Biomedical subjects

K Takeuchi

Publications and source records attributed to K Takeuchi.

At least 163 records · Page 9Linked to original sources

PubMed2001

Prediction of functional recovery in patients with myocardial infarction after revascularization--comparison of low-dose dobutamine stress echocardiography with fluorine-18 fluorodeoxyglucose positron emission tomography.

The present study investigated the agreement between low-dose dobutamine stress echocardiography (LDDSE) and fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET) and compared each technique's ability to detect myocardial viability and predict functional recovery in 30 patients. All patients underwent revascularization, followed by echocardiography 5+/-3 months. Of the 390 segments analyzed by echocardiography before revascularization, 110 (28%) had abnormal wall motion. LDDSE showed viability in 66 sites of the 110 dyssynergic segments and 58 of these viable segments recovered their wall motion. With FDG-PET, 78 of the 110 dyssynergic segments were diagnosed as viable and 62 of these showed improvement of the wall motion. The sensitivities for LDDSE and FDG-PET to assess functional recovery were 84% and 90%, respectively; specificities were 80% and 64%, respectively. Positive predictive values for LDDSE and FDG-PET were 88% and 79%; negative predictive values were 75% and 78%, respectively. Both methods had good sensitivity for detecting improvement in regional function after revascularization, but LDDSE had a higher specificity for detecting viability and a better positive predictive value for left ventricular functional recovery.

Aged↗

PubMed2001

Relationship between doppler-derived left ventricular diastolic function and exercise capacity in patients with myocardial infarction.

Doppler echocardiographic indices of left ventricular (LV) diastolic function are widely used to evaluate the cardiac function of patients with cardiac disease. However, there have been few reports about the relationship between Doppler indices and exercise capacity and so 44 patients with myocardial infarction were investigated by cardiopulmonary exercise testing and 2-D and Doppler echocardiography. Diastolic performance was assessed using Doppler transmitral flow velocity and pulmonary venous flow velocity. The ratio of peak E wave velocity and peak A wave velocity (E/A) correlated with peak oxygen consumption (peak Vo2) (R=0.72), and there was a negative correlation between the deceleration time of E velocity (Dct) and peak Vo2 or anaerobic threshold (AT) (R=-0.65, -0.62, respectively). The ratio of peak S wave velocity and peak D wave velocity (S/D) negatively correlated with peak Vo2 (R=-0.58). Left ventricular ejection fraction did not correlate to exercise capacity. These results suggest that the Doppler echocardiographic indices of LV diastolic function correlate with exercise capacity in patients with mild cardiac dysfunction.

Aged↗

PubMed2001

Effects of smoking on myocardial injury in patients with conservatively treated acute myocardial infarction: a study with resting 123I-15-iodophenyl 3-methyl pentadecanoic acid/201Tl myocardial single photon emission computed tomography.

Many reports have demonstrated that smokers who have suffered an acute myocardial infarction (AMI) have a better prognosis than nonsmokers. The present study investigated the effects of current smoking on myocardial injury with resting 123I-15-iodophenyl 3-methyl pentadecanoic acid (BMIPP)/201Tl myocardial single photon emission computed tomography in 103 patients with conservatively treated AMI. The left ventricular myocardium was divided into 9 segments and BMIPP and 201Tl defects were scored using a 5-point grading system (0 = normal and 4 = no uptake). The sum of the defect scores was defined as the total defect score. There was no significant difference in either the baseline severity of the coronary artery disease or the total defect scores for BMIPP and 201Tl between the current smoker and nonsmoker groups. The difference between the total defect scores for BMIPP and 201Tl tended to be larger in the current smoker group than in the nonsmoker group (2.0 +/- 1.9 vs 1.3 +/- 1.6, p = 0.056). Forty-one (53%) of 77 patients in the current smoker group exhibited a BMIPP/201Tl mismatch, whereas only 8 (31%) of 26 patients in the nonsmoker group did (p = 0.047). In conclusion, current smokers had more likelihood of salvageable myocardium in areas at risk, as demonstrated by BMIPP/201Tl mismatch, in AMI than nonsmokers.

Adult↗

PubMed2001

Activation of mitogen-activated protein kinases in the non-ischemic myocardium of an acute myocardial infarction in rats.

