A bibliometric analysis of publications on burn sepsis using VOSviewer.

Background: Sepsis is one of the most common complications in burn patients and causes high morbidity, especially in those with severe burns. Nevertheless, there are no formal criteria for diagnosing and treating burn sepsis. Therefore, this bibliometric analysis is applied to reveal research trends in this field and predicts its possible hot spots. Methods: We screened relevant literature on burn sepsis that met the inclusion criteria of the Web of Sciences (WOS) database and analyzed publication trends and research hot spots in related fields using VOSviewer software. Results: From 1981 to 2022, we screened 2,486 documents that met the requirements and analyzed them bibliometrically. The American scholar Herndon DN had a much higher h-index [47] than other authors. Most published, cited, and h-indexed publications are from the USA (Np: 1193, Nc: 42154, H: 98). The second most publishing country is China, but the second most cited and h-indexed country is Germany. Burns also outperforms other journals in this field (Np: 376, Nc: 8019, H: 46). "Biomarkers" is a newly emerging keyword (cluster "clinical research," APY was 2018.16), and clinically relevant research in burn sepsis maybe a future research trend. Conclusions: Sepsis in burn patients has unique pathophysiological characteristics and the general diagnostic criteria for sepsis lack specificity. Consequently, we must establish a database and construct an intelligent predictive model to help achieve a more individualized and precise early diagnosis and treatment of burn sepsis. This may also be an important development direction for future research in this field.

The Prognostic Value of Circulating Cell-Free DNA in Colorectal Cancer: A Meta-Analysis.

BACKGROUND: Circulating cell-free DNA (cfDNA) is a promising candidate biomarker for detection, monitoring and survival prediction of colorectal cancer (CRC). However, its prognostic significance for patients with CRC remains controversial. To derive a precise estimation of the prognostic significance of cfDNA, a meta-analysis was performed. METHODS: We made a systematic search in data base of the Science Citation Index Embase and Pubmed for studies reporting prognostic data of cfDNA in CRC patients. The data of cfDNA on recurrences-free survival (RFS) and overall survival (OS) were extracted and measured in hazard rates (HRs) and 95% confident intervals (CIs). Subgroup analyses were carried out as well. Finally, the meta-analysis is accompanied with nine studies including 19 subunits. RESULTS: The pooled HRs with 95% CIs revealed strong associations between cfDNA and RFS (HR [95%CI]=2.78[2.08-3.72], I(2)=32.23%, n=7) along with OS (HR [95%CI]=3.03[2.51-3.66], I(2)=29.24%, n=12) in patients with CRC. Entire subgroup analyses indicated strong prognostic value of cfDNA irrespective tumor stage, study size, tumor markers, detection methods and marker origin. CONCLUSIONS: All the results exhibits that appearance of cfDNA in blood is an indicator for adverse RFS and OS in CRC patients.

[Study on molecular mechanism of Euodiae Fructus on liver toxicity in MICE].

OBJECTIVE: To study the molecular mechanism of extracts from Euodia rutaecarpa on hepatotoxicity in mice. METHOD: Totally 30 KM mice were divided into 3 groups and orally administrated extracts from E. rutaecarpa for consecutively 15 days. The expressions of Erkl/2, CDK8, CK1e, Stat3 and Src were detected by Western blotting method. RESULT: The extracts from E. rutaecarpa could up-regulated Erkl/2, CDK8 and CK1e expressions (P <0.01) and down-regulate Stat3 and Src (P <0.01). CONCLUSION: The molecular mechanism of E. rutaecarpa on hepatotoxicity may be correlated with Erkl/2, CDK8, CKle, Stat3 and Src signal molecules.

ADAMTS-1 expression in rat myocardium after ischemic preconditioning: age-associated differences.

