Resolution of herpes zoster-induced small bowel pseudo-obstruction by epidural nerve block: A case report.

BACKGROUND: When herpes zoster is complicated with paralytic ileus, this mostly involves acute intestinal pseudo-obstruction of Ogilvie's syndrome manifesting as obvious dilatation of the cecum and right colon; small intestinal obstruction is rare. Here, we present a patient with a very rare case of small bowel pseudo-obstruction. CASE SUMMARY: A 76-year-old female patient complained of right upper quadrant pain. Two days later, a blistering, right-sided rash of the thoracoabdominal dermatome (T5-T10) emerged in conjunction with small intestinal dilatation and the inability to defecate. Computed tomography of the abdomen confirmed small bowel pseudo-obstruction. Antiviral therapy, gastrointestinal decompression, and enemas proved unproductive. After 4 d of stagnation, an epidural block was performed for pain relief and prompted the passage of gas and stool, resolving the obstructive problem. Three days later, the rash appeared dry and crusted, and the pain diminished. After 5 d, no abnormality was visible by gastroenteroscopy, and the patient was discharged on day 7. CONCLUSION: This case shows that herpes zoster may induce small bowel pseudo-obstruction in addition to colonic pseudo-obstruction. Epidural block can not only treat intercostal neuralgia but also resolve small bowel pseudo-obstruction caused by herpes zoster.

Curcumin alleviates oxidative stress and inhibits apoptosis in diabetic cardiomyopathy via Sirt1-Foxo1 and PI3K-Akt signalling pathways.

Diabetes is a disorder of glucose metabolism, and over 90% are type 2 diabetes. Diabetic cardiomyopathy (DCM) is one of the type 2 diabetes complications, usually accompanied by changes in myocardial structure and function, together with cardiomyocyte apoptosis. Our study investigated the effect of curcumin on regulating oxidative stress (OS) and apoptosis in DCM. In vivo, diabetes was induced in an experimental rat model by streptozoticin (STZ) together with high-glucose and high-fat (HG/HF) diet feeding. In vitro, H9c2 cardiomyocytes were cultured with high-glucose and saturated free fatty acid palmitate. Curcumin was orally or directly administered to rats or cells, respectively. Streptozoticin -induced diabetic rats showed metabolism abnormalities and elevated markers of OS (superoxide dismutase [SOD], malondialdehyde [MDA], gp91phox , Cyt-Cyto C), enhanced cell apoptosis (Bax/Bcl-2, Cleaved caspase-3, TUNEL-positive cells), together with reduced Akt phosphorylation and increased Foxo1 acetylation. Curcumin attenuated the myocardial dysfunction, OS and apoptosis in the heart of diabetic rats. Curcumin treatment also enhanced phosphorylation of Akt and inhibited acetylation of Foxo1. These results strongly suggest that apoptosis was increased in the heart of diabetic rats, and curcumin played a role in diabetic cardiomyopathy treatment by modulating the Sirt1-Foxo1 and PI3K-Akt pathways.

Optimal Dexmedetomidine Dose to Prevent Emergence Agitation Under Sevoflurane and Remifentanil Anesthesia During Pediatric Tonsillectomy and Adenoidectomy.

