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This work demonstrates a mixed-dimensional piezoelectric-gated transistor in the microscale that could be used as a millinewton force sensor. The force-sensing transistor consists of 1D piezoelectric zinc oxide (ZnO) nanorods (NRs) as the gate control and multilayer tungsten diselenide (WSe 2) as the transistor channel. The applied mechanical force on piezoelectric NRs can induce a drain-source current change (Δ I ds) on the WSe 2 channel. The different doping types of the WSe 2 channel have been found to lead to different directions of Δ I ds. The pressure from the calibration weight of 5 g has been observed to result in an ∼30% I ds change for ZnO NRs on the p-type doped WSe 2 device and an ∼-10% I ds change for the device with an n-type doped WSe 2. The outcome of this work would be useful for applications in future human-machine interfaces and smart biomedical tools.

This work demonstrates a mixed-dimensional piezoelectric-gated transistor in the microscale that could be used as a millinewton force sensor. The force-sensing transistor consists of 1D piezoelectric zinc oxide (ZnO) nanorods (NRs) as the gate control and multilayer tungsten diselenide (WSe

A 128 $\times $ 128 single-photon avalanche diode (SPAD) motion detection-triggered time-of-flight (ToF) sensor is implemented in STMicroelectronics 40 nm CMOS SPAD foundry process. The sensor combines vision and ToF ranging functions to acquire depth frames only when inter-frame intensity changes are detected. The 40 $\mu \text{m}\,\,\times $ 20 $\mu \text{m}$ pixels integrate two 16-bit time-gated counters to acquire ToF histograms and repurpose them to compare two vision frames without the requirement for additional out-of-pixel frame memory resources. An embedded column-parallel ToF and vision processor performs on-chip vision frame comparison and binary frame output compression as well as controlling the time-resolved histogram sampling. The sensor achieves a maximum 32.5 kframes/s in vision modality and 500 frames/s in motion detection-triggered ToF over a measured 3.5 m distance with 1.5 cm accuracy. The vision function reduces the sensor power consumption by 70% over continuous ToF operation and allows the sensor to gate the ToF laser emitter to reduce the system power when no motion activity is observed.

In this work, we present a novel force-sensing device with zinc oxide nanorods (ZnO NRs) integrated with a metal-oxide-semiconductor (MOS) capacitor and encapsulated with Kapton tape. The details of the fabrication process and working principle of the integrated ZnO NRs-MOS capacitor as a force sensor and nanogenerator have been discussed. The fabricated ZnO-MOS device is tested for both the open-circuit and resistor-connected mode. For an input force in the range of 1–32 N, the open-circuit output voltage of the device is measured to be in the range of 60–100 mV for different device configurations. In the resistor-connected mode, the maximum output power of 0.6 pW is obtained with a 1 MΩ external resistor and input force of 8 N. In addition, the influence of different seed layers (Ag and ZnO) and the patterning geometry of the ZnO nanorods on the output voltage of ZnO-MOS device have been investigated by experiments. An equivalent circuit model of the device has been developed to study the influence of the geometry of ZnO NRs and Kapton tape on the ZnO-MOS device voltage output. This study could be an example of integrating piezoelectric nanomaterials on traditional electronic devices and could inspire novel designs and fabrication methods for nanoscale self-powered force sensors and nanogenerators.

Bacterial growth in microfluidic droplets is relevant in biotechnology, in microbial ecology, and in understanding stochastic population dynamics in small populations. However, it has proved challenging to automate measurement of absolute bacterial numbers within droplets, forcing the use of proxy measures for population size. Here we present a microfluidic device and imaging protocol that allows high-resolution imaging of thousands of droplets, such that individual bacteria stay in the focal plane and can be counted automatically. Using this approach, we track the stochastic growth of hundreds of replicate Escherichia coli populations within droplets. We find that, for early times, the statistics of the growth trajectories obey the predictions of the Bellman–Harris model, in which there is no inheritance of division time. Our approach should allow further testing of models for stochastic growth dynamics, as well as contributing to broader applications of droplet-based bacterial culture.

