Anoxygenic phototroph of the Chloroflexota uses a type I reaction centre.

Scientific exploration of phototrophic bacteria over nearly 200 years has revealed large phylogenetic gaps between known phototrophic groups that limit understanding of how phototrophy evolved and diversified1,2. Here, through Boreal Shield lake water incubations, we cultivated an anoxygenic phototrophic bacterium from a previously unknown order within the Chloroflexota phylum that represents a highly novel transition form in the evolution of photosynthesis. Unlike all other known phototrophs, this bacterium uses a type I reaction centre (RCI) for light energy conversion yet belongs to the same bacterial phylum as organisms that use a type II reaction centre (RCII) for phototrophy. Using physiological, phylogenomic and environmental metatranscriptomic data, we demonstrate active RCI-utilizing metabolism by the strain alongside usage of chlorosomes3 and bacteriochlorophylls4 related to those of RCII-utilizing Chloroflexota members. Despite using different reaction centres, our phylogenomic data provide strong evidence that RCI-utilizing and RCII-utilizing Chloroflexia members inherited phototrophy from a most recent common phototrophic ancestor. The Chloroflexota phylum preserves an evolutionary record of the use of contrasting phototrophic modes among genetically related bacteria, giving new context for exploring the diversification of phototrophy on Earth.

Prophylactic trimethoprim-sulfadiazine during chemotherapy in dogs with lymphoma and osteosarcoma: a double-blind, placebo-controlled study.

BACKGROUND: The administration of chemotherapy is associated with risk for morbidity. Management of chemotherapy-related morbidity in veterinary oncology has been primarily supportive. HYPOTHESIS: The purpose of this study was to evaluate the effect of prophylactic antimicrobial use on chemotherapy-associated morbidity in dogs with lymphoma or osteosarcoma. ANIMALS: Dogs presenting with histologically confirmed osteosarcoma or lymphoma were eligible. METHODS: Patients were randomized to receive placebo or trimethoprim-sulfadiazine for 14 days after their first doxorubicin chemotherapy. Both owner and clinician were blinded with respect to treatment. Patient assessment included CBC, physical examination and performance, and toxicosis grading on days 7 and 14. Investigated outcomes were hospitalization, suspicion of infection, gastrointestinal toxicity, neutropenia, nonhematologic toxicity, and quality of life. RESULTS: Seventy-three dogs were enrolled; 34 had osteosarcoma, and 39 had lymphoma. Dogs receiving trimethoprim-sulfadiazine (n = 36) had a significantly reduced hospitalization rate (P = .03), nonhematologic toxicity (P = 0.039), grade 2-4 nonhematologic toxicity (P < .0001), grade 2-4 gastrointestinal toxicity (P = .007). and altered performance (P = .015). By group, dogs with osteosarcoma (n = 34) that received the antimicrobial experienced fewer occurrences of nonhematologic toxicity (P = .02) and less severe nonhematologic toxicity (P = .038). Dogs with lymphoma (n = 39) had significant reductions in the occurrence of hospitalization (P = .035), severity of nonhematologic toxicity (P = .036), and alterations of performance (P = .015). CONCLUSIONS: The use of prophylactic trimethoprim-sulfadiazine has benefit in reducing morbidity in dogs with osteosarcoma or lymphoma during the first 14 days after treatment with doxorubicin.

The effects of electroconvulsive shock on retinal activity.

Two experiments are reported examining the effects of electroconvulsive shock (ECS) on the electroretinogram (ERG) and the retinal oscillatory potentials (OPs) in the albino rat. Immediately after the induction of generalised seizure activity, both the ERG and the OPs were always preserved basically intact, despite minor alterations to their waveforms. In Experiment 1, it was found that small changes in amplitude of the ERG were recorded following ECS, but these were most likely artifactual. The only other notable finding was a temporary decrease in latency of the b-wave of the ERG. In Experiment 2, a slight overall attenuation in the amplitude of the OPs was observed. This was associated with a paradoxical decrease in the latencies of all three OP subcomponents similar to that found for the ERG b-wave. It is concluded that ECS does not interfere to any marked extent with either the transduction of the visual signal or its processing within the various retinal layers. This implies that the blockade of the afferent volley that occurs following ECS must be confined to the optic pathway or to the occipital cortex itself.

