Percutaneous Radiofrequency Lesioning of the Suprascapular Nerve for the Management of Chronic Shoulder Pain: A Case Series

Purpose: The objective of this study was to retrospectively evaluate the analgesic effects of continuous radiofrequency lesioning of the suprascapular nerve (SSN) for chronic shoulder pain. The authors sought to obtain insight into the time-sensitive analgesic success and complications of this therapy. Patients and methods: This study was a retrospective case series involving patients with unremitting shoulder pain that had lasted for at least 12 months. Patients were selected if they showed a reduction of at least 50% in pain intensity during the anesthetic phase after SSN block, no additional motor weakness of the shoulder, and pain relief lasting for less than 2 months after separate treatments of the SSN with depot corticosteroids and pulsed radiofrequency. Nine patients were referred to the Arnold Pain Management Center. Of these nine patients, six patients who had significant chronic shoulder pain unresponsive to oral medications and intra-articular injections and who were not considered surgical candidates were selected. These patients were treated with a single radiofrequency lesion of the SSN at 80$^\circ$C for 60 seconds. The primary outcome was a reduction in pain intensity by 50%, as determined by the numeric rating scale, and duration of this effect. The secondary outcome was improvement in either the passive or the active range of motion (ROM). Patients were also monitored for adverse effects such as weakness or increased pain. Results: The pooled mean numeric rating scale score before the procedure was 7.2 $\pm$ 1.2; this fell to 3.0 $\pm$ 0.9 at 5–7 weeks post procedure. The duration of pain relief ranged from 3 to 18 months, and all patients underwent at least one additional treatment. The change in baseline ROM improved from an average of 60$^\circ$ $\pm$ 28$^\circ$ (flexion) and 58$^\circ$ $\pm$ 28$^\circ$ (abduction) to 99$^\circ$ $\pm$ 46$^\circ$ (flexion) and 107$^\circ$ $\pm$ 39$^\circ$ (abduction). No adverse side effects were observed. Conclusion: Continuous radiofrequency lesioning of the SSN seems to be an effective treatment for chronic shoulder pain. There can be improved ROM of the shoulder following this treatment. More formal, controlled studies are required to confirm these observations

The essential mycobacterial genes, fabG1 and fabG4, encode 3-oxoacyl-thioester reductases that are functional in yeast mitochondrial fatty acid synthase type 2

Mycobacterium tuberculosis represents a severe threat to human health worldwide. Therefore, it is important to expand our knowledge of vital mycobacterial processes, such as that effected by fatty acid synthase type 2 (FASII), as well as to uncover novel ones. Mycobacterial FASII undertakes mycolic acid biosynthesis, which relies on a set of essential enzymes, including 3-oxoacyl-AcpM reductase FabG1/Rv1483. However, the M. tuberculosis genome encodes four additional FabG homologs, designated FabG2–FabG5, whose functions have hitherto not been characterized in detail. Of the four candidates, FabG4/Rv0242c was recently shown to be essential for the survival of M. bovis BCG. The present work was initiated by assessing the suitability of yeast oar1Δ mutant cells lacking mitochondrial 3-oxoacyl-ACP reductase activity to act as a surrogate system for expressing FabG1/MabA directed to the mitochondria. Mutant yeast cells producing this targeted FabG1 variant were essentially wild type for all of the chronicled phenotype characteristics, including respiratory growth on glycerol medium, cytochrome assembly and lipoid acid production. This indicated that within the framework of de novo fatty acid biosynthesis in yeast mitochondria, FabG1 was able to act on shorter (C4) acyl substrates than was previously proposed (C8–20) during mycolic acid biosynthesis in M. tuberculosis. Thereafter, FabG2–FabG5 were expressed as mitochondrial proteins in the oar1Δ strain, and FabG4 was found to complement the mutant phenotype and contain high levels of 3-oxoacyl-thioester reductase activity. Hence, like FabG1, FabG4 is also an essential, physiologically functional 3-oxoacyl-thioester reductase, albeit the latter’s involvement in mycobacterial FASII remains to be explored

A C. elegans Model for Mitochondrial Fatty Acid Synthase II: The Longevity-Associated Gene W09H1.5/mecr-1 Encodes a 2-trans-Enoyl-Thioester Reductase

Our recognition of the mitochondria as being important sites of fatty acid biosynthesis is continuously unfolding, especially in light of new data becoming available on compromised fatty acid synthase type 2 (FASII) in mammals. For example, perturbed regulation of murine 17β-HSD8 encoding a component of the mitochondrial FASII enzyme 3-oxoacyl-thioester reductase is implicated in polycystic kidney disease. In addition, over-expression in mice of the Mecr gene coding for 2-trans-enoyl-thioester reductase, also of mitochondrial FASII, leads to impaired heart function. However, mouse knockouts for mitochondrial FASII have hitherto not been reported and, hence, there is a need to develop alternate metazoan models such as nematodes or fruit flies. Here, the identification of Caenorhabditis elegans W09H1.5/MECR-1 as a 2-trans-enoyl-thioester reductase of mitochondrial FASII is reported. To identify MECR-1, Saccharomyces cerevisiae etr1Δ mutant cells were employed that are devoid of mitochondrial 2-trans-enoyl-thioester reductase Etr1p. These yeast mutants fail to synthesize sufficient levels of lipoic acid or form cytochrome complexes, and cannot respire or grow on non-fermentable carbon sources. A mutant yeast strain ectopically expressing nematode mecr-1 was shown to contain reductase activity and resemble the self-complemented mutant strain for these phenotype characteristics. Since MECR-1 was not intentionally targeted for compartmentalization using a yeast mitochondrial leader sequence, this inferred that the protein represented a physiologically functional mitochondrial 2-trans-enoyl-thioester reductase. In accordance with published findings, RNAi-mediated knockdown of mecr-1 in C. elegans resulted in life span extension, presumably due to mitochondrial dysfunction. Moreover, old mecr-1(RNAi) worms had better internal organ appearance and were more mobile than control worms, indicating a reduced physiological age. This is the first report on RNAi work dedicated specifically to curtailing mitochondrial FASII in metazoans. The availability of affected survivors will help to position C. elegans as an excellent model for future pursuits in the emerging field of mitochondrial FASII research

Maximal subgroups in finite and profinite groups

Abstract. We prove that if a finitely generated profinite group G is not generated with positive probability by finitely many random elements, then every finite group F is obtained as a quotient of an open subgroup of G. The proof involves the study of maximal subgroups of profinite groups, as well as techniques from finite permutation groups and finite Chevalley groups. Confirming a conjecture from Ann. of Math. 137 (1993), 203–220, we then prove that a finite group G has at most |G | c maximal soluble subgroups, and show that this result is rather useful in various enumeration problems. 1