Cachexia and sarcopenia: emerging syndromes of importance in dogs and cats

Cachexia is the loss of lean body mass (LBM) that affects a large proportion of dogs and cats with congestive heart failure (CHF), chronic kidney disease (CKD), cancer, and a variety of other chronic diseases. Sarcopenia, the loss of LBM that occurs with aging, is a related syndrome, although sarcopenia occurs in the absence of disease. As many of the diseases associated with muscle loss are more common in aging, cachexia and sarcopenia often are concurrent problems. Both cachexia and sarcopenia have important clinical implications because they are associated with increased morbidity and mortality. The pathophysiology of these 2 syndromes is complex and multifactorial, but recent studies have provided new information that has helped to clarify mechanisms and identify potential new targets for treatment. Newly identified mechanisms and pathways that mediate cachexia appear to act by increasing energy requirements, decreasing energy intake, impairing nutrient absorption, and causing metabolic alterations. Whereas cachexia and sarcopenia are important areas of research for drug development in people, they are only beginning to be recognized in veterinary medicine. Greater awareness and earlier diagnosis will help provide practical approaches to managing body weight and lean tissue in dogs and cats, as well as more directed targets for treatment.     

Health Factors Associated with Microchip Insertion in Horses

The objectives of this study were to characterize the inflammatory response after microchip insertion, evaluate pain response and swelling at the microchip insertion site, and measure migration of the microchips. Eighteen mature Quarter Horse mares were separated by expected parturition dates and then assigned randomly to treatment groups. The microchip group (n = 7) had microchips inserted using a sterile needle and syringe; the sham group (n = 7) had a needle inserted but no microchip; and the control group (n = 4) had no insertion. The inflammatory response was measured over a 2-week period by measuring dermal temperature, response to pressure, and swelling at the insertion site and plasma serum amyloid A (SAA). For the migration component of the study, radiographs of the seven microchipped horses were taken over 6 months after insertion. These radiographs allowed measurement between a select vertebral point and the microchip. The microchip and sham insertion did not cause a detectable increase in temperature. Algometer readings, used to quantify pressure necessary to induce a pain threshold response, indicated that microchip insertion area was more sensitive than sham insertion at 2 hours, day 1, and day 3 post insertion. Visible swelling began 2 hours postinsertion and resolved by day 3. SAA concentrations were affected by day following insertion, but not by treatment group. Increases in SAA concentration could not be matched with local insertion reactions. Migration was not detected in any of the horses during the 6 months within a 0.7-cm margin of error.     

The Effect of Glucosamine and Chondroitin on Stressed Equine Cartilage Explants

Effective prevention and treatment of osteoarthritis for horses is still needed. This research tests the ability of glucosamine and chondroitin sulfate (GLN/CS) to mitigate inflammatory and mechanical stress in vitro. In this study, GLN/CS mediate this effect by a decrease of the synthesis of nitric oxide (NO) and a decrease of proteoglycan release from the extracellular matrix in stressed cartilage explants. Explants were cultured with interleukin-1 (IL-1) + mechanical trauma with and without GLN/CS. NO and prostaglandin E2 were measured as indicators of an inflammatory response. Glycosaminoglycans were measured as an indicator of cartilage breakdown. NO levels in the stressed explants with GLN/CS treatment were lower than the IL-1 + mechanical impact treatment alone and did not differ from control group. The glycosaminoglycan release was also lower in the GLN/CS treatment than the IL-1 + mechanical impact treatment, although the prostaglandin E2 concentration was not affected. This study offers some evidence that GLN/CS treatment can partially mitigate the catabolic response to inflammatory stress and mechanical trauma in equine cartilage explants. These results provide additional support for the continued study on the benefit of GLN/CS for horses with cartilage degeneration.     

