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Primary abandonment of the sac in the management of scrotal hernias: a dual-institution experience of short-term outcomes

Nikolian, V C; Pereira, X; Arias-Espinosa, L; Bazarian, A N; Porter, C G; Henning, J R; Malcher, F
PURPOSE/OBJECTIVE:Management of scrotal hernias presents as a common challenge, with operative interventions to address these hernias associated with higher rates of morbidity compared to those of less-complex pathology. Surgeons have advocated for the use of techniques such as primary abandonment of the distal sac as a potential means to reduce complications for operative intervention, with preliminary findings demonstrating feasibility. We sought to assess outcomes related to primary sac abandonment among patients undergoing minimally invasive (MIS) repair of scrotal hernias. METHODS:A review of prospectively maintained databases among two academic hernia centers was conducted to identify patients who underwent MIS inguinal hernia repairs with primary sac abandonment. Patient demographics, hernia risk factors, intraoperative factors, and postoperative outcomes were evaluated. Short-term outcomes related to patient-reported experiences and surgical-site occurrences requiring procedural intervention were queried. RESULTS:Sixty-seven male patients [median age: 51.6 years; interquartile range (IQR): 45-65 years] underwent inguinal hernia repair with primary sac abandonment. Anatomic polypropylene mesh was used in 98.5% cases. Rates of postoperative complications were low and included postoperative urinary retention (6%), clinically identified or patient-reported seromas/hematomas within a 30-day follow-up period (23.9%), deep venous thrombosis (1.5%), and pelvic hematoma (1.5%). No seromas or hematomas necessitated procedural interventions, with resolution of symptoms within three months of their operation date. CONCLUSION/CONCLUSIONS:We report a multi-center experience of patients managed with primary abandonment of the sac technique during repair of inguinoscrotal hernias. Utilization of this technique appears to be safe and reproducible with a low burden of short-term complications.
PMID: 38502368
ISSN: 1248-9204
CID: 5640402

Robotic Primary and Revisional Hiatal Hernia Repair is Safe and Associated with Favorable Perioperative Outcomes: A Single Institution Experience

Rodier, Simon; Henning, Justin; Kukreja, Janvi; Mohammedi, Taher; Shah, Paresh; Damani, Tanuja
PMID: 37417969
ISSN: 1557-9034
CID: 5539432

Laparoscopic repair of incarcerated diaphragmatic hernia containing right colon after radiofrequency ablation for hepatocellular carcinoma [Meeting Abstract]

Sethi, M; Henning, J; Parikh, M S
Aims: Local ablative therapies, such as radiofrequency ablation (RFA) and microwave ablation (MWA), are commonly used to treat patients with unrespectable or recurrent hepatocellular carcinoma (HCC). These therapies are generally safe and well tolerated, yet complications related to mechanical or thermal damage may result. This case highlights a very rare complication after local ablative therapy for HCC, namely diaphragmatic perforation, and demonstrates a step-by-step laparoscopic repair. Methods: This is the case of an 81-year-old female with segment 4B hepatocellular carcinoma diagnosed in 2008, treated with laparoscopic radiofrequency ablation. The disease recurred in 2012 and subsequent microwave ablation and trans-arterial chemoembolization were performed. One year later, the patient developed severe right upper quadrant abdominal pain. CT scan showed incarcerated colon and cecum herniating through the right diaphragm with associated colonic obstruction. The patient was taken to the OR for laparoscopic repair of the diaphragm and possible bowel resection. With the patient in the right lateral decubitus position, the terminal ileum, cecum, and right colon were reduced and the diaphragm repaired with 0-prolene sutures in a horizontal mattress fashion. A 34 French chest tube was placed. Upon further inspection, the right colon appeared gangrenous. The patient was then repositioned into the supine position and a laparoscopic right hemicolectomy was performed. Results: The patient was extubated on postoperative day 1. Recovery was complicated by a subdiaphragmatic abscess, which responded to percutaneous drainage and antibiotics. The patient was subsequently discharged to a subacute rehab facility. Conclusion: With only a few cases cited in the literature, diaphragmatic perforation is an uncommon complication of local ablative therapies for HCC. The mechanism of injury is presumably thermal injury to the diaphragm. In cases of acute right upper quadrant abdominal pain after RFA or MWA, this rare but serious complication should remain in the differential
EMBASE:72210249
ISSN: 0930-2794
CID: 2049612

