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1.
World J Clin Cases ; 12(4): 795-800, 2024 Feb 06.
Artigo em Inglês | MEDLINE | ID: mdl-38322680

RESUMO

BACKGROUND: The majority of gastric neuroendocrine tumors (G-NENs) are present in various lesions under endoscopy, and they can be polypoid uplifts, submucosal tumors or papules, erosions, and ulcers. The lesions are mostly confined to the mucosal or submucosal layer, usually less than 2 cm, and exclusively localized to the gastric body or fundus. In type 1 G-NENs, about 22% of cases have no visible lesions under an endoscope, and such lesions can only be detected via biopsies (microcarcinoids). CASE SUMMARY: A 67-year-old female patient with appetite loss for more than half a year and personal history of hyperthyroidism was admitted to our hospital. After admission, a random multi-point biopsy was performed on the gastric body, fundus, angle, and antrum through gastroscopy. Pathological examination showed chronic severe atrophic gastritis in the fundus and body of the stomach. The small curvature of the gastric body, the anterior wall of the gastric body, and the posterior wall of the gastric body displayed proliferation of intestinal chromaffin cells. The curvature of the gastric body showed neuroendocrine tumor G1 (carcinoid), while the antrum and angle of the stomach showed mild atrophic gastritis with mild intestinal metaplasia. Immunohistochemical examination showed that the greater curvature of the gastric body was Syn (+), CgA (+), and Ki-67 (+, approximately 1%), which is consistent with neuroendocrine tumors (grade 1). Regular gastroscopy and biopsy should be performed every one to two years to monitor G-NENs. CONCLUSION: In the case under study, the patient did not have any visible raised lesions under a gastroscope, and the lesions were found only after a random biopsy. This article combines the endoscopic manifestations and clinical features of the lesions in this case to improve the diagnosis of G-NENs.

2.
Yi Chuan ; 45(5): 395-408, 2023 May 20.
Artigo em Inglês | MEDLINE | ID: mdl-37194587

RESUMO

STIM1 (stromal interaction molecule 1) is one of the key components of the store operated Ca2+ entry channel (SOCE), which is located on the endoplasmic reticulum membrane and highly expressed in most kinds of tumors. STIM1 promotes tumorigenesis and metastasis by modulating the formation of invadopodia, promoting angiogenesis, mediating inflammatory response, altering the cytoskeleton and cell dynamics. However, the roles and mechanism of STIM1 in different tumors have not been fully elucidated. In this review, we summarize the latest progress and mechanisms of STIM1 in tumorigenesis and metastasis, thereby providing insights and references for the study on STIM1 in the field of cancer biology in the future.


Assuntos
Cálcio , Carcinogênese , Humanos , Molécula 1 de Interação Estromal/genética , Molécula 1 de Interação Estromal/metabolismo , Carcinogênese/genética , Cálcio/metabolismo , Sinalização do Cálcio/fisiologia , Proteínas de Neoplasias/genética
3.
Inorg Chem ; 55(4): 1412-22, 2016 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-26811966

RESUMO

Two new dinuclear Ru(II) polypyridyl complexes containing three and ten methylene chains in their bridging linkers are synthesized and characterized. Their calf thymus DNA-binding and plasmid DNA photocleavage behaviors are comparatively studied with a previously reported, six-methylene-containing analog by absorption and luminescence spectroscopy, steady-state emission quenching by [Fe(CN)6](4-), DNA competitive binding with ethidium bromide, DNA viscosity measurements, DNA thermal denaturation, and agarose gel electrophoresis analyses. Theoretical calculations applying the density functional theory (DFT) method for the three complexes are also performed to understand experimentally observed DNA binding properties. The results show that the two complexes partially intercalate between the base pairs of DNA. Cellular uptake and colocalization studies have demonstrated that the complexes could enter HeLa cells efficiently and localize within lysosomes. The in-vitro antitumor activity against HeLa and MCF-7 tumor cells of the complexes are studied by MTT cytotoxic analysis. A new method, high-content analysis (HCA), is also used to assess cytotoxicity, apoptosis and cell cycle arrest of the three complexes. The results show that the lengths of the alkyl linkers could effectively tune their biological properties and that HCA is suitable for rapidly identifying cytotoxicity and can be substituted for MTT assays to evaluate the cell cytotoxicity of chemotherapeutic agents.


