Changes in miR-222 expression, DNA repair capacity, and MDM2-p53 axis in association with low-dose benzene genotoxicity and hematotoxicity.

Mechanisms for hematotoxicity and health effects from exposure to low doses of benzene (BZ) remain to be identified. To address the information gap, our investigation was focused onto using appropriate populations and cell cultures to investigate novel BZ-induced effects such as disruption of DNA repair capacity (DRC). From our study, abnormal miRNAs were identified and validated using lymphocytes from 56 BZ-poisoned workers and 53 controls.

Aberrant lncRNA Profiles Are Associated With Chronic Benzene Poisoning and Acute Myelocytic Leukemia.

Objective: This study investigates the mechanisms of benzene hematotoxicity.

Methods: We used microarray to detect expression profiles of long non-coding RNAs (lncRNAs) and mRNAs in peripheral lymphocytes from chronic benzene poisoning, acute myelocytic leukemia, and healthy controls. The lncRNAs and mRNAs were validated using real-time quantitative PCR (RT-qPCR).

[Pathology and neurophysiology analysis for peripheral neuropathy of four patients with chemicals poisoning].

Objective: To study the nerve electromyogram results by analysing the pathological characters of 4 cases diagnosed as peripheral neuropathy caused by n-hexane and arsenic.

Methods: The nerve electromyogram examination and pathology data of 4 patients, who had been diagnosed as toxic chemicals peripheral neuropathy, were studied retrospectively.

Results: Two patients in this group were exposed to n-hexane, their nerve electromyogram examinations and biopsy pathology of superficial peroneal nerve indicated the peripheral neuropathy was mainly manifests the lesion of medullary sheath.

Case of interstitial lung disease possibly induced by exposure to iron dust.

Interstitial lung diseases are primarily attributable to occupational or environmental exposures to dusts and irritants. We report on a case of interstitial lung disease, possibly secondary to iron exposure. Our male patient presented with cough and shortness of breath of more than 20 years' duration after his occupational exposure had ended.

[Establishment of acute pulmonary edema model induced by high concentrations of nitrogen dioxide in rats].

Objective: To establish the rats model of acute pulmonary edema induced by inhalation of high concentrations of nitrogen dioxide (NO2).

Methods: 38 SD rats were divided into the experimental group (n = 30) and the control group (n = 8). 30 rats in the experimental group were exposed to (6747.

[Preliminary experimental research on glucocorticoid for treatment of nitrogen dioxide induced acute pulmonary edema in rats].

Objective: To investigate the therapeutic effect of glucocorticoids on the acute pulmonary edema in rats induced by nitrogen dioxide (NO₂).

Methods: Thirty SD female rats were randomly equally divided into 5 groups: normal control group, NO₂ exposed group, high-, middle- and low-dose of glucocorticoids treated group (6 rats per group). 6 rats in the normal control group were exposed to room air for 30 min, and the other rats to NO₂.