Background: Emergence agitation (EA) is a common pediatric complication after sevoflurane anesthesia that can be prevented with dexmedetomidine. However, an inappropriate dose of dexmedetomidine can cause prolonged sedation and cardiovascular complications. Thus, we evaluated the optimal dose (ED95) of dexmedetomidine for preventing EA with sevoflurane and remifentanil anesthesia after pediatric tonsillectomy and adenoidectomy. Methods: We enrolled American Society of Anesthesiologists (ASA) I and II children 3-7 years of age who underwent tonsillectomy with adenoidectomy. During induction, dexmedetomidine was infused for 10 min. Anesthesia was induced with sevoflurane and maintained with sevoflurane and remifentanil, resulting in a bispectral spectrum index (BIS) range from 40 to 60. Extubation time, surgical and anesthetic duration time, and duration time in the postanesthesia care unit (PACU) stay were recorded. EA [measured with Pediatric Anaesthesia Emergence Delirium (PAED) scores] and pain [measured with Face, Legs, Activity, Cry, Consolability (FLACC) scores] were assessed at extubation (E0), 15 min after extubation (E1), and 30 min after extubation (E2). If EA occurred, the next surgical procedure included increased dexmedetomidine by 0.1 µg/kg, and if not, the drug was reduced by 0.1 µg/kg. Results: The 50% effective dose (ED50) of dexmedetomidine for preventing EA after sevoflurane and remifentanil anesthesia for tonsillectomy and adenoidectomy was 0.13 µg/kg, and its 95% confidence interval is 0.09-0.19 µg/kg; ED95 was 0.30 µg/kg, and its 95% confidence interval is 0.21-1.00 µg/kg. Conclusion: Intravenous dexmedetomidine infusion at ED50 (0.13 µg/kg) or ED95 (0.30 µg/kg) during induction for 10 min can prevent half or almost all EA after sevoflurane and remifentanil anesthesia during pediatric tonsillectomy and adenoidectomy.

Endothelial progenitor cells attenuate the lung ischemia/reperfusion injury following lung transplantation via the endothelial nitric oxide synthase pathway.

OBJECTIVE: Endothelial progenitor cells (EPCs) can improve endothelial integrity. This study aimed to examine the effects and the mechanism of EPCs on lung ischemia-reperfusion injury (LIRI). METHODS: Wistar rats were randomized into the sham or the left lung transplantation group. The recipients were randomized and treated with vehicle as the LIRI group, with EPC as the EPC group, or with N5-(1-iminoethyl)-l-ornithine-pretreated EPC as the EPC/L group (n = 8 per group). The ratios of arterial oxygen partial pressure to fractional inspiratory oxygen were measured. The lung wet-to-dry weight ratios, protein levels, and injury, as well as the levels of plasma cytokines, were examined. The levels of endothelin (ET)-1, endothelial nitric oxide synthase (eNOS), phosphorylated eNOS, inducible NOS, phosphorylated myosin light chain, nuclear factor-κBp65, Bax, Bcl-2, cleaved caspase-3, and myeloperoxidase in the graft lungs were detected. RESULTS: Compared with the LIRI group, EPC treatment significantly increased the ratios of arterial oxygen partial pressure to fractional inspiratory oxygen and decreased the lung wet-to-dry weight ratios and protein levels in the grafts, accompanied by increasing eNOS expression and phosphorylation, but decreasing endothelin-1, inducible NOS, phosphorylated nuclear factor-kBp65, phosphorylated myosin light chain expression, and myeloperoxidase activity. EPCs reduced lung tissue damage and apoptosis associated with decreased levels of Bax and cleaved caspase-3 expression, but increased Bcl-2 expression. EPC treatment significantly reduced the levels of serum proinflammatory factors, but elevated levels of interleukin-10. In contrast, the protective effect of EPCs were mitigated and abrogated by N5-(1-iminoethyl)-l-ornithine pretreatment. CONCLUSIONS: Data indicated that EPC ameliorated LIRI by increasing eNOS expression.

Effect of preoperative inhaled budesonide on pulmonary injury after cardiopulmonary bypass: A randomized pilot study.

BACKGROUND: Cardiopulmonary bypass can result in lung injury. This prospective, double-blinded, randomized trial aimed to evaluate the protective effect of inhaled budesonide on lung injury after cardiopulmonary bypass. METHODS: Sixty patients, aged 25 to 65 years, requiring cardiopulmonary bypass were randomized to groups treated with saline or budesonide inhalation preoperatively. The respiratory mechanics were recorded. Bronchoalveolar lavage fluid was collected before cardiopulmonary bypass and after sternal closure. Serum and bronchoalveolar lavage fluid levels of proinflammatory and anti-inflammatory factors were analyzed. The primary end point was the lowest ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen after cardiopulmonary bypass. The durations of ventilation and postoperative recovery time were noted. RESULTS: Budesonide significantly improved respiratory mechanics after cardiopulmonary bypass. Budesonide improved the partial pressure of arterial oxygen to the fraction of inspired oxygen ratio from 8 to 48 hours after the operation. Budesonide shortened the durations of mechanical ventilation and postoperative recovery time. Budesonide decreased the levels of proinflammatory factors while increasing the levels of anti-inflammatory factors in bronchoalveolar lavage fluid and serum (all P < .05). The macrophage and neutrophil counts, and protein and elastase concentrations were decreased by budesonide treatment. CONCLUSIONS: Budesonide treatment shortened the durations of mechanical ventilation, inhibited local and systemic inflammation, and improved respiratory function after cardiopulmonary bypass.

