The effectiveness of curvilinear supine position on the incidence of pressure injuries and interface pressure among surgical patients.

BACKGROUND: Intraoperative pressure injury is still a major problem of perioperative nursing. Reducing the peak interface pressure is a valid clinical intervention for reducing the incidence of intraoperative pressure injuries. However, studies of repositioning and pressure-redistributing for surgical patients are still lacking. In this context we aimed to evaluate the effect of a curvilinear supine position on incidence of pressure injury with surgical patients in a hospital setting. METHODS: This was a prospective, randomized, controlled study, carried out from May to December 2016, included 104 surgical patients from a university hospital in China (experimental group, n = 52; control group, n = 52). Incidence of pressure injury, interface pressure, comfort and satisfaction scores from surgeons, anesthesiologists, OR nurses were recorded. Mann-Whitney U Chi-square test was used for difference of pressure injury's incidence and mixed linear model was used for interface pressure. RESULTS: Overall the intervention group had significant fewer intraoperative pressure injuries than the control group (0 patients [0%] vs. 9 patients [17.65%], p = 0.002). Compared with control group, the experimental group had significantly lower interface pressures in the sacrum and heel regions (F = 23.81, p < 0.001; F = 60.71, p < 0.001). The subjects felt comfortable in two groups were 40(80%) vs. 3(5.88%) (experimental group vs. control group), respectively (p < 0.001). CONCLUSIONS: Curvilinear supine position could significantly decrease the incidence of perioperative pressure injuries in surgical patients with surgery duration more than three hours. Considering these results, we recommend that curvilinear supine position use as effective interventions to inform perioperative care delivery, reducing perioperative pressure injuries. These findings may serve to guide the application of pressure redistribution in the surgical positioning of patients during prolonged surgery.

Effects of Curvilinear Supine Position on Tissue Interface Pressure: A Prospective Before-and-After Study.

PURPOSE: To determine whether a curvilinear supine position increases the contact area between the subject and the surgical table, reduces interface pressures within contact areas, and improves comfort. DESIGN: This observational study was completed to establish proof-of-concept to determine differences between 2 positions (supine and curvilinear) on interface pressure of 5 at-risk anatomical locations, overall contact area, and subjects' comfort level. SUBJECTS AND SETTING: The study was conducted at the operating theater of a tertiary teaching hospital in Wuhan, China. The sample comprised 145 healthy Asian volunteers between 18 and 60 years of age. METHODS: Subjects were placed in the supine and curvilinear supine positions on a surgical table. Contact area and peak interface pressures of 5 at-risk anatomical locations (occiput, scapula, sacrum, calf, and heel) were measured using a pressure mapping system, and the mean and maximum pressures of the overall contact area were calculated. Comfort was assessed by self-report using a Likert scale of 1 to 5. The Wilcoxon paired signed rank test was used to compare differences between the 2 positions, and the Spearman correlation analysis was used to identify associations among outcome variables. RESULTS: Results indicated that whole-body (overall) maximum, average interface pressures, and maximum interface pressures of the sacrum and the heel were decreased significantly, with contact area and comfort-level score increasing from 2438.71 to 2709.68 cm and 3.00 to 4.00, respectively (P < .001). Statistically significant associations were found between the contact area and measures of body morphology; correlation coefficients varied from 0.409 to 0.740 (P < .001). CONCLUSIONS: Curvilinear supine position increased overall contact area with the support surface, reduced interface pressures over contact areas (bony prominences), improved comfort, and enhanced pressure redistribution. Additional research is needed to determine if these effects will reduce intraoperative pressure injury occurrence.

Chaihushugan decoction exerts antiepileptic effects by increasing hippocampal glutamate metabolism in pentylenetetrazole-kindled rats.