BACKGROUND: It has been found that cardiac protection afforded by ischemic preconditioning (IPC) is significantly reduced in the senescent myocardium. ADAMTS-1 (a disintesrin and metalloprotease with thrombospondin type 1 motifs) has been shown to inhibit angiogenesis in a variety of in vitro and in vivo assays. The aim of this study was to investigate the age-associated differences in ADAMTS-1 protein expression in rat myocardium after ischemic preconditioning. METHODS: Sixty-four young (4 months) and old (24 months) male Sprague-Dawley rats were randomly assigned to an IPC group (40 rats) or a sham group (rats). A model of delayed IPC was induced and rats were sacrificed and myocardial samples were harvested from the ischemic-reperfused region for immunohistochemical detection of ADAMTS-1 at serial time points after IPC. A model of myocardial infarction was produced by ligation of the left anterior descending coronary artery in additional sets of young and old rats after sham or IPC procedures, then age-associated myocardial infarction survival after IPC was calculated. RESULTS: ADAMTS-1 expression increased significantly in old rats compared to young rats (P < 0.05). The mean densities of ADAMTS-1 protein at 0, 6, 12, and 24 hours in young-IPC group after IPC were 0.05 ± 0.01, 0.13 ± 0.03, 0.16 ± 0.04, and 0.12 ± 0.03 vs. 0.07 ± 0.03, 0.20 ± 0.03, 0.24 ± 0.05, and 0.21 ± 0.04 in old-IPC group. IPC resulted in diminished survival rates (5/35 vs. 6/14, old-IPC group vs. old-sham group, P < 0.05), reduced left ventricular fractional shortening ((13.9 ± 2.8)% vs. (18.3 ± 2.3)%, P < 0.05) and increased the myocardial infarction size ((37.9 ± 3.2)% vs. (32.8 ± 5.1)%, P < 0.05) in the older rats. CONCLUSIONS: Cardioprotection with IPC is attenuated in the older heart. ADAMTS-1 expression induced by IPC is greater in old rats. Over-expression of anti-angiogenic factors might be a potential mechanism behind reduced protection after IPC associated with aging.

[Ischemia preconditioning attenuated myocardial ischemia via upregulating the expression of adiponectin in rat].

OBJECTIVE: To investigate whether adiponectin plays a role in the protection of myocardium in the rat myocardial ischemia preconditioning (IPC) model. METHOD: Infarct size was measured by Masson's Trichrome staining, the expression of protein and mRNA of adiponectin at 0, 6, 12 and 24 h after IPC was examined by immunohistochemistry and quantitative real time RT-PCR, plasma levels of adiponectin at above mentioned four time points after IPC were detected by ELISA in IPC and MI rats. RESULT: Infarct size was smaller in IPC than in MI rats (20% ± 2% vs. 31% ± 3%, P < 0.05). The expression of adiponectin mRNA at 6 h and 12 h after IPC was 2.2 and 2.1 times higher than in Sham rats at respective time points (P < 0.05). Immunohistochemistry staining evidenced increased adiponectin expression in the ischemic area and weak expression of adiponectin in non-ischemic area (P < 0.05). Compared to the sham group, the plasma level of adiponectin increased significantly at 0, 6 and 12 h after IPC (0 h: 7.40 ± 0.47 vs. 10.90 ± 1.74; 6 h: 8.18 ± 1.41 vs. 10.98 ± 1.74; 12 h: 6.97 ± 1.02 vs. 9.31 ± 0.96, P < 0.05). CONCLUSION: IPC reduced infarction size, upregulated the myocardial expression of adiponectin at mRNA and protein levels, and increased plasma adiponectin concentration, suggesting that the adiponectin may play a critical role in the protective effect of IPC.

[Effect of ischemia preconditioning on pro- and anti- angiogenic molecule expression and functional arteries formation].

OBJECTIVE: to observe the effect of ischemia preconditioning (IPC) on the expression of pro-angiogenic VEGF, PDGF and anti-angiogenic ADAMTS-1, and arteriogenesis. METHODS: rat heart IPC model was made by 4 circles of occluding the LAD for 6 min followed by 6 min of reperfusion. The expression of VEGF, PDGF-B and ADAMTS-1 in the ischemic area was examined with immunohistochemistry at 6, 12 and 24 h after IPC. IPC plus myocardial infarction model was induced by LAD ligation 24 h after IPC, 14 days later, the anti-SM-α-actin antibody was used to detect the mature neovascularization in the border of the infracted area. RESULTS: VEGF, PDGF-B and ADAMTS-1 were significantly upregulated in the ischemic area in IPC group compared with the control group (P < 0.05). Density of mature arteries was also significantly increased in IPC plus MI group than that in MI group (P < 0.05). CONCLUSION: IPC promoted the formation of mature new arteries which may be modulated by upregulating VEGF, PDGF-B, and ADAMTS-1 expressions.

Novel mitochondrial DNA mutations associated with Chinese familial hypertrophic cardiomyopathy.

