[Clinical characteristics of anti-CV2 antibody-associated neurological diseases].

This study reviewed the clinical data of patients who were hospitalized in the Department of Neurology of Henan Provincial People's Hospital from January 2017 to October 2020. A total of 46 patients with positive serum anti-CV2 antibody were included. The average age of the patients was (54±15) years old, with a male to female ratio of 1.88∶1. Twenty-six patients were diagnosed with paraneoplastic neurological syndrome (PNS). The most malignant tumors were thymoma, small cell lung cancer, and prostate cancer. The most common PNS included myasthenia gravis, subacute cerebellar degeneration, and subacute/chronic sensorimotor neuropathies. Twenty non-PNS patients exhibited subacute/old cerebral infarction, Parkinson's disease, Alzheimer's disease, and so on. Among them, brain magnetic resonance imaging (MRI) of 10 cases showed different degrees of white matter demyelination, some of which were accompanied by brain atrophy. The current study found that the positive predictive value of anti-CV2 antibody for the diagnosis of PNS was 56.5%, which was relatively weak. As an accompanying antibody, it may be a coincidence, and it may also be related to the involvement of family members in the pathological process of the diseases.

[Jaridonin, a new diterpenoid from Isodon rubescens, induces cell cycle arrest in gastric cancer cells through activating ataxia telangiectasia mutated kinase].

OBJECTIVE: To study the effects of Jaridonin, a novel diterpenoid from isodon rubescens, on the cell cycle of human gastric cancer cells and its molecular mechanism of action. METHODS: Flow cytometry was used to analyze the cell cycle distribution and expression of ataxia telangiectasia mutated kinase (ATM) after Jaridonin treatment. Western blot was performed to detect the expression of cell cycle-related proteins. RESULTS: The results of flow cytometry showed that the percentages of MGC-803 cells in G(2)/M phase at 6 hours after 0, 10, 20 µmol/L Jaridonin-treatment were (10.8±2.2)%, (18.2±2.5)%, (27.3±3.2)%, respectively; those at 12 hours after Jaridonin-treatment were (12.0±1.5)%, (24.1±2.0)% and (39.7±5.2)%, respectively, indicating a G2/M phase arrest of MGC-803 cells was resulted in a time- and dose-dependent manner. The expressions of ATM, Chk1, Chk2, phosphorylated Cdc2 and CDK2 were up-regulated in the MGC-803 cells after Jaridonin treatment, while the levels of Cdc2 and CDK2 were decreased. KU-55933, an inhibitor of ATM, reversed the expression of relevant proteins and G(2)/M phase arrest induced by Jaridonin. CONCLUSIONS: Jaridonin can significantly induce G(2)/M arrest in gastric cancer MGC-803 cells. Its mechanism may be related to the activation of ATM and Chk1/2, and inactivation of Cdc2 and CDK2 phosphorylation.

Studies on the mutagenicity of hair dyes made in China.

A total of 13 commercial hair dye products made in China were tested for mutagenicity in 2 short-term bioassays, the histidine-requiring mutants of Salmonella typhimurium (strains TA98 and TA100) and the micronucleus test with mouse bone-marrow polychromatic erythrocyte cells in vivo. The results showed that the 13 hair dyes were not mutagenic in strains TA98 and TA100 with and without S-9. In the micronucleus test, no mutagenic effect was observed.

Metabolism of 1,2,3,4-, 1,2,3,5-, and 1,2,4,5-tetrachlorobenzene in the rat.

Adult male rats were given orally single doses of 14C-labeled 1,2,3,4-, 1,2,3,5-, or 1,2,4,5-tetrachlorobenzene (TCB) at 10 mg/kg body weight, and were housed in individual metabolism cages to collect urine and feces for radioassay. For 1,2,3,4- and 1,2,3,5-TCB, approximately 46-51% of the doses were excreted in urine and feces within 48 h after administration. During the same period only 8% of the administered 1,2,4,5-tetrachlorobenzene was excreted. Analysis of urine indicted that the tetrachlorobenzenes were biotransformed to a number of polar compounds. The metabolites for each of the three TCBs in decreasing order of quantities were as follows: 1,2,3,4-TCB, to 2,3,4,5- and 2,3,4,6-tetrachlorophenol and a trace of tetrachlorothiophenol and 2,3,4-trichlorophenol; 1,2,3,5-TCB, to 2,3,4,6-tetrachlorophenol, isomeric hydroxythrichlorothiophenols, and a trichlorophenol; 1,2,4,5-TCB, to 2,3,5,6-tetrachlorophenol, tetrachloroquinol, and a trichlorophenol.