Biomedical subjects

Qian Jiang

Publications and source records attributed to Qian Jiang.

At least 19 recordsLinked to original sources

PubMed2026

Phosphoproteomic Analysis of GAP50-Deficient Parasites Reveals the Inner Membrane Complex Is Involved in Ion Regulation in Toxoplasma gondii.

The Alveolata group of organisms is characterized by a vesicular structure located beneath the plasma membrane. In apicomplexa, this structure is known as the inner membrane complex (IMC). The IMC acts as a scaffold during the budding of the daughter parasite and is utilized as a rigid base for the glideosome. In this study, we discovered that the phosphatase activity of GAP50 is crucial for its function in the biogenesis of the IMC. Through further phosphoproteomic analysis of parasites lacking GAP50, we identified that an NIPA family transporter is localized in the IMC. Knocking out TgNIPA1 significantly impairs the robust growth of the parasites. Additionally, expressing TgNIPA1 in a Salmonella strain lacking magnesium transporters could rescue the growth phenotype of bacteria under low magnesium conditions, indicating that it functions as an active magnesium transporter. Our results strongly suggest that the flattened vesicles of the IMC may play important roles in ion regulation in T. gondii.

Toxoplasma↗

PubMed2007

RGS4 modulates serotonin signaling in prefrontal cortex and links to serotonin dysfunction in a rat model of schizophrenia.

Regulator of G protein signaling 4 (RGS4) has recently been identified as one of the genes linked to the susceptibility of schizophrenia. However, the functional roles of RGS4 and how it may be involved in the pathophysiology of schizophrenia remain largely unknown. In this study, we investigated the possible impact of RGS4 on the function of serotonin and dopamine receptors, two main targets for schizophrenia treatment. Activation of serotonin 5-HT(1A) receptors or dopamine D(4) receptors down-regulates the function of NMDA receptor (NMDAR) channel, a key player controlling cognition and emotion, in pyramidal neurons of prefrontal cortex (PFC). Blocking RGS4 function significantly potentiated the 5-HT(1A) regulation of NMDAR current; conversely, overexpression of RGS4 attenuated the 5-HT(1A) effect. In contrast, the D(4) regulation of NMDAR current was not altered by RGS4 manipulation. Moreover, the 5-HT(1A) regulation of NMDA receptors was significantly enhanced in a subset of PFC pyramidal neurons from rats treated with subchronic phencyclidine, an animal model of schizophrenia, which was found to be associated with specifically decreased RGS4 expression in these cells. Thus, our study has revealed an important coupling of RGS4 to serotonin signaling in cortical neurons and provided a molecular and cellular mechanism underlying the potential involvement of RGS4 in the pathophysiology of schizophrenia.

Animals↗

PubMed2006

Generalized n-photon resonant 2n-wave mixing in an (n+1)-level system with phase-conjugate geometry.

A generalized scheme for phase-conjugate resonant 2n-wave mixing, which has a high efficiency and is easy for phase matching, is proposed. As a new type of coherent laser spectroscopy this approach can be employed for studying highly excited atomic states or states with a high angular momentum. To demonstrate its feasibility we have studied the doubly excited autoionizing Rydberg states of Ba by phase-conjugate six-wave mixing, and have furthermore achieved eight-wave mixing in Na. This method may find wide application in related areas such as coherent transient spectroscopy, Autler-Townes spectroscopy and electromagnetically induced transparency. In particular, it may provide new insights into the nature of highly excited states.

Journal Article↗

PubMed2006

Neurotrophic factors stabilize microtubules and protect against rotenone toxicity on dopaminergic neurons.

