Transcriptome analysis reveals the key network of axillary bud outgrowth modulated by topping in citrus.

Topping, an important tree shaping and pruning technique, can promote the outgrowth of citrus axillary buds. However, the underlying molecular mechanism is still unclear. In this study, spring shoots of Citrus reticulata 'Huagan No.2' were topped and transcriptome was compared between axillary buds of topped and untopped shoots at 6 and 11 days after topping (DAT). 1944 and 2394 differentially expressed genes (DEGs) were found at 6 and 11 DAT, respectively. KEGG analysis revealed that many DEGs were related to starch and sucrose metabolism, signal transduction of auxin, cytokinin and abscisic acid. Specially, transcript levels of auxin synthesis, transport, and signaling-related genes (SAURs and ARF5), cytokinin signal transduction related genes (CRE1, AHP and Type-A ARRs), ABA signal responsive genes (PYL and ABF) were up-regulated by topping; while transcript levels of auxin receptor TIR1, auxin responsive genes AUX/IAAs, ABA signal transduction related gene PP2Cs and synthesis related genes NCED3 were down-regulated. On the other hand, the contents of sucrose and fructose in axillary buds of topped shoots were significantly higher than those in untopped shoots; transcript levels of 16 genes related to sucrose synthase, hexokinase, sucrose phosphate synthase, endoglucanase and glucosidase, were up-regulated in axillary buds after topping. In addition, transcript levels of genes related to trehalose 6-phosphate metabolism and glycolysis/tricarboxylic acid (TCA) cycle, as well to some transcription factors including Pkinase, Pkinase_Tyr, Kinesin, AP2/ERF, P450, MYB, NAC and Cyclin_c, significantly responded to topping. Taken together, the present results suggested that topping promoted citrus axillary bud outgrowth through comprehensively regulating plant hormone and carbohydrate metabolism, as well as signal transduction. These results deepened our understanding of citrus axillary bud outgrowth by topping and laid a foundation for further research on the molecular mechanisms of citrus axillary bud outgrowth.

Molecular physiology for the increase of soluble sugar accumulation in citrus fruits under drought stress.

To investigate the mechanism for drought promoting soluble sugar accumulation will be conducive to the enhancement of citrus fruit quality as well as stress tolerance. Fruit sucrose mainly derives from source leaves. Its accumulation in citrus fruit cell vacuole involves in two processes of unloading in the fruit segment membrane (SM) and translocating to the vacuole of fruit juice sacs (JS). Here, transcript levels of 47 sugar metabolism- and transport-related genes were compared in fruit SM or JS between drought and control treatments. Results indicated that transcript levels of cell wall invertase genes (CwINV2/6) and sucrose synthase genes (SUS2/6) in the SM were significantly increased by the drought. Moreover, transcript levels of SWEET genes (CsSWEET1/2/4/5/9) and monosaccharide transporter gene (CsPMT3) were significantly increased in SM under drought treatment. On the other hand, SUS1/3 and vacuolar invertase (VINV) transcript levels were significantly increased in JS by drought; CsPMT4, sucrose transporter gene 2 (CsSUT2), tonoplast monosaccharide transporter gene 2 (CsTMT2), sugar transport protein gene 1 (CsSTP1), two citrus type I V-PPase genes (CsVPP1, and CsVPP2) were also significantly increased in drought treated JS. Collectively, the imposition of drought stress resulted in more soluble sugar accumulation through enhancing sucrose download by enhancing sink strength- and transport ability-related genes, such as CwINV2/6, SUS2/6, CsSWEET1/2/4/5/9, and CsPMT3, in fruit SM, and soluble sugar storage ability by increasing transcript levels of genes, such as CsPMT4, VINV, CsSUT2, CsTMT2, CsSTP1, CsVPP1, and CsVPP2, in fruit JS.

Effectively removing gaseous polycyclic aromatic hydrocarbons (PAHs) by willow catkins: Do you still dislike the catkins floating?

