Objective To investigate the frequency distribution of Val762Ala(T2444C)polymorphism among Han Chinese population in Gansu province,and to explore its relation to the suseeptibihty to gastric cancer. Methods A hospital-based,case-control study was performed involving 138 patients with gastric cancer and 110 healthy controls by PCR-RFLP method.Logistic regression and Chisquare analyses were used to assess OR and 95% CI. Results PARP-1762Ala allele was overexpressed in gastric cancer cases(11.5%)compared with controls(4.5%)(OR=3.012,95%CI 1.054-8.603,P=0.033).Statistic analysis showed increaged risk for gastric cancer patients with the 762Ala allele.Conclusion PARP-1 Val762Ala(T2444C)is related to the risk of gastric cancer,PARP-1762Ala allele could be used as a susceptibility marker for the development of gastric cancer.

Neural stem cells were labeled with superparamagnetic iron oxide (SPIO) and tracked by MRI in vitro and in vivo after implantation. Rat neural stem cells were labeled with SPIO combined with PLL by the means of receptor-mediated endocytosis. Prussian blue staining and electron microscopy were conducted to identify the iron particles in these neural stem cells. SPIO-labeled cells were tracked by 4.7T MRI in vivo and in vitro after implantation. The subjects were divided into 5 groups, including 5 x 10(5) labeled cells cultured for one day after labeling, 5 x 10(5) same phase unlabeled cells, cell culture medium with 25 mug Fe/mL SPIO, cell culture medium without SPIO and distilled water. MRI scanning sequences included T(1)WI, T(2)WI and T(2)*WI. R(2) and R(2)* of labeled cells were calculated. The results showed: (1) Neural stem cells could be labeled with SPIO and labeling efficiency was 100%. Prussian blue staining showed numerous blue-stained iron particles in the cytoplasm; (2) The average percentage change of signal intensity of labeled cells on T(1)WI in 4.7T MRI was 24.06%, T2WI 50.66% and T(2)*WI 53.70% respectively; (3) T2 of labeled cells and unlabeled cells in 4.7T MRI was 516 ms and 77 ms respectively, R(2) was 1.94 s(-1) and 12.98 s(-1) respectively, and T(2)* was 109 ms and 22.9 ms, R(2)* was 9.17 s(-1) and 43.67 s(-1) respectively; (4) Remarkable low signal area on T(2)WI and T(2)*WI could exist for nearly 7 weeks and then disappeared gradually in the left brain transplanted with labeled cells, however no signal change in the right brain implanted with unlabeled cells. It was concluded that neural stem cells could be labeled effectively with SPIO. R2 and R(2)* of labeled cells were increased obviously. MRI can be used to track labeled cells in vitro and in vivo.

The basic mechanical properties of a Radial Shock Wave Therapy Equipment (RSWTE) were experimentally studied in this paper. The output energy of the RSWTE working on the operation frequency of 10 Hz was measured by dynamic pressure transducer under the conditions of different operation pressure. The results showed that both operation pressure and operation frequency have effects on the output energy of the equipment. The output energy increases with the increase of operation pressure, and the magnitude of increased energy decreases with higher operation of frequency. With the increase of operation frequency, the output energy rises up in condition of lower operation pressure and drops off in condition of higher operation pressure. The accurate medical treatment should be selected with the optimized energy and condition according to the treatment requirement to different illness in clinical medical applications.
Equipment Design ; High-Energy Shock Waves ; Physical Therapy Modalities ; instrumentation ; Pressure

OBJECTIVETo examine the spatiotemporal profiles and localization of CysLT1R, CysLT2R and GPR17 in mice with 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-induced Parkinson disease (PD).

METHODSPD model was induced by subcutaneous injection of MPTP (25 mg/kg) for 5 d in adult male C57BL/6 mice. At d10 after MPTP injection, the expression and cellular localization of CysLT1R, CysLT2R and GPR17 in the substantia nigra were detected by immunohistochemistry and immunofluorescence.

