Distinct Histopathological Changes Research Articles

Examining the effect of Helicobacter pylori cagPAI variety on gene expression pattern related to gastric cancer.

We aimed to determine possible association between heterogeneity of Helicobacter pylori cytotoxin-associated gene pathogenicity island and gene expression profiles in patients with distinct histopathological changes. Gastric biopsies were obtained from seventy five patients. Microbiological and pathological examinations were done and intactness of Helicobacter pylori cagPAI was determined by PCR using 11 pairs of primers flanking cagζ-cagA regions and cagPAI empty site. Alterations at mRNA levels of eight genes were investigated by real-time PCR and their association with cagPAI intactness and histopathological changes examined statistically. A larger proportion of cagPAI positive strains colonized patients with SAG (52.4%), followed by CG (33.3%), and IM (14.3%). Intact cagPAI was found in 87.5% of the strains obtained from patients with SAG, while significantly lower frequency was detected among those with CG (12.5%) and IM (0%). No significant difference was found among thestudied histological groups and fold changes in gene expression of gastric biopsies of Helicobacter pylori infected patients with distinct cagPAI status. However, in each histological group, the strains with more complete gene cluster induced (ErbB2, CCNE1, CTNNB1, and MMP7 in SAG and IM groups) or reduced (TP53, in CG group) expression of the GC associated genes in relatively higher levels. APC, TP53 and E-cadherin were down-regulated in patients with SAG and IM compared with CG patients, irrespective to the status of cagPAI integrity. Helicobacter pylori strains that carry more complete cagPAI segment could induce remarkably higher levels of mRNA changes of GC associated genes in all histopathological groups.

Comparative Histopathology of Bovine Acute Interstitial Pneumonia and Bovine Respiratory Syncytial Virus-Associated Interstitial Pneumonia

Acute interstitial pneumonia (AIP) is a significant disease of cattle and many aetiologies have been implicated on the basis of the characteristic pathological lesions. Bovine respiratory syncytial virus (BRSV) is one of the key aetiological factors in bovine respiratory disease complex and several studies have suggested, controversially, that BRSV may be an underlying cause of bovine AIP. BRSV infection is known to cause several distinctive histopathological changes, including epithelial syncytia formation and intracytoplasmic viral inclusions. However, distinguishing bovine AIP from BRSV-related pneumonia by clinical presentation, gross pathology or histopathology can sometimes be challenging. In order to identify the potential distinguishing features, we compared the histopathological findings of AIP that were, and were not, associated with BRSV infection in naturally occurring cases. We found that multinucleated giant cells were more frequently identified in cattle with AIP while bronchiolitis was more common in BRSV-infected cattle. However, this was not considered a sole indicator of either disease group. Statistically, we identified that a combination of several histopathological features, including alveolar septal necrosis, presence of multinucleated giant cells and bronchiolitis, can serve as an excellent indicator for distinguishing between idiopathic AIP and BRSV-related pneumonia, with a strong statistical significance (P=0.0004). Based on the results of this retrospective study, we present a histopathological scoring system for predicting BRSV-associated AIP.

Pulmonary Parenchymal Changes in COVID-19 Survivors

BackgroundAs the COVID-19 pandemic moves into the survivorship phase, questions regarding long-term lung damage remain unanswered. Previous histopathologic studies are limited to autopsy reports. We studied lung specimens from COVID-19 survivors who underwent elective lung resections to determine whether postacute histopathologic changes are present. MethodsThis multicenter observational study included 11 adult COVID-19 survivors who had recovered but subsequently underwent unrelated elective lung resection for indeterminate lung nodules or lung cancer. We compared these against an age- and procedure-matched control group who never contracted COVID-19 (n = 5) and an end-stage COVID-19 group (n = 3). A blinded pulmonary pathologist examined the lung parenchyma focusing on 4 compartments: airways, alveoli, interstitium, and vasculature. ResultsElective lung resection was performed in 11 COVID-19 survivors with asymptomatic (n = 4), moderate (n = 4), and severe (n = 3) COVID-19 infections at a median 68.5 days (range 24-142 days) after the COVID-19 diagnosis. The most common operation was lobectomy (75%). Histopathologic examination identified no differences between the lung parenchyma of COVID-19 survivors and controls across all compartments examined. Conversely, patients in the end-stage COVID-19 group showed fibrotic diffuse alveolar damage with intra-alveolar macrophages, organizing pneumonia, and focal interstitial emphysema. ConclusionsIn this study to examine the lung parenchyma of COVID-19 survivors, we did not find distinct postacute histopathologic changes to suggest permanent pulmonary damage. These results are reassuring for COVID-19 survivors who recover and become asymptomatic.