Effect of Parenteral Selenium Administration to Sheep on Prevalence and Recovery from Footrot

Background: Insufficient intake of selenium (Se) is common in many regions, and can contribute to increased susceptibility to and prolonged recovery from infectious diseases. Objective: To determine the effect of Se administration in decreasing the severity and prevalence of footrot in sheep. Animals: Thirty‐eight footrot‐affected and 19 nonaffected sheep from a commercial flock of known high incidence of footrot. Methods: Placebo‐controlled, prospective, 15‐month clinical trial. Footrot‐affected sheep were randomly assigned into 2 groups (n = 19) and injected with either 5 mg Se (footrot [FR]‐Se) or saline (FR‐Sal) at 1‐month intervals for the duration of the study. Unaffected sheep (controls) received no treatment. Sheep feet were examined, trimmed, and scored for footrot with a scale of 0 (no footrot) to 4 (extensive) at 0, 3, 6, 9, and 15 months. Sheep were also bled at time 0 and then at 3, 6, and 15 months to assess whole blood Se concentrations. Results: At time 0, control sheep (255 ± 11 ng/mL) had higher (P < .05) whole blood Se concentrations compared with FR‐Se (205 ± 12 ng/mL) and FR‐Sal (211 ± 14 ng/mL) sheep. By 6 months, FR‐Se sheep (317 ± 9 ng/mL) had whole blood Se concentrations greater (P < .05) than both control (281 ± 14 ng/mL) and FR‐Sal (277 ± 16 ng/mL) sheep. FR‐Se ewes showed a faster decline in highest lesion score at 3 (P= .012) and 6 (P= .0036) months, and a greater decrease in the number of feet with foot score >0 at 6 (P= .020) months compared with FR‐Sal ewes. Sheep with blood Se concentrations <300 ng/mL were at 3.5 times greater risk (1.1–12.1 confidence interval, odds ratio) for FR, although this relationship was only significant (P= .04) at 6 months of the study. Conclusions and Clinical Importance: In sheep with footrot, improved Se status in conjunction with routine control practices result in more rapid improvement of foot lesions.     

MiR-155在脂多糖诱导的RAW264.7巨噬细胞炎症反应中的表达研究

[目的]探讨miR-155在脂多糖(LPS)诱导的RAW264.7巨噬细胞炎症反应中的表达及糖皮质激素(GCs)的干预影响。[方法]体外培养RAW 264.7巨噬细胞,分别用浓度为10.0、1.0、0.1μg/ml LPS刺激RAW 264.7巨噬细胞,于2、6、12、24、36 h 5个时间点收集上清用ELISA检测白介素-6(IL-6)蛋白浓度;实时定量-PCR检测miR-155在2、6、12、36 h 4个时间点的表达变化。[结果]IL-6在各浓度LPS处理组、各时间点其含量均高于对照组(CK);miR-155的表达在各时间点LPS组均高于LPS+GCs和CK。[结论]LPS可以诱导RAW264.7巨噬细胞的炎症反应,炎症反应时miR-155高表达,糖皮质激素可抑制miR-155的表达。     

Butyrylcholinesterase as a marker of inflammation and liver injury in the acute and subclinical phases of canine ehrlichiosis

The aim of this study was to evaluate the role of butyrylcholinesterase (BChE) as a marker of inflammation and liver injury in the acute and subclinical phases of canine ehrlichiosis. Forty-two serum samples of dogs naturally infected with Ehrlichia canis were used, of which 24 were from animals with the acute phase of the disease and 18 with subclinical disease. In addition, sera from 17 healthy dogs were used as negative controls. The hematocrit, BChE activity, hepatic injury (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)), nitric oxide, and cytokines levels were evaluated. The BChE activity was significantly elevated (P < 0.05) in dogs with the acute phase of the disease when compared to healthy animals. However, there was a reduction on BChE activity on dogs with subclinical disease compared to the other two groups. AST and ALT levels were significantly higher (P < 0.05) in the acute phase, as well as the inflammatory mediators (NO_x, TNF-α, INF-γ, IL-4, IL-6) when compared to the control group. On the other hand, IL-10 levels were lower in the acute phase. Based on these results, we are able to conclude that the acute infection caused by E. canis in dogs leads to an increase on seric BChE activity and some inflammatory mediators. Therefore, this enzyme might be used as a marker of acute inflammatory response in dogs naturally infected by this bacterium.     

