The Global and Regional Prevalence of Hospital-Acquired Carbapenem-Resistant Klebsiella pneumoniae Infection: A Systematic Review and Meta-analysis.

Background: Due to scarce therapeutic options, hospital-acquired infections caused by Klebsiella pneumoniae (KP), particularly carbapenem-resistant KP (CRKP), pose enormous threat to patients' health worldwide. This study aimed to characterize the epidemiology and risk factors of CRKP among nosocomial KP infections. Method: MEDLINE, Embase, PubMed, and Google Scholar were searched for studies reporting CRKP prevalence from inception to 30 March 2023. Data from eligible publications were extracted and subjected to meta-analysis to obtain global, regional, and country-specific estimates. To determine the cause of heterogeneity among the selected studies, prespecified subgroup analyses and meta-regression were also performed. Odds ratios of CRKP-associated risk factors were pooled by a DerSimonian and Laird random-effects method. Results: We retained 61 articles across 14 countries and territories. The global prevalence of CRKP among patients with KP infections was 28.69% (95% CI, 26.53%-30.86%). South Asia had the highest CRKP prevalence at 66.04% (95% CI, 54.22%-77.85%), while high-income North America had the lowest prevalence at 14.29% (95% CI, 6.50%-22.0%). In the country/territory level, Greece had the highest prevalence at 70.61% (95% CI, 56.77%-84.45%), followed by India at 67.62% (95% CI, 53.74%-81.79%) and Taiwan at 67.54% (95% CI, 58.65%-76.14%). Hospital-acquired CRKP infections were associated with the following factors: hematologic malignancies, corticosteroid therapies, intensive care unit stays, mechanical ventilations, central venous catheter implantations, previous hospitalization, and antibiotic-related exposures (antifungals, carbapenems, quinolones, and cephalosporins). Conclusions: Study findings highlight the importance of routine surveillance to control carbapenem resistance and suggest that patients with nosocomial KP infection have a very high prevalence of CRKP.

The incidence of brain trauma caused by road injuries: Results from the Global Burden of Disease Study 2019.

BACKGROUND: Road collisions are a significant source of traumatic brain injury (TBI). We aimed to determine the pattern of road injury related TBI (RI-TBI) incidence, as well as its temporal trends. METHODS: We collected detailed information on RI-TBI between 1990 and 2019, derived from the Global Burden of Disease Study 2019. Estimated annual percentage changes (EAPCs) of RI-TBI age standardized incidence rate (ASIR), by sex, region, and cause of road injuries, were assessed to quantify the temporal trends of RI-TBI burden. RESULTS: Globally, incident cases of RI-TBI increased 68.1% from 6,900,000 in 1990 to 11,600,000 in 2019. The overall ASIR increased by an average of 0.43% (95% CI 0.30%-0.56%) per year during this period. The ASIR of RI-TBI due to cyclist, motorcyclist and other road injuries increased between 1990 and 2019; the corresponding EAPCs were 0.56 (95% CI 0.37-0.75), 1.60 (95% CI 1.35-1.86), and 0.75 (95% CI 0.59-0.91), respectively. In contrast, the ASIR of RI-TBI due to motor vehicle and pedestrian decreased with an EAPC of -0.12 and -0.14 respectively. The changing pattern for RI-TBI was heterogeneous across countries and regions. The most pronounced increases were observed in Mexico (EAPC = 3.74), followed by China (EAPC = 2.45) and Lesotho (EAPC = 1.91). CONCLUSIONS: RI-TBI remains a major public health concern worldwide, although road safety legislations have contributed to the decreasing incidence in some countries. We found an unfavorable trend in several countries with a relatively low socio-demographic index, suggesting that much more targeted and specific approaches should be adopted in these areas to forestall the increase in RI-TBI.

Increased Susceptibility of Mice Lacking Renin-b to Angiotensin II-Induced Organ Damage.

