To determine the relationship between cerebral Glc metabolism and glutamatergic neuronal function, we used 13 C NMR spectroscopy to measure, simultaneously, the rates of the tricarboxylic acid cycle and Gln synthesis in the rat cortex in vivo. From these measurements, we calculated the rates of oxidative Glc metabolism and glutamate-neurotransmitter cycling between neurons and astrocytes (a quantitative measure of glutamatergic neuronal activity). By measuring the rates of the tricarboxylic acid cycle and Gln synthesis over a range of synaptic activity, we have determined the stoichiometry between oxidative Glc metabolism and glutamateneurotransmitter cycling in the cortex to be close to 1:1. This finding indicates that the majority of cortical energy production supports functional (synaptic) glutamatergic neuronal activity. Another implication of this result is that brain activation studies, which map cortical oxidative Glc metabolism, provide a quantitative measure of synaptic glutamate release.Glc metabolism is the major pathway of energy production in the mature brain (1). During brain activation, increases in Glc metabolism directly form the basis of brain functional mapping by using both 2-deoxyglucose autoradiography (2, 3) and positron-emission tomography (4) and indirectly influence signal changes observed with functional MRI (5). Despite the extensive use of these methods for mapping brain function, the mechanism linking Glc metabolism and functional neuronal activity and the fraction of cerebral energy production that supports neuronal function are still unknown.Glutamate is the major excitatory neurotransmitter in the brain (6), and a high percentage of cortical neurons are glutamatergic (7). It has been proposed that a neuronalastrocytic neurotransmitter cycle exists in the brain in which glutamate from the neuronal pool is released into the synaptic cleft as a neurotransmitter, taken up by astrocytes, converted to Gln, and returned to the neuron in this synaptically inactive form where it is converted back to glutamate (6). The development of in vivo 13 C NMR spectroscopy has enabled the direct investigation of cerebral glutamate metabolism (8, 9). We recently have shown that the rate of glutamateneurotransmitter cycling between neurons and astrocytes can be calculated by using the flux of the 13 C label from glutamate to Gln in the rat brain in vivo during a [1-13 C]Glc infusion (10). Thus, we can obtain an in vivo measure of glutamatergic neuronal activity. In the same experiment, the flux of the 13 C label from [1-13 C]Glc into glutamate yields a simultaneous in vivo measurement of the cerebral tricarboxylic acid (TCA) cycle rate, from which oxidative Glc consumption can be derived (11,12). Therefore, by using the combined measurement of these two fluxes, we can determine quantitatively the stoichiometry between cerebral Glc metabolism and glutamatergic-synaptic activity in vivo.In the present study, we have used direct 13 C NMR spectroscopy to determine the cerebral (primarily cortical)...

The cerebral tricarboxylic acid (TCA) cycle rate and the rate of glutamine synthesis were measured in rats in vivo under normal physiological and hyperammonemic conditions using 13 C NMR spectroscopy. In the hyperammonemic animals, blood ammonia levels were raised from control values of Ϸ0.05 mM to Ϸ0.35 mM by an intravenous ammonium acetate infusion. Once a steady-state of cerebral metabolites was established, a [1-13 C]glucose infusion was initiated, and 13 C NMR spectra acquired continuously on a 7-tesla spectrometer to monitor 13 C labeling of cerebral metabolites. The time courses of glutamate and glutamine C-4 labeling were fitted to a mathematical model to yield TCA cycle rate (V TCA ) and the f lux from glutamate to glutamine through the glutamine synthetase pathway (V gln ). Under hyperammonemia the value of V TCA was 0.57 ؎ 0.16 mol͞min per g (mean ؎ SD, n ‫؍‬ 6) and was not significantly different (unpaired t test; P > 0.10) from that measured in the control animals (0.46 ؎ 0.12 mol͞min per g, n ‫؍‬ 5). Therefore, the TCA cycle rate was not significantly altered by hyperammonemia. The measured rate of glutamine synthesis under hyperammonemia was 0.43 ؎ 0.14 mol͞min per g (mean ؎ SD, n ‫؍‬ 6), which was significantly higher (unpaired t test; P < 0.01) than that measured in the control group (0.21 ؎ 0.04 mol͞ min per g, n ‫؍‬ 5). We propose that the majority of the glutamine synthetase f lux under normal physiological conditions results from neurotransmitter substrate cycling between neurons and glia. Under hyperammonemia the observed increase in glutamine synthesis is comparable to the expected increase in ammonia transport into the brain and reported measurements of glutamine eff lux under such conditions. Thus, under conditions of elevated plasma ammonia an increase in the rate of glutamine synthesis occurs as a means of ammonia detoxification, and this is superimposed on the constant rate of neurotransmitter cycling through glutamine synthetase.Glutamine synthetase in the brain is predominantly an astrocytic enzyme that catalyzes the formation of glutamine from glutamate and ammonia. It has been suggested that this pathway forms part of a neurotransmitter cycle between neurons and glia (1). In this cycle, astrocytes take up neurotransmitter glutamate from the synaptic cleft, convert it to glutamine via glutamine synthetase, and release this glutamine into the extracellular space for uptake by neurons, where it is converted back to glutamate primarily by glutaminase. ␥-Aminobutyric acid (GABA) released from inhibitory neurons also may be taken up by astrocytes, converted to glutamate, and recycled to neruons in the same way. The function of such a cycle would be to remove the synaptically active metabolite from the synaptic cleft and to recycle the carbon skeletons back to the neuronal pool by a synaptically inactive form.While ammonia is a normal constituent of tissue, elevated concentrations of blood and brain ammonia have been found to interfere with cerebral energy metabolism and may redu...