The floating catkins generated by willow and poplar trees have been criticized for spreading germ and causing fire for decades. It has been found that catkins are with a hollow tubular structure, which made us wonder if the floating catkins can adsorb atmospheric pollutions. Thus, we conducted a project in Harbin, China to investigate whether and how willow catkins could adsorb atmospheric polycyclic aromatic hydrocarbons (PAHs). The results suggest that both the catkins floating in the air and on the ground preferred to adsorb gaseous PAHs rather than particulate PAHs. Moreover, 3- and 4-ring PAHs were the dominating compositions adsorbed by catkins, which significantly increased with exposure time. The gas/catkins partition (KCG) was defined, which explained why 3-ring PAHs are more easily adsorbed by catkins than by airborne particles when their subcooled liquid vapor pressure is high (log PL > -1.73). The removal loading of atmospheric PAHs by catkins were estimated as 1.03 kg/year in the center city of Harbin, which may well explain the phenomenon that levels of gaseous and total (particle + gas) PAHs are relatively low in the months with catkins floating reported in peer-reviewed papers.

Genome-wide analysis of citrus TCP transcription factors and their responses to abiotic stresses.

BACKGROUND: Citrus is one of the most important fruit crops in the world, and it is worthy to conduct more research on artificially controlling citrus plant growth and development to adapt to different cultivation patterns and environmental conditions. The plant-specific TEOSINTE BRANCHED1, CYCOLOIDEA, and PROLIFERATING CELL FACTORS (TCP) transcription factors are crucial regulators controlling plant growth and development, as well as responding to abiotic stresses. However, the information about citrus TCP transcription factors remains unclear. RESULTS: In this study, twenty putative TCP genes (CsTCPs) with the TCP domain were explored from Citrus sinensis genome, of which eleven (CsTCP3, - 4, - 5, - 6, - 10, - 11, - 15, - 16, - 18, - 19, - 20), five (CsTCP1, - 2, - 7, - 9, - 13), and four genes (CsTCP8, - 12, - 14, - 17) were unevenly distributed on chromosomes and divided into three subclades. Cis-acting element analysis indicated that most CsTCPs contained many phytohormone- and environment-responsive elements in promoter regions. All of CsTCPs were predominantly expressed in vegetative tissues or organs (stem, leaf, thorn, and bud) instead of reproductive tissues or organs (flower, fruit, and seed). Combined with collinearity analysis, CsTCP3, CsTCP9, and CsTCP13 may take part in leaf development; CsTCP12 and CsTCP14 may function in shoot branching, leaf development, or thorn development; CsTCP15 may participate in the development of stem, leaf, or thorn. In mature leaf, transcript levels of two CsTCPs (CsTCP19, - 20) were significantly increased while transcript levels of eight CsTCPs (CsTCP2, - 5, - 6, - 7, - 8, - 9, - 10, - 13) were significantly decreased by shading; except for two CsTCPs (CsTCP11, - 19), CsTCPs' transcript levels were significantly influenced by low temperature; moreover, transcript levels of two CsTCPs (CsTCP11, - 12) were significantly increased while five CsTCPs' (CsTCP14, - 16, - 18, - 19, - 20) transcript levels were significantly reduced by drought. CONCLUSIONS: This study provides significant clues for research on roles of CsTCPs in regulating citrus plant growth and development, as well as responding to abiotic stresses.

[Adenovirus pneumonia with hemophagocytic lymphohistiocytosis in children: a clinical analysis of 7 children].

OBJECTIVE: To study the clinical features of children with adenovirus pneumonia and hemophagocytic lymphohistiocytosis (HLH). METHODS: A retrospective analysis was performed on the mediacal data of 7 children with adenovirus pneumonia and HLH from March to September, 2019. RESULTS: The age of these children ranged from 11 months to 5 years, and among these children, 5 were aged <2 years and 5 were boys. None of these children had underlying diseases. All children were hospitalized due to persistent high fever and cough, and the peak temperature of fever was 39°C to 41°C. With disease progression, 7 children developed hepatomegaly and 6 developed splenomegaly. Routine blood test results showed reductions in two or three lineages of blood cells, with increases in serum ferritin (SF), C-reactive protein (CRP), procalcitonin (PCT), and lactate dehydrogenase (LDH). Phagocytosis of blood cells was observed in 6 children. Radiological examination of lungs showed pneumonia changes. All 7 children were diagnosed with human adenovirus type 7 infection based on pathogenic metagenome detection. No abnormality was found by HLH gene detection and the children were diagnosed with secondary HLH. All children received intravenous immunoglobulin. Among these children, 4 received dexamethasone and etoposide chemotherapy, 3 received dexamethasone alone, and 4 received plasma exchange. Of the 7 children, 2 died and 5 were recovered. Compared with those who survived, the children who died had significantly greater reductions in the three lineages of blood cells and significantly greater increases in serum levels of CRP, PCT, SF, and LDH. CONCLUSIONS: The children with adenovirus pneumonia and HLH have main clinical features of persistent high fever, progressive reductions in two or three lineages of peripheral blood cells, and involvement of other organ systems, including hepatosplenomegaly. Significant increases in serum levels of CRP, PCT, SF, and LDH may suggest a poor prognosis.

