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Zoster sine herpete (ZSH) is one of the atypical clinical manifestations of herpes zoster (HZ), which stems from infection and reactivation of the varicella-zoster virus (VZV) in the cranial nerve, spinal nerve, viscera, or autonomic nerve. Patients with ZSH display variable symptoms, such as neuralgia, however, different from HZ, ZSH show no zoster, which makes clinical diagnosis difficult. ZSH not only causes initial symptoms, such as neuropathic pain in the affected nerve, Bell palsy, and Ramsay Hunt syndrome, but also postherpetic neuralgia and fatal complications such as VZV encephalitis and stroke. The misdiagnosis of ZSH and tardy antiviral treatment may lead to severe ZSH sequelae. We review the publications related to ZSH, especially its diagnosis with VZV DNA and/or anti-VZV immunoglobulin (IgG and IgM). More work about ZSH, especially ZSH epidemiological survey and guidelines for its diagnosis and treatment, are needed because most of the present studies are case reports.
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Objective@#To analyze effects of pulse contour cardiac output (PiCCO) monitoring technology in amelioration of myocardial damage in fluid resuscitation of patients with large area burn in the early stage.@*Methods@#From November 2015 to November 2017, medical data of 52 patients with large area burn hospitalized in our unit, meeting the inclusion criteria, were analyzed retrospectively. Twenty-seven patients (18 males and 9 females) with age of (43±10)years in tradition group hospitalized from November 2015 to November 2016 were monitored by traditional monitoring methods for fluid resuscitation, and 25 patients (18 males and 7 females) with age of (44±10)years in PiCCO group hospitalized from December 2016 to November 2017 were monitored by traditional monitoring methods and PiCCO monitoring equipment for fluid resuscitation. Fluid infusion coefficients and total fluid replacement volume of patients in both groups at the first and second post burn hour (PBH) 24, as well as the levels of N terminal pro B type natriuretic peptide (NT-proBNP), cardiac troponin T (cTnT), and creatine kinase MB (CK-MB) immediately on admission and post burn day (PBD) 1, 2, 3, 4, 5, 6, and 7 were recorded. Data were processed with analysis of variance for repeated measurement, chi-square test, t test and Bonferroni correction, and Mann-Whitney U test and Bonferroni correction.@*Results@#(1) The fluid infusion coefficients of patients in tradition group at the first and second PBH 24 were respectively (1.42±0.10) and (0.94±0.14)mL·kg-1·% total body surface area (TBSA)-1, and those in PiCCO group were respectively (1.76±0.14) and (0.85±0.08) mL·kg-1·%TBSA-1. Fluid infusion coefficient and total fluid replacement volume at the first PBH 24 of patients in PiCCO group were significantly higher than those in tradition group (t=-9.775, -4.769, P<0.01). Fluid infusion coefficient at the second PBH 24 of patients in PiCCO group was significantly lower than that in tradition group (t=2.682, P<0.05). There was no statistically significant difference in total fluid replacement volume at the second PBH 24 in patients between the two groups (t=1.167, P>0.05). (2) Immediately on admission and PBD 1, 2, 3, 4, 5, 6, and 7, the levels of NT-proBNP of patients in tradition group were respectively 518 (320, 763), 236 (98, 250), 139 (62, 231), 172 (104, 185), 296 (225, 341), 727 (642, 921), 1 840 (1 357, 2 081), 1 005 (671, 1 297) pg/mL, and those in PiCCO group were respectively 444 (206, 601), 66 (29, 73), 54(28, 75), 139(101, 175), 199 (106, 279), 576 (333, 837), 833 (466, 1 080), 485 (225, 710) pg/mL. The levels of NT-proBNP of patients in PiCCO group on PBD 1, 2, 6, and 7 were significantly lower than those in tradition group (Z=-5.004, -3.967, -5.285, -4.626, P<0.01). The levels of NT-proBNP immediately on admission and PBD 3, 4, and 5 in patients between the two groups were close (Z=-0.834, -0.806, -2.665, -2.153, P>0.05). (3) Immediately on admission and PBD 1, 2, 3, 4, 5, 6, and 7, the levels of cTnT of patients in tradition group were respectively (42±15), (21±12), (17±7), (11±4), (12±4), (94±32), (88±23), (42±23) pg/L, and those in PiCCO group were respectively (37±15), (9±3), (10±3), (13±3), (12±5), (85±30), (60±26), (22±14) pg/L. The levels of cTnT of patients in PiCCO group on PBD 1, 2, 6, and 7 were significantly lower than those in tradition group (t=5.227, 4.751, 4.239, 3.845, P<0.01). The levels of cTnT immediately on admission and PBD 3, 4, and 5 of patients between the two groups were close (t=1.098, -1.562, -0.117, 1.107, P>0.05). (4) The levels of CK-MB of patients in PiCCO group on PBD 3, 6, and 7 were significantly lower than those in tradition group (t=3.123, 4.103, 3.178, P<0.05 or P<0.01). The levels of CK-MB immediately on admission and PBD 1, 2, 4, and 5 in patients between the two groups were close (t=0.351, 1.868, 1.100, 0.798, 2.094, P>0.05).@*Conclusions@#PiCCO monitoring technology can monitor and guide fluid resuscitation of patients with large area burn in the early stage more scientifically and reasonably, and the effect of reducing myocardial damage is better than traditional monitoring methods.
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Pulse contour cardiac output (PiCCO) monitor as an invasive monitoring technology has been widely applied to various kinds of critical patients. It can reliably reflect actual hemodynamics of critical patients and monitor parameters such as cardiac output. Fluid resuscitation is of great importance for patients with large area of burns. On account of its easy operation as well as precise and comprehensive parameters, PiCCO has been widely used in circulation monitoring of patients with large area of burns. This article briefly introduces PiCCO monitor technology and reviews its application in fluid resuscitation monitoring, diagnosis and identification of pneumonedema in patients with large area of burns, as well as the new theory and knowledge.