Parkinson disease is characterized by the selective degeneration of dopaminergic (DA) neurons in substantia nigra. Long term epidemiological studies have implicated exposure to agricultural pesticides as a significant risk factor. Systemic administration of rotenone, a widely used pesticide, causes selective degeneration of nigral DA neurons and Parkinson disease-like symptoms in rats. Our previous study has shown that the microtubule depolymerizing activity of rotenone plays a critical role in its selective toxicity on DA neurons. Rotenone toxicity is mimicked by the microtubule-depolymerizing drug colchicine and attenuated by the microtubule-stabilizing agent taxol. Here we show that nerve growth factor (NGF) significantly reduced rotenone toxicity on TH(+) neurons in midbrain neuronal cultures. The protective effect of NGF was completely abolished by inhibiting the microtubule-associated protein kinase kinase (MEK) and partially reversed by blocking phosphatidylinositol 3-kinase. In addition, NGF decreased colchicine toxicity on TH(+) neurons in a manner dependent on MEK but not phosphatidylinositol 3-kinase. The protective effect of NGF against rotenone toxicity was occluded by the microtubule-stabilizing drug taxol. In a MEK-dependent manner, NGF significantly attenuated rotenone- or colchicine-induced microtubule depolymerization and ensuing accumulation of vesicles in the soma and elevation in protein carbonyls. Moreover, other neurotrophic factors such as brain-derived neurotrophic factor and glia cell line-derived neurotrophic factor also reduced rotenone- or colchicine-induced microtubule depolymerization and death of TH(+) through a MEK-dependent mechanism. Thus, our results suggest that neurotrophic factors activate the microtubule-associated protein kinase pathway to stabilize microtubules, and this action significantly attenuates rotenone toxicity on dopaminergic neurons.

Animals↗

PubMed2006

Activation of group III metabotropic glutamate receptors attenuates rotenone toxicity on dopaminergic neurons through a microtubule-dependent mechanism.

Systemic administration of rotenone, a widely used pesticide, causes selective degeneration of nigral dopaminergic (DA) neurons and Parkinson's disease-like symptoms in animal models. Our previous study has shown that the microtubule-depolymerizing activity of rotenone plays a critical role in its selective toxicity on tyrosine hydroxylase-positive (TH+) neurons in rat embryonic midbrain neuronal cultures. Here, we show that application of group III metabotropic glutamate receptor (mGluRIII) agonists (e.g., L-AP-4) significantly reduced rotenone toxicity on midbrain TH+ neurons in culture. The protective effect of L-AP-4 was abolished by pharmacological inhibition of the microtubule-associated protein (MAP) kinase kinase (MEK) or overexpression of dominant-negative MEK1, suggesting its dependence on the MAP kinase cascade. We found that L-AP-4 induced a rapid and transient activation of the MAP kinase extracellular signal-regulated kinase (ERK) through a pathway mediated by dynamin, beta-arrestin 2, and Src. ERK activated in this manner targeted cytosolic rather than nuclear substrates. Consistent with this, L-AP-4 significantly attenuated rotenone- or colchicine-induced microtubule depolymerization in an MEK-dependent manner. Moreover, L-AP-4 decreased colchicine toxicity on TH+ neurons in an MEK-dependent manner as well. The protective effect of L-AP-4 against rotenone toxicity was occluded by the microtubule-stabilizing agent Taxol. Together, these results suggest that activation of group III metabotropic glutamate receptors attenuates the selective toxicity of rotenone on DA neurons by activating the MAP kinase pathway to stabilize microtubules. These findings may offer a novel neuroprotective approach against rotenone-induced parkinsonism.

Animals↗

PubMed2006

Parkin suppresses the expression of monoamine oxidases.