The effects of electroconvulsive shock on the primary cortical auditory potential.

BACKGROUND: Recording of evoked potentials provides an ideal method of quantifying the acute changes in neurophysiological activity that occur following the administration of electroconvulsive shock (ECS) or electroconvulsive therapy. METHODS: Serial recordings of the primary cortical auditory evoked potential (PCAEP) were made from 20 adult male albino rats starting immediately after the induction of generalized seizure activity by ECS. RESULTS: Directly after ECS, the PCAEP was abolished; however, an auditory potential that superficially resembled an abnormal PCAEP was invariably present during this period. On analysis, it was shown that this response was of probable thalamic origin, which had become unmasked due to the temporary absence of the normally dominant cortical potential. Within 1 min, the genuine PCAEP had begun to reappear, and its normal morphology was then rapidly restored. CONCLUSIONS: It was concluded that the principal site of action of ECS on the PCAEP may lie quite discretely within the cortex, while auditory activity generated in brain stem and subcortical locations is largely immune to its effects. It is suggested that the loss of the cortical waveform following ECS may be due to epileptogenic events responsible for the development of the paroxysmal depolarization shift, which temporarily block the formation of the postsynaptic PCAEP. The relevance of these findings for an understanding of the therapeutic efficacy of electroconvulsive therapy is discussed.

The effects of electroconvulsive shock on the short-latency somatosensory evoked potential in the rat.

The effects of electroconvulsive shock (ECS) were examined on the short-latency somatosensory evoked potential (SEP) in the awake rat. Immediately after the induction of generalized seizure activity (GSA), the primary cortical response was lost although the preceding far field thalamic component appeared to be preserved basically intact. Within 1 minute the cortical potential had begun to reemerge, albeit with an attenuated amplitude and a prolonged latency. Recordings made at 2 and 3 minutes revealed evidence of a slight postictal enhancement of the cortical potential. Within 6 minutes, a near normal waveform had been restored. It is concluded that the principal site of impact of ECS resides at the cortical level and that the somatosensory impulse is, therefore, able to traverse the central pathways unimpeded by GSA until it is finally blocked at the primary sensory cortex. The present findings are compared to previous attempts to record cortical SEPs from patients undergoing electroconvulsive therapy (ECT). It is presumed that the failure of ECT to abolish the SEP in these circumstances was due either to the protective role played by concurrent medication or because of a post-ECS delay in restarting the recordings. The relevance of the findings to an understanding of the physiology of electrical stunning is discussed.

The relationship between the putative optic pathway potential and the electroretinogram.

The putative optic pathway flash visual evoked potential (FVEP) and the electroretinogram (ERG) were recorded consecutively in the lightly anesthetised rat. The purpose was to test the hypothesis that the optic pathway FVEP is only an artifact created by distorted volume-conducted retinal activity. A comparison of the timing of the ERG with that of the optic pathway FVEP confirmed this suspicion. It is shown that there is a close temporal correspondence between individual subcomponents of the optic pathway potential and those of the ERG (i.e., the a-wave, b-wave, and the oscillatory potentials). In addition, it was found that when ERG currents are recorded far field from the vicinity of the optic nerve or tract, they acquire a triphasic positive-negative-positive waveform, thereby heightening the illusion that the optic pathway FVEP is a genuine compound action potential. It is concluded that experimental findings derived from the recording of the optic pathway FVEP must be treated with caution.

The effects of electroconvulsive shock on the flash visual evoked potential in the rat.

The effects of electroconvulsive shock (ECS) on the flash visual evoked potential (FVEP) were studied in the awake albino rat. Immediately after the induction of generalised seizure activity, the FVEP was totally abolished although accidentally averaged rhythmic epileptiform activity was often present in the trace. During the second recording, a potential had reappeared but this response was suspected of being a superior colliculus FVEP masquerading as a cortical response. By the third recording, the genuine cortical FVEP had returned, albert with an abnormally large amplitude. The waveform subsequently remained significantly distorted although it had regained an approximately normal morphology within 6-7 min of the administration of ECS. It was not possible to identify the principal site of action of ECS but it was concluded that ECS may impact on activity generated at more than one location within the optic pathways. The present findings are compared with a number of previous animal and human studies where the FVEP was apparently preserved following ECS and attempts are made to explain the discrepancy in results. The relevance of the present findings for understanding the pathophysiology of electrical stunning and of the loss or impairment of consciousness during generalised epileptic seizures is also discussed.