Several cardiac and renal diseases are attributed to a dysregulation of the renin-angiotensin system. Renin, the rate-limiting enzyme of the renin-angiotensin system, has 2 isoforms. The classical renin isoform (renin-a) encoding preprorenin is mainly confined to the juxtaglomerular cells and released into the circulation upon stimulation. Alternatively, renin-b is predicted to remain intracellular and is expressed in the brain, heart, and adrenal gland. In the brain, ablation of renin-b (Ren-bNull mice) results in increased brain renin-angiotensin system activity. However, the consequences of renin-b ablation in tissues outside the brain remain unknown. Therefore, we hypothesized that renin-b protects from hypertensive cardiac and renal end-organ damage in mice. Ren-bNull mice exhibited normal blood pressure at baseline. Thus, we induced hypertension by using a slow pressor dose of Ang II (angiotensin II). Ang II increased blood pressure in both wild type and Ren-bNull to the same degree. Although the blood pressure between Ren-bNull and wild-type mice was elevated equally, 4-week infusion of Ang II resulted in exacerbated cardiac remodeling in Ren-bNull mice compared with wild type. Ren-bNull mice also exhibited a modest increase in renal glomerular matrix deposition, elevated plasma aldosterone, and a modestly enhanced dipsogenic response to Ang II. Interestingly, ablation of renin-b strongly suppressed plasma renin, but renal cortical renin mRNA was preserved. Altogether, these data indicate that renin-b might play a protective role in the heart, and thus renin-b could be a potential target to treat hypertensive heart disease.

Reduced mRNA Expression of RGS2 (Regulator of G Protein Signaling-2) in the Placenta Is Associated With Human Preeclampsia and Sufficient to Cause Features of the Disorder in Mice.

Cascade-specific termination of G protein signaling is catalyzed by the RGS (regulator of G protein signaling) family members, including RGS2. Angiotensin, vasopressin, and endothelin are implicated in preeclampsia, and RGS2 is known to inhibit G protein cascades activated by these hormones. Mutations in RGS2 are associated with human hypertension and increased risk of developing preeclampsia and its sequelae. RGS family members are known to influence maternal vascular function, but the role of RGS2 within the placenta has not been explored. Here, we hypothesized that reduced expression of RGS2 within the placenta represents a risk factor for the development of preeclampsia. Although cAMP/CREB signaling was enriched in placentas from human pregnancies affected by preeclampsia compared with clinically matched controls and RGS2 is known to be a CREB-responsive gene, RGS2 mRNA was reduced in placentas from pregnancies affected by preeclampsia. Experimentally reducing Rgs2 expression within the feto-placental unit was sufficient to induce preeclampsia-like phenotypes in pregnant wild-type C57BL/6J mice. Stimulation of RGS2 transcription within immortalized human HTR8/SVneo trophoblasts by cAMP/CREB signaling was discovered to be dependent on the activity of histone deacetylase activity, and more specifically, HDAC9 (histone deacetylase-9), and HDAC9 expression was reduced in placentas from human pregnancies affected by preeclampsia. We conclude that reduced expression of RGS2 within the placenta may mechanistically contribute to preeclampsia. More generally, this work identifies RGS2 as an HDAC9-dependent CREB-responsive gene, which may contribute to reduced RGS2 expression in placenta during preeclampsia.

Dexamethasone protects the glycocalyx on the kidney microvascular endothelium during severe acute pancreatitis.

OBJECTIVE: This study demonstrated that dexamethasone (DEX) protects the endothelial glycocalyx from damage induced by the inflammatory stimulus tumor necrosis factor-α (TNF-α) during severe acute pancreatitis (SAP), and improves the renal microcirculation. METHODS: Ninety mice were evenly divided into 3 groups (Sham, SAP, and SAP+DEX). The SAP mice model was established by ligature of pancreatic duct and intraperitoneal injection of cerulein. Renal perfusion and function, and morphological changes of the glycocalyx were evaluated by laser Doppler velocimetry, electron microscopy, and histopathology (hematoxylin and eosin (H&E) staining), respectively. Serum levels of syndecan-1 and TNF-α were assessed by enzyme-linked immunosorbent assay (ELISA). The protective effects of dexamethasone on the glycocalyx and renal microcirculation were evaluated. RESULTS: Significantly high levels of serum TNF-α were detected 3 h after the onset of SAP. These levels might induce degradation of the glycocalyx and kidney hypoperfusion, resulting in kidney microcirculation dysfunction. The application of dexamethasone reduced the degradation of the glycocalyx and improved perfusion of kidney. CONCLUSIONS: Dexamethasone protects the endothelial glycocalyx from inflammatory degradation possibly initiated by TNF-α during SAP. This is might be a significant discovery that helps to prevent tissue edema and hypoperfusion in the future.