A WSe2 field effect transistor integrated with a lead zirconium titanate (PZT) pyroelectric device has been designed, fabricated, and tested and is described as the integrated pyroelectric device. The integrated device has been compared to a standalone pyroelectric device, which consists of PZT sandwiched between platinum electrodes. A pyroelectric coefficient of 1.755 × 10−4 C/m2K has been realized for our thin-film PZT (650 nm). The integrated device amplifies the output of the standalone device by over ten orders of magnitude as the current density calculated for the devices is 16 nA/mm2 and 1 nA/mm2, respectively. The interplay between the pyro- and ferro-induced polarization of the integrated device has been studied. From our observations, the ferroelectric gating controls directly the drain-source current output of the integrated device, showing anti-clockwise hysteresis behavior. The device shows promise for application in infrared sensing.

In this study, ZnO nanowires with diameters ranging from 50 nm to 500 nm have been synthesized hydrothermally on Ag and ZnO seed layers deposited by electron beam evaporation. ZnO nanowires grown on hetero and homo interfaces have been studied by comparing the growth characteristics of (a) ZnO nanowires on the Ag seed layer and (b) ZnO nanowires grown on the ZnO seed layer, respectively. The surface morphology of the as-evaporated seed layers before the nanowire growth has been investigated. Electron backscatter diffraction (EBSD) has been employed to examine the crystallinity of ZnO nanowires. In addition, the integrity of the Ag–ZnO heterointerface has been investigated using high-resolution transmission electron microscopy (HR-TEM). The length, diameter, density, and alignment of nanowires grown on Ag and ZnO seed layers have been studied as a function of growth time from 0.5 hours to 18 hours and precursor concentration from 5 mM to 18 mM. Furthermore, for both the Ag–ZnO nanowire heterostructure and ZnO–ZnO nanowire homostructure, the role of defects in the optical properties in the wavelength range of 517 nm to 900 nm has been studied using photoluminescence (PL) spectroscopy.

A novel patterning method for the selective growth of ZnO nanorods has been developed, which can avoid any etching steps and longtime lift-off processes. In the simplified process, the deposition of a titanium buffer layer is omitted, and a 50 nm ZnO thin-film seed layer is deposited by e-beam evaporation directly onto the silicon patterned with the photoresist. The omitted titanium buffer layer has been observed to result in the absence of the ZnO seed layer on the photoresist. Then, the ZnO nanorods with diameters ranging from 50 to 500 nm have been found to grow hydrothermally only on the regions without the photoresist. The photoresist remains on the substrate after the hydrothermal growth, which can protect areas from the polluted solution and unwanted nanorods. After all processes, the photoresist can be removed easily by the solvent without any unwanted damage of nanorods. With this simplified method, ZnO nanorods can be synthesized and patterned with only one step of lithography, which can be used for novel ZnO based devices.

A 128 x 128 SPAD motion detection-triggered time of flight (ToF) sensor is implemented in 40nm CMOS. The sensor combines vision and ToF ranging functions to only acquire depth frames when inter-frame intensity changes are detected. The 40µm x 20µm pixel integrates two 16-bit time-gated counters to acquire ToF histograms and repurposes them to compare two vision frames without requirement for additional out-of-pixel frame memory resources. An embedded ToF and vision processor performs on-chip vision frame comparison and binary frame output compression as well as controlling the time-resolved histogram sampling. The sensor achieves a maximum 20kfps in vision modality and 500fps in motion detection-triggered ToF over a measured 2.55m range with 1.6cm accuracy. The vision function reduces the sensor power consumption by 70% over continuous ToF operation and allows the sensor to gate the ToF laser emitter to reduce the system power when no motion activity is observed.

Mongolian gerbils of the seizure-sensitive strain exhibit epileptic seizures in relation to changes in the environment, a characteristic which has been increased to about 100% by inbreeding. The seizures vary from animal to animal but are rather stable in the individual animal, which makes it possible to study the neuron densities in the hippocampus of the gerbil in relation to seizure type and seizure intensity. Five groups of gerbils with seizures ranging from minor movements and motor arrest to intense generalized convulsions were investigated with a quantitative method including cell counting by light microscope and estimation of possible brain shrinkage, as well as determination of nucleoli and nuclei diameters. The cell densities were determined in different areas of the pyramidal cells of the hippocampus (H-fields). The study discloses a reduction of cell densities in fields H2 and H3 in relation to intense generalized convulsions. It is suggested that the reduction in cell density in field H2 is a result of seizure activity, whereas the field H3 cell loss can be the result of both the hypoxia and the seizure activity.

