Histological Damage (histological + damage)

Distribution by Scientific Domains


Selected Abstracts


On-line glucose and lactate monitoring in rat striatum: effect of malonate and correlation with histological damage

JOURNAL OF NEUROCHEMISTRY, Issue 2003
J. Skjoeth-Rasmussen
Microdialysis of glucose, lactate and glycerol was performed to monitor brain insults and to predict brain injury in a rat model using the mitochondrial toxin malonate (5,100 mm). Striatal dialysates were analyzed off-line using a CMA 600 microdialysis analyzer or on-line using flow-injection analysis and biosensors for glucose and lactate. Histological damage was evaluated using stereological principles. Lactate (baseline ca. 1 mm) was dose-dependently increased, reaching a maximum of five- to six-fold increase, whereas glucose (baseline 1,2 mm) was decreased (>50%) by malonate >20 mm. These changes were reversible upon perfusion with normal Ringer's. Transient increases in glycerol (four- to eight-fold) were only observed in some rats, and were not dose-dependent. Histological damage was related to the perfused malonate concentration, but was not significantly correlated with lactate or glycerol changes. [source]


Effect of experimentally induced Escherichia coli epididymo-orchitis and ciprofloxacin treatment on rat spermatogenesis

INTERNATIONAL JOURNAL OF UROLOGY, Issue 3 2007
Aslan Demir
Abstract: We investigated the effects of epididymo-orchitis and ciprofloxacin on rat testicular histology and spermatogenesis. The control group underwent left orchiectomy. The second group received oral ciprofloxacin (150 mg/kg/day) for 10 days. Escherichia coli (106 cfu/mL, 0.1 mL) was injected into the proximal right ductus deferens in the third group. The fourth group received ciprofloxacin treatment 48 h after E. coli inoculation. In groups 3 and 4, bilateral orchiectomy was performed 14 days after the challenge. In healthy rats, ciprofloxacin caused recognizable histological damage associated with a mild decrease in testicular volume and sperm concentration. Infected testicles in groups 3 and 4 revealed severe histological damage associated with severe testicular atrophy and impaired spermatogenesis that were more significant in infected rats which received ciprofloxacin treatment. Contralateral testicles in these animals showed similar histopathological changes to a lesser extent. The results of our study suggest a gonadotoxic potential for ciprofloxacin and this potential in humans should be addressed with further studies. [source]


MRI tissue characterization of experimental cerebral ischemia in rat

JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 4 2003
Hamid Soltanian-Zadeh PhD
Abstract Purpose To extend the ISODATA image segmentation method to characterize tissue damage in stroke, by generating an MRI score for each tissue that corresponds to its histological damage. Materials and Methods After preprocessing and segmentation (using ISODATA clustering), the proposed method scores tissue regions between 1 and 100. Score 1 is assigned to normal brain matter (white or gray matter), and score 100 to cerebrospinal fluid (CSF). Lesion zones are assigned a score based on their relative levels of similarities to normal brain matter and CSF. To evaluate the method, 15 rats were imaged by a 7T MRI system at one of three time points (acute, subacute, chronic) after MCA occlusion. Then they were killed and their brains were sliced and prepared for histological studies. MRI of two or three slices of each rat brain (using two DWI (b = 400, b = 800), one PDWI, one T2WI, and one T1WI) was performed, and an MRI score between 1 and 100 was determined for each region. Segmented regions were mapped onto the histology images and scored on a scale of 1,10 by an experienced pathologist. The MRI scores were validated by comparison with histology scores. To this end, correlation coefficients between the two scores (MRI and histology) were determined. Results Experimental results showed excellent correlations between MRI and histology scores at different time points. Depending on the reference tissue (gray matter or white matter) used in the standardization, the correlation coefficients ranged from 0.73 (P < 0.0001) to 0.78 (P < 0.0001) using the entire dataset, including acute, subacute, and chronic time points. This suggests that the proposed multiparametric approach accurately identified and characterized ischemic tissue in a rat model of cerebral ischemia at different stages of stroke evolution. Conclusion The proposed approach scores tissue regions and characterizes them using unsupervised clustering and multiparametric image analysis techniques. The method can be used for a variety of applications in the field of computer-aided diagnosis and treatment, including evaluation of response to treatment. For example, volume changes for different zones of the lesion over time (e.g., tissue recovery) can be evaluated. J. Magn. Reson. Imaging 2003;17:398,409. © 2003 Wiley-Liss, Inc. [source]


