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Histological Abnormalities (histological + abnormality)
Selected AbstractsDevelopmental anatomy of reeler mutant mouseDEVELOPMENT GROWTH & DIFFERENTIATION, Issue 3 2009Yu Katsuyama The reeler mouse is one of the most famous spontaneously occurring mutants in the research field of neuroscience, and this mutant has been used as a model animal to understand mammalian brain development. The classical observations emphasized that laminar structures of the reeler brain are highly disrupted. Molecular cloning of Reelin, the gene responsible for reeler mutant provided insights into biochemistry of Reelin signal, and some models had been proposed to explain the function of Reelin signal in brain development. However, recent reports of reeler found that non-laminated structures in the central nervous system are also affected by the mutation, making function of Reelin signal more controversial. In this review, we summarized reported morphological and histological abnormalities throughout the central nervous system of the reeler comparing to those of the normal mouse. Based on this overview of the reeler abnormalities, we discuss possible function of Reelin signal in the neuronal migration and other morphological events in mouse development. [source] Exposure to the polychlorinated biphenyl mixture Aroclor® 1254 alters melanocyte and tail muscle morphology in developing Xenopus laevis tadpolesENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 2 2003Marla A. Fisher Abstract Polychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants that have damaging effects on both ecosystem and human health. Numerous studies have shown that exposure to PCBs can alter growth and development of aquatic organisms, including frogs. In this report, developing Xenopus laevis tadpoles were exposed to the PCB mixture Aroclor® 1254. Tadpoles were exposed from 5 through 9 d postfertilization to either 0, 1, 10, 50, or 100 ppm Aroclor 1254. Exposure to an acute, high concentration of Aroclor 1254 (10, 50, and 100 ppm) caused statistically significant reductions in survival and body size. In addition, tadpoles exposed to these higher concentrations showed histological abnormalities, including aberrant tail tip, myotomal, and melanocyte morphologies. Described adverse health effects associated with PCB exposure of developing frogs will serve as useful health endpoints in ongoing and future molecular-based studies that correlate health effects with changes in gene expression. [source] Intrahepatic hepatitis C viral RNA status of serum polymerase chain reaction,negative individuals with histological changes on liver biopsyHEPATOLOGY, Issue 6 2001Sharon Barrett For individuals testing anti-HCV positive but negative for HCV RNA in serum, diagnosis remains unclear. Debate exists over whether these individuals have resolved infection or have similar clinical, histological, and virological profiles as serum PCR,positive individuals. The aim of this study was to assess the significance of histological changes in the liver of 33 serum PCR,negative women by investigation of clinical, histological, and intrahepatic HCV RNA status. For comparison, clinical and histological data from 100 serum PCR,positive women is presented. Viral RNA status was determined in snap-frozen liver biopsies using a sensitive nested PCR with an internal control. Although serum PCR,positive and ,negative individuals shared similar age at diagnosis, source, and duration of infection, they differed from a clinical, histological, and virological perspective. Mean serum ALT levels were significantly lower in serum PCR,negative women (27.4 IU/L ± 18 vs. 58.7 IU/L ± 40 P < .001). Similarly, although inflammation (82%) and mild fibrosis (15%) were observed in PCR,negative biopsies, the mean HAI/fibrosis scores were significantly lower than in serum PCR,positive biopsies (1.9 ± 1.5/0.15 ± 0.4 vs. 4.2 ± 1.4/1.1 ± 1.3, respectively). Finally, HCV RNA was not detectable in serum PCR,negative liver biopsies but was detectable in all serum PCR,positive control biopsies. In conclusion, serum PCR,negative individuals may have mild histological abnormalities more suggestive of nonspecific reactive changes, steatosis or nonalcoholic steatohepatitis rather than chronic HCV, even when significant antibody responses are present in serum. Negative serum PCR status appears to reflect cleared past-exposure in liver. [source] Disruption of FRNK expression by gene targeting of the intronic promoter within the focal adhesion kinase geneJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 4 2007Haruko Hayasaka Abstract FRNK, a non-catalytic variant of focal adhesion kinase (FAK), is expressed in major blood vessels throughout mouse development and is postulated to play a role in regulating cell adhesion