Cyelocryotherapy using nitrogen monoxide was performed on 28 patients (28 eyes) with secondary glaucoma following penetrating keratoplasty, which had failed to respond to anti-glaucoma drugs and routine filtering procedures. All patients were followed up for more than one year. Intraoeular pressure was well under control in 89% of the eyes. The graft remained clear in 85%. The effective visual function was preserved in 82%. Our study showed that timely intervention, precisely controlled temperature) timing, extent of cryotherapy, and post-operative use of anti-rejection agents were key factors to suceess. Over-treatment, which may lead to atrophy of the eye, must be avoided. The effort should not be given up following under-treat-ment in the initial procedure.

Objectives To investigate the parmacokinetic characteristics of Meropenem used during the shock phase of severely burned patients. Methods The concentration of Meropenem in the plasma, blister and urine of 11 burn patients during the shock phase (S group) were determined by high performance liquid chromatography after the iv injection of Meropenem. Pharmacokinetic parameters were thus produced by 3P97 software. 6 healthy volunteers served as control group (C group). The t test was used to analyze difference between pharmacokinetic parameters of burned patients and healthy volunteers. Results Compared to those in control group, pharmacokinetic parameters of Meropenem in S group showed significant difference, such as prolonged elimination half-life (t1/2?):[(2 29?0 54)h vs (1 34?0 16)h] and decreased clearance(CLs): [(11 34?3 08)L? h-1 vs (18 76?4 60)L?h -1 ], and enlarged area under the serum concentration versus time curve(AUC):[(47 85?16 15)?g?h?ml -1 vs (27 54?10 76)?g?h?ml -1 ]. Conclusions Meropenem at the dose 500mg iv 3/d can show good activity (both in plasma and wound tissues)against most of pathogens which are common in burn clinic. The intervals should be prolonged when maximum dosage of Meropenem was administered in burn patients during the shock phases.

Objective To study the dynamic change of polysaccharide from Asarum insigne in Guizhou during different harvest period and its hemostatic effect. Methods Asarum insigne polysaccharide was extracted by water isolation and alcohol precipitation. We measured the polysaccharide content by UV spectrophotometry after impurity and purification and detected the bleeding and clotting time by tail cutting and slide methods in mice. Results There was significant variation in polysaccharide content of Asarum insigne at different harvest time, which was at a higher level in June(1. 78%-1. 82%). The bleeding time in mice of normal control group was (6. 73±1. 21) min,and that in mice treated with refined polysaccharide at high dose was (4. 91±1. 58) min,the difference between two groups was statistically significant(P<0. 01). The clotting time in mice of normal control group was (7. 27±2. 09) min,and that in the refined polysaccharide at middle and high dose groups was (3. 96±1. 78) min and (3. 27±1. 61) min,respectively. The latter two groups were obviously different from the normal control group(P<0. 05 or P<0. 01). Conclusion The polysaccharide is an active hemostatic substance in Asarum insigne and the optimum harvest time of it is in June for the clinical use.

Objective To screen and analyze nucleotide variants in 5'-untranslated region(5'-UTR)in voltage-gated sodium channel α1-subunit gene(SCN1A)in patients with Dravet syndrome and to evaluate the association of the variants with disease.Methods Peripheral blood of 24 patients with Dravet syndrome and 100 unrelated normal persons were collected and genomic DNA was extracted.PCR-sequencing of SCN1 A 5'-UTR in these DNA was performed.To evaluate the possibility of mutation inducing disease,bioinformatics analysis was applied to analyze the conservation of the sequences around the mutation site and predict the potential transcription elements.Results The nucleotide variant of 166.642.520G→A in exon 2 was identified in two patients,but not in normal controls.The mutation was a de novo mutation in a patient with early-onset.In the second proband,the mutation was also carried by his clinically asymptomatic mother.The nucleotide site 166.642.520 was moderately conserved in mammals(62.5%).The average nucleotide identity rate between human and other mammals species in the region adjacent to 166.642.520 was 88.5%.Two potential transcription regulatory elements were predicted on the sequence with the mutation of 166.642.520G>A,and only one on the sequence with wild-type.Conclusions The mutation 166.642.520G>A may be associated with Dravet syndrome and further studied should be performed to verify it and demonstrate its pathogenic mechanisms.