Efficacy of Xuebijing Injection () on Cardiopulmonary Bypass-Associated Pulmonary Injury: A Prospective, Single-center, Randomized, Double Blinded Trial.

OBJECTIVE: To evaluate the efficacy of Xuebijing Injection (, XBJ) on the lung injury induced by cardiopulmonary bypass (CPB). METHODS: Fifty patients undergoing CPB were randomized to either the saline group or XBJ group according to a random number table (25 cases in each group). The patients in the saline group received saline and patients in XBJ group received XBJ at 12 h prior to the operation, at the beginning of the operation, and at 12 h after the second injection. The PaO2/FiO2 at extubation 3 days post-operation, duration of ventilation in the intensive care unit (ICU), and lengths of stay in the ICU and hospital were recorded. The levels of inflammatory mediators including interleukin (IL)-1ß, IL-8, IL-10, and C-reactive protein (CRP) in bronchoalveolar lavage fluid (BALF) and plasma were measured. The neutrophil count and elastase neutrophil elastase in BALF were also measured. In addition, adverse events were monitored. RESULTS: The PaO2/FiO2 in the XBJ group was higher than that in the saline group from 12 to 72 h post-operation (all P<0.05). The blood levels of IL-1ß, IL-8, and CRP in the XBJ group from 12 to 72 h were all significantly lower than those in the saline group (all P<0.05). In contrast, the level of the anti-inflammatory cytokine IL-10 was significantly higher in the XBJ group than in the saline group (P<0.05). In addition, 4 patients presented with atelectasis in the saline group and none in the XBJ group. Ten patients experienced mild acute respiratory distress syndrome (ARDS) during hospitalization, and 5 patients with mild ARDS were in the XBJ group (P<0.05). CONCLUSION: XBJ shows protective potential against lung injury in patients who undergo CPB surgery, possibly through the downregulation of inflammatory mediators, reduction in neutrophil infiltration, and upregulation of IL-10 (Trial registry: ChiCTR-TRC-14004628).

Adiponectin protects against lung ischemia-reperfusion injury in rats with type 2 diabetes mellitus.

Adiponectin (APN) has been associated with the pathogenesis of acute brain, liver and heart injury. However, the role of APN in lung ischemia-reperfusion injury (LIRI) in diabetes mellitus remains unclear. To investigate this, the present study evaluated the effects of APN on lung dysfunction and pathological alterations in rats with type 2 diabetes mellitus via lung ischemia/reperfusion (I/R). The lung­protective effects of APN globular domain (gAPN) in rats with type 2 diabetes mellitus were also investigated by measuring the oxygenation index, inflammatory cytokines, lung edema, histopathology, oxidative stress, apoptosis and the protein expression levels of phosphorylated 5'adenosine monophosphate­activated protein kinase (p­AMPK), endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS). The results of the present study demonstrated that the diabetes mellitus rats + I/R (DIR) group exhibited greater concentrations of tumor necrosis factor­α and interleukin­6, and increases in the wet­weight to dry­weight ratio, lung injury score, oxidative stress and cellular apoptosis. These effects were accompanied by lower pulmonary oxygenation compared with the normal rat + I/R (NIR) group (P<0.05). Additionally, all of these alterations were attenuated in the NIR + gAPN and DIR + gAPN groups compared with in the NIR and DIR groups, respectively. In the DIR group, the expression levels of p­AMPK/AMPK and eNOS were significantly downregulated, and the levels of iNOS were upregulated, compared with those of the NIR group. Treatment with APN activated AMPK, increased eNOS expression and attenuated iNOS expression. The results of the present study demonstrated that APN exerted protective effects against LIRI via its anti­inflammatory, antioxidative stress and anti­apoptotic activities. These protective effects of APN were eliminated in rats with type 2 diabetes mellitus, in which LIRI was exacerbated. The present study indicated that APN may be a potential therapeutic agent for LIRI in type 2 diabetes mellitus.

