLUSIONS: Gastric ulcerogenic and healing responses were altered in arthritic rats. The ulcerogenic response to indomethacin was increased while that to HCl/ethanol was decreased. These changes in ulcerogenic responses may both be accounted for by increased production of NO/iNOS, with the latter also being partially related to elevated production of PGs/COX-2. Moreover, the healing of gastric ulcers was also delayed in arthritic rats, but the mechanism was related to neither NO nor PGs.

Animals↗
PubMed2000

Induction therapy consisting of alternating cycles of ranimustine, vincristine, melphalan, dexamethasone and interferon alpha (ROAD-IN) and a randomized comparison of interferon alpha maintenance in multiple myeloma: a co-operative study in Japan.

This pilot study evaluated the efficacy of a new combination chemotherapy with a newly developed nitrosourea derivative ranimustine and evaluated the efficacy of interferon alpha (IFN-alpha) maintenance in previously untreated patients with multiple myeloma (MM). The induction therapy (ROAD-IN) was a 6-week regimen consisting of chemotherapy with ranimustine, vincristine (Oncovin), melphalan (Alkeran) and dexamethasone starting on day 1 and IFN-alpha, which was administered three times weekly for 3 weeks starting on day 22. This was repeated for three cycles. The responders were subsequently randomized into two groups that received or did not receive IFN-alpha as maintenance therapy. Of the 164 patients registered, 161 were evaluated. An objective response to induction therapy was seen in 75% of patients; complete remission (CR) in 38 (24%) and partial remission (PR) in 82 (51%). The median survival for all patients was 3.6 years from registration. The survival of responders (CR + PR) was significantly better than that of non-responders (median survival 4.3 years vs. 1.4 years; 7-year survival rate 32% vs. 9%; P < 0.0001). The IFN-alpha maintenance did not show any advantage for either response duration or survival. This pilot study demonstrated that a comparatively short period of induction therapy with the ROAD-IN regimen produced a rather high response rate and a similar survival rate to those achieved with other longer induction regimens, and that good responders to the initial therapy survived significantly longer than non-responders.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2000

Significance of lung resistance-related protein in the clinical outcome of acute leukaemic patients with reference to P-glycoprotein.

Lung resistance-related protein (LRP) overexpression in leukaemic blast cells from acute leukaemia patients and the effect of LRP or P-glycoprotein (P-gp) on the clinical outcome of acute leukaemia were investigated individually by dividing patients into four groups. The complete remission rate of group I (LRP and P-gp both negative) was 81.7%, group II (only LRP positive) 87.5%, group III (only P-gp positive) 87.1% and group IV (LRP and P-gp both positive) 40.0%. There were no statistical differences between group I and groups II or III, but a significant difference was observed between groups I, II or III and group IV. Median overall survival in group IV was significantly shorter (4.6 months) than in groups I, II or III, although no significant differences were observed between group I and groups II or III (18.9, 20.5 and 31.8 months). There was a tendency for disease-free survival in group III to be longer than that in groups I, II or IV. The reasons for these findings are discussed. Our present results indicate that the co-existence of LRP and P-gp strongly influenced the effectiveness of induction chemotherapy and long-term prognosis, whereas the isolated presence of LRP or P-gp did not.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed2000

Regulatory mechanism of acid secretion in the damaged stomach: role of endogenous nitric oxide.

