Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morbidity and mortality resulting from cardiotoxic complications of anticancer therapy is still unacceptably high. Despite advances in the understanding of the pathomechanisms of cardiotoxicity, in prevention and detection of these complications, progressive ventricular dysfunction in cancer survivors represents a great therapeutic problem. Ventricular dysfunction is a life-threatening complication particularly in patients treated with anthracycline cytostatics. Anthracycline-induced loss of myocytes leads to an inadequate ventricular hypertrophy, which produces a rise in left ventricular (LV) afterload and deterioration of ventricular contractility culminating in heart failure. Efficacy of angiotensin-converting enzyme (ACE) inhibitors for the treatment of asymptomatic and symptomatic LV dysfunction in various clinical settings has been confirmed in a number of controlled, randomized trials. Until now, there are only few published data supporting the use of ACE inhibitors to treat patients with ventricular dysfunction-induced by anthracyclines. Cardio-protection with ACE inhibitors in children and adolescents treated with anthracyclines in contrast to ACE inhibition in adults after anthracycline therapy is a controversial topic. Evidence from the recent follow up study indicates a progressive deterioration of left ventricular wall thinning in childhood cancer survivors treated with enalapril. The ongoing large controlled, double blind, randomized trials will provide an important information concerning the efficacy of ACE inhibitors to prevent progression of ventricular dysfunction in paediatric oncologic patients.
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PMID:[ACE inhibitors in the treatment of ventricular dysfunction caused by cardiotoxic cytostatics]. 1509 72

The disease progression in oral submucous fibrosis (OSF) seems to be in a biphasic manner, along both fibroblastic and keratinocytic lineages. The epithelial malignancy is considered to be a sequel of connective tissue changes. "Atrophy" of epithelium makes it amenable to the effect of oral carcinogens. This concept looks rather simplistic in the light of the current understanding of epithelial cell biology. So the concept of epithelial "atrophy" needs redressal against the backdrop of recent investigations. 12 cases of clinically and histologically advanced OSF cases (M:F = 4:8) who were habitual areca-quid chewers comprise the study group. 5 (M:F=1:4) non-OSF, non-areca-nut chewing healthy volunteers, constituted the control group. Biopsy was done and the sections were processed for light and electron microscopy. Cell countings were made based on established criteria for apoptosis and necrosis under the high resolution of a TEM and electron micrographs were taken. The Apoptotic Index (A1) calculated for the diseased mucosa was 3.0 +/- 1.3 and for the control was 2.1 +/- 1.5 (X2 = 1.21, df= 1, p>0.05). The necrotic indices (NI) were respectively, 2.5 +/- 0.6 and 2.0 +/- 1.3 (X2 = 0.24, df = 1, p>0.05). The Absolute Cell death Index (ACI), which is the cumulative figure of apoptosis and necrosis indices, was 5.5 and 4.2 respectively for diseased and normal samples (X2 = 1.8, df = 1, p>0.05). The inability to compute an increased ACI in OSF epithelium, when compared to normal, goes against the concept of epithelial "atrophy". Atrophy envisages an increased apoptotic cell death of keratinocytes, induced by the same signals that caused atrophy and this may contribute to loss of cell of an entire organ. This basic concept in pathology seems to be unfounded with disease. This prompted us for an alternative concept in favour of a reduced proliferation index of the adult stem cell compartment of the oral epithelium. So this study favours the concept of epithelial hypoplasia, rather than atrophy, which causes thinning of surface epithelium in advanced OSF.
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PMID:Cell death does not herald epithelial involution ("atrophy") in oral sub mucous fibrosis: a TEM study. 1568 90

Epidemiologic studies suggest that dietary complex carbohydrates are protective against colorectal cancer but dietary protein may increase risk. However, experimental data to support these relationships are scant. We have shown in rats that consumption of a high-protein (25% casein) diet for 4 wk resulted in a twofold increase in damage to colonocyte DNA compared with a low-protein (15% casein) diet. This was associated with thinning of the colonic mucous barrier and increased levels of fecal p-cresol. Addition of resistant starch as a high-amylose maize starch to the diet increased cecal short-chain fatty acid pools and attenuated DNA damage, suggesting protection against genotoxic agents. In humans, this could translate to altered risk of colonic cancer.
Nutr Cancer 2005
PMID:Resistant starch attenuates colonic DNA damage induced by higher dietary protein in rats. 1574 29