Budesonide instillation immediately after reperfusion ameliorates ischemia/reperfusion-induced injury in the transplanted lung of rat.

PURPOSE: Lung ischemia-reperfusion injury (LIRI) after lung transplantation can lead to primary graft dysfunction. Budesonide can improve endothelial function to reduce lung injury. This study was aimed to examine the effects of budesonide on LIRI and potential mechanisms. METHODS: Wistar rats were randomized and transplanted with syngeneic left lung or received the sham surgery. The recipients were instilled with saline or budesonide immediately after reperfusion. The mean arterial pressure (MAP), blood gas, and lung histology were analyzed. The ratios of wet to dry lung weights, the levels of total proteins, tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, and IL-10, and neutrophil elastase in bronchoalveolar lavage fluid (BALF) were measured. The levels of malondialdehyde (MDA), myeloperoxidase (MPO), and xanthine oxidase (XO) in the lung, and the levels of plasma lymphocyte function-associated antigen (LFA)-1 and P-selectin were determined. RESULTS: Compared with the saline group, treatment with budesonide significantly increased blood PaO2, but reduced PaCO2, and mitigated lung damages after reperfusion, the levels of BALF proteins, and the ratios of wet to dry lung weights in rats. Furthermore, treatment with budesonide significantly decreased the levels of MDA, MPO, and XO in the lung and the levels of TNF-α, IL-1ß, IL-6, and neutrophil elastase, but increased IL-10 in the BALF, accompanied by significantly reduced levels of serum P-selectin and LFA-1 in rats. CONCLUSIONS: Budesonide effectively mitigated LIRI and ameliorated the lung function by attenuating oxidative stress and inflammation following syngeneic lung transplantation.

Low dose of dexmedetomidine as an adjuvant to bupivacaine in cesarean surgery provides better intraoperative somato-visceral sensory block characteristics and postoperative analgesia.

OBJECT: In this study, we aimed to investigate the beneficial effects of dexmedetomidine on somato-visceral sensory block characteristcs, postoperative analgesia and stress response of intrathecal bupivacaine administration in women undergoing cesarean section, and to find out which dose is better. METHODS: Sixty parturients with the American Society of Anesthesiologists (ASA) physical status I or II were anesthetized with intrathecal bupivacaine(10mg) alone or in combination with dexmedetomidine (3 µg and 5 µg) to undergo cesarean section. The anesthetic parameters, postoperative analgesia and stress responses were monitored. RESULTS: Co-administration of dexmedetomidine(3 µg and 5 µg) prolonged the duration of motor and sensory block compared with bupivacaine(10mg) alone. Less supplemental dose of lidocaine and fentanyl were required in dexmedetomidine(3 µg and 5 µg) co-administration groups. Visceral traction response and abdominal muscle relaxation in operation were better in dexmedetomidine(3 µg and 5 µg) co-administration groups. No difference in haemodynamics was detected among groups. There was no significant difference in Apgar scores, neonatal umbilical pH, oxygen pressure, carbon dioxide pressure and lactate level among groups. Postoperative plasma IL-6 and cortisol levels were lower in dexmedetomidine(3 µg and 5 µg) co-administration groups. At 6 hour after operation the visual analogue scale (VAS) was smaller in dexmedetomidine(3 µg and 5 µg) co-administration groups. The uterine contraction pain at 6 and 12 hour after operation and supplemental analgesics had no difference across three groups. No difference of side effects(shivering, nausea and vomiting, itching), the first anal aerofluxus time and intraoperation tramadol dose were detected among the three groups. CONCLUSION: The use of dexmedetomidine especially at the dose of 3µg as an adjuvant to bupivacaine in cesarean surgery provides better intraoperative somato-visceral sensory block characteristcs and postoperative analgesia, which produced no influence on Apgar scores, side effects and stress response.

