Objective To explore the causes and preventive measures of symptomatic intracranial hemorrhage in 217 patients with acute cerebral ischemic stroke treated with local intra-arterial urokinase. Methods From February1999 to June 2004, 217 patients were treated for acute ischemic stroke with local intra-arterial urokinase in our hospital. Factors associated with symptomatic intracranial hemorrhage of intra-arterial thrombolysis were analyzed by Stepwise logistic regression to identify some factors relating the prediction symptomatic intracranial hemorrhage. Results Symptomatic intracranial hemorrhage occurred in 8 cases (3.7%). Predictors of the symptomatic intracranial hemorrhage were the elevated systolic blood pressure before therapy (odds ratio, 1.096; 95% CI, 1.006 to 1.194) and urokinase (UK) treatment (odds ratio , 1.068; 95% CL, 1.053 to 1.247). Risk of secondary symptomatic intracranial hemorrhage was increased with elevated systolic blood pressure. Other factors like age, initial treating time, NIHSS, diabetes and collateral circulation did not predict the symptomatic intracranial hemorrhage respectively. Conclusions Predictors of symptomatic intracranial hemorrhage after local intra-arterial infusion of urokinase for acute ischemic stroke were the elevated systolic blood pressure before therapy and urokinase (UK) treatment.

The formation mechanism of kidney stones is complex. It is generally recognized that abnormal urine conditions or renal tubular epithelial cell damage, together with other factors cause the formation of renal papillary subepithelial calcium plaques (Randall’s plaques) or stone crystals that block the renal tubules (Randall’s plugs), and then oversaturated crystals gathering on Randall's plaque or plug and forming stones. However, there are many pathophysiological changes and manifestations, such as renal papillary anchoring stones, renal papillary crypts, renal papillary tip erosion, and exogenous renal papilla Renal papillary lesions, which may be an early manifestations before the formation of kidney stones. The study of renal papillary calcium plaque is very important for the pathogenesis of kidney stones, as well as the prevention and treatment of patients with stones. By focusing on the development process of Randall plaque theory, the formation and transformation mechanism of Randall plaque, as well as the manifestations and clinical treatment of the above mentioned different types of renal papillary calcium plaque lesions, this article reviewed three aspects of stone formation, including Randall’s plaque, renal papillary lesions with stones, and renal papillary lesions related to stone.

Objective:To study the effect of Pterostilbene on endoplasmic reticulum stress and apoptosis in human renal tubular epithelial cells (HK-2 cells) induced by oxalate.Methods:From January 2019 to January 2020, HK-2 cells were divided into a control group (cultured with normal medium), an oxalate group (cultured with a medium containing 4 mmol/L of oxalate), and an intervention group of Pterostilbene (containing 4 mmol/L of oxalate + Pterostilbene 5, 10, and 20 μmol/L mixed medium were cultured at the same time), and the following tests were performed after 12 hours of treatment. Pterostilbene (5, 10, and 20 μmol/L) intervention group for cell viability test, lactate dehydrogenase cytotoxicity test, reduced glutathione, superoxide dismutase, malondialdehyde, hydrogen peroxide enzyme, total antioxidant capacity detection experiments to explore the degree of oxidative damage, and Western blotting experiments to explore the protein expression of ATF6, GRP78, DDIT3, caspase12, Clevead caspase 3/9; Pterostilbene (10 μmol/L) intervention group to detect mitochondrial membrane potential, caspase 3 enzyme activity, apoptosis rate, reactive oxygen detection to detect the apoptosis, reactive oxygen level, and qRT-PCR to detect ATF6, GRP78, DDIT3 of cells mRNA expression.Results:CCK-8 and lactate dehydrogenase toxicity test results showed that the cell activity of the oxalate group was significantly lower than that of the control group [(45.6±3.1)% vs. 100.0%, P<0.001]; the lactate dehydrogenase [(330.2±11.1)U/L vs. (2.6±6.7) U/L, P<0.001] of the oxalate group was higher than that of the control group increased obviously; the cell viability[ (57.2±1.7)%, (67.2±3.4)%, (78.9±1.8)%] of Pterostilbene intervention group (5, 10, 20 μmol/L) significantly increased compared with oxalate group ( P<0.05); lactate dehydrogenase [(288.1±4.3)U/L, (260.9±5.5)U, (202.7±10.2)U/L] in Pterostilbene intervention group (5, 10, 20 μmol/L ) was significantly lower than oxalate group ( P<0.05). The results of the five biochemical indexes of malondialdehyde, reduced glutathione, total superoxide dismutase, catalase, and total antioxidant capacity showed that the cell damage state was consistent with the experimental results of CCK-8 and lactate dehydrogenase. The active oxygen test results showed that the oxalate group had a significantly higher active oxygen level (76.3±4.9 vs. 6.2±1.7, P<0.01); the active oxygen level (39.5±5.4) of the Pterostilbene intervention group(10 μmol/L) was significantly lower than oxalate group ( P<0.01). The flow cytometry and caspase3 enzyme activity showed an increase in apoptosis rate and caspase3 activity in line with the trend of reactive oxygen levels. Mitochondrial membrane potential results showed that the oxalate group had a significantly lower mitochondrial membrane potential (0.76±0.15 vs. 7.84±0.26, P<0.01), and the mitochondrial membrane potential (2.26±0.27) of the Pterostilbene intervention group (10 μmol/L) was significantly higher than oxalate group( P<0.01). Western blot analysis showed that the relative expression of ATF6, DDIT3, GRP78, caspase12 and Cleaved caspase3/9 protein in the oxalate group was significantly higher than that in the control group. The relative expression of ATF6, DDIT3, GRP78, caspase12, Cleaved caspase3/9 protein in the Pterostilbene intervention group was significantly lower than that in the oxalate group ( P<0.05). qRT-PCR results showed that the mRNA expression trends of ATF6, DDIT3 and GRP78 in the three groups were consistent with the results of Western blotting. Conclusion:Pterostilbene can effectively inhibit the endoplasmic reticulum stress and apoptosis of HK-2 cells induced by oxalate.