The present article overviews the regulatory mechanism of acid secretion in the stomach after damage with taurocholate (TC), one of the bile acids. Mucosal exposure of a rat stomach to 20 mmol/L TC for 30 min caused a decrease of acid secretion with a concomitant increase in nitric oxide (NO) and prostaglandin (PG) E2 (PGE2) as well as Ca2+ in the luminal contents. Prior administration of N(G)-nitro-L-arginine methyl ester (L-NAME), as well as indomethacin, significantly attenuated the reduction of acid secretion by TC and acid secretion was even increased in the presence of L-NAME. The acid stimulatory effect of L-NAME in the damaged stomach was not mimicked by aminoguanidine and was antagonized by co-administration of L-arginine but not D-arginine. Increased NO release in the damaged stomach was suppressed by pretreatment with L-NAME or co-application of EGTA and the latter also inhibited the increase in luminal Ca2+. The enhanced acid secretory response in the presence of L-NAME was also inhibited by cimetidine, FPL-52694 (a mast cell stabilizer) or sensory deafferentation. Mucosal exposure to TC caused an increase in luminal histamine output, together with a decrease in the number of mucosal mast cells in the stomach. These changes were prevented by FPL-52694 and sensory deafferentation and were also partly suppressed by indomethacin. In addition, the acid stimulatory action of L-NAME in the damaged stomach was significantly mitigated when indomethacin was administered together with L-NAME. We conclude that: (i) damage in the stomach may activate acid a stimulatory pathway in addition to a PG-, NO- and Ca2+-dependent inhibitory mechanism, but the latter effect overcomes the former, resulting in a decrease in acid secretion; (ii) acid stimulation in the damaged stomach is mediated by histamine released from the mucosal mast cell, a process interacting with capsaicin-sensitive sensory nerves; (iii) the increase in luminal Ca2+ plays a role in increasing NO production and, hence, in regulating acid secretion; and (iv) PG may have a dual role in the regulation of acid secretion in the damaged stomach: an inhibitory effect at the parietal cell and an excitatory effect, probably through enhancing the release of mucosal histamine.

Animals↗
PubMed2000

A pilot study of intermittent androgen ablation in advanced prostate cancer in Japanese men.

BACKGROUND: Permanent androgen ablation has been the mainstay of treatment for advanced prostate cancer. However, the favorable outcome seen in recent pilot studies of intermittent androgen ablation raises the possibility of overtreatment. METHODS: This study included 35 Japanese men with advanced prostate cancer. Initial androgen ablation continued for 2 months after PSA levels decreased to <4.0 ng/ml, then was withdrawn. Androgen ablation was reinstituted 2 months after PSA reached levels >10 ng/ml, when indicated clinically or on patient request. Cycling continued until androgen independence was reached. RESULTS: Mean follow-up was 21.0 months, representing an average of 2.5 cycles. Nine patients developed androgen independence at an average of 16.0 months following androgen ablation; three of these have died. Six of the nine patients with early biochemical progression had elevated alkaline phosphatase levels at entry; five of these exhibited a flare in alkaline phosphatase activity after initiation of androgen ablation. Mean bone mineral density (BMD) in the lumbar spines of 17 patients was 81.5 mg/cm3 at 23 months following therapy. The BMD of 10 of these patients was normal for their age. Four patients suffered bone fractures, none pathological. CONCLUSIONS: Intermittent androgen ablation may be an option for patients with advanced prostate cancer and may be especially beneficial for those with initially low BMD levels. Patients with elevated alkaline phosphatase levels at entry or a flare in its activity may not be ideal candidates. Whether prolonging time to androgen independence will provide benefit remains to be investigated in a randomized, prospective study.

Adenocarcinoma↗
PubMed2000

Infrequent involvement of the anterior base in low-risk patients with clinically localized prostate cancer and its possible significance in definitive radiation therapy.

BACKGROUND: The zonal distribution and location of tumors in different subgroups of Japanese patients with clinically localized prostate cancer have not been fully described. The appropriate radiation treatment volume thus remains unclear. METHODS: Radical prostatectomy specimens of 141 consecutive patients with clinically localized prostate cancer were examined by the whole organ step-section technique. The zonal distribution and location of tumors at different levels of the gland were investigated after stratification into patient subgroups based on preoperative clinicopathological findings and risk group assessment. RESULTS: The median tumor volume was 2.8 cm3; 72 patients (51.1%) had pathologically organ-confined disease (pT2). Higher risk groups showed a statistically significant increase in tumor volume and a decrease in the rate of pathologically confirmed organ confinement. Involvement of the anterior base was found infrequently in certain patient subgroups: in only one of 20 patients (5%) with preoperative PSA <4.0 ng/ml, in three of 19 patients (15.8%) with specimen Gleason scores of 2-4 and in two of 32 patients (6.3%) identified as low-risk. CONCLUSIONS: Infrequent involvement of the anterior base in low-risk patients may be an intrinsic feature of clinically localized prostate cancer. Treatment volume modifications in these patients that reduce the radiation dose to the anterior base may be justified to avoid acute and late genitourinary toxicities.