Inflammatory Immune Responses and Gut Microbiota Changes Following Campylobacter coli Infection of IL-10-/- Mice with Chronic Colitis.

Human infections with the food-borne enteropathogens Campylobacter are progressively rising. Recent evidence revealed that pre-existing intestinal inflammation facilitates enteropathogenic infection subsequently exacerbating the underlying disease. Given that only little is known about C. coli–host interactions and particularly during intestinal inflammation, the aim of the present study was to survey gastrointestinal colonization properties, gut microbiota changes and pro-inflammatory sequelae upon peroral C. coli-infection of IL-10-/- mice with chronic colitis. C. coli colonized the gastrointestinal tract of mice with varying efficiencies until day 28 post-infection and induced macroscopic and microscopic inflammatory changes as indicated by shorter colonic lengths, more distinct histopathological changes in the colonic mucosa and higher numbers of apoptotic colonic epithelial cells when compared to mock-infected controls. Furthermore, not only colonic innate and adaptive immune cell responses, but also enhanced systemic TNF-α secretion could be observed following C. coli as opposed to mock challenge. Notably, C. coli induced intestinal inflammatory sequelae were accompanied with gut microbiota shifts towards higher commensal enterobacterial loads in the infected gut lumen. Moreover, the pathogen translocated from the intestinal tract to extra-intestinal tissue sites in some cases, but never to systemic compartments. Hence, C. coli accelerates inflammatory immune responses in IL-10-/- mice with chronic colitis.

Small-for-gestational age placentas associate with an increased risk of adverse outcomes in pregnancies complicated by either type I or type II pre-gestational diabetes mellitus

Introduction One-fifth of pregnancies with pre-gestational diabetes mellitus (pre-DM) yield placentas <10th percentile small for gestational age (SGA), compared to a non-diabetic population. We hypothesized that SGA placentas of women with pre-DM, whether type I (T1DM) or type II (T2DM), exhibit distinct histopathological changes and pregnancy outcomes compared to pre-DM pregnancies with an AGA placenta. Methods We conducted a retrospective, cohort study of placentas from pregnant women enrolled in the Diabetes in Pregnancy Program at Brown University between 2003 and 2011, by comparing pre-DM patients with SGA placentas to pre-DM patients with AGA placental weights. Results The SGA placenta groups were associated with an increased risk for adverse clinical outcomes, compared to AGA placentas in pregnancies complicated by either T1DM or T2DM. Compared to their AGA pre-DM counterparts, T1DM, SGA placentas show increased peri-villous fibrin/fibrinoid deposition, thrombosis in fetal blood vessels, and meconium staining. Moreover, the histopathology of SGA placentas from T2DM is characterized by decidual vasculopathy, accelerated villous maturity, and erythroblastosis, compared to T2DM AGA placentas. The contrasting placental pathologies between the two pre-DM SGA phenotypes evolved independent of patient demographics and were unrelated to indicators of the glycemic control present at early gestational ages. Discussion A sub-population of pre-DM women with either T1DM or T2DM diabetes that have an SGA placenta are at increased risk for adverse clinical outcomes in pregnancy, compared to pre-DM women with AGA placental weights.

BAP1-inactivated melanocytic tumor with preserved BAP1 expression? Morphology to the rescue!

BAP1-inactivated melanocytic tumors typically present with distinctive histopathological changes and loss of nuclear BAP1 protein expression. Rare cases exhibit the typical morphology but with preserved expression of BAP1. In the current issue of Journal of Cutaneous Pathology, Linos et al. describe such a case and provide a comprehensive molecular-genetic exploration to explain such a phenomenon.

