The trypsin inhibitor activity of processed foods can be determined by measuring the loss of activity of added trypsin under standard conditions. Observed values are not usually independent of the degree of inhibition, and averaging over a range of inhibition levels or extrapolation to zero inhibition may not produce a more reliable value. A somewhat modified method is described which has been tested in two laboratories and used for large numbers of different samples on a routine basis; its application and limitations are discussed.
Nontoxigenic and bacteriophage-sensitive bacterial cultures have been isolated from toxigenic Clostridium botulinum type C, strain 468C, after treatment with either ultraviolet light or acridine orange. Two bacteriophages, designated CEbeta and CE(gamma), were isolated from toxigenic strain 468C. Both of these bacteriophages were capable of infecting the nontoxigenic type C cultures, but only bacteriophage CEbeta was involved in the change from nontoxigenicity to toxigenicity.
Summary
Neuregulin 1 (Nrg1) is a susceptibility gene of schizophrenia, a disabling mental illness that affects 1% of the general population. Here we show that ctoNrg1 mice, which mimic high levels of NRG1 observed in forebrain regions of schizophrenic patients, exhibit behavioral deficits and hypofunction of glutamatergic and GABAergic pathways. Intriguingly, these deficits were diminished when NRG1 expression returned to normal in adult mice that had been symptomatic, suggesting that damage which occurred during development is recoverable. Conversely, increase of NRG1 in adulthood was sufficient to cause glutamatergic impairment and behavioral deficits. We found that the glutamatergic impairment by NRG1 overexpression required LIM domain kinase 1 (LIMK1), which was activated in mutant mice, identifying a novel pathological mechanism. These observations demonstrate that synaptic dysfunction and behavioral deficits require continuous NRG1 abnormality in adulthood, suggesting that relevant schizophrenia may benefit from therapeutic intervention to restore NRG1 signaling.
Rosen served as lead for writing -original draft and writingreview and editing. Leslie A. Morland contributed equally to writing -review and editing and served in a supporting role for writing -original draft. Lisa H. Glassman served as lead for writing -review and editing and served in a supporting role for writing -original draft. Brian P. Marx served in a supporting role for conceptualization and writing -review and editing. Kendra Weaver served in a supporting role for conceptualization, data curation, and writing -review and editing. Clifford A. Smith served as lead for data curation and served in a supporting role for conceptualization and writing -review and editing. Stacey Pollack served in a supporting role for writing -review and editing. Paula P. Schnurr served in a supporting role for conceptualization and writing -review and editing. Craig S. Rosen, Leslie A. Morland, and Lisa H. Glassman contributed to conceptualization equally. Craig S. Rosen and Clifford A. Smith contributed to formal analysis equally. Craig S. Rosen and Leslie A. Morland contributed to project administration equally. The views expressed are those of the authors and do not necessarily reflect the position of the U.S. Veterans Health Administration or the government of the United States.
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