RESULTSCysLT1R, CysLT22 and GPR17 were normally localized in TH-positive dopaminergic neurons and microglia, while CysLT2R was also expressed in astrocytes. In dopaminergic neurons, approximately 91% co-expressed GPR17, 77% co-expressed CysLT1R and 52% co-expressed CysLT2R. Compared with the control group, TH-positive cells in the substantia nigra were significantly reduced in PD mice. CysLT1R, CysLT2R and GPR17-positive cells were significantly reduced; and CysLT1R, CysLT2R, GPR17-positive dopaminergic neurons were also significantly reduced in the PD group. In the striatum, both CysLT1R and GPR17 were normally expressed in neurons; whereas CysLT2R was expressed in astrocytes. In PD striatum, CysLT1R and GPR17-positive cells were decreased, but CysLT2R expression was significantly increased which mainly expressed in the proliferating astrocytes.

CONCLUSIONCysLT1R, CysLT2R and GPR17 may be involved in the MPTP-induced PD damage in mice.

Animals ; Brain ; metabolism ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins ; metabolism ; Parkinson Disease ; metabolism ; Receptors, G-Protein-Coupled ; metabolism ; Receptors, Leukotriene ; metabolism

Neural stem cells were labeled with superparamagnetic iron oxide (SPIO) and tracked by MRI in vitro and in vivo after implantation. Rat neural stem cells were labeled with SPIO combined with PLL by the means of receptor-mediated endocytosis. Prussian blue staining and electron microscopy were conducted to identify the iron particles in these neural stem cells. SPIO-labeled cells were tracked by 4.7T MRI in vivo and in vitro after implantation. The subjects were divided into 5 groups, including 5× 105 labeled cells cultured for one day after labeling, 5 × 105 same phase unlabeled cells, cell culture medium with 25 μg Fe/mL SPIO, cell culture medium without SPIO and distilled water. MRI scanning sequences included T1WI, T2WI and T2*WI. R2 and R2* of labeled cells were calculated. The results showed: (1) Neural stem cells could be labeled with SPIO and labeling efficiency was 100%. Prussian blue staining showed numerous blue-stained iron particles in the cytoplasm; (2) The average percentage change of signal intensity of labeled cells on T1WI in 4.7T MRI was 24.06%, T2WI 50.66% and T2*WI 53.70% respectively; (3) T2 of labeled cells and unlabeled cells in 4.7T MRI was 516 ms and 77 ms respectively, R2 was 1.94 s-1 and 12.98 s-1 respectively, and T2* was 109 ms and 22.9 ms, R2* was 9.17 s-1 and 43.67 s-1 respectively; (4) Remarkable low signal area on T2WI and T2*WI could exist for nearly 7 weeks and then disappeared gradually in the left brain transplanted with labeled cells, however no signal change in the right brain implanted with unlabeled cells. It was concluded that neural stem cells could be labeled effectively with SPIO. R2 and R2* of labeled cells were increased obviously. MRI can be used to track labeled cells in vitro and in vivo.

Objective:To evaluate the clinical value of prenatal molecular diagnostic technology in preventing hereditary diseases through analysis of prenatal diagnostic characteristics in 22 monogenic skeletal disorders pedigrees.Methods:This study retrospectively analyzed prenatal molecular diagnostic results of 22 pedigrees with monogenic skeletal disorders who were admitted to Department of Osteoporosis and Bone Diseases in our hospital from January 2014 to July 2021.Results:Among 22 pedigrees, there were 10 pedigrees with X-linked hypophosphatemic rickets due to PHEX gene mutations, in which 8 fetuses were found to carry pathogenic variants; 6 pedigrees with osteopetrosis, including 3 cases of CLCN7 gene mutation, 2 TCIRG1 gene mutation, and 1 CTSK gene mutation, were detected to have 2 affected fetuses and 1 carrier. There were 4 cases of osteogenesis imperfecta, including 2 cases of COL1A1 gene mutation, 1 case of COL1A2 gene mutation, and 1 case of SERPINF1 gene mutation, in which 1 affected fetus and 1 carrier were found; only one case of osteoarthritis with mild chondrodysplasia caused by COL2A1 gene mutation was found to harbor pathogenic variant in fetus; 1 case of hypophosphatasia due to ALPL gene mutation was not detected to carry pathogenic variant in fetus. By the time of follow-up, all 12 affected fetuses were terminated, and the remaining 10 fetuses except for one case still in pregnancy were born in good condition.Conclusion:Prenatal molecular diagnosis may confirm whether the fetus carries pathogenic variants at the first and second trimesters. For monogenic skeletal disorders that comply with Mendel′s law of separation, prenatal diagnosis can be determined by calculating the probability of recurrence of offspring. In addition, for families with de novo mutations in the offspring, it is necessary to pay attention to whether there are mosaic mutations in the parents.