[Drug-Resistant Mechanism of Multiple Myeloma and Its Therapy Combined with HDACi -Review].

Drug resistance of multiple myeloma(MM) has become more and more common, and greatly decreased the survival rate of these patients. The occurence of drug-resistance involves in many factors such as bone marrow microenveronment, tumor cell self-metabolism, cytokines, specific targets and so on. In this review, the potential mechanisms of resistance to glucocorticoid/proteasome inhibitor/immunomodulatory druges are briefly expounded in the aspect of tumor cell self-metabolism, including the changes of heat slock protein expression, mRNA expression, related cytokine levels and down-regulation of thalidomid-effecting site CRBN expression. In this review, the researches on the effect of histone deacetylase inhibitors(HDACi) combined with glucocorticoid, proteasome inhibitors, immunomodulatory drugs and monoclonal antibodies on multiple myeloma, specially, drug-resistant multiple myeloma are also summarized.

Epidural Co-Administration of Dexmedetomidine and Levobupivacaine Improves the Gastrointestinal Motility Function after Colonic Resection in Comparison to Co-Administration of Morphine and Levobupivacaine.

UNLABELLED: Gastrointestinal motility may be impaired after intestinal surgery. Epidural morphine is effective in controlling postoperative pain, but can further reduce gastrointestinal motility. Here, we aimed to investigate the effects of epidural dexmedetomidine on gastrointestinal motility in patients undergoing colonic resection. Seventy-four patients undergoing colonic resection were enrolled in this clinical trial and allocated randomly to treatment with dexmedetomidine (D group) or morphine (M group). The D group received a loading dose epidural administration of 3 ml dexmedetomidine (0.5 µg kg(-1)) and then a continuous epidural administration of 80 µg dexmedetomidine in 150 ml levobupivacaine (0.125%) at 3 ml h(-1) for two days. The M group received a loading dose epidural administration of 3 ml morphine (0.03 mg kg(-1)) and then a continuous epidural administration of 4.5 mg morphine in 150 ml levobupivacaine at 3 ml h(-1) for two days. Verbal rating score (VRS), postoperative analgesic requirements, side effects related to analgesia, the time to postoperative first flatus (FFL) and first feces (FFE) were recorded. VRS and postoperative analgesic requirements were not significantly different between treatment groups. In contrast, the time to FFL and time to FFE were significant longer in M group in comparison to D group (P < 0.05). Moreover, patients in M group had a significantly higher incidence of nausea, vomiting, and pruritus (P < 0.05). No patients showed neurologic deficits in either group. In comparison to morphine, epidural dexmedetomidine is safe and beneficial for the recovery of gastrointestinal motility after colonic resection when used as an adjunct with levobupivacaine for postoperative pain control. TRIAL REGISTRATION: Chinese Clinical Trial Registry ChiCTR-TRC-14004644.

Hypercapnic acidosis confers antioxidant and anti-apoptosis effects against ventilator-induced lung injury.

Hypercapnic acidosis may attenuate ventilator-induced lung oxidative stress injury and alveolar cell apoptosis, but the underlying mechanisms are poorly understood. We examined the effects of hypercapnic acidosis on the role of apoptosis signal-regulating kinase 1 (ASK1), which activates the c-Jun N-terminal kinase (JNK) and p38 cascade in both apoptosis and oxidative reactions, in high-pressure ventilation stimulated rat lungs. Rats were ventilated with a peak inspiratory pressure (PIP) of 30 cmH2O for 4 h and randomly given FiCO2 to achieve normocapnia (PaCO2 at 35-45 mm Hg) or hypercapnia (PaCO2 at 80-100 mm Hg); normally ventilated rats with PIP of 15 cmH2O were used as controls. Lung injury was quantified by gas exchange, microvascular leaks, histology, levels of inflammatory cytokines, and pulmonary oxidative reactions. Apoptosis through the ASK1-JNK/p38 mitogen-activated protein kinase (MAPK) cascade in type II alveolar epithelial cells (AECIIs) were evaluated by examination of caspase-3 activation. The results showed that injurious ventilation caused significant lung injury, including deteriorative oxygenation, changes of histology, and the release of inflammatory cytokines. In addition, the high-pressure mechanical stretch also induced apoptosis and caspase-3 activation in the AECIIs. Hypercapnia attenuated these responses, suppressing the ASK1 signal pathways with its downstream kinase phosphorylation of p38 MAPK and JNK, and caspase-3 activation. Thus, hypercapnia can attenuate cell apoptosis and oxidative stress damage in rat lungs during injurious ventilation, at least in part, due to the suppression of the ASK1-JNK/p38 MAPK pathways.