and signaling in vascular smooth muscle cells (VSMCs). The FRNK transcriptional start site lies within an intron of the FAK gene, suggesting that the FRNK gene is a "gene within a gene". Here, we identified a 1 kb intronic sequence of the FAK gene that is necessary for endogenous FRNK expression. Deletion of this sequence in gene-targeted mice abolished FRNK expression, showing the direct involvement of the FAK intron in the regulation of FRNK expression. The level of FAK expression was normal in the FRNK-deficient mice, indicating that FAK and FRNK are transcriptionally regulated by distinct promoters. The FRNK-deficient mice were viable, fertile, and displayed no obvious histological abnormalities in any of the major blood vessels. Western blot analysis showed that FRNK,deficient and wild-type (WT) cells had comparable levels of steady-state and adhesion-dependent FAK autophosphorylation. Despite the fact that ectopic expression of FRNK suppresses focal adhesion formation in cultured cells, these results suggest that endogenous FRNK is not essential for development or the formation of the mouse vasculature. J. Cell. Biochem. 102: 947,954, 2007. © 2007 Wiley-Liss, Inc. [source] Hepatitis C virus infection in Egyptian children: single centre experienceJOURNAL OF VIRAL HEPATITIS, Issue 5 2004M. S. El-Raziky Summary., The outcome of hepatitis C virus (HCV) infection acquired in childhood is uncertain because of the diversity of the epidemiological and clinical features of infection and disease. The aim of this study was to determine the outcome of HCV infection in 105 Egyptian children who tested positive for HCV antibody (anti-HCV). The data of 105 anti-HCV-positive children presenting to the Pediatric Hepatology Unit, Cairo University Children's Hospital, between 1995 and 2002, were retrospectively analysed for risk factors. Seventy-four children with available polymerase chain reaction results were further analysed clinically, serologically and histologically. The age range was 1.3,22 years, with a mean of 11.2 ± 4.9 years. History of blood transfusion was found in 81 children (77%). HCV RNA was detected in 58.1% of 74 children. Persistently elevated alanine aminotransferase (ALT) levels were present in 40 patients (54.1%). Hepatitis B virus markers (HBsAg and/or anti-HBc) were detected in 18 patients (24.3%). Twenty-six of the 43 HCV RNA-positive children underwent a diagnostic liver biopsy that showed chronic hepatitis in 19 patients (73.1%), cirrhosis in one case only (3.8%), and normal biopsy findings in seven children (26.9%). Blood transfusion remains a major risk of HCV transmission among Egyptian children. HCV infection is not always benign in the childhood period. ALT levels remain elevated in half of the children and histological abnormalities are detected in three quarters of HCV RNA-positive cases. [source] Recurrent autoimmune hepatitis after liver transplantation: Diagnostic criteria, risk factors, and outcomeLIVER TRANSPLANTATION, Issue 4 2001Stefan G. Hübscher MD Approximately 20% to 30% of patients undergoing liver transplantation for autoimmune hepatitis (AIH) develop features of recurrent disease. Diagnostic criteria for recurrent AIH are similar to those used in the nontransplanted liver and include, in varying combinations, biochemical, serological, and histological abnormalities and steroid dependency. However, these criteria are more difficult to apply in the liver allograft because of potential interactions between recurrent AIH and other complications of liver transplantation, particularly rejection, and the uncertain effects of long-term immunosuppression. In the absence of other reliable diagnostic markers, a number of studies have used the histological finding of chronic hepatitis as the main or sole criterion for diagnosing recurrent AIH. However, this also lacks diagnostic specificity because there are many other possible causes of chronic hepatitis in the liver allograft. In addition, approximately 20% to 40% of biopsies performed on patients as part of routine annual review have histological features of chronic hepatitis, for which no definite cause can be identified. Risk factors that have been associated with the development of recurrent AIH include suboptimal immunosuppression, HLA phenotype, disease type and severity in the native liver, and duration of follow up. In many cases in which recurrent AIH seems to be related to underimmunosuppression, biochemical and histological features rapidly resolve once adequate immunosuppression is restored. However, in other cases, recurrent AIH behaves more aggressively, with progression to cirrhosis and graft failure. Areas that require further study include developing uniform criteria for the diagnosis of recurrent AIH, identifying risk factors for severe recurrent disease, and