Anticonvulsant and Neuroprotective Effects of Paeonol in Epileptic Rats.

Paeonol is the main active compound in the root bark extract of the peony tree, and it has antioxidative and anti-inflammatory effects. Recent studies have reported the neuroprotective effects of paeonol including its capacity in improving impaired memory. However, the effect of paeonol on epilepsy is yet to be demystified. We aimed to investigate the therapeutic effect of paeonol in epilepsy and its relationship with oxidative stress damage and neuronal loss in the rat brain to reveal the underlying mechanisms of epileptic seizures. A rat model for chronic epilepsy was established, and the seizure scores of the rats in different groups were recorded. The seizure duration and the seizure onset latency were used to evaluate the anticonvulsant effects of paeonol. Terminal deoxynucleotidyl transferase dUTP nick end-labeling staining, Nissl staining and H/E staining were used to evaluate the effects of paeonol on neuronal loss and apoptosis in epileptic rats. The colorimetric assessment of malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, catalase activity and total antioxidant capacity of paeonol were used in assessing paeonol's effect on oxidative stress in epileptic rats. Evaluation of Caspase-3 mRNA and protein expression levels were determined using western blot and quantitative real-time (RT-q)PCR. In this study, we found that paeonol reduced the seizure scores of epileptic rats and attenuated the duration and onset latency of seizures. Paeonol can also increase the activities of total antioxidant capacity, SOD and catalase activity and reduce MDA content as well. This suggests that paeonol can improve the level of oxidative stress in rats. More significantly, paeonol can improve neuronal loss and apoptosis in epileptic rats. These results indicate that paeonol has anticonvulsant and neuroprotective effects in epileptic rats. This effect may be caused by reducing oxidative stress.

Gradual replacement of all previously circulating respiratory syncytial virus A strain with the novel ON1 genotype in Lanzhou from 2010 to 2017.

ON1 is a novel genotype of human respiratory syncytial virus (HRSV) subtype A, in children with acute respiratory tract infections (ARTIs). However, there is not much data on the prevalence and clinical and molecular characterization in China.Our study is based on the children who had respiratory infections positive for RSV-A admitted by Gansu Provincial Maternity and Child-care Hospital in Lanzhou (northwestern China) during the last 7 epidemic seasons from 2010 to 2017.In our study, different strains of the novel RSV-A genotype ON1, first identified in Canada in December 2010, were first detected in Gansu Provincial Maternity and Child-care Hospital in August 2012 and then followed by an abrupt expansion in the number of ON1 variants in the beginning of 2014 and eventually replaced all other RSV-A strains from 2015 to 2017. ON1 is characterized by a 72-nt duplication in the C-terminal region of the highly variable attachment glycoprotein (G), predicted to lengthen the polypeptide with 24 amino acids, including a 23-aa duplication, which likely changes antigenicity. New N-glycosylation sites occurred within the 23-aa duplication and 24-aa insertion of the ON1 viruses in our study. Notably, RSV infections occurred later, but peaked sooner from the 2014/2015 to 2016/2017 epidemic seasons, compared with the previous 4 seasons.Our study concluded that genotype ON1 has caused larger outbreaks and became the predominate genotype for HRSV subgroup A in Lanzhou from 2013 to 2017, and became the sole genotype of RSV-A in 2015/2016 and 2016/2017. Our data indicate that northwest of China and the world will eventually be dominated by the ON1 RSV-A genotype, including the possibility for vaccine development. Based on trends seen in RSV-B BA genotype, which predominated for decades, there is a possibility to develop a vaccine for children in the next 10 years.