The effects of generalized seizure activity on the cerebellar auditory potential.

The effects of generalized seizure activity (GSA) on the primary cortical component of the cerebellar auditory evoked potential [CERAEP] were studied in the awake rat. GSA was induced by electroconvulsive shock (ECS) [80 mA for 600 ms]. CERAEPs proved largely resistant to GSA, even during the ictal period. Any minor alterations to the waveform were very transient and normal morphology was restored within 1-2 min after ECS. Overall, there was a mean decrease in amplitude of 2.6 microV associated with an increase in latency of 0.2 ms. These findings are consistent with those of GSA on the fast and slow components of the brainstem auditory evoked potential and imply that activity generated in the more caudal parts of the central auditory system is largely invulnerable to GSA. In contrast, a later component of the CERAEP waveform of uncertain origin was totally abolished by the action of ECS.

The temporal relationship between the brainstem and primary cortical auditory evoked potentials.

Many methods are employed in order to define more precisely the generators of an evoked potential (EP) waveform. One technique is to compare the timing of an EP whose origin is well established with that of one whose origin is less certain. In the present article, the latency of the primary cortical auditory evoked potential (PCAEP) was compared to each of the seven subcomponents which compose the brainstem auditory evoked potential (BAEP). The data for this comparison was derived from a retrospective analysis of previous recordings of the PCAEP and BAEP. Central auditory conduction time (CACT) was calculated by subtracting the latency of the cochlear nucleus BAEP component (wave III) from that of the PCAEP. It was found that CACT in humans is 12 msec which is more than double that of central somatosensory conduction time. The interpeak latencies between BAEP waves V, VI, and VII and the PCAEP were also calculated. It was deduced that all three waves must have an origin rather more caudally within the central auditory system than is commonly supposed. In addition, it is demonstrated that the early components of the middle latency AEP (No and Na) largely reside within the time domain between the termination of the BAEP components and the PCAEP which would be consistent with their being far field reflections of midbrain and subcortical auditory activity. It is concluded that as the afferent volley ascends the central auditory pathways, it generates not a sequence of high frequency BAEP responses but rather a succession of slower post-synaptic waves. The only means of reconciling the timing of the BAEP waves with that of the PCAEP is to assume that the generation of all the BAEP components must be largely restricted to a quite confined region within the auditory nerve and the lower half of the pons.

The effects of low-pass filtering on the primary cortical auditory potential of the rat.

The effects of low-pass filtering on the primary cortical auditory evoked potential (CAEP) were studied using the rat as subject. The CAEP is the potential which is generated by the arrival of the afferent volley in the primary auditory projection area. Recordings were made from animals which were totally awake and those which were anaesthetised with pentobarbital. A total of 9 recordings were obtained from each subject. The high-pass (low-frequency) filter remained fixed at 3.2 Hz while the low-pass (high-frequency) filter was set at 32, 80, 160, 320, 800 Hz and 1.6, 3.2, 8 and 16 kHz. The CAEP recorded from the awake animal consisted of a primary positivity (P1) followed by a later secondary positivity (P2). In the anaesthetised subjects, only the P1 potential was present. As the bandpass was progressively opened, there was at first a quite steep decline in latency associated with a gradual increase in amplitude. After the low-pass filter setting had been raised to 320 Hz, the amplitude of components P1 and P2 when awake and of P1 when anaesthetised had stabilized and thereafter there was no additional increase. Likewise, the latency of P2 for the awake subjects subsequently remained constant. In contrast, the latency of P1 recorded from both awake and anaesthetised subjects showed a continuing small decline as the bandpass was extended to 3.2-16 kHz. It is probable that this phenomenon did not represent a further genuine decrease in the latency of P1 but was more likely an artefact caused by the distorting effects of a cluster of late high-frequency components of the brainstem auditory evoked potential generated temporally contiguous to P1. It was concluded that a bandpass of 3.2-320 Hz is optimal for recording both early and late components of the CAEP and that low-pass filtering had an essentially uniform effect on the waveform irrespective of the subject's state of arousal.

