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Schizophrenia is a chronic, disabling neuropsychiatric disorder characterised by positive, negative and cognitive symptoms. The aetiology is not known, although genetic, imaging and pathological studies have implicated both neurodevelopmental and neurodegenerative processes. The substantia nigra is a basal ganglia nucleus responsible for the production of dopamine and projection of dopaminergic neurons to the striatum. The substantia nigra is implicated in schizophrenia as dopamine has been heavily implicated in the dopamine hypothesis of schizophrenia and the prevalent psychotic symptoms and the monoamine theory of depression, and is a target for the development of new therapies. Studies into the major dopamine delivery pathways in the brain will therefore provide a strong base in improving knowledge of these psychiatric disorders. This post-mortem study examines the cytoarchitecture of dopaminergic neurons of the substantia nigra in schizophrenia (n = 12) and depression (n = 13) compared to matched controls (n = 13). Measures of nucleolar volume, nuclear length and nuclear area were taken in patients with chronic schizophrenia and major depressive disorder against matched controls. Astrocyte density was decreased in schizophrenia compared to controls (p = 0.030), with no change in oligodendrocyte density observed. Significantly increased nuclear cross-sectional area (p = 0.017) and length (p = 0.021), and increased nucleolar volume (p = 0.037) in dopaminergic neurons were observed in schizophrenia patients compared with controls, suggesting nuclear pleomorphic changes. No changes were observed in depression cases compared to control group. These changes may reflect pathological alterations in gene expression, neuronal structure and function in schizophrenia.

PURPOSE OF REVIEW: Munchausen syndrome by proxy (MBP) is a complicated form of child maltreatment. Difficulties remain in properly defining the condition, as well as in detection and differentiation from organic illness. This review will discuss the epidemiology and diagnosis of MBP, as well as the role of the physician in sorting out these cases. RECENT FINDINGS: Several recent case studies, including two in which children were diagnosed with celiac disease, add to our knowledge of the protean manifestations of MBP. There is growth in our understanding of how sudden infant death syndrome (SIDS) and the symptom complex seen in acute life-threatening events (ALTEs) may in fact represent manifestations of MBP. Recent legal issues in the United Kingdom pose concern for all physicians engaged in child protection work. SUMMARY: In spite of these challenges, the high mortality and recidivism rates associated with MBP make it imperative that pediatricians be familiar with the condition, the subtle signs and symptoms with which it may present, and methods to best protect the children in their care. Language: en

The study objectives, based on federal and state legislative language, were to objectively define symptoms and signs commonly agreed on by "prudent laypersons" as "emergency medical conditions." After comprehensive tabulation of symptom classifications from the International Classification of Diseases (ICD-9), we performed a survey of nonmedical laypersons. Data analysis included descriptive statistics, proportional calculations, and 95% confidence intervals. A minority of symptoms and signs (25/87, 29%) were considered emergency medical conditions by more than half of nonmedical survey respondents who were self-defined as prudent laypersons. The leading conditions deemed emergencies were loss of consciousness, seizure, no recognition of one side of the body, paralysis, shock, gangrene, coughing blood, trouble breathing, chest pain, and choking. Pain, except for renal colic or chest pain, was not considered an emergency. No symptoms or signs specifically related to gynecologic disorders were considered emergencies. Most symptoms and signs tabulated in the diagnostic coding manual, ICD-9, are not considered emergency medical conditions by self-designated prudent laypersons. These include many conditions that are commonly investigated and treated in the emergency department setting. Use of the prudent layperson standard for reimbursable emergency health services may not reflect the actual scope of symptoms necessitating emergency care.

