OBJECTIVE: A review of the literature on coccygectomy and our patients was performed to assess the effectiveness of coccygectomy for chronic refractory coccygodynia. METHODS: An English language PubMed search was conducted with the terms "coccygodynia" and "coccygectomy" from January 1980 to January 2012. We retrospectively reviewed the medical records and performed telephone questionnaire on 61 patients who underwent coccygectomy at UCDMC between 1997 and 2009. RESULTS: There were 28 case series from 1980 to 2012 for a total of 742 patients who underwent coccygectomy following failed conservative management. The mean age ranged from 26.4 to 52.8 years. The most common cause was direct trauma (58.5%) with a male:female ratio of 1:5.2. Most patients (84%) had a good to excellent outcome after coccygectomy. The most common complication is wound infection (10.0%). The overall complication rate was 13.3%. Similarly, 84.6% of patients from our own surgical case series reported good to excellent outcomes with 11.5% wound infection. CONCLUSION: Coccygectomy is an effective treatment for chronic refractory coccygodynia. The surgery isrelatively simple to perform but precaution must be taken to avoid wound infection.
Humans ; Medical Records ; Surveys and Questionnaires ; Retrospective Studies ; Telephone ; Wound Infection

Azoospermia/surgery* ; Humans ; Male ; Vas Deferens ; Vasectomy

The induction of interleukin (IL)-32 in bone marrow (BM) inflammation is crucial in graft versus host disease (GvHD) that is a common side effect of allogeneic BM transplantation. Clinical trials on α-1 antitrypsin (AAT) in patients with GvHD are based on the preliminary human and mouse studies on AAT reducing the severity of GvHD. Proteinase 3 (PR3) is an IL-32-binding protein that was isolated from human urine. IL-32 primarily induces inflammatory cytokines in myeloid cells, probably due to PR3 expression on the membrane of the myeloid lineage cells. The inhibitory activity of AAT on serine proteinases may explain the anti-inflammatory effect of AAT on GvHD. However, the anti-inflammatory activity of AAT on BM cells remains unclear. Mouse BM cells were treated with IL-32γ and different inflammatory stimuli to investigate the anti-inflammatory activity of AAT. Recombinant AAT-Fc fusion protein inhibited IL-32γ-induced IL-6 expression in BM cells, but failed to suppress that induced by other stimuli. In addition, the binding of IL-32γ to PR3 was abrogated by AAT-Fc. The data suggest that the specific anti-inflammatory effect of AAT in mouse BM cells is due to the blocking of IL-32 binding to membrane PR3.
Animals ; Bone Marrow Cells* ; Bone Marrow* ; Cytokines* ; Graft vs Host Disease ; Humans ; Inflammation ; Interleukin-6 ; Interleukins ; Membranes ; Mice* ; Myeloblastin ; Myeloid Cells ; Serine Proteases

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) is a positive-sense singlestranded RNA (+ssRNA) that causes coronavirus disease 2019 (COVID-19). The viral genome encodes twelve genes for viral replication and infection. The third open reading frame is the spike (S) gene that encodes for the spike glycoprotein interacting with specific cell surface receptor – angiotensin converting enzyme 2 (ACE2) – on the host cell membrane. Most recent studies identified a single point mutation in S gene. A single point mutation in S gene leading to an amino acid substitution at codon 614 from an aspartic acid 614 into glycine (D614G) resulted in greater infectivity compared to the wild type SARS-CoV2. We were interested in investigating the mutation region of S gene of SARS-CoV2 from Korean COVID-19 patients. New mutation sites were found in the critical receptor binding domain (RBD) of S gene, which is adjacent to the aforementioned D614G mutation residue. This specific sequence data demonstrated the active progression of SARS-CoV2 by mutations in the RBD of S gene.The sequence information of new mutations is critical to the development of recombinant SARS-CoV2 spike antigens, which may be required to improve and advance the strategy against a wide range of possible SARS-CoV2 mutations.