Hybrid Vibration and UV Fluorescence Technology for Rapid Imaging and Guidance for Manual Removal of Fish Bones from Fish Floss.

The objective of the proposed human-machine cooperation (HMC) workstation is to both rapidly detect calcium-based fish bones in masses of minced fish floss and visually guide operators in approaching and removing the detected fish bones by hand based on the detection of fingernails or plastic-based gloves. Because vibration is a separation mechanism that can prevent absorption or scattering in thick fish floss for UV fluorescence detection, the design of the HMC workstation included a vibration unit together with an optical box and display screens. The system was tested with commonly used fish (swordfish, salmon, tuna, and cod) representing various cooking conditions (raw meat, steam-cooked meat, and fish floss), their bones, and contaminating materials such as derived from gloves made of various types of plastic (polyvinylchloride, emulsion, and rubber) commonly used in the removal of fish bones. These aspects were each investigated using the spectrum analyzer and the optical box to obtain and analyze the fluorescence spectra and images. The filter was mounted on a charge-coupled device, and its transmission-wavelength window was based on the characteristic band for fish bones observed in the spectra. Gray-level AI algorithm was utilized to generate white marker rectangles. The vibration unit supports two mechanisms of air and downstream separation to improve the imaging screening of fish bones inside the considerable flow of fish floss. Notably, under 310 nm ultraviolet B (UVB) excitation, the fluorescence peaks of the raw fillets, steam-cooked meat, and fish floss were observed at for bands at longer wavelengths (500-600 nm), whereas those of the calcium and plastic materials occurred in shorter wavelength bands (400-500 nm). Perfect accuracy of 100% was achieved with the detection of 20 fish bones in 2 kg of fish floss, and the long test time of around 10-12 min results from the manual removal of these fish bones.

Triglyceride is a Good Biomarker of Increased Injury Severity on a High Fat Diet Rat After Traumatic Brain Injury.

Injury severity is correlated with poor prognosis after traumatic brain injury (TBI). It is not known whether triglycerides (TGs) or total cholesterol (TC) is good biomarker of increased injury of neuroinflammation and apoptosis in a high fat diet (HFD)-treated rat after TBI episodes. Five-week-old male Sprague-Dawley (SD) rats were fed a HFD for 8 weeks. The anesthetized male SD rats were divided into three sub-groups: sham-operated and TBI with 1.6 atm or with 2.4 atm fluid percussion injury (FPI). Cell infarction volume (triphenyltetrazolium chloride stain), tumor necrosis factor-alpha (TNF-α) expression in the microglia (OX42 marker) and astrocytes (Glial fibrillary acidic protein marker), TNF-α receptor expression in the neurons (TNFR1 and TNFR2 markers), and the extent of neuronal apoptosis (TUNEL marker) were evaluated by immunofluorescence, and the functional outcome was assessed by an inclined plane test. These tests were performed 72 h after TBI. Serum triglyceride and cholesterol levels were measured at 24, 48 and 72 h after TBI. The FPI with 2.4 atm significantly increased body weight loss, infarction volume, neuronal apoptosis and TNF-α expression in the microglia and astrocytes, and it decreased the maximum grasp degree and TNFR1 and TNFR2 expression in neurons at the 3rd day following TBI. The serum TG level was positively correlated with FPI force, infarction volume, Neu-N-TUNEL, GFAP-TNFα, and OX42-TNFα Simultaneously; the serum TG level was negatively correlated with Neu-N-TNFR1 and Neu-N-TNFR2. TG is a good biomarker of increased injury for neuroinflammation and apoptosis at the 3rd day after TBI in HFD rats.

Effects of a High-Fat Diet on Neuroinflammation and Apoptosis in Acute Stage After Moderate Traumatic Brain Injury in Rats.