The laboratory rat has been used as an animal model to investigate the effects of cocaine on body temperature and to determine if abuse of the drug is a risk factor in the pathogenesis of exercise-induced heat stroke. Animals were trained to run on a treadmill which was enclosed so that the ambient temperature could be regulated. Exercise at ambient temperatures of 20 and 30 degrees C led to a similar rise in core temperature of approximately 1 degrees C, although the starting core temperature was higher in the rats at 30 degrees C (38.5 +/- 0.10 degrees C compared to 37.9 +/- 0.06 degrees C). Cocaine (20 mg/kg) led to a transient fall in core temperature in the 20 degrees C group; the temperature then rapidly recovered, so that after 60 min exercise there was no significant difference between these and the control animals. At the higher ambient temperature cocaine augmented the rise in core temperature during running, although the animals had regained thermal balance by 30 min and core temperature was maintained at 40.2 +/- 0.13 degrees C until the end of the exercise period. The dopamine D1 receptor antagonist SCH 23390 (0.1, 0.3 or 1.0 mg/kg) led to suppression of spontaneous motor activity so that the rats could be persuaded to exercise for only 30-45 min after treatment. Pretreatment with the antagonist did not affect the rise in core temperature induced by cocaine at 30 degrees C which again stabilized by 30 min at 40.0 +/- 0.12 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Publisher Summary During exposure to high ambient temperatures, the thermoregulatory centers in the brain and spinal cord activate appropriate physiological and behavioral responses to maintain the core temperature at the normal level of 37°C in the face of the external heat load. In addition to the hot environment, other factors have been implicated in the pathogenesis of classical heat stroke. Notable among these is the concomitant use of prescription drugs or exposure to exogenous chemicals, many of which are commonly used in agriculture and industry. Although there is evidence for secondary centers in the spinal cord, the major control of body temperature is exercised by neurones located in the rostra1 hypothalamus in the preoptic/anterior hypothalamic nuclear complex. The sites and mechanisms of action of exogenous substances, which interfere with normal temperature regulation, have been extensively studied in animals but far less completely in human subjects. The focus is primarily on brain function during heat exposure.

Hot flushes are frequently incapacitating to the patient and the severe vasomotor disturbances may seriously impair normal daily life. This review attempts to provide an understanding of the pathophysiology of the hot flush as a basis for rationale therapy for each individual patient. The physiological mechanisms controlling body temperature are discussed briefly, and the changes in the system which precipitate the menopausal hot flush are detailed. The neuroendocrine events leading to the onset of the flushing syndrome are then considered. Finally, the therapeutic strategies which may be used in the management of the affected patient are discussed.

The laboratory rat is being studied as a model to determine if abuse of cocaine constitutes a risk factor in the pathogenesis of stress or exertion induced heatstroke. During running on a treadmill for 60 min under thermoneutral conditions (Ta 22 degrees C) a rise in core temperature of approximately 1 degree C was recorded. Injection of cocaine (10 or 20 mg/kg IP) or its vehicle (0.9% NaCl solution) did not modify the running behavior or the core temperature change. Cocaine (30 mg/kg IP) led to a significant increase in the core temperature (compared to animals treated with saline or the lower doses of cocaine) at 45 and 60 min. The rats recovered rapidly following cessation of exercise. Repeated (3) injections of cocaine (30 mg/kg) at 7-day intervals did not alter the magnitude of the final hyperthermia, i.e., neither tolerance nor potentiation were in evidence.

The laboratory rat is being developed as a model to determine whether abuse of cocaine constitutes a risk factor in the pathogenesis of stress or exertion-induced heatstroke. Under thermoneutral conditions (Ta 20 degrees C) cocaine (10-40 mg/kg i.p.) caused a dose-dependent fall in core temperature ranging from 0.45 +/- 0.18 to 1.77 +/- 0.26 degrees C. When the ambient temperature (Ta) was increased to 35 degrees C, cocaine (10-40 mg/kg i.p.) led to a dose-dependent hyperthermia (0.3 +/- 0.08 to 1.43 +/- 0.43 degrees C). Repeated injection of cocaine (40 mg/kg at Ta 20 degrees C or 20 mg/kg at Ta 40 degrees C) on days 1, 3, 8, 15, and 23 did not alter the magnitude of the temperature change compared to that following the first injection, i.e., neither tolerance nor potentiation occurred.

Opiate receptor binding was studied in seizure sensitive (SS) and seizure resistant (SR) strains of the Mongolian gerbil. Cryostat sections of the brain were labeled with [3H]-dihydromorphine, subjected to autoradiography and analysed by microdensitometry. SS gerbils, prior to seizure induction, demonstrated overall greater brain opiate binding when compared to SR animals. Immediately following a seizure, binding in the interpeduncular nucleus fell to levels found in SR animals. The increased opiate binding in the SS (pre-seizure) compared to SR gerbils could reflect a deficit of endogenous ligand which could underlie the seizure diathesis in the gerbil.