OBJECTIVE: To investigate the antiepileptic effects of Chaihushugan decoction (CHSGD) in rats with pentylenetetrazole (PTZ)-induced seizures and to discuss the impact of CHSGD on glutamate metabolism, a hypothesized underlying mechanism of seizure reduction. METHODS: Fifty Wistar rats were divided randomly into either control (n = 10) or experimental (n = 40) groups. Rats in the control group were administered physiological saline intraperitoneally. A subconvulsive dose of PTZ (35 mg/kg) was administered intraperitoneally to rats in the experimental group to induce seizures. The fully PTZ-kindled rats were then randomly divided into five subgroups (n = 8 each) based on the following treatment categories: physiological saline, VPA (200 mg/kg), CHSGD (2.5 g/kg), CHSGD (5 g/kg), or CHSGD (10 g/kg), administered orally once per day, respectively. On day 28 following initiation of drug treatment, seizures were monitored. The rats were then sacrificed, and hippocampal dissections were performed for subsequent studies. RESULTS: CHSGD significantly prolonged the latency of myoclonic, clonic, and tonic seizures, while decreasing overall seizure rates in the kindled rats. The measured concentrations of 2-[N-(7-nitrobenz-2-oxa-1,3-diazo-4-yl) amino]-2-deoxy-d-glucose (2-NBDG) and glutamate were significantly lower in the hippocampi of kindled rats in groups treated with CHSGD compared with those treated with PTZ alone. In addition, CHSGD was found to up-regulate both the expression of glutamate transporter-1 (GLT-1) protein and the activity of glutamine synthetase (GS) in the hippocampi of kindled rats. CONCLUSION: These results suggest that CHSGD has antiepileptic effects on PTZ-induced seizures. The results further suggest an increase in glutamate metabolism at the synaptic cleft is a putative underlying mechanism of seizure reduction.

Activation of brain indoleamine 2,3-dioxygenase contributes to epilepsy-associated depressive-like behavior in rats with chronic temporal lobe epilepsy.

BACKGROUND: Depression has most often been diagnosed in patients with temporal lobe epilepsy (TLE), but the mechanism underlying this association remains unclear. In this study, we report that indoleamine 2,3-dioxygenase 1 (IDO1), a rate-limiting enzyme in tryptophan metabolism, plays a key role in epilepsy-associated depressive-like behavior. METHODS: Rats which develop chronic epilepsy following pilocarpine status epilepticus exhibited a set of interictal disorders consistent with depressive-like behavior. Changes of depressive behavior were examined by taste preference test and forced swim test; brain IL-1ß, IL-6 and IDO1 expression were quantified using real-time reverse transcriptase PCR; brain kynurenine/tryptophan and serotonin/tryptophan ratios were analyzed by liquid chromatography-mass spectrometry. Oral gavage of minocycline or subcutaneous injection of 1-methyltryptophan (1-MT) were used to inhibite IDO1 expression. RESULTS: We observed the induction of IL-1ß and IL-6 expression in rats with chronic TLE, which further induced the upregulation of IDO1 expression in the hippocampus. The upregulation of IDO1 subsequently increased the kynurenine/tryptophan ratio and decreased the serotonin/tryptophan ratio in the hippocampus, which contributed to epilepsy-associated depressive-like behavior. The blockade of IDO1 activation prevented the development of depressive-like behavior but failed to influence spontaneous seizures. This effect was achieved either indirectly, through the anti-inflammatory tetracycline derivative minocycline, or directly, through the IDO antagonist 1-MT, which normalizes kynurenine/tryptophan and serotonin/tryptophan ratios. CONCLUSION: Brain IDO1 activity plays a key role in epileptic rats with epilepsy-associated depressive-like behavior.

Social support, coping strategies and health-related quality of life among primary caregivers of stroke survivors in China.

AIMS AND OBJECTIVES: To examine the relationships of social support and coping strategies to health-related quality of life among primary caregivers of stroke survivors in China. BACKGROUND: Caring for a stroke survivor is highly stressful, which can negatively affect a caregiver's physical and psychological well-being. Stroke caregivers generally report more somatic symptoms, depressive symptoms, sleep disorders and social isolation. They generally have poorer quality of life than the general population. DESIGN: A cross-sectional, descriptive, correlational study. METHODS: A quasi-random, point of reference sample of 121 survivor-caregiver dyads was recruited from three community health centres and six health service stations in a city in central China. Data were collected in face-to-face interviews at participants' homes using structured questionnaires. RESULTS: Higher educational levels, planning and active coping were positively associated with health-related quality of life. The number of chronic conditions, hours of care per day and functional dependence of the survivor were negatively related to quality of life. CONCLUSION: Active coping strategies predicted better health-related quality of life. Findings suggest that intervention programmes should be developed to enhance caregivers of stroke survivors' coping skills and improve social support for these caregivers in China. RELEVANCE TO CLINICAL PRACTICE: Community healthcare providers may need to help caregivers strengthen strategies that are effective (planning, active coping, seeking instrumental and emotional support) and change those that are not helpful (venting, denial and self-blame).

