Erfahrungen über den Croup

Ohne Zusammenfassung     

Additional surgical procedure is a risk factor for surgical site infections after laparoscopic cholecystectomy

Purpose

Surgical site infections (SSI) are associated with increased costs and length of hospital stay, readmission rates, and mortality. The aim of this study was to identify risk factors for SSI in patients undergoing laparoscopic cholecystectomy.

Methods

Analysis of 35,432 laparoscopic cholecystectomies of a prospective multicenter database was performed. Risk factors for SSI were identified among demographic data, preoperative patients’ history, and operative data using multivariate analysis.

Results

SSIs after laparoscopic cholecystectomy were seen in 0.8 % (n?=?291) of the patients. Multivariate analysis identified the following parameters as risk factors for SSI: additional surgical procedure (odds ratio [OR] 4.0, 95 % confidence interval [CI] 2.2–7.5), age over 55 years (OR 2.4 [1.8–3.2]), conversion to open procedure (OR 2.6 [1.9–3.6]), postoperative hematoma (OR 1.9 [1.2–3.1]), duration of operation >60 min (OR 2.5 [1.7–3.6], cystic stump insufficiency (OR 12.5 [4.2–37.2]), gallbladder perforation (OR 6.2 [2.4–16.1]), gallbladder empyema (OR 1.7 [1.1–2.7]), and surgical revision (OR 15.7 [10.4–23.7]. SSIs were associated with a significantly prolonged hospital stay (p?<?0.001), higher postoperative mortality (p?<?0.001), and increased rate of surgical revision (p?<?0.001).

Conclusions

Additional surgical procedure was identified as a strong risk factor for SSI after laparoscopic cholecystectomy. Furthermore, operation time >60 min, age >55 years, conversion to open procedure, cystic stump insufficiency, postoperative hematoma, gallbladder perforation, gallbladder empyema, or surgical revision were identified as specific risk factors for SSI after laparoscopic cholecystectomy.     

Neurturin shares receptors and signal transduction pathways with glial cell line-derived neurotrophic factor in sympathetic neurons

Neurturin (NTN) is a neurotrophic factor that shares homology with glial cell line-derived neurotrophic factor (GDNF). Recently, a receptor complex has been identified for GDNF that includes the Ret tyrosine kinase receptor and a glycosylphosphatidylinositol-linked protein termed “GDNFRα.” However, differences in the phenotype of Ret and GDNF knockout animals suggest that Ret has at least one additional ligand. In this report, we demonstrate that NTN induces Ret phosphorylation in primary cultures of rat superior cervical ganglion (SCG) neurons. NTN also caused Ret phosphorylation in fibroblasts that were transfected stably with Ret and GDNFRα but not in cells expressing Ret alone. A glycosylphosphatidylinositol-linked protein also was important for NTN and GDNF signaling in SCG neurons; phosphatidylinositol-specific phospholipase C treatment of SCG cultures reduced the ability of NTN to phosphorylate Ret and the ability of NTN or GDNF to activate the mitogen-activated protein kinase pathway. NTN and GDNF also caused sustained activation of Ret and the mitogen-activated protein kinase pathway in SCG neurons. Finally, both NTN and GDNF activated the phosphatidylinositol 3-kinase pathway in SCG neurons, which may be important for the ability of NTN and GDNF to promote neuronal survival. These data indicate that NTN is a physiologically relevant ligand for the Ret receptor and suggest that NTN may have a critical role in the development of many neuronal populations.     

Can a clinical test of hamstring strength identify football players at risk of hamstring strain?

Purpose  

To demonstrate the potential for a simple clinical test of hamstring muscle strength to identify susceptibility to muscle strain injury.     

Microanatomy and ultrastructure of the excretory system of two pelagic opisthobranch species (Gastropoda: Gymnosomata and Thecosomata)

The microanatomy and ultrastructure of the excretory system of Pneumoderma sp. (Gymnosomata) and Creseis virgula Rang, 1828 (Thecosomata) have been investigated by means of semithin serial sections, reconstructions and transmission electron microscopy. The studies revealed a functional metanephridial system consisting of a heart with a single ventricle and auricle in a pericardial cavity and a single kidney in both species. Podocytes in the atrial wall of the pericardial epithelium are the site of ultrafiltration, whereas the flat epithelium of the kidney with numerous basal infoldings and a dense microvillous border on the luminal surface suggests modification of the ultrafiltrate. In Pneumoderma sp., additional loci of ultrafiltration with identical fine structure (meandering slits with diaphragms covered by extracellular matrix) occur in the solitary rhogocytes (pore cells). The presence of podocytes situated on the atrial wall in representatives of two higher opisthobranch taxa contradicts former ideas on the loss of the primary site of ultrafiltration in the ancestors of the Opisthobranchia.     