As one of the signal transduction pathways related to myocardial remodeling, mitogen-activated protein kinases (MAPKs) possibly play an important role in ischemic heart disease, but it is still unknown whether myocardial MAPKs are activated in the non-ischemic region of an acute myocardial infarction (AMI). Therefore, the present study investigated the myocardial activity of extracellular signal-regulated kinases (ERKs), c-Jun NH2 terminal kinases (JNKs) and p38MAPK during the acute phase of an infarction of the rat heart, and measured the geometrical ventricular changes by echocardiography. All MAPKs were significantly activated in the ischemic myocardium (IM), non-ischemic septal wall (SW), and right ventricular wall (RV). Furthermore, the activation patterns of MAPKs differed in each region. The activation of p44ERK, JNKs and p38MAPK in the IM occurred rapidly after myocardial ischemia, followed by those in the SW and RV. The activator protein-1 DNA binding activities of the IM, SW and RV increased significantly at I day after coronary ligation. Echocardiography showed increased SW motion and RV dilatation. In conclusion, this is the first in vivo evidence that myocardial MAPKs are activated in the non-ischemic region of an AMI. Echocardiographic results suggest that acceleration of workload and/or stretch may partially induce the activation of MAPKs.

Animals↗

PubMed2001

[Gastrointestinal sparing anti-inflammatory drugs--COX-2 selective inhibitors and NO-releasing NSAIDs].

The use of NSAIDs is associated with a wide array of alterations in the gastrointestinal integrity and function. Various approaches have been taken to develop NSAIDs with reduced gastrointestinal toxicity, and few have successfully reduced the incidence of adverse reactions. These include COX-2 selective inhibitors and NO-releasing NSAIDs. Much has been written about the potential of COX-2 inhibitors as antiinflammatory agents that lack the gastrointestinal side effects of traditional NSAIDs. COX-2 expression is most evident at sites of inflammation, while COX-1 accounts for most of the PG synthesis in the normal gastrointestinal tract. However, there are distinct examples of circumstances in which COX-2-derived PGs play a role in the maintenance of the mucosal integrity, and the differentiation of COX-1 and COX-2 is not quite as clear as has been suggested. On the other hand, the rational behind the NO-releasing NSAIDs is that NO released from the derivatives exerts beneficial effects on the gastrointestinal mucosa. The present article overviews the roles of COX and NO in housekeeping functions of the gastrointestinal mucosa in various circumstances and the effects of gastrointestinal sparing NSAIDs, such as COX-2 selective inhibitors and NO-releasing NSAIDs, on the ulcerogenic and healing responses in the gastrointestinal mucosa.

Animals↗

PubMed2001

[Gastrointestinal cytoprotection by prostaglandin E and EP receptor subtypes].

Endogenous prostaglandins (PGs) play important roles in modulating the mucosal integrity and various functions of the gastrointestinal tract. Among them, E-type PGs are most effective in these actions. This article reviews recent studies dealing with the relationship of the cytoprotective action of PGE2- and EP-receptor subtypes in the gastrointestinal mucosa. PGE2 exerts gastric cytoprotection against HCl/ethanol and indomethacin. These effects were mimicked by only EP1 agonists and attenuated by EP1 antagonists. Likewise, the adaptive cytoprotection induced by a mild irritant was attenuated by EP1 antagonists as well as indomethacin. On the other hand, the protective effect of dmPGE2 against indomethacin-induced small intestinal lesions was mimicked by only EP3 and EP4 agonists. Similar results were obtained in EP-receptor knockout mice; i.e., PGE2 failed to exhibit both direct and adaptive cytoprotection in EP1-receptor knockout mice, while the protective action in both the duodenum and small intestine was hampered in EP3-receptor knockout mice. The underlying mechanism related to these actions of PGE2 in the stomach, duodenum or small intestine may be related to inhibition of stomach contraction, stimulation of duodenal alkaline secretion, or suppression of bacterial translocation due to inhibition of intestinal contraction as well as stimulation of mucus secretion, respectively.

Animals↗

PubMed2001

Differential effects among thiazolidinediones on the transcription of thromboxane receptor and angiotensin II type 1 receptor genes.