On-line glucose and lactate monitoring in rat striatum: effect of malonate and correlation with histological damage

JOURNAL OF NEUROCHEMISTRY, Issue 2003
J. Skjoeth-Rasmussen
Microdialysis of glucose, lactate and glycerol was performed to monitor brain insults and to predict brain injury in a rat model using the mitochondrial toxin malonate (5,100 mm). Striatal dialysates were analyzed off-line using a CMA 600 microdialysis analyzer or on-line using flow-injection analysis and biosensors for glucose and lactate. Histological damage was evaluated using stereological principles. Lactate (baseline ca. 1 mm) was dose-dependently increased, reaching a maximum of five- to six-fold increase, whereas glucose (baseline 1,2 mm) was decreased (>50%) by malonate >20 mm. These changes were reversible upon perfusion with normal Ringer's. Transient increases in glycerol (four- to eight-fold) were only observed in some rats, and were not dose-dependent. Histological damage was related to the perfused malonate concentration, but was not significantly correlated with lactate or glycerol changes. [source]


Low-intensity pulsed ultrasound (LIPUS) increases the articular cartilage type II collagen in a rat osteoarthritis model

JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 3 2010
Kiyohito Naito
Abstract In this study, the effect of low-intensity pulsed ultrasound (LIPUS) on cartilage was evaluated in a rat osteoarthritis (OA) model using serum biomarkers such as CTX-II (type II collagen degradation) and CPII (type II collagen synthesis) as well as histological criteria (Mankin score and immunohistochemical type II collagen staining). OA was surgically induced in the knee joint of rats by anterior cruciate/medial collateral ligament transection and medial meniscus resection (ACLT,+,MMx). Animals were divided into three groups: sham-operated group (Sham), ACLT,+,MMx group without LIPUS (,LIPUS), and ACLT,+,MMx group with LIPUS (+LIPUS; 30 mW/cm2, 20 min/day for 28 days). CTX-II levels were elevated in both ,LIPUS and +LIPUS groups compared to that in the Sham group after the operation, but there was no significant difference between +LIPUS and ,LIPUS groups, suggesting that LIPUS does not affect the degradation of type II collagen in this model. In contrast, CPII was significantly increased in +LIPUS group compared to ,LIPUS and Sham. Moreover, histological damage on the cartilage (Mankin score) was ameliorated by LIPUS, and type II collagen was immunohistochemically increased by LIPUS in the cartilage of an OA model. Of interest, mRNA expression of type II collagen was enhanced by LIPUS in chondrocytes. Together these observations suggest that LIPUS is likely to increase the type II collagen synthesis in articular cartilage, possibly via the activation of chondrocytes and induction of type II collagen mRNA expression, thereby exhibiting chondroprotective action in a rat OA model. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:361,369, 2010 [source]


Low p38 MAPK and JNK activation in cultured hepatocytes of DRH rats; a strain highly resistant to hepatocarcinogenesis