Aged↗
PubMed2000

Alterations of the PPP1R3 gene in hematological malignancies.

PPP1R3 (protein phosphatase 1, regulatory subunit 3) is a candidate tumor suppressor gene at chromosome 7q31, since nonsense and missense mutations of the PPP1R3 gene have been detected in a variety of human cancers. Loss of chromosome 7q is a recurrent abnormality in hematological malignancies, especially of myeloid lineage, and a common region of 7q deletions has been mapped to 7q31. Thus, it has been suggested that 7q31 harbors a tumor suppressor gene whose functional loss contributes to leukemogenesis. To evaluate the possible involvement of the PPP1R3 gene in the development of hematological malignancies, we examined 72 leukemia and lymphoma cell lines for alterations of the PPP1R3 gene by PCR-SSCP and direct sequence analyses. Mutations were detected in 1 (2.8%) of 36 myeloid cell lines, 4 (20.0%) of 20 B-lineage lymphoid cell lines and none of 16 T-lineage lymphoid cell lines. All the mutations were heterozygous, and they consisted of two missense mutations and three silent mutations. The PPP1R3 gene was expressed in cell lines of various cell lineages. These results indicate that PPP1R3 is not a major target of 7q deletions in myeloid leukemia, however, alterations of the PPP1R3 gene may contribute to the development of a subset of hematological malignancies.

Amino Acid Substitution↗
PubMed2000

Differential antinociceptive effects of endomorphin-1 and endomorphin-2 in the mouse.

Two highly selective mu-opioid receptor agonists, endomorphin-1 and endomorphin-2, have been identified and postulated to be endogenous mu-opioid receptor ligands. We determined the antinociceptive effects of these two ligands at the supraspinal level in mice with the tail-flick and hot-plate responses. The i.c.v. injection of endomorphin-1 and -2 inhibited the tail-flick and hot-plate responses in a dose-dependent manner. The endomorphin-1 was found to be 3.3- and 2.4-fold more potent than endomorphin-2 in inhibiting the tail-flick and hot-plate responses, respectively. The antinociception induced by endomorphin-1 was blocked by i.c.v. pretreatment with the mu-opioid receptor antagonist beta-funaltrexamine but not by the kappa-opioid receptor antagonist nor-binaltorphimine, the delta(1)-opioid antagonist 7-benzylidene naltrexamine, or the delta(2)-opioid receptor antagonist naltriben. In contrast, the antinociception induced by endomorphin-2 was blocked by i.c.v. pretreatment with beta-funaltrexamine or nor-binaltorphimine but not by 7-benzylidene naltrexamine or naltriben. The inhibition of the tail-flick response induced by endomorphin-2 was blocked by pretreatment with an antiserum against dynorphin A(1-17) but not by antisera against Met-enkephalin, Leu-enkephalin, or beta-endorphin. None of these antisera reduced the endomorphin-1-induced tail-flick inhibition. We propose that endomorphin-1 produces antinociception by stimulating one type of mu-opioid receptor, whereas endomorphin-2 initially stimulates different mu-opioid receptors, which subsequently induce the release of dynorphins that act on kappa-opioid receptors to produce antinociception.

Analgesics↗
PubMed2000

[Clinical evaluation of rhG-CSF in patients with neutropenia induced by chemotherapy for multiple myeloma].

