Differentials and trends in emergency department visits due to alcohol intoxication and co-occurring conditions among students in a U.S. public university.

BACKGROUND: Few studies have explored the epidemiology of students presenting to the emergency department (ED) as a consequence of hazardous drinking. This study examined differentials and trends in ED visits following alcohol intoxication and co-occurring conditions among students presenting to a major U.S. university health system. METHODS: The ED electronic medical records from academic years 2010-2015 were queried for student visits and their records were linked to the university's student admission datasets. Student alcohol-related visits were identified based on ICD-9 codes. Student characteristics and trends in the rate of alcohol intoxication per 100 ED student visits were analyzed. A random sample of 600 student clinical records were reviewed to validate diagnostic codes. RESULTS: There were 9616 student ED visits (48% males) to the ED of which 1001 (10.4%) visits involved alcohol intoxication. Two thirds of ED visits with alcohol intoxication had a co-occurring diagnosis, with injuries (24%) being the most common condition. The rate of alcohol intoxication varied greatly by student demographics and campus-related factors. There was a linear increase in the rate of alcohol intoxication from 7.9% in 2009-10 to 12.3% in 2014-15 (p<0.01). The increase was greater among female students, students below 20 years of age, Asian students, and student athletes. In the sample reviewed, only two thirds of ED visits with alcohol intoxication were recorded by diagnostic codes. CONCLUSION: The rate of ED visits following alcohol intoxication varied by student demographic characteristics and campus-related factors with a rising trend over the study period.

Direct Bonding of Chitosan Biomaterials to Tissues Using Transglutaminase for Surgical Repair or Device Implantation.

Natural biomaterials, such as chitosan and collagen, are useful for biomedical applications because they are biocompatible, mechanically robust, and biodegradable, but it is difficult to rapidly and tightly bond them to living tissues. In this study, we demonstrate that the microbial transglutaminase (mTG), can be used to rapidly (<5 min) bond chitosan and collagen biomaterials to the surfaces of hepatic, cardiac, and dermal tissues, as well as to functionalized polydimethylsiloxane (PDMS) materials that are used in medical products. The mTG-bonded chitosan patches effectively sealed intestinal perforations, and a newly developed two-component mTG-bonded chitosan spray effectively repaired ruptures in a breathing lung when tested ex vivo. The mechanical strength of mTG-catalyzed chitosan adhesive bonds were comparable to those generated by commonly used surgical glues. These results suggest that mTG preparations may be broadly employed to bond various types of organic materials, including polysaccharides, proteins, and functionalized inorganic polymers to living tissues, which may open new avenues for biomedical engineering, medical device integration, and tissue repair.

Atorvastatin reduces functional deficits caused by photodynamic therapy in rats.

Clinical studies have indicated that photodynamic therapy (PDT) significantly prolonged the median survival of patients with gliomas. Experimental studies demonstrate that increasing optical energy and photosensitizer dose leads to increased volume of tumor necrosis. However, increasing the light dose delivered to the tumor may increase the risks of inducing permanent neurological deficits. In the current study, we sought to test the behavioral deficits induced in normal rats by brain PDT and the neurorestorative effects of atorvastatin on PDT-induced behavioral deficits. Considering its potential as a combination treatment of brain tumors, we investigated both in vitro and in vivo whether atorvastatin treatment promotes brain tumor growth. Non-tumored Fischer rats received PDT (n=18). Nine of the PDT-treated animals were treated with atorvastatin. Control animals underwent the same surgical procedure, but did not receive Photofrin and laser light. PDT-treated animals had significant behavioral deficits on days 2, 5, 7, 9 and 14 after PDT, compared with surgery controls. PDT-treated animals receiving atorvastatin displayed significantly ameliorated behavioral deficits on days 7, 9 and 14 after PDT, compared to PDT-treated rats. In vitro tumor cell viability and growth were evaluated. Atorvastatin did not affect the growth of glioma cells. Fischer rats with intracranial 7-day-old 9L glioma tumor cell implantation were randomly subjected to no treatment, PDT alone, atorvastatin alone, or combined treatment with atorvastatin and PDT (6 rats/group). Our data indicate that atorvastatin did not promote tumor growth in either PDT treated and non-treated rats. However, atorvastatin significantly reduced the cell damage caused by PDT. To further test the mechanisms underlying the atorvastatin-mediated reduction of functional deficits, we investigated the effects of atorvastatin on angiogenesis and synaptogenesis. Our data demonstrate that atorvastatin significantly induced angiogenesis and synaptogenesis in the PDT-damaged brain tissue. Our data indicate that PDT induces functional deficits. Atorvastatin treatment promotes functional restoration after PDT, but does not promote glioma growth in vitro and in vivo. Atorvastatin reduces astrocyte and endothelial cell damage caused by PDT and induces angiogenesis and synaptogenesis after PDT. Thus consideration and further testing of the combination of atorvastatin and PDT for the treatment of glioma is warranted.

