OBJECTIVETo explore the distribution of the main clinical symptoms and signs of primary biliary cirrhosis (PBC) in a population of individuals with positivity for anti-mitochondrial antibody-M2 (AMA-M2).

METHODSA total of 20 970 persons who participated in routine health examinations at our hospital were tested for presence and level of antinuclear antibodies (ANAs) using an indirect immunofluorescence (IIF) assay and of AMA-M2 by western blotting. The chi-square test was used for statistical analysis.

RESULTSTiters of ANAs more than 1:320 were detected in 1 243 of all the study participants, with 156 of those individuals having detectable AMA-M2.The overall rate ofAMA-M2 positivity was 0.74%, with a significantly higher rate among female subjects (males:0.3% (32/10 550) vs.females:1.2% (124/10 420); x2=55.85, P less than 0.05). Among the AMA-M2-positive population there were 66 cases of abnormal liver function, 58 cases of increased alkaline phosphatase, 72 cases of abnormal findings for routine blood testing, 47 cases of gallbladder disease history, 49 cases of diabetes history, 22 cases of allergy, 75 cases of abdominal discomfort, 38 cases of weakness, 3 cases of jaundice, and 11 cases of pruritus. There were significant differences between the AMA-M2-negative individuals and the AMA-M2-positive individuals.

CONCLUSIONAmong the general population, individuals with substandard states of health, such as those with abnormal findings in routine blood tests and abnormal liver function, should be screened for AMA-M2. This screening will facilitate early diagnosis of PBC and timely initiation of disease management, improving the patient's life quality of life and prolonging their life.

Biomarkers ; Blotting, Western ; Female ; Fluorescent Antibody Technique, Indirect ; Humans ; Liver Cirrhosis, Biliary ; metabolism ; Male ; Pruritus ; Quality of Life

Plasticity in the glutamatergic synapses on striatal medium spiny neurons (MSNs) is not only essential for behavioral adaptation but also extremely vulnerable to drugs of abuse. Modulation on these synapses by even a single exposure to an addictive drug may interfere with the plasticity required by behavioral learning and thus produce impairment. In the present work, we found that the negative reinforcement learning, escaping mild foot-shocks by correct nose-poking, was impaired by a single in vivo exposure to 20 mg/kg cocaine 24 h before the learning in mice. Either a single exposure to cocaine or reinforcement learning potentiates the glutamatergic synapses on MSNs expressing the striatal dopamine 1 (D1) receptor (D1-MSNs). However, 24 h after the cocaine exposure, the potentiation required for reinforcement learning was disrupted. Specific manipulation of the activity of striatal D1-MSNs in D1-cre mice demonstrated that activation of these MSNs impaired reinforcement learning in normal D1-cre mice, but inhibition of these neurons reversed the reinforcement learning impairment induced by cocaine. The results suggest that cocaine potentiates the activity of direct pathway neurons in the dorsomedial striatum and this potentiation might disrupt the potentiation produced during and required for reinforcement learning.