Kidney stones are mixed by various inorganic salts and organic matter according to certain rules. The process of crystal nucleation, growth and aggregation is the key step of kidney stone formation. The different crystal structures will bring about the different formation process and physicochemical properties of kidney stones. It is of great significance to study the crystal structures and formation characteristics of kidney stone to clarify the causes of it and prevent the recurrence of it. In this paper, based on the microstructure and crystal structure of kidney stones, the distribution of different crystals and components in kidney stones, the nucleation and growth process of crystal forming kidney stones, and the different treatment methods based on crystal structure are reviewed in recent years.

Objective To investigate the problems during using, standard and quality management of the POCT glucose meters in hospital, to analyze the solutions, and to provide reference data for improving the test level of POCT in hospital.Methods The amount, brand and application of portable glucose meters in the hospital were obtained by 3 rounds of surveillance from May to July in 2013.All of those glucose meters were taken part in external quality assessment of Clinical Laboratory Center of National Health and Family Planning Commission.The test results of those glucose meters were compared with that of automatic biochemical analyzer, the comparison results were then analyzed.Results The POCT glucose meters possessed 5 brands in our hospital, and the amount and type of glucose meters in some clinical departments were often changed.When 4 brands which were detected as quality control samples by ministry of health, the accuracy of detection results of 3 concentration of brand Ⅲ were substandard, the CV% of two levels were 11.9%and 10.1%respectively, the remaining 3 brands were in line with the requirements.The qualified percentages of 3 times of comparison were 85.0%, 92.0%and 97.4%.Conclusions The hospital should select the brand of portable glucose meters reasonably, correct use of glucose meters, and it is very necessary to build indoor and interstitial quality evaluation system, at the same time, suggesting the hospital to establish the POCT quality management team, to carry out the instrument comparison periodically, so to guarantee the accurate, reliable results of POCT in hospital.

Oxalate is an organic dicarboxylic acid that is a common component of plant foods.The kidneys are essential organs for oxalate excretion,but excessive oxalates may induce kidney stones.Jupiter micro-tubule associated homolog 2(JPT2)is a critical molecule in Ca2+mobilization,and its intrinsic mecha-nism in oxalate exposure and kidney stones remains unclear.This study aimed to reveal the mechanism of JPT2 in oxalate exposure and kidney stones.Genetic approaches were used to control JPT2 expression in cells and mice,and theJPT2 mechanism of action was analyzed using transcriptomics and untargeted metabolomics.The results showed that oxalate exposure triggered the upregulation of JPT2,which is involved in nicotinic acid adenine dinucleotide phosphate(NAADP)-mediated Ca2+mobilization.Tran-scriptomic analysis revealed that cell adhesion and macrophage inflammatory polarization were inhibited by JPT2 knockdown,and these were dominated by phosphatidylinositol 3-kinase(PI3K)/AKT signaling,respectively.Untargeted metabolomics indicated that JPT2 knockdown inhibited the produc-tion of succinic acid semialdehyde(SSA)in macrophages.Furthermore,JPT2 deficiency in mice inhibited kidney stones mineralization.In conclusion,this study demonstrates that oxalate exposure facilitates kidney stones by promoting crystal-cell adhesion,and modulating macrophage metabolism and in-flammatory polarization via JPT2/PI3K/AKT signaling.