Preventive and therapeutic effects of penehyclidine hydrochloride on morphine-induced increased bladder pressure, urinary bladder sphincter pressure and histological damage in rabbits.

BACKGROUND: Morphine has become the preferred drug for analgesia. However, analgesic doses of morphine can result in urinary retention, which is an intractable problem in clinical practice. Though bladder catheterization is one available therapeutic option, data supporting the technique's effectiveness are controversial. As a novel anti-cholinergic medicine developed in China, penehyclidine hydrochloride (PHC) exhibits greater selectivity for M(3)/M(1) receptors than M(2) receptors. Therefore, this study aimed to determine the efficacy of PHC in treating urinary retention. METHODS: Thirty-two healthy male New Zealand white rabbits were randomly divided in four groups (n = 8 each) as follows: control group (C group), PHC low-dose group (PL group, 0.01 mg/kg of PHC intramuscularly), PHC middle-dose group (PM group, 0.02 mg/kg of PHC intramuscularly), and PHC high-dose group (PH group, 0.05 mg/kg of PHC intramuscularly). All rabbits were injected intravenously with morphine (1 mg/kg) to induce urinary retention and different doses of PHC were injected intramuscularly in the PL, PM and PH groups. In the C group, 1 ml saline was administered instead of PHC. The bladder pressure and the bladder sphincter pressure were recorded at different time points. The plasma concentration of PHC was measured at different time points with high performance liquid chromatography. Arterial blood pressure and heart rate (HR) were recorded at different time points. RESULTS: Bladder pressure and urinary bladder sphincter pressure rose significantly from 30 minutes after morphine administration until the end of the experiment. PHC markedly attenuated the elevations in pressure induced by morphine. Morphometric analysis also revealed histological damage, erythrocytes and ruptures of the microcirculation in regions of the submucosa and smooth muscle. Morphometric damage was ameliorated with PHC but not with saline. Hemodynamic data (mean arterial pressure (MAP) and HR) did not differ between groups over the observation period. CONCLUSIONS: This study demonstrated that intravenous morphine significantly increased bladder pressure and urinary bladder sphincter pressure and induced histological damage in the bladder and urinary bladder sphincter. Importantly, preliminary data showed that PHC could decrease the extent of these changes.

{µ-6,6'-Dimeth-oxy-2,2'-[butane-1,4-diylbis(nitrilo-methanylyl-idene)]diphenolato}trinitratocopper(II)samarium(III).

In the monomeric dinuclear title complex, [CuSm(C(20)H(22)N(2)O(4))(NO(3))(3)], the four-coordinate Cu(II) ion has a square-planar geometry involving two O atoms and two N atoms of the deprotonated Schiff base ligand. The Sm(III) ion is ten-coordinate, chelated by four O donor atoms of the Schiff base and two O atoms each from three bidentate nitrate groups, one of which is disordered over two sites in a 0.55 (7):0.45 (7) ratio.

Chronic ß-adrenoceptor antagonists upregulate the rat alveolar macrophage adrenergic system through the ß1-subtype.

