The present study discovered that (a) the ethanolic extract of Cortex Magnoliae Officinalis had 20% greater antimicrobial activities against M. smegmatis than streptomycin; (b) the boiled extract of Cortex Magnoliae Officinalis demonstrated comparable activities to streptomycin (c) the synergism of magnonol and honokiol had comparable effects to those of streptomycin; (d) the aerial parts of rodent tuber had antimicrobial activities against S. aureus. Among the tested 107 extracts, Cortex Magnoliae Officinalis had (1) potent antimicrobial activities against S. aureus, B. subtilis, M. smegmatis and C. albicans and (2) highest antioxidant activities in DPPH assay regardless extraction methods. Cortex Magnoliae Officinalis is likely a potential medicinal plant resource for developing effective antimicrobials and antioxidants. Results From a Hypothesis Generating Case-Control Study: Herpes Family Viruses and Schizophrenia Among Military Personnel Background: Herpes family viruses can cause central nervous system inflammatory changes that can present with symptoms indistinguishable from schizophrenia and therefore are of interest in schizophrenia research. Most existing studies of herpes viruses have used small populations and postdiagnosis specimens. As part of a larger research program, we conducted a hypothesis-generating case-control study of selected herpes virus antibodies among individuals discharged from the US military with schizophrenia and pre- and postdiagnosis sera. Methods: Cases (n = 180) were servicemembers hospitalized and discharged from military service with schizophrenia. Controls, 3:1 matched on several factors, were members not discharged. The military routinely collects and stores members' serum specimens. We used microplate enzyme immunoassay to measure immunoglobulin G (IgG) antibody levels to 6 herpes viruses in pre- and postdiagnosis specimens. Conditional logistic regression was used, and the measure of association was the hazard ratio (HR). Results: Overall, we found a significant association between human herpes virus type 6 and schizophrenia, with an HR of 1.17 (95% confidence interval [CI] = 1.04, 1.32). Women and blacks had significant negative associations with herpes simplex virus type 2 and cytomegalovirus; among blacks, there was a significant positive association with herpes simplex virus type 1. Among men, there was a HHV-6 temporal effect with an HR of 1.41 (95% CI = 1.02, 1.96) for sera drawn 6–12 months before diagnosis. Discussion: Findings from previous studies of herpes family viruses and schizophrenia have been inconsistent. Our study is based on a larger population than most previous studies and used serum specimens collected before onset of illness. This study adds to the body of knowledge and provides testable hypotheses for follow-on studies. Recent research has focused on infectious agents as potential players in the etiologic pathway of chronic diseases, [1] [2] [3] including psychiatric illnesses such as schizophrenia. [4] [5] [6] [7] [8] [9] [10] Due to their potential neurotropism and latency, viral organisms in particular are considered possible agents in many chronic central nervous system (CNS) disorders. 2, [11] [12] [13] Encephalitis and other conditions leading to CNS inflammatory changes often present with symptoms that are difficult to distinguish from new-onset schizophrenia. As ) are of prime interest in schizophrenia research. 14 Although laboratory-based research into herpes family viruses as possible etiologic agents for schizophrenia goes back decades, [15] [16] [17] [18] [19] [20] [21] [22] ascertaining the nature of a possible etiologic association between infection and schizophrenia is highly challenging. There have been few consistent findings between studies, which could be due to many factors, including the heterogeneity of schizophrenia itself, the use of different immunologic assays across the studies and over time as technology changes, focusing attention on a variety of different infections, and the possibility that maternal infection occurring at the right time during pregnancy may be enough to increase the risk of psychosis in offspring. 23 There is more information regarding risks associated with maternal, neonatal, or childhood infection and schizophrenia than for adult infection, with a number of studies reporting increased risk of schizophrenia among persons exposed in utero to a number of infections [24] [25] [26] or born after epidemic. 27 Little is known about potential mechanisms of action for herpes family virus infections and risk of schizophrenia.