Treatment with chlorous acid to inhibit spores of Alicyclobacillus acidoterrestris in aqueous suspension and on apples.

AIM: To test the efficacy of a chemical (chlorous acid) for reducing the numbers of viable Alicyclobacillus acidoterrestris spores in laboratory media and on apples. METHODS AND RESULTS: Alicyclobacillus acidoterrestris spores in aqueous suspension and on apple surfaces of four different cultivars were treated with 268 ppm chlorous acid. Treatment with 268 ppm chlorous acid sharply reduced the numbers of spores of A. acidoterrestris in laboratory media by 1.6, 4.3, and 7.0 log(10) reductions for 5, 10, and 15 min treatments, respectively. Chlorous acid also effectively reduced the spore load on apple surfaces. Alicyclobacillus acidoterrestris spore counts were significantly reduced by about 5 log(10) after 10 min treatment on four different apple cultivars ('Red Delicious', 'Golden Delicious',' Gala', and 'Fuji'). There was no synergistic effect on spore reduction when chlorous acid treatment was combined with heat. CONCLUSIONS: These results show that chlorous acid is highly efficacious against A. acidoterrestris spores on apple surfaces. SIGNIFICANCE AND IMPACT OF THE STUDY: Chlorous acid can be used as an alternative sanitizer of chlorine to control a major A. acidoterrestris contamination source in juice processing plants.

Protective effect of green tea extract on ischemia/reperfusion-induced brain injury in Mongolian gerbils.

Free radical-induced oxidative damages of macromolecules and cell death are important factors in the pathogenesis of ischemia/reperfusion brain injury. In the present study, an investigation as to whether green tea extract reduces ischemia/reperfusion-induced brain injury in Mongolian gerbils was conducted. The effect of green tea on the ischemia/reperfusion-induced production of hydrogen peroxide, lipid peroxidation and oxidative DNA damage (formation of 8-hydroxydeoxyguanosine), and cell death in addition to locomotor activity was studied. Two doses (0.5 or 2%) of green tea extract were added into the drinking water and to be accessed by animals ad libitum for 3 weeks prior to the induction of ischemia. A global ischemia was induced by the bilateral occlusion of the common carotid arteries for 5 min. Reperfusion was achieved by releasing the occlusion and restoring blood circulation for 48 h. The infarction volumes were 112+/-31 mm(3) and 76+/-11 mm(3) in the 0.5 and 2% green tea pretreated animals compared to 189+/-12 mm(3) in the ischemia/reperfusion animals. Green tea extract also reduced the levels of ischemia/reperfusion-induced hydrogen peroxide (from 1470+/-170 to 1034+/-46 and 555+/-30 nmole/mg protein), lipid peroxidation products (from 1410+/-210 to 930+/-40 and 330+/-20 nmole/mg protein) and 8-oxodG (from 3.9+/-0.1 to 2.8+/-0.3 and1.9+/-0.3 ng/microg DNA, x10(-2)) by pretreatment of 0.5 or 2% green tea for 3 weeks, respectively. Moreover, green tea also reduced the number of ischemia/reperfusion-induced apoptotic cells (from 59+/-12 to 37+/-8, 15+/-11 apoptotic cells/high power field in the striatum region) and locomotor activity (from 15140+/-2940 to 3900+/-600 and 4100+/-1200). This study therefore suggests that green tea may be a useful agent for the prevention of cerebral ischemia damage.

Involvement of cortical damage in the ischemia/reperfusion-induced memory impairment of Wistar rats.

The effect of ischemia/reperfusion-induced neuronal damage on the memory impairment were investigated using active avoidance and Morris water maze tasks in Wistar rats. Focal ischemia was induced by 1 h occlusion of the right middle cerebral artery (MCA) of Wistar male rats. Reperfusion was induced by releasing the occlusion and restoring the blood circulation for 24 h. The acquisition and preservation memory tested by active avoidance showed a significant difference between the sham and ischemia/reperfusion group. The water maze acquisition performance was also significant difference between sham and ischemia/reperfusion groups in both latency and moving distance. The infarction volume was increased by the ischemia/reperfusion. Furthermore, the cresyl violet staining of the ischemia/reperfusion brain showed severe neuronal damage (pyramidal cell loss) in the cortex in addition to the striatum lesion of brain. This study shows that pyramidal cell damage in the cortex lesion may be partially related to memorial disturbance in the ischemia/reperfusion brain injury.

Neuroprotective effect of green tea extract in experimental ischemia-reperfusion brain injury.

Eicosanoids accumulation and formation of oxygen free radicals have been implicated in the pathogenesis of ischemia/reperfusion brain injury. In the present study, we examined whether green tea extract protects against ischemia/reperfusion-induced brain injury by minimizing eicosanoid accumulation and oxygen radical-induced oxidative damage in the brain. Green tea extract (0.5%) was orally administered to Wistar rats for 3 weeks before induction of ischemia. Ischemia was induced by the occlusion of middle cerebral arteries for 60 min and reperfusion was achieved for 24 h. Infarction volume in the ipsilateral hemisphere of ischemia/reperfusion animals was 114 +/- 16 mm(3) in the 0.5% green tea pretreated animals compared to 180 +/- 54 mm(3) in left hemisphere of nontreated animals. Green tea extract (0.5%) also reduced ischemia/reperfusion-induced eicosanoid concentration: Leukotriene C(4) (from 245 +/- 51 to186 +/- 22), prostoglandin E(2) (from 306 +/- 71 to 212 +/- 43) and thromboxane A(2) (327 +/- 69 to 251 +/- 87 ng/mg protein). Ischemia/reperfusion-induced increases of hydrogen peroxide level (from 688 +/- 76 to 501 +/- 99 nmole/mg protein), lipid peroxidation products (from 1010 +/- 110 to 820 +/- 70 nmole/mg protein) and 8-oxodG formation (from 1.3 +/- 0.3 to 0.8 +/- 0.2 ng/microg DNA, x10(-2)) were also reduced. Moreover, 0.5% green tea extract also reduced the apoptotic cell number (from 44 +/- 11 to 29 +/- 1 in the striatum, and from 72 +/- 11 to 42 +/- 5 apoptotic cells/high power field in the cortex region). Green tea extract pretreatment also promoted recovery from the ischemia/reperfusion-induced inhibition of active avoidance. The present study shows that the minimizing effect of green tea extract on the eicosanoid accumulation and oxidative damage in addition to the reduction of neuronal cell death could eventually result in protective effect on the ischemia/reperfusion-induced brain injury and behavior deficit.

A case of rectal cancer with sternal metastasis as initial presentation.

Colorectal cancer with bone metastasis as initial manifestation is a very rare event. We have reported a case of rectal cancer presenting with sternal metastasis. A 30 year-old man was evaluated due to pain in the sternal area with a bulging mass. History and physical examination did not suggest any specific disease. A radionuclide bone scan revealed increased uptake in the sternal area, right 6th rib, and sacrum. Microscopic examination of a biopsy specimen from the sternum showed metastatic adenocarcinoma. A barium enema and CT scan of the pelvis suggested carcinoma of the upper rectum. Adenocarcinoma of the rectosigmoid junction area was demonstrated by colonoscopic examination with biopsy. He received palliative transverse colostomy for obstruction without further treatment.