Postischemic neuroprotection in the ischemia-tolerant state gerbil hippocampus is associated with increased ligand binding to inhibitory GABA<Subscript>A</Subscript> receptors

Excitotoxic activation of glutamate receptors is thought to play a key role in delayed neuronal death (DND) of highly vulnerable hippocampal CA1 neurons after transient global ischemia. DND can be prevented by a short sublethal preconditioning (PC) stimulus. Recently, we demonstrated that ischemic PC, but not a single period of 5-min ischemia elicits a transient up-regulation of hippocampal [(3)H]muscimol binding to GABA(A) receptors. This indicates that activation of the GABAergic system may participate in the acquisition of neuroprotection. The present study was designed to test whether postischemic modulation of receptor binding also occurs in the ischemia-tolerant state, i.e., after a PC stimulus of 2.5-min ischemia and a subsequent normally lethal period of 5-min ischemia 4 days apart. Using receptor autoradiography, [(3)H]AMPA and [(3)H]muscimol binding to excitatory AMPA and inhibitory GABA(A) receptors was analyzed in hippocampal subfields CA1, CA3 and dentate gyrus at recirculation intervals of 30 min, 8, 24, 48, 96 h and 3 weeks. Postischemic hippocampal ligand binding to AMPA receptors remained unchanged at any time point investigated, but [(3)H]muscimol binding to GABA(A) receptors in CA1 neurons rendered tolerant to ischemia was up-regulated between 30 min and 48 h of recirculation. Our data suggest that a relative shift between excitatory and inhibitory neurotransmission may promote postischemic survival of CA1 neurons.     

Pronounced arterial collateralization was induced after permanent rat cerebral four-vessel occlusion. Relation to neuropathology and capillary ultrastructure

The present study investigates chronic changes in cerebral arterial vessel system, microvasculature, and brain histopathology using an adult rat model based on permanent and stepwise occlusion of four cerebral vessels. Digital subtraction angiography (DSA) was performed to study chronic changes in arterial cerebral vessel system after permanent vessel occlusion. Long-lasting functional changes such as NMDA-, AMPA- and GABA(A)-receptor binding were detected in hippocampus and dentate gyrus using autoradiography. Structural changes in cerebral capillaries were investigated using light- and electron microscopy. Chronic cerebral oligemia did not cause any significant changes in the densities of excitatory glutamate and inhibitory GABA(A) receptors. By electron microscopy we could document, however, that most capillaries in vessel-occluded animals shrank, the endothelial cells were prominent with enlarged nuclei and increased cytoplasm, and the basal membrane was thickened. In contrast to the degenerative changes in brain capillaries, pronounced arterial collateralization was disclosed by DSA after chronic brain vessel occlusion. The model of chronic occlusion of four cerebral vessels is characterized by capillary degeneration and arterial collateralization proceeding in parallel. Thus, this rat model may be useful in investigations of long-lasting compensatory mechanisms contributing to cerebrovascular or neurodegenerative disorders.     

Band 3 nullVIENNA,a novel homozygous SLC4A1 p.Ser477X variant causing severe hemolytic anemia,dyserythropoiesis and complete distal renal tubular acidosis

We describe the second patient with anionic exchanger 1/band 3 null phenotype (band 3 null^VIENNA), which was caused by a novel nonsense mutation c.1430C>A (p.Ser477X) in exon 12 of SLC4A1. We also update on the previous band 3 null^COIMBRA patient, thereby elucidating the physiological implications of total loss of AE1/band 3. Besides transfusion‐dependent severe hemolytic anemia and complete distal renal tubular acidosis, dyserythropoiesis was identified in the band 3 null^VIENNA patient, suggesting a role for band 3 in erythropoiesis. Moreover, we also, for the first time, report that long‐term survival is possible in band 3 null patients.