Microbial community regulation and performance enhancement in gas biofilters by interrupting bacterial communication.

BACKGROUND: Controlling excess biomass accumulation and clogging is important for maintaining the performance of gas biofilters and reducing energy consumption. Interruption of bacterial communication (quorum quenching) can modulate gene expression and alter biofilm properties. However, whether the problem of excess biomass accumulation in gas biofilters can be addressed by interrupting bacterial communication remains unknown. RESULTS: In this study, parallel laboratory-scale gas biofilters were operated with Rhodococcus sp. BH4 (QQBF) and without Rhodococcus sp. BH4 (BF) to explore the effects of quorum quenching (QQ) bacteria on biomass accumulation and clogging. QQBF showed lower biomass accumulation (109 kg/m3) and superior operational stability (85-96%) than BF (170 kg/m3; 63-92%) at the end of the operation. Compared to BF, the QQBF biofilm had lower adhesion strength and decreased extracellular polymeric substance production, leading to easier detachment of biomass from filler surface into the leachate. Meanwhile, the relative abundance of quorum sensing (QS)-related species was found to decrease from 67 (BF) to 56% (QQBF). The QS function genes were also found a lower relative abundance in QQBF, compared with BF. Moreover, although both biofilters presented aromatic compounds removal performance, the keystone species in QQBF played an important role in maintaining biofilm stability, while the keystone species in BF exhibited great potential for biofilm formation. Finally, the possible influencing mechanism of Rhodococcus sp. BH4 on biofilm adhesion was demonstrated. Overall, the results of this study achieved excess biomass control while maintaining stable biofiltration performance (without interrupting operation) and greatly promoted the use of QQ technology in bioreactors. Video Abstract.

The role of PTEN in primary sensory neurons in processing itch and thermal information in mice.

PTEN is known as a tumor suppressor and plays essential roles in brain development. Here, we report that PTEN in primary sensory neurons is involved in processing itch and thermal information in adult mice. Deletion of PTEN in the dorsal root ganglia (DRG) is achieved in adult Drg11-CreER: PTENflox/flox (PTEN CKO) mice with oral administration of tamoxifen, and CKO mice develop pathological itch and elevated itch responses on exposure to various pruritogens. PTEN deletion leads to ectopic expression of TRPV1 and MrgprA3 in IB4+ non-peptidergic DRG neurons, and the TRPV1 is responsive to capsaicin. Importantly, the elevated itch responses are no longer present in Drg11-CreER: PTENflox/flox: TRPV1flox/flox (PTEN: TRPV1 dCKO) mice. In addition, thermal stimulation is enhanced in PTEN CKO mice but blunted in dCKO mice. PTEN-involved regulation of itch-related gene expression in DRG neurons provides insights for understanding molecular mechanism of itch and thermal sensation at the spinal level.

Extracellular signal-regulated kinase (ERK) activation is required for itch sensation in the spinal cord.

BACKGROUND: Itch, chronic itch in particular, can have a significant negative impact on an individual's quality of life. However, the molecular mechanisms underlying itch processing in the central nervous system remain largely unknown. RESULTS: We report here that activation of ERK signaling in the spinal cord is required for itch sensation. ERK activation, as revealed by anti-phosphorylated ERK1/2 immunostaining, is observed in the spinal dorsal horn of mice treated with intradermal injections of histamine and compound 48/80 but not chloroquine or SLIGRL-NH2, indicating that ERK activation only occurs in histamine-dependent acute itch. In addition, ERK activation is also observed in 2, 4-dinitrofluorobenzene (DNFB)-induced itch. Consistently, intrathecal administration of the ERK phosphorylation inhibitor U0126 dramatically reduces the scratching behaviors induced by histamine and DNFB, but not by chloroquine. Furthermore, administration of the histamine receptor H1 antagonist chlorpheniramine decreases the scratching behaviors and ERK activation induced by histamine, but has no effect on DNFB-induced itch responses. Finally, the patch-clamp recording shows that in histamine-, chloroquine- and DNFB-treated mice the spontaneous excitatory postsynaptic current (sEPSC) of dorsal horn neurons is increased, and the decrease of action potential threshold is largely prevented by bathing of U0126 in histamine- and DNFB-treated mice but not those treated with chloroquine. CONCLUSION: Our results demonstrate a critical role for ERK activation in itch sensation at the spinal level.