Mutations of parkin are linked to early onset Parkinson disease. Here we show that stable transfection of parkin in the human dopaminergic neuroblastoma cell line SH-SY5Y markedly reduced the activities of both monoamine oxidase (MAO) A and B. The amount of 3,4-dihydroxyphenylacetic acid, which is produced during dopamine oxidation by MAO, was greatly reduced by parkin overexpression. Radioligand binding assays showed that MAO binding sites were decreased accordingly. Consistent with these, MAO-B protein level was much lower, whereas the amount of MAO-A protein was not determined due to the lack of a suitable antibody. Co-transfection of either MAO with parkin in HEK293 cells did not significantly alter ubiquitination and degradation of each MAO. When we measured MAO expression by real-time quantitative reverse transcription-PCR, marked reductions were seen in SH-SY5Y cells stably expressing parkin compared with the parental cells or a control line stably transfected with luciferase. In addition, parkin mutants defective in E3 ligase activity exhibited different effects on MAO expression. We found that parkin also significantly decreased mRNA levels of both MAOs in the mouse fibroblast cell line NIH3T3. Furthermore, MAO expression was significantly increased in human B lymphocyte cell lines derived from Parkinson disease patients with homozygous but not heterozygous deletion of exon 4 of parkin. Together these results suggest that parkin suppresses MAO expression. This function may limit the production of reactive oxygen species generated by MAO in dopamine oxidation and would, thus, be beneficial to the survival of dopaminergic neurons.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2006

Long-term effect of early discharge on sEPSC and [Ca2+]i in developing neurons.

To study the long-term changes induced in immature rat cortical neuronal cultures by transient exposure to an Mg(2+)-free treatment, at cultured day 6, cells were assigned into three groups, based on the mediums they were transiently exposed to as follows: control group 1 (CONT1) was exposed to Dulbecco's Modified Eagle's Medium (DMEM), control group 2 was exposed to a physiological solution (PS), and the magnesium-free physiological solution group (MGFPS) was exposed to the same medium as CONT2 except for the removal of magnesium. Following a 3-h exposure, the amplitude and frequency of spontaneous excitatory postsynaptic currents (sEPSC) were recorded and intracellular calcium concentrations ([Ca2+]i) were measured. Compared to the CONT1 and CONT2 groups, the MGFPS group displayed a significantly greater amplitude (at d6, d7, d9, and d12) and frequency (at d6, d7, and d9) of sEPSC (p<0.05). Also, both the resting and peak intracellular calcium levels were significantly greater in the MGFPS group at days 6, 7, 9, 12 and 17 (p<0.05). The rise time (time from resting level to peak level of intracellular calcium following NMDA application) was significantly shorter in the MGFPS group at culture days 7 and 17 and significantly longer at culture day 12 (p<0.05). Finally, we compared the percentage of cortical neurons expressing neuron-specific enolase (NSE) and found that there were no significant differences in the number of NSE positive neurons among three groups at days 7, 12, and 17. Our results suggests that there are long-term changes in sEPSCs and [Ca2+]i in cultured rat cortical neurons following exposure to Mg2+-free environment without cell loss.

Analysis of Variance↗

PubMed2006

[Syndrome inappropriate ADH secretion after allogeneic hematopoietic stem cell transplantation: a case report and literature review].

OBJECTIVE: To study the syndrome of inappropriate ADH secretion (SIADH) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) and the possible etiology. METHODS: The clinical manifestation, laboratory examination, treatment and outcome of a patient with refractory anemia with excess blasts after allo-HSCT were presented. RESULTS: Hyperacute graft-versus-host disease (GVHD) was developed in the patient after allo-HSCT followed by severe hyponatraemia (lowest serum sodium 103.7 mmol/L), natriuresis, hypo-osmolality of plasma, hyper-osmolality of urine, coma and twitch at day 17 after allo-HSCT. SIADH was diagnosed. The clinical condition was improved after restriction of water and administration of hypertonic saline, but SIADH was not controlled completely. Afterwards, graft failure was developed. Hyperacute GVHD and graft rejection occurred again after the second transplant. The patient died of secondary infection. CONCLUSION: SIADH after allo-HSCT is a rare fatal acute complication of central nervous system. Numerous transplant-related causes are probably associated with the development of SIADH. Early accurate diagnosis and treatment promptly is of great importance.