The changes in cutaneous and body temperature and cutaneous conductance during hot flushes in eight postmenopausal women were studied. The vasomotor changes occurred approx. 45 sec after the patients experienced the initial subjective symptoms of the attacks. The rise in skin conductance appeared to be a more reliable index of the flushing episode than did the change in skin temperature. On the basis of the changes recorded it is suggested that the hot flush syndrome may represent a specific thermoregulatory disorder rather than being due to a non-specific central autonomic discharge. The episodes may be triggered by a neuroendocrine imbalance following the disruption of ovarian function and fall in estrogen production. In assessing the frequency and severity of hot flushes, and the effects of treatment, objective measurements of skin and core temperature and skin conductance should replace subjective criteria.

The naturally epileptic Mongolian gerbil was used to investigate the epileptogenic properties of beta-endorphin, dynorphin, met-enkephalin and morphine. The results indicate that opioid induced "seizures" are different from naturally spontaneous seizures in the gerbil in respect to EEG recording and motor behavior. Evidence for a protective role in preventing seizures is also presented.

Injections of muscimol (12.5 or 25 ng bilaterally), a GABAA agonist, into the posterior nuclei of the thalamus suppressed generalized convulsive seizures in the spontaneously epileptic Mongolian gerbil. This anticonvulsant effect was dose-dependent and was reversed by picrotoxin (10 ng bilaterally), a GABAA antagonist. Bilateral intrathalamic injections of 1-baclofen (50 ng), an agonist of the GABAB receptor, were ineffective in suppressing seizures in this model. These results suggest that GABAergic transmission within the thalamus is involved in the control or the genesis of some generalized convulsive seizures.

Central injections of apomorphine (10, 20 or 40 μg) into the lateral ventricle or the rostral hypothalamus produced a dose-dependent hypothermie response in the rat. Systemic injections of apomorphine caused a fall in temperature which could be antagonized by pretreatment with pimozide (5 and 20 μg) injected into the rostral hypothalamus, but was not altered when pimozide (20 μg) was given in the lateral ventricle. Tolerance developed to the hypothermie effects of systemic or rostral hypothalamic injections of apomorphine when the same dose was repeated 24 or 48 hr later. However, no tolerance was observed upon repeated administration into the lateral ventricle. Behavioral thermoregulation studies showed that injection of apomorphine into the rostral hypothalamus caused the animals to stay under a heat lamp for a significantly shorter time than saline controls, indicating that the hypothermie effect of apomorphine is due to a downward shift in the thermoregulatory set point. It is suggested that apomorphine may be inducing a hypothermie effect via two different types of dopamine receptors at two different sites: (1) in the rostral hypothalamus, where receptors exhibit tolerance development and where the temperature change is due to a downward shift in the set point; and (2) in areas surrounding the lateral ventricle, where the receptors do not manifest tolerance. A relay from the lateral ventricular sites to the rostral hypothalamus is also a possibility though this cannot be determined from the present data.

Behavioural thermoregulation studies, in which rats were exposed to a heat lamp, indicated that the fall in temperature induced by systemic injection of histidine is due to activation of efferent heat loss pathways. This response was blocked by injection of the H 2 -receptor antagonist, burimamide into the third ventricle. The hypothermia following intraventricular injection of histamine appears to be due to a lowering of the set point of the rostral hypothalamic thermostat. Pyrilamine, an H 1 -receptor antagonist, prevented this effect of histamine.

1. 1. A method for assessing the set temperature regulating behavioural thermoregulation in the fish Chromus chromus is described. 2. 2. Cholinergic stimulation of the brain, both muscarinic and nicotinic, lowered the thermoregulatory set point. 3. 3. Histamine raised the set temperature by an action on H1-receptors. 4. 4. Increasing brain catecholamines, with l-Dopa, also raised the set temperature but it was not possible to distinguish between dopaminergic or noradrenergic components of this response.