Arginine vasopressin infusion is sufficient to model clinical features of preeclampsia in mice.

Copeptin, a marker of arginine vasopressin (AVP) secretion, is elevated throughout human pregnancies complicated by preeclampsia (PE), and AVP infusion throughout gestation is sufficient to induce the major phenotypes of PE in mice. Thus, we hypothesized a role for AVP in the pathogenesis of PE. AVP infusion into pregnant C57BL/6J mice resulted in hypertension, renal glomerular endotheliosis, intrauterine growth restriction, decreased placental growth factor (PGF), altered placental morphology, placental oxidative stress, and placental gene expression consistent with human PE. Interestingly, these changes occurred despite a lack of placental hypoxia or elevations in placental fms-like tyrosine kinase-1 (FLT1). Coinfusion of AVP receptor antagonists and time-restricted infusion of AVP uncovered a mid-gestational role for the AVPR1A receptor in the observed renal pathologies, versus mid- and late-gestational roles for the AVPR2 receptor in the blood pressure and fetal phenotypes. These findings demonstrate that AVP is sufficient to initiate phenotypes of PE in the absence of placental hypoxia, and indicate that AVP may mechanistically (independently, and possibly synergistically with hypoxia) contribute to the development of clinical signs of PE in specific subtypes of human PE. Additionally, they identify divergent and gestational time-specific signaling mechanisms that mediate the development of PE phenotypes in response to AVP.

Angiotensin AT1A receptors expressed in vasopressin-producing cells of the supraoptic nucleus contribute to osmotic control of vasopressin.

Angiotensin II (ANG) stimulates the release of arginine vasopressin (AVP) from the neurohypophysis through activation of the AT1 receptor within the brain, although it remains unclear whether AT1 receptors expressed on AVP-expressing neurons directly mediate this control. We explored the hypothesis that ANG acts through AT1A receptors expressed directly on AVP-producing cells to regulate AVP secretion. In situ hybridization and transgenic mice demonstrated localization of AVP and AT1A mRNA in the supraoptic nucleus (SON) and the paraventricular nucleus (PVN), but coexpression of both AVP and AT1A mRNA was only observed in the SON. Mice harboring a conditional allele for the gene encoding the AT1A receptor (AT1Aflox) were then crossed with AVP-Cre mice to generate mice that lack AT1A in all cells that express the AVP gene (AT1AAVP-KO). AT1AAVP-KO mice exhibited spontaneously increased plasma and serum osmolality but no changes in fluid or salt-intake behaviors, hematocrit, or total body water. AT1AAVP-KO mice exhibited reduced AVP secretion (estimated by measurement of copeptin) in response to osmotic stimuli such as acute hypertonic saline loading and in response to chronic intracerebroventricular ANG infusion. However, the effects of these receptors on AVP release were masked by complex stimuli such as overnight dehydration and DOCA-salt treatment, which simultaneously induce osmotic, volemic, and pressor stresses. Collectively, these data support the expression of AT1A in AVP-producing cells of the SON but not the PVN, and a role for AT1A receptors in these cells in the osmotic regulation of AVP secretion.

Severe traumatic hemorrhagic shock induces compromised immune barrier function of the mesenteric lymph node leading to an increase in intestinal bacterial translocation.

Critically ill patients have increased susceptibility to translocation of gut bacteria. However, the mechanisms are complicated and remain unclear, and the aim of this study was to explore these mechanisms. Rats exposed to different levels of shock were orally administrated with bioluminescent Citrobacter. We found that severe shock caused an increase in bacterial translocation to the visceral organs, such as liver, spleen and blood, compared with mild shock. Surprisingly, bacterial translocation to mesenteric lymph node (MLN) was unchanged between the two shock groups. Various methods, including flow cytometry, a co-culture model and western blots, were used to evaluate MLN-associated immune function. Specifically, we focused on mesenteric lymph node dendritic cells (MLN-DCs), the critical antigen presenting cells involved in the construction of the immune barrier in MLN. We also found that severe shock impaired the phenotypic maturation of MLN-DCs and induced a tolerogenic phenotype. Furthermore, co-culture assays of DCs with naive CD4+ T cells showed that DCs subject to severe shock were more inclined to polarize native CD4+ T cells into Th2 and Treg cells. This study successfully reproduced the clinical phenomenon of severe shock resulting in increased bacterial translocation to extraintestinal tissues, and this may be related to the compromised immune barrier function of MLN, as maturation and function of MLN-DC's were badly impaired.