Adolescent↗

PubMed2006

[Alterations in coagulation in patients during transplant conditioning regimen before allogeneic hematopoietic stem cell transplantation].

OBJECTIVE: To evaluate the alterations in coagulation in patients during conditioning with modified busulfan plus cyclophosphamide (BU/CY) +/- antithymocyte globulin (ATG) regimen before allogeneic hematopoietic stem cell transplantation (allo-HSCT), and to assess the effect of ATG on coagulation system. METHODS: Thirty-five patients with various hematological malignancies undergoing allo-HSCT were assessed. Of them, 19 patients with HLA-matched sibling donors (group A) were conditioned with modified BU/CY regimen, 16 with HLA-mismatched family members or HLA-matched unrelated donors (group B) were conditioned with modified BU/CY + ATG regimen. Blood samples were collected before the beginning of conditioning till d + 1 after allo-HSCT. The following parameters were measured: prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (Fg), antithrombin (AT), D-Dimer, fibrin degradation product (FDP), platelet (BPC), liver enzymes and bilirubin. FVIII: C, FIX: C, FXI: C and FXII: C in prolonged APTT blood samples were also determined. Clinical hemorrhagic symptoms were monitored. RESULTS: During conditioning, temporary lengthening of APTT, persistent rising in Fg and declining of BPC were observed in the two groups. Alterations of Fg and BPC were more significant in group B than in group A. Transient D-Dimer increase occurred only in group B on administration of ATG. Among intrinsic pathway coagulation factors, FXII: C and FXI: C were commonly decreased while APTT prolonged. No difference between the two groups was found with regard to PT, FDP, AT and liver parameters which remained in normal ranges. Most of patients in the two groups did not have overt bleeding manifestations. CONCLUSIONS: Modified BU/CY +/- ATG conditioning regimen can induce subclinical alterations in coagulation. The regimen containing ATG has more significant effect on coagulation parameters.

Adolescent↗

PubMed2005

Activation of dopamine D4 receptors induces synaptic translocation of Ca2+/calmodulin-dependent protein kinase II in cultured prefrontal cortical neurons.

One of the important targets of dopamine D4 receptors in prefrontal cortex (PFC) is the multifunctional Ca2+/calmodulin-dependent protein kinase II (CaMKII). In the present study, we investigated the effect of D4 receptor activation on subcellular localization of CaMKII. We found that activation of D4 receptors, but not D2 receptors, induced a rapid translocation of alpha-CaMKII from cytosol to postsynaptic sites in cultured PFC neurons. Activated CaMKII (Thr286 phospho-CaMKII) was also redistributed to postsynaptic sites after D4 receptor stimulation. The translocation was blocked by inhibiting the phospholipase C/inositol 1,4,5-trisphosphate receptor/Ca2+ signaling. Point mutation of the calmodulin binding site (Ala302), but not the autophosphorylation site (Thr286), of alpha-CaMKII prevented the D4-induced CaMKII translocation. Moreover, D4 receptors failed to induce CaMKII translocation in the presence of an actin stabilizer, and D4 activation reduced the binding of CaMKII to F-actin. Concomitant with the synaptic accumulation of alpha-CaMKII in response to D4 receptor activation, a D4-induced increase in the CaMKII phosphorylation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor glutamate receptor 1 (GluR1) subunits and the amplitude of AMPA receptor-mediated excitatory postsynaptic currents was also observed. Thus, our results show that D4 receptor activation induces the synaptic translocation of CaMKII through a mechanism involving Ca2+/calmodulin and F-actin, which facilitates the regulation of synaptic targets of CaMKII, such as AMPA receptors.

Animals↗

PubMed2005

[Disease transformation in imatinib mesylate treated Philadelphia chromosome-positive chronic myelogenous leukemia patients achieved cytogenetic remissions].