Assuntos
DNA/metabolismo , Compostos de Rutênio/metabolismo , Ensaios de Seleção de Medicamentos Antitumorais , Eletroforese em Gel de Ágar , Células HeLa , Humanos , Técnicas In Vitro , Células MCF-7 , Processos Fotoquímicos , Compostos de Rutênio/farmacologia
4.
Zhongguo Shi Yan Xue Ye Xue Za Zhi ; 23(5): 1464-8, 2015 Oct.
Artigo em Chinês | MEDLINE | ID: mdl-26524058

RESUMO

OBJECTIVE: To explore the molecular mechanism of erythrocyte pyruvate kinase deficiency (PKD). METHODS: Targeted sequence capture and next-generation sequencing (NGS) were used to detect the regions of exon and exon-intron boundarie of PKLR gene in a clinical suspected PKD patient. The protein function of mutant gene was forecasted by the SIFT and PolyPhen-2 databank, after the mutation of PKLR gene in the patient was detected by the NGS technology, its genotype was confirmed by Sanger sequencing. RESULTS: The patient was found to have peculiar double heterozygous mutations: 661 G>A (Asp221Asn) of exon 5 and 1528 C>T (Arg510Ter) of exon 10, resulting in amino acid substitution Asp221Asn and Arg510Ter, these mutations were also further confirmed by Sanger sequencing. The complex mutations were infrequent and each of them was able to cause diseases. CONCLUSION: The complex mutations of both 661 G>A and 1528 C>T of PKLR gene are the molecular mechanism of PKD. Simultaneous existance of above-mentioned complex mutations in PDK patient was never been previously reported at home and abroad.


Assuntos
Anemia Hemolítica Congênita não Esferocítica/genética , Sequenciamento de Nucleotídeos em Larga Escala , Mutação , Piruvato Quinase/deficiência , Piruvato Quinase/genética , Erros Inatos do Metabolismo dos Piruvatos/genética , Éxons , Genótipo , Humanos , Íntrons
6.
Zhongguo Zhen Jiu ; 29(5): 365-9, 2009 May.
Artigo em Chinês | MEDLINE | ID: mdl-19489492

RESUMO

OBJECTIVE: To evaluate the therapeutic effect of Chuzhen therapy on insomnia through clinical randomized controlled trials. METHODS: Sixty cases of insomnia were randomly divided into a Chuzhen group (n=30) and an acupuncture group (n=30). Acupoints of Bazhen (Baihui Bazhen, Fengfu Bazhen, Shendao Bazhen) and Hechelu [from Dazhui (GV 14) to Mingmen (GV 4)] in the Chuzhen group, and Baihui (GV 20), Sishencong (EX-HN 1), etc. in the acupuncture group were selected, respectively. Four weeks treatments were carried out in the two groups, once daily for 5 times on week days. Three months after treatment, they were followed up and the therapeutic effects were assessed by the effective rate of sleep improvement and Pittsburgh Sleep Quality Index (PSQI). RESULTS: After treatment, the sleep quality in the two groups was improved, but there were no differences in the effective rate of sleep improvement and PSQI between the two groups (all P > 0.05). Three months after treatment, the total effective rate of 85.2% in the Chuzhen group was better than 78.6% in the acupuncture group (P < 0.05). The total cumulative score of PSQI, sleep effectiveness and the factors of sleep obstacle in the Chuzhen group were significantly different from those in the acupuncture group (all P < 0.05). CONCLUSION: Chuzhen therapy can increase long-term sleep quality and living quality through improving the effective rate of sleep and reducing the score of PSQI in the patients of insomnia.


Assuntos
Terapia por Acupuntura , Distúrbios do Início e da Manutenção do Sono/terapia , Pontos de Acupuntura , Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Distúrbios do Início e da Manutenção do Sono/fisiopatologia , Adulto Jovem
7.
Zhongguo Shi Yan Xue Ye Xue Za Zhi ; 15(2): 242-7, 2007 Apr.
Artigo em Chinês | MEDLINE | ID: mdl-17493324

RESUMO

This study was aimed to investigate the regulative effect of ERK and p38 signal transduction pathway on cell cycle of CML. The mRNA and protein expression of ERK, p38, cyclin D(2), cyclin E and p27 (ERK and p38 were Phosph-ERK and Phosph-P38) in CML cells and K562 cell lines were detected by RT-PCR and Western blot, respectively; cell cycle was determined by FCM, and their relationship was analyzed. The results showed that the mRNA and protein expressions of ERK, p38, cyclin D(2) and cyclin E in CML cells and K562 cells increased (P<0.01) and the expression of p27 decreased (P<0.01). There was positive correlation between the protein expressions of cyclin D(2) and the protein expression of ERK, p38 and cyclin E, but there was negative correlation between the protein expressions of cyclin D(2) and the protein expression of p27. The percentage of cells in G(0)/G(1) phase was decreased and the percentage of cells in S phase was increased, there was significant difference as compared with control (P<0.05). It is concluded that increase of the mRNA expression and protein activity of ERK and p38 activate the cell cycle-regulating proteins such as cyclin D(2), cyclin E, p27 which results in shortening of G(0)/G(1) phase, switching cell to S phase through G(1)/S check point quickly and accelerating cell cycle progression and cell proliferation, and eventually leads to occurrence of CML.


Assuntos
Ciclo Celular/fisiologia , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Leucemia Mielogênica Crônica BCR-ABL Positiva/metabolismo , Transdução de Sinais , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Adulto , Células Cultivadas , Feminino , Humanos , Células K562 , Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia , Masculino , Pessoa de Meia-Idade
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