Vascular recovery promoted by atorvastatin and simvastatin after experimental intracerebral hemorrhage: magnetic resonance imaging and histological study.

OBJECT: Longitudinal multiparametric MR imaging and histological studies were performed on simvastatin- or atorvastatin-treated rats to evaluate vascular repair mechanisms after experimental intracerebral hemorrhage (ICH). METHODS: Primary ICH was induced in adult Wistar rats by direct infusion of 100 µl of autologous blood into the striatal region adjacent to the subventricular zone. Atorvastatin (2 mg/kg), simvastatin (2 mg/kg), or phosphate-buffered saline was given orally at 24 hours post-ICH and continued daily for 7 days. The temporal evolution of ICH in each group was assessed by MR imaging measurements of T2, T1(sat), and cerebral blood flow in brain areas corresponding to the bulk of the hemorrhage (core) and edematous border (rim). Rats were killed after the final MR imaging examination at 28 days, and histological studies were performed. A small group of sham-operated animals was also studied. Neurobehavioral testing was performed in all animals. Analysis of variance methods were used to compare results from the treatment and control groups, with significance inferred at p ≤ 0.05. RESULTS: Using histological indices, animals treated with simvastatin and atorvastatin had significantly increased angiogenesis and synaptogenesis in the hematoma rim compared with the control group (p ≤ 0.05). The statin-treated animals exhibited significantly increased cerebral blood flow in the hematoma rim at 4 weeks, while blood-brain barrier permeability (T1(sat)) and edema (T2) in the corresponding regions were reduced. Both statin-treated groups showed significant neurological improvement from 2 weeks post-ICH onward. CONCLUSIONS: The results of the present study demonstrate that simvastatin and atorvastatin significantly improve the recovery of rats from ICH, possibly via angiogenesis and synaptic plasticity. In addition, in vivo multiparametric MR imaging measurements over time can be effectively applied to the experimental ICH model for longitudinal assessment of the therapeutic intervention.

Improvement in recovery after experimental intracerebral hemorrhage using a selective cathepsin B and L inhibitor.

OBJECT: This study investigates a potential novel application of a selective cathepsin B and L inhibitor in experimental intracerebral hemorrhage (ICH) in rats. METHODS: Forty adult male Wistar rats received an ICH by stereotactic injection of 100 µl of autologous blood or sham via needle insertion into the right striatum. The rats were treated with a selective cathepsin B and L inhibitor (CP-1) or 1% dimethyl sulfoxide sterile saline intravenously at 2 and 4 hours after injury. Modified neurological severity scores were obtained and corner turn tests were performed at 1, 4, 7, and 14 days after ICH. The rats were sacrificed at 3 and 14 days after ICH for immunohistological analysis of tissue loss, neurogenesis, angiogenesis, and apoptosis. RESULTS: The animals treated with CP-1 demonstrated significantly reduced apoptosis as well as tissue loss compared with controls (p < 0.05 for each). Neurological function as assessed by modified neurological severity score and corner turn tests showed improvement after CP-1 treatment at 7 and 14 days (p < 0.05). Angiogenesis and neurogenesis parameters demonstrated improvement after CP-1 treatment compared with controls (p < 0.05) at 14 days. CONCLUSIONS: This study is the first report of treatment of ICH with a selective cathepsin B and L inhibitor. Cathepsin B and L inhibition has been shown to be beneficial after cerebral ischemia, likely because of its upstream regulation of the other prominent cysteine proteases, calpains, and caspases. While ICH may not induce a major component of ischemia, the cellular stress in the border zone may activate these proteolytic pathways. The observation that cathepsin B and L blockade is efficacious in this model is provocative for further investigation.