It is in the belief that the Secretary of State for Employment's call for new thinking about industrial training needs to include the views and experience of professional industrial trainers that this article has been prepared. The object of the article is to broaden the scope of the debate and to set out constructive ideas about: • The principles and objectives of industrial training • Methods of achieving these objectives • Establishing national training standards

Opioid agonists were used to investigate the modulation of seizures mediated by mu, kappa and delta opiate receptors in the seizure-sensitive Mongolian gerbil. Morphine (1.0-25 mg/kg, s.c.) were used as prototypic agonists for mu, kappa and delta opiate receptors. Each opioid decreased the incidence and severity of the seizure as compared to control values. The anticonvulsant effects of morphine (10 mg/kg, s.c.) and ketocyclazocine (0.5 mg/kg, s.c.) were reversed by naloxone (1.0 mg/kg, s.c.), while the anticonvulsant effects of N-allylnormetazocine (2 mg/kg, s.c.) were not significantly changed by naloxone. Additionally, abnormal behavior was observed following administration of the opioids. Morphine (10 mg/kg, s.c.) produced excitation and hyperresponsiveness with intermittent cataleptic-like states. Ketocyclazocine (10 mg/kg, s.c.) predominantly produced a stuporous, immobile state, accompanied by some loss of posture. N-allylnormetazocine (10 mg/kg, s.c.) produced ataxia and stereotypic side-to-side head nodding . Naloxone was able to reverse the behavioral effects produced by morphine and ketocyclazocine but not those produced by N-allylnormetazocine. The data presented are consistent with earlier studies which demonstrated the anticonvulsant effects of beta-endorphin in the gerbil. This study further suggests that opioids have a protective role against seizure activity in the gerbil and the opioid anticonvulsant effect is not specific to one type of opioid agonist.

The possibility of a role for the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in seizure disorders has been strengthened by biochemical studies showing that various nervous system depressant drugs can modulate GABA receptor binding in vitro. In particular, two classes of anticonvulsant agents, the benzodiazepines and the barbiturates, have modulatory receptor sites on the GABA receptor-ionophore protein complex of the postsynaptic membrane. Furthermore, it is well established that direct block of GABA function causes seizures and that augmentation of GABA function can protect against seizure activity. Direct evidence for altered GABA synaptic markers has been obtained in some animal models of epilepsy, as well as in human focal epilepsy. We present preliminary evidence for a deficit in benzodiazepine receptor binding in the midbrain of seizure-susceptible Mongolian gerbils. These data would be consistent with an impairment of GABA-mediated inhibitory synaptic transmission that contributes to susceptibility to the genesis or spread of seizures in some kinds of epilepsy.

The fall in core temperature induced by a fixed dose of ethanol (1 g x kg-1 i.p.) was an exponential function of the ambient temperature over the range 0-18 degrees C. In rats acclimated to 4 degrees C for 7 days the dose response curve relating the fall in body temperature to ethanol was markedly attenuated. The hypothermic effect of ethanol declined exponentially over 20 days of exposure to 4 degrees C and by the 20th day the fall was no greater than in saline injected controls. Blood ethanol concentrations were similar in acclimated and non-acclimated rats indicating that pharmacokinetic factors do not account for the altered responses. Although the time course of the development of resistance to the hypothermic effect of ethanol parallels that of cold acclimation to 4 degrees C, and the development of non-shivering thermogenesis, the attenuated drug effect does not appear to be due to the altered metabolic activity of brown adipose tissue. It is suggested that the modulation of the effect of ethanol in lowering the thermoregulatory set point results from central nervous system adaptation to the environmental thermal stress.

The seizure sensitive Mongolian gerbil, a genetic model of epilepsy, has been used to investigate the effects of prior spontaneous seizures on the threshold for pentylenetetrazole (PTZ) and maximum electroshock (MES) induced convulsions. In animals which had spontaneous epileptic seizures prior to testing the threshold for PTZ induced convulsions was raised compared to non-seized animals. This inhibitory effect of a spontaneous seizure was not observed for MES convulsions. Pretreatment with naltrexone, an opioid antagonist, attenuated the post-ictal inhibitory effect on PTZ induced convulsions. It is concluded that a spontaneous seizure in the epileptic gerbil leads to non-specific post-ictal inhibition of seizure sensitivity. Endogenous opioids may exert a modulatory action in mediating this phenomenon.

Δ 9 -THC was injected daily for 6 days into gerbils from our breeding colony that exhibit spontaneous epileptiform seizures. At a dose of 20 mg/kg no effect was seen on the latency, duration or severity of the seizures induced after 1 and 6 days of treatment. Δ 9 -THC (50 mg/kg) completely abolished the seizures after a single injection but tolerance developed to this effect so that no protection was afforded after 6 daily doses. Severe toxin signs were evident at the higher dose level with marked depression of spontaneous motor activity. The toxic effects increased progressively with chronic treatment and half the animals failed to survive.

