Identification of spin effects in the anomalous Righi-Leduc effect in ferromagnetic metals.

The emerging of spin caloritronics leads to a series of new spin-thermal related effects, such as spin Seebeck effect (SSE), spin Nernst effect (SNE) and their corresponding inverse effects. Anomalous Righi-Leduc effect (ARLE) describes that a transverse temperature gradient can be induced by a longitudinal heat flow in ferromagnets. The driving force and the response of the ARLE are all involved with heat. It is curious if spin effects mediate the heat transport and provide extra influence. In this work, we investigate the ARLE and the interplay between the heat current, charge current, and spin current via linear response theory. We identified that spin effects do have clear roles in heat transport, which can be confirmed by phase shifts of voltage output varying with the direction of magnetization. Our formulas fit the experimental data very well. Moreover, we discuss more configuration of magnetization which is expected to be tested in the future. It should be emphasized that the present formalism including spin effects is out of the theory based on magnon transport, which may be conspicuous in the devices within the spin diffusion length.

[Influence of omega-3 polyunsaturated fatty acids on inflammation-related parameters in lung tissue of rats with severe scald].

OBJECTIVE: To study the effect of omega-3 polyunsaturated fatty acids (omega-3 PUFA) on inflammation in lung tissue of rats with severe scald and its mechanism. METHODS: Seventy-two adult SD rats were divided into sham scald group (SS, n = 8), treatment group 1 (T1, n = 32), treatment group 2 (T2, n = 32) according to the random number table. Rats in T1 group and T2 group were inflicted with 30% TBSA full-thickness scald, and then they were respectively injected with 100 g/L omega-3 PUFA (1 mL/kg) and 200 g/L long-chain fatty acid (2 mL/kg) via tail vein within 5 minutes after burn. The above two fatty acids with equivalent calories were continuously injected for 10 days (once a day). On post burn day (PBD) 1, 4, 7, and 10, serum level of TNF-alpha and level of macrophage inflammatory protein 1alpha (MIP-lalpha) in lung homogenate of T1 and T2 groups were detected, the levels of NF-kappaBp65 and macrophage migration inhibitory factor (MIF) in lung tissue of T1 and T2 groups were observed with immunohistochemical staining (recorded as score). Above-mentioned parameters were also determined in SS group. Data were processed with t test. RESULTS: The levels of 4 parameters in T1 and T2 groups on PBD 1, 4, 7, 10 were higher than those in SS group (with t values from 3.411 to 8.782, P values all below 0.01), and those in T1 group on PBD 4, 7, 10 were lower than those in T2 group (with t values from 2. 321 to 2.785, P values all below 0.05). The serum level of TNF-alpha and levels of MIP-1alpha, NF-kappaBp65, and MIF in lung tissue in SS group was respectively (0.96 +/- 0.32) ng/mL, (76 +/- 16) pg/mL, 0.24 +/- 0.03, 1.31 +/- 0.03, and those in T1 and T2 groups all peaked on PBD 7 [(2.43 +/- 0.32) ng/mL, (210 +/- 56) pg/mL, 4.23 +/- 2.15, 4.69 +/- 1.83; (3.15 +/- 0.54) ng/mL, (274 +/- 64) pg/mL, 5.15 +/- 2.31, 5.37 +/- 2.16]. CONCLUSIONS: Omega-3 PUFA can effectively reduce serum level of TNF-alpha and levels of MIP-1alpha, NF-kappaBp65, and MIF in lung tissue of rats with severe scald, showing that it has a protective effect against injury of lung tissue.

[Analysis of drug resistance and risk factors of Enterobacteriaceae in burn units].

OBJECTIVE: To study the risk factors of infection of extended-spectrum beta-lactamases (ESBL)-producing strains and drug resistance of Enterobacteriaceae that infected burn patients. METHODS: A retrospective study was performed on clinical information of 92 patients with Enterobacteriaceae infection in our burn unit from January 2001 to December 2008. The distribution and drug resistance of Enterobacteriaceae, and the detection rate, drug resistance of ESBL-producing strains, and its risk factors of nosocomial infection were analyzed. Data were processed with Chi-square test. RESULTS: One hundred and nine strains of Enterobacteriaceae were isolated, with 38 (34.9%) strains of Enterobacter cloacae, 25 (22.9%) strains of Escherichia coli, 22 (20.2%) strains of Klebsiella pneumoniae, 13 (11.9%) strains of Proteus mirabilis, and 11 (10.1%) other strains of Enterobacteriaceae. Enterobacteriaceae were moderately or highly resistant to antibiotics except imipenem, resistance rate of which was less than 8.0%. ESBL-producing strains accounted for 44.0% in Escherichia coli, and 77.3% in Klebsiella pneumoniae. Drug-resistance rate of ESBL-producing strains to antibiotics was obviously higher than that of non ESBL-producing strains. Length of hospital stay longer than 20 days, and use of the third-generation cephalosporin longer than 5 days, quinolone antibiotics longer than 7 days, and topical antibiotics longer than 5 days were the risk factors of nosocomial infection caused by ESBL-producing strains, comparing with non ESBL-producing strains, the difference was statistically significant (with chi2 value respectively 5.491, 4.441, 15.186, 4.938, P values all below 0.05). CONCLUSIONS: Enterobacteriaceae strains in burn unit of our hospital are highly drug resistant, with high lactamase-producing rates, calling for intense monitor to control the risk factors that predispose the infection of ESBL-producing strains in order to lower the infection rate.