Allicin ameliorates intraintestinal bacterial translocation after trauma/hemorrhagic shock in rats: The role of mesenteric lymph node dendritic cell.

BACKGROUND: Intestinal dendritic cells play important roles in regulating the function of the intestinal immune barrier and the intestinal bacterial translocation. In this study, we aim to investigate the effects of allicin on the function of mesenteric lymph node-dendritic cells after trauma/hemorrhagic shock. METHODS: One hundred and eight-four Sprague-Dawley rats were randomly assigned into a sham group (n = 46), sham + allicin group (n = 46), trauma/hemorrhagic shock group (n = 46), and trauma/hemorrhagic shock + allicin group (n = 46). Studies were performed on an in vivo model of spontaneously breathing rats with induced trauma/hemorrhagic shock. Allicin was diluted in resuscitation fluid and was administered through the right jugular vein. Flow cytometry was used to determine the expression of CD80, CD86, and major histocompatibility complex II (MHC II) on the surface of mesenteric lymph node-dendritic cells, as well as apoptosis. Intraintestinal bacterial translocation was monitored by using bioluminescent citrobacter. Intestinal permeability tests were conducted by using both FITC-Dextran and Ussing-Chember assay. RESULT: CD80 and MHC-II expression levels were downregulated in the trauma/hemorrhagic shock group compared with the sham and sham + allicin groups; however, the expression was upregulated after allicin treatment. Also, allicin could ameliorate the trauma/hemorrhagic shock-induced increase in early apoptosis of mesenteric lymph node-dendritic cells. A significant increase was observed in the permeability of the intestinal barrier after severe traumatic shock, along with an obvious intraintestinal bacterial translocation to mesenteric lymph node. No difference was noticed in the bacterial translocation in mesenteric lymph node in the trauma/hemorrhagic shock group compared with trauma/hemorrhagic shock + allicin group (P = .589), which indicated allicin could not block bacterial translocation into mesenteric lymph node after trauma/hemorrhagic shock. However, it may increase the capacity of mesenteric lymph node to block intraintestinal bacterial translocation to extraintestinal organs as a statistical difference was noticed in the bacterial translocation in liver, blood, and spleen between trauma/hemorrhagic shock and trauma/hemorrhagic shock + allicin groups (P < .05). CONCLUSION: Trauma/hemorrhagic shock resulted in a decrease of mature mesenteric lymph node-dendritic cells. Allicin treatment could block intraintestinal bacterial translocation through increasing the immunologic barrier function of mesenteric lymph node by modulating dendritic cells maturation.

Alterations in the expression of Hs1-associated protein X-1 in the rat retina after optic nerve crush.

HS-1-associated protein X-1 (Hax-1) has been suggested to be expressed in various rodent and human tissues. Accumulating evidence has demonstrated that Hax­1 exerts an anti­apoptotic effect in neurological diseases. Furthermore, it has also been reported that Hax­1 interacts with various apoptosis­associated proteins, including high temperature-regulated A2 (HtrA2) and caspase­3. Previous studies have indicated that abnormal expression of Hax­1 may be associated with the development of the nervous system and with the pathophysiology of neurological diseases, including traumatic brain injury and cerebral ischemia. The present study reported temporal­spatial patterns of Hax­1 in rat retina following optic nerve crush (ONC). Using western blotting and double­immunofluorescence, significant upregulation of Hax­1 was observed in retinal ganglion cells (RGCs) in the retina following ONC. Increased Hax­1 expression was demonstrated to be accompanied by upregulation of active­caspase­3 and HtrA2 following ONC. In addition, Hax-1 co­localized with active caspase­3 and HtrA2 in RGCs following ONC. Terminal deoxynucleotidyl transferase­mediated biotinylated-dUTP nick­end labeling staining suggested that Hax­1 was involved in RGC apoptosis following ONC. Thus, these results suggested that Hax­1 may participate in regulating RGC apoptosis via interacting with caspase­3 and HtrA2 following ONC.

Impact of misplaced subclavian vein catheter into jugular vein on transpulmonary thermodilution measurement variables.