Acute Urinary Retention Caused by an Ovarian Teratoma-A Unique Pediatric Presentation and Review

Binder, Zachary; Iwata, Kathryn; Mojica, Michael; Ginsburg, Howard B; Henning, Justin; Strubel, Naomi; Kahn, Philip
BACKGROUND: Acute urinary retention (AUR) is a rare diagnosis both in pediatric and adult female populations, especially when compared to adult males. AUR occurs in women at a rate of 7 in 100,000 per year in a 1:13 female to male ratio. Multiple studies have shown that within the pediatric population AUR is far less common in females and is caused by different pathologies than AUR in adult women. CASE REPORT: We report the case of an 11 year-old prepubescent female who presented to the emergency department with acute urinary retention found to be caused by a mature cystic ovarian teratoma. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Our case is unique in that it describes an ovarian mass leading to AUR which has not previously been described in the pediatric literature. We will review the causes of AUR in the pediatric female population and compare these to the causes of AUR in other populations.
PMID: 26275742
ISSN: 0736-4679
CID: 1721912

Patterns of Traumatic Injury in New York City Prisoners Requiring Hospital Admission

Henning, Justin; Frangos, Spiros; Simon, Ronald; Pachter, H Leon; Bholat, Omar S
Bellevue Hospital's prison ward cares for male prisoners requiring medical attention that exceeds the capabilities of New York City Department of Correction (NYC-DOC) infirmaries. This study evaluated the injury patterns that occur in this patient population. Data were collected on consecutive prisoners transferred from NYC-DOC for traumatic injuries from June 1, 2003, to June 1, 2006, and analyzed by retrospective chart review. Overall, 251 patients were evaluated for traumatic injuries. Injury mechanisms were violent (75.7%), nonviolent (23.5%), and self-inflicted (0.8%). Of the 241 (96%) patients admitted, 213 (84.9%) required operative intervention. The most common injuries were mandible fractures (46.5%) and facial fractures (14.9%).
PMID: 25559630
ISSN: 1078-3458
CID: 1428832

Dendritic cells limit fibro-inflammatory injury in NASH

Henning, Justin R; Graffeo, Christopher S; Rehman, Adeel; Fallon, Nina C; Zambirinis, Constantinos P; Ochi, Atsuo; Barilla, Rocky; Jamal, Mohsin; Deutsch, Michael; Greco, Stephanie; Ego-Osuala, Melvin; Saeed, Usama Bin; Rao, Raghavendra S; Badar, Sana; Quesada, Juan P; Acehan, Devrim; Miller, George
Non-alcoholic steatohepatitis (NASH) is the most common etiology of chronic liver dysfunction in the United States and can progress to cirrhosis and liver failure. Inflammatory insult resulting from fatty infiltration of the liver is central to disease pathogenesis. Dendritic cells (DC) are antigen presenting cells with an emerging role in hepatic inflammation. We postulated that DC are important in the progression of NASH. We found that intrahepatic DC expand and mature in NASH liver and assume an activated immune-phenotype. However, rather than mitigating the severity of NASH, DC depletion markedly exacerbated intrahepatic fibro-inflammation. Our mechanistic studies support a regulatory role for DC in NASH by limiting sterile inflammation via their role in clearance of apoptotic cells and necrotic debris. We found that DC limit CD8(+) T cell expansion and restrict Toll-like receptor expression and cytokine production in innate immune effector cells in NASH, including Kupffer cells, neutrophils, and inflammatory monocytes. Consistent with their regulatory role in NASH, during the recovery phase of disease, ablation of DC populations results in delayed resolution of intrahepatic inflammation and fibroplasia. Conclusion: Our findings support a role for DC in modulating NASH. Targeting DC functional properties may hold promise for therapeutic intervention in NASH. (HEPATOLOGY 2013.).
PMCID:3638069
PMID: 23322710
ISSN: 0270-9139
CID: 302922