Objective:To investigate the expression at protein level and diagnostic value of histone acetyltransferase MYST2 in pancreatic cancer.Methods:From December 1st, 2017 to June 30th, 2020, at Peking Union Medical College Hospital, a total of 54 cases of pancreatic cancer tissues and corresponding paracancerous pancreatic tissues (>5 cm from the surgical margin) resected and confirmed by pathology were collected. ASPC1 and BXPC3 pancreatic cancer cell lines were knocked down (ASPC1 and BXPC3 knockdown group), CFPAC1 and SW1990 pancreatic cancer cell lines were overexpressed (CFPAC1 and SW1990 overexpression group), the untreated ASPC1, BXPC3, CFPAC1 and SW1990 were set as blank vector control group. The expression at protein level of MYST2 was detected by Western blotting in patients with different degrees of pathological differentiation, human normal pancreatic duct epithelial cell line HPDE, human pancreatic cancer cell lines ASPC1, BXPC3, CFPAC1 and SW1990, knockdown group, overexpression group and blank vector control group. The cell proliferation, migration, invasion and colony formation ability of the knockdown group, overexpression group and blank vector control group were determined by real-time cellular analysis, Transwell migration and invasion test, and plate colony formation assay. MYST2 immunohistochemical scoring was performed on pancreatic cancer tissues and para cancer tissues. Receiver operating characteristic curve was drawn to analyze the value of different MYST2 protein expression levels in the diagnosis of pancreatic cancer. Independent sample t test and variance analysis were used for statistical analysis. Results:Among the pathological slides of 54 cases of pancreatic cancer, 13 cases were highly differentiated, 24 cases were moderately differentiated, 15 cases were poorly differentiated and 2 cases were undifferentiated, the MYST2 expression at protein level in pancreatic cancer cells was 3.12±1.67, 2.87±1.59, 2.12±1.03 and 1.08±0.34, respectively, and the difference was statistically significant ( F=1.241, P<0.05). The MYST2 expression levels of ASPC1, BXPC3, CFPAC1 and SW1990 were all higher than that of normal pancreatic ductal epithelial cell lines HPDE (1.41±0.47, 1.40±0.93, 1.13±0.62 and 1.71±0.46 vs. 0.82±0.25), and the differences were statistically significant( t=1.625, 1.577, 1.319 and 1.832, all P<0.05). The MYST2 expression level of BXPC3 knockdown group was lower than that of BXPC3 blank vector control group (0.39±0.12 vs. 0.75±0.34); that of ASPC1 knockdown group was lower than that of ASPC1 blank vector control group (0.43±0.22 vs. 0.82±0.48); that of CFPAC1 overexpression group was higher than that of CFPAC1 blank vector control group (1.38±0.45 vs. 0.82±0.37); that of SW1990 overexpression group was higher than that of SW1990 blank vector control group (1.34±0.65 vs. 0.51±0.22), and the differences were statistically significant ( t=1.414, 1.378, 1.319 and 1.934, all P<0.05). The cell proliferation of ASPC1 knockdown group was slower than that of ASPC1 blank vector control group, and the proliferation peak at 80 h was lower than that of blank vector control group (1.02±0.77 vs. 4.31±2.45); the cell proliferation of BXPC3 knockdown group was slower than that of BXPC3 blank vector control group, and the proliferation peak at 80 h was lower than that of blank vector control group (0.91±0.24 vs. 2.84±0.53); the proliferation of pancreatic cancer cells in SW1990 overexpression group was faster than that of SW1990 blank vector control group, and the proliferation peak at 80 h was higher than that of blank vector control group (3.10±0.67 vs. 1.04±0.17); the proliferation of pancreatic cancer cells in CFPAC1 overexpression group was faster than that that of CFPAC1 