BACKGROUND: A high-fat diet (HFD) is correlated with a higher risk of metabolic syndrome. The effect of HFD on neuroinflammation and apoptosis in acute stage after traumatic brain injury (TBI) in rats is not well known. MATERIALS AND METHODS: Five-week-old male Sprague-Dawley (SD) rats were fed a HFD or normal diet (ND) for 8 weeks. Anesthetized male SD rats were divided into two subgroups: sham-operated and TBI. Motor function was measured using an inclined plane. The numbers of apoptotic neurons (markers Neu-N, TUNEL, caspase-3), activated astrocytes (marker GFAP) and microglia (marker OX42), and TNF-α expression in microglia and astrocytes in the ischemic cortex were investigated using an immunofluorescence assay. All of the parameters were measured on the 3rd day after TBI. RESULTS: Rats fed a HFD for 8 weeks had higher body weight, serum cholesterol, and triglycerides. TBI-induced motor deficits, neuronal decrease, neuronal apoptosis, astrocyte and microglia activation, and TNF-α expression in microglia and astrocytes in the ischemia cortex were significantly increased in ND and HFD rats compared to sham rats. However, these parameters were not significantly different between the ND and HFD TBI groups, except motor deficit. CONCLUSIONS: HFD has no significant effects on neuronal apoptosis or neuroinflammation in acute stage compared with ND for 8 weeks after moderate TBI in experimental rats.

The Neuroprotective Effects of Simvastatin on High Cholesterol Following Traumatic Brain Injury in Rats.

BACKGROUND: High cholesterol has been correlated with a greater risk of cerebrovascular diseases. Whether pre-existing high cholesterol exacerbates traumatic brain injury (TBI), and whether treatment with the cholesterol-lowering agent simvastatin has neuroprotective effects, especially anti-neuroinflammatory effects, after TBI are not well investigated. METHODS: Five-week-old male Sprague-Dawley rats were fed a high-fat diet for 8 weeks to induce hypercholesterolemia. Anesthetized male Sprague-Dawley rats were divided into 5 groups, including the sham-operated control, TBI control, and TBI with simvastatin treatment (4 mg/kg, 10 mg/kg, or 20 mg/kg) groups. Simvastatin was intraperitoneally injected at 0, 24, and 48 hours after TBI. Motor function was measured using an inclined plane. Neuronal apoptosis (maker Neu-N, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling), tumor necrosis factor-α expression in microglia (marker OX42) and astrocytes (marker glial fibrillary acidic protein), and Tumor necrosis factor-alpha receptor (TNFR) 1 and TNFR2 expression in neurons in the ischemic cortex were investigated using an immunofluorescence assay. All of the parameters were measured on the third day after TBI. RESULTS: TBI significantly increased the serum levels of cholesterol. The TBI-induced motor deficit was significantly attenuated by 4, 10, and 20 mg/kg simvastatin therapy on the third day after TBI. TBI-induced neuronal TNFR1 activation and apoptosis, as well as tumor necrosis factor-α expression in astrocytes in the ischemic cortex, were significantly attenuated by simvastatin, particularly when 20 mg/kg was administered. Simultaneously, the serum cholesterol remained high despite simvastatin treatment. CONCLUSIONS: The neuroprotection effects of simvastatin on the pre-existing hypercholesterolemia during TBI in rats may be related to its anti-neuroinflammatory effects but not to its cholesterol-lowing effects.

Simvastatin Therapy in the Acute Stage of Traumatic Brain Injury Attenuates Brain Trauma-Induced Depression-Like Behavior in Rats by Reducing Neuroinflammation in the Hippocampus.

BACKGROUND: The antidepressant-like effects of simvastatin on traumatic brain injury (TBI) remain unclear. The present study aimed to investigate the neuroprotective effects of simvastatin and determine whether simvastatin attenuates TBI-induced depression-like behavior and, more specifically, acts as an antineuroinflammatory. METHODS: Anesthetized male Sprague-Dawley rats were divided into five groups: sham-operated controls, TBI controls, and TBI treatment with simvastatin 4, 10, or 20 mg/kg. Simvastatin was intraperitoneally injected 0, 24, and 48 h after TBI. The motor function was measured using an inclined plane, and depression-like behavior was evaluated using forced swimming tests. Neuronal apoptosis (markers: NeuN, TUNEL, caspase-3), microglia (marker: OX42) and astrocyte (marker: GFAP) activation, and TNF-α expression in the microglia and astrocytes of the hippocampal CA3 area were investigated using immunofluorescence assay. All parameters were measured on the 4th, 8th, and 15th day, or only on the 15th day after TBI. RESULTS: TBI-induced depression-like behavior, which increased duration of immobility, was significantly attenuated by 20 mg simvastatin therapy on day 15 after TBI. TBI-induced neuronal apoptosis, microglia and astrocyte activation, and TNF-α expression in the microglia and astrocytes of the CA3 area of the hippocampus were significantly reduced by simvastatin treatment, particularly when 20 mg/kg was administered for 3 days. CONCLUSIONS: Intraperitoneal injection of simvastatin attenuated TBI in rats during the acute stage by reducing neuronal apoptosis, microglia, and TNF-α expression, thereby resulting in a reduction of depressive-like behavior. Our results suggest that simvastatin may be a promising treatment for TBI-induced depression-like behavior.