Effect of cholinesterase inhibitor galanthamine on circulating tumor necrosis factor alpha in rats with lipopolysaccharide-induced peritonitis.

BACKGROUND: The nervous system, through the vagus nerve and its neurotransmitter acetylcholine, can down-regulate the systemic inflammation in vivo, and recently, a role of brain cholinergic mechanisms in activating this cholinergic anti-inflammatory pathway has been indicated. Galanthamine is a cholinesterase inhibitor and one of the centrally acting cholinergic agents available in clinic. This study aimed to evaluate the effect of galanthamine on circulating tumor necrosis factor alpha (TNF-alpha) in rats with lipopolysaccharide-induced peritonitis and the possible role of the vagus nerve in the action of galanthamine. METHODS: Rat models of lipopolysaccharide-induced peritonitis and bilateral cervical vagotomy were produced. In the experiment 1, the rats were randomly divided into control group, peritonitis group, and peritonitis groups treated with three dosages of galanthamine. In the experiment 2, the rats were randomly divided into sham group, sham plus peritonitis group, sham plus peritonitis group treated with galanthamine, vagotomy plus peritonitis group, and vagotomy plus peritonitis group treated with galanthamine. The levels of plasma TNF-alpha were determined in every group. RESULTS: The level of circulating TNF-alpha was significantly increased in rats after intraperitoneal injection of endotoxin. Galanthamine treatment decreased the level of circulating TNF-alpha in rats with lipopolysaccharide-induced peritonitis, and there was significant difference compared with rats with lipopolysaccharide-induced peritonitis without treatment. The 3 mg/kg dosage of galanthamine had the most significant inhibition on circulating TNF-alpha level at all the three tested doses. Galanthamine obviously decreased the TNF-alpha level in rats with lipopolysaccharide-induced peritonitis with sham operation, but could not decrease the TNF-alpha level in rats with lipopolysaccharide-induced peritonitis with vagotomy. CONCLUSION: Cholinesterase inhibitor galanthamine has an inhibitory effect on TNF-alpha release in rats with lipopolysaccharide-induced peritonitis, and the vagus nerve plays a role in the process of the action of galanthamine.

Risk factors for urban road traffic injuries in Hangzhou, China.

OBJECTIVE: To investigate factors that most influence urban road traffic injuries (RTI) mortality and morbidity. METHODS: The study used linked police and hospital records of RTI patients in the city of Hangzhou during the 3-year period 2004-2006. Three RTI outcome groups were included: (1) fatally injured; (2) severely injured; and (3) mildly injured persons. RESULTS: High risks for fatal road traffic accidents (RTA) were found on urban links, over weekend, during night hours, in male drivers who drove old vehicles without using seat belts, and at exceeding speeds, or with night time accidents and bad weather condition. In case of higher risk for all urban road users on urban junctions, the numbers on mildly injury cases were increasing. The highest combined risk for dying or being severely injured was found in male drivers driving at excessive speed, on urban links, and with night time accidents. CONCLUSIONS: Intensifying safety education of motor vehicle drivers, enhancing traffic management and keeping balance of "person-vehicle-road" system will greatly reduce the urban traffic accidents and casualties.

Research progress in mechanism of traumatic brain injury affecting speed of fracture healing.

In patients who have sustained traumatic brain injury with associated extremity fracture, there is often a clinical perception that the rate of new bone formation around the fracture site increases.(1) An overgrowth of callus is observed and ectopic ossification even occurs in the muscle,(2) but the mechanism remains unclear. Whether this rapidly-formed new bone is fracture callus or a variant of heterotopic ossification, a common complication of traumatic brain injury, is the subject of some debates.(3) It is generally believed that the process of fracture healing is a recapitulation of normal embryonic osteogenesis,(4) i.e. ,a series of changes in the intracellular and extracellular matrix, which start from the injury of cells, blood vessels and bone matrix to a complete reconstruction of the bone.(5) It is a complex process influenced by multi-level and multi-route regulations of the general and local environments in the body, and many growth factors participate in this process, which is the base of bone healing;(6) whatever methods are used to promote bone healing, they are based on accelerating the changes of growth factors.(7) So it is worth making a thorough study on the mechanism, by which traumatic brain injury influences the expression levels of growth factors and consequently affects the speed of bone healing.