Quantitative myocardial tissue characterization by cardiac magnetic resonance in heart transplant patients with suspected cardiac rejection.

Distinct histopathologic changes occur in acute cellular rejection (ACR), antibody-mediated rejection (AMR), and biopsy-negative rejection (BNR). Cardiovascular magnetic resonance (CMR)-based myocardial tissue characterization can be used to quantify these changes. We assessed T1, T2, and extracellular volume fraction (ECV) by CMR in patients with subtypes of rejection. T1, T2, and ECV were quantified at the mid-ventricular level and compared between patients with and without rejection. The association between quantitative tissue characteristics and the combined outcome of death, retransplantation, heart failure hospitalization, or myocardial infarction was evaluated with a Cox-proportional hazards model. In 46 patients, mean age 53.3±13.7years, 71.7% male, at a median of 7.4years from transplant, average myocardial T1 was increased in BNR compared with no rejection (1057 vs 1012msec, P=.006). Average myocardial T2 was elevated in all types of rejection, P<.05. In a cox-proportional hazards model, higher T2 values were associated with an increase in the combined clinical outcome (adjusted HR 1.21, 95% CI 1.06-1.37, P=.004) after adjusting for left ventricular mass index. Myocardial tissue characteristics are abnormal in all subtypes of rejection, and abnormal T2 quantified by CMR provides additional prognostic value.

Transient use of a systemic adenosine kinase inhibitor attenuates epilepsy development in mice.

Over one-third of all patients with epilepsy are refractory to treatment and there is an urgent need to develop new drugs that can prevent the development and progression of epilepsy. Epileptogenesis is characterized by distinct histopathologic and biochemical changes, which include astrogliosis and increased expression of the adenosine-metabolizing enzyme adenosine kinase (ADK; EC 2.7.1.20). Increased expression of ADK contributes to epileptogenesis and is therefore a target for therapeutic intervention. We tested the prediction that the transient use of an ADK inhibitor administered during the latent phase of epileptogenesis can mitigate the development of epilepsy. We used the intrahippocampal kainic acid (KA) mouse model of temporal lobe epilepsy, which is characterized by ipsilateral hippocampal sclerosis with granule cell dispersion and the development of recurrent hippocampal paroxysmal discharges (HPDs). KA-injected mice were treated with the ADK inhibitor 5-iodotubercidin (5-ITU, 1.6mg/kg, b.i.d., i.p.) during the latent phase of epileptogenesis from day 3-8 after injury; the period when gradual increases in hippocampal ADK expression begin to manifest. HPDs were assessed at 6 and 9weeks after KA administration followed by epilepsy histopathology including assessment of granule cell dispersion, astrogliosis, and ADK expression. 5-ITU significantly reduced the percent time in seizures by at least 80% in 56% of mice at 6weeks post-KA. This reduction in seizure activity was maintained in 40% of 5-ITU-treated mice at 9weeks. 5-ITU also suppressed granule cell dispersion and prevented maladaptive ADK increases in these protected mice. Our results show that the transient use of a small-molecule ADK inhibitor, given during the early stages of epileptogenesis, has antiepileptogenic disease-modifying properties, which provides the rationale for further investigation into the development of a novel class of antiepileptogenic ADK inhibitors with increased efficacy for epilepsy prevention.

Antibiotic Resistance Among Helicobacter pylori Strains Isolated from Patients with Gastric Pathologies Towards Metronidazole, Clarithromycin, and Ciprofloxacin