Role of Fatty-Acid synthesis in dendritic cell generation and function

Rehman, Adeel; Hemmert, Keith C; Ochi, Atsuo; Jamal, Mohsin; Henning, Justin R; Barilla, Rocky; Quesada, Juan P; Zambirinis, Constantinos P; Tang, Kerry; Ego-Osuala, Melvin; Rao, Raghavendra S; Greco, Stephanie; Deutsch, Michael; Narayan, Suchithra; Pachter, H Leon; Graffeo, Christopher S; Acehan, Devrim; Miller, George
Dendritic cells (DC) are professional APCs that regulate innate and adaptive immunity. The role of fatty-acid synthesis in DC development and function is uncertain. We found that blockade of fatty-acid synthesis markedly decreases dendropoiesis in the liver and in primary and secondary lymphoid organs in mice. Human DC development from PBMC precursors was also diminished by blockade of fatty-acid synthesis. This was associated with higher rates of apoptosis in precursor cells and increased expression of cleaved caspase-3 and BCL-xL and downregulation of cyclin B1. Further, blockade of fatty-acid synthesis decreased DC expression of MHC class II, ICAM-1, B7-1, and B7-2 but increased their production of selected proinflammatory cytokines including IL-12 and MCP-1. Accordingly, inhibition of fatty-acid synthesis enhanced DC capacity to activate allogeneic as well as Ag-restricted CD4(+) and CD8(+) T cells and induce CTL responses. Further, blockade of fatty-acid synthesis increased DC expression of Notch ligands and enhanced their ability to activate NK cell immune phenotype and IFN-gamma production. Because endoplasmic reticulum (ER) stress can augment the immunogenic function of APC, we postulated that this may account for the higher DC immunogenicity. We found that inhibition of fatty-acid synthesis resulted in elevated expression of numerous markers of ER stress in humans and mice and was associated with increased MAPK and Akt signaling. Further, lowering ER stress by 4-phenylbutyrate mitigated the enhanced immune stimulation associated with fatty-acid synthesis blockade. Our findings elucidate the role of fatty-acid synthesis in DC development and function and have implications to the design of DC vaccines for immunotherapy.
PMCID:3633656
PMID: 23536633
ISSN: 0022-1767
CID: 302912

Toll-like receptor 7 regulates pancreatic carcinogenesis in mice and humans

Ochi, Atsuo; Graffeo, Christopher S; Zambirinis, Constantinos P; Rehman, Adeel; Hackman, Michael; Fallon, Nina; Barilla, Rocky M; Henning, Justin R; Jamal, Mohsin; Rao, Raghavendra; Greco, Stephanie; Deutsch, Michael; Medina-Zea, Marco V; Bin Saeed, Usama; Ego-Osuala, Melvin O; Hajdu, Cristina; Miller, George
Pancreatic ductal adenocarcinoma is an aggressive cancer that interacts with stromal cells to produce a highly inflammatory tumor microenvironment that promotes tumor growth and invasiveness. The precise interplay between tumor and stroma remains poorly understood. TLRs mediate interactions between environmental stimuli and innate immunity and trigger proinflammatory signaling cascades. Our finding that TLR7 expression is upregulated in both epithelial and stromal compartments in human and murine pancreatic cancer led us to postulate that carcinogenesis is dependent on TLR7 signaling. In a mouse model of pancreatic cancer, TLR7 ligation vigorously accelerated tumor progression and induced loss of expression of PTEN, p16, and cyclin D1 and upregulation of p21, p27, p53, c-Myc, SHPTP1, TGF-beta, PPARgamma, and cyclin B1. Furthermore, TLR7 ligation induced STAT3 activation and interfaced with Notch as well as canonical NF-kappaB and MAP kinase pathways, but downregulated expression of Notch target genes. Moreover, blockade of TLR7 protected against carcinogenesis. Since pancreatic tumorigenesis requires stromal expansion, we proposed that TLR7 ligation modulates pancreatic cancer by driving stromal inflammation. Accordingly, we found that mice lacking TLR7 exclusively within their inflammatory cells were protected from neoplasia. These data suggest that targeting TLR7 holds promise for treatment of human pancreatic cancer.
PMCID:3484447
PMID: 23023703
ISSN: 0021-9738
CID: 210732

Dendritic Cell Populations With Different Concentrations of Lipid Regulate Tolerance and Immunity in Mouse and Human Liver

Ibrahim, J; Nguyen, AH; Rehman, A; Ochi, A; Jamal, M; Graffeo, CS; Henning, JR; Zambirinis, CP; Fallon, N; Barilla, R; Badar, S; Mitchell, A; Rao, R