MOLECULAR CARCINOGENESIS, Issue 9 2007
Satoshi Honmo
Abstract DRH rats are a hepatocarcinogenesis-resistant strain isolated from hepatocarcinogenesis-sensitive Donryu rats, and the liver of DRH shows less histological damage and fewer/smaller neoplastic hepatic lesions by the treatment with hepatocarcinogens. To investigate the mechanism of the resistance, the properties of hepatocytes of DRH and Donryu were compared. In primary culture, DRH hepatocytes exhibited higher proliferation and less apoptosis than Donryu hepatocytes in the presence of EGF and insulin. However, such difference was not correlated to the degree of DNA damage associated with cell culture or cell cycle checkpoint function. Although the mitogen-activated protein kinases [EGF receptor (EGFR) and extracellular signal regulating kinases (ERK1/2)] were activated to the same degree, the stress-activated protein kinases [p38 mitogen-activated protein kinase (p38) and c- jun N-terminal kinase (JNK)] were activated to a lesser degree in the DRH hepatocytes. Treatment with 2-acetylaminofluorene (2-AAF) in vivo also resulted in less JNK and p38 activation in the DRH livers. Furthermore, apoptosis signal-regulating kinase 1 (ASK1) was inhibited by the lysate from the DRH but not by the Donryu hepatocytes. The low activation of the stress-activated protein kinases may be linked to the resistance to cellular stress, which may underlie the hepatocarcinogenesis-resistance in DRH rats. © 2007 Wiley-Liss, Inc. [source]


Endogenous and exogenous ghrelin enhance the colonic and gastric manifestations of dextran sodium sulphate-induced colitis in mice

NEUROGASTROENTEROLOGY & MOTILITY, Issue 1 2009
B. De Smet
Abstract, Ghrelin is an important orexigenic peptide that not only exerts gastroprokinetic but also immunoregulatory effects. This study aimed to assess the role of endogenous and exogenous ghrelin in the pathogenesis of colitis and in the disturbances of gastric emptying and colonic contractility during this process. Dextran sodium sulphate colitis was induced for 5 days in (i) ghrelin+/+ and ghrelin,/, mice and clinical and histological parameters were monitored at days 5, 10 and 26 and (ii) in Naval Medical Research Institute non-inbred Swiss (NMRI) mice treated with ghrelin (100 nmol kg,1) twice daily for 5 or 10 days. Neural contractility changes were measured in colonic smooth muscle strips, whereas gastric emptying was measured with the 14C octanoic acid breath test. Inflammation increased ghrelin plasma levels. Body weight loss, histological damage, myeloperoxidase activity and IL-1, levels were attenuated in ghrelin,/, mice. Whereas absence of ghrelin did not affect changes in colonic contractility, gastric emptying in the acute phase was accelerated in ghrelin+/+ but not in ghrelin,/, mice. In agreement with the studies in ghrelin knockout mice, 10 days treatment of NMRI mice with exogenous ghrelin enhanced the clinical disease activity and promoted infiltration of neutrophils and colonic IL-1, levels. Unexpectedly, ghrelin treatment decreased excitatory and inhibitory neural responses in the colon of healthy but not of inflamed NMRI mice. Endogenous ghrelin enhances the course of the inflammatory process and is involved in the disturbances of gastric emptying associated with colitis. Treatment with exogenous ghrelin aggravates colitis, thereby limiting the potential therapeutic properties of ghrelin during intestinal inflammation. [source]


Type 4 phosphodiesterase inhibitor suppresses experimental bladder inflammation

BJU INTERNATIONAL, Issue 10 2008
Takeya Kitta
OBJECTIVE To evaluate the effects of orally administered YM976, a specific inhibitor of type 4 phosphodiesterase (PDE4), on bladder activity in a rat model with hydrochloric acid (HCl)-induced cystitis (IC), hypothesizing that a PDE4 inhibitor might suppress bladder overactivity and bladder pain responses in bladder-hypersensitive disorders such as IC. MATERIALS AND METHODS Wistar rats with HCl-induced IC were treated with YM976 or vehicle and their voiding observed and assessed by cystometry. The severity of bladder inflammation (BI) was quantified using the BI index (BII), which comprises three factors (oedema, leukocyte infiltration and haemorrhage). Nociceptive neural activity was also examined using an immunohistochemical study of spinal c-fos expression. RESULTS YM976 significantly reduced the number of voids, and the volume per void was significantly higher than in control (vehicle) group. Cystometry showed a significant increase in bladder capacity, voided volume and voiding efficiency, and a decrease in the amplitude of voiding pressure in rats treated with YM976. All BII scores were significantly lower in the YM976 than in the control group. c-fos expression in the spine was less in the YM976 than in the control group. CONCLUSIONS Oral administration of YM976 significantly improved the voiding behaviour and histological damage in rats with IC induced by HCl. These results indicate that PDE4 inhibitor might be effective in relieving bladder symptoms with IC. [source]