In an investigation of the auditory cortex response to speech, six subjects were studied using echo-planar functional magnetic resonance imaging (fMRI) at 2.1T. The subjects were asked to listen to English nouns presented at various rates ranging from 0 words per minute (wpm) to 130 wpm while fMRI images encompassing their primary and posterior superior secondary auditory cortices were acquired. An asymmetric spin echo imaging sequence was used with an induced T2 weighting of 50 ms to allow for transverse relaxation effects. Images were acquired in two or four axial-oblique slices with a repetition time of 3.75 or 7.5 s, in plane resolution of 6 x 3 mm, and a slice thickness of 5 mm. Localized activation centered over grey matter was consistently observed in all subjects in the transverse temporal gyrus (TTG), the transverse temporal sulcus (TTS), and the posterior superior aspect of the superior temporal gyrus (STG). The total activate volume and the integrated signal response in bilateral primary and posterior superior secondary auditory cortices increased with increasing rate of word presentation, peaking at 90 wpm (with some intersubject variability) with a subsequent fall at 130 wpm. There were no significant differences in the rate dependence of the signal response in bilateral primary and bilateral posterior superior secondary auditory cortices (P < 0.05).

Aim: Perforation peritonitis is the most common surgical emergency encountered by surgeons in India. The etiology and sites of perforation shows wide geographical variation. The objective of the study was to find the spectrum of perforation peritonitis & highlight its management at Maharishi Markendeshwar Institute of Medical Sciences & Research, Mullana (MMIMSR).Methods: 93 Operated patients of perforation peritonitis were studied retrospectively in terms of clinical presentation, duration, operative findings and postoperative morbidity and mortality over a period of two years between 2011 to 2013 at MMIMSR Mullana. All the patients had undergone emergency laparatomy under general anesthesia and sites of perforation were identified & managed.Results: The most common cause of perforation peritonititis noticed in our series was peptic ulcer perforation 43 cases (46%), followed by ileal perforation 30 cases (32%), appendicular perforation 6 cases (6.4%), gallbladder perforation 5 cases (5.3%) and all the jejunal perforation 6cases (6.4%) was post traumatic. Large bowel and malignant perforation were least common in our series. Highest no. of perforation noticed in upper part of Gastro intestinal tract as compared to western countries where perforations are seen in distal parts. Mortality was of 11 cases (11.8%) & morbidity was noticed in 55 cases (59%).Conclusion: Peptic ulcer perforation peritonitis is the leading etiology. Mortality is comparable to that of best centre. Aggressive resuscitation and early minimum surgery are required to avoid the high morbidity and mortality. Major complication noticed was wound infection and dehiscence.Bangladesh Journal of Medical Science Vol.15(1) 2016 p.70-73

Highly active bimetallic NiPd/MIL‐101, CuPd/MIL‐101 and CoPd/MIL‐101 alloy nanoparticle catalysts stabilized by MIL‐101 framework, (M/Pd atomic ratio=95:5, M=Ni, Cu and Co) were synthesized, and their catalytic activity for Suzuki reaction at moderate reaction conditions was explored. In contrary to monometallic counterparts, a significant enhancement in catalytic activity, with excellent yields for biaryls (upto 97 %), was observed with these bimetallic NiPd/MIL‐101, CuPd/MIL‐101 and CoPd/MIL‐101 alloy nanoparticle catalysts. Among these catalysts, NiPd/MIL‐101 and CuPd/MIL‐101 displayed highest catalytic activity for the synthesis of biaryls for a wide range of substituted aryl halides and arylboronic acids with electron donating and electron withdrawing substituents, whereas CoPd/MIL‐101 was found to be poorly active. Worthy to mention that, NiPd/MIL‐101 and CuPd/MIL‐101 displayed ca 20 times higher TOF (h−1) than the Pd/MIL‐101 catalyst. The observed high catalytic activity displayed by NiPd/MIL‐101 and CuPd/MIL‐101 was attributed to the synergistic effect due to electronic charge transfer from Ni or Cu to Pd, and high dispersion of NiPd and CuPd nanoparticles on MIL‐101 frameworks.

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