Objective To observe the effect of artemether in the control of prevalence and acute infection of Schistosoma japonicum in humans in high endemic areas. Methods During the transmission season (May-October), the residents in the pilot village took artemether with a 15- day interval to prevent the infection of S. japonicum. Results By the end of the transmission season, the egg positive rate was 0.83% and no acute case occurred in the artemether group, while 15.01% and 3 acute cases were observed in the placebo group. Conclusions Oral administration of artemether at a 15-day interval shows an effective protection from infection of S. japonicum, with a protection rate of 94.47% in residents of a high endemic area and it also shows marked effect to prevent acute schistosomiasis.

Objective: To explore the effects of cardiac support on delayed resuscitation in extensively burned patients with shock. Methods: Clinical data of 62 extensively burned patients with shock on admission, admitted to the 159th Hospital of PLA (hereinafter referred to as our hospital) from January 2012 to January 2017, were retrospectively analyzed. They were divided into cardiac support group (n=35) and control group (n=27) according to the use of deslanoside and ulinastatin. All patients were treated with routine fluid resuscitation based on the formula of the Third Military Medical University till post injury hour (PIH) 48. Patients in cardiac support group were given slow intravenous injection of deslanoside which was added in 20 mL 100 g/L glucose injection with first dose of 0.4 to 0.6 mg, 0.2 to 0.4 mg per 6 to 8 h, no more than 1.6 mg daily, and slow intravenous injection of 1×10⁵U ulinastatin which was added in 100 mL 50 g/L glucose injection, once per 12 h. Other treatments of patients in the two groups followed the same conventional procedures of our hospital. The following data of the two groups of patients were collected. (1) The data of urine volume per hour within PIH 48, heart rate, mean arterial pressure (MAP), central venous pressure (CVP), blood lactic acid, base excess, hematocrit, and albumin at PIH 48 were recorded. (2) The input volumes of electrolyte, colloid within the first and second 24 hours post burn and the total fluid input volumes within PIH 48 were recorded. (3) The data of creatine kinase, creatine kinase isoenzyme-MB, lactate dehydrogenase, total bile acid, alanine aminotransferase, aspartate aminotransferase, β₂-microglobulin, urea nitrogen, and creatinine at PIH 48 were recorded. (4) The complications including cardiac failure, pulmonary edema, pleural effusion, seroperitoneum, renal failure, sepsis, and death were also recorded. Data were processed with independent sample ttest, Fisher′s exact test, Pearson chi-square test, or continuous correction chi-square test. Results: (1) There were no statistically significant differences in urine volume within PIH 48, heart rate, MAP, CVP, hematocrit, or albumin at PIH 48 between the patients of two groups (t=0.150, 0.488, 0.805, 0.562, 1.742, 0.696, P>0.05). While the levels of blood lactic acid and base excess were respectively (4.2±2.2) and (-4.3±2.0) mmol/L in patients of cardiac support group, which were significantly better than (5.9±1.7) and (-6.0±3.1) mmol/L in patients of control group (t=3.249, 2.480, P<0.05 or P<0.01). (2) There was no statistically significant difference in input volume of colloid within the first 24 hours post burn between the patients of two groups (t=0.642, P>0.05). The input volume of electrolyte within the first 24 hours post burn, the input volumes of electrolyte and colloid within the second 24 hours post burn, and the total fluid input volume within PIH 48 of patients in cardiac support group were significantly less than those in control group (t=2.703, 4.223, 3.437, 2.515, P<0.05 or P<0.01). (3) The levels of creatine kinase, creatine kinase isoenzyme-MB, lactate dehydrogenase, total bile acid, alanine aminotransferase, aspartate aminotransferase, β₂-microglobulin, urea nitrogen, and creatinine of patients in cardiac support group at PIH 48 were significantly lower than those in control group (t=3.066, 3.963, 3.225, 2.943, 2.431, 3.084, 4.052, 2.915, 3.353, P<0.05 or P<0.01). (4) The occurrences of pleural effusion and seroperitoneum and mortality of patients in cardiac support group were significantly lower than those in control group (χ²=5.514, 6.984, 4.798, P<0.05 or P<0.01). There were no statistically significant differences in cardiac failure, pulmonary edema, renal failure, and sepsis between the patients of two groups [χ²=1.314 (sepsis), P>0.05]. Conclusions The cardiotonic and cardiac protection treatments in delayed resuscitation of extensively burned patients with shock contribute to improving the cellular anonic metabolism, reducing the volume of fluid resuscitation, and mitigating the ischemic and hypoxic damage to organs, so as to lay foundation for decreasing further complication incidences and mortality.