Background: The extent of antibiotic resistance among Helicobacter pylori strains influences current clinical therapeutic regimens in each region. Objectives: This cross-sectional study aimed to determine the resistance property and minimum inhibitory concentration (MIC50-90) of Helicobacter pylori strains toward metronidazole, clarithromycin, and ciprofloxacin in patients with distinct gastric histopathological changes in Tehran, Iran. Methods: This study was conducted on 170 patients suffering from gastric complications in three hospitals in Tehran from October 2014 until March 2015. Two separate biopsy samples were collected from each patient and used for pathological and microbiological examinations. Antimicrobial susceptibility tests were performed by agar dilution method according to the CLSI guidelines. The MIC values and susceptibility to varying concentrations of metronidazole (4 to 64 µg/mL), ciprofloxacin (0.5 to 16 µg/mL), and clarithromycin (0.25 to 16 µg/mL) were determined based on EUCAST recommendations. Results: Our results indicated the infection with H. pylori in a frequency of 32% (55/170) among the study patients (female, 51% and male, 49%). Endoscopic findings indicated that 42% of the patients suffered from peptic ulcers, 33% from duodenal ulcers, and 25% with a non-ulcer disease. Pathological findings indicated 58% of the patients had chronic gastritis, 33% had active chronic gastritis, and 9% suffered from intestinal metaplasia. In terms of antibiotic susceptibility, nearly 76.3%, 49%, and 45.5% of the strains were resistant to metronidazole, clarithromycin, and ciprofloxacin, respectively. The MIC values at which the growth of 50% and 90% of the strains was inhibited (MIC50-90) were 32 - 64 µg/mL for metronidazole, 0.5 - 16 µg/mL for clarithromycin, and 2 - 16 µg/mL for ciprofloxacin. Conclusions: The overall resistance levels were relatively high among the study patients. Accordingly, the administration of other anti-Helicobacter drugs, as well as more appropriate therapeutic regimens based on laboratory results, is recommended in patients with a history of treatment failure.

Consensus statement on surgical pathology of the aorta from the Society for Cardiovascular Pathology and the Association For European Cardiovascular Pathology: II. Noninflammatory degenerative diseases - nomenclature and diagnostic criteria.

Surgical aortic specimens are usually examined in Pathology Departments as a result of treatment of aneurysms or dissections. A number of diseases, genetic syndromes (Marfan syndrome, Loeys-Dietz syndrome, etc.), and vasculopathic aging processes involved in vascular injury can cause both distinct and nonspecific histopathologic changes with degeneration of the media as a common denominator. Terminology for these changes has varied over time leading to confusion and inconsistencies. This consensus document has established a revised, unified nomenclature for the variety of noninflammatory degenerative aortic histopathologies seen in such specimens. Older terms such as cystic medial necrosis and medionecrosis are replaced by more technically accurate terms such as mucoid extracellular matrix accumulation (MEMA), elastic fiber fragmentation and/or loss, and smooth muscle cell nuclei loss. A straightforward system of grading is presented to gauge the extent of medial degeneration and synoptic reporting tables are provided. Herein we present a standardized nomenclature that is accessible to general pathologists and useful for future publications describing these entities.

Anti-Inflammatory Properties of NAP in Acute Toxoplasma gondii-Induced Ileitis in Mice

The octapeptide NAP has been shown to exert neuroprotective properties. Here, we investigated potential anti-inflammatory effects of NAP in an acute ileitis model. To address this, C57BL/6j mice were perorally infected with Toxoplasma gondii (day 0). Within 1 week postinfection (p.i.), placebo (PLC)-treated mice developed acute ileitis due to Th1-type immune responses. Mice that were subjected to intraperitoneal NAP treatment from day 1 until day 6 p.i., however, developed less distinct macroscopic and microscopic disease as indicated by less body weight loss, less distinct histopathological ileal changes, and lower ileal apoptotic, but higher proliferating cell numbers, less abundance of neutrophils, macrophages, monocytes, and T lymphocytes, but higher numbers of regulatory T cells in the ileal mucosa and lamina propria, and lower concentrations of pro-inflammatory mediators in the ilea as compared to PLC controls at day 7 p.i. Remarkably, NAP-mediated anti-inflammatory effects could also be observed in extra-intestinal compartments including liver and spleen. Strikingly, lower MCP-1, TNF, and IL-12p70 serum concentrations in NAP as compared to PLC-treated mice at day 7 p.i. indicate a pronounced systemic anti-inflammatory effect of NAP in acute ileitis. These findings provide first evidence for NAP as a potential novel treatment option in intestinal inflammation.

