Functional Outcome Of Bristow-Latarjet Procedure In Post-Traumatic Recurrent Anterior Shoulder Instability.

BACKGROUND: Due to its lack of bony support, the shoulder joint has the broadest range of motion out of all the joints in the body. Instead, one of the joints that dislocate most frequently is the shoulder joint. Multiple pathologic abnormalities, including the traumatic separation of the anterior-inferior capsule-labral complex from the glenoid rim, are caused by repeated anterior glenohumeral dislocation. The objective of the study is to ascertain the Bristow-LATARJET procedure's efficacy in situations of recurrent post-traumatic anterior shoulder instability. METHODS: From 31 January 2020 to 31 July 2020, a descriptive case series was undertaken in the orthopaedic surgery department of the Lahore General Hospital. For this study, 71 patients who met the inclusion and exclusion criteria were recruited, and all interventions were conducted while the patients were lying in a beach chair while under general anaesthesia. The Delto-pectoral incision surgical technique was applied. For 12 weeks, all patients underwent clinical follow-up, and the results were documented. RESULTS: There were 50(70.4%) males and 21(29.6%) females in this study & the mean age of the patients were 34.64±10.73. There were 37(52.1%) patients among them the outcome of treatment (Rowe Scale at 12th week) was excellent, among 21(29.6%) it was good, among 8(11.3%) it was fair and among 5 (7.0%) it was poor. There was a significant association between the outcome of treatment (Rowe scale at 12th week) and age groups (p-value: 0.000). CONCLUSIONS: The Bristow-LATARJET procedure is deemed to be a very productive, safe, and problem-free procedure for curing post-traumatic reoccurring traumatic anterior shoulder instability.

Possible neurotoxicity of the anesthetic propofol: evidence for the inhibition of complex II of the respiratory chain in area CA3 of rat hippocampal slices.

Propofol is the most frequently used intravenous anesthetic for induction and maintenance of anesthesia. Propofol acts first and formost as a GABAA-agonist, but effects on other neuronal receptors and voltage-gated ion channels have been described. Besides its direct effect on neurotransmission, propofol-dependent impairment of mitochondrial function in neurons has been suggested to be responsible for neurotoxicity and postoperative brain dysfunction. To clarify the potential neurotoxic effect in more detail, we investigated the effects of propofol on neuronal energy metabolism of hippocampal slices of the stratum pyramidale of area CA3 at different activity states. We combined oxygen-measurements, electrophysiology and flavin adenine dinucleotide (FAD)-imaging with computational modeling to uncover molecular targets in mitochondrial energy metabolism that are directly inhibited by propofol. We found that high concentrations of propofol (100 µM) significantly decrease population spikes, paired pulse ratio, the cerebral metabolic rate of oxygen consumption (CMRO2), frequency and power of gamma oscillations and increase FAD-oxidation. Model-based simulation of mitochondrial FAD redox state at inhibition of different respiratory chain (RC) complexes and the pyruvate-dehydrogenase show that the alterations in FAD-autofluorescence during propofol administration can be explained with a strong direct inhibition of the complex II (cxII) of the RC. While this inhibition may not affect ATP availability under normal conditions, it may have an impact at high energy demand. Our data support the notion that propofol may lead to neurotoxicity and neuronal dysfunction by directly affecting the energy metabolism in neurons.

Monoamines block kainate- and carbachol-induced gamma-oscillations but augment stimulus-induced gamma-oscillations in rat hippocampus in vitro.

Monoamines are implicated in a cognitive processes in a variety of brain regions, including the hippocampal formation, where storage and retrieval of information are facilitated by synchronous network activities. We have investigated the effects of norepinephrine, serotonin, and dopamine on carbachol-, kainate-, and stimulus-induced hippocampal gamma-oscillations employing combined extra- and intracellular recordings. Monoamines dose-dependently and reversibly suppressed kainate- and carbachol-induced gamma-oscillations while increasing the frequency. The effect of serotonin was mimicked by fenfluramine, which releases serotonin from presynaptic terminals. Forskolin also suppressed kainate- and carbachol-induced gamma-oscillations. This effect was mimicked by 8-Br-cAMP and isoproterenol, an agonist of noradrenergic beta-receptor suggesting that the monoamines-mediated suppression of these oscillations could involve intracellular cyclic adenosine 3',5'-cyclic monophosphate (AMP). By contrast, stimulus-induced gamma-oscillations were dose-dependently augmented in power and duration after monoamines application. Intracellular recordings from pyramidal cells revealed that monoamines prolonged the stimulus-induced depolarization and membrane potential oscillations. Stimulus-induced gamma-oscillations were also suppressed by isoproterenol, the D1 agonist SKF-38393 forskolin, and 8-Br-cAMP. This suggests that the augmentation of stimulus-induced gamma-oscillations by monoamines involves--at least in part-different classes of cells than in case of carbachol- and kainate-induced gamma-oscillations.