Protective effect of raloxifene on lipopolysaccharide and acid- induced acute lung injury in rats.

AIM: To evaluate the protective effect of oral raloxifene on acute lung injury. METHODS: Thirty adult, male Sprague-Dawley rats each weighing 180-210 g were used and divided into 3 groups: the raloxifene-lipopolysaccharide (LPS)-HCl group (n=10), the LPS-raloxifene-HCl group (n=10), and the placebo group (n=10). All the rats were injected intraperitoneally (ip) with 5 mg/kg LPS, and raloxifene (30 mg/kg) was orally administered 1 h before and 14 h after LPS injection into the raloxifene-LPS-HCl and the LPS-raloxifene-HCl groups, respectively; the placebo group received nothing. Sixteen hours after LPS injection, all the animals were anesthetized and the femoral artery was cannulated. All the rats received a direct intratracheal (IT) injection of HCl (pH 1.2; 0.5 mL/kg). The mean arterial pressure (MAP) and blood gas concentrations were measured. Fifteen rats (5 in each group, respectively) underwent a micro positron emission tomography (microPET) scan of the thorax 4 h after HCl instillation. The wet/dry (W/D) weight ratio determination and histopathological examination were also performed. RESULTS: The rats in the LPS-raloxifene-HCl group had a lower [18F]fluorodeoxyglucose uptake compared with the rats in the placebo group (4.67+/-1.33 vs 9.01+/-1.58, respectively, P<0.01). The rats in the LPS-raloxifene-HCl group also had a lower histological lung injury score (8.20+/-1.23 vs 12.6+/-0.97, respectively, P<0.01) and W/D weight ratio (5.335+/-0.198 vs 5.886+/-0.257, respectively, P<0.01) compared to the placebo group. The rats in this group also showed better pulmonary gas exchange and more stable mean arterial pressure (MAP) compared to the placebo group. CONCLUSION: Raloxifene provides a significant protective effect on acute lung injury in rats induced first by LPS ip injection and then by HCl IT instillation.

Basic fibroblast growth factor alleviates brain injury following global ischemia reperfusion in rabbits.

The aim of this study was to explore the protective effect of basic fibroblast growth factor (bFGF) on brain injury following global ischemia reperfusion and its mechanisms. Brain injury following global ischemia was induced by four vessels occlusion and systemic hypotension. Twenty-four rabbits were randomized into three groups: group A, only dissection of vessels; group B, intravenous infusion of normal saline after reperfusion for 6 h; group C, 30 microg/kg bFGF injected intravenously at the onset of reperfusion, then infused with 10 microg/(kg.h) for 6 h. Serum neuron specific enolase (NSE), S-100B, tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), interleukin-8 (IL-8) were measured before ischemia, 30 min after ischemia, 0.5, 1, 3, 6 h after reperfusion. Brain water content was determined and cerebral histopathological damages were compared. NSE and S-100B were increased 1 h after reperfusion and reached their peaks 6 h after reperfusion, but were much higher in group B than those in group C 3, 6 h after reperfusion. In groups B and C, TNF-alpha was increased after ischemia and IL-1 and IL-8 were increased significantly 0.5 h after reperfusion, then reached their peaks 6 h, 3 h, 6 h after reperfusion respectively. TNF-alpha and IL-8 at the time points of 1 h and 3 h and IL-1 at 3 h and 6 h in group C were correspondingly lower than those in group B. These indices in group A were nearly unchanged. There were less severe cerebral histopathological damages in group C compared with group B, but no difference in brain water content. It could be concluded that bFGF alleviates brain injury following global ischemia and reperfusion by down-regulating expression of inflammatory factors and inhibiting their activities.