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Using paired serum samples obtained from patients with illness associated with increases in anti-human coronavirus OC43 (HCoV-OC43) or anti-HCoV-229E antibodies, we examined the possibility of false-positive results detected in a recombinant severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) nucleocapsid protein immunoglobulin G enzyme-linked immunosorbent assay (ELISA). Three of the 21 and 1 of the 7 convalescent-phase serum samples from persons with increases in antibodies against HCoV-OC43 and HCoV-229E, respectively, tested positive by the recombinant SARS-CoV nucleocapsid protein-based ELISA. None of these samples were found to contain a specific antibody in the recombinant SARS-CoV spike polypeptide-based Western blot assay.

Background Patients with vasospastic angina (VA) may have recurrent chest symptoms and life-threatening arrhythmias. Despite regular medications, many VA patients experience recurrent episodes of VA. In this study, we evaluate clinical and angiographic predictors of recurrent VA. Patients and methods From January 2010 to May 2018, a total of 858 patients who underwent ergonovine provocation test were retrospectively reviewed. We excluded the patients who had negative results of provocation test, follow up duration less than 1 month and poor medication compliance. The recurrent-VA group consisted of patients who were re-hospitalized, visited the emergency room, or had repeated coronary angiographies because of chest pain. Results A total of 858 patients who underwent ergonovine provocation tests between January 2010 to May 2018 were retrospectively reviewed. Of them, 162 (mean follow-up duration, 3.0 years) were eligible for our study. The patients were divided into two groups: recurrent-VA (n=33, 20.4%) and stable-VA groups (n=129, 79.6%). Compared with the stable-VA group, the recurrent-VA group consisted mostly of men (93.9% vs. 75.2%, P=0.01), and had low LDL-cholesterol levels (93±27 mg/dl vs. 108±31 mg/dl, P=0.01). In the angiographic findings, a degree of coronary artery disease (CAD) and the site and number of spasm-positive vessels showed no difference between the two groups. Nicorandil was more frequently prescribed at discharge in the stable-VA group (15.2% vs. 35.7%, P=0.02). In the multivariate analysis, the male sex (odds ratio [OR], 5.87; 95% confidence interval [CI], 1.31–26.22; P=0.02) and non-use of nicorandil (OR, 3.51; 95% CI, 1.25–9.84; P=0.01) were the independent predictive factors in the recurrent-VA group. In the Kaplan-Meier analysis, men who did not use nicorandil (n=85, 52.5%) had higher incidences of recurrent angina compared to the other group (n=77, 47.5%). (30.6% vs. 6.6%; p Univariate and multivariate analysis Refractory VA (n=33) Stable VA (n=129) Odds ratio [95% CI] P value univariate Odds ratio [95% CI] P value multivariate Age 0.86 ng/ml, n (%) 2 (7.1) 3 (2.7) 2.74 [0.43–17.27] 0.08 NA NS LDL-C Kaplan-Meier curves Conclusions Male sex and non-use of nicorandil were independent predictors of recurrent VA.

Platelet monoamine oxidase B (MAO B) activity and concentration were studied in a small sample of alcoholic families (n = 8) and in 20 unrelated, nonalcoholic controls. Complex segregation analyses of familial data indicated that both activity and concentration are controlled by a single major gene locus with a multifactorial background effect accounting for 0-50% of the variance. When the alcoholic family members (n = 24) were compared with the controls, all determinations of activity display significant differences, whereas MAO B concentration levels showed no difference. These results indicated that the lowered MAO B activities frequently reported among alcoholics do not reflect a change in the number of MAO B macromolecules expressed in platelets, but could be caused by the presence of an inhibitor or by a polymorphic or variant form of the enzyme.