In a previous study we have shown that high levels of dietary protein (as casein) result in increased levels of colonic DNA damage, measured by the comet assay, and thinning of the colonic mucus layer in rats when dietary resistant starch (RS) is negligible. Feeding RS abolishes these effects. This study aimed to establish whether a diet high in protein as cooked red meat would have similar effects and whether RS was protective. Rats were fed a diet containing 15% or 25% casein or 25% cooked lean red beef, each with or without the addition of 48% high amylose maize starch (a rich source of RS) for four weeks. As expected, high dietary casein caused a 2-fold increase in colonic DNA damage compared with a low casein diet and reduced the thickness of the colonic mucus layer by 41%. High levels of cooked meat caused 26% greater DNA damage than the high casein diet but reduced mucus thickness to a similar degree to casein. Addition of RS to the diet abolished the increase in DNA damage and the loss of colonic mucus thickness induced by either high protein diet. Cecal and fecal short chain fatty acid pools were also increased by inclusion of RS in the diet. Because DNA damage is an early step in the initiation of cancer, these findings suggest that increased DNA damage due to high dietary protein as cooked red meat or casein could increase colorectal cancer risk but inclusion of resistant starch in the diet could significantly reduce that risk.
Cancer Biol Ther 2006 Mar
PMID:Resistant starch prevents colonic DNA damage induced by high dietary cooked red meat or casein in rats. 1662 72

Dysfunctional vascular smooth muscle cell (VSMC) behaviour contributes to the pathogenesis of atherosclerosis and restenosis. Increased rates of VSMC apoptosis are thought to lead to thinning of the fibrous atherosclerotic plaque and thereby instability, while migration of VSMCs to the intima, and inappropriate VSMC proliferation, contribute to intimal thickening that occurs in atherosclerosis and restenosis. Studies, mainly in cancer and neuronal cells, have demonstrated that cell-cell adhesion by the cadherin:catenin complex modulates apoptosis, migration and proliferation. In contrast, until recently the involvement of this complex in the regulation of VSMC behaviour was relatively unstudied. In this review, evidence for the regulation of VSMC apoptosis, migration and proliferation by the cadherin:catenin complex will be discussed.
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PMID:Cadherin:catenin complex: a novel regulator of vascular smooth muscle cell behaviour. 1643 74

Sulfur mustard is an alkylating agent that reacts with ocular, respiratory, cutaneous, and bone marrow tissues, resulting in early and late toxic effects. We compare these effects based on the experience in Iranian veterans exposed to the agent during the Iran-Iraq conflict (1983-88). The first clinical manifestations of sulfur mustard poisoning occurred in the eyes with a sensation of grittiness, lacrimation, photophobia, blepharospasm, and corneal ulceration. Respiratory effects appeared as rhinorhea, laryngitis, tracheobronchitis, and dyspnoea. Skin lesions varied from erythema to bullous necrotization. Initial leukocytosis and lymphopenia returned to normal within four weeks in recovered patients, but marked cytopenia with bone marrow failure occurred in fatal cases. Late toxic effects of sulfur mustard were most commonly found in lungs, skin and eyes. Main respiratory complications were chronic obstructive pulmonary disease, bronchiectasis, asthma, large airway narrowing, and pulmonary fibrosis. Late skin lesions were hyperpigmentation, dry skin, atrophy, and hypopigmentation. Fifteen of the severely intoxicated patients were diagnosed with delayed keratitis, having corneal vascularization, thinning, and epithelial defect. Respiratory complications exacerbated over time, while cutaneous and ocular lesions decreased or remained constant. Both the severity and frequency of bronchiectatic lesions increased during long-term follow-up. The only deteriorating cutaneous complication was dry skin. The maximum incidence of delayed kaeratitis was observed 15 to 20 years after initial exposure. Being suggested as the main cause ofassociated with malignancies and recurrent infections, natural killer cells were significantly lower 16 to 20 years after intoxication.
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PMID:Comparison of early and late toxic effects of sulfur mustard in Iranian veterans. 1704 Feb 11

