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 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 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.

Monitoring by compressed spectral array in prolonged coma.

Compressed spectral array (CSA) transforms the electroencephalogram into a succinct graphic display of changes in frequency and amplitude. We used CSA to monitor 51 comatose patients for at least 15 hours daily for up to 49 days. The crucial CSA feature was the presence or absence of a peak of activity within the theta or alpha frequency range (4.0 to 13 Hz). Persistence or return of this peak in the first 10 days of coma was seen in all patients who made a good recovery; continued absence of the peak for 10 days, or its return and loss, was associated with death or a residual disability.

The effect of pentobarbital on the auditory evoked response in the brainstem of the rat.

The effect of pentobarbital on the auditory evoked response in the brainstem was studied in 20 male rats. Auditory evoked responses were recorded at regular intervals from the onset of a surgical level of anaesthesia until the return of spontaneous movement. There were small (less than 0.1 msec) but significant increases in the mean latency of each of the four major waves of the auditory evoked response under barbiturate anaesthesia. This is consistent with the effect of pentobarbital on far-field potentials generated from subthalamic locations in the somatosensory system. The mean transmission time in the brainstem, measured as the wave I-IV interpeak latency, increased significantly from 2.11 msec when the animals were awake to 2.15 msec when they were anaesthetized. The effect of pentobarbital on the amplitudes of the four waves was more complex than that on the latencies. Overall, there was an increase in the amplitude of wave I under barbiturate anaesthesia while wave II remained constant and wave III decreased. Wave IV was the component most affected by pentobarbital. In most animals there was either a marked reduction in amplitude or a complete abolition of this wave for one or more intervals during the period of anaesthesia.

The effects of chloralose on the brainstem auditory evoked potential of the rat.

The effects of alpha-chloralose were examined on the brainstem auditory evoked potential of the rat. Subjects were given one of four different doses of chloralose. These were a sedative dose (50 mg/kg), an anaesthetic dose (100 mg/kg), a usually fatal dose (150 mg/kg) or an invariably fatal dose (200 mg/kg). Recordings were made 60 min later. There was no evidence of any dose-dependent increase or decrease in the amplitudes of the four principal components (waves I, II, III and IV) of the brainstem auditory potential. There were only minor dose-dependent increases in latency. These were less than 0.1 msec for waves I, II and III and just over 0.1 msec for wave IV. Wave IV was the component which was most sensitive to chloralose, although this was apparent only at a large dose. In general, the latencies showed little or no difference from those recorded previously from awake animals. The results are discussed in relation to a series of experiments, where animals were initially immobilized with chloralose in order to study the effects of a variety of pharmacological agents on the brainstem auditory potential.

Cloning of high-affinity methionine transport genes from Salmonella typhimurium.

At least one of the genes encoding a methionine transport system in Salmonella typhimurium has been cloned on a 15 kbp fragment in the lambda 1059 vector, and the region responsible for the transport activity was subcloned in a set of plasmids with inserts ranging from 1.4 to 4.2 kbp in the multicopy plasmid pUC8. Two proteins of Mr 34 and 40 kDa were expressed from the larger inserts.

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.

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.

A thalamic component of the cervical evoked potential in man.

Somatosensory evoked potentials (SEPs) were recorded simultaneously from scalp and neck locations following median nerve stimulation. By subtracting the latency of the major negative peak of the cervical SEP (N13) from that of the primary cortical response (N20), the central somatosensory conduction time was calculated (5.9 ms). On the descending slope of the cervical SEP was superimposed a positive potential of probable thalamic origin (P17). By subtracting the latency of N13 from that of P17 and P17 from that of N20 respectively, the transit time for the afferent volley both within the brainstem (3.9 ms) and the thalamo-cortical radiation (2.0 ms) was obtained.

Somatosensory evoked potentials after experimental head injury in the awake rat.

Experimental acceleration concussion was induced in 30 male rats who were immobilized with curare, artificially ventilated but not anaesthetised. Serial recordings of cortical somatosensory evoked potentials (SEPs) were made from the onset of concussion and for the following 30 min. Immediately after the head blow the initial three components of the SEP (P1, N1 and P2) were all either absent or markedly increased in latency. The late negative component (N2) was always abolished. All components reappeared and returned to approximately pre-concussion latencies within 5-6 min. The most persisting abnormality was in N2 whose post-concussion amplitude stabilized and remained depressed at only 50% of baseline value. The results suggest that experimental head injury produces a significant abnormality in every component of the evoked potential. The findings are therefore inconsistent with the theory that concussion differentially affects the diffuse nonspecific pathways whose activity is mediated by the reticular formation while leaving the lemniscal system comparatively intact. It is also shown that the morphology of the post-concussion SEP waveform can be quite accurately simulated by recording SEPs from normal animals at high rates of stimulation (50/s). This implies that the pathophysiology of concussion involves a temporary dysfunction in synaptic transmission although the level at which this is occurring has yet to be determined.

Somatosensory evoked potentials after head injury. The significance of the double peak.

The calculation of central somatosensory conduction time by subtracting the peak latency of the cervical potential from that of the initial cortical response in patients in posttraumatic coma provides both a reliable indication of outcome plus an assessment of brain damage. The interpretation of such recordings is confounded in a minority of patients by the presence in the cortical SEP of a biphasic cortical negativity, giving the impression that the initial cortical response (N20) has bifurcated into two subcomponents. Depending upon which subcomponent is assumed to be N20, an individual recording may ambiguously appear to have a central conduction time either within normal limits or very abnormally prolonged. The aetiology and significance of this double peak phenomenon was studied in 30 patients with severe head trauma. It is concluded that the first of the subcomponents invariably represents the genuine N20 potential irrespective of its relative amplitude. The second subcomponent is assumed to be N25, a minor cortical potential which can be recorded in only a limited number of normal subjects. The double peak effect appears to be created by a distortion in the early cortical waveform probably due to the characteristic reduction in its amplitude following head injury.

Somatosensory evoked potentials following severe head injury: loss of the thalamic potential with brain death.

The thalamic component (P17) of the short-latency somatosensory evoked potential (SEP) was assessed to determine its usefulness in patients with severe head injury. Subjects were a group of patients admitted to the Auckland Hospital Critical Care Unit who subsequently died from head injury. In all instances where brain death was unequivocally established and a SEP recording made in close temporal proximity to the time of brain death the P17 potential was absent. When there was evidence of continuing brainstem activity and particularly where prolonged survival occurred following the last SEP recording the P17 potential remained intact bilaterally. This study shows that the presence or absence of the thalamic component of the short-latency SEP provides a reliable electrophysiological measure of brainstem function in patients where brain death has been suspected.

A possible thalamic component of the auditory evoked potential in the rat.

An attempt is described to identify a thalamic component of the auditory evoked potential in the rat. Auditory potentials were recorded simultaneously from skull locations over the thalamus and the primary auditory cortex. From over the thalamus a slow positive response was recorded with a mean peak latency of 7.3 ms. This preceded the primary cortical response by 1.2 ms. It is concluded that this potential is a more likely candidate for a thalamic response than either a late high frequency component of the brainstem auditory evoked potential or else one of the early components of the middle latency auditory evoked potential.

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.

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.

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.

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 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.