Bis[(2,2-dimethyl­propano­yloxy)meth­yl] {[2-(6-amino-9H-purin-9-yl)eth­oxy]meth­yl}phospho­nate–succinic acid (2/1)

The title compound, C20H32N5O8P·0.5C4H6O4, is composed of two 9-{2-[bis­(pivaloyloxymeth­oxy)phosphinylmeth­oxy]eth­yl}adenine, commonly known as adefovir dipivoxil (AD), mol­ecules linked to the carb­oxy­lic acid groups of succinic acid (SA). The asymmetric unit contains one mol­ecule of AD and half a mol­ecule of SA, which sits on an inversion center. Both adenine units in the two AD mol­ecules make AD–SA N—H⋯O and SA–AD O—H⋯N hydrogen bonds to SA. In addition, the inter­molecular AD–AD N—H⋯O—P hydrogen bond serves to stabilize the cocrystal. There is also a π–π stacking inter­action [inter­planar spacing 3.34 (19) Å] between adjacent inversion-related adenine groups

The role of phosphodiesterase 3 in endotoxin-induced acute kidney injury

Background: Acute kidney injury frequently accompanies sepsis. Endotoxin is known to reduce tissue levels of cAMP and low levels of cAMP have been associated with renal injury. We, therefore, hypothesized that endotoxin induced renal injury by activating phosphodiesterase 3 (PDE3) which metabolizes cAMP and that amrinone an inhibitor of PDE3 would prevent the renal injury. Methods: Animals were divided into three groups (n = 7/group): 1) Control (0.9% NaCl infusion without LPS); 2) LPS (0.9% NaCl infusion with LPS); 3) Amrinone+LPS (Amrinone infusion with LPS). Either lipopolysaccharide (LPS) or vehicle was injected via the jugular vein and the rats followed for 3 hours. We explored the expression of PDE3 isoenzymes and the concentrations of cAMP in the tissue. Results: The PDE3B gene but not PDE3A was upregulated in the kidney of LPS group. Immunohistochemistry also showed that PDE3B was expressed in the distal tubule in the controls and LPS caused PDE3B expression in the proximal as well. However, PDE3A was not expressed in the kidney either in the control or LPS treated groups. Tissue level of cAMP was decreased after LPS and was associated with an increase in blood urea nitrogen, creatinine, ultrastructural proximal tubular changes, and expression of inducible nitric oxide synthase (iNOS) in the endotoxemic kidney. In septic animals the phosphodiesterase 3 inhibitor, amrinone, preserved the tissue cAMP level, renal structural changes, and attenuated the increased blood urea nitrogen, creatinine, and iNOS expression in the kidney. Conclusion: These findings suggest a significant role for PDE3B as an important mediator of LPS-induced acute kidney injury

Metal/graphene sheets as p-type transparent conducting electrodes in GaN light emitting diodes

We demonstrate the use of graphene based transparent sheets as a p-type current spreading layer in GaN light emitting diodes (LEDs). Very thin Ni/Au was inserted between graphene and p-type GaN to reduce contact resistance, which reduced contact resistance from similar to 5.5 to similar to 0.6 Omega/ cm(2), with no critical optical loss. As a result, LEDs with metal-graphene provided current spreading and injection into the p-type GaN layer, enabling three times enhanced electroluminescent intensity compared with those with graphene alone. We confirmed very strong blue light emission in a large area of the metal-graphene layer by analyzing image brightness.open281

The effect of heating insufflation gas on acid-base alterations and core temperature during laparoscopic major abdominal surgery

BACKGROUND: Carbon dioxide (CO(2)) has different biophysical properties under different thermal conditions, which may affect its rate of absorption in the blood and the related adverse events. The present study was aimed to investigate the effects of heating of CO(2) on acid-base balance using Stewart's physiochemical approach, and body temperature during laparoscopy. METHODS: Thirty adult patients undergoing laparoscopic major abdominal surgery were randomized to receive either room temperature CO(2) (control group, n = 15) or heated CO(2) (heated group, n = 15). The acid-base parameters were measured 10 min after the induction of anesthesia (T1), 40 min after pneumoperitoneum (T2), at the end of surgery (T3) and 1 h after surgery (T4). Body temperature was measured at 15-min intervals until the end of the surgery. RESULTS: There were no significant differences in pH, PaCO(2), the apparent strong ion difference, the strong ion gap, bicarbonate ion, or lactate between two groups throughout the whole investigation period. At T2, pH was decreased whereas PaCO(2) was increased in both groups compared with T1 but these changes were not significantly different. Body temperatures in the heated group were significantly higher than those in the control group from 30 to 90 min after pneumoperitoneum. CONCLUSIONS: The heating of insufflating CO(2) did not affect changes in the acid-base status and PaCO(2) in patients undergoing laparoscopic abdominal surgery when the ventilator was set to maintain constant end-tidal CO(2). However, the heated CO(2) reduced the decrease in the core body temperature 30 min after the pneumoperitoneum.ope

Atelectasis Induced by Thoracotomy Causes Lung Injury during Mechanical Ventilation in Endotoxemic Rats

Atelectasis can impair arterial oxygenation and decrease lung compliance. However, the effects of atelectasis on endotoxemic lungs during ventilation have not been well studied. We hypothesized that ventilation at low volumes below functional residual capacity (FRC) would accentuate lung injury in lipopolysaccharide (LPS)-pretreated rats. LPS-pretreated rats were ventilated with room air at 85 breaths/min for 2 hr at a tidal volume of 10 mL/kg with or without thoracotomy. Positive end-expiratory pressure (PEEP) was applied to restore FRC in the thoracotomy group. While LPS or thoracotomy alone did not cause significant injury, the combination of endotoxemia and thoracotomy caused significant hypoxemia and hypercapnia. The injury was observed along with a marked accumulation of inflammatory cells in the interstitium of the lungs, predominantly comprising neutrophils and mononuclear cells. Immunohistochemistry showed increased inducible nitric oxide synthase (iNOS) expression in mononuclear cells accumulated in the interstitium in the injury group. Pretreatment with PEEP or an iNOS inhibitor (1400 W) attenuated hypoxemia, hypercapnia, and the accumulation of inflammatory cells in the lung. In conclusion, the data suggest that atelectasis induced by thoracotomy causes lung injury during mechanical ventilation in endotoxemic rats through iNOS expression