determining optimal levels of immunosuppression that minimize the impact of disease recurrence without exposing patients to the risks of overimmunosuppression. [source] Incidence and significance of microscopic pathological lesions found in pedicle and recipient vessels used in microsurgical breast reconstructionMICROSURGERY, Issue 1 2003H.H. El-Mrakby M.D. The purpose of this study was to assess the incidence of abnormal vascular histology and to determine whether or not this was correlated with the incidence of postoperative microvascular problems. The microvascular histology of both donor and recipient vessels was studied in 38 patients (40 flaps) undergoing breast reconstruction with free TRAM flaps. Preoperative risk factors were assessed and correlated with histological changes in vessels, and both were tested against anastomotic complications. Thrombosis of either the artery or the vein of the flap was seen in 6 cases (15%), and of these, two flaps failed completely and one suffered partial necrosis. The occlusion affected the arterial anastomosis in 3 patients, and the venous anastomosis in 2 patients, while both the artery and the vein were thrombosed in one case. Preoperative risk factors such as smoking, obesity, radiotherapy, and chemotherapy were not associated with a significantly higher incidence of thrombosis or with significant histological abnormalities in vessels (P value varied between 0.3,0.06). Microvascular histology showed variable degrees of pathological changes in six flaps (15%); nevertheless, in this group, only one flap suffered a venous thrombosis, which ended in total flap loss. Among those with one or more risk factors (24 patients), only 2 had some evidence of histological abnormality of the blood vessels used for the microvascular anastomosis (P = 0.2). © 2003 Wiley-Liss, Inc. MICROSURGERY 23:6,9 2003 [source] Pathological and clinical significance of increased intraepithelial lymphocytes (IELs) in small bowel mucosa,APMIS, Issue 6 2005Review article Intestinal intraepithelial lymphocytes (IELs) belong to a unique T-cell population interspersed between epithelial cells of both the small and large intestine. It is becoming increasingly recognised that an increased number of IELs with a normal villous architecture is within the wide spectrum of histological abnormalities observed in coeliac disease. An increased number of IELs is the earliest pathological change following gluten challenge and a high IEL count may be the only sign of gluten sensitivity. Therefore, the finding of a raised IEL count with normal villous architecture is of sufficient clinical importance to be reported in routine small bowel biopsies. However, it is evident that not all small intestinal biopsy specimens showing increased IELs are explained by gluten sensitivity. Increased IELs in small bowel mucosa have also been associated with autoimmune disorders, tropical sprue, food protein intolerance, Helicobacter pylori -associated gastritis, peptic duodenitis, parasitic and viral infections, as well as the development of intestinal lymphoma. Histological examination of a biopsy specimen of the small bowel remains the diagnostic gold standard for coeliac disease. There will be an ever increasing demand for histological confirmation of gluten sensitivity in patients in whom the classic microscopic appearance of flattened villi may not have fully developed. The more widespread recognition by histopathologists of the pattern of injury manifested by increased numbers of IELs in intestinal biopsy specimens will certainly help in early diagnosis of coeliac disease, lessen diagnostic confusion and influence the modern practice of gastrointestinal tract medicine. This review discusses some of the recent developments in clinical pathology pertaining to increased IELs in small bowel mucosal biopsies. [source] Tolerance of Atlantic salmon (Salmo salar) to dietborne endosulfan assessed by haematology, biochemistry, histology and growthAQUACULTURE NUTRITION, Issue 5 2010A.-K. LUNDEBYE Abstract The inclusion of plant-based ingredients in commercial fish feeds may pose a challenge because of the presence of undesirable substances, such as the pesticide endosulfan. Waterborne endosulfan is highly toxic to fish, whereas dietborne exposure has varied toxicity in different species. To investigate the systemic effects of endosulfan exposure, quadruplicate groups of Atlantic salmon (Salmo salar) were fed either 0 (control), 0.005 mg kg,1; the European Union's maximum limit, or 10 or 20 times this level (0.05 and 0.1 mg kg,1 respectively) for 95 days. There were no significant differences (P > 0.05) in liver somatic index, spleen somatic index, condition factor or growth among treatments. There were no indications of liver damage in fish from any of the groups in the biomarkers measured: plasma aspartate aminotransferase, plasma alanine aminotransferase and histopathology. Similarly, there were no apparent treatment-related effects on the haematological parameters Hct, Hb, mean corpuscular volume, mean corpuscular haemoglobin concentration and mean corpuscular haemoglobin, and blood sodium, potassium, calcium and chloride levels were not significantly (P > 0.05) different among groups. Lipid digestibility, but not energy, protein, or glycogen digestibility, was significantly (P < 0.05) reduced at the highest exposure concentration. However, no significant differences were observed in lipid production value or lipid efficiency ratio. In contrast to previous studies, clinical histological abnormalities were not observed in the intestine, liver or spleen of endosulfan-treated fish. [source] Sequential developmental changes in holoprosencephalic mouse embryos exposed to ethanol during the gastrulation period,BIRTH DEFECTS RESEARCH, Issue 7 2007Daisuke Higashiyama Abstract BACKGROUND: Prenatal exposure to ethanol induces holoprosencephalic malformations in both humans and laboratory animals. However, its teratogenic window for inducing holoprosencephaly is narrow, and the teratogenic mechanism is not well understood. In the present study, we examined the morphological changes in the craniofacial structures of mouse embryos/fetuses at intervals following ethanol treatment and evaluated gene expression patterns in the embryos. METHODS: Pregnant C57BL/6J mice were given two doses of ethanol (30 mg/kg in total) on the morning (7:00 and 11:00 AM) of day 7. The fetuses were observed at E10.5 and E15.5 grossly and/or histologically. The expression of Shh and Nkx2.1 gene transcripts was examined at E8.5 by in situ hybridization. RESULTS: Gross and histological abnormalities of the brain and face were found in ethanol-exposed fetuses, and their midline structures were most frequently affected. The midline commissural fibers were often lacking in ethanol-exposed fetuses, even in those cases without external gross malformations. In situ hybridization revealed down-regulation of Shh and Nkx2.1 genes in ethanol-exposed embryos. CONCLUSIONS: The results indicate that ethanol may perturb the expression of some developmental genes at a critical stage of embryonic development and induce holoprosencephaly and other midline craniofacial malformations, including histological brain abnormalities. Birth Defects Research (Part A), 2007. © 2007 Wiley-Liss, Inc. [source] Gestational Hypoxia Induces White Matter Damage in Neonatal Rats: A New Model of Periventricular LeukomalaciaBRAIN PATHOLOGY, Issue 1 2004Olivier Baud In the premature infant, periventricular leukomalacia, usually related to hypoxic-ischemic white matter damage, is the main cause of neurological impairment. We hypothesized that protracted prenatal hypoxia might induce white matter damage during the perinatal period. Pregnant Sparague-Dawley rats were placed in a chamber supplied with hypoxic gas (10% O2 -90% N2) from embryonic day 5(E5) to E20. Neonatal rat brains were investigated by histology, immunocytochemistry, western blotting, in situ hybridization, DNA fragmentation analysis, and in vivo magnetic resonance imaging (MRI). Body weight of pups subjected to prenatal hypoxia was 10 to 30% lower from p0 to P14 than in controls. Specific white matter cysts wear detected between p0 and p7 in pups subjected to prenatal hypoxia, in addition to abnormal extra-cellular matrix, increased lipid peroxidation, white matter cell death detected by TUNEL and increased activated macrophage counts in white matter. Subsequently, gliotic scars and delayed myelination primarily involving immature oligodendrocytes were seen In vivo MRI with T1, T2, and diffusion sequences disclosed similar findings immediately after birth, showing strong correlations with histological abnormalities. We speculate that protracted prenatal hypoxia in rat induces abnormalities. We speculate that protracted prenatal hypoxia in rat induces white matter damage occurring through local inflammatory response and oxidative stress linked to re-oxygenation during the perinatal period. [source] Significance of high-risk human papillomavirus detection by polymerase chain reaction in primary cervical cancer screeningCYTOPATHOLOGY, Issue 2 2001Y. L. Oh Significance of high-risk human papillomavirus detection by polymerase chain reaction in primary cervical cancer screening The purposes of this study were to evaluate the incidence of high-risk human papillomavirus (HPV) infection by polymerase chain reaction (PCR) and to assess its diagnostic usefulness in primary cervical screening. PCR testing for HPV type 16, 18, 31 and 33 was performed on 1305 specimens obtained during routine cervical cancer screening. We analysed the concurrent cervical smears and