Adiponectin Single Nucleotide Polymorphisms and Serum Levels Are Relevant to Prognosis of Patients With Aneurysmal Subarachnoid Hemorrhages.

To investigate the association of adiponectin gene polymorphisms and its levels with aneurysmal subarachnoid hemorrhages (aSAHs) prognosis. This case-control study enrolled 138 patients with aSAH and 102 healthy controls as case group and control group, respectively. Prognosis of case group was evaluated using Glasgow Outcome Scale. Polymerase chain reaction-restriction fragment length polymorphism was used to examine the genotypes of 45T>G and -11377C>G. Enzyme-linked immunosorbent assay was used to detect adiponectin levels. Logistic regression analysis was applied to assess the association of adiponectin gene polymorphism with aSAH prognosis. Case group had increased GG genotype and G allele genotype frequencies of 45T>G and -11377C>G compared with control group (all P < 0.01). In case group, TT genotype had the highest adiponectin level compared with both TG and GC genotypes (both P < 0.05). As for -11377C>G, GG genotype had the lowest adiponectin levels, followed by CG genotype and CC genotype in both groups (P < 0.05). In general, case group had decreased adiponectin levels compared with control group (P < 0.05). Univariate analysis showed that hypertension, Hunt-Hess grade, aneurysm size, aneurysms multiplicity and -11377C>G were associated with aSAH prognosis, while multivariate logistic regression analysis confirmed that hypertension, Hunt-Hess grade, residual flow in aneurysms and aneurysm size were independent risk factors for aSAH prognosis. Decreased adiponectin levels may be a pathological index for aSAH, which may be explain by the G allele of -11377C>G in adiponectin. Moreover, hypertension, Hunt-Hess grade, residual flow in aneurysms and aneurysm size may be independent risk factors for aSAH prognosis.

[Mid-term outcome of endoscopic greater saphenous vein harvesting in coronary artery bypass grafting].

OBJECTIVE: To evaluate the mid-term clinical outcome of endoscopic greater saphenous vein harvesting (EVH) in coronary artery bypass grafting (CABG). Method A total of 205 patients receiving off-pump CABG between July, 2012 and April, 2013 at our department were enrolled in this study, including 66 patients (35 male and 31 female patients with a mean age of 60.3±7.92 years) undergoing EVH and 139 patients (109 male and 30 female patients with a mean age of 59.20±8.37 years) undergoing open greater saphenous vein harvesting (OVH). RESULTS: The surgical procedures were completed smoothly in all the cases. The perioperative mortality rates was 3.03% (2/66) in EVH group, as compared with 3.60% (5/139) in OVH group (P=1.00). Acute myocardial infarction (AMI) occurred during the perioperative period in 3 (2.16%) patients in OVH group and in 1 (1.52%) patient in EVH group. Perioperative low cardiac output syndrome was diagnosed in 4 (2.88%) patients in OVH group and in 2 (3.03%) in EVH group (P>0.05). During the follow-up, 8 (8.80%) patients in OVH group and 5 (8.06%) in EVH group had recurrent angina (P=0.93). No patients experienced AMI during the follow-up. The 2-year patency rate of the venous grafts was 83.59% in OVH group and 82.22% in EVH group (P=0.73). CONCLUSION: EVH has significant advantage in reducing the complications of the incision in the lower limbs. The mid-term patency rates of venous grafts are similar between OVH and EVH, but the long-term patency rate needs further evaluation.

The molecular basis of the genesis of basal tone in internal anal sphincter.

Smooth muscle sphincters exhibit basal tone and control passage of contents through organs such as the gastrointestinal tract; loss of this tone leads to disorders such as faecal incontinence. However, the molecular mechanisms underlying this tone remain unknown. Here, we show that deletion of myosin light-chain kinases (MLCK) in the smooth muscle cells from internal anal sphincter (IAS-SMCs) abolishes basal tone, impairing defecation. Pharmacological regulation of ryanodine receptors (RyRs), L-type voltage-dependent Ca(2+) channels (VDCCs) or TMEM16A Ca(2+)-activated Cl(-) channels significantly changes global cytosolic Ca(2+) concentration ([Ca(2+)]i) and the tone. TMEM16A deletion in IAS-SMCs abolishes the effects of modulators for TMEM16A or VDCCs on a RyR-mediated rise in global [Ca(2+)]i and impairs the tone and defecation. Hence, MLCK activation in IAS-SMCs caused by a global rise in [Ca(2+)]i via a RyR-TMEM16A-VDCC signalling module sets the basal tone. Targeting this module may lead to new treatments for diseases like faecal incontinence.