Objective: To survey the prevalence of drug resistant HIV-1 in Shandong province in 2013-2015. Methods: WHO truncated sequential sampling technique was adopted by using 77 and 53 samples of newly diagnosed as HIV-1 positive and aged 16-25 years in Shandong province in 2013 and 2015. RNA was prepared and HIV-1 pol region was amplified by RT-PCR and nested PCR. Pol genetic mutation associated with drug resistance was analyzed. Results: The success rates for sequence acquisition of the survey were 100% (77/77) and 94% (50/53) in 2013 and 2015, and the main subtype was CRF01_AE. A total of 2 surveillance drug-resistance mutation(SDRMs) and 3 SDRMs were found by analyzing the 47 sequences each year, sampled in 2013 and 2015, indicating that the prevalence of drug resistant HIV-1 stains was low in 2013, and moderate in 2015. A total of 5 individuals with drug resistant HIV-1 stains found in this study were mainly infected by homosexual transmission (3 cases), and the other two samples were different: one was infected by heterosexual transmission, the other was infected by IDU. The subtype was CRF01_AE (2 cases) , CRF07_BC (2 cases) and B (1 case) . SDRMs for protease inhibitor (PIs), nucleotide HIV-reverse transcriptase inhibitor (NRTIs) and non-NRTI (NNRTIs) were all found in the individuals with drug resistant HIV-1 stains. Conclusion CRF01_AE were the main HIV-1 subtypes of recently reported HIV-infected individuals in Shandong province, and the HIV-1 drug resistant strains transmission was catalogued as at low and moderate prevalence level in 2013 and 2015.

Objective To evaluate the biological effect of a kind of protective cover against inhalation of depleted uranium (DU) dust particles. Methods At 1 and 3 d after inhalation of DU dust particles, uranium concentrations in the blood, lung, bronchia, kidney, and liver of the rats in the protected group and non protected group were measured and the efficiency of protection was calculated. Results Uranium levels in all tissues and fluids of the rats in the protected group decreased significantly to 71.2%-96.1% as compared with those in non protected group. Conclusion The protective cover is effective to reduce the harm due to inhalation of DU dust particles.

