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A large percentage of diabetic patients also have other components of metabolic syndrome, which is a group of cardiovascular (CV) hazard factors related to both diabetes mellitus (DM) and cardiovascular diseases (CVD). We do not know about the prevalence of CV risk factors in diabetic patients in Upper Egypt. We aimed to assess the CV risk factors in type 2 diabetic patients in Upper Egypt villages.<br /><br /> We conducted a cross-sectional study that included 800 patients with type 2 DM. We classified the participants into three groups according to the hemoglobin A1c (HbA1c) levels. We assessed the prevalence of other cardiovascular risk factors and their association with HbA1c levels through a detailed history, full clinical examination, and laboratory tests.<br /><br /> We found that 75% of the participants were males, 25.5% elderly, 60.25% had hypertension, 60.75% had dyslipidemia, 33.25% were overweight or obese, 19.75% had a family history of coronary artery disease (CAD), 55.75% had established CVD, 42.5% were smokers,associated CV risk factors. The clustering of cardiovascular risk factors showed a significant association with higher HbA1c levels. These findings require the thought of associated CV risk factors in choosing medical treatments to optimize glycemic control and multifactorial intervention to improve CV risk.Non-small cell lung cancer (NSCLC) patients with anaplastic lymphoma kinase (ALK) rearrangement benefit from treatment with ALK inhibitors. Therefore, the identification of druggable ALK fusions is necessary for NSCLC treatment. More than 90 fusion partners of ALK have been reported in NSCLC patients, but the striatin gene (STRN)-ALK fusion has rarely been reported. Moreover, the response of STRN-ALK fusion patients treated with ALK inhibitors remains to be explored. A 64-year-old Chinese male with no history of smoking or alcohol consumption was diagnosed as stage IVB lung adenocarcinoma (LADC) (cT4N3M1c) in October 2018. Next-generation sequencing (NGS) targeting 425 cancer-related genes was performed on the plasma and supernatant of pleural effusion samples and revealed an STRN-ALK fusion. The patient received alectinib (600 mg, twice daily) as the first-line treatment with an excellent response exceeding 19 months. This is the first report of a NSCLC patient harboring an STRN-ALK fusion and exhibiting an excellent response to alectinib treatment. This case provides valuable information for therapeutic decision-making of patients with STRN-ALK fusions. [https://www.selleckchem.com/products/740-y-p-pdgfr-740y-p.html https://www.selleckchem.com/products/740-y-p-pdgfr-740y-p.html] Furthermore, this case also highlighted the advantage of performing targeted NGS on circulating tumor DNA for the identification and analysis of rare, druggable genomic alterations.<br /><br /> Hepatocellular carcinoma (HCC) is the most common malignant tumor worldwide with high morbidity and mortality rates. We aimed to examine the expression of chromobox 6 (CBX6) in HCC and analyze its correlation with clinicopathological features of HCC patients. Moreover, the role of CBX6 in the HCC cell proliferation, invasion and metastasis and the potential mechanism underlying HCC metastasis were also investigated.<br /><br /> We used quantitative polymerase chain reaction (qRT-PCR) and Western blot to evaluate the expression levels of CBX6 in HCC cell lines. Furthermore, the expression of CBX6 in HCC and the adjacent non-tumor tissues was assessed by immunohistochemistry (IHC). Cell proliferation was evaluated using MTT assay, cell migration and invasion were measured using wound healing and transwell assays. Finally, we detected the expression of target proteins in HCC cell lines transfected with CBX6 overexpression plasmid or CBX6 shRNA plasmid by Western blot.<br /><br /> We found that the expression of CBX6 was increaseds ability of HCC cells through regulating transcription factors snail/zeb1-mediated EMT mechanism, which indicated that the protein could serve as a novel therapeutic target for the treatment of HCC.Most patients diagnosed with hepatocellular carcinoma (HCC) have advanced diseases, and many are not eligible for curative therapies. There is growing evidence suggesting that the combination treatment of PD-1/PD-L1 inhibitors and tyrosine kinase inhibitors (TKIs) is becoming a prospective trend for advanced HCC. For those HCC patients with sorafenib resistance, the efficacy of regorafenib combined with PD-1/PD-L1 inhibitors remains unclear. Herein, we represent a case of HCC with lung metastasis in the setting of Hepatitis B virus (HBV)-induced liver cirrhosis responding dramatically to the sequential treatment with regorafenib followed by PD-1 inhibitor after initial liver resection. A 51-year-old man diagnosed with alpha fetoprotein (AFP)-negative HCC underwent liver resection in September 2015 and was found to have solitary liver recurrence and multiple lung metastases in March 2017. He received microwave coagulation therapy (MCT) and trans-arterial chemoembolization (TACE) for liver tumor and treatment was started with sorafenib 400 mg twice daily for controlling lung metastases. In December 2018, an abdominal computerized tomography (CT) scan showed two new lesions in the liver. In March 2019, disease progression of lung metastases was measured and he received 160 mg regorafenib once daily. After a short period of partial response, in December 2019, due to the progression of the disease, he started treatment with regorafenib 160 mg in combination with sintilimab (PD-1 inhibitor) (200 mg, 3 weeks as a cycle). Surprisingly, after five cycles of sintilimab injection, he showed complete response in target lesions. There was no clinical evidence of disease progression, and the side-effects were mild. The current overall survival (OS) is 58 months. Data from this clinical case report suggest that sequential treatment with regorafenib followed by PD-1 inhibitor is a promising therapeutic option for sorafenib-refractory cases of HCCs.<br /><br /> Peptide drugs provide promising regimes in bladder cancer. In order to identify potentialbioactive peptides involved in bladder cancer, we performed the present study.<br /><br /> Liquid chromatography/mass spectrometry assay was used to compare the endogenous peptides between bladder cancer and normal control. The potential biological functions of these dysregulated peptides are assessed by GO analysis and KEGG pathway analysis of their precursors. The SMART and UniProt databases are used to identify the sequences of the dysregulated peptides located in the functional domains. The Open Targets Platform database was used to investigate the precursors related to metabolic diseases.<br /><br /> A total of 9 up-regulated peptides and 110 down-regulated peptides in bladder cancer compared with normal control were identified (fold change &gt; 1.2, <br /><br /> &lt; 0.05). The MW of these dysregulated peptides ranged from 500 Da to 2500 Da and the MW of all identified peptides was below 3500 Da. The GO and KEGG pathway analysis indicated that these dysregulated peptides could play an important role in bladder cancer.