[Effects of heterotherapy for homopathy on the metabolism path of glutamate in the pentylenetetrazol-kindled seizure rats' hippocampus].

OBJECTIVE: To investigate and compare the effects of Compound Chaihu Shugan Decoction (CHSGD, "treatment from Gan") and Dingxian Pill (DXP, "treatment from the sputum") on the metabolism path of glutamate in the pentylenetetrazol-kindled seizure rats' hippocampus, thus exploring the molecular mechanism of "heterotherapy for homopathy". METHODS: A chronic kindling seizures rat model was established by intraperitoneal injecting pentylenetetrazol (PTZ). Totally 24 fully kindled seizure rats were randomized into four groups, i.e., the model control group, the Sodium Valproate (VPA) group, the DXP group, and the CHSGD group. They were respectively treated with normal saline, VPA, CHSGD, and DXP, respectively. Rats in the control group were treated with normal saline by peritoneal injection and by gastrogavage. After intragastric administration for 4 successive weeks, the glutamate (Glu) levels in the hippocampus were detected by high performance liquid chromatography (HPLC). The expressions of glutamate transporter-1 (GLT-1) proteins were detected by Western blot. The activity of glutamine synthetase (GS) was detected by using GS detection kit. RESULTS: Compared with the control group, the content of Glu in the model group significantly increased, and the expression of GLT-1 and the activity of GS significantly decreased (P < 0.01). Compared with the model group, the content of Glu in each medication group significantly decreased, and the protein expression of GLT-1 as well as the activity of GS significantly increased (P < 0.01). But when compared between the CHSGD group and the DXP group, the content of Glu was lower and the activity of GS was higher in the CHSGD group than in the DXP group (P < 0.01), while there was no statistical difference in the expression of GLT-1 between the two groups (P > 0.05). CONCLUSIONS: CHSGD ("treatment from Gan") and DXP ("treatment from the sputum") could both decrease the level of Glu and raise the expression of GLT-1 and the activity of GS, indicating that CHSGD and DXP both could regulate the metabolism path of Glu to affect the level of the Glu in the brain. But the effects of CHSGD were superior to those of DXP in decreasing the content of Glu and up-regulating the activity of GS, suggesting that there were some different effects targets between the two compounds on the metabolism path of Glu, which may be one of possible molecular mechanisms for treating epilepsy by heterotherapy for homopathy.

Update on transfusion-related acute lung injury: an overview of its pathogenesis and management.

Transfusion-related acute lung injury (TRALI) is a severe adverse event and a leading cause of transfusion-associated death. Its poor associated prognosis is due, in large part, to the current dearth of effective therapeutic strategies. Hence, an urgent need exists for effective management strategies for the prevention and treatment of associated lung edema. Recently, various preclinical and clinical studies have advanced the current knowledge regarding TRALI pathogenesis. In fact, the application of this knowledge to patient management has successfully decreased TRALI-associated morbidity. This article reviews the most relevant data and recent progress related to TRALI pathogenesis. Based on the existing two-hit theory, a novel three-step pathogenesis model composed of a priming step, pulmonary reaction, and effector phase is postulated to explain the process of TRALI. TRALI pathogenesis stage-specific management strategies based on clinical studies and preclinical models are summarized with an explication of their models of prevention and experimental drugs. The primary aim of this review is to provide useful insights regarding the underlying pathogenesis of TRALI to inform the development of preventive or therapeutic alternatives.

Kakonein restores hyperglycemia-induced macrophage digestion dysfunction through regulation of cathepsin B-dependent NLRP3 inflammasome activation.

In hyperglycemia-induced complications, macrophages play important roles in disease progression, and altered digestion is a key feature that dictates macrophage function. Recent evidence indicates that kakonein (Ka) possesses anti-inflammatory activities for hyperglycemia-induced complication. In this study, we established a mouse model of Nlrp3+/+ and Nlrp3-/- hyperglycemia and administering Ka, primary culture macrophages were tested by engulfing and digesting microbes. The role of macrophages in the cathepsin B-NLRP3 pathway involved in the mechanism of Ka in restoring macrophage digestion function was investigated using biochemical analyses, molecular biotechnology, and microbiology. Ka restored the function of macrophage digestion, which were same characterized by Nlrp3-/- mice. Meanwhile, kakonein could decrease NLRP3 inflammasome products expression and NLRP3/ASC or NLRP3/Casp1 colocalization in macrophage. Interestingly, Ka suppressed inflammasome response not by reducing NLRP3 and ASC expression but by reducing cathepsin B release and activation. And Ka restored macrophage digestion and inhibited NLRP3 inflammasome activation consistent with cathepsin B inhibitor. It is concluded that Ka reduced the release of lysosomal cathepsin B and consequently inhibited NLRP3 inflammasome activation to prevent macrophage digestion. Hence, Ka may contribute to new targets for treatment of hyperglycemia-associated dysfunction of macrophage digestion and development of innovative drugs.

