CHAPTER XII COMBINED OPERATIONS: THE SACO AND PETTEE MACHINE SHOPS, 1897-1912

1950 ◽  
pp. 404-454
1999 ◽  
Author(s):  
W.K. Sieber ◽  
G.M. Piacitelli ◽  
R.T. Hughes ◽  
R.A. Glaser ◽  
J.D. Catalano ◽  
...  

Soon after his accession to the English throne William’s two navies started combined operations against the common enemy France. The Nine Years War had broken out, and this was followed after a short interval by the War of the Spanish Succession. Combined naval operations by two allies were nothing uncommon in those days. Anglo- French fleets had fought the Dutch in no fewer than four fierce battles in 1672 and 1673. French and Dutch squadrons had cooperated against the English Navy in 1666, and much earlier in 1596 and 16252727 Anglo- Dutch fleets jointly attacked Spanish ports (1). In these examples cooperation never lasted long nor was it very close. Problems concerning the command structure were seldom satisfactorily solved. Allies regularly changed sides during the 17th century. The Glorious Revolution, however, can be treated as a turning point. England became involved in a generations-long struggle against France. The Dutch Republic under William III had already started to fight Louis XIV’s urge for expansion, more than 15 years earlier. Both countries almost became traditional allies. Right from the beginning in 1689 detailed arrangements were made for naval cooperation, long-standing ones as later developments showed.


Hand ◽  
2021 ◽  
pp. 155894472098807
Author(s):  
Momodou L. Jammeh ◽  
J. Westley Ohman ◽  
Chandu Vemuri ◽  
Ahmmad A. Abuirqeba ◽  
Robert W. Thompson

Background: The clinical outcomes of reoperations for recurrent neurogenic thoracic outlet syndrome (NTOS) remain undefined. Methods: From 2009 to 2019, 90 patients with recurrent NTOS underwent anatomically complete supraclavicular reoperation after previous operation(s) performed at other institutions using either supraclavicular (Prev-SC = 48), transaxillary (Prev-TA = 31), or multiple/combination (Prev-MC = 11) approaches. Prospectively maintained data were analyzed retrospectively. Results: The mean patient age was 39.9 ± 1.4 years, 72% were female, and the mean interval after previous operation was 4.1 ± 0.6 years. The mean Disabilities of the Arm, Shoulder, and Hand (QuickDASH) score was 62 ± 2, reflecting substantial preoperative disability. Residual scalene muscle was present in 100% Prev-TA, 79% Prev-SC, and 55% Prev-MC ( P < .05). Retained/residual first rib was present in 90% Prev-TA, 75% Prev-SC, and 55% Prev-MC ( P < .05). There were no differences in operative time (overall 210 ± 5 minutes), length of hospital stay (4.7 ± 0.2 days), or 30-day readmissions (7%). During follow-up of 5.6 ± 0.3 years, the improvement in QuickDASH scores was 21 ± 2 (36% ± 3%) ( P < .01) and patient-rated outcomes were excellent in 10%, good in 36%, fair in 43%, and poor in 11%. Conclusions: Anatomically complete decompression for recurrent NTOS can be safely and effectively accomplished by supraclavicular reoperation, regardless of the type of previous operation. Residual scalene muscle and retained/residual first rib are more frequently encountered after transaxillary operations than after supraclavicular or multiple/combined operations. Supraclavicular reoperation can achieve significant symptom reduction and functional improvement for approximately 90% of patients with recurrent NTOS.


Author(s):  
Gennadii Oborskyi ◽  
Alexandr Orgiyan ◽  
Volodymyr Tonkonogyi ◽  
Albakush Aymen ◽  
Anna Balaniuk

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0243391
Author(s):  
Elma H. Akand ◽  
Stephen J. Maher ◽  
John M. Murray

Human immunodeficiency virus (HIV) is subject to immune selective pressure soon after it establishes infection at the founder stage. As an individual progresses from the founder to chronic stage of infection, immune pressure forces a history of mutations that are embedded in envelope sequences. Determining this pathway of coevolving mutations can assist in understanding what is different with the founder virus and the essential pathways it takes to maintain infection. We have combined operations research and bioinformatics methods to extract key networks of mutations that differentiate founder and chronic stages for 156 subtype B and 107 subtype C envelope (gp160) sequences. The chronic networks for both subtypes revealed strikingly different hub-and-spoke topologies compared to the less structured transmission networks. This suggests that the hub nodes are impacted by the immune response and the resulting loss of fitness is compensated by mutations at the spoke positions. The major hubs in the chronic C network occur at positions 12, 137 (within the N136 glycan), and 822, and at position 306 for subtype B. While both founder networks had a more heterogeneous connected network structure, interestingly founder B subnetworks around positions 640 and 837 preferentially contained CD4 and coreceptor binding domains. Finally, we observed a differential effect of glycosylation between founder and chronic subtype B where the latter had mutational pathways significantly driven by N-glycosylation. Our study provides insights into the mutational pathways HIV takes to evade the immune response, and presents features more likely to establish founder infection, valuable for effective vaccine design.


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