11 results match your criteria: "The Chongqing Hospital of Traditional Chinese Medicine[Affiliation]"

We specifically discuss the mechanisms of the pathogenesis, diagnosis, and management of blastic plasmacytoid dendritic cell neoplasm (BPDCN), a rare but aggressive haematologic malignancy characterized by frequent skin manifestations and systemic dissemination. The article enriches our understanding of BPDCN through detailed case reports showing the clinical, immunophenotypic, and histopathological features that are critical for diagnosing this disease. These cases highlight the essential role of pathologists in employing advanced immunophenotyping techniques to accurately identify the disease early in its course and guide treatment decisions.

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Metabolic Enzyme SLC27A5 Regulates PIP4K2A pre-mRNA Splicing as a Noncanonical Mechanism to Suppress Hepatocellular Carcinoma Metastasis.

Adv Sci (Weinh)

February 2024

Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400010, China.

Article Synopsis
  • - The enzyme SLC27A5, important for transporting fatty acids and bile acids in the liver, is often found at low levels in hepatocellular carcinoma (HCC) patients, which correlates with poor outcomes.
  • - This study reveals that SLC27A5 also plays a role in regulating mRNA splicing, which helps inhibit the spread of HCC, independent of its metabolic functions.
  • - Restoring levels of SLC27A5 can reduce HCC metastasis by decreasing the production of a specific mRNA isoform (PIP4K2A-S), suggesting that targeting this isoform could be a new strategy in treating HCC related to SLC27A5 deficiency.
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Previous studies reported that the codeletion of PTEN and SOCS3 can greatly enhance the capacity of axon regeneration after central nervous system (CNS) injury. Moreover, the promotion of functional recovery can be improved by rehabilitative training under a use-dependent plasticity mechanism after CNS injury. However, few studies have reported the interaction between these mechanisms after spinal cord injury (SCI).

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Many studies have confirmed that the classical cadherin (CDH) gene family may be involved in the development and progression of various tumors. However, the comprehensive assays of CDH family members in lung adenocarcinoma (LUAD) were rarely reported. In this study, our group analyzed TCGA datasets and identified 18 dysregulated CDH members in LUAD specimens.

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Background: The role of dysfunction of , a recently identified tumor suppressor gene, has not yet been established in lung cancer. In our previous study, it was reported that expression is downregulated in lung cancer tissues and that overexpression inhibits the proliferation of non-small-cell lung cancer cells. The results can be found in the APJC and journals.

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Objectives: To investigate molecular mechanisms of nicastrin () mutations inducing acne inversa (AI).

Methods: New and old lesional and non-lesional skin samples were obtained from an AI patient. Healthy skin samples were obtained from the buttocks of 100 non-AI patients.

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Objective: This study is designed to explore permeability of ethosomes encapsulated with 5-florouracil (5-FU) mediated by CO fractional laser on hypertrophic scar tissues. Moreover, therapeutic and duration effect of CO fractional laser combined with 5-FU encapsulated ethosomes in rabbit ear hypertrophic scar model will be evaluated.

Methods: The permeated amount of 5-FU and retention contents of 5-FU were both determined by high-performance liquid chromatography (HPLC).

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Two novel Co(II) complexes with two different Schiff bases: inhibiting growth of human skin cancer cells.

Braz J Med Biol Res

July 2017

Department of Dermatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.

Using two flexible Schiff bases, H2L1 and H2L2, two new cobalt II (Co(II))-coordination compounds, namely, Py3CoL1 (1) and Py3CoL2 (2) (Py=pyridine, L1=3,5-ClC6H2(O)C=NC6H3(O)-4-NO2, L2=3,5-BrC6H2(O)C=NC6H3(O)-4-NO2) have been synthesized under solvothermal conditions. Single crystal X-ray structural analysis revealed that compounds 1 and 2 are both six-coordinate in a distorted octahedral geometry, and the 1D chain structure was formed by the π…π and C-H…O interactions or C-H…Cl interaction. The in vitro antitumor activities of 1, 2 and their corresponding organic ligands Py, L1, and L2 were studied and evaluated, in which three human skin cancer cell lines (A-431, HT-144 and SK-MEL-30) were used in the screening tests.

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Local injection of Lenti-Olig2 at lesion site promotes functional recovery of spinal cord injury in rats.

CNS Neurosci Ther

June 2017

State Key Laboratory of Trauma, Burns and Combined Injury, Department of Research Institute of Surgery, Daping Hospital, The Third Military Medical University, Chongqing, China.

Aims: Olig2 is one of the most critical factors during CNS development, which belongs to b-HLH transcription factor family. Previous reports have shown that Olig2 regulates the remyelination processes in CNS demyelination diseases models. However, the role of Olig2 in contusion spinal cord injury (SCI) and the possible therapeutic effects remain obscure.

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Overexpression of MCPH1 inhibits uncontrolled cell growth by promoting cell apoptosis and arresting the cell cycle in S and G2/M phase in lung cancer cells.

Oncol Lett

January 2016

Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing 400014, P.R. China; Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing 400014, P.R. China.

Microcephalin (MCPH1/BRIT1) is a large nuclear protein that is involved in the early cellular response to DNA damage, the expression of which is reduced in a variety of types of human tumors. A recent study by our group demonstrated that MCPH1 expression is markedly decreased in lung cancer. However, it remains unclear whether inducing the expression of MCPH1 may ameliorate lung cancer, and, if so, which mechanisms underlie this process.

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