Hydrogen sulfide-induced enhancement of gastric fundus smooth muscle tone is mediated by voltage-dependent potassium and calcium channels in mice.

AIM: To investigate the effect of hydrogen sulfide (H2S) on smooth muscle motility in the gastric fundus. METHODS: The expression of cystathionine ß-synthase (CBS) and cystathionine γ-lyase (CSE) in cultured smooth muscle cells from the gastric fundus was examined by the immunocytochemistry technique. The tension of the gastric fundus smooth muscle was recorded by an isometric force transducer under the condition of isometric contraction with each end of the smooth muscle strip tied with a silk thread. Intracellular recording was used to identify whether hydrogen sulfide affects the resting membrane potential of the gastric fundus in vitro. Cells were freshly separated from the gastric fundus of mice using a variety of enzyme digestion methods and whole-cell patch-clamp technique was used to find the effects of hydrogen sulfide on voltage-dependent potassium channel and calcium channel. Calcium imaging with fura-3AM loading was used to investigate the mechanism by which hydrogen sulfide regulates gastric fundus motility in cultured smooth muscle cells. RESULTS: We found that both CBS and CSE were expressed in the cultured smooth muscle cells from the gastric fundus and that H2S increased the smooth muscle tension of the gastric fundus in mice at low concentrations. In addition, nicardipine and aminooxyacetic acid (AOAA), a CBS inhibitor, reduced the tension, whereas Nω-nitro-L-arginine methyl ester, a nonspecific nitric oxide synthase, increased the tension. The AOAA-induced relaxation was significantly recovered by H2S, and the NaHS-induced increase in tonic contraction was blocked by 5 mmol/L 4-aminopyridine and 1 µmol/L nicardipine. NaHS significantly depolarized the membrane potential and inhibited the voltage-dependent potassium currents. Moreover, NaHS increased L-type Ca(2+) currents and caused an elevation in intracellular calcium ([Ca(2+)]i). CONCLUSION: These findings suggest that H2S may be an excitatory modulator in the gastric fundus in mice. The excitatory effect is mediated by voltage-dependent potassium and L-type calcium channels.

S-Nitrosylation of proline-rich tyrosine kinase 2 involves its activation induced by oxygen-glucose deprivation.

Previous studies have demonstrated that activation of proline-rich tyrosine kinase 2 (PYK2) in cerebral ischemia is involved in the modulation of N-methyl-d-aspartate-type (NMDA) glutamate receptor activity and Ca(2+) dynamics, resulting in ischemic neuron death ultimately. A number of reports indicate that PYK2 is a redox sensitive kinase that must be activated by an estrogen-induced reactive oxygen species (ROS). However, the mechanism of PYK2 activation remains incompletely illustrated. Accumulating attention is focused on nitric oxide (NO, a free radical) which plays a critical role in cellular signal transduction through stimulus-coupled S-nitrosylation of cysteine residues. Here we reported that PYK2 over-expressed in human embryonic kidney (HEK293) cells was S-nitrosylated (forming SNO-PYK2) by reacting with GSNO, an exogenous NO donor, at one critical cysteine residue (Cys534) with a biotin switch assay. Moreover, our results showed that S-nitrosylation and phosphorylation of PYK2 over-expressed in SH-SY5Y cells was significantly increased after oxygen-glucose deprivation (OGD). We further investigated whether the activation (phosphorylation) of PYK2 was associated with S-nitrosylation following SH-SY5Y cells OGD. Our results showed that the cysteine534 residue (site of S-nitrosylation) mutant PYK2 over-expressed in SH-SY5Y cells diminished S-nitrosylation of PYK2 and inhibited its phosphorylation induced by OGD. In addition, overexpression of the mutant PYK2 protein could prevent nuclear accumulation and abrogate neuronal cell death compared to wild type PYK2 in SH-SY5Y cells induced by OGD. These data suggest that the activation of PYK2 following OGD may be modulated by S-nitrosylation, which provides a new avenue for stroke therapy by targeting the post-translational modification machinery.