Objective: To investigate the role of hexokinase Ⅱ in the changes of autophagic flow in cardiomyocytes of mice with ischemia-hypoxia in vitro. Methods: The hearts of totally six male and female C57BL/6 mice aged from 1 to 2 days were isolated to culture primary cardiomyocytes which were used for the following experiments. (1) The cells were divided into 6 groups according to the random number table (the same grouping method below), i. e., normal control 3, 6, and 9 h groups and ischemia-hypoxia 3, 6, and 9 h groups, with 4 wells in each group. After being regularly cultured for 48 h with Dulbecco′s modified Eagle medium/nutrient mixture F12 (DMEM/F12) medium (the same regular culture condition below), the cells in normal control 3, 6, and 9 h groups were cultured with replaced fresh DMEM/F12 medium for 3, 6, and 9 h, respectively, and the cells in ischemia-hypoxia 3, 6, and 9 h groups were cultured with replaced sugar-free serum-free medium in the low-oxygen incubator with a volume fraction of 1% oxygen and a volume fraction of 5% carbon dioxide at 37 ℃ (the same hypoxic culture condition below) for 3, 6, and 9 h, respectively. Cell viability was measured by the cell counting kit 8 (CCK-8) method. (2) The cells were grouped and treated the same as those in experiment (1), with 1 well in each group. Western blotting was used to detect the protein expressions of microtubule-associated protein 1 light chain 3 Ⅰ (LC3Ⅰ), LC3Ⅱ, p62, and hexokinase Ⅱ. (3) The cells were divided into normal control group, simple ischemia-hypoxia 9 h group, and ischemia-hypoxia 9 h+ 2-deoxyglucose (2-DG) group, with 4 wells in each group. After a regular culture for 48 h, the cells in normal control group were cultured with replaced fresh DMEM/F12 medium for 9 h; the cells in simple ischemia-hypoxia 9 h group were replaced with sugar-free serum-free medium, and the cells in ischemia-hypoxia 9 h+ 2-DG group were replaced with sugar-free serum-free medium in which 2-DG was dissolved in a concentration of 10 mmol/L (20 μmol), and then they were cultured with hypoxia for 9 h. Cell viability was measured by CCK-8 method. (4) The cells were grouped and treated the same as those in experiment (3), with 1 well in each group. Western blotting was used to detect the protein expressions of LC3Ⅰ, LC3Ⅱ, and p62. (5) The cells were grouped and treated the same as those in experiment (3), with 2 wells in each group. Transmission electron microscope was used to observe autophagosomes/autolysosomes in cardiomyocytes. (6) The cells were divided into normal control group, simple ischemia-hypoxia 9 h group, ischemia-hypoxia 9 h+ hexosinase Ⅱ small interfering RNA1 (HK-ⅡsiRNA1) group, and ischemia-hypoxia 9 h+ HK-ⅡsiRNA2 group, with 4 wells in each group. The cells in normal control group and simple ischemia-hypoxia 9 h group were regularly cultured for 48 h, and the cells in ischemia-hypoxia 9 h+ HK-ⅡsiRNA1 group and ischemia-hypoxia 9 h+ HK-ⅡsiRNA2 group were respectively transfected with 200 nmol/L HK-ⅡsiRNA1 and HK-ⅡsiRNA2 and then also cultured for 48 h. The cells in normal control group were cultured with replaced fresh DMEM/F12 medium for 9 h, and the cells in simple ischemia-hypoxia 9 h group, ischemia-hypoxia 9 h+ HK-ⅡsiRNA1 group, and ischemia-hypoxia 9 h+ HK-ⅡsiRNA2 group were cultured with replaced sugar-free serum-free medium and hypoxia for 9 h. Cell viability was measured by CCK-8 method. (7) The cells were grouped and treated the same as those in experiment (6), with 1 well in each group. Western blotting was used to detect the protein expressions of LC3Ⅰ, LC3Ⅱ, p62, and hexokinase Ⅱ. Except for experiment (5), each experiment was repeated 3 times. Data were processed with one-way analysis of variance and lest significant difference t test, and Bonferroni correction. Results: (1) The viabilities of cardiomyocytes in ischemia-hypoxia 3, 6, and 9 h groups were 0.450±0.022, 0.385±0.010, and 0.335±0.015, respectively, which were significantly lower than 0.662±0.026, 0.656±0.028, and 0.661±0.021 of the corresponding normal control 3, 6, and 9 h groups, respectively (t=6.21, 9.12, 12.48, P<0.01). (2) Compared with those of corresponding normal control 3, 6, and 9 h groups, the LC3Ⅱ/Ⅰ ratio and protein expressions of p62 and hexokinase Ⅱ in cardiomyocytes of ischemia-hypoxia 3, 6, and 9 h groups were significantly increased (t_{3 h}=16.15, 10.99, 5.30, t_{6 h}=6.79, 10.42, 9.42, t_{9 h}=15.76, 16.51, 7.20, P<0.05 or P<0.01). (3) The viability of cardiomyocytes in simple ischemia-hypoxia 9 h group was 0.353±0.022, which was significantly lower than 0.673±0.027 of normal control group (t=9.29, P<0.01). The viability of cardiomyocytes in ischemia-hypoxia 9 h+ 2-DG group was 0.472±0.025, which was significantly higher than that of simple ischemia-hypoxia 9 h group (t=3.60, P<0.05). (4) Compared with those of normal control group, the LC3Ⅱ/Ⅰ ratio and protein expression of p62 in cardiomyocytes of simple ischemia-hypoxia 9 h group were significantly increased (t=9.45, 8.40, P<0.01). Compared with those of simple ischemia-hypoxia 9 h group, the LC3Ⅱ/Ⅰratio and protein expression of p62 in cardiomyocytes of ischemia-hypoxia 9 h+ 2-DG group were significantly decreased (t=4.39, 4.74, P<0.05). (5) In cardiomyocytes of normal control group, only single autophagosome/autolysosome with bilayer membrane structure was observed. Compared with that of normal control group, the number of autophagosome/autolysosome with bilayer membrane structure in cardiomyocytes of simple ischemia-hypoxia 9 h group was increased significantly. Compared with that of simple ischemia-hypoxia 9 h group, the number of autophagosome/autolysosome with bilayer membrane structure in cardiomyocytes of ischemia-hypoxia 9 h+ 2-DG group was significantly decreased. (6) The viability of cardiomyocytes in simple ischemia-hypoxia 9 h group was 0.358±0.023, which was significantly lower than 0.673±0.026 in normal control group (t=9.12, P<0.01). The viabilities of cardiomyocytes in ischemia-hypoxia 9 h+ HK-ⅡsiRNA1 group and ischemia-hypoxia 9 h+ HK-ⅡsiRNA2 group were 0.487±0.027 and 0.493±0.022, respectively, which were significantly higher than the viability in simple ischemia-hypoxia 9 h group (t=3.63, 4.28, P<0.05). (7) Compared with those of normal control group, the LC3Ⅱ/Ⅰratio and protein expressions of p62 and hexokinase Ⅱ in cardiomyocytes of simple ischemia-hypoxia 9 h group were significantly increased (t=6.08, 6.31, 4.83, P<0.05 or P<0.01). Compared with those of simple ischemia-hypoxia 9 h group, the LC3Ⅱ/Ⅰ ratio and protein expressions of p62 and hexokinase Ⅱ in cardiomyocytes of ischemia-hypoxia 9 h+ HK-ⅡsiRNA1 group and ischemia-hypoxia 9 h+ HK-ⅡsiRNA2 group were significantly decreased (t=5.10, 7.76, 15.33, 4.17, 8.42, 12.11, P<0.05 or P<0.01). Conclusions Ischemia-hypoxia upregulates the expression level of hexokinase Ⅱ protein in mouse cardiomyocytes cultured in vitro, which decreases the viability of cardiomyocytes by impairing autophagic flow. To inhibit the activity of hexokinase Ⅱ or its expression can alleviate the ischemia-hypoxia damage of cardiomyocytes.