Pulmonary coagulation and fibrinolysis abnormalities that favor fibrin deposition in the lungs of mouse antibody-mediated transfusion-related acute lung injury.

Transfusion­related acute lung injury (TRALI) is a life­threatening disease caused by blood transfusion. However, its pathogenesis is poorly understood and specific therapies are not available. Experimental and clinical studies have indicated that alveolar fibrin deposition serves a pathological role in acute lung injuries. The present study investigated whether pulmonary fibrin deposition occurs in a TRALI mouse model and the possible mechanisms underlying this deposition. The TRALI model was established by priming male Balb/c mice with lipopolysaccharide (LPS) 18 h prior to injection of an anti­major histocompatibility complex class I (MHC­I) antibody. Untreated mice and mice administered LPS plus isotype antibody served as controls. At 2 h after TRALI induction, blood and lung tissue were collected. Disease characteristics were assessed based on lung tissue histology, inflammatory responses and alterations in the alveolar­capillary barrier. Immunofluorescence staining was used to detect pulmonary fibrin deposition, platelets and fibrin­platelet interactions. Levels of plasminogen activator inhibitor­1 (PAI­1), thrombin­antithrombin complex (TATc), tissue factor pathway inhibitor (TFPI), coagulation factor activity and fibrin degradation product (FDP) in lung tissue homogenates were measured. Severe lung injury, increased inflammatory responses and a damaged alveolar­capillary barrier in the LPS­primed, anti­MHC­I antibody­administered mice indicated that the TRALI model was successfully established. Fibrin deposition, fibrin­platelet interactions and platelets accumulation in the lungs of mouse models were clearly promoted. Additionally, levels of TATc, coagulation factor V (FV), TFPI and PAI­1 were elevated, whereas FDP level was decreased in TRALI mice. In conclusion, both impaired fibrinolysis and enhanced coagulation, which might be induced by boosted FV activity, increased pulmonary platelets accumulation and enhanced fibrin­platelet interactions and contributed to pulmonary fibrin deposition in TRALI mice. The results provided a therapeutic rationale to target abnormalities in either coagulation or fibrinolysis pathways for antibody­mediated TRALI.

Analysis of therapeutic potential of preclinical models based on DR3/TL1A pathway modulation (Review).

Death receptor 3 (DR3) and its corresponding ligand, tumor necrosis factor-like ligand 1A (TL1A), belong to the tumor necrosis factor superfamily. Signaling via this receptor-ligand pair results in pro-inflammatory and anti-inflammatory effects. Effector lymphocytes can be activated to exert pro-inflammatory activity by triggering the DR3/TL1A pathway. By contrast, DR3/TL1A signaling also induces expansion of the suppressive function of regulatory T cells, which serve an important role in exerting anti-inflammatory functions and maintaining immune homeostasis. Preclinical evidence indicates that neutralizing and agonistic antibodies, as well as ligand-based approaches targeting the DR3/TL1A pathway, may be used to treat diseases, including inflammatory and immune-mediated diseases. Accumulating evidence has suggested that modulating the DR3/TL1A pathway is a promising therapeutic approach for patients with these diseases. This review discusses preclinical models to gauge the progress of therapeutic strategies for diseases involving the DR3/TL1A pathway to aid in drug development.

Rheological and Aging Properties of Composite Modified Bitumen by Styrene-Butadiene-Styrene and Desulfurized Crumb Rubber.