Impairment of thalamo-cortical network activities in animal models of multiple sclerosis

Introduction: Infiltration of immune cells, demyelination, axonal damage and neuronal degeneration are all indicative of the impaired interplay between the immuneandnervous systemduringmultiple sclerosis (MS). The neuroinflammatory events and resulting alterations in neuronal excitability can cause changes in synaptic network function. The aim of this study was to evaluate the hypothesis that distinct histopathological changes like inflammation or demyelination can lead to alterations in neuronal network activities in thalamo-cortical network system. Methods: Control and cuprizone treated mice (general demyelination in the CNS) unilaterally equipped with micro-wire arrays (MWA, 1 array, 8 electrodes and one reference/array per brain region) in the 4th layer of the auditory cortex (AC-IV) and ventral part of the Medial Geniculate Nucleus (MGNv) of the thalamus. Unit activities were recorded before, during and after the presentation of auditory stimuli (2.5 and 10 kHz, 6 times each). The spikes of individual neurons were sorted by a time-amplitude window discrimination and principal component analysis and verified through quantification of cluster analysis. Baseline as well as stimulus-related neuronal firing rates were analyzed and compared between the demyelinated, remyelinating and remyelinated mice. Results: Compared to control mice, demyelinated mice show decreased neuronal activities, but with the time during remyelination, the activity comes back. In addition to that, the control mice show neuronal response to high frequency (10 kHz) auditory stimuli, but the cuprizone treated mice are not able to discriminate between high (10 kHz) and low frequency (2.5 kHz) auditory stimuli. Conclusion: Neurons in auditory cortex and auditory thalamus possess response specificity and discrimination properties. But after cuprizone treatment, sensory responsiveness is abolished and slowly recovers with remyelination, although discrimination properties and specificity remain impaired. Acknowledgements: This work is supported by the CRC TR 128, B6, Meuth, Pape and Budde.

Radical antioxidants limit blood–brain barrier activation and ameliorate disease in models of multiple sclerosis

Introduction: Infiltration of immune cells, demyelination, axonal damage and neuronal degeneration are all indicative of the impaired interplay between the immuneandnervous systemduringmultiple sclerosis (MS). The neuroinflammatory events and resulting alterations in neuronal excitability can cause changes in synaptic network function. The aim of this study was to evaluate the hypothesis that distinct histopathological changes like inflammation or demyelination can lead to alterations in neuronal network activities in thalamo-cortical network system. Methods: Control and cuprizone treated mice (general demyelination in the CNS) unilaterally equipped with micro-wire arrays (MWA, 1 array, 8 electrodes and one reference/array per brain region) in the 4th layer of the auditory cortex (AC-IV) and ventral part of the Medial Geniculate Nucleus (MGNv) of the thalamus. Unit activities were recorded before, during and after the presentation of auditory stimuli (2.5 and 10 kHz, 6 times each). The spikes of individual neurons were sorted by a time-amplitude window discrimination and principal component analysis and verified through quantification of cluster analysis. Baseline as well as stimulus-related neuronal firing rates were analyzed and compared between the demyelinated, remyelinating and remyelinated mice. Results: Compared to control mice, demyelinated mice show decreased neuronal activities, but with the time during remyelination, the activity comes back. In addition to that, the control mice show neuronal response to high frequency (10 kHz) auditory stimuli, but the cuprizone treated mice are not able to discriminate between high (10 kHz) and low frequency (2.5 kHz) auditory stimuli. Conclusion: Neurons in auditory cortex and auditory thalamus possess response specificity and discrimination properties. But after cuprizone treatment, sensory responsiveness is abolished and slowly recovers with remyelination, although discrimination properties and specificity remain impaired. Acknowledgements: This work is supported by the CRC TR 128, B6, Meuth, Pape and Budde.

