Analyzing treatment aggressiveness and identifying high‐risk patients in diabetic foot ulcer return to care

Rates of diabetes and its associated comorbidities have been increasing in the United States, with diabetic foot ulcer treatment representing a large cost to the patient and healthcare system. These ulcers often result in multiple hospital admissions. This study examined readmissions following inpatient care for a diabetic foot ulcer and identified modifiable factors associated with all‐cause 30‐day readmissions to the inpatient or emergency department (ED) setting. We hypothesized that patients undergoing aggressive treatment would have lower 30‐day readmission rates. We identified patient discharge records containing International Classification of Disease ninth revision codes for both diabetes mellitus and distal foot ulcer in the State Inpatient and Emergency Department databases from the Agency for Healthcare Research and Quality, Healthcare Cost and Utilization Project in Florida and New York, 2011–2012. All‐cause 30‐day return to care visits (ED or inpatient) were analyzed. Patient demographics and treatment characteristics were evaluated using univariate and multivariable regression models. The cohort included 25,911 discharges, having a mean age of 63 and an average of 3.8 comorbidities. The overall rate of return to care was 30%, and 21% of subjects underwent a toe or midfoot amputation during their index stay. The most common diagnosis codes upon readmission were diabetes mellitus (19%) and infection (13%). Patients with a toe or midfoot amputation procedure were less likely to be readmitted within 30 days (odds ratio: 0.78; 95% confidence interval: 0.73, 0.84). Presence of comorbidities, black and Hispanic ethnicities, and Medicare and Medicaid payer status were also associated with higher odds of readmission following initial hospitalization (p < 0.05). The study suggests that there are many factors that affect readmission rates for diabetic foot ulcer patients. Understanding patients at high‐risk for readmission can improve counseling and treatment strategies for this fragile patient population.     

腰椎后外侧融合椎弓根钉对相邻节段椎间盘影响的三维有限元分析

目的利用三维有限元法分析腰椎不同运动状态时椎弓根钉的置入位置对邻近节段椎间盘应力的影响。方法利用三维建模软件建立正常人有效性腰骶椎(L_3~S_1)模型。根据椎弓根钉在椎体的位置,分别建立融合模型A、B、C。并根据不同工况对这3种模型施加相应的预载荷及扭矩,分析比较不同腰椎轴向运动时相邻节段椎间盘应力的变化情况。结果成功建立正常有效的L_3~S_1三维有限元模型及椎弓根钉棒系统融合固定三维有限元模型。在后伸状态下,模型A的L_3/L_4椎间盘应力明显增加,而模型B、C较融合前无明显变化;在侧曲状态中,模型B、C的L_3/L_4椎间盘应力变化不大,而模型A显著增加;在其余状态中,3个模型的L_3/L_4椎间盘应力均升高,其中以模型A增加最为明显。3个模型在所有状态下L_5/S_1椎间盘的应力均较融合前略有升高,其中模型B、C应力的变化小于模型A。结论椎弓根钉尖端位于椎体上1/3区域会显著增加融合节段上位邻近椎间盘应力,进而引起相邻节段退变;腰椎融合术不会明显增加邻近下位椎间盘的应力。     

IL-13 induces expression of CD36 in human monocytes through PPARgamma activation

The class B scavenger receptor CD36 is a component of the pattern recognition receptors on monocytes that recognizes a variety of molecules. CD36 expression in monocytes depends on exposure to soluble mediators. We demonstrate here that CD36 expression is induced in human monocytes following exposure to IL-13, a Th2 cytokine, via the peroxisome proliferator-activated receptor (PPAR)gamma pathway. Induction of CD36 protein was paralleled by an increase in CD36 mRNA. The PPARgamma pathway was demonstrated using transfection of a PPARgamma expression plasmid into the murine macrophage cell line RAW264.7, expressing very low levels of PPARgamma, and in peritoneal macrophages from PPARgamma-conditional null mice. We also show that CD36 induction by IL-13 via PPARgamma is dependent on phospholipase A2 activation and that IL-13 induces the production of endogenous 15-deoxy-Delta12,14-prostaglandin J2, an endogenous PPARgamma ligand, and its nuclear localization in human monocytes. Finally, we demonstrate that CD36 and PPARgamma are involved in IL-13-mediated phagocytosis of Plasmodium falciparum-parasitized erythrocytes. These results reveal a novel role for PPARgamma in the alternative activation of monocytes by IL-13, suggesting that endogenous PPARgamma ligands, produced by phospholipase A2 activation, could contribute to the biochemical and cellular functions of CD36.     