A randomized controlled study of patients with multiple myeloma was performed to evaluate the efficacy and safety of recombinant human granulocyte colony-stimulating factor (rhG-CSF:KW-2228) in treating neutropenia induced by chemotherapy, and its influence on the dose intensity of, and response rate to, chemotherapy. As a rule, 3 courses of chemotherapy at intervals of 4 weeks were administered both to the untreated and KW-2228-treated groups. Among 98 eligible patients evaluated for neutrophil recovery, a markedly reduced duration of neutropenia was observed during each course in the KW-2228 treated group. No significant difference distinguished the two groups in terms of incidence or duration of infection. However, febrile neutropenia appeared only in the untreated group. There was no significant difference in terms of response rate or dose intensity. However, only patients in the untreated group withdrew from the study due to protracted neutropenia. These results demonstrated that KW-2228 is effective and safe, and has a significant effect on the acceleration of neutrophil recovery in patients with neutropenia induced by chemotherapy for multiple myeloma, and is useful for the completion of chemotherapy regimens.

Adolescent↗
PubMed2000

Delineation of the frequently deleted region on chromosome arm 13q in B-cell non-Hodgkin's lymphoma.

The loss of a specific chromosomal region provides a clue to the elucidation of the putative tumor suppressor gene implicated in the pathogenesis and progression of tumors. To delineate the specific region(s) involved in lymphomagenesis, we performed a survey of loss of heterozygosity for 11 polymorphic microsatellite loci scattered on variable chromosome arms. We examined 20 primary lymphoma samples, including both indolent and aggressive B-cell non-Hodgkin's lymphoma (B-NHL) and Hodgkin's disease (HD), and found a significant number of B-NHLs with loss of genetic material on chromosome arm 13q at the RB1 locus (50%; 4 of 8 informative cases for the RB1 locus). To specify the 13q deletion and to narrow the critical deleted region, we examined the same 20 lymphomas by intensive microsatellite mapping analysis using 12 microsatellite markers, mapping from 13q12.3 to 13q14. We confirmed the frequent 13q14 deletion to be in the vicinity of the RB1 locus (50% of the informative NHLs for at least 1 of 12 microsatellite loci; 5 of 10 aggressive NHLs and 2 of 4 indolent NHLs, but none of 6 HDs) and determined a subchromosomal region deleted in lymphoma on 13q14 defined by D13S164-D13S273, which is an overlapped region frequently lost in chronic lymphocytic leukemia. Taken together, our data indicate that the 13q alterations are present in a wide variety of NHLs including both indolent and aggressive B-NHLs, suggesting that loss of genetic material at chromosome band 13q14 may play an important role in the formation or development of a wide variety of mature lymphoid malignancies.

Adult↗
PubMed2000

[Efficacy and safety of cefozopran (CZOP) monotherapy and combination therapy with CZOP and amikacin (AMK) for infections accompanying hematological diseases].

We evaluated efficacy and safety of monotherapy with CZOP (1-2 g x 2/day) and combination therapy with CZOP (1-2 g x 2/day) and AMK (200 mg x 2/day) for infections in patients with hematological diseases. Efficacy was evaluated in 71 patients of monotherapy group and 70 patients of combination therapy group. Underlying diseases were mostly leukemia and lymphoma. Infections included sepsis, suspected sepsis, pneumonia and so on. Efficacy in CZOP monotherapy was excellent in 21 patients (31.3%), good in 23 patients (34.3%), fair in 5 patients (7.5%) and the efficacy rate was 65.7%. On the other hand, in combination therapy, each was 14 patients (21.2%), 23 patients (34.8%), 12 patients (18.2%) and the efficacy rate was 56.1%. Side effects such as eruption were noted in 2 patients. Abnormal laboratory findings were noted in 9 patients. All side effects as well as abnormal laboratory findings were minimal. It was concluded that CZOP monotherapy was effective in the treatment of various infections accompanying hematological diseases.

Adolescent↗
PubMed2000

[A case of left renal cell carcinoma in a young male adult with left varicocele].

