The Hospital for the Ruptured and Crippled: Knight to Gibney, 1870-1887.
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SUBMITTER: Levine DB
PROVIDER: S-EPMC2504108 | biostudies-other | 2006 Feb
REPOSITORIES: biostudies-other
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Project description:In 1912, the Hospital for the Ruptured and Crippled (R & C) moved to its third location since its founding in 1863. It was a newly constructed six-story building on 42nd Street between Second Avenue and First Avenue. At the time Dr. Virgil Gibney, the second Surgeon-in-Chief, was 65 years of age and had already served 25 years in that position. The building housed a New York City public school since the length of stay of the children, many afflicted with tuberculosis and poliomyelitis, might be over 1-2 years. The large number of immigrants in the city led to very challenging social conditions that saw changes made in the first two decades of the twentieth century. When this country entered World War I in 1917, the physician staff was significantly affected as many volunteered for military service. Soldiers, sailors, and marines were treated at R & C, and military physicians were educated in orthopedics and hernia care on the wards and in the outpatient department. Because of declining health in 1924, Dr. Gibney retired and was replaced as Surgeon-in-Chief by his long-term friend and colleague, Dr. William B. Coley in January 1925.
| S-EPMC2504267 | biostudies-other
Project description:In 1939, the 75th anniversary program marking the founding of the Hospital for the Ruptured and Crippled (R & C), the oldest orthopaedic hospital in the nation, was held at the hospital site in New York City. Dr. Philip D. Wilson, Surgeon-in-Chief since 1935, used this event to mark the return of the hospital to its leadership role in the country. When the Hospital for the Ruptured and Crippled first opened its doors on May 1, 1863, the name of the hospital was not unusual; it described the type of patients treated. In 1940, the Board of Managers with guidance from Dr. Wilson changed the name to the Hospital for Special Surgery (HSS). In 1941, with Britain engaged in a European war, Dr. Wilson felt there was a need for the Americans to support the British. He personally organized the American Hospital in Britain, a privately funded voluntary unit, to help care for the wounded. After the United States actually entered World War II in December 1941, HSS quickly organized support at all levels with a significant number of professional and auxiliary staff, eventually enlisting in the military. Even with such staff turnover, the hospital continued to function under Dr. Wilson's leadership. After the war ended in 1945, Wilson forged ahead to further restore HSS as a leader in musculoskeletal medicine and surgery.
| S-EPMC2642546 | biostudies-other
Project description:In January 1925, the Board of Managers of the New York Society for the Relief of the Ruptured and Crippled appointed William Bradley Coley, M.D., age 63, Surgeon-in-Chief of the Hospital for the Ruptured and Crippled (R & C) to succeed Virgil P. Gibney who submitted his resignation the month before. It would be the first time a general surgeon held that position at the oldest orthopedic hospital in the nation, now known as Hospital for Special Surgery (HSS). Coley had been on staff for 36 years and was world famous for introducing use of toxins to treat malignant tumors, particularly sarcomas. A graduate of Yale College and Harvard Medical College, Coley interned at New York Hospital and was appointed, soon after, to the staff of the New York Cancer Hospital (now Memorial Sloan Kettering Cancer Center) located at that time at 106th Street on the West Side of New York. With his mentor Dr. William Bull, Coley perfected the surgical treatment of hernias at R & C. He was instrumental in raising funds for his alma maters, Yale, Harvard and Memorial Hospital. His crusade in immunology as a method of treatment for malignant tumors later fell out of acceptance in the medical establishment. After his death in 1936, an attempt to revive interest in use of immunotherapy for inoperable malignancies was carried out by his daughter, Helen Coley Nauts, who pursued this objective until her death at age 93 in 2000. Coley's health deteriorated in his later years, and in 1933, he resigned as chief of Bone Tumors at Memorial Hospital and Surgeon-in-Chief at R & C, being succeeded at Ruptured and Crippled as Surgeon-in-Chief by Dr. Eugene H. Pool. William Bradley Coley died of intestinal infarction in 1936 and was buried in Sharon, Connecticut.