[Protective effects of enteral immuno-nutrition on intestinal mucosa injury in burned rats].

OBJECTIVE: To investigate the protective effects of enteral immuno-nutrition on intestinal mucosa injury following severe burn. METHODS: Sixty-four Wistar rats with 30% total body surface area (TBSA) full-thickness burn were randomly divided into enteral nutrition (EN, n=32) group and enteral immuno-nutrition (EIN, n=32) group. Another 8 Wistar rats were used as normal control group. The concentration of secretory immunoglobulin A (sIgA) in intestinal mucosa, the blood levels of diamine oxidase (DAO) activity and tumor necrosis factor-alpha (TNF-alpha) were determined, and the expression of TNF-alpha mRNA in intestinal mucosa was determined by reverse transcription polymerase chain reaction (PT-PCR) in control group and on 1st, 4th, 7th, and 10th day postburn in EN and EIN group. RESULTS: Compared with that of before injury, the blood levels of DAO activity, TNF-alpha content, the concentration of sIgA and the expression of TNF-alpha mRNA in intestinal mucosa were significantly increased in both EN and EIN groups (P<0.05 or P<0.01). However, the blood levels DAO activity, TNF-alpha content, the concentration of sIgA on 4th, 7th and 10th postinjury days and the expression of TNF-alpha mRNA in intestinal mucosa on 1st, 4th, 7th and 10th days postinjury in EIN group were significantly lower than those in EN group (P<0.05 or P<0.01). CONCLUSION: EIN can ameliorate the damage of the intestinal mucosa in burned rats compared with EN group. This might be related to an increase in the sIgA level and reduction of the expression of TNF-alpha mRNA in intestinal mucosa.

[The influence of changes in the levels of calcitonin gene-related peptide and neuropeptide Y on cardiac function of severe burn patients during shock stage].

OBJECTIVE: To investigate the influence of the changes in the levels of calcitonin gene-related peptide (CGRP) and neuropeptide Y (NPY) on cardiac function of severe burn patients during shock stage. METHODS: Sixty severe burn patients with total burn surface area larger than 30% were enrolled as experiment group (E group) , and they received fluid resuscitation and debridement during shock stage. Sixty healthy volunteers were enrolled as control group (C group). The changes in the plasma level of CGRP, NPY and cTnT in E and C groups were observed at 1, 3, 6, 12, 24, 48 post-burn hours (PBH). The correlation among the CGRP, NPY and cTnT in the C group were analyzed. RESULTS: At 3 PBH, the plasma level of CGRP in E group (28 +/- 6) ng/L was lower than that in C group (55 +/- 7) ng/L , and it reached the lowest level at 12 PBH (15 +/- 4)ng/L . It was still lower than that in C group at 48 PBH (P < 0.05). The levels of NPY and cTnT in E group were significantly increased at 1PBH [(136 +/- 20) ng/L, (0.41 +/- 0.08) microg/L] compared with that in C group[ (86 +/- 13) ng/L, (0.16 +/- 0.06) microg/L], peaking at 12PBH [(189 +/- 31) ng/L, (1.78 +/- 0. 47) microg/L], and remaining higher than those in C group at 48PBH. There exhibited obvious negative correlation between the changes in the level of CGRP and cTnT ( r = -0.76, P < 0.01), while obvious positive correlation was found between the changes in level of NPY and cTnT ( r = 0.79, P < 0.01). CONCLUSION: The decrease in CGRP level and the increase in NPY level might play important roles in myocardial injury during shock stage of severe burn patients.

Ligustrazine attenuates acute lung injury after burn trauma.

Acute lung injury is a common complication in patients with extensive burns in which the burned area exceeds 30% of the total body surface area (TBSA). This study was undertaken to evaluate the effect of Ligustrazine on burn-induced lung injury as well as the release of interleukin-8 (IL-8) in rats to characterize the role of Ligustrazine and IL-8 in lung injury after burn trauma. Sprague-dawley rats were divided into three groups: (1) sham group, rats who underwent sham burn; (2) control group, rats given third-degree burns over 30% TBSA and lactated Ringer solution for resuscitation; and (3) Ligustrazine group, rats given burn injury and lactated Ringer's solution with Ligustrazine inside for resuscitation. Pulmonary injury was assessed at 24 h by pulmonary capillary permeability determined with fluorescein isothiocyanate-labeled albumin and lung histologic analysis, and lung myeloperoxidase (MPO) activity as well as lung wet/dry weight ratio. The IL-8 levels were measured in serum by enzyme-linked immunosorbent assay. These studies showed that burn trauma results in increased pulmonary leakage permeability and lung wet/dry ratio, elevated serum IL-8 levels and MPO activity, and worsened histologic condition. Ligustrazine inhibited these changes, prevented burn-mediated lung injury, and the production of IL-8. This will likely provide further evidence for ligustrazine as a therapeutic strategy in burn-induced lung injury.