Increased risk of new-onset depression in patients with traumatic brain injury and hyperlipidemia: the important role of statin medications.

OBJECTIVE: Depression is a common complication after traumatic brain injury (TBI). This study aimed to evaluate the risk of hyperlipidemia for new-onset depression after TBI and the role of statin medications using a longitudinal population database. METHOD: A matched longitudinal cohort study of 3,792 subjects (1,264 TBI patients [ICD-9-CM code: 801-804 and 850-854] with preexisting hyperlipidemia [ICD-9-CM code: 272.0, 272.1, 272.2, 272.4] and 2,528 age- and sex-matched TBI patients without hyperlipidemia) was conducted using the Taiwan Longitudinal Health Insurance Database from January 2001 to December 2008. The incidence and hazard ratios (HRs) for the development of new-onset depression (ICD-9-CM code: 296.2X-296.3X, 300.4, and 311.X) after TBI were compared between the 2 groups. RESULTS: The incidence rate of depression in TBI with preexisting hyperlipidemia was 136.61 per 10,000 person-years. TBI patients with preexisting hyperlipidemia had a 1.72-fold increased incidence rate ratio compared with those without hyperlipidemia (P = .0056). A Cox model showed hyperlipidemia to be an independent predictor of depression (HR = 1.61; 95% CI, 1.03-2.53). TBI patients with hyperlipidemia who were not treated with statins experienced a 1.95-fold incidence risk ratio (P = .0017) and higher risk of new-onset depression (HR = 1.61; 95% CI, 1.03-2.53) compared to TBI patients without hyperlipidemia. CONCLUSIONS: Preexisting hyperlipidemia could be an independent predictor of new-onset depression in TBI patients, and TBI patients with preexisting hyperlipidemia who were not treated with statins presented a higher risk of new-onset depression than TBI patients without hyperlipidemia. Our findings may provide some insight into the important role of statin medications in the development of new-onset depression in patients with traumatic brain injury.

One-Year Mortality after Traumatic Brain Injury in Liver Cirrhosis Patients--A Ten-Year Population-Based Study.

This study investigated the 1-year mortality of patients who underwent brain surgery following traumatic brain injury (TBI) who also had alcoholic and/or nonalcoholic liver cirrhosis (LC) using a nationwide database in Taiwan. A longitudinal cohort study matched by propensity score with age, gender, length of ICU stay, HTN, DM, MI, stroke, HF, renal diseases, and year of TBI diagnosis in TBI patients with alcoholic and/or nonalcoholic LC and TBI patients without LC was conducted using the National Health Insurance Research Database in Taiwan between January 1997 and December 2007. The main outcome studied was 1-year mortality. In total, 7296 subjects (2432 TBI patients with LC and 4864 TBI patients without LC) were enrolled in this study. The main findings were (1) TBI patients with LC had a higher 1-year mortality (52.18% vs 30.61%) and a 1.75-fold increased risk of mortality (95% CI 1.61-1.90) compared with non-LC TBI patients, (2) renal diseases and HF are risk factors, but hypertension could be a protective factor in cirrhotic TBI patients, and (3) TBI patients with non-alcoholic LC and the coexistence of alcoholic and nonalcoholic LC had higher 1-year mortality compared with TBI patients with alcoholic cirrhosis. This study showed that patients with LC who have undergone brain surgery might have higher risk of 1-year mortality than those without LC. In addition, nonalcoholic and the coexistence of alcoholic and nonalcoholic LC show higher 1-year mortality risk than alcoholic in TBI patients with LC, especially in those with comorbidities of hypertension, diabetes mellitus, and stroke.