Spinal cord pathology in chronic experimentalToxoplasma gondiiinfection

Infection with the protozoan Toxoplasma (T.) gondii causes chronic infection of the central nervous system and can lead to life-threatening encephalomyelitis in immunocompromised patients. While infection with T. gondii has long time been considered asymptomatic in immunocompetent hosts, this view is challenged by recent reports describing links between seropositivity and behavioral alterations. However, past and current researches are mainly focused on the brain during Toxoplasma encephalitis, neglecting the spinal cord as a key structure conveying brain signals into motion. Therefore, our study aimed to fill the gap and describes the spinal cord pathology in an experimental murine model of toxoplasmosis. In the spinal cord, we found distinct histopathological changes, inflammatory foci and T. gondii cysts similar to the brain. Furthermore, the recruitment of immune cells from the periphery was detected. Moreover, resident microglia as well as recruited monocytes displayed an increased MHC classes I and II expression. Additionally, the expression of pro- and anti-inflammatory cytokines was enhanced in the brain as well as in the spinal cord. In summary, the pathology observed in the spinal cord was similar to the previously described changes in the brain during the infection. This study provides the first detailed description of histopathological and immunological alterations due to experimental T. gondii induced myelitis in mice. Thus, our comparison raises awareness of the importance of the spinal cord in chronic T. gondii infection.

Gastro-intestinal toxicity of chemotherapeutics in colorectal cancer: the role of inflammation.

Chemotherapy-induced diarrhea (CID) is a common and often severe side effect experienced by colorectal cancer (CRC) patients during their treatment. As chemotherapy regimens evolve to include more efficacious agents, CID is increasingly becoming a major cause of dose limiting toxicity and merits further investigation. Inflammation is a key factor behind gastrointestinal (GI) toxicity of chemotherapy. Different chemotherapeutic agents activate a diverse range of pro-inflammatory pathways culminating in distinct histopathological changes in the small intestine and colonic mucosa. Here we review the current understanding of the mechanisms behind GI toxicity and the mucositis associated with systemic treatment of CRC. Insights into the inflammatory response activated during this process gained from various models of GI toxicity are discussed. The inflammatory processes contributing to the GI toxicity of chemotherapeutic agents are increasingly being recognised as having an important role in the development of anti-tumor immunity, thus conferring added benefit against tumor recurrence and improving patient survival. We review the basic mechanisms involved in the promotion of immunogenic cell death and its relevance in the treatment of colorectal cancer. Finally, the impact of CID on patient outcomes and therapeutic strategies to prevent or minimise the effect of GI toxicity and mucositis are discussed.

Effects of illegal cyanide fishing on vitellogenin in the freshwater African catfish, Clarias gariepinus (Burchell, 1822)

The effects of cyanide, used in illegal fishing, on one of the most economically important Nile fishes, the African catfish (Clarias gariepinus), were studied. Cyanide impacts were evaluated in terms of biochemical, molecular and histopathological characteristics. After exposure to sublethal concentration (0.05mg/l) of potassium cyanide (KCN) for two and four weeks, GOT (glutamate oxaloacetate transaminase) was significantly increased in both male and female, while GPT (glutamate pyruvate transaminase), total plasma protein, phosphoprotein phosphorus (Vgt) in serum, vitellogenin gene expression (Vtg mRNA) and estrogen receptors (ER mRNA) were significantly decreased in female. On the other hand, male C. gariepinus showed a significant increase in Vtg and Vtg mRNA. Liver, testis and ovaries showed distinct histopathological changes. It was concluded that, cyanide caused damaging effects to fish and can cause serious disturbance in the natural reproduction and a drastic decline in fish population. Therefore, it is recommended that, the use of cyanide compounds must be prohibited to conserve the fisheries resources.