OBJECTIVETo retrospectively analyze the risk factors and clinical manifestations of myocardial damage of patients with severe burn in order to provide evidence for its prevention and treatment.

METHODSTwo hundred and fifty-two patients with severe burn admitted to 5 burn centers from January 2010 to June 2015, conforming to the study criteria, were treated in accordance with the fluid resuscitation formula of the Third Military Medical University. According to the creatine kinase isoenzyme-MB (CK-MB) level before treatment on admission, patients were divided into non-myocardial damage group (n=118, CK-MB level less than 75 U/mL) and myocardial damage group (n=134, CK-MB level higher than or equal to 75 U/mL). Data of patients in two groups were collected and evaluated such as gender, age, body mass, number of patients with chemical burn, admission time after injury, total burn area, full-thickness burn area, number of patients with inhalation injury, levels of haemoglobin, hematocrit, and blood lactate on admission and at post injury hour (PIH) 24 and 48, volumes of urine output and fluid input at PIH 24 and 48, levels of creatinine, urea nitrogen, total bile acid, diamine oxidase on admission and at PIH 24 and 48, and mortality. Furthermore, patients were divided into three groups, i. e. less than 50% total body surface area (TBSA) group (n=110), larger than or equal to 50% TBSA and less than 80% TBSA group (n=83), and larger than or equal to 80% TBSA group (n=59) according to the total burn area, and the incidence rates of myocardial damage in patients of three groups were recorded. Data were processed with chi-square test, t test, Wilcoxon test, analysis of variance for repeated measurement, and the values of P were adjusted by Bonferroni. Basic data of 252 patients were processed with binary logistic regression analysis. Receiver operating characteristic curve of total burn area of 252 patients was drawn to predict myocardial damage.