Auditory evoked potentials recorded from different skull locations in the rat.

Auditory evoked potentials were recorded from different skull sites in the rat. From over the cerebellum, the inferior colliculus, the thalamus and the auditory cortex, a series of discrete slow potentials of positive polarity were identified. The timing of these waveforms was compared with each other and with the high frequency components of the brainstem auditory evoked potential. Potentials recorded from over the inferior colliculus and the thalamus consisted of two possible responses, one of which predominated in an individual animal. Tentative origins for these slow potentials include the cerebellar cortex, the termination of the lateral lemniscus, the brachium of the inferior colliculus, the medial geniculate body, the auditory radiations and primary auditory cortex. It is concluded that as the afferent volley ascends the central auditory pathways, it generates initially the fast waves of the brainstem auditory potential followed by a series of slow positivities.

Impairment of the gustatory engram by generalised seizure activity without associated loss of conditioned taste aversion.

Three experiments are reported concerning the disruption of conditioned taste aversion (CTA) by generalised seizure activity (GSA) induced by electroconvulsive shock (ECS). Rats were taught CTAs by pairing either strong or weak taste cues (10% or 2.5% sucrose solutions) with either strong (0.15 M) or weak (0.05 M) doses of LiCl. In Experiment 1 it is shown that a 2.5% sucrose cue combined with a weak dose of LiCl will reproduce the disruptive effect of GSA when the CTA is established using a 10% sucrose cue. Likewise, a CTA acquired using a 2.5% sucrose cue paired with a strong dose of LiCl will simulate the failure of GSA to disrupt a CTA which has been established with a 10% sucrose cue. These findings support the theory that GSA acts to disrupt CTA by weakening the gustatory engram and an apparent inability to disrupt CTA by GSA does not necessarily signify that the gustatory engram itself remains intact. In Experiment 2, a CTA was established to a 2.5% sucrose cue using the more toxic dose of LiCl. It is shown that GSA will cause a substantial learning loss irrespective of whether it is interpolated within the taste-illness interval, or after the aversion has been acquired. It is concluded that the gustatory engram continues to reside in an active labile state even after the CTA has been established. In Experiment 3 it was estimated that the memory of the 2.5% sucrose cue must have been reduced to just over half of its original strength in order to create the learning loss reported in Experiment 2.

Increase in mortality rates due to aircraft noise.

In a study using data from the 1970-1980 decade, we find that people near Los Angeles International Airport (LAX) suffer a 5% increase in mortality rates due to increases in a number of fatal diseases. We comment also on the effect of changes in noise level over the last decade. It is found that there is an 18% increase in cardiovascular deaths, for people over 75 at a 97% confidence level, in areas around the airport. Approximately 200,000 people are involved in the study, split into two groups, test and control, near LAX. The two areas were adjusted to be alike in race, age and economic level. The number of suicides in the age bracket 45-54 was increased by the jet noise by over 100% at a 99% confidence level. Total accidental deaths increased by over 60% in the age group above 75 at a 96% confidence level. If we add together all increases there are an average of 24 extra deaths due to aircraft, primarily jet, noise in the high noise area. If we included all people living within the extended high noise contour, there is reason to believe that there is an increase of over 60 deaths in the LAX area per year.

A possible collicular component of the auditory evoked potential and its relationship to brainstem and cerebellar auditory potentials.

Auditory evoked potentials were recorded from the rat using skull screw electrodes inserted over the inferior colliculus and the cerebellum. In addition, brainstem auditory evoked potentials (BAEPs) were also recorded. The response recorded from over the inferior colliculus consisted of a slow positive potential with one of two possible peak latencies. The mean latency of the earlier potential was 5.6 ms and that of the later potential was 6.4 ms. A hypothetical generator for the first collicular potential is the termination of the lateral lemniscus in the ventrolateral inferior colliculus, while the later collicular potential could have its origins within the brachium of the inferior colliculus. None of the principal nor minor BAEP waves corresponded to either of the collicular responses. Nor did the trough of negativity between BAEP waves IV and V which is often thought to reflect activity generated within the midbrain. The potential recorded over the cerebellum also consisted of a slow positivity but with a slightly sharper contour than that of the collicular response. The mean latency of the cerebellar potential was 4.9 ms. As there was no temporal relationship between collicular and cerebellar potentials, the present study provided no support for the theory that cerebellar auditory potentials are artefactual and simply far field reflections of activity generated in the inferior colliculus. Judging by the timing of the BAEP waves, it is also concluded that the afferent volley most likely projects to the cerebellum via a collateral pathway branching off the caudal part of the lateral lemniscus.