A high-density graphene-sulfur assembly: a promising cathode for compact Li-S batteries.

This work reports a high-density graphene/sulfur assembly for compact Li-S batteries with high volumetric capacity, which retains good structural stability and conductivity. This dense assembly was prepared by a reduction-triggered self-assembly of graphene oxide with simultaneous deposition of sulfur, followed by unique evaporation-induced spatial volume shrinkage. This assembly has an ultrahigh density, delivering an unprecedented volumetric capacity that is much higher than common carbon/sulfur cathodes. In particular, the unique spatial confinement derived from the shrinkage of the graphene/sulfur assembly is favorable for stabilizing sulfur cathodes.

Gastric nNOS reduction accompanied by natriuretic peptides signaling pathway upregulation in diabetic mice.

AIM: To investigate the relationship between neuronal nitric oxide synthase (nNOS) expression and the natriuretic peptide signaling pathway in the gastric fundus of streptozotocin (STZ)-induced diabetic mice. METHODS: Diabetic mice were induced by injection of STZ solution. Immunofluorescence labeling of HuC/D, nNOS and natriuretic peptide receptor-A, B, C (NPRs) in the gastric fundus (GF) was used to observe nNOS expression and whether NPRs exist on enteric neurons. The expression levels of nNOS and NPRs in the diabetic GF were examined by western blotting. An isometric force transducer recorded the electric field stimulation (EFS)-induced relaxation and contraction in the diabetic GF. An intracellular recording method assessed EFS-induced inhibitory junction potentials (IJP) on the GF. GF smooth muscles acquired from normal mice were incubated with different concentrations of the NPRs agonist C-type natriuretic peptide (CNP) for 24 h, after which their nNOS expressions were detected by western blotting. RESULTS: Eight weeks after injection, 43 diabetic mice were obtained from mouse models injected with STZ. Immunofluorescence indicated that the number of NOS neurons was significantly decreased and that nNOS expression was significantly downregulated in the diabetic GF. The results of physiological and electrophysiological assays showed that the EFS-induced relaxation that mainly caused by NO was significantly reduced, while the contraction was enhanced in the diabetic GF. EFS-induced IJP showed that L-NAME sensitive IJP in the diabetic GF was significantly reduced compared with control mice. However, both NPR-A and NPR-B were detected on enteric neurons, and their expression levels were upregulated in the diabetic GF. The nNOS expression level was downregulated dose-dependently in GF smooth muscle tissues exposed to CNP. CONCLUSION: These findings suggested that upregulation of the NPs signaling pathway may be involved in GF neuropathy caused by diabetes by decreasing nNOS expression.

Voltage dependent potassium channel remodeling in murine intestinal smooth muscle hypertrophy induced by partial obstruction.

Partial obstruction of the small intestine causes obvious hypertrophy of smooth muscle cells and motility disorder in the bowel proximate to the obstruction. To identify electric remodeling of hypertrophic smooth muscles in partially obstructed murine small intestine, the patch-clamp and intracellular microelectrode recording methods were used to identify the possible electric remodeling and Western blot, immunofluorescence and immunoprecipitation were utilized to examine the channel protein expression and phosphorylation level changes in this research. After 14 days of obstruction, partial obstruction caused obvious smooth muscle hypertrophy in the proximally located intestine. The slow waves of intestinal smooth muscles in the dilated region were significantly suppressed, their amplitude and frequency were reduced, whilst the resting membrane potentials were depolarized compared with normal and sham animals. The current density of voltage dependent potassium channel (KV) was significantly decreased in the hypertrophic smooth muscle cells and the voltage sensitivity of KV activation was altered. The sensitivity of KV currents (IKV) to TEA, a nonselective potassium channel blocker, increased significantly, but the sensitivity of IKv to 4-AP, a KV blocker, stays the same. The protein levels of KV4.3 and KV2.2 were up-regulated in the hypertrophic smooth muscle cell membrane. The serine and threonine phosphorylation levels of KV4.3 and KV2.2 were significantly increased in the hypertrophic smooth muscle cells. Thus this study represents the first identification of KV channel remodeling in murine small intestinal smooth muscle hypertrophy induced by partial obstruction. The enhanced phosphorylations of KV4.3 and KV2.2 may be involved in this process.