| S-EPMC2504278 | biostudies-other
Project description:In 1933, for the second time in the history of the Hospital for the Ruptured and Crippled (R & C), a general surgeon, Eugene Hillhouse Pool, MD, was appointed Surgeon-in-Chief by the Board of Managers of the New York Society for the Relief of the Ruptured and Crippled. R & C (whose name was changed to the Hospital for Special Surgery in 1940), then the oldest orthopaedic hospital in the country, was losing ground as the leading orthopaedic center in the nation. The R & C Board charged Dr. Pool with the task of recruiting the nation's best orthopaedic surgeon to become the next Surgeon-in-Chief. Phillip D. Wilson, MD, from the Massachusetts General Hospital in Boston and the Harvard Medical School was selected and agreed to accept this challenge. He joined the staff of the Hospital for the Ruptured and Crippled in the spring of 1934 as Director of Surgery and replaced Dr. Pool as Surgeon-in-Chief the next year. It was the time of the Great Depression, which added a heavy financial toll to the daily operations of the hospital. With a clear and courageous vision, Dr. Wilson reorganized the hospital, its staff responsibilities, professional education and care of patients. He established orthopaedic fellowships to support young orthopaedic surgeons interested in conducting research and assisted them with the initiation of their new practices. Recognizing that the treatment of crippling conditions and hernia were becoming separate specialties, one of his first decisions was to restructure the Hernia Department to become the General Surgery Department. His World War I experiences in Europe helped develop his expertise in the fields of fractures, war trauma and amputations, providing a broad foundation in musculoskeletal diseases that was to be beneficial to him in his future role as the leader of R & C.
| S-EPMC2553161 | biostudies-other
Project description:Neisseria gonorrhoeae (gonococci) and Neisseria meningitidis (meningococci) are human pathogens that cause gonorrhea and meningococcal meningitis, respectively. Both N. gonorrhoeae and N. meningitidis release a number of small peptidoglycan (PG) fragments, including proinflammatory PG monomers, although N. meningitidis releases fewer PG monomers. The PG fragments released by N. gonorrhoeae and N. meningitidis are generated in the periplasm during cell wall remodeling, and a majority of these fragments are transported into the cytoplasm by an inner membrane permease, AmpG; however, a portion of the PG fragments are released into the extracellular environment through unknown mechanisms. We previously reported that the expression of meningococcal ampG in N. gonorrhoeae reduced PG monomer release by gonococci. This finding suggested that the efficiency of AmpG-mediated PG fragment recycling regulates the amount of PG fragments released into the extracellular milieu. We determined that three AmpG residues near the C-terminal end of the protein modulate AmpG's efficiency. We also investigated the association between PG fragment recycling and release in two species of human-associated nonpathogenic Neisseria: N. sicca and N. mucosa Both N. sicca and N. mucosa release lower levels of PG fragments and are more efficient at recycling PG fragments than N. gonorrhoeae Our results suggest that N. gonorrhoeae has evolved to increase the amounts of toxic PG fragments released by reducing its PG recycling efficiency.Neisseria gonorrhoeae and Neisseria meningitidis are human pathogens that cause highly inflammatory diseases, although N. meningitidis is also frequently found as a normal member of the nasopharyngeal microbiota. Nonpathogenic Neisseria, such as N. sicca and N. mucosa, also colonize the nasopharynx without causing disease. Although all four species release peptidoglycan fragments, N. gonorrhoeae is the least efficient at recycling and releases the largest amount of proinflammatory peptidoglycan monomers, partly due to differences in the recycling permease AmpG. Studying the interplay between bacterial physiology (peptidoglycan metabolism) and pathogenesis (release of toxic monomers) leads to an increased understanding of how different bacterial species maintain asymptomatic colonization or cause disease and may contribute to efforts to mitigate disease.