Altered lung function relates to inflammation in an acute LPS mouse model

Preclinical in vivo models of lipopolysaccharide (LPS) -induced acute lung injury are commonly used to recapitulate pathophysiological features of chronic obstructive pulmonary disease and acute exacerbations. The LPS-induced lung inflammation is well described; however, whether the inflammatory response relates temporally to specific alterations in lung function has not been elucidated.We have investigated the effects of acute LPS inhalation in mice up to 96 h post LPS. Quantitation of inflammatory cells and inflammatory mediators in bronchoalveolar lavage fluid and non-invasive and invasive lung function measurements were performed at corresponding time points. The inhibitory effect of the glucocorticoid, budesonide, on LPS-induced lung inflammation and lung function was determined.LPS inhalation induced distinct histopathological changes, and infiltration of inflammatory cells to the lungs peaked at 48 h. At this time point, significantly increased inflammatory mediators and significantly altered lung capacity and mechanics parameters were observed. Budesonide given per os prevented the LPS-induced lung inflammation and lung dysfunction.These results demonstrate a temporal relationship between the peak of inflammatory cell influx and significant impairment of lung function, suggestive of a causative role of inflammation. These results allow better understanding of the functional consequences of lung inflammation in respiratory diseases.

Genomic Amplification of hTERC in Paraffin-embedded Tissues of Cervical Intraepithelial Neoplasia and Invasive Cancer

Cervical lesions and invasive cervical carcinomas are frequently associated with the amplification of chromosome 3q, which harbors the human telomerase gene hTERC. The differential diagnosis between low-grade and high-grade cervical lesions has been a clinical challenge in cytopathology. In the current study, we evaluated hTERC amplification by fluorescence in situ hybridization in cervical lesions with distinct histopathological changes and assessed the potential application of this technology in diagnosis. We showed that the frequency of genomic amplification of hTERC increased with the severity of the disease, with no marked difference between disease-free cervical squamous epithelium and Grade I cervical intraepithelial neoplasia(CIN)1, but that there were significant differences between these 2 stages and the CIN2, CIN3, and squamous cell carcinoma lesions. The difference between CIN1 and CIN2 would be of great importance for differential diagnosis in the clinic. In addition, hTERC amplification status exhibited a sensitivity of 59.42%, a specificity of 85.29%, an accuracy of 67.96%, a positive prediction value of 89.13%, and a negative prediction value of 68.42% in distinguishing CIN1 from CIN2/3 lesions. Therefore, hTERC amplification within cervical lesions can be accurately assessed by fluorescence in situ hybridization analysis on paraffin tissue microarrays. This technique may be clinically applied to differentiate between CIN1 and CIN2/3 lesions in paraffin-embedded biopsy tissues.

Unusual imaging features of completely isolated enteric duplication in a child

We report a case of completely isolated enteric duplication in an 18-month-old boy in whom US revealed a reniform abdominal mass with a pseudokidney sign that had no connection to adjacent organs. Distinctive histopathological changes of the duplication account for these unusual imaging features. Our case represents a diagnostic challenge in this rare entity. To our knowledge, this is a unique case.

Polychlorinated Biphenyls Affect Thyroid Function and Induce Autoimmunity in Sprague-Dawley Rats

Polychlorinated biphenyls (PCBs) have been reported to cause a variety of toxic effects. In order to assess the thyroid function after exposure to PCBs and investigate whether PCBs induce autoimmune process in the thyroid gland, we determined the levels of serum thyroid hormones (FT3, FT4, and T4), thyroid-stimulating hormone (TSH), and thyroid peroxidase antibody (TPOAb) in Sprague-Dawley rats treated with a commercial mixture of PCBs, Aroclor 1,254 (PCBs group), or the antithyroid drug, propylthiouracil (PTU group). The histopathology of the thyroid was also examined. Serum FT3, FT4, and T4 concentrations were significantly reduced, while TSH values were dramatically increased in PCBs group and PTU group compared with control rats (p < 0.05). TPOAb levels were significantly elevated in PCBs-treated rats (p < 0.05) but not in PTU group (p > 0.05). In contrast to the controls, treatment with PCBs lead to distinct histopathological changes in the thyroid gland, such as hyperplasia of the epithelia in follicles, colloid content reduction, vascularization, and lymphocytic infiltration in the perifollicular areas, whereas the major changes in the thyroid in PTU-treated rats were follicles shrinkage or collapse and colloid content reduction compatible with induced hypothyroidism. The results indicate that PCBs affect thyroid function via the induction of autoimmunity, which is a mechanism different from the effect of antithyroid drug on the thyroid gland.