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BACKGROUND: In critical care medicine, mesenteric ischemia (MI) is a life-threatening disease that can be present in both critically ill patients and those undergoing major surgery. For the first time, we report a case of concealed MI with a long course after knee arthroplasty. CASE SUMMARY: A male patient underwent left total knee arthroplasty for gouty arthritis and developed a persistent fever and persistently high levels of serum infection markers after surgery. He was considered to have a periprosthetic site infection and treated with antibiotics and colchicine, periprosthetic debridement was performed, and the spacer was replaced, but no improvement was seen. At 54 d after arthroplasty, the patient developed gastrointestinal symptoms of nausea and vomiting, abdominal distention, and subsequently, cloudiness of consciousness, and hypotensive shock. Finally, the patient was diagnosed with ascending colonic mesentery ischemia with necrosis after laparotomy, which improved after right hemicolectomy. CONCLUSION: Concealed MI without gastrointestinal symptoms after major surgery is rare and easily misdiagnosed. Orthopedic surgeons need to be aware of this complication.
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BACKGROUND: Osteochondritis dissecans (OCD) is a rare disease of unclear cause characterized by subchondral bone damage and overlying cartilage defects. The current report presents the results of subchondral bone as a novel target for implantation of peripheral blood stem cells (PBSCs) in the treatment of OCD. CASE SUMMARY: A 16-year-old patient diagnosed with OCD underwent subchondral bone implantation of PBSCs. Four months later, the patient's visual analog scale scores, Western Ontario and McMaster University osteoarthritis index, and whole-organ magnetic resonance imaging score improved significantly, and regeneration of cartilage and subchondral bone was observed on magnetic resonance imaging. CONCLUSION: This is the first case of OCD treated with subchondral bone as an implantation target of PBSCs, which highlights the importance of subchondral bone for cartilage repair. This treatment could be a potential option for articular cartilage and subchondral bone recovery in OCD.
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Past studies have shown that the Src homology 2-containing inositol 5-phosphatase 2 (SHIP2) is commonly downregulated in gastric cancer, which contributes to elevated activation of PI3K/Akt signaling, proliferation and tumorigenesis of gastric cancer cells. However, the mechanisms underlying the reduced expression of SHIP2 in gastric cancer remain unclear. While gene copy number variation analysis and exon sequencing indicated the absence of genomic alterations of SHIP2, bisulfite genomic sequencing (BGS) showed promoter hypomethylation of SHIP2 in gastric cancer cells. Analysis of transcriptional activity of SHIP2 promoter revealed Specificity protein 1 (Sp1) was responsible for the regulation of SHIP2 expression in gastric cancer cells. Furthermore, Sp1 expression, but not Sp3, was frequently downregulated in gastric cancer compared with normal gastric mucosa, which was associated with a paralleled reduction in SHIP2 levels in gastric cancer. Moreover, overexpression of Sp1 inhibited cell proliferation, induced apoptosis, suppressed cell motility and invasion in gastric cancer cells in vitro, which was, at least in part, due to transcriptional activation of SHIP2 mediated by Sp1, thereby inactivating Akt. Collectively, these results indicate that decreased expression of transcription factor Sp1 contributes to suppression of SHIP2 in gastric cancer cells.
Assuntos
Regulação para Baixo/genética , Regulação Neoplásica da Expressão Gênica , Fosfatidilinositol-3,4,5-Trifosfato 5-Fosfatases/genética , Fator de Transcrição Sp1/metabolismo , Neoplasias Gástricas/genética , Linhagem Celular Tumoral , Humanos , Mutação/genética , Fosfatidilinositol-3,4,5-Trifosfato 5-Fosfatases/metabolismo , Regiões Promotoras Genéticas , Transcrição GênicaRESUMO
BACKGROUND: The Src homology 2-containing inositol 5-phosphatase 2 (SHIP2) is implicated in diabetes, arthrosclerosis, and cancer. However, the role of SHIP2 in human gastric cancer remains unclear. METHODS: The expression levels of SHIP2 in gastric cancer tissues, a panel of gastric cancer cell lines, and normal gastric epithelial cells were analyzed by immunohistochemistry (IHC), Western blot, and real-time quantitative RT-PCR (qRT-PCR). Gastric cancer cells with either overexpressed SHIP2 or co-overexpressed SHIP2 and Akt were analyzed to determine cell proliferation, colony formation, apoptosis, cell migration, and invasion assays. Normal gastric epithelial cells with knockdown SHIP2 or co-knockdown SHIP2 and Akt were subjected by anchorage-independent growth assays. The effect of SHIP2 on tumor growth in vivo was detected by xenograft tumorigenesis assays. RESULTS: SHIP2 was commonly downregulated in gastric cancer compared with normal gastric mucosa, and overexpression of SHIP2 inhibited cell proliferation, induced apoptosis, suppressed cell motility and invasion in gastric cancer cells in vitro, and retarded the growth of xenograft gastric tumors in vivo, while knockdown of SHIP2 in normal gastric epithelial cells promoted anchorage-independent growth. Moreover, overexpression of SHIP2 inactivated Akt, and upregulated p21, p27, and the pro-apoptotic protein Bim. Restoring Akt activation in gastric cancer cells largely blocked the inhibition of PI3K/Akt signaling by SHIP2 and reversed the inhibitory effect of SHIP2 on tumorigenesis and proliferation. CONCLUSIONS: This study demonstrates, for the first time, that SHIP2 is frequently downregulated in gastric cancer, and reduced SHIP2 expression promotes tumorigenesis and proliferation of gastric cancer via activation of the PI3K/Akt signaling.