Pattern visual evoked potential luminance and multiple sclerosis.

Pattern visual evoked potentials (PVEPs) were recorded from 111 patients classified as having possible, probable or definite multiple sclerosis. Patients were stimulated with a checkerboard pattern using high and low luminances in order to test the hypothesis that an attenuated pattern luminance increases the detection rate of PVEP abnormalities. With increasing certainty of diagnosis, there was a concomitant increase in the incidence of PVEP abnormalities. However, there was no evidence that stimulating with a lower luminance pattern enhanced the sensitivity of the test. The same findings were also apparent when the patient data was analyzed according to the presence or absence of a history of optic neuritis or other visual symptoms. It is concluded that, within the luminance limits used in this study, the role of varied luminance in detecting demyelinating lesions in the optic nerves using the PVEP is minimal, although there was some limited evidence that a high level of luminance may be more appropriate than a low level.

The effects of low-pass filtering on the flash visual evoked potential of the albino rat.

Flash visual evoked potentials (FVEPs) were recorded from the rat in order to determine the effects of low-pass filtering on the wave form. The low-frequency (high pass) filter remained fixed at 3.2 Hz while the setting of the high-frequency (low-pass) filter was progressively raised from 32 Hz to 3.2 kHz. The amplitude of the primary cortical potential (P30) steadily increased while its latency decreased until asymptotic values were recorded with a low-pass cut-off of 320 Hz. Thereafter, there was little additional change in wave form. It is concluded that a bandpass of 3.2-320 Hz is optimal to record the primary cortical response of the FVEP, and this is consistent with the theory that the P30 potential is generated by comparatively slow post-synaptic activity. In a second experiment the effects of low-pass filtering were examined on the later and more labile secondary components of the FVEP wave form. These were found to be less responsive to low-pass filtering than the early components and assumed a near optimal configuration when the high-frequency cut-off was raised to 80 Hz. The high-frequency filter setting which is most appropriate to record the primary component of the FVEP therefore appears to be more than adequate also to record the secondary responses. It is also shown that the same principles of low-pass filtering on the FVEP will apply irrespective of whether the subject is awake or anaesthetised.

Auditory potentials elicited by the grass photic stimulator in the rat.

Flash visual evoked potentials were recorded from the rat to determine whether the Grass photic stimulator could generate an auditory component of the waveform. When the click associated with each lamp flash remained unmuffled, the primary response of the visual cortex (P30) was preceded by an earlier positivity with a latency between 6-8 ms. When the photic stimulator lamp was subsequently insulated in order to deaden the sound of the click, the P30 potential remained intact while the earlier response disappeared. It is concluded that the photic stimulator is capable of eliciting a distinct auditory potential of probable collicular origin.

The effects of low pass filtering on central somatosensory conduction time.

Central Somatosensory conduction time (CSCT) in the rat was measured by simultaneously recording the cortical somatosensory evoked potential (SEP) and cervical SEP and then subtracting the peak latency of the cervical response from that of the primary cortical response. The low frequency (high pass) filter of the recording system was kept fixed at 3.2 Hz but the high frequency cut-off was progressively raised from 32 to 16 kHz to examine the effects of low pass filtering on the two waveforms from which CSCT is derived. With a bandpass of 3.2-32 Hz, no activity could be reliably identified in either the cortical or cervical traces. With subsequent rises in the high frequency filter, the amplitude of both potentials increased with a concomitant decrease in their latencies. Stable values were obtained with a bandpass of 3.2-3.2 kHz and there was little additional change in waveform configuration. In contrast to the waveforms, low pass filtering had only minimal effects on CSCT and near constant values (in the range 3.6-4.1 ms) were obtained regardless of the setting of the low pass filter. I concluded that low pass filtering has a largely uniform effect on somatosensory activity generated in both primary cortical and cervico-medullary locations.