OBJECTIVE: The subclavian vein (SCV) is usually used to inject the indicator of cold saline for a transpulmonary thermodilution (TPTD) measurement. The SCV catheter being misplaced into the internal jugular (IJV) vein is a common occurrence. The present study explores the influence of a misplaced SCV catheter on TPTD variables. METHODS: Thirteen severe acute pancreatitis (SAP) patients with malposition of the SCV catheter were enrolled in this study. TPTD variables including cardiac index (CI), global end-diastolic volume index (GEDVI), intrathoracic blood volume index (ITBVI), and extravascular lung water index (EVLWI) were obtained after injection of cold saline via the misplaced SCV catheter. Then, the misplaced SCV catheter was removed and IJV access was constructed for a further set of TPTD variables. Comparisons were made between the TPTD results measured through the IJV and misplaced SCV accesses. RESULTS: A total of 104 measurements were made from TPTD curves after injection of cold saline via the IJV and misplaced SCV accesses. Bland-Altman analysis demonstrated an overestimation of +111.40 ml/m(2) (limits of agreement: 6.13 and 216.70 ml/m(2)) for GEDVI and ITBVI after a misplaced SCV injection. There were no significant influences on CI and EVLWI. The biases of +0.17 L/(min·m(2)) for CI and +0.17 ml/kg for EVLWI were revealed by Bland-Altman analysis. CONCLUSIONS: The malposition of an SCV catheter does influence the accuracy of TPTD variables, especially GEDVI and ITBVI. The position of the SCV catheter should be confirmed by chest X-ray in order to make good use of the TPTD measurements.

Successful Resolution of Gastric Outlet Obstruction Caused by Pancreatic Pseudocyst or Walled-Off Necrosis After Acute Pancreatitis: The Role of Percutaneous Catheter Drainage.

OBJECTIVE: Delayed gastric emptying (DGE) in patients with acute pancreatitis (AP) can be caused by gastroparesis or gastric outlet obstruction, which may occur when pancreatic pseudocyst (PP) or walled-off necrosis (WON) compresses the stomach. The aim of the study was to explore a proper surgical treatment. METHODS: From June 2010 to June 2013, 25 of 148 patients with AP suffered DGE. Among them, 12 were caused by gastroparesis, 1 was a result of obstruction from a Candida albicans plug, and 12 were gastric outlet obstruction (GOO) compressed by PP (n = 8) or WON (n = 4), which were treated by percutaneous catheter drainage (PCD). RESULTS: All 12 cases of compressing GOO achieved resolution by PCD after 6 [1.86] and 37.25 [12.02] days for PP and WON, respectively. Five cases developed intracystic infection, 3 cases had pancreatic fistulae whereas 2 achieved resolution and 1 underwent a pseudocyst jejunostomy. CONCLUSIONS: Gastric outlet obstruction caused by a PP or WON is a major cause of DGE in patients with AP. Percutaneous catheter drainage with multiple sites, large-bore tubing, and lavage may be a good therapy due to high safety and minimal invasiveness.

The hydrocortisone protection of glycocalyx on the intestinal capillary endothelium during severe acute pancreatitis.

Malfunctioning of the intestinal microcirculation secondary to severe acute pancreatitis (SAP) can cause injuries to the intestinal mucosal barrier, translocation of gut flora, and sepsis. The glycocalyx on the vascular endothelium helps maintain its normal function through multiple mechanisms, including regulation of vascular permeability and inhibition of intercellular adhesion. It is unknown that whether pancreatitis inflicts injuries to the intestinal mucosal barrier through damaging glycocalyx or stabilizing glycocalyx can be a potential therapeutic target in maintaining the integrity of the intestinal mucosal barrier during SAP. Injecting sodium taurocholate into the pancreatic duct of Sprague-Dawley rats induced SAP. Intestinal perfusion, changes in endothelial glycocalyx, and the associated molecular mechanisms were assessed by laser Doppler velocimetry, electron microscopy, and the levels of heparan sulfate, syndacan-1, and tumor necrosis factor-α (TNF-α) in the superior mesenteric vein. Protective effects of hydrocortisone treatment in the intestinal microcirculation during SAP were evaluated. Degradation of the glycocalyx in intestinal vascular endothelium developed 3 h after the onset of SAP in rats. By 12 h, significant reduction of intestinal perfusion was observed. The concomitant elevated levels of TNF-α in the superior mesenteric vein suggest that TNF-α is involved in the degradation of the glycocalyx. With the use of hydrocortisone, intestinal perfusion was improved and the degradation of glycocalyx was reduced. The degradation of glycocalyx is involved in the malfunction of the intestinal microcirculation. The massive release of TNF-α participates in this process and leads to glycocalyx degradation. Hydrocortisone may be a good therapy to prevent this process.