Peroxisome proliferator-activated receptor (PPAR)-gamma ligands thiazolidinediones (TZDs) have recently been reported to be anti-hypertensive and anti-atherosclerotic. We have previously shown that one of the TZDs troglitazone significantly suppressed the transcription of both thromboxane receptor (TXR) and angiotensin II type 1 receptor (AT1R) genes in vascular smooth muscle cells (VSMCs) by activating PPAR-gamma. In the present study, we compared the effects of troglitazone and other TZDs on the transcription of these genes. TXR and AT1R mRNAs in rat VSMCs were determined by semi-quantitative RT-PCR. Luciferase chimeric constructs containing either the 989-bp rat TXR gene promoter or the 1,969-bp rat AT1R gene promoter were transiently transfected into VSMCs. The cells were incubated with troglitazone, RS-1455 (a derivative of troglitazone which does not contain the hindered phenol resembling alpha-tocopherol), pioglitazone, or rosiglitazone for 12 h before harvesting. mRNA expression levels of TXR and AT1R were significantly decreased by troglitazone in contrast to rosiglitazone. TXR gene and AT1R gene transcription was significantly suppressed by troglitazone in a dose-dependent manner, while RS-1455 was less potent. Pioglitazone and rosiglitazone weakly suppressed the transcription of both genes in a manner almost similar to RS-1455. We have shown that troglitazone suppresses transcription of both the TXR and AT1R genes more potently than other TZDs. The structure of troglitazone and RS-1455 is identical except the hindered phenol, which is recently recognized to function as an antioxidant. Moreover, we have shown that the potency for activating PPAR-gamma is almost identical between troglitazone and RS-1455. We therefore speculate that the strong transcriptional suppression of the TXR and AT1R genes by troglitazone may be mediated in part by its antioxidant effect.

Animals↗

PubMed2001

Abundant expression of platelet-derived growth factor in spiral arteries in decidua associated with pregnancy-induced hypertension and its relevance to atherosis.

OBJECTIVE: To elucidate the role of platelet-derived growth factor (PDGF) in the pathophysiology of pregnancy-induced hypertension (PIH) in which the spiral arteries of the decidua demonstrate the atherosclerotic change. DESIGN AND METHODS: We determined serum levels of PDGF and PDGF expression in the decidua as well as serum levels of 17 beta-estradiol (E2) and progesterone (P4) both in normotensive cases and in PIH cases. Furthermore, we investigated whether sex steroid hormones could interact with PDGF in cultured vascular smooth muscle cells (SMC) by immunohistochemical staining for proliferating cell nuclear antigen. RESULTS: Serum PDGF levels were higher (P<0.01) but serum E2 levels were lower (P<0.01) in PIH cases compared with normotensive cases. There was no statistically significant difference between serum P4 levels in PIH cases and those in normotensive cases. Immunohistochemical staining for PDGF in SMC of spiral arteries was more prominent in PIH cases than in normotensive cases. The proliferative potential of cultured SMC was stimulated by PDGF, but inhibited by concomitant treatment with PDGF and E2. CONCLUSIONS: PDGF is suggested to play an important role in the pathophysiology of PIH through its stimulatory effect on vascular SMC proliferation which may elicit the atherosclerotic change in the spiral arteries of the placenta.

Adult↗

PubMed2001

Novel method for assessing myocardial perfusion: visualization and measurement of intramyocardial coronary blood flow in the entire left ventricular wall using contrast enhanced, high frequency Doppler echocardiography.

Using a high frequency ultrasonic transducer, intramyocardial coronary blood flow (IM-CBF) can be visualized and evaluated during hemodynamic changes in the anterior wall and septum of the left ventricle (LV). We tested the hypothesis that detection and quantitative measurement of IM-CBF of entire LV segments are feasible using a high frequency ultrasonic transducer in conjunction with intravenous contrast injection in vivo. A 3 - 8 MHz transducer was used to image and measure IM-CBF in 10 anesthetized dogs. We obtained a color Doppler image of IM-CBF in the LV short-axis view after intravenous Levovist injection (25 mg/ml). The IM-CBF velocity was recorded using spectral Doppler in the antero-septal and infero-posterior wall of closed chest dogs and in the entire LV after opening the chest. A significant increase in IM-CBF velocity was observed in all LV regions after adenosine 5'- triphosphate (ATP) administration. After Levovist(TM) injection, the visualization of IM-CBF was improved and the spectral Doppler pattern of coronary flow velocity was clarified compared to baseline. IM-CBF was assessed in the antero-septal region of the LV before and after left anterior descending coronary artery occlusion. A high frequency ultrasonic transducer in conjunction with intravenous contrast injection improved IM-CBF visualization, enabling quantitative evaluation of the intramyocardial coronary circulation in the entire LV after coronary occlusion and hyperemia. This study may represent a step towards noninvasive assessment of myocardial perfusion before and after coronary reperfusion.

Animals↗

PubMed2001

Concentration of nitric oxide (NO) in spinal fluid of chronic spinal disease.