Investigation of the effects of peppermint oil and valerian on rat liver and cultured human liver cells

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2003
Liem T Vo
Summary 1.,The aim of the present study was to investigate the effects of peppermint oil and valerian on rat liver and cultured human hepatoma cells. 2.,Rats received a single oral dose of peppermint oil (8.3,830 µL/kg) or valerian (0.31,18.6 g/kg), or daily oral doses of 83 µL/kg peppermint oil or 3.1 g/kg valerian for 28 days. After 24 h, rats were anaesthetized and measurements made of bile flow, liver function and in vivo sinusoidal area. Livers were then removed for histology. 3.,Bile flow was unaffected by any treatment, except acute high-dose peppermint oil (830 µL/kg; 70% increase in flow). No change in liver enzyme activity was found, except for a 45% increase in alkaline phosphatase after chronic peppermint oil. No change in sinusoidal area in vivo or in histology was found following any treatment, although pretreatment with carbon tetrachloride reduced sinusoidal bed area and produced histological damage. Incubation of human hepatoma cells with 0.5 µL/mL (but not 0.05 µL/mL) peppermint oil or 20 mg/mL (but not 2 mg/mL) valerian resulted in increased cell death. 4.,In conclusion, the present study demonstrated in vitro toxicity of high doses of valerian and peppermint oil in cultured human hepatoma cells and, at doses 2,3 orders of magnitude greater than those recommended for human use, an increase in rat bile flow after acute peppermint oil and an increase in alkaline phosphatase after chronic peppermint oil. [source]


Guidelines for the treatment of chronic hepatitis and cirrhosis due to hepatitis C virus infection for the fiscal year 2008 in Japan

HEPATOLOGY RESEARCH, Issue 1 2010
Hiromitsu Kumada
In the 2008 guidelines for the treatment of patients with chronic hepatitis C, pegylated interferon (Peg-IFN) combined with ribavirin for 48 weeks are indicated for treatment-naive patients infected with hepatitis C virus (HCV) of genotype 1. Treatment is continued for an additional 24 weeks (72 weeks total) in the patients who have remained positive for HCV RNA detectable by the real-time polymerase chain reaction at 12 weeks after the start of treatment, but who turn negative for HCV RNA during 13,36 weeks on treatment. Re-treatment is aimed to either eradicate HCV or normalize transaminase levels for preventing the development of hepatocellular carcinoma (HCC). For patients with compensated cirrhosis, the clearance of HCV RNA is aimed toward improving histological damages and decreasing the development of HCC. The recommended therapeutic regimen is the initial daily dose of 6 million international units (MIU) IFN continued for 2,8 weeks that is extended to longer than 48 weeks, if possible. IFN dose is reduced to 3 MIU daily in patients who fail to clear HCV RNA by 12 weeks for preventing the development of HCC. Splenectomy or embolization of the splenic artery is recommended to patients with platelet counts of less than 50 × 103/mm3 prior to the commencement of IFN treatment. When the prevention of HCC is at issue, not only IFN, but also liver supportive therapy such as stronger neo-minophagen C, ursodeoxycholic acid, phlebotomy, branched chain amino acids (BCAA), either alone or in combination, are given. In patients with decompensated cirrhosis, by contrast, reversal to compensation is attempted. [source]