[Glomuvenous malformation: a clinicopathological analysis of 31 cases].

Objective: To investigate the clinicopathological features of glomuvenous malformation (GVM). Methods: Thirty-one cases of GVM diagnosed at the Henan Provincial People's Hospital from January 2011 to December 2021 were collected. Their clinical and pathological features were analyzed. The expression of relevant markers was examined using immunohistochemistry. The patients were also followed up. Results: There were 16 males and 15 females in this study, with an average age of 11 years (range, 1-52 years). The locations of the disease included 13 cases in the limbs (8 cases in the upper limbs, 5 cases in the lower limbs), 9 cases in the trunks, and 9 cases in the foot (toes or subungual area). Twenty-seven of the cases were solitary and 4 were multifocal. The lesions were characterized by blue-purple papules or plaques on the skin surface, which grew slowly. The lumps became larger and appeared to be conspicuous. Microscopically, GVM mainly involved the dermis and subcutaneous tissue, with an overall ill-defined border. There were scattered or clustered irregular dilated vein-like lumens, with thin walls and various sizes. A single or multiple layers of relatively uniform cubic/glomus cells were present at the abnormal wall, with scattered small nests of the glomus cells. The endothelial cells in the wall of abnormal lumen were flat or absent. Immunohistochemistry showed that glomus cells strongly expressed SMA, h-caldesmon, and collagen IV. Malformed vascular endothelial cells expressed CD31, CD34 and ERG. No postoperative recurrence was found in the 12 cases. Conclusions: GVM is an uncommon type of simple venous malformation in the superficial soft tissue and different from the classical glomus tumor. Morphologically, one or more layers of glomus cells grow around the dilated venous malformation-like lumen, which can be combined with common venous malformations.

[The application of 3-dimensional shear wave elastography in the therapeutic effect evaluation of neoadjuvant chemotherapy for Her-2 positive breast cancer patients].

Objective: To investigate the clinic value of ultrasound 3-dimensional shear wave elastography (3D-SWE) in therapeutic effect evaluation of neoadjuvant chemotherapy (NAC) for HER-2 positive breast cancer patients. Methods: A total of 43 lesions from 43 HER-2 positive breast cancer patients were selected and all of the lesions were confirmed by biopsy. Ultrasound examination was performed routinely before each chemotherapy cycle. The interested regions were selected under the 3-dimensional (3D) elasticity and gray-scale mode, the relevant data such as shear waves in the transverse, longitudinal and coronal sections of the mass were generated automatically. According to the histopathological results, the patients were divided into the pathological complete remission (pCR) group and the incomplete remission (non-pCR) group. The maximum elastic hardness value (Emax) and the reduction degree (ΔEmax) of the lesions in the two groups were measured and compared in each cycle of NAC. The accuracy of 3D-SWE technique for predicting the efficacy of NAC was evaluated using indicators such as sensitivity, specificity and area under the receiver operating characteristic (ROC) curve. Results: The clinicopathologic features between pCR group (18 cases) and non-pCR Group (25 cases) were not significantly different (P>0.05). Compared with pre-chemotherapy, the Emax values of pCR group and non-pCR Group during chemotherapy were declined (P<0.05). Moreover, the Emax values of pCR group before and after chemotherapy were lower than those of non-pCR group (P<0.05). At the end of the first cycle of chemotherapy, the predictive specificity, sensitivity and area under the curve (AUC) of pCR group were 72.0%, 83.3% and 0.838 (95%CI=0.680~0.930) respectively when the cutoff value of Emax was 118 kPa. At the end of the second cycle, the predictive specificity, sensitivity and AUC of pCR group were 76.0%, 83.3% and 0.863 (95%CI=0.720~0.940) respectively when the cutoff value of Emax was 87 kPa. At the end of the third cycle, the predictive specificity and sensitivity and the AUC of the pCR group were 88.0%, 77.8% and 0.893 (95%CI=0.760~0.970) when the cutoff value of Emax was 57 kPa. At the end of the fourth cycle of chemotherapy, the predictive specificity, sensitivity and AUC of pCR group were 92.5%, 88.9% and 0.960 (95%CI=0.850~0.990) respectively when the cutoff value of Emax was 30 kPa. After one cycle of NAC, the predictive sensitivity and specificity and AUC of pCR group were 88.0%, 60.0%, and 0.719 (95%CI=0.620~0.890) when the cutoff value of ΔEmax was 16.8%. After two cycles, the predictive sensitivity, specificity and AUC of pCR group were 55.5%, 80.0% and 0.712 (95%CI=0.550~0.840) when the cutoff value of ΔEmax was 34.9%. After three cycles, the predictive sensitivity, specificity and AUC of pCR group were 67.4%, 81.2% and 0.779 (95%CI=0.680~0.930) when the cutoff value of ΔEmax was 55.2%. After four cycles, the predictive sensitivity, specificity and AUC of pCR group was 72.3%, 92.0% and 0.831 (95%CI=0.690~0.930) when the cutoff value of ΔEmax was 75.1%. Conclusion: The Emax and ΔEmax values measured by 3D-SWE technology can predict the curative effect of NAC for breast cancer.