Corticotropin-releasing factor (CRF) receptor type 1-dependent modulation of synaptic plasticity

Mobile phones signals are pulse-modulated microwaves, and EEG studies suggest that the extremely low-frequency (ELF) pulse modulation has sleep effects. However, 'talk', 'listen' and 'standby' modes differ in the ELF (2, 8, and 217Hz) spectral components and specific absorption rates, but no sleep study has differentiated these modes. We used a GSM900 mobile phone controlled by a base-station simulator and a test SIM card to simulate these three specific modes, transmitted at 12.5% (23dBm) of maximum power. At weekly intervals, 10 healthy young adults, sleep restricted to 6h, were randomly and single-blind exposed to one of: talk, listen, standby and sham (nil signal) modes, for 30 min, at 13:30 h, whilst lying in a sound-proof, lit bedroom, with a thermally insulated silent phone beside the right ear. Bipolar EEGs were recorded continuously, and subjective ratings of sleepiness obtained every 3 min (before, during and after exposure). After exposure the phone and base-station were switched off, the bedroom darkened, and a 90 min sleep opportunity followed. We report on sleep onset using: (i) visually scored latency to onset of stage 2 sleep, (ii) EEG power spectral analysis. There was no condition effect for subjective sleepiness. Post-exposure, sleep latency after talk mode was markedly and significantly delayed beyond listen and sham modes. This condition effect over time was also quite evident in 1-4Hz EEG frontal power, which is a frequency range particularly sensitive to sleep onset. It is possible that 2, 8, 217Hz modulation may differentially affect sleep onset.     

An immunohistochemical approach to differentiate hepatic lipidosis from hepatic phospholipidosis in rats

Hepatocellular vacuolation can be a diagnostic challenge since cytoplasmic accumulations of various substances (lipid, water, phospholipids, glycogen, and plasma) can have a similar morphology. Cytoplasmic accumulation of phospholipids following administration of cationic amphiphilic drugs (CAD) can be particularly difficult to differentiate from nonphosphorylated lipid accumulations at the light microscopic level. Histochemical methods (Sudan Black, Oil Red-O, Nile Blue, etc.) can be used to identify both nonphosphorylated and/or phosphorylated lipid accumulations, but these techniques require non-paraffin-embedded tissue and are only moderately sensitive. Thus, electron microscopy is often utilized to achieve a definitive diagnosis based upon the characteristic morphologic features of phospholipid accumulations; however, this is a low throughput and labor intense procedure. In this report, we describe the use of immunohistochemical staining for LAMP-2 (a lysosome-associated protein) and adipophilin (a protein that forms the membrane around non-lysosomal lipid droplets) to differentiate phospholipidosis and lipidosis, respectively in the livers of rats. This staining procedure can be performed on formalin-fixed paraffin embedded tissues, is more sensitive than histochemistry, and easier to perform than ultrastructural evaluation.     

Re-expression of a developmentally restricted potassium channel in autoimmune demyelination: Kv1.4 is implicated in oligodendroglial proliferation

Mechanisms of lesion repair in multiple sclerosis are incompletely understood. To some degree, remyelination can occur, associated with an increase of proliferating oligodendroglial cells. Recently, the expression of potassium channels has been implicated in the control of oligodendrocyte precursor cell proliferation in vitro. We investigated the expression of Kv1.4 potassium channels in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Confocal microscopy revealed expression of Kv1.4 in AN2-positive oligodendrocyte precursor cells and premyelinating oligodendrocytes in vitro but neither in mature oligodendrocytes nor in the spinal cords of healthy adult mice. After induction of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, Kv1.4 immunoreactivity was detected in or around lesions already during disease onset with a peak early and a subsequent decrease in the late phase of the disease. Kv1.4 expression was confined to 2',3'-cyclic nucleotide 3'-phosphodiesterase-positive oligodendroglial cells, which were actively proliferating and ensheathed naked axons. After a demyelinating episode, the number of Kv1.4 and 2',3'-cyclic nucleotide 3'-phosphodiesterase double-positive cells was greatly reduced in ciliary neurotrophic factor knockout mice, a model with impaired lesion repair. In summary, the re-expression of an oligodendroglial potassium channel may have a functional implication on oligodendroglial cell cycle progression, thus influencing tissue repair in experimental autoimmune encephalomyelitis and multiple sclerosis.