We studied total nitric oxide (nitrite + nitrate) (NO) levels in cerebrospinal fluid (CSF) of chronic spinal diseases in nonsmokers (133 patients: 76 men and 57 women; mean age, 63 years; range, 15-92 years) by the Griess method to clarify the role of NO in different spinal diseases. The extent of compression in terms of numbers of disc level at the compressed spinal nerve and neurological evaluation were also assessed according to the Japanese Orthopaedic Association scores. The spinal diseases included cervical myelopathy and radiculopathy (cervical disease group), ossification of yellow ligament (thoracic disease group), and lumbar disc herniation, lumbar canal stenosis and lumbar spondylolisthesis (lumbar disease group). NO levels in the spinal disease groups (4.98+/-2.28 micromol/l: mean +/- SD) were significantly higher than that in the control group (2.53+/-0.94 micromol/l). An inverse correlation was detected between the elevated levels of NO and the grade of clinical symptoms in the cervical disorders. The number of disc level at the compressed spinal nerve was positively correlated with elevated NO levels in CSF in the cervical and lumbar disorder groups. These results indicate that nerve compression may elevate NO levels in CSF, and that NO concentration in the CSF might be a useful marker of damage to nervous system in spinal disorders.

Adolescent↗

PubMed2001

Development of interferon-alpha resistant subline from human chronic myelogenous leukemia cell line KT-1.

OBJECTIVE: Interferon-alpha (IFN-alpha) is one of the most effective therapeutic agents for a number of hematological malignancies, including chronic myelogenous leukemia (CML). Nevertheless, its efficacy is limited because of the development of resistance to IFN-alpha therapy. Previously, we established the novel human CML cell line KT-1, which is sensitive to the antiproliferative effects of IFN-alpha. Here, we report the establishment of an IFN-alpha-resistant subline, KT-1/A3R alpha 1000, by culturing KT-1/A3 cells (IFN-alpha-sensitive subline of KT-1) with increasing concentrations of IFN-alpha, in order to analyze the mechanism of acquisition of IFN-alpha resistance in CML cells after IFN-alpha therapy. SUBJECTS AND METHODS: We developed an IFN-alpha-resistant tumor cell variant, KT-1/A3R alpha 1000, from the KT-1/A3 cell line by culturing cells with increasing concentrations of IFN-alpha. This subline was examined for its ability to proliferate and its resistance to apoptosis in high concentrations of IFN-alpha. The induction of the ISGF3 complex in response to IFN-alpha alpha in KT-1/A3R alpha 1000 was compared with that in the parental cell. RESULTS: The levels of interferon-stimulated gene factor 3 components (STAT1, STAT2, and p48) proteins and STAT2 tyrosine phosphorylation induced after IFN-alpha treatment were unchanged, but formation of the ISGF3 complex was remarkably reduced in KT-1/A3R alpha 1000 cells compared to parental cells. CONCLUSION: The KT-1/A3R alpha 1000 subline is a useful model for studying the mechanism of IFN-alpha resistance after IFN-alpha therapy.

Antineoplastic Agents↗

PubMed2001

Gastrointestinal sparing anti-inflammatory drugs--effects on ulcerogenic and healing responses.

The use of nonsteroidal antiinflammatory drugs (NSAIDs) is associated with a wide array of alterations in gastrointestinal integrity and function. Various approaches have been taken to developing NSAIDs with reduced gastrointestinal toxicity, and few have been successfully reduced the incidence of adverse reactions. These include cyclooxygenase-2 (COX-2) selective inhibitors and nitric oxide (NO)-releasing NSAIDs. Especially, much has been written about the potential of COX-2 inhibitors as anti-inflammatory and analgesic agents that lack the gastrointestinal side effects of traditional NSAIDs. COX-2 expression is most evident at sites of inflammation, while COX-1 accounts for the majority of prostaglandin synthesis in the normal gastrointestinal tract. However, there are distinct examples of circumstances in which COX-2-derived prostaglandins play a role in the maintenance of gastrointestinal mucosal integrity, particularly when the mucosa is injured, and the delineation of COX-1 and COX-2 might not be quite as clear as has been suggested. On the other hand, the rational behind the NO-releasing NSAIDs is that the NO released from the derivatives will exert beneficial effects on the gastrointestinal mucosa. This approach has been successfully demonstrated to lessen the incidence of gastrointestinal damage and to promote the healing of gastric ulcers. The present article overviews the roles of COX and NO in housekeeping functions of the gastrointestinal mucosa in various circumstances, and the effects of gastrointestinal sparing NSAIDs, mainly COX-2 selective inhibitors and NO-releasing derivatives of NSAIDs, on the ulcerogenic and healing responses in the gastrointestinal mucosa of experimental animals.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2001

Lifestyle and sociodemographic risk factors for death among middle-aged and elderly residents in japan from a five-year follow-up cohort study.