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To construct a pUCP18/lasRantisense plasmid carrying the reversed gene and analyze its effect on the virulence of Pseudomonas aeruginosus, LasR gene was amplified from the genome of Pseudomonas aeruginosus by PCR and reversely recombined with plasmid pUCP18. The recombinant pUCP18/lasRantisense was verified by enzyme digestion, PCR and sequencing. The biological effects of pUCP18/lasRantisense were examined by using RT-PCR, NAD method and the assay of pyocyanin. Our results showed that the expected full length lasR fragment (721 bp) was extended from Pseudomonas aeruginosus gene with PCR. And it is consistent with LasR gene of Pseudomonas aeruginosa in GenBank (No. NC_002516). The recombinant plasmid was successfully constructed and transferred into Pseudomonas aeruginosus. The antisense nucleic acid of LasR gene could reduce the virulence of Pseudomonas aeruginosus and might serve as a new target site for treatment purpose.
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The LasR gene was amplified from the genome of Pseudomonas aeruginosus by PCR and recombined with plasmid pUCP18 reversely. The recombinant pUCP18/lasRantisense was verified with restriction analysis, PCR and sequence and was transformed in Pseudomonas aeruginosus. The biological effect of pUCP18/lasRantisense was detected by RT-PCR, NAD method and the assay of pyocyanin. The air tubes of rats were infected by pUCP18/lasRantisense strain and then carried on histopathologic slide check. Expected full length LasR fragment (721bp) can be extended from Pseudomonas aeruginosus gene with PCR technology. And it is consistent with LasR gene of Pseudomonas aeruginosa covered in GenBank (NO. NC_002516). The recombinant plasmid was constructed and transformed into Pseudomonas aeruginosus sucessfully. Compared with the rats which were infected by standard strain, the bronchitis of the rats which were infected by pUCP18/lasRantisense strain was obviously eased. It can be concluded that the antisensenucleic acid of LasR gene can depress the virulence of Pseudomonas aeruginosus and reveal a new target site for treatment.
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To investigate the killing effect of PNP/MeP-dR suicide gene system on hepatoma cells,pcDNA3. 0/PNP, an eukaryotic expression vector harboring E. coli PNP gene, was transfected into human hepatoma HepG2 cells by liposome-mediated method. A HepG2 cell line with stable PNP gene expression, HepG2/PNP, was established with presence of G418 selection. The cell growth curves were determined with trypan blue staining. The sensitivity of HepG2/PNP to MePdR and bystander effects were assayed by MTT and FCM methods. The enzymatic activity of the product of PNP gene was determined by HPLC method. The cytotoxic effects of MeP-dR on HepG2/PNP cells were obvious (IC50 =4.5μmol/L) and all HepG2/PNP cells were killed 4 days after the treatment with 100μmol/L MeP～dR. In mixed cultures containing increasing percentages of HepG2/PNP cells, total population killing was demonstrated when HepG2/PNP cells accounted for as few as 5% of all HepG2 cells 8 days after the treatment with 100μmol MeP-dR. Highpressure liquid chromatography (HPLC) demonstrated that the PNP enzyme could convert MePdR into 6-MP. PNP/MeP-dR suicide gene system had an advantage over traditional suicide gene systems for hepatoma gene therapy. Our e results suggest that high-level bystander effects of this system result in significant anti-tumor responses to hepatoma gene therapy, especially in vivo.
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Objective To investigate whether microtubule disassembly plays an important role in the pathogenesis of the opening of mitochondria permeability transition pore (MPTP) in hypoxic cardiomyocytes and the decrease of its activity, resulting in its hypoxic injury. Methods Neonatal rat cardiomyocytes in primary culture were randomized as normoxia group (A), hypoxic group (B), normoxia treated with microtubule destabilizing agent (Colchicine) group (C), hypoxia treated with microtubule stabilizing agent (Taxol) group (D). At 0.5, 1, 3, 6, 12 h after treatment, polymeric tubulin was detected by immunofluorescence and Western blotting, mitochondria permeability transition pore (MPTP) open by coloading with calcein AM and cobalt chloride, and the activity of cells by measuring the mitochondrial-dependent reduction of MTT to formazan. Results Early microtubule disassembly, MPTP open and activity decrease of cardiomyocytes in both groups B and C were observed at 0.5 h after treatment. These phenomena all became more and more significant with the prolongation of treatment. However, microtubule disassembly, MPTP open and activity decrease of cardiomyocytes of group D were significantly lower than those of group B. Conclusion Microtubule disassembly happened at 0.5 h after hypoxic treatment. Microtubule stabling agent Taxol and destabilizing agent Colchicine can regulate microtubule integrity efficiently. The microtubule damage plays an important role in the hypoxic injury of cardiomyocytes.
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Objective To investigate the protective effect of glycine (Gly) on hypoxic injury to murine cardiomyocytes and the mechanisms. Methods The survival rate of cardiomyocyte survival was detected by trypan blue exclusion and lactate dehydrogenase (LDH) with an ultraviolet spectrophotometer. Ca 2+ changes in the cardiomyocytes were detected by laser confocal microscopy. Results Glycine markedly improved the survival rate of cardiomyocytes and decreased the release of LDH in cardiomyocytes after hypoxia. The protective effect was in a dose-dependent manner. Glycine could also block calcium overload after hypoxia. Conclusion Glycine has the protective effect on cardiomyocytes through the improvement of survival rate, decrease of LDH release, and blockage of calcium overload after hypoxia.