BACKGROUND: Previous studies demonstrate that macrophages synthesis and release catecholamines, which regulate the immune responses in an autocrine manner. These responses are mediated in part by ß-adrenoceptors expressed on macrophages. Some ß-adrenoceptor antagonists are commonly used in clinical conditions. Here we investigated whether the chronic administration of ß-adrenoceptor antagonists upregulate adrenergic system of alveolar macrophage and the potential mechanims. METHODS: Propranolol (30 mg/kg·d) or atenolol (5 mg/kg·d) was administered by gavage to rats for 4 weeks. Then alveolar macrophages were isolated and the expression of ß(1) or ß(2)-adrenoceptor was detected by flow cytometric analysis. Dopamine ß-hydroxylase expression was assessed by Western blot assay and the concentrations of noradrenaline, IL-6, and TNF-α in cell supernatants were measured using ELISA after 2 h or 24 h exposure of alveolar macrophages to 100 ng/ml lipopolysaccharide (LPS). RESULTS: Propranolol increased the mean fluorescence intensity (MFI) of ß(1), ß(2)-adrenoceptor and the frequency of ß(1)-,ß(2)- adrenoceptor positive macrophages. However, only the MFI of ß(1)-adrenoceptor and the frequency of ß(1)-adrenoceptor positive macrophages were increased by atenolol. Furthermore, both propranolol and atenolol promoted LPS-mediated dopamine ß-hydroxylase protein expression and increased noradrenaline production in rat alveolar macrophages. This was accompanied by increased LPS-mediated IL-6 and TNF-α production in cell supernatants of alveolar macrophages. CONCLUSION: These findings demonstrate that propranolol or atenolol upregulates alveolar macrophage adrenergic system, and the response may be ß(1)-adrenergic receptor subtype dependent.

Propofol improved neurobehavioral outcome of cerebral ischemia-reperfusion rats by regulating Bcl-2 and Bax expression.

Propofol is an intravenous anesthetic with neuroprotective effects against cerebral ischemia-reperfusion (I/R) injury. Few studies regarding the neuroprotective and neurobehavioral effects of propofol have been conducted, and the underlying mechanisms are still unclear. Because I/R may result in neuronal apoptosis, the apoptosis regulatory genes B-cell leukemia-2 (Bcl-2) and Bcl-2-associated X protein (Bax) may be involved in the neuroprotective process. In this study, 120 Wistar rats were randomly divided into three groups (sham, I/R-induced, and propofol-treated). Cerebral ischemia was induced by clamping the bilateral common carotid arteries for 10min. Propofol (1.0mg/kg/min) was administered intravenously for 1h before the induction of ischemia. Neuronal damage was evaluated by neurobehavioral scores and histological examination of the brain sections at the level of the dorsal hippocampus at 6h, 24h, 48h, 72h, 4days, 5days, 6days, and 7days after I/R. The apoptotic rate of hippocampal neurons was detected by flow cytometry. The expression of Bcl-2 and Bax was evaluated using immunohistochemical and Western blot methods. The results of this study showed that neurobehavioral scores were higher in propofol-treated rats compared with I/R-induced rats with no propofol treatment. Moreover, the hippocampal expression of Bcl-2 was significantly higher, while the expression of Bax was significantly lower in propofol-treated rats compared with I/R-induced rats at 24h after ischemia. Hence, this study suggests that the neuroprotective effects of propofol against neuronal apoptosis may be a consequence of the regulation of Bcl-2 and Bax.

Propofol inhibited the delayed rectifier potassium current (I(k)) via activation of protein kinase C epsilon in rat parietal cortical neurons.

Propofol has been shown to exert neuroprotective effects. Delayed rectifier potassium current (I(K)) was reported to be closely related to neuronal damage. This study was designed to test the effects of propofol on I(K) in rat parietal cortical neurons and the involvement of PKC in this activity. Whole-cell patch-clamp recordings were performed in rat parietal cortical neurons. The amplitudes of I(K) were recorded before and after the addition of different concentrations of propofol. Propofol concentration-dependently inhibited I(K) with an IC50 value of 36.3±2.7 µM. Moreover, propofol caused a downward shift of the I-V curve of I(K) in a concentration dependent manner. The kinetics of I(K) was altered by propofol, with decreased activation and delayed recovery of I(K). Pretreatment with calphostin-C (a non-selective inhibitor of PKC) or PKC epsilon translocation inhibitor peptide (PKC epsilon inhibitor) abrogated the inhibition of I(K) by propofol. In conclusion, propofol inhibited I(K) via the activation of PKC epsilon in rat cerebral parietal cortical neurons.

