OBJECTIVEThe inflammatory and immune systems are altered in type 2 diabetes. Here, the aim was to profile the immune and inflammatory response in subjects with prediabetes and diabetes in a large population-representative sample. RESEARCH DESIGN AND METHODSIn total, 15,010 individuals were analyzed from the population-based Gutenberg Health Study. Glucose status was classified according to HbA 1c concentration and history of diagnosis. All samples were analyzed for white blood cells (WBCs), granulocytes, lymphocytes, monocytes, platelets, C-reactive protein (CRP), albumin, fibrinogen, and hematocrit. Interleukin-18 (IL-18), IL-1 receptor antagonist (IL-1RA), and neopterin concentrations were determined in a subcohort. RESULTSIn total, 7,584 men and 7,426 women were analyzed (range 35-74 years), with 1,425 and 1,299 having prediabetes and diabetes, respectively. Biomarkers showed varying dynamics from normoglycemic via subjects with prediabetes to subjects with diabetes: 1) gradual increase (WBCs, granulocytes, monocytes, IL-1RA, IL-18, and fibrinogen), 2) increase with subclinical disease only (lymphocytes and CRP), 3) increase from prediabetes to diabetes only (neopterin), and 4) no variation with glucose status (hematocrit). The strongest relative differences were found for CRP, IL-1RA, and fibrinogen concentrations. Several inflammatory and immune markers were associated with the glucose status independent from cardiovascular risk factors and comorbidities, varied with disease severity and the presence of disease-specific complications in the diabetes subcohort. CONCLUSIONSThe inflammatory and immune biomarker profile varies with the development and progression of type 2 diabetes. Markers of inflammation and immunity enable differentiation between the early preclinical and clinical phases of the disease, disease complications, and progression.Type 2 diabetes and its disease-associated complications represent an important and increasing public health burden worldwide (1). Obesity, which leads to metabolic and adipocyte stress, is the most important predisposing factor for type 2 diabetes (2). Obesity-associated insulin resistance, activation of the innate immune system, and chronic increased production of cytokines and adipokines are an

Pectus excavatum and pectus carinatum represent the most frequent chest wall deformations. However, the pathogenesis is still poorly understood and research results remain inconsistent. To focus on the recent state of knowledge, we summarize and critically discuss the pathological concepts based on the history of these entities, beginning with the first description in the sixteenth century. Based on the early clinical descriptions, we review and discuss the different pathogenetic hypotheses. To open new perspectives for the potential pathomechanisms, the embryonic and foetal development of the ribs and the sternum is highlighted following the understanding that the origin of these deformities is given by the disruption in the maturation of the parasternal region. In the second, different therapeutical techniques are highlighted and based on the pathogenetic hypotheses and the embryological knowledge potential new biomaterial-based perspectives with interesting insights for tissue engineering-based treatment options are presented.

Mesothelial cells play a crucial physiological role in friction less gliding of the serosa and the maintenance of anantiadhesive surface. The formation of postoperative adhesions results from a cascade of events and is regulated by various cellular and humoral factors. Therefore, optimization or functionalization of barrier materials by developments interacting with this cascade on a structural or pharmacological level could give an innovative input for future strategies in peritoneal adhesion prevention. For this purpose, the proper understanding of the formal pathogenesis of adhesion formation is essential. Based on the physiology of the serosa and the pathophysiology of adhesion formation, the available barriers in current clinical practice as well as new innovations are discussed in the present review.

2-Ammoniumethanethiolate, (-)SCH(2)CH(2)NH(3)(+), the first structurally characterized zwitterionic ammoniumthiolate, is the stable form of cysteamine (HL) in the solid state and in aqueous solution. Reactions of ZnCl(2), Cd(Oac)(2), and HgCl(2) with cysteamine and NaOH in a 1:2:2 ratio, respectively, lead to the homoleptic complexes ML(2). Their single-crystal X-ray structures demonstrate basic differences in the coordination chemistry of Zn(II), Cd(II), and Hg(II). While chelating N,S-coordination modes are found for all metal ions, Zn(II) forms a mononuclear complex with a distorted tetrahedral Zn(N(2)S(2)) coordination mode, whereas Hg(II) displays a dimer with Hg(N(2)S(2)) coordinated monomers being connected by two long Hg...S contacts. Solid-state (199)Hg NMR spectra of HgL(2) and [Hg(HL)(2)]Cl(2) reveal a low-field shift of the signals with increasing coordination number. Strong and nearly symmetric Cd-S-Cd bridges in solid CdL(2) lead to a chain structure, Cd(II) displaying a distorted square pyramidal Cd(N(2)S(3)) coordination mode. The ab initio [MP2/LANL2DZ(d,f)] structures of isolated ML(2) show a change from a distorted tetrahedral to bisphenoidal coordination mode in the sequence Zn(II)-Cd(II)-Hg(II). A natural bond orbital analysis showed a high ionic character for the M-S bonds and suggests that the S-M-S fragment is best described by a 3c4e bond. The strength of the M...N interactions and the stability of ML(2) toward decomposition to M and L-L decreases in the sequence Zn > Cd > Hg. Ab initio calculations further suggest that a tetrahedral S-M-S angle stabilizes Zn(II) against substitution by Cd(II) and Hg(II) in a M(N(2)S(2)) environment. Such geometry is provided in zinc-finger proteins, as was found by a database survey.

Peritoneal adhesions remain a relevant clinical problem despite the currently available prophylactic barrier materials. So far, the physical separation of traumatized serosa areas using barriers represents the most important clinical strategy for adhesion prevention. However, the optimal material has not yet been found. Further optimization or pharmacological functionalization of these barriers could give an innovative input for peritoneal adhesion prevention. Therefore, a more complete understanding of pathogenesis is required. On the basis of the pathophysiology of adhesion formation the main barriers currently in clinical practice as well as new innovations are discussed in the present review. Physiologically, mesothelial cells play a decisive role in providing a frictionless gliding surface on the serosa. Adhesion formation results from a cascade of events and is regulated by a variety of cellular and humoral factors. The main clinically applied strategy for adhesion prevention is based on the use of liquid or solid adhesion barriers to separate physically any denuded tissue. Both animal and human trials have not yet been able to identify the optimal barrier to prevent adhesion formation in a sustainable way. Therefore, further developments are required for effective prevention of postoperative adhesion formation. To reach this goal the combination of structural modification and pharmacological functionalization of barrier materials should be addressed. Achieving this aim requires the interaction between basic research, materials science and clinical expertise.