Percutaneous coronary intervention for poor coronary microcirculation reperfusion of patients with stable angina pectoris.

Percutaneous coronary intervention (PCI) has been extensively applied to repair the forward flow of diseased coronary artery and can achieve significant curative results. However, some patients with acute myocardial infarction (AMI) develop non-perfusion or poor perfusion of cardiac muscle tissue after PCI, which increases the incidence of cardiovascular events and the death rate. PCI can dredge narrowed or infarct-related artery (IRA) and thus induce full reperfusion of ischemic myocardium. It is found in practice that some cases of AMI still have no perfusion or poor perfusion in myocardial tissue even though coronary angiography suggests opened coronary artery after PCI, which increases the incidence of vascular events and mortality. Therefore, to explore the detailed mechanism of PCI in treating coronary microcirculation of patients with stable angina pectoris, we selected 140 patients with stable angina pectoris for PCI, observing the index of microcirculatory resistance (IMR) of descending branch and changes of myocardial injury markers and left ventricular systolic function, and made a subgroup analysis based on the correlation between clinical indexes, IMR and other variables of diabetic and non-diabetic patients, PCI-related and non-PCI-related myocardial infarction patients. The results suggest that IMR of anterior descending branch after PCI was higher compared to that before PCI, and the difference was significant (P less than 0.05); creatine kinase-MB (CK-MB), myohemoglobin and high sensitive troponin T were all increased after PCI, and the difference was also significant (P less than 0.05); brain natriuretic peptide (BNP) level became higher after PCI, with significant difference (P less than 0.05); left ventricular ejection fraction (LVEF) declined after PCI, and the difference before and after PCI was statistically significant (P less than 0.05). Moreover, subgroup analysis results of the three groups all demonstrated statistically significant differences. PCI can effectively increase microcirculatory resistance of patients with stable angina pectoris, especially those who develop both stable angina pectoris and diabetes. Patients with higher microcirculatory resistance before PCI are more likely to develop PCI-related myocardial infarction after PCI.

Overexpression, purification, and pharmacologic evaluation of anticancer activity of ribosomal protein L24 from the giant panda (Ailuropoda melanoleuca).

The ribosomal protein L24 (RPL24) belongs to the L24E family of ribosomal proteins and is located in the cytoplasm. The purpose of this study was to investigate the structure and anti-cancer function of RPL24 of the giant panda (Ailuropoda melanoleuca). The complementary DNA of RPL24 was cloned successfully using reverse transcription-polymerase chain reaction technology. We constructed a recombinant expression vector containing RPL24 complementary DNA and overexpressed it in Escherichia coli using pET28a plasmids. The expression product obtained was purified using Ni-chelating affinity chromatography. The results indicated that the length of the fragment cloned is 509 bp, and it contains an open-reading frame of 474 bp encoding 157 amino acids. Primary structure analysis revealed that the molecular weight of the putative RPL24 protein is 17.78 kDa with a theoretical isoelectric point of 11.86. The RPL24 gene is readily expressed in E. coli, and the RPL24 fused with the N-terminal histidine-tagged protein to give rise to the accumulation of an expected 23.51-kDa polypeptide. The inhibitory rate in mice treated with 0.1 mg/mL RPL24, the highest of 3 doses administered, can reach 67.662%, which may be comparable to the response to mannatide. The histology of organs with tumors showed that the tissues in the RPL24 group displayed a looser arrangement compared with that in the control group. Furthermore, no obvious damage was apparent in other organs, such as heart, lung, and kidney. The data showed that the recombinant RPL24 had time and dose dependency on the cell growth inhibition rate. Human laryngeal carcinoma Hep-2 cells treated with 0.3125-10 µg/mL RPL24 for 24 h displayed significant cell growth inhibition (P < 0.05; N = 6) in assays using 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide compared with that in control (untreated) cells. By contrast, human hepatoma Hep G-2 cells displayed no significant change (P > 0.05; N = 6) from control (untreated) cells. RPL24 has time and dose dependency on Hep-2 cell growth inhibition. The data indicate that the effect at low concentrations is better than that at high concentrations, and the concentration of 0.625 µg/mL provides the best rate of growth inhibition. Further research is ongoing to determine the bioactive principles of recombinant RPL24 protein that are responsible for its anticancer activity.