A novel, recovery, and reproducible minimally invasive cardiopulmonary bypass model with lung injury in rats.

BACKGROUND: Cardiopulmonary bypass (CPB) has been shown to be associated with a systemic inflammatory response leading to postoperative organ dysfunction. Elucidating the underlying mechanisms and developing protective strategies for the pathophysiological consequences of CPB have been hampered due to the absence of a satisfactory recovery animal model. The purpose of this study was to establish a good rat model of CPB to study the pathophysiology of potential complications. METHODS: Twenty adult male Sprague-Dawley rats weighing 450-560 g were randomly divided into a CPB group (n = 10) and a control group (n = 10). All rats were anaesthetized and mechanically ventilated. The carotid artery and jugular vein were cannulated. The blood was drained from the right atrium via the right jugular and transferred by a miniaturized roller pump to a hollow fiber oxygenator and back to the rat via the left carotid artery. Priming consisted of 8 ml of homologous blood and 8 ml of colloid. The surface of the hollow fiber oxygenator was 0.075 m(2). CPB was conducted for 60 minutes at a flow rate of 100-120 ml× kg(-1)×min(-1) in the CPB group. Oxygen flow/perfusion flow was 0.8 to 1.0, and the mean arterial pressure remained 60-80 mmHg. Blood gas analysis, hemodynamic investigations, and lung histology were subsequently examined. RESULTS: All CPB rats recovered from the operative process without incident. Normal cardiac function after successful weaning was confirmed by electrocardiography and blood pressure measurements. Mean arterial pressure remained stable. The results of blood gas analysis at different times were within the normal range. Levels of IL-1ß and TNF-α were higher in the lung tissue in the CPB group (P < 0.005). Histological examination revealed marked increases in interstitial congestion, edema, and inflammation in the CPB group. CONCLUSION: This novel, recovery, and reproducible minimally invasive CPB model may open the field for various studies on the pathophysiological process of CPB and systemic ischemia-reperfusion injury in vivo.

Total liquid ventilation reduces oleic acid-induced lung injury in piglets.

BACKGROUND: Pediatric patients are susceptible to lung injury that does not respond to traditional therapies. Total liquid ventilation has been developed as an alternative ventilatory strategy for severe lung injury. The aim of this study is to investigate the effect of total liquid ventilation on oleic acid (OA)-induced lung injury in piglets. METHODS: Twelve Chinese immature piglets were induced acute lung injury by OA. Twelve piglets were randomly treated with conventional gas ventilation (control group) or total liquid ventilation (study group) for 240 minutes. Samples for blood gas analysis were collected before, and at 60-minute intervals after OA-induced lung injury. The degree of lung injury was quantified by histologic examination. The inflammatory cells and the levels of IL-1ß, IL-6, IL-10 and TNF-α in plasma, tissue and bronchoalveolar lavage were analyzed. RESULTS: Neutrophil and macrophage counts in bronchoalveolar lavage were significantly decreased in the study group (P < 0.05). The total lung injury score was also reduced in the study group (P < 0.05). The concentrations of IL-1ß, IL-6, IL-10 and TNF-α in plasma, tissue and bronchoalveolar lavage were significantly reduced in the study group (P < 0.05). CONCLUSIONS: Total liquid ventilation reduces biochemical and histologic OA-induced lung injury in piglets.

Different regulatory effects of hydrogen sulfide and nitric oxide on gastric motility in mice.