RESULTS(1) There were no statistically significant differences in age, body mass, number of patients with chemical burn, number of patients with inhalation injury, and full-thickness burn area between two groups (with t values respectively 0.20 and 0.31, χ(2) values respectively 0.49 and 4.10, Z=1.42, P values above 0.05). There were statistically significant differences in gender, admission time after injury, and total burn area of patients between two groups (χ(2)=5.00, with t values respectively 2.44 and 3.13, P<0.05 or P<0.01). (2) Gender, admission time after injury, and total burn area were independent risk factors related to myocardial damage in the patients (with odds ratios respectively 2.608, 3.620, and 1.030; 95% confidence intervals respectively 1.315-5.175, 1.916-6.839, and 1.011-1.049; P values below 0.01). (3) The incidence rates of myocardial damage of patients in less than 50% TBSA group, larger than or equal to 50% TBSA and less than 80% TBSA group, and larger than or equal to 80% TBSA group were 38.2% (42/110), 54.2% (45/83), and 61.0% (36/59) respectively, and there was statistically significant difference among them (χ(2)=9.46, P<0.05). (4) The total area under receiver operating characteristic curve of total burn area to predict myocardial damage of 252 patients was 0.706 (with 95% confidence interval 0.641-0.772, P<0.01), and 51.5% TBSA was chosen as the optimal threshold value, with sensitivity of 62.6% and specificity of 65.3%. (5) Compared with those in non-myocardial damage group, except the levels of haemoglobin and hematocrit at PIH 48 (with t values respectively -0.76 and -0.61, P values above 0.05), the levels of haemoglobin, hematocrit, and blood lactate of patients in myocardial damage group were significantly increased at each time point (with t values from -2.80 to -2.06, P<0.05 or P<0.01). Compared with those in non-myocardial damage group, the volume of urine output of patients was significantly declined (with t values respectively 2.05 and 3.68, P<0.05 or P<0.01), while the volume of fluid input of patients was not obviously changed in myocardial damage group at PIH 24 and 48 (with t values respectively 1.01 and 1.08, P values above 0.05). (6) Compared with those in non-myocardial damage group, the level of creatinine of patients was significantly increased on admission and at PIH 24 and 48 (with Z values from -2.91 to -1.99, P<0.05 or P<0.01), the level of urea nitrogen of patients was only significantly increased at PIH 24 and 48 (with t values respectively -4.75 and -5.24, P values below 0.01), the level of total bile acid of patients was not obviously changed on admission and at PIH 24 and 48 (with t values from -0.81 to -0.20, P values above 0.05), and the level of diamine oxidase of patients was only significantly increased on admission and PIH 24 in myocardial damage group (with t values respectively -3.97 and -2.02, P<0.05 or P<0.01). (7) Compared with that in myocardial damage group, the mortality of patients in non-myocardial damage group was significantly declined (χ(2)=5.81, P<0.05).

CONCLUSIONSPatients with severe burn have high incidence of myocardial damage, which may be predicted by total burn area. Severely burned patients with myocardial damage are more likely to suffer from decline of effective circulating volume, tissue oxygenation disorders, and damage in other organs in shock stage.

Body Surface Area ; Burn Units ; Burns ; pathology ; Fluid Therapy ; Hematocrit ; Hemoglobins ; analysis ; Humans ; Lactic Acid ; blood ; Myocardium ; pathology ; Retrospective Studies ; Shock