The retinoblastoma gene was the first tumour suppressor gene identified that was altered not only in retinoblastomas but has been described in a wide variety of human neoplasms. The retinoblastoma gene encodes a nuclear phosphoprotein that in its hypophosphorylated state plays an important role in regulating the cell cycle, thus preventing from tumour formation. Expression of retinoblastoma gene protein product (pRB) was investigated in 118 formalin-fixed, paraffin-embedded cervical tissues by immunohistochemistry using commercially available antibody directed against RB protein. Ten normal ectocervical epithelium, 16 cervical intraepithelial neoplasia (CIN) I, 13 CIN II, 14 CIN III, 53 invasive squamous cell carcinoma, 11 adenocarcinoma and 1 small cell carcinoma were selected for this study. The proportions of pRB-positive cells as well as the extent of pRB expression in ectocervical squamous epithelium were assessed and compared among the lesions. The pRB expression was observed in 100% of normal ectocervical epithelium (n=10), 100% of CIN lesions (n=43) and 98.5% of invasive carcinoma of the uterine cervix (n=65) and were statistically significant when CIN or CIN/invasive were compared to normal cases (P < 0.01, P < 0.05 respectively). While in invasive squamous cell carcinoma (SCC), 81.8% (9/11) pRB-positive cells were found in much higher percentages in well differentiated SCC compared to 64.3% (18/28) of moderately differentiated cases and only 7.1% (1/14) of poorly differentiated SCC (P < 0.01, respectively). The results of this study suggest that loss of RB protein expression is rare in carcinoma of the uterine cervix and this protein may be important in the pathogenesis of cervical carcinoma.

Monoamine oxidase A and B (MAO A and B) are the major neurotransmitter-degrading enzymes in the central nervous system and in peripheral tissues. MAO A and B cDNAs from human, rat, and bovine species have been cloned and their deduced amino acid sequences compared. Comparison of A and B forms of the enzyme shows approximately 70% sequence identity, whereas comparison of the A or B forms across species reveals a higher sequence identity of 87%. Within these sequences, several functional regions have been identified that contain crucial amino acid residues participating in flavin adenine dinucleotide (FAD) or substrate binding. These include a dinucleotide-binding site, a second FAD-binding site, a fingerprint site, the FAD covalent-binding site, an active site, and the membrane-anchoring site. The specific residues that play a role in FAD or substrate binding were identified by comparing sequences in wild-type and variants of MAO with those in soluble flavoproteins of known structures. The genes that encode MAO A and B are closely aligned on the X chromosome (Xp11.23), and have identical exon-intron organization. Immunocytochemical localization studies of MAO A and B in primate brain showed distribution in distinct neurons with diverse physiological functions. A defective MAO A gene has been reported to associate with abnormal aggressive behavior. A deleterious role played by MAO B is the activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a proneurotoxin that can cause a parkinsonian syndrome in mammals. Deprenyl, an inhibitor of MAO B, has been used for the treatment of early-stage Parkinson's disease and provides protection of neurons from age-related decay.

Somatic cell hybrids formed by the fusion of mouse hepatoma (BWTG3) and rat fibroblast (JF1) cells exhibit the extinction of mouse AFP gene expression. Analysis of HindIII digests clearly shows that both mouse and rat AFP genes are present in the hybrids. DNA-RNA hybridization data show that AFP mRNA is virtually absent in the somatic cell hybrids. Our studies indicate, therefore, that extinction of mouse AFP gene expression in somatic cell hybrids (BJ01, BJ50, and BJ140) occurs in the presence of the rat genes and that the mechanism of extinction involves processes that result in the loss of AFP mRNA. We propose that the mechanism may involve either the inhibition of transcription or an inhibition of the processing of the mRNA transcript.

Elementary image analysis techniques have been used in the analysis of microscope pictures of histochemically labeled tissues. Tissues were treated with labeling substances having specificity for a molecular species of pharmacologic interest. Either fluorescent or dense labels were used in different situations. The objective of analysis is to measure the extent or intensity of labeling, or to describe the number or geometric properties of the labeled structures. The experiments reported here demonstrate the conversion of qualitative pictorial data to quantitative data which can be related to drug effects in a manner familiar to biomedical researchers.