A 25-year-old man presented to our hospital with the chief complaint of left-sided painless scrotal swelling. Varicocele was diagnosed and high ligation was performed. Two months later, he noticed asymptomatic gross hematuria. Transabdominal ultrasonography and abdominal computed tomographic scanning showed a left renal tumor measuring more than 10 cm in diameter. Radical nephrectomy (thoraco-abdominal approach) was performed and pathological diagnosis was granular cell carcinoma (G2, pT2, INF alpha, pNX, pMX). He then received intramuscular injections of interferon-alpha 3 million units on three days per week. The frequency of renal cell carcinoma was reported to be about 1-3% for individuals in the 20s in the recent Japanese literature, and renal cell carcinoma in a young man with left varicocele is very rare.

Adenocarcinoma↗
PubMed2000

Differential mechanisms mediating descending pain controls for antinociception induced by supraspinally administered endomorphin-1 and endomorphin-2 in the mouse.

We have previously demonstrated that both endomorphin-1 and endomorphin-2 produce their antinociception by the stimulation of mu-opioid receptors. However, the antinociception induced by endomorphin-2 contains an additional component, which is mediated by the release of dynorphin A (1-17) acting on kappa-opioid receptors. These studies were done to determine whether the antinociception induced by endomorphin-1 and endomorphin-2 given supraspinally was mediated by the activation of different descending pain control pathways in the mouse. Specific receptor antagonists or antisera against endogenous opioid peptides were injected intrathecally to block the receptors or bind the released endogenous opioid peptides, and endomorphin-1 or endomorphin-2 was then administered i.c.v. to activate the descending pain control systems to produce antinociception. The tail-flick response was used as antinociceptive test. The blockade of the alpha(2)-adrenoceptors and 5-hydroxytryptamine receptors in the spinal cord by i.t. injection of yohimbine and methysergide, respectively, inhibited the antinociception induced by i.c.v.-administered endomorphin-1 and endomorphin-2. However, the antinociception induced by endomorphin-2 was inhibited by i.t. pretreatment with delta(2)-opioid receptor antagonist naltriben or kappa-opioid receptor antagonist nor-binaltorphimine, but not by the mu-opioid receptor antagonist D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH(2) or the delta(1)-opioid receptor antagonist 7-benzylidene naltrexamine. Intrathecal pretreatment with antiserum against Met-enkephalin attenuated the antinociception induced by i.c.v.-administered endomorphin-2, but not endomorphin-1. Furthermore, i.t. pretreatment with antiserum against dynorphin A (1-17) also inhibited the antinociception induced by i.c.v.-administered endomorphin-2, but not endomorphin-1. Intrathecal pretreatment with antiserum against Leu-enkephalin or beta-endorphin did not inhibit i.c.v.-administered endomorphin-1- or endomorphin-2-induced antinociception. The results indicate that, like other opioid micro-receptor agonists, morphine, and [D-Ala(2), N-Me-Phe(4), Gly(5)-ol]-enkephalin, endomorphin-1 and endomorphin-2 given i.c.v. produce antinociception by activating spinipetal noradrenergic and serotonergic pathways for producing antinociception. However, the antinociception induced by endomorphin-2 given i.c.v. also contains other components, which are mediated by the release of Met-enkephalin and dynorphin A (1-17) acting on opioid delta(2)- and kappa-receptors, respectively, in the spinal cord.

Adrenergic alpha-Antagonists↗
PubMed2000

Consensus Conference on the Treatment of Aplastic Anemia.

This article presents guidelines for the diagnosis and treatment of aplastic anemia (AA) established by a consensus panel of investigators from various countries. The panel used the scientific evidence presented during the Consensus Conference forum and found in the scientific literature to prepare guidelines categorized as immunosuppressive therapy, unrelated bone marrow transplantation in patients with AA, and myelodysplasia/acute myeloid leukemia after immunosuppressive therapy.

Anemia, Aplastic↗