| S-EPMC5055606 | biostudies-literature
Project description:BackgroundA brain arteriovenous malformation (BAVM) is a tangle of abnormal blood vessels connecting the arteries and veins in the brain and is associated with a higher risk for intracerebral hemorrhage (ICH). RNA sequencing technology has been recently used to investigate the mechanism of diseases owing to its ability to identify the gene changes on a transcriptome-wide level. This study aims to gain insights into the potential mechanism involved in BAVM rupture.MethodsSixty-five BAVM nidus samples were collected, among which 28 were ruptured and 37 were un-ruptured. Then, next-generation RNA sequencing was performed on all of them to obtain differential expressed genes (DEGs) between the two groups. In addition, bioinformatics analysis was performed to evaluate the involved biological processes and pathways by GO and KEGG analysis. Finally, we performed a univariate Cox regression analysis to obtain the early rupture-prone DEGs.ResultsA total of 951 genes were differentially expressed between the ruptured and un-ruptured BAVM groups, of which 740 genes were upregulated and 211 genes were downregulated in ruptured BAVMs. Then, bioinformatics analysis showed the biological processes and pathways related to the inflammatory processes and extracellular matrix organization were significantly enriched. Meanwhile, some downregulated genes are involved in cell adhesion and genes participating in response to muscle activity and the terms of nervous system development. Finally, one hundred twenty-five genes, many were involved in inflammation, were correlated with the early rupture of BAVMs.ConclusionsThe upregulated genes in the ruptured BAVM group were involved in inflammatory processes and extracellular matrix organization. Some of the downregulated genes participated in cell adhesion and myofibril assembly, indicating the role of enhanced inflammation and reduced inflammation vessel strength in BAVMs rupture.
| S-EPMC9161579 | biostudies-literature
Project description:Submitral aneurysm is a rare entity, with around few hundred cases reported till date. Presentation can be varied. We describe here a case of submitral aneurysm in a young male with rupture into the left atrium cavity.
| S-EPMC5067383 | biostudies-literature
Project description:ObjectiveVascular surgeons treating patients with ruptured abdominal aortic aneurysm must make rapid treatment decisions and sometimes lack immediate access to endovascular devices meeting the anatomic specifications of the patient at hand. We hypothesized that endovascular treatment of ruptured abdominal aortic aneurysm (rEVAR) outside manufacturer instructions-for-use (IFU) guidelines would have similar in-hospital mortality compared to patients treated on-IFU or with an infrarenal clamp during open repair (ruptured open aortic aneurysm repair [rOAR]).MethodsVascular Quality Initiative datasets for endovascular and open aortic repair were queried for patients presenting with ruptured infrarenal AAA between 2013-2018. Graft-specific IFU criteria were correlated with case-specific proximal neck dimension data to classify rEVAR cases as on- or off-IFU. Univariate comparisons between the on- and off-IFU groups were performed for demographic, operative and in-hospital outcome variables. To investigate mortality differences between rEVAR and rOAR approaches, coarsened exact matching was used to match patients receiving off-IFU rEVAR with those receiving complex rEVAR (requiring at least one visceral stent or scallop) or rOAR with infrarenal, suprarenal or supraceliac clamps. A multivariable logistic regression was used to identify factors independently associated with in-hospital mortality.Results621 patients were treated with rEVAR, with 65% classified as on-IFU and 35% off-IFU. The off-IFU group was more frequently female (25% vs. 18%, P = 0.05) and had larger aneurysms (76 vs. 72 mm, P= 0.01) but otherwise was not statistically different from the on-IFU cohort. In-hospital mortality was significantly higher in patients treated off-IFU vs. on-IFU (22% vs. 14%, P= 0.02). Off-IFU rEVAR was associated with longer operative times (135 min vs. 120 min, P= 0.004) and increased intraoperative blood product utilization (2 units vs. 1 unit, P= 0.002). When off-IFU patients were matched to complex rEVAR and rOAR patients, no baseline differences were found between the groups. Overall in-hospital complications associated with off-IFU were reduced compared to more complex strategies (43% vs. 60-81%, P< 0.001) and in-hospital mortality was significantly lower for off-IFU rEVAR patients compared to the supraceliac clamp group (18% vs. 38%, P= 0.006). However, there was no significantly increased mortality associated with complex rEVAR, infrarenal rOAR or suprarenal rOAR compared to off-IFU rEVAR (all P> 0.05). This finding persisted in a multivariate logistic regression.ConclusionsOff-IFU rEVAR yields inferior in-hospital survival compared to on-IFU rEVAR but remains associated with reduced in-hospital complications when compared with more complex repair strategies. When compared with matched patients undergoing rOAR with an infrarenal or suprarenal clamp, survival was no different from off-IFU rEVAR. Taken together with the growing available evidence suggesting reduced long-term durability of off-IFU EVAR, these data suggest that a patient's comorbidity burden should be key in making the decision to pursue off-IFU rEVAR over a more complex repair when proximal neck violations are anticipated preoperatively.