1. Hypertrophic cardiomyopathy (HCM) is a genetic disorder that has a complex set of symptoms and potentially devastating consequences. Increasing evidence indicates that mitochondrial DNA (mtDNA) mutations are responsible for the development of HCM, but the mtDNA mutations appear to differ considerably among different populations and regions. 2. In the present study, three families with HCM were found and investigated: one in Shandong province and two in the Chongqing region of China. The entire mtDNA genome from the 18 affected and 66 unaffected family members was sequenced directly and the mtDNA mutations were determined. 3. The frequency of haplogroup M10 was significantly higher in family members with HCM (HCM group) than in unaffected family members (normal group). Three mtDNA mutations were found with a significantly higher frequency in affected individuals than in unaffected family individuals, namely G7697A in the cytochrome c oxidase subunit II gene (P < 0.0001; odds ratio (OR) 227.5; 95% confidence interval (CI) 23.6­2194.8) and T12477C (P = 0.0037; OR 5.6; 95% CI 1.8­17.6) and G13135A in the NADH dehydrogenase 5 gene (P < 0.0001; OR 26.0; 95% CI 6.9­98.3), suggesting that these mutations are probably associated with susceptibility to HCM. In addition, mitochondrial Complex I activity was markedly decreased in the HCM group, suggesting that these mutations most likely affect mitochondrial respiratory function. 4. In conclusion, the results of the present study imply that mtDNA mutations G7697A, T12477C and G13135A are genetic factors that indicate a susceptibility to HCM and that could be used for the large-scale screening of genetic markers as well as the early diagnosis of HCM.

Adiponectin protects against cerebral ischemia-reperfusion injury through anti-inflammatory action.

Adiponectin (APN), a circulating adipose-derived hormone regulating inflammation and energy metabolism, has beneficial actions on cardio- and cerebrovascular disorders. Hypoadiponectinemia is associated with ischemic cerebrovascular disease, however, little is known about the cerebroprotective action of APN as well as its molecular mechanisms. In the present study, the role of APN in the pathogenesis of acute cerebral injury was investigated. Rats were divided into three groups: (i) a sham operation group; (ii) an ischemia/reperfusion (I/R) group, rats were subjected to 1 h middle cerebral artery occlusion followed by 23 h reperfusion (I/R); (iii) a APN-treated group, two bolus of 5 microg APN was administered through jugular vein before and after operation. I/R resulted in obvious cerebral infarct size, neurological deficits, and increased expression of endogenous immunoglobin G and matrix metalloproteinase 9, which can be significantly diminished by administration of APN. We also found that APN can significantly inhibited cerebral expression of myeloperoxidase, a distinct indicator of inflammatory cell infiltration, and inflammatory cytokines, interleukin (IL)-1beta, tumor necrosis factor-alpha and IL-8 in response to I/R, suggesting that APN exerts potent anti-inflammatory actions. Furthermore, nuclear factor (NF)-kappaB (p65), a critical transcription factor involved in inflammatory reactions, was observed predominantly located in the nucleus after I/R, whereas APN can obviously inhibit its translocation from cytoplasm into the nucleus. Results of this study demonstrate that APN exerts a potent cerebroprotective function through its anti-inflammatory action, and NF-kappaB (p65) is a key component in this process. APN might be potential molecular targets for ischemic stroke therapy.

Concentrations of antioxidant vitamins in maternal and cord serum and their effect on birth outcomes.

BACKGROUND: Emerging evidence indicates that maternal oxidative stress during pregnancy could impair fetal growth and that antioxidant vitamins (e.g. vitamins A, E and C) have a significant role in maintaining physiological processes of pregnancy and growth. AIMS: To determine the concentrations of vitamins A, E, and C in pair-matched maternal and cord serum samples of neonate, and thus to investigate the relationship between maternal serum levels of these vitamins at delivery and birth outcomes. METHODS: A total of 143 mother-neonate pairs were recruited into the cross-sectional descriptive study. Demographic information was investigated by questionnaire. After delivery, both cord and maternal blood were collected for quantification of serum levels of vitamins A, E and C by HPLC. RESULTS: Maternal serum levels of vitamins A and E were significantly higher than those in cord serum. In contrast, vitamin C level in cord serum was significantly higher than that in maternal serum. Further, we found that maternal vitamin A status was significantly correlated to both birth weight (r=0.19, p=0.0419) and birth height (r=0.21, p=0.0311), and these were manifested by these findings: (i) per 250.2 g reduction in birth weight concomitant with 1 micromol/L increase in maternal serum vitamin A level (p<0.01; 95% CI: 56.9-451.5); and (ii) per 1% increase in the ratio of serum vitamin A level of neonate to mother concomitant with 0.8 cm increase in birth height (p=0.049; 95% CI: 0.004-1.639). CONCLUSION: Maternal vitamin A, but not vitamins E and C, during pregnancy had a significant effect on birth outcomes. Further studies are necessary to investigate the role of these antioxidant vitamins in fetal growth at various gestation stages.