Taking advantage of crumb rubber from waste tires to modify bitumen is widely for the environmentally friendly and sustainable development of pavement. This study investigated the modification mechanism, rheological, and aging properties of styrene-butadiene-styrene (SBS)/desulfurized crumb rubber (DCR) composite modified bitumen (SBS/DCRMB). Morphological features and chemical characteristics were assessed by fluorescence intensity measurement and gel permeation chromatography (GPC), respectively, and results demonstrated that the DCR and SBS modifier in SBS/DCRMB had been vulcanized and formed a three-dimensional network structure. Moreover, a comparison of the GPC elution curve showed the residual bitumen hardly changed due to carbon black released from DCR of SBS/DCRMB during the aging process of SBS/DCRMB, and the polymer molecules condensed to larger units. However, the remaining bitumen in SBSMB had changed evidently and the polymer degraded to smaller molecules. Meanwhile the rheological testing results, including multiple stress creep recovery, linear amplitude sweep and bending beam rheometer, declared that the SBS/DCRMB is superior to SBSMB before and after aging.

[Effect of Chaihu Shugan Tang on excitability in different brain regions of pentylenetetrazole-kindled chronic epileptic rats].

OBJECTIVE: To study the effect of the Chinese compound prescription Chaihu Shugan Tang (CHSGT) on the excitability in the cerebral cortex and hippocampus (different brain regions) of pentetrazole (PTZ)-kindled chronic epileptic rats. METHOD: To establish the model of chronic kindling rats intraperitoneal injected with pentylenetet. Fully kindled rats were randomized into control and experimental groups for intragastric administration of normal saline (control, model), Sodium Valproate and CHSGT at the high, medium and low doses for 4 consecutive weeks. The content of 2-NBDG, the glutamate (Glu) and the aspartate (Asp) in different brain regions of rats were detected by fluorescence imaging techniques and HPLC assay respectively. RESULT: CHSGT at the high, medium and low doses all significantly decreased the content of 2-NBDG, the Glu and the Asp in different brain regions of chronic epileptic rats (P < 0.01). CONCLUSION: CHSGT can inhibit the excitability in different brain regions of PTZ-induced epileptic rats, by decreasing the level of excitatory neurotransmitter maybe one of its antiepileptic mechanisms.

Nitrogen-doped dual mesoporous carbon for the selective oxidation of ethylbenzene.

A nanocasting method to fabricate nitrogen-doped dual mesoporous carbon is proposed by the carbonization of nitrile functional ionic liquid (FIL) grafted SBA-15 for the first time. These carbon materials have high nitrogen content (12.8%), large specific surface areas (763 m(2) g(-1)) and uniform rod morphologies, which are derived from FILs grafted on the surface of SBA-15. Furthermore, by adjusting the impregnation amount of ionic liquids on SBA-15, pore structures of these carbon materials can be adjusted from single to dual mesopores. The developed dual mesoporous carbon materials exhibit good catalytic performance in the selective oxidation of ethylbenzene, ascribed to the promoting effects of nitrogen-doping, high surface area and dual mesostructure. It may be concluded that the dual mesostructure has an advantage over a single mesostructure to obtain a fast mass transport rate, resulting in higher acetophenone yield.

Saikosaponin a mediates the anticonvulsant properties in the HNC models of AE and SE by inhibiting NMDA receptor current and persistent sodium current.

Epilepsy is one of the most common neurological disorders, yet its treatment remains unsatisfactory. Saikosaponin a (SSa), a triterpene saponin derived from Bupleurum chinensis DC., has been demonstrated to have significant antiepileptic activity in a variety of epilepsy models in vivo. However, the electrophysiological activities and mechanisms of the antiepileptic properties of SSa remain unclear. In this study, whole-cell current-clamp recordings were used to evaluate the anticonvulsant activities of SSa in the hippocampal neuronal culture (HNC) models of acquired epilepsy (AE) and status epilepticus (SE). Whole-cell voltage-clamp recordings were used to evaluate the modulation effects of SSa on NMDA-evoked current and sodium currents in cultured hippocampal neurons. We found that SSa effectively terminated spontaneous recurrent epileptiform discharges (SREDs) in the HNC model of AE and continuous epileptiform high-frequency bursts (SE) in the HNC model of SE, in a concentration-dependent manner with an IC(50) of 0.42 µM and 0.62 µM, respectively. Furthermore, SSa significantly reduced the peak amplitude of NMDA-evoked current and the peak current amplitude of I(NaP). These results suggest for the first time that the inhibitions of NMDA receptor current and I(NaP) may be the underlying mechanisms of SSa's anticonvulsant properties, including the suppression of SREDs and SE in the HNC models of AE and SE. In addition, effectively abolishing the refractory SE implies that SSa may be a potential anticonvulsant candidate for the clinical treatment of epilepsy.