Full Airway Drainage by Fiber Bronchoscopy Through Artificial Airway in the Treatment of Occult Traumatic Atelectasis.

The objective of this study is to investigate the effects of full airway drainage by fiber bronchoscopy through artificial airway in the treatment of traumatic atelectasis with occult manifestations. From May 2006 to May 2011, 40 cases of occult traumatic atelectasis were enrolled into our prospective study. Group A (n = 18) received drainage by nasal bronchoscope; group B underwent airway drainage by fiber bronchoscopy through artificial airway (n = 22). The effects of treatment were evaluated by the incidence of adult respiratory distress syndrome (ARDS), lung abscess, and the average length of hospital stay. Compared with nasal fiber-optic treatment, airway drainage by fiber bronchoscopy through artificial airway reduced the incidence of ARDS (p = 0.013) and lung abscess (p = 0.062) and shortened the mean length of stay (p = 0.018). Making the decision to create an artificial airway timely and carry out lung lavage by fiber bronchoscopy through artificial airway played a significant role in the treatment of occult traumatic atelectasis.

Six cases of severe acute pancreatitis complicated with vancomycin-resistant enterococcus enteritis.

OBJECTIVE: The objective of this study was to explore the clinical manifestations and possible mechanisms of vancomycin-resistant enterococcus (VRE)-induced severe enteritis and extraenteric disseminations. METHODS: In six patients with severe acute pancreatitis (SAP) complicated with acute infectious diarrhea, VRE was confirmed by bacterial genotyping, minimum inhibitory concentration testing, and empiric linezolid treatment. Samples collected from stools and peripancreatic effusions were used to compare the genotypes of VRE by pulsed-field gel electrophoresis and multilocus sequence typing and to validate the suspected extraenteric disseminations caused by VRE. To further elucidate the mechanisms of VRE-inflicted enteric mucosal injury, in vitro infection of human intestinal Caco-2 cell line with VRE was performed followed by inflammatory cytokine assays and morphological characterization by electron microscopy. RESULTS: All six VRE strains isolated from stool samples caused severe enteritis in SAP patients. The same strains further inflicted significant damage and induced inflammatory reactions in Caco-2 cells. Homologous assays demonstrated high homology between samples from stool and peripancreatic effusions in two patients, indicating the occurrence of extraenteric disseminations. CONCLUSIONS: Alterations in drug resistance and virulence of enterococci, part of the symbiotic bacteria, during the course of SAP may cause inflammatory injuries to enteric epithelium, resulting in enteritis and extraenteric disseminations.

Early enteral nutrition with polymeric feeds was associated with chylous ascites in patients with severe acute pancreatitis.

OBJECTIVE: Chylous ascites (CA) may be involved in the pathological process of severe acute pancreatitis (SAP), but the underlying mechanisms remain unknown. This study investigated the incidence of CA in patients with SAP and its relationship with enteral nutrition (EN). METHODS: A retrospective review of 85 patients with SAP admitted to our hospital was performed. Patients starting EN within 72 hours after the onset of SAP were classified as the early EN (EEN) group, and others, as the later EN group. The incidences of CA and prognosis in the EEN and later EN groups were examined with nutrition preparation of polymeric formula or semielemental feed. RESULTS: Thirteen (15.29%) of 85 patients were identified with CA. A higher incidence of CA was observed in EEN patients who received polymeric formula (9 of 33, P < 0.05). All patients with CA were successfully treated with a modified medium-chain triglyceride diet. Consequently, there were no differences in intensive care unit stay and in mortality rates in patients with or without CA. CONCLUSIONS: There was a higher incidence of CA associated with early enteral feeding of polymeric formula in patients with SAP. Future studies are warranted to confirm our findings and evaluate better enteral feeding options to avoid CA.

[Synthesis and luminescence properties of Mg2Y8Si6O26 : Ce3+, Mn2+ phosphor].