Effects of therapeutic hypercapnia on inflammation and apoptosis after hepatic ischemia-reperfusion injury in rats.

BACKGROUND: Therapeutic hypercapnia (TH) has been demonstrated to protect several organs ischemia-reperfusion injury. The study aimed to investigate the effects of therapeutic hypercapnia on hepatic ischemia-reperfusion injury (HIRI). METHODS: Thirty adult male Wistar rats weighing (250+/-20) g were randomized into 3 groups (n=10 in each), group C (control group), group A (hypercapnia group) and group B (CO2 preconditioning group). A segmental ischemia of the liver was induced by interrupting the blood vessels including the bile duct to the median and left lateral lobes for 60 minutes and all the animals were sacrificed after 240 minutes observation period of reperfusion. Mean arterial pressure (MAP) and the blood gases were measured before ischemia (baseline) and at 30, 60, 120, 180 and 240 minutes after reperfusion. Arterial blood samples were obtained for determination of serum levels of TNF-alpha, IL-10, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The histopathology of liver tissues was evaluated by light microscopy. The NF-kappaB expression and apoptotic hepatocytes were respectively determined by immunohistochemistry and TUNEL assay. RESULTS: The serum levels of liver enzymes and TNF-alpha were significantly decreased while the IL-10 level was significantly increased in groups A and B than in group C (P<0.05), and group B surpassed group A (P<0.05). The histopathological scores, the NF-kappaB immunohistochemical score (IHS) and apoptotic index were significantly lower in groups A and B than in group C (P<0.05), and the decrease in group B was more obvious than in group A (P<0.05). CONCLUSION: Therapeutic hypercapnia attenuates ischemia-reperfusion injury to the liver. Moreover, the effects of CO2 preconditioning are outstandingly notable.

[Construction of eukaryote expression vector carrying human pulmonary surfactant-associated protein C and its expression in vitro].

OBJECTIVE: To clone human pulmonary surfactant-associated protein C (SP-C) and construct an eukaryote expression vector pcDNA3.1(+)/SP-C, and then to examine the SP-C expression in vitro, which may provide a reliable way of massive production of SP-C. METHODS: The total RNA of normal lung tissue neighboring lung cancer from patients undergoing operation was extracted, and SP-C cDNA was then obtained by reverse transcription-polymerase chain reaction (RT-PCR). Both SP-C cDNA sequence and plasmid pcDNA3.1(+) were digested with NotI and XhoI, then connected by T4 DNA ligase after recycling agarose. After identification by restriction analysis and DNA sequencing, the recombinant was transfected into human breast cancer MCF-7 cells by using lipofectin reagent, and then the expression of SP-C was examined by RT-PCR and Western blotting. RESULTS: Human SP-C cDNA could be correctly cloned into the plasmid pcDNA3.1(+), and SP-C protein may be expressed in MCF-7 cells after transfection. CONCLUSION: By in vitro recombination, the eukaryote expression vector pcDNA3.1(+)/SP-C was successfully constructed and expressed SP-C in vitro, which rendered preparation for the construction of specific expression vector of human SP-C, and it laid the foundation of massive production of SP-C through mammary gland bioreactor.

{µ(2)-6,6'-Dimeth-oxy-2,2'-[butane-1,4-diylbis(nitrilo-methyl-idyne)]diphenolato}trinitratocopper(II)neodymium(III).

In the title complex, [CuNd(C(20)H(22)N(2)O(4))(NO(3))(3)], the Cu(II) ion is coordinated in a distorted square-planar environment by two O atoms and two N atoms of a tetra-dentate Schiff base ligand. The Nd(III) ion is ten-coordinated by three bis-chelating nitrate groups and four O atoms of the Schiff base ligand. The atoms of one of the nitrato ligands are disordered over two sets of sites, with refined occupancies of 0.567 (13) and 0.433 (17).