Previous studies have shown increased levels of colonocyte DNA damage (as measured by the comet assay) and thinning of the colonic mucus layer in rats fed higher dietary protein as casein or red meat with highly digestible starch. Feeding resistant starch (RS) as high amylose maize starch (HAMS) opposed these changes. However, the dietary level of HAMS was relatively high (48% by weight) so this study was conducted to establish whether HAMS had the same effects at lower dietary levels. Adult male rats were fed a diet containing 25% casein with 0%, 10%, 20%, 30% or 40% HAMS for 4 wk. DNA single strand breaks and 8-hydroxyguanosine levels were measured in isolated colonocytes by the comet assay. As expected, comet tail moment was greatest and the mucus barrier thinnest in rats fed 0% HAMS. DNA damage was reduced and the mucus barrier thickened in a logarithmic dose-dependent manner by HAMS. There was no significant difference in 8-hydroxyguanosine between dietary groups. Caecal and fecal short chain fatty acid (SCFA) pools rose with the increased level of dietary HAMS. DNA damage of colonocytes correlated negatively with caecal SCFA but the strongest correlation was with caecal butyrate, which is consistent with the proposed role of this SCFA in promoting a normal cell phenotype. These data show that HAMS prevents protein-induced colonic DNA damage in a dose-dependent manner. Inclusion of 10% HAMS was found to be sufficient to oppose colonocyte DNA damage, and to increase caecal and fecal SCFA pools.
Cancer Biol Ther 2007 Feb
PMID:Dose-dependent reduction of dietary protein-induced colonocyte DNA damage by resistant starch in rats correlates more highly with caecal butyrate than with other short chain fatty acids. 1742 35

Automatic centromere identification and polarity assignment are two key factors in the automatic karyotyping of human chromosomes. A multi-stage rule-based computer scheme has been investigated to automatically detect centomeres and determine polarities for both abnormal and normal metaphase chromosomes. The scheme first implements a modified thinning algorithm to identify the medial axis of a chromosome and extracts three feature profiles. Based on a set of pre-optimized classification rules, the scheme adaptively identifies the centromere and then assigns corresponding polarity. An image dataset of 2287 chromosomes acquired from 24 abnormal and 26 normal Giemsa metaphase cells is utilized to optimize and test the scheme. The overall accuracy is 91.4% for centromere identification and 97.4% for polarity assignment. The experimental results demonstrate that our scheme can be successfully applied to diverse chromosomes, which include those severely bent and abnormal chromosomes extracted from cancer cells.
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PMID:A rule-based computer scheme for centromere identification and polarity assignment of metaphase chromosomes. 1808 9

Tumor vascularity is an important factor that has been shown to correlate with tumor malignancy and was demonstrated as a prognostic indicator for a wide range of cancers. Three-dimensional (3-D) power Doppler ultrasound (PDUS) offers a convenient tool for investigators to inspect the signals of blood flow and vascular structures in breast cancer. In this paper, a new computer-aided diagnosis (CAD) system for quantifying Doppler ultrasound images based on 3-D thinning algorithm and neural network is proposed. We extracted the skeleton of blood vessels from 3-D PDUS data to facilitate the capturing of morphological changes. Nine features including vessel-to-volume ratio, number of vascular trees, length of vessels, number of branching, mean of radius, number of cycles, and three tortuosity measures, were extracted from the thinning result. Benign and malignant tumors can therefore be differentiated by a score computed by a multilayered perceptron (MLP) neural network using these features as parameters. The proposed system was tested on 221 breast tumors, including 110 benign and 111 malignant lesions. The accuracy, sensitivity, specificity, and positive and negative predictive values were 88.69% (196/221), 91.89% (102/111), 85.45% (94/110), 86.44% (102/118), and 91.26% (94/103), respectively. The Az value of the ROC curve was 0.94. The results demonstrate a correlation between the morphology of blood vessels and tumor malignancy, indicating that the newly proposed method can retrieves a high accuracy in the classification of benign and malignant breast tumors.
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PMID:Analysis of tumor vascularity using three-dimensional power Doppler ultrasound images. 1833 28

An 82-year-old diabetic female had been aware of gradually enlarging, painless scalp depressions in the bilateral parietal regions for more than 6 years. She had no history of head injury, or inflammatory or malignant disease. Her family history was unremarkable for hereditary bone disease. She had diabetes mellitus which had been well controlled with orally administered drugs. Blood examination showed normal renal and liver functions with normal serum calcium, magnesium, and phosphorus concentrations, in addition to normal parathyroid hormone and calcitonin levels. Neuroimaging including skull radiography, head computed tomography, and magnetic resonance imaging demonstrated symmetric thinning in the bilateral parietal bones attributed to loss of diploe and thinning of the outer table. The inner table was intact without associated soft tissue mass or vascular lesions. Technetium-99m methylene diphosphate systemic bone scintigraphy showed mild hypoaccumulation in the affected calvarium on the left. No other pathological findings were found by systemic examination. She underwent open biopsy for histological verification which revealed homogeneous membranous bone tissue with regressed diploe, absence of osteoblasts, absence of osteoclastic appearance, and absence of findings of underlying malignancy. There was no markedly fibrovascular connective tissue typical of Gorham-Stout disease. Calvarial thinning in the present case may have been caused by an undetermined complex mechanism.
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PMID:Idiopathic calvarial thinning. 1857 36


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