OBJECTIVE: To report disease transformation in 3 imatinib mesylate treated Philadelphia chromosome-positive chronic myelogenous leukemia (Ph(+)CML) patients who achieved cytogenetic response. METHODS: Hematologic examinations and bone marrow G-banding karyotyping were evaluated at regular intervals in 3 patients with Ph(+)CML who achieved hematologic responses during continuous imatinib therapy, including 1 patient in first chronic phase (case 1), 1 patient in second chronic phase (case 2) and 1 patient in accelerated phase (case 3). RESULTS: Case 1, case 2 and case 3 achieved complete cytogenetic response after 4, 3 and 6 months of imatinib therapy respectively. Though under continuously imatinib treatment, they developed acute lymphoblastic leukemia, acute myelogenous leukemia and extramedullary blast crisis in the following 12, 6 and 0 months respectively. Cytogenetic studies of bone marrow in the crisis period showed that cells in case 1 and case 3 had a complete cytogenetic response (Ph(+)cell=0), but case 2 had 20% Ph(+) cells. CONCLUSION: Acute leukemia or extramedullary blast crisis with Ph(-) cells or dominant Ph(-) cells in bone marrow may occur in the patients with Ph(+)CML after imatinib therapy.

Adult↗

PubMed2005

[Analysis of ABL tyrosine kinase point mutations in imatinib treated chronic myelogenous leukemia patients].

OBJECTIVE: To evaluate ABL tyrosine kinase point mutations in imatinib treated chronic myelogenous leukemia (CML) patients. METHODS: A total of 45 bone marrow samples from 30 CML patients were included in this work. The patients were in accelerated/blast phase (AP/BP) or late-chronic phase (CP) at the start of imatinib and usually showed resistance to imatinib. ABL kinase domain of BCR-ABL allele was amplified by nested reverse transcriptase-polymerase chain reaction technique, followed by direct sequencing and sequence homologous analyzing. RESULTS: The ABL point mutation was detected in 13 of 30 patients, 12 of them had progressed to advanced phase, The other patient who was in late chronic phase showed point mutation when she was at 45th months of imatinib treatment, but she was still in complete cytogenetic remission at 50th months and is doing well. 4 patients had Glu255Lys mutation and 4 had Gly250Glu, the other types of mutation were Phe359Cys, Glu355Gly, Met244Val, Tyr253His and Asp276Gly, each was tested in one patient. 11/12 patients who progressed to advanced disease and showed point mutation were collected samples in advanced stage, 8 patients showed homozygote mutation, and 3 patients had a mixture of wild and mutant type. In advanced stage patients, mutations were detected in a median of 5 months (ranged 0.5-30 months), it appeared much earlier than that in late CP patients (25.5 months, ranged 11-45 months, P < 0.05). In 4/7 followed up patients, the intensity of point mutation increased gradually within 7-15 months before disease progression. 6 patients did not showed ABL point mutation while their disease were in progression. CONCLUSIONS: Abl kinase point mutation is one of the main mechanisms of CML secondary resistance to imatinib. Long term regular monitoring of ABL kinase point mutation is necessary during imatinib treatment.

Adolescent↗

PubMed2005

Selective vulnerability of dopaminergic neurons to microtubule depolymerization.

Parkinson disease (PD) is characterized by the specific degeneration of dopaminergic (DA) neurons in substantia nigra and has been linked to a variety of environmental and genetic factors. Rotenone, an environmental PD toxin, exhibited much greater toxicity to DA neurons in midbrain neuronal cultures than to non-DA neurons. The effect was significantly decreased by the microtubule-stabilizing drug taxol and mimicked by microtubule-depolymerizing agents such as colchicine or nocodazole. Microtubule depolymerization disrupted vesicular transport along microtubules and caused the accumulation of dopamine vesicles in the soma. This led to increased oxidative stress due to oxidation of cytosolic dopamine leaked from vesicles. Inhibition of dopamine metabolism significantly reduced rotenone toxicity. Thus, our results suggest that microtubule depolymerization induced by PD toxins such as rotenone plays a key role in the selective death of dopaminergic neurons.