Pre-existing hyperlipidaemia increased the risk of new-onset anxiety disorders after traumatic brain injury: a 14-year population-based study.

OBJECTIVES: Anxiety disorders (ADs) are common after traumatic brain injury (TBI). However, the risk factors of new-onset ADs remain unclear. This study was aimed at evaluating the incidence and risk factors for new-onset ADs, including pre-existing hyperlipidaemia and three major comorbidities (diabetes mellitus, hypertension and cardiovascular disease), in patients with TBI. SETTING: A matched cohort study was conducted using the Taiwan Longitudinal Health Insurance Database between January 1997 and December 2010. PARTICIPANTS: A total of 3822 participants (1274 patients with TBI with hyperlipidaemia and 2548 age-matched and gender-matched patients with TBI without hyperlipidaemia). OUTCOME MEASURES: The incidence and HRs for the development of new-onset ADs after TBI were compared between the two groups. RESULTS: The overall incidence rate of new-onset ADs for patients with TBI with hyperlipidaemia is 142.03/10 000 person-years (PYs). Patients with TBI with hyperlipidaemia have a 1.60-fold incidence rate ratio (p<0.0001) and increased HR of ADs (1.58, 95% CI 1.24 to 2.02) compared with those without hyperlipidaemia. The incidence rates of ADs for males and females with hyperlipidaemia, respectively, were 142.12 and 292.32/10 000 PYs, which were higher than those without hyperlipidaemia (93.03 and 171.68/10 000 PYs, respectively). Stratified by age group, hyperlipidaemia is a risk factor of ADs for patients with TBI aged 65 years or younger. CONCLUSIONS: Pre-existing hyperlipidaemia is an independent predictor of new-onset ADs in patients with TBI, even when controlling for other demographic and clinical variables. Female patients with pre-existing hyperlipidaemia had significantly higher risk of new-onset ADs than males, especially between the ages of 35 and 65 years.

Misdiagnosis of spontaneous cervical epidural haemorrhage.

Spontaneous spinal epidural haemorrhage is a rare condition. The initial clinical manifestations are variable. Nonetheless, most spinal cord lesions result in paraparesis or quadriparesis, but not hemi-paresis, if motor function is involved. We report on a 69-year-old man who presented initially with right-side limb weakness. He was initially misdiagnosed at emergency room with a cerebral stroke and treated inappropriately with heparin. One day after admission, correct diagnosis of acute spinal epidural haematoma was based on the repeated neurological examination and cervical magnetic resonance imaging study. The patient underwent emergency surgical decompression and hematoma removal. The pathogenesis of the haematoma could have been due to hypertension, increased abdominal pressure and anticoagulant therapy. We emphasize that patients with hemi-paresis on initial presentation could have an acute spinal epidural haemorrhage. We also draw the misdiagnosis to the attention of the reader because early recognition of spontaneous spinal epidural haematoma is very important for prompt and appropriate treatment to improve the overall prognosis.

Virtual bronchoscopy for diagnosis of recurrent respiratory papillomatosis.

Virtual bronchoscopy is a new method for viewing helical/spiral computed tomography (CT) images of the tracheobronchial trees. Using commercially available software to process the CT data, the tracheobronchial trees can be inspected through a series of three-dimensional images. Recently, this technique has been increasingly used to detect benign and malignant airway stenosis. We report the findings of virtual bronchoscopy in a 41-year-old man with recurrent respiratory papillomatosis (RRP). Several tiny nodules were evident in the lower trachea. Fiberoptic bronchoscopy was performed 1 month later during a planned surgery for laryngeal papillomas, and the findings were in agreement with virtual bronchoscopy. Detection of intrabronchial spreading in RRP is important since peripheral seeding of RRP can cause complications, including recurrent pneumonia, obstructive atelectasis, hemoptysis, and, rarely, may degenerate to squamous cell carcinoma. Virtual bronchoscopy is an alternative method for inspecting the tracheobronchial trees in patients with RRP when laryngeal papillomas impede fiberoptic bronchoscopy.