| S-EPMC9843606 | biostudies-literature
Project description:The outbreak of novel and recent coronavirus disease 2019, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, has made an emergency throughout the world. In India, the outspread of the pandemic was observed on 3 March 2020, and after that exponential growth in the cases was observed in the country. Owing to the widespread transmission, high population density, high testing capacity and ineffective treatment, a continuous rise in cases was observed due to the pandemic in India. In this paper, we have discussed the trend and spread of COVID-19 spread in India with time, history of initial confirmed cases, the impact of phased manner lockdown, age- and gender-wise trend of cases and comparison of cases with the other most affected countries. The study uses exploratory data analysis to describe the current situation of COVID-19 cases in India till 16 August 2020, with the help of data from the Ministry of Health and Family Welfare, Government of India (GOI) and the World Health Organization (WHO). As of August 16, the total number of confirmed cases in India crossed 2.5 million marks with over 50,000 causalities. With more patients recovering and being discharged from hospitals and home isolation (in case of mild and moderate cases), the total recoveries have crossed the 1.8 million mark with a recovery rate of more than 70% and case fatality rate of 1.94% which is maintained below the global average and is on a continuous positive slide. The study also enlightens the preventive and stringent measures taken by India to combat the COVID-19 situation along with the future prospects. The GOI is following its proactive and preemptive approach for management, prevention and containment of COVID-19 in collaboration with the WHO.
| S-EPMC7456788 | biostudies-literature
Project description:BACKGROUND AND PURPOSE:Carotid plaques are a strong risk factor for ischemic stroke, and plaque rupture poses an even higher risk. Although many studies have investigated the pathogenic mechanisms of carotid plaque formation, few have studied the differences in molecular mechanisms underlying the rupture and non-rupture of carotid plaques. In addition, since early diagnosis and treatment of carotid plaque rupture are critical for the prevention of ischemic stroke, many studies have sought to identify the important target molecules involved in the rupture. However, a target molecule critical in symptomatic ruptured plaques is yet to be identified. METHODS:A total of 79 carotid plaques were consecutively collected, and microscopically divided into ruptured and non-ruptured groups. Quantitative polymerase chain reaction array, proteomics, and immunohistochemistry were performed to compare the differences in molecular mechanisms between ruptured and non-ruptured plaques. Enzyme-linked immunosorbent assay was used to measure the differences in ATP-binding cassette subfamily A member 1 (ABCA1) levels in the serum. RESULTS:The expression of several mRNAs and proteins, including ABCA1, was higher in ruptured plaques than non-ruptured plaques. In contrast, the expression of other proteins, including β-actin, was lower in ruptured plaques than non-ruptured plaques. The increased expression of ABCA1 was consistent across several experiments, ABCA1 was positive only in the serum of patients with symptomatic ruptured plaques. CONCLUSIONS:This study introduces a plausible molecular mechanism underlying carotid plaque rupture, suggesting that ABCA1 plays a role in symptomatic rupture. Further study of ABCA1 is needed to confirm this hypothesis.
| S-EPMC5836578 | biostudies-literature