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Surgical post-operative adhesions can lead to serious clinical complications. Barrier agent is the broad usage for the prevention of post-operative adhesions. This study aimed to evaluate the reducing adhesion efficacy of non-animal hyaluronic acid (HA) hydrogel in pigs undergoing conventional laparotomy pelvic surgery. HA hydrogel was applied to eighteen female pigs who underwent conventional laparotomy. The adhesion degrees and histopathology were evaluated in bilateral uterine horns as well as peritoneal sidewall excision. In the present study, all animals survived and had no complications after the surgery. The histopathological observations were demonstrated that HA obviously improved laparotomy pelvic surgery-induced adhesion in peritoneal sidewall and uterine horn. The anastomotic healing score of injury + HA group was significantly lower than the injury alone group. We conclude HA hydrogel can attenuate the post-operative adhesions in porcine.

Dipeptidyl peptidase-4 inhibitors (or gliptins), a class of antidiabetic drugs, have recently been shown to have protective actions in the central nervous system. Their cellular and molecular mechanisms responsible for these effects are largely unknown. In the present study, two structurally different gliptins, sitagliptin and vildagliptin, were examined for their therapeutic actions in a controlled cortical impact (CCI) model of moderate traumatic brain injury (TBI) in mice. Early post-CCI treatment with sitagliptin, but not vildagliptin, significantly reduced body asymmetry, locomotor hyperactivity, and brain lesion volume. Sitagliptin attenuated post-CCI microglial deramification in the ipsilateral dorsolateral (DL) striatum, while vildagliptin had no effect. Sitagliptin also reduced striatal expression of galectin-3 and monocyte chemoattractant protein 1(MCP-1), and increased the cortical and striatal levels of the anti-inflammatory cytokine IL-10 on the ipsilateral side. These data support a differential protective effect of sitagliptin against TBI, possibly mediated by an anti-inflammatory effect in striatum to preserve connective network. Both sitagliptin and vildagliptin produced similar increases of active glucagon-like peptide-1 (GLP-1) in blood and brain. Increasing active GLP-1 may not be the sole molecular mechanisms for the neurotherapeutic effect of sitagliptin in TBI.

It is generally understood that continuing neuroinflammation after ischemic stroke can exacerbate the brain damage. During the inflammatory hematogenous recruitment process, the monocytes and macrophages are activated into proinflammatory M1 and anti-inflammatory M2 cell types. Inhibition of soluble epoxide hydrolase (sEH) activity has been reported to regulate monocytes/macrophages, and attenuates neuroinflammation. This study aimed to evaluate whether a selective sEH inhibitor, 12-(3-adamantan-1-yl-ureido)-dodecanoic acid (AUDA), can regulate monocyte/macrophage polarization and improve motor function in the rats with ischemic stroke induced by middle cerebral artery occlusion. We measured the infarct volume with 2,3,5-triphenyltetrazolium chloride staining and used the rotarod test to assess motor performance in rats. The monocyte/macrophage activation and mRNA expression of proinflammatory mediators were measured by flow cytometry and reverse-transcription quantitative PCR, respectively. Our results showed better neurological function and less infarct volume in the rats treated with AUDA. Compared with the vehicle group, the AUDA-treated group showed a reduction in M1 monocyte/macrophage activation and proinflammatory mRNA expressions in the infarct cortex of rats. Our data suggest that the sEH inhibition may regulate monocyte/macrophage polarization and improve neurological outcome after ischemic stroke.