blank vector control group, and the proliferation peak at 80 h was higher than that of blank vector control group (5.45±1.13 vs. 1.01±0.29), and the differences were statistically significant ( t=1.427, 1.316, 1.292 and 1.501, all P<0.05). In the test of migration ability, the number of cells passed through the Transwell chamber of ASPC1 knockdown group was less than that of ASPC1 blank vector control group (34.08±17.62 vs. 118.76±5.31); that of BXPC3 knockdown group was less than that of BXPC3 blank vector control group (18.62±9.64 vs. 57.90±12.67); that of SW1990 overexpression group was more than that of SW1990 blank vector control group (134.84±24.65 vs. 37.82±6.73); that of CFPAC1 overexpression group was more than that of CFPAC1 blank vector control group (65.79±27.46 vs. 11.68±5.13), and the differences were statistically significant ( t=1.475, 1.322, 1.437 and 1.219, all P<0.05). In the test of invasion ability, the number of cells passed through the Transwell chamber of ASPC1 knockdown group was less than that of ASPC1 blank vector control group (9.79±5.75 vs. 45.76±12.71); that of BXPC3 knockdown group was less than that of BXPC3 blank vector control group (23.46±11.13 vs. 84.92±17.65); that of SW1990 overexpression group was more than that of SW1990 blank vector control group (156.42±34.50 vs. 42.13±22.17); that of CFPAC1 overexpression group was more than that of CFPAC1 blank vector control group (112.64±47.82 vs. 39.09±17.23), and the differences were statistically significant ( t=1.324, 1.635, 1.423 and 1.119, all P<0.05). The number of colony formation of the ASPC1 knockdown group was less than that of ASPC1 blank vector control group (13.15±6.42 vs. 86.79±35.17); that of BXPC3 knockdown group was less than that of BXPC3 blank vector control group (14.93±9.30 vs. 52.93±15.76); that of SW1990 overexpression group was more than that of SW1990 blank vector control group (129.10±57.31 vs. 62.42±37.43); that of CFPAC1 overexpression group was more than that of CFPAC1 blank vector control group (157.98±66.45 vs. 74.35±34.69), and the differences were statistically significant ( t=1.148, 1.290, 1.274 and 1.462, all P<0.05). The MYST2 score of pancreatic cancer tissues was higher than that of adjacent paracancerous pancreatic tissues (3.04±2.23 vs. 1.32 ± 0.70), and the difference was statistically significant ( t=3.479, P<0.05). When the total immunohistochemistry score of MYST2 was 3 point, the area under the curve was the largest (0.888, 95% confidence interval 0.827 to 0.948), and the Youden index was 0.56. Conclusion:MYST2 is associated with the proliferation, invasion and migration of pancreatic cancer cells, and promotes the development of pancreatic cancer.

Grey matter (GM) alterations may contribute to cognitive decline in individuals with white matter hyperintensities (WMH) but no consensus has yet emerged. Here, we investigated cortical thickness and grey matter volume in 23 WMH patients with mild cognitive impairment (WMH-MCI), 43 WMH patients without cognitive impairment, and 55 healthy controls. Both WMH groups showed GM atrophy in the bilateral thalamus, fronto-insular cortices, and several parietal-temporal regions, and the WMH-MCI group showed more extensive and severe GM atrophy. The GM atrophy in the thalamus and fronto-insular cortices was associated with cognitive decline in the WMH-MCI patients and may mediate the relationship between WMH and cognition in WMH patients. Furthermore, the main results were well replicated in an independent dataset from the Alzheimer's Disease Neuroimaging Initiative database and in other control analyses. These comprehensive results provide robust evidence of specific GM alterations underlying WMH and subsequent cognitive impairment.