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1.
Journal of Leukemia & Lymphoma ; (12): 630-633, 2021.
Artigo em Chinês | WPRIM | ID: wpr-907225

RESUMO

Angioimmunoblastic T-cell lymphoma (AITL) is an aggressive peripheral T-cell lymphoma (PTCL) that originates from follicular helper T cells (TFH). It has the highest incidence in PTCL which is second only to PTCL-not otherwise specified (PTCL-NOS). Its clinicopathological diagnosis is difficult, it is easy to be misdiagnosed and missed, and the prognosis is poor. This article reviews the pathogenesis, clinical and pathological characteristics as well as treatment progress of AITL, in order to provide a reasonable basis for clinical diagnosis and treatment of the disease.

2.
Journal of International Oncology ; (12): 568-571, 2021.
Artigo em Chinês | WPRIM | ID: wpr-907582

RESUMO

Small cell lung cancer (SCLC), as a pathological type with high malignancy, presents a high risk of early brain metastasis. Prophylactic cranial irradiation (PCI) can reduce the risk of brain metastasis in patients with SCLC, however, the incidence of brain structural and functional damage caused by PCI is high, and their clinical symptoms are not typical. The existing treatment methods can relieve some clinical symptoms, but can not effectively reverse the process of brain injury, which reduces the survival benefit of patients. In-depth understanding the mechanisms of PCI neurotoxicity and exploring effective strategies for ptevention and treatment are of great value in improving prognosis of SCLC.

3.
Acta Physiologica Sinica ; (6): 62-68, 2011.
Artigo em Chinês | WPRIM | ID: wpr-337703

RESUMO

TGFβ/smad pathway is recognized as an important signal pathway to promote the pathogenesis of atherosclerosis (AS). Peroxisome proliferator-activated receptor γ (PPARγ) activation is considered to be important in modulating AS. Herein, we investigated the regulation of PPARγ on c-Ski, the repressor of TGFβ/smad pathway, in rat AS model and cultured vascular smooth muscle cells (VSMCs). c-Ski mRNA and protein expression were detected by real-time PCR and Western blot, respectively, in vivo and in vitro with treatment of PPARγ agonist rosiglitazone and antagonist GW9662. The proliferation and collagen secretion of VSMCs after c-Ski transfection were investigated. The underlying mechanism was further investigated by online program NUBIScan and luciferase reporter gene analysis. Results showed that both mRNA and protein expressions of c-Ski in the AS lesions was down-regulated in vivo, while in cultured VSMCs, c-Ski transfection significantly suppressed the proliferation and collagen secretion of rat VSMCs. Rosiglitazone significantly up-regulated mRNA and protein levels of c-Ski in VSMCs, which could be blocked by GW9662. Online NUBIScan analysis suggested possible PPARγ binding sites in the promoter region of c-Ski. In addition, luciferase activity of c-Ski reporter gene was also increased obviously in the presence of rosiglitazone. These results indicate that c-Ski is one of the newly found target genes of PPARγ and thus involved in the anti-AS effect of PPARγ.


Assuntos
Animais , Masculino , Ratos , Anilidas , Farmacologia , Aterosclerose , Células Cultivadas , Músculo Liso Vascular , Biologia Celular , Miócitos de Músculo Liso , Metabolismo , PPAR gama , Fisiologia , Proteínas Proto-Oncogênicas , Genética , Metabolismo , RNA Mensageiro , Genética , Metabolismo , Ratos Wistar , Proteínas Repressoras , Genética , Metabolismo , Transdução de Sinais , Proteínas Smad , Metabolismo , Tiazolidinedionas , Farmacologia , Fator de Crescimento Transformador beta , Metabolismo , Regulação para Cima
4.
Chinese Acupuncture & Moxibustion ; (12): 533-536, 2010.
Artigo em Chinês | WPRIM | ID: wpr-254933

RESUMO

<p><b>OBJECTIVE</b>To observe the therapeutic effect of acpuncture treatment for chronic fatigue syndrome (CFS).</p><p><b>METHODS</b>Nighty cases of CFS were randomly divided into an observation group and a control group, 45 cases in each group. The observation group was treated with acupunture at Renying (ST 9), Fengfu (GV 16), Baihui (GV 20); the control group was treated with 250 mL 5% Glucose injectio combined with 20 mL Shenmai injectio. Fatigue Scale (FS) was used to compare the scores between the two groups after treatment.</p><p><b>RESULTS</b>The total scores in the observation group were 9.37 +/- 2.33 and 5.41 +/- 1.96 before and after treatment respectively, and in the control group, they were 9.08 +/- 2.27 and 7.34 +/- 2.03 respectively. FS brainwork integral, physical fatigue integral, and total integral all decreased after treatment in two groups (all P < 0.001), and it decreased much more obviously in the observation group (P < 0.05, P < 0.01).</p><p><b>CONCLUSION</b>Both of the acpuncture treatment and Shenmai injectio are able to decrease fatigue scale score, improve the fatigue symptoms of CFS patients, and the effect of acupucture treatment is obviously superior to that of Shenmai injectio.</p>


Assuntos
Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Terapia por Acupuntura , Síndrome de Fadiga Crônica , Terapêutica , Resultado do Tratamento
5.
Acta Physiologica Sinica ; (6): 555-559, 2010.
Artigo em Chinês | WPRIM | ID: wpr-337712