Chien-Fu Yeh,1–3,* Tung‐Yueh Chuang,4,* Yu-Wen Hung,5 Ming-Ying Lan,2,3 Ching-Han Tsai,4 Hao-Xiang Huang,4 Yung-Yang Lin1,4,6–8 1Institute of Brain Science, National Yang-Ming University, Taipei 11221, Taiwan; 2Department of Otorhinolaryngology, National Yang-Ming University, Taipei 11221, Taiwan; 3Department of Otolaryngology-Head and Neck Surgery, Taipei Veterans General Hospital, Taipei 11217, Taiwan; 4Department of Critical Care Medicine, Taipei Veterans General Hospital, Taipei 11217, Taiwan; 5Institute of Cellular and System Medicine, National Health Research Institutes, Miaoli County 35053, Taiwan; 6Institute of Physiology, National Yang-Ming University, Taipei 11221, Taiwan; 7Institute of Clinical Medicine, National Yang-Ming University, Taipei 11221, Taiwan; 8Department of Neurology, Neurological Institute, Taipei Veterans General Hospital, Taipei 11217, Taiwan*These authors contributed equally to this workCorrespondence: Yung-Yang LinDepartment of Critical Care Medicine, Taipei Veterans General Hospital, No. 201, Sec. 2, Shipai Rd., Taipei 11217, TaiwanTel +886-2-2871-2121Fax +886-2-2875-7890Email g2000kev@gmail.comBackground: Ischemic stroke triggers inflammatory responses and oxidative stress in the brain, and microglia polarization affects the degree of neuroinflammation. It has been reported that the inhibition of soluble epoxide hydrolase (sEH) activity protects brain tissue. However, the anti-inflammatory and antioxidative effects of sEH inhibition in the ischemic brain are not fully understood. This study aimed to investigate the effects of a selective sEH inhibitor, 12-(3-adamantan-1-yl-ureido)-dodecanoic acid (AUDA), after ischemic stroke.Methods: Adult male rats with middle cerebral artery occlusion (MCAO) were administered with AUDA or a vehicle. Behavioral outcome, infarct volume, microglia polarization, and gene expression were assessed.Results: Rats treated with AUDA showed better behavioral outcomes and smaller infarct volumes after MCAO. After AUDA treatment, a reduction of M1 microglia and an increase of M2 microglia occurred at the ischemic cortex of rats. Additionally, there was an increase in the mRNA expressions of antioxidant enzymes and anti-inflammatory interleukin-10, and pro-inflammatory mediators were decreased after AUDA administration. Heme oxygenase-1 was mainly expressed by neurons, and AUDA was found to improve the survival of neurons.Conclusion: The results of this study provided novel and significant insights into how AUDA can improve outcomes and modulate inflammation and oxidative stress after ischemic stroke.Keywords: ischemic stroke, microglia polarization, middle cerebral artery occlusion, soluble epoxide hydrolase, anti-inflammation, antioxidant

Background/Aim: Middle cerebral artery occlusion (MCAO) in rodents is an essential animal model for research focusing on ischemic stroke. To date, several kinds of surgical methods for MCAO have been developed and the craniotomy method has the advantage of direct visualization of the middle cerebral artery (MCA). MCAO at a more proximal site produces better surgical results, but it is a more invasive technique. The aim of this study was to evolve the surgical technique for simulating ischemic cerebral cortex injury in rats. Materials and Methods: To approach proximal MCA with a less invasive procedure, a modified surgical technique for MCAO in rats was developed. Besides, rats receiving the modified and conventional method were compared with regard to infarct volume and by behavioral tests. Results: Following craniotomy, we proposed that the inferior edge of the craniotomy should be enlarged with fine forceps. This modified surgical method induces larger infarct volume, significant behavioral impairment and can induce ischemic stroke. Additionally, it does not significantly increase the operation time, and has produced no obvious complications. Conclusion: This modified surgical technique may serve as a practical method for performing MCAO.

Introduction The introduction of universal health insurance coverage aims to provide equal accessibility and affordability of health care, but whether such a policy eliminates health inequalities has not been conclusively determined. This research aims to examine the healthcare outcomes of oral cancer and determine whether the universal coverage system in Taiwan has reduced health inequality. Methods Linking the databases of the National Cancer Registry with the National Mortality Registry in Taiwan, we stratified patients with oral squamous cell carcinoma by gender and income to estimate the incidence rate, cumulative incidence rate aged from 20 to 79 (CIR20-79), life expectancy, and expected years of life lost (EYLL). The difficulties with asymmetries and short follow-up periods were resolved through applying survival analysis extrapolation methods. Results While all people showed a general improvement in life expectancy after the introduction of the NHI, the estimated change in EYLL's of the high-, middle-, and low-income female patients were found to have +0.3, -0.5 and -7 years of EYLL, respectively, indicating a reduction in health inequality. Improvements for the male patients were unremarkable. There was no drop in the CIR20-79 of oral cancer in disadvantaged groups as in those with higher incomes. Conclusions Universal coverage alone may not reduce health inequality across different income groups for oral cancer unless effective preventive measures are implemented for economically disadvantaged regions.

Pompe disease is a rare inherited metabolic disorder of glycogen metabolism caused by mutations in the GAA gene, encoding the acid α-1,4 glucosidase. Successful diagnosis of Pompe disease is achieved by clinical and biochemical evaluation followed by confirmation with DNA testing. Here, we report a male infant with a prenatal onset of cardiac symptoms and enzyme testing consistent with Pompe disease, but DNA testing by Sanger sequencing revealed no pathogenic variants. Due to the strong indication from clinical, enzymatic, and histological studies (despite the absence of molecular confirmation by traditional Sanger sequencing), enzyme replacement therapy (ERT) for Pompe disease was initiated. Reanalysis of the patient's DNA sample using next generation sequencing (NGS) of a panel of target genes causing glycogen storage disorders demonstrated compound heterozygosity for a point mutation and an exonic deletion in the GAA gene. This case illustrates the value of astute clinical judgement in patient management as well as the power of target capture deep NGS in the simultaneous detection of both a point mutation and a heterozygous exonic deletion by correcting pitfalls of the traditional PCR based sequencing, namely; allele dropout and the inability to detect exonic deletions.