Autoradiography was used to examine opioid receptor binding in the Mongolian gerbil, a genetic model of the epilepsies. Coronal brain sections of seizure-resistant (SR) and seizure-sensitive (SS) (both pre- and post-seizure conditions) gerbils were labeled with [3H]dihydromorphine. SS (pre-seizure) gerbils demonstrated overall greater brain opioid binding when compared to SR animals. The periaqueductal gray, substantia nigra and medial geniculate body were specific areas in SS (pre-seizure) gerbils which demonstrated highly significant increases in opioid binding compared to SR animals (% increase vs SR were 98%, 91.3% and 42.9%, respectively). Scatchard analysis demonstrated that the increase in opioid binding was due to an increase in the total number of receptors without a significant change in receptor affinity (i.e. periaqueductal gray area: total number of binding sites was 12.7 (SR) and 18.0 fmol/mg tissue (SS pre-seizure), while Kd values were 4.0 (SR) and 4.0 mM (SS pre-seizure). Opioid binding was also increased in the SS (post-seizure) animals when compared to SR animals, especially in the substantia nigra. However, when compared to SS (pre-seizure) gerbils, there was a general but not significant, decrease in opioid binding in SS post-seizure gerbils. The increased opioid binding in the SS (pre-seizure) gerbil compared to SR gerbils could reflect an up-regulation due to a deficit in endogenous ligand (e.g. a deficit in synthesis or decreased release) which could underlie the seizure diathesis in the gerbil.

Human urine samples obtained before and after active and passive exposure to marijuana were analyzed by immune kits (Roche, Amersham, and Syva) and gas chromatography/mass spectrometry (GC/MS). Seven of eight subjects were positive for the entire five-day test period with one immune kit. The latter correlated with GC/MS in 98% of the samples. Passive inhalation experiments under conditions likely to reflect realistic exposure resulted consistently in less than 10 ng/mL of cannabinoids. The 10-100-ng/mL cannabinoid concentration range essential for detection of occasional and moderate marijuana users is thus unaffected by realistic passive inhalation.

Withdrawal hypothermia can be induced in rats by injection of naltrexone 72 h after subcutaneous implantation of a morphine pellet. At 45 days after implantation the same dose of naltrexone is without effect on body temperature and the animals are normally sensitive to the hypothermic effect of acute morphine administration. This acute administration of morphine re-sensitizes the animals to naltrexone so that administration of the antagonist again causes withdrawal hypothermia. These results are consistent with the view that narcotic dependence can be reinstated in previously dependent, but not naive, animals by acute administration of the narcotic.

The mechanism by which systemic injection of histidine induces hypothermia has been studied in rats. Injection of histidine directly into the rostral hypothalamic thermoregulatory centers, at sites at which histamine causes hypothermia, had no effect on body temperature. Systemic histidine laoding did not change the hypothalamic or whole brain levels of norepinephrine, dopamine or 5-HT, indicating that the fall in temperature is not due to depletion of these amines which are known to be involved in thermoregulation. Blood pressure measurements showed that when histidine was administered to rats pretreated with a peripherally acting histidine decarboxylase inhibitor no appreciable amount of systemic histamine was formed. It is concluded that the hypothermic effect of histidine is due to the increased formation of histamine in the brain.

Azomorphine products were synthesized and structures determined. A purified derivative was condensed with keyhole limpet hemocyanin and rabbit antisera generated. IgG was purified by Cellex azomorphine. Quantitative inhibition of morphine azobenzoic acid quenching of antibody fluorescence was shown by increasing concentrations of native morphine but not its surrogates. These results were confirmed by radioimmune assay experiments in which methadone and dextromethorphan were essentially unrecognized by crude morphine antisera regardles of hapten concentrations.

1. 1.|Central injections of dopamine (50–600 μm) induce a dose dependent hypothermic response in the rat, with lateral ventricular injections being much more effective than those into the rostral hypothalamus. 2. 2.|Tolerance develops to this hypothermic response. 3. 3.|The hypothermia following lateral ventricular injections of dopamine in the morphine dependent rat can be blocked by injection of pimozide systemically, into the lateral ventricle or into the rostral hypothalamus. 4. 4.|Behavioral thermoregulatory responses indicate that the hypothermia is due to a lowering of the set point of the central thermostats.