Mitochondrial DNA haplogroups in a Chinese Uygur population and their potential association with longevity.

1. The haplogroups and polymorphisms of mitochondrial (mt) DNA are associated with longevity. This association is highly geographically dependent. The aim of the present study was to determine the relationship between mtDNA haplogroups, single nucleotide polymorphisms (SNPs) and longevity in the Chinese Uygur population. 2. Ninety-eight Uygur Chinese subjects aged over 90 years (vitality 90+) and 117 healthy young controls living in the Xinjiang Uygur Autonomous Region of China were chosen for the present study. Frequencies of mtDNA haplogroups and SNPs in the subjects were analysed using polymerase chain reaction. The entire mtDNA genome was sequenced and the mtDNA haplogroups and SNPs were determined. 3. Nine haplogroups were identified in the Chinese Uygur population and the frequency of haplogroup J was higher in control subjects than in the vitality 90+ group (odds ratio = 0.384; 95% confidence interval = 0.163-0.906; P = 0.025). Interestingly, most of the SNPs were in the D-loop region, with frequencies higher in the control group than in the vitality 90+ group. 4. In conclusion, mtDNA haplogroups are potentially associated with longevity in the Uygur Chinese population and the D-loop region is strongly involved in ageing-related events.

Novel mutations of mitochondrial DNA associated with type 2 diabetes in Chinese Han population.

Mitochondrial single nucleotide polymorphisms (mtSNPs) have been reported to associate with type-2 diabetes mellitus (T2DM), but mtSNPs appear to be considerably different among different populations and regions. To determine mtSNPs in Chinese Han patients with T2DM, the entire sequences of the mitochondrial genomes from 72 T2DM Chinese (59 +/- 4 years) and 50 age-matched healthy subjects (controls) in Chongqing region of Western China were directly sequenced and mtSNPs were analyzed. We found that M8, M9, D, G, R and A haplogroups exist in Chinese Han population and the frequency of haplogroup M9 was significantly higher in patients with T2DM than in the controls (p = 0.0006, OR 0.06 [95% CI 0.008-0.476]). MtSNPs T3394C in NADH dehydrogenase subunit 1 (ND1), G4491A in ND2, T16189C and T16519C were found with significantly higher frequency in patients with T2DM than in the controls (T16189C, p = 0.0045; T16519C, p < 0.0001; T3394C, p = 0.0015; G4491A, p = 0.0015). In contrast, the frequency of C5178A in ND2 and A10398G in ND3 was higher in the controls than in patients with T2DM (C5178A, p = 0.014; A10398G, p = 0.0011). Our results indicate that mtSNPs T3394C, G4491A, T16189C and T16519C show susceptible tendency to T2DM and mtSNPs C5178A and A10398G seem to be genetic factors for against T2DM. These mtSNPs determined in our study is useful and could be used for early diagnosis and prevention of T2DM in Chinese Han population.

Expression of human myoglobin in H9c2 cells enhances toxicity to added hydrogen peroxide.

Hydrogen peroxide (H2O2) is implicated in cardiac myocyte (CM) damage during myocardial ischemia-reperfusion (IR) injury. Myoglobin (Mb) is present in CM at significant concentrations and reacts with H2O2 to yield one- and two-electron oxidants that may promote myocardial injury. Paradoxically, hearts from mice lacking Mb are more susceptible to H2O2-induced dysfunction than the corresponding controls [U. Flogel, A. Godecke, L.O. Klotz, J. Schrader, Role of myoglobin in the anti-oxidant defense of the heart, FASEB J. 18 (2004) 1156-1158]. We have overexpressed wild-type or Y103F variant of human Mb in cultured CMs to test whether Mb protects against H2O2 insult. Contrary to expectation, cells expressing WT or the Y103F Mb show increased mitochondrial dysfunction and apoptosis, and decreased ATP in response to H2O2 that follows the order native < Y103F Mb < WT human Mb consistent with the increasing pro-oxidant activity for these proteins. These data indicate that (i) Mb promotes oxidative damage to cultured CM and (ii) Mb may be a useful target for the design of inhibitors of myocardial IR injury.