NO and H2S are gaseous signaling molecules that modulate smooth muscle motility. We aimed to identify expressions of enzymes that catalyze H2S and NO generation in mouse gastric smooth muscle, and determine relationships between endogenous H2S and NO in regulation of smooth muscle motility. Western blotting and immunocytochemistry methods were used to track expressions of neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), cystathionine ß-synthase (CBS) and cystathionine γ-lyase (CSE) in gastric smooth muscles. Smooth muscle motility was recorded by isometric force transducers. cGMP production was measured by a specific radioimmunoassay. We found that CBS, CSE, eNOS, and nNOS were all expressed in mice gastric antral smooth muscle tissues, and in cultured gastric antral smooth muscle cells. AOAA significantly inhibited smooth muscle contractions in the gastric antrum, which was significantly recovered by NaHS, while PAG had no significant effect. l-NAME enhanced contractions. NaHS at low concentrations increased basal tension but decreased it at high concentrations. SNP significantly inhibited the contractions, which could be recovered by NaHS both in the absence and presence of CuSO4. ODQ did not block NaHS-induced excitatory effect, while IBMX partially blocked this effect. cGMP production in smooth muscle was significantly increased by SNP but was not affected by NaHS. All these results suggest that endogenous H2S and NO appear to play opposite roles in regulating gastric motility and their effects may be via separate signal transduction pathways. Intracellular H2S/NO levels may be maintained in a state of balance to warrant normal smooth muscle motility.

Switchable transport strategy to deposit active Fe/Fe3C cores into hollow microporous carbons for efficient chromium removal.

Magnetic hollow structures with microporous shell and highly dispersed active cores (Fe/Fe3 C nanoparticles) are rationally designed and fabricated by solution-phase switchable transport of active iron species combined with a solid-state thermolysis technique, thus allowing selective encapsulation of functional Fe/Fe3 C nanoparticles in the interior cavity. These engineered functional materials show high loading (≈54 wt%) of Fe, excellent chromium removal capability (100 mg g(-1)), fast adsorption rate (8766 mL mg(-1) h(-1)), and easy magnetic separation property (63.25 emu g(-1)). During the adsorption process, the internal highly dispersed Fe/Fe3 C nanoparticles supply a driving force for facilitating Cr(VI) diffusion inward, thus improving the adsorption rate and the adsorption capacity. At the same time, the external microporous carbon shell can also efficiently trap guest Cr(VI) ions and protect Fe/Fe3 C nanoparticles from corrosion and subsequent leaching problems.

Atrial natriuretic peptide attenuates inflammatory responses on oleic acid-induced acute lung injury model in rats.

BACKGROUND: An inflammatory response leading to organ dysfunction and failure continues to be a major problem after injury in many clinical conditions such as sepsis, severe burns, and trauma. It is increasingly recognized that atrial natriuretic peptide (ANP) possesses a broad range of biological activities, including effects on endothelial function and inflammation. A recent study has revealed that ANP exerts anti-inflammatory effects. In this study we tested the effects of human ANP (hANP) on lung injury in a model of oleic acid (OA)-induced acute lung injury (ALI) in rats. METHODS: Rats were randomly assigned to three groups (n = 6 in each group). Rats in the control group received a 0.9% solution of NaCl (1 ml × kg(-1) × h(-1)) by continuous intravenous infusion, after 30 minutes a 0.9% solution of NaCl (1 ml/kg) was injected intravenously, and then the 0.9% NaCl infusion was restarted. Rats in the ALI group received a 0.9% NaCl solution (1 ml × kg(-1) × h(-1)) intravenous infusion, after 30 minutes OA was injected intravenously (0.1 ml/kg), and then the 0.9% NaCl infusion was restarted. Rats in the hANP-treated ALI group received a hANP (0.1 µg × kg(-1) × min(-1)) infusion, after 30 minutes OA was injected intravenously (0.1 ml/kg), and then the hANP infusion was restarted. The anti-inflammation effects of hANP were evaluated by histological examination and determination of serum cytokine levels. RESULTS: Serum interleukin (IL)-1ß, IL-6, IL-10 and tumor necrosis factor (TNF) α were increased in the ALI group at six hours. The levels of all factors were significantly lower in the hANP treated rats (P < 0.005). Similarly, levels of IL-1ß, IL-6, IL-10 and TNF-α were higher in the lung tissue in the ALI group at six hours. hANP treatment significantly reduced the levels of these factors in the lungs (P < 0.005). Histological examination revealed marked reduction in interstitial congestion, edema, and inflammation. CONCLUSION: hANP can attenuate inflammation in an OA-induced lung injury in rat model.