To examine the relationship between lifestyle and sociodemographic risk factors and mortality, a population-based prospective cohort study was conducted in two areas of Gunma Prefecture, Japan, and a cohort consisting of 11,565 subjects aged 40-69 at baseline in 1993 was followed. During the five-year follow-up period, 201 men and 103 women died. The relative risks (RRs) of risk factors were estimated by the Cox proportional-hazards model. Significant RRs with multivariate adjustment for all-cause mortality was observed for body mass index (BMI). The curve for the relationship between BMI and all-cause mortality was L-shaped in men and U-shaped in women, with the lowest RRs at a BMI of 22-25 in both men and women. Other significant RRs for all-cause mortality were observed for obesity in the subjects' 30's in both men and women (RR: 2.42 and RR: 2.75), poor perceived health status in men (RR: 4.55), and having had a health examination in the past three years in both men and women (RR: 0.49 and RR: 0.46). These results suggested that increased risk of death was independently associated with a lower BMI, obesity in the subjects' 30's, and not undergoing health examinations, among both men and women, and poor perceived health status among men.

Adult↗

PubMed2001

Evidence of primary beta-cell destruction by T-cells and beta-cell differentiation from pancreatic ductal cells in diabetes associated with active autoimmune chronic pancreatitis.

OBJECTIVE: Diabetes associated with autoimmune chronic pancreatitis (ACP) is a subtype of diabetes that is responsive to corticosteroid treatment of progressive endocrine and exocrine dysfunction. However, little is known about pathological changes of islet and exocrine pancreas in ACP. RESEARCH DESIGN AND METHODS: We examined pancreatic specimens obtained on biopsy from four diabetic men with ACP (mean [range]: age 62 years [48-78], duration of ACP 3 months [1-5], duration of diabetes 1 month [0-3]) morphologically, immunohistochemically, and morphometrically. RESULTS: The pancreatic specimens in all cases exhibited inflammatory cell infiltration surrounding ductal cells and extensive fibrosis. Some islets were infiltrated with mononuclear cells with disrupted beta-cells. The subsets of T-cells infiltrated to the islets were mainly CD8(+). Islet beta-cell volume was decreased; the mean percentage area of beta-cells in the islets in four cases with ACP were 16% (range 13-20) (P = 0.0015 vs. type 2 diabetic patients, 48% [27-73], n = 8; P = 0.0002 vs. nondiabetic control subjects, 58% [39-77], n = 7). Preserved ductal cells were surrounded predominantly by CD8(+) or CD4(+) T-cells. Some cytokeratin 19-positive ductal cells contained insulin and glucagon, representing upregulated differentiation of islet cells from ductal cells. Insulin promoter factor-1 (IPF-1) was hyperexpressed in insulin-containing ductal cells. CONCLUSIONS: Diabetes associated with ACP is caused by T-cell-mediated mechanisms primarily involving islet beta-cells as well as pancreatic ductal cells. In ACP, ductal islet precursor cells were associated with IPF-1 hyperexpression, suggesting a critical role of IPF-1 on islet cell differentiation and eventual beta-cell restoration.

Acute Disease↗

PubMed2001

Adult colonic intussusception: a case report.

Intussusception accounts for almost all cases of intestinal obstruction in children. In contrast, intussusception in adults is relatively rare. An 86-year-old Japanese female with rectal bleeding came to our hospital via ambulance. At first, colonoscopy findings revealed the sigmoid colon cancer. Ultrasonography showed a hypoechoic mass with a multiple concentric ring sign. Computed tomography showed a round fluid-filled cystic structure. Colon contrast studies demonstrated stenosis in the rectosigmoid colon. A laparotomy was performed. The sigmoid colon was intussuscepted to the rectosigmoid colon. We employed both rectosigmoid and sigmoid colon resection. The resected specimen showed that the disease was advanced sigmoid colon cancer with ulcer formation due to an ischemic change. Tumor was 4.5 cm x 2.0 cm in size. The disease was histopathologically diagnosed as advanced sigmoid colon cancer, well-differentiated adenocarcinoma. We report here a case of adult intussusception due to the sigmoid colon cancer.