Effects of HSP90 on complement-mediated hypoxia/reoxygenation injury of H9c2 cardiomyocytes during hypoxic postconditioning

AIM To investigate the effects and mechanisms of heat shock protein 90 （HSP90） on complement-mediated hypoxia/reoxygenation （H/R） injury of rat H9c2 cardiomyocytes during hypoxic postconditioning （HPC）. METHODS Rat H9c2 cardiomyocytes were divided into 7 groups according to different treatments： （1） control group （cultured for 10 h under normal oxygen）； （2） H/R group （hypoxia for 4 h and reoxygenation for 6 h）； （3） HPC group （3 cycles of 5 min H/R after hypoxia for 4 h， followed by reoxygenation for 6 h）； （4） HPC+geldanamycin （GA） group （1 μmol/L HSP90 inhibitor GA was added 20 min before HPC）； （5） negative control group （empty plasmid was transfected before HPC）； （6） C3 over-expression group （C3a plasmid was transfected before HPC）； （7） C5 over-expression group （C5a plasmid was transfected before HPC）. Morphological changes of the H9c2 cells were detected by Hoechst 33242 staining. The effects of HPC on the apoptosis of H9c2 cells were examined by flow cytometry. The protein levels of HSP90， C3a， C5a， NF-κB p65， TNF-α， IL-1β， IL-6， Bcl-2 and Bax were determined by Western blot. RESULTS With up-regulation of HSP90， HPC significantly reduced H/R-induced apoptosis of the H9c2 cells， inhibited the expression of C3a， C5a， NF-κB p65， TNF-α， IL-1β， IL-6 and Bax， and increased the expression of Bcl-2. These effects were blocked by GA. The inhibitory effects of HPC on NF-κB p65 expression and H9c2 cell apoptosis were offset after over-expression of C3a or C5a. CONCLUSION HSP90 attenuates H/R injury of H9c2 cardiomyocytes by inhibiting complement-NF-κB signaling pathway during HPC.     

Polymerase chain reaction screening for DNA viruses in paraffin-embedded brains from dogs with necrotizing meningoencephalitis, necrotizing leukoencephalitis, and granulomatous meningoencephalitis

The objective of this investigation was to determine whether or not herpesvirus (herpes-), adenovirus (adeno-), or canine parvovirus DNA is present in the brains of dogs with necrotizing meningoencephalitis (NME), necrotizing leukoencephalitis (NLE), and granulomatous meningoencephalitis (GME). Paraffin-embedded brain specimens from 12 histopathologically confirmed dogs with NME, 3 with NLE, and 7 with GME were screened for viral DNA with degenerate herpes- and adenovirus polymerase chain reaction (PCR) and a canine parvovirus-specific PCR. Positive-control specimens included genomic viral DNA and paraffin-embedded tissues from dogs with confirmed herpes-, adeno-, or canine parvovirus infections. Herpes-, adeno-, or canine parvovirus DNA was amplified by PCR from the corresponding positive-control specimens. Negative controls included 7 dogs with various brain disorders and produced no viral amplicons. The 22 dogs with NME, NLE, and GME were negative for viral DNA. Additional studies testing for other viruses or inherited genetic mutations are warranted to gain insight into the etiologies of NME, NLE, and GME. We discuss potential etiologies and provide a clinical and histopathologic overview of these common canine encephalitides.     

黄瓜嫩果皮色与色素含量的关系

试材为不同皮色的8个黄瓜品种和以其为亲本配制的10个组合。将上述材料设区种植,每小区30株。先按果色差异对照色谱目测分类,再随机抽样测定色素含量。雌花开花至商品瓜成熟(约7～10 d)取样,沿果实纵向削下宽1 cm,厚0.2cm左右的表皮,用打孔器(直径0.56 cm)取圆片20片,在80％的丙酮液中遮光浸提24 h,用721型分光光度计比色。