Cell Death↗

PubMed2005

Microtubule regulation of N-methyl-D-aspartate receptor channels in neurons.

N-Methyl-D-aspartate (NMDA) receptors (NMDARs), which play a key role in synaptic plasticity, are dynamically regulated by many signaling molecules and scaffolding proteins. Although actin cytoskeleton has been implicated in regulating NMDAR stability in synaptic membrane, the role of microtubules in regulating NMDAR trafficking and function is largely unclear. Here we show that microtubule-depolymerizing agents inhibited NMDA receptor-mediated ionic and synaptic currents in cortical pyramidal neurons. This effect was Ca(2+)-independent, required GTP, and was more prominent in the presence of high NMDA concentrations. The NR2B subunit-containing NMDA receptor was the primary target of microtubules. The effect of microtubule depolymerizers on NMDAR currents was blocked by cellular knockdown of the kinesin motor protein KIF17, which transports NR2B-containing vesicles along microtubule in neuronal dendrites. Neuromodulators that can stabilize microtubules, such as brain-derived neurotrophic factor, significantly attenuated the microtubule depolymerizer-induced reduction of NMDAR currents. Moreover, immunocytochemical studies show that microtubule depolymerizers decreased the number of surface NR2B subunits on dendrites, which was prevented by the microtubule stabilizer. Taken together, these results suggest that interfering with microtubule assembly suppresses NMDAR function through a mechanism dependent on kinesin-based dendritic transport of NMDA receptors.

Animals↗

PubMed2005

Serotonin 5-HT1A receptors regulate NMDA receptor channels through a microtubule-dependent mechanism.

The serotonin system and NMDA receptors (NMDARs) in prefrontal cortex (PFC) are both critically involved in the regulation of cognition and emotion under normal and pathological conditions; however, the interactions between them are essentially unknown. Here we show that serotonin, by activating 5-HT(1A) receptors, inhibited NMDA receptor-mediated ionic and synaptic currents in PFC pyramidal neurons, and the NR2B subunit-containing NMDA receptor is the primary target of 5-HT(1A) receptors. This effect of 5-HT(1A) receptors was blocked by agents that interfere with microtubule assembly, as well as by cellular knock-down of the kinesin motor protein KIF17 (kinesin superfamily member 17), which transports NR2B-containing vesicles along microtubule in neuronal dendrites. Inhibition of either CaMKII (calcium/calmodulin-dependent kinase II) or MEK/ERK (mitogen-activated protein kinase kinase/extracellular signal-regulated kinase) abolished the 5-HT(1A) modulation of NMDAR currents. Biochemical evidence also indicates that 5-HT(1A) activation reduced microtubule stability, which was abolished by CaMKII or MEK inhibitors. Moreover, immunocytochemical studies show that 5-HT(1A) activation decreased the number of surface NR2B subunits on dendrites, which was prevented by the microtubule stabilizer. Together, these results suggest that serotonin suppresses NMDAR function through a mechanism dependent on microtubule/kinesin-based dendritic transport of NMDA receptors that is regulated by CaMKII and ERK signaling pathways. The 5-HT(1A)-NMDAR interaction provides a potential mechanism underlying the role of serotonin in controlling emotional and cognitive processes subserved by PFC.

Animals↗

PubMed2005

Regulation of NMDA receptors by neuregulin signaling in prefrontal cortex.