A basic phosphoprotein defined by a monoclonal antibody named AF5 was found to be highly abundant in human hepatocellular carcinoma by Western immunoblotting. Under the same conditions, the levels of this phosphoprotein were low or undetectable in normal liver extracts. The AF5 antibody was used to screen a cDNA expression library of a human hepatoma cell line named FOCUS. A 960-base-pair cDNA was isolated and found to be a partial cDNA encoding the human protein-tyrosine kinase substrate p36, also known as lipocortin II. p36 expression was highly abundant in hepatocellular carcinomas at both the transcript and protein levels. Its expression was not induced significantly during rat liver regeneration following a partial hepatectomy. These results suggest that the induction of p36 expression is associated with malignant transformation of hepatocytes. p36 was previously shown to be phosphorylated upon transformation of normal fibroblasts by retroviral oncogenes without significant modulation of expression. We report here the initial description of the association of increased p36 expression with malignant transformation.

Study objectives To determine whether an association exists between aortic calcification viewed on plain chest radiography and coronary artery disease. Methods Retrospective review of all chest radiographs obtained from consecutive patients undergoing coronary angiography at a primary cardiac center during 1999. Plain chest radiographs were reviewed by blinded radiologists, and interobserver consistency was measured. The presence or absence of aortic arch calcification was abstracted and compared with the results of coronary angiography. Results Of 654 cases, 329 of 360 patients with aortic arch calcification vs 241 of 294 patients without aortic arch calcification had coronary artery disease demonstrated on angiography. The 9% absolute difference in proportions was significant (p = 0.0003). The relative risk (measured by risk ratio) was 1.11 (95% confidence interval, 1.05 to 1.19). Conclusion Several objective signs ( eg , hypertension, hyperlipidemia, and ECG changes) have been associated previously with the presence of coronary artery disease. This study further suggests an association between coronary disease and aortic arch calcification on plain chest radiography. These results may assist primary-care providers performing routine health assessments as well as emergency practitioners evaluating patients with potential angina.

We analyzed the status of retinoblastoma and p53 genes in 10 human hepatoma cell lines. Polyclonal anti-peptide antibodies generated against peptides homologous to COOH-terminal and leucine-zipper domains of the retinoblastoma protein allowed us to identify two cell lines (Hep 3B and FOCUS) with abnormal expression. The same cell lines have both lacked p53 expression. In contrast to the retinoblastoma gene, the expression of the p53 gene was abnormal in six additional cell lines. Indeed, only the Hep G2 hepatoblastoma cell line (and its derivative Hep G2/2215) appeared to have normal p53 and retinoblastoma gene expression. Our studies indicate that p53 abnormalities are common but retinoblastoma gene aberrations are rare in human hepatoma cell lines.

There is little information regarding the molecular mechanisms of hepatocarcinogenesis. We studied the p53 gene at the DNA, RNA, and protein level in seven human hepatocellular carcinoma (HCC)-derived cell lines; six of seven showed p53 abnormalities. By Southern blotting, the p53 gene was found to be partially deleted in Hep 3B and rearranged in SK-HEP-1 cells. Transcripts of the p53 gene were undetectable in Hep 3B as well as in FOCUS cells that had no apparent deletion or rearrangement of the p53 gene. Immunoprecipitation after [35S]methionine labeling of HCC cells demonstrated that p53 protein was absent in Hep 3B and FOCUS and reduced in concentration in PLC/PRF/5 cells. p53 synthesized by Mahlavu cells showed a slower migration on SDS/polyacrylamide gels suggesting it was an abnormal protein. In Huh7 cells, p53 protein had a prolonged half-life leading to its accumulation in the nuclei; increased levels of p53 protein were also found by immunoblotting. The p53 gene and its expression appeared to be unaltered in the hepatoblastoma-derived Hep G2 cell line. We found that the loss of p53 expression did not occur as a late in vitro event in the FOCUS cell line because p53 protein was also nondetectable at an early passage. We conclude that the loss of p53 expression or the presence of abnormal forms of the protein are frequently associated with HCC cell lines. These observations suggest that alterations in p53 may be important events in the transformation of hepatocytes to the malignant phenotype.