RESUMO

The aim of this study is to investigate the effect of (S)-4-carboxy-3-hydroxy-phenylglycine [(S)-4C3HPG], a mixed group I glutamate metabotropic receptor antagonist and a group II agonist, on impairment in a cortical impact model of traumatic brain injury (TBI) in mice and to elucidate the possible mechanisms. Mice were injected (i.p.) with saline, 1 mg/kg (S)-4C3HPG, 5 mg/kg (S)-4C3HPG and 10 mg/kg (S)-4C3HPG (n=10 per group), respectively, at 30 min before moderate TBI. Neurological deficit scores, water content in injured brain and glutamate concentration in cerebral spinal fluid (CSF) were detected at 24 h after TBI. The expressions of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) mRNA in injured cortex were also detected by real-time RT-PCR. The results showed that the neurological deficits and cerebral edema were significantly attenuated in mice pretreated with (S)-4C3HPG (5 and 10 mg/kg respectively) compared with those in mice pretreated with saline. Furthermore, (S)-4C3HPG treatment also decreased the glutamate concentration in CSF and the expressions of TNF-α and IL-1β mRNA remarkably in a dose-dependent manner. These results suggest that (S)-4C3HPG treatment attenuates cortical impact-induced brain injury possibly via suppression of glutamate release and inhibition of excessive inflammatory cytokine production. These findings highlight the potential benefit of glutamate metabotropic receptor ligand for preventing TBI.


Assuntos
Animais , Masculino , Camundongos , Lesões Encefálicas , Tratamento Farmacológico , Metabolismo , Citocinas , Metabolismo , Ácido Glutâmico , Líquido Cefalorraquidiano , Glicina , Usos Terapêuticos , Camundongos Endogâmicos C57BL , Receptores de Glutamato Metabotrópico
6.
Acta Physiologica Sinica ; (6): 254-258, 2008.
Artigo em Chinês | WPRIM | ID: wpr-316732

RESUMO

Recently, activation of the adenosine A2A receptors has been shown to exert protection against peripheral tissue injuries but aggravation in the central nervous system (CNS) injuries. To explore the different effects of adenosine A2A receptors and try to perform some new treatment strategies for peripheral tissue and CNS traumas, we constructed the mouse models of skin trauma, skin combined radiation-impaired wound and traumatic brain injury (TBI), respectively. Wild type mice and A2A receptor gene knockout mice were both used in the experiments. In skin trauma and combined radiation-impaired wound models, the time of wound healing was observed, while in TBI model, neurological deficit scores, water content in injured brain and glutamate concentration in cerebral spinal fluid (CSF) were detected at 24 h after TBI. The results showed that in skin trauma and combined radiation-impaired wound models, CGS21680 (an agonist of the A2A receptors) promoted while A2A receptor gene knockout delayed the course of skin wound healing. On the contrary, in TBI model, A2A receptor gene knockout, not CGS21680, showed a protective role by inhibition of glutamate release. These data further indicate that promoting glutamate release may account for the different effects of A2A receptor activation in CNS injury and peripheral tissue injury models. These findings may provide some experimental evidence and a new strategy for clinical treatment of peripheral tissue damages by agonists of A2A receptors, while treatment of CNS injuries by antagonists of A2A receptors.


Assuntos
Animais , Camundongos , Adenosina , Farmacologia , Encéfalo , Patologia , Lesões Encefálicas , Modelos Animais de Doenças , Ácido Glutâmico , Líquido Cefalorraquidiano , Camundongos Knockout , Fenetilaminas , Farmacologia , Receptor A2A de Adenosina , Genética , Fisiologia , Cicatrização
7.
Chinese Journal of Hematology ; (12): 174-177, 2007.
Artigo em Chinês | WPRIM | ID: wpr-328389

RESUMO

<p><b>OBJECTIVE</b>To establish a mice model with selective inactivation adenosine A2A receptors (A2ARs) in peripheral white blood cells (PWBC).</p><p><b>METHODS</b>A2ARs were selectively inactivated in PWBCs by transplanting bone marrow cells (BMCs) from A2AR knockout (KO) mice into their wild type (WT) littermates after a single total body irradiation of 9.5 Gy or fractionated total body irradiation of 6.2 Gy x 2. The efficiency of reconstitution of bone marrow-derived cells in chimeric mice was assessed.</p><p><b>RESULTS</b>PCR band patterns changed from the recipient pattern (one band of 330 bp) to the donor (two bands of 300 and 330 bp) pattern. Immunohistochemistry analysis showed that 10.21% of cells were A2AR+ in PWBCs in KO--> WT mice, whereas 96.72% of cells were A2AR+ in WT mice. The survival rates of mice irradiated with 6.2 Gy x 2 and transplanted with more than 6 x 10(6) BMCs were about 91%.</p><p><b>CONCLUSION</b>A murine model of selective inactivation adenosine A2A receptors in PWBCs was established successfully.</p>


Assuntos
Animais , Camundongos , Deleção de Genes , Camundongos Endogâmicos C57BL , Camundongos Knockout , Modelos Animais , Receptor A2A de Adenosina , Genética
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