Recent linkage studies have identified a significant association of the neuregulin gene with schizophrenia, but how neuregulin is involved in schizophrenia is primarily unknown. Aberrant NMDA receptor functions have been implicated in the pathophysiology of schizophrenia. Therefore, we hypothesize that neuregulin, which is present in glutamatergic synaptic vesicles, may affect NMDA receptor functions via actions on its ErbB receptors enriched in postsynaptic densities, hence participating in emotional regulation and cognitive processes that are impaired in schizophrenia. To test this, we examined the regulation of NMDA receptor currents by neuregulin signaling pathways in prefrontal cortex (PFC), a prominent area affected in schizophrenia. We found that bath perfusion of neuregulin significantly reduced whole-cell NMDA receptor currents in acutely isolated and cultured PFC pyramidal neurons and decreased NMDA receptor-mediated EPSCs in PFC slices. The effect of neuregulin was mainly blocked by application of the ErbB receptor tyrosine kinase inhibitor, phospholipase C (PLC) inhibitor, IP3 receptor (IP3R) antagonist, or Ca2+ chelators. The neuregulin regulation of NMDA receptor currents was also markedly attenuated in cultured neurons transfected with mutant forms of Ras or a dominant-negative form of MEK1 (mitogen-activated protein kinase kinase 1). Moreover, the neuregulin effect was prevented by agents that stabilize or disrupt actin polymerization but not by agents that interfere with microtubule assembly. Furthermore, neuregulin treatment increased the abundance of internalized NMDA receptors in cultured PFC neurons, which was also sensitive to agents affecting actin cytoskeleton. Together, our study suggests that both PLC/IP3R/Ca2+ and Ras/MEK/ERK (extracellular signal-regulated kinase) signaling pathways are involved in the neuregulin-induced reduction of NMDA receptor currents, which is likely through enhancing NR1 internalization via an actin-dependent mechanism.

Animals↗

PubMed2005

[Methotrexate for treatment of graft versus host disease after allogeneic hematopoietic stem cell transplantation].

OBJECTIVE: To evaluate the efficacy and safety of low-dose methotrexate in patients with graft versus host disease (GVHD) after allogeneic hematopoietic stem cell transplantation (Allo-HSCT). METHODS: Thirty-one patients with minor or moderate grade acute GVHD (aGVHD), chronic GVHD (cGVHD) or GVHD post donor lymphocyte infusion (post-DLI GVHD) after Allo-HSCT received intravenously administrated methotrexate at a dose of 5 or 10mg every 5 to 7 days until achieving complete or partial responses, treatment failure or intolerable side effects. RESULTS: The overall response rate was 93.8% (15/16 patients) in patients with aGVHD, 75% (12/16 patients) in patients with cGVHD and 100% (2/2 in patients) with post-DLI GVHD. The response rate for GVHD involving organs was 100% in skin, 60% in gut, 71% in liver, 75% in mouth and 100% in eyes. Side effects were minor. During the therapy, the other immunosuppressive agents were reduced. CONCLUSION: Short-term low-dose methotrexate is a tolerable and effective regimen for patients with minor or moderate grade aGVHD, cGVHD or post-DLI GVHD after Allo-HSCT.

Adolescent↗

PubMed2005

[Analysis of pathogenesis of pneumonia post allogeneic hematopoietic stem cell transplantation].

OBJECTIVE: To analyse the clinical features and pathogenesis of pneumonia post allogeneic hematopoietic stem cell transplantation (HSCT). METHODS: Analysis was made of 255 patients of recipients of allo-HSCT from 1998 to 2001. RESULTS: Seventy-two episodes of pneumonia occurred in 66 patients with the morbidity of 25.9%; 50 (75%) patients were cured. Twelve episodes (16.7%) were caused by mixed infection of bacteria and fungi; 22 episodes (30.6%) were caused by cytomegalovirus infection and 36 episodes (50.0%) were classified as idiopathic pneumonia syndrome. The total mortility of pneumonia post allo-HSCT in our institute was 22.7%. The occurrence of chronic graft-versus-host disease was significantly high in idiopathic pneumonia syndrome, in which good response to immune suppressive therapy was observed. CONCLUSION: Pneumonia post allo-HSCT is a common complication, of which pathogenesis includes infection and non-infection. Its clinical outcome could be improved by specific therapy.

Adolescent↗