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

Delamination of Layered Zeolite Precursors under Mild Conditions: Synthesis of UCB-1 via Fluoride/Chloride Anion-Promoted Exfoliation

New material UCB-1 is synthesized via the delamination of zeolite precursor MCM-22 (P) at pH 9 using an aqueous solution of cetyltrimethylammonium bromide, tetrabutylammonium fluoride, and tetrabutylammonium chloride at 353 K. Characterization by powder X-ray diffraction, transmission electron microscopy, and nitrogen physisorption at 77 K indicates the same degree of delamination in UCB-1 as previously reported for delaminated zeolite precursors, which require a pH of greater than 13.5 and sonication in order to achieve exfoliation. UCB-1 consists of a high degree of structural integrity via ^(29)Si MAS NMR and Fourier transform infrared spectroscopies, and no detectable formation of amorphous silica phase via transmission electron microscopy. Porosimetry measurements demonstrate a lack of hysteresis in the N_2 adsorption/desorption isotherms and macroporosity in UCB-1. The new method is generalizable to a variety of Si:Al ratios and leads to delaminated zeolite precursor materials lacking amorphization

Successful Treatment of Cutaneous Lesions of Dermatomyositis with Topical Pimecrolimus

Dermatomyositis (DM) is an idiopathic inflammatory process characterized by proximal muscle weakness and cutaneous lesions, such as the Gottron's sign, heliotrope rash, and erythematous photosensitive rash. Administration of systemic agents for the treatment of underlying systemic diseases leads to remission of the cutaneous lesions in many cases. However, cutaneous lesions may remain refractory to treatment. Pimecrolimus is a calcineurin inhibitor with combined anti-inflammatory and immunomodulatory activity. It has high affinity to the skin and low permeation potential, even in patients with acute skin inflammation and in those undergoing post-topical corticosteroid therapy. We herein report two DM patients whose cutaneous lesions were refractory to conventional treatment but showed dramatic response to topical pimecrolimus. The clinical outcomes suggest that topical pimecrolimus may be a good therapeutic alternative for the management of the cutaneous lesions of DM

Network Clustering Revealed the Systemic Alterations of Mitochondrial Protein Expression

The mitochondrial protein repertoire varies depending on the cellular state. Protein component modifications caused by mitochondrial DNA (mtDNA) depletion are related to a wide range of human diseases; however, little is known about how nuclear-encoded mitochondrial proteins (mt proteome) changes under such dysfunctional states. In this study, we investigated the systemic alterations of mtDNA-depleted (ρ0) mitochondria by using network analysis of gene expression data. By modularizing the quantified proteomics data into protein functional networks, systemic properties of mitochondrial dysfunction were analyzed. We discovered that up-regulated and down-regulated proteins were organized into two predominant subnetworks that exhibited distinct biological processes. The down-regulated network modules are involved in typical mitochondrial functions, while up-regulated proteins are responsible for mtDNA repair and regulation of mt protein expression and transport. Furthermore, comparisons of proteome and transcriptome data revealed that ρ0 cells attempted to compensate for mtDNA depletion by modulating the coordinated expression/transport of mt proteins. Our results demonstrate that mt protein composition changed to remodel the functional organization of mitochondrial protein networks in response to dysfunctional cellular states. Human mt protein functional networks provide a framework for understanding how cells respond to mitochondrial dysfunctions