biopsy, and correlated them with the HPV infection status. We also evaluated histologically-proven cases with ASCUS smears according to HPV infection. HPV DNA was identified in eight (0.7%) of 1144 cytologically normal patients; nine (10.5%) of 86 ASCUS; seven (25.0%) of 28 LSIL; 26 (78.8%) of 33 HSIL; and in all of three squamous cell carcinomas (SCC). HPV positivity was significantly associated with cytohistological diagnosis for HSIL of more. In addition, HPV-positive ASCUS cases were found to be associated with histological abnormality rather than HPV-negative. The results indicate that high-risk HPV testing by PCR could be a useful adjunct tool for Pap smear in primary cervical screening. The combination of Pap smear and high-risk HPV testing by PCR might reduce unnecessary colposcopy-guided biopsy of women with cytological diagnosis of ASCUS. [source] Hepatic arterial flow becomes the primary supply of sinusoids following partial portal vein ligation in ratsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2006Yukihiro Yokoyama Abstract Background and Aim:, Partial portal vein ligation (PPVL) is a commonly used procedure to induce prehepatic portal hypertension in animal models. The aim of this study was to test the hypothesis that the hepatic arterial flow becomes the primary source feeding the sinusoids in the liver after PPVL. Methods:, Sprague,Dawley rats underwent either sham operation or partial portal vein ligation (PPVL). The number of vessels in the liver at 2 weeks postoperatively was determined by factor VIII immunolocalization and the gene expression of angiogenic factors was assessed by RT-PCR. The total hepatic arterial supply to the liver was measured using the fluorescent microsphere injection technique. To further test the hypothesis, two additional groups of rats underwent hepatic artery ligation (HAL) or PPVL plus HAL (PPHAL). The integrity of hepatic microcirculation was then evaluated in all four groups by intravital microscopy. Results:, At 2 weeks after operation, the number of vessels detected by factor VIII staining was significantly higher in PPVL compared to sham. Densitometric analysis of RT-PCR bands revealed a significant increase of vascular endothelial growth factor gene expression in PPVL compared to sham. Arterial flow to the liver measured by fluorescent microspheres was increased by 190% in PPVL compared to sham. When all four groups were compared, no prominent histological abnormality was observed in sham, HAL, and PPVL groups; however, PPHAL livers showed focal necrosis and inflammatory cell infiltration around the portal triads. Additionally, only the PPHAL livers showed a decreased sinusoidal diameter and significantly lower perfusion index (PPHAL 42.9 ± 6.1; sham 85.7 ± 7.0, PPVL 80.2 ± 6.5, HAL 70.9 ± 4.5). Conclusions:, These results suggest that the hepatic artery flow becomes the primary source for the blood supply of sinusoids and the compensatory change in the hepatic arterial system plays a critical role in maintaining microcirculatory perfusion following the restriction of the portal vein flow by PPVL. [source] Incidence and significance of microscopic pathological lesions found in pedicle and recipient vessels used in microsurgical breast reconstructionMICROSURGERY, Issue 1 2003H.H. El-Mrakby M.D. The purpose of this study was to assess the incidence of abnormal vascular histology and to determine whether or not this was correlated with the incidence of postoperative microvascular problems. The microvascular histology of both donor and recipient vessels was studied in 38 patients (40 flaps) undergoing breast reconstruction with free TRAM flaps. Preoperative risk factors were assessed and correlated with histological changes in vessels, and both were tested against anastomotic complications. Thrombosis of either the artery or the vein of the flap was seen in 6 cases (15%), and of these, two flaps failed completely and one suffered partial necrosis. The occlusion affected the arterial anastomosis in 3 patients, and the venous anastomosis in 2 patients, while both the artery and the vein were thrombosed in one case. Preoperative risk factors such as smoking, obesity, radiotherapy, and chemotherapy were not associated with a significantly higher incidence of thrombosis or with significant histological abnormalities in vessels (P value varied between 0.3,0.06). Microvascular histology showed variable degrees of pathological changes in six flaps (15%); nevertheless, in this group, only one flap suffered a venous thrombosis, which ended in total flap loss. Among those with one or more risk factors (24 patients), only 2 had some evidence of histological abnormality of the blood vessels used for the microvascular anastomosis (P = 0.2). © 2003 Wiley-Liss, Inc. MICROSURGERY 23:6,9 2003 [source] | ||||||||||||||||||||||