Aged↗

PubMed2001

Somatic alterations of the DPC4 and Madr2 genes in colorectal cancers and relationship to metastasis.

The DPC4 and Madr2 genes are located at 18q21, and the LOH on chromosome 18q21 has been shown to occur frequently in colorectal cancers. To investigate the role of these genes in advanced colorectal cancers, we analyzed 29 colorectal specimens for alterations in the DPC4 and Madr2 genes. Twelve (63.2%) of 19 informative primary colorectal cancers showed allelic loss of chromosome 18q21.3 marker. An alteration of the DPC4 gene sequence was identified in 6 (20.7%) of 29 colorectal carcinomas, and the distinct Madr2 gene mobility shifts were present in 3 (10.3%) cancers. Somatic mutations were identified in these tumors by sequencing analysis. DPC4 gene alterations of 4 cases were detected in Mad homology 2 domains. There was no significant correlation between the somatic alteration of Madr2 and clinicopathological findings. However, the frequency of DPC4 mutation was significantly higher in tumors associated with liver metastasis than in those without such metastasis. Our findings suggest that somatic alteration of the DPC4 gene may play a role in tumorigenesis and liver metastasis of human colorectal cancers.

Chi-Square Distribution↗

PubMed2001

Penetration of Escherichia coli O157:H7 into lettuce as influenced by modified atmosphere and temperature.

The effects of temperature and atmospheric oxygen concentration on the respiration rate of iceberg lettuce and Escherichia coli O157:H7 cells attachment to and penetration into damaged lettuce tissues were evaluated. Respiration rate of lettuce decreased as the temperature was reduced from 37 to 10 degrees C. Reducing the temperature further to 4 degrees C did not affect the respiration rate of lettuce. Respiration rate was also reduced by lowering the atmospheric oxygen concentration. Lettuce was submerged in E. coli O157:H7 inoculum at 4, 10, 22, or 37 degrees C under 21 or 2.7% oxygen. Attachment and penetration of E. coli O157:H7 were not related to the respiration rate. The greatest numbers of E. coli O157:H7 cells attached to damaged lettuce tissues at 22 degrees C at both oxygen concentrations. More cells were attached under 21% oxygen than under 2.7% oxygen at each temperature, but this difference was small. Penetration of E. coli O157:H7 into lettuce tissue was determined by immunostaining with a fluorescein isothiocyanate-labeled antibody. Under 21% oxygen, E. coli O157:H7 cells showed greatest penetration when lettuce was held at 4 degrees C, compared to 10, 22. or 37 degrees C, and were detected at an average of 101 microm below the surfaces of cut tissues. However, under 2.7% oxygen, there were no differences in degree of penetration among four incubation temperatures. The degree of E. coli O157:H7 penetration into lettuce tissue at 4 or 22 degrees C was greater under 21% oxygen than under 2.7% oxygen; however, no difference was observed at 37 degrees C. Conditions that promote pathogen penetration into tissue could decrease the effectiveness of decontamination treatments.

Bacterial Adhesion↗

PubMed2001

Confocal microscopy and microbial viability detection for food research.

Confocal microscopy offers several advantages over other conventional microscopic techniques as a tool for studying the interaction of bacteria with food and the role of food microstructure in product quality and safety. When using confocal microscopy, samples can be observed without extensive preparation processes, which allows for the evaluation of food without introducing artifacts. In addition, observations can be made in three dimensions without physically sectioning the specimen. The confocal microscope can be used to follow changes over a period of time, such as the development of the food structure or changes in microbial population during a process. Microbial attachment to and detachment from food and food contact surfaces with complex three-dimensional (3-D) structures can be observed in situ. The fate of microbial populations in food system depends on processing, distribution, and storage conditions as well as decontamination procedures that are applied to inactivate and remove them. The ability to determine the physiological status of microorganisms without disrupting their physical relationship with a food system can be useful for determining the means by which microorganisms survive decontamination treatments. Conventional culturing techniques can detect viable cells; however, these techniques lack the ability to locate viable cells in respect to the microscopic structures of food. Various microscopic methods take advantage of physiological changes in bacterial cells that are associated with the viability to assess the physiologic status of individual cells while retaining the ability to locate the cell within a food tissue system. This paper reviews the application of confocal microscopy in food research and direct observation of viable bacteria with emphasis on their use in food microbiology.

Bacteria↗