Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori is a Gram-negative spiral-shaped bacterium that colonizes over half of the world's population. Chronic H. pylori infection is associated with increased risk for numerous disease outcomes including gastritis, dysplasia, neoplasia, B-cell lymphoma of mucosal-associated lymphoid tissue (MALT lymphoma), and invasive adenocarcinoma. The complex interactions that occur between pathogen and host are dynamic and exquisitely regulated, and the relationship between H. pylori and its human host are no exception. To successfully colonize, and subsequently persist, within the human stomach H. pylori must temporally regulate numerous genes to ensure localization to the gastric lumen and coordinated expression of virulence factors to subvert the host's innate and adaptive immune response. H. pylori achieves this precise gene regulation by sensing subtle environmental changes including host-mediated alterations in nutrient availability and responding with dramatic global changes in gene expression. Recent studies revealed that the presence or absence of numerous metal ions encountered in the lumen of the stomach, or within host tissues, including nickel, iron, copper and zinc, can influence regulatory networks to alter gene expression in H. pylori. These expression changes modulate the deployment of bacterial virulence factors that can ultimately influence disease outcome. In this review we will discuss the environmental stimuli that are detected by H. pylori as well as the trans regulatory elements, specifically the transcription regulators and transcription factors, that allow for these significant transcriptional shifts.
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PMID:Metalloregulation of Helicobacter pylori physiology and pathogenesis. 2638 55

Patients with underlying malignancy who develop new skin findings while acutely ill often require skin biopsy for histologic evaluation and/or culture to reach a diagnosis. Here, we present the case of a 53-year-old male with relapsed diffuse large B-cell lymphoma on chemotherapy who developed new skin lesions on the leg. On exam, there were 2 nickel-sized, erythematous to violaceous round plaques with central necrotic cores on the right lower leg with relatively nonspecific clinical features for which the initial differential diagnosis was broad. Consensus on a diagnosis was reached upon histologic evaluation of his skin biopsy in the context of his clinical setting. This diagnosis led to a change in treatment plan, with subsequent clinical improvement.
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PMID:A 53-Year-Old Male with Relapsed Diffuse Large B-Cell Lymphoma on Chemotherapy with a New Leg Lesion. 2945 99

The purpose of this research is to go a step further study on the reproductive toxicities and the underlying mechanisms induced by nickel nanoparticles (NiNPs), and the possible protective action of vitamin C. Animal experiment was designed according to the one-generation reproductive toxicity standard, and rats were exposed to NiNPs through gavage. Ultrastructural, reactive oxygen species (ROS), oxidant and antioxidant enzymes, and cell apoptosis-related factors in the testicular tissue were analyzed. In contrast with the control group, the activity of surperoxide dismutase (SOD), catalase (CAT) and gonad-stimulating hormone (GSH) was reduced, while the content of nitric oxide (NO), malondialdehyde (MDA) and ROS was increased in the NiNPs treated animals. As the doses of NiNPs increase, the mRNA of apoptotic related factor Caspase-9, Caspase-8 and Caspase-3 showed an obviously upregulation. Protein expression of Bcl-2-associated X Protein (Bax) and apoptosis inducing factor (AIF) was significantly unregulated. After addition of antioxidants-vitamin C, the toxicity was reduced. Injured testicular tissue indicated that NiNPs exposure could damage the reproductive system. Our results suggest that NiNPs induce significant reproductive toxicities. The cellular apoptosis might be induced by caspase family proteinases, but the regulator factor (factor associated suicide (Fas), B-cell lymphoma-2 (Bcl-2), Bax, BH3-interacting domain death agonist (Bid) and AIF protein) might not be involved in this process. Thus, the mechanism of reproductive toxicity of NiNPs on rat testes involves in the induction of oxidative stress, which further results in cell apoptosis. Antioxidants-vitamin C shows a significant inhibition on the reproductive toxicities induced by NiNPs.
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PMID:Mechanisms underlying nickel nanoparticle induced reproductive toxicity and chemo-protective effects of vitamin C in male rats. 3047 9