Mg2Y8Si6O26 : Ce3+, Mn2+ phosphor was synthesized by the high temperature solid-state reaction, and the structure and luminescence properties were characterized by X-ray diffraction (XRD) and fluorescence spectrophotometer. The XRD pattern demonstrated that the synthetic material belongs to the hexagonal phase of Mg2Y8Si6O26 crystal without detectable impurity and space group P6(3)/m. The excitation and emission spectrum showed that there exist two lattice positions for Ce3+ in Mg2Y8Si6O26 crystal and their luminescence properties were compared. There are two emission peaks at 400 and 600 nm in the emission spectra under excitation at 286 nm, which come from Ce3+ and Mn2+ emission, respectively. It was demonstrated that there exists energy transfer between Ce3+ and Mn2+. The white light can be achieved by changing Mn2+ concentration. It can be used as a potential single-phased white phosphor excited by ultraviolet light.

[Synthesis and upconversion luminescence properties of BaIn6 Y2O13 : Yb3+, Er3+].

BaIn6 Y2O13 phosphors with different doping concentrations of Yb3+ and Er3+ were prepared via the high temperature solid-state reaction method. XRD data showed that BaIn6 Y2O13 phosphors belong to hexagonal system and the introduction of doping agent Yb3+ and Er3+ did not change the lattice structure of the host. The upconversion emission spectrum and power were measured by 971 nm LD laser with different excitation powers and the energy efficiencies of the samples were calculated. The obtained data showed that the ratio of green power to red power kept decreasing with the increase in doping agent concentration when the excitation density remains constant, increasing with the increase in the excitation density at the same concentration of doping agent. The analyses revealed that the former was attributed to the increasing cross relaxation between Er3+ ions, while the latter came from the raise of the energy transfer between Yb3+ and Er3+ ions and the excited state absorption of Er3+ ions due to the higher excitation density. With the increase in the excitation density, at the beginning the green luminescence power was proportional to the square of the excitation power, which agrees with the reported result. The maximum values of the fluorescence efficiencies of the samples were obtained as 0.38% (the doping concentrations of Yb3+ and Er3+ are 3%, 1%)and 0.06% (the doping concentrations of Yb3+ and Er3+ are 9%, 3%). It can be attributed to the long lifetime of 4 I13/2 energy level so it can gather a large number of electrons and reduce the population of ground state, resulting in lower pump efficiency.

Development and characterization of 109 polymorphic EST-SSRs derived from the Chinese bayberry (Myrica rubra, Myricaceae) transcriptome.

PREMISE OF THE STUDY: In Chinese bayberry (Myrica rubra), the available simple sequence repeat (SSR) markers are insufficient to meet the developing demand for genetic and molecular breeding research. This study was aimed at developing a large number of polymorphic expressed sequence tag (EST)-SSRs from the transcriptome of Chinese bayberry. • METHODS AND RESULTS: Five hundred ninety-four compound EST-SSRs and 5557 noncompound ones were identified from 41239 unigene sequences generated from the transcriptome of M. rubra cv. Biqi. Using 10 Chinese bayberry cultivars, 109 polymorphic EST-SSRs were screened from 412 selected. In total, they generated 389 alleles, with a polymorphism ratio of 93.8%. In addition, it was observed that the polymorphism levels of compound EST-SSRs were somewhat lower than those of noncompound ones. • CONCLUSIONS: The 109 polymorphic EST-SSRs developed from the Chinese bayberry transcriptome should greatly promote the development of genetic and molecular breeding studies in this as well as other Myricaceae species.

Surgical intervention of severe post-ERCP-pancreatitis accompanied with duodenum perforation.

Endoscopic retrograde cholangiopancreatography (ERCP) is a procedure widely used to diagnose and treat conditions of biliary or pancreatic ductal system. The post-ERCP severe acute pancreatitis (SAP) accompanied with duodenum perforation is rare but serious, remaining a challenge in clinic. In this study we report two such cases. Two Chinese women were treated for clinical suspicion of bile duct obstruction and underwent ERCP after admission. Both developed duodenum perforation and SAP after ERCP, and were managed in the intensive care unit (ICU) and required an organ-failure support. The surgical intervention of the peri-pancreatic debridement with lumber-abdominal compound incisions and postoperative washing and drainage was performed, and the two patients recovered well. The therapeutic effect of the peri-pancreatic debridement with lumber-abdominal compound incisions combined with postoperative washing and drainage in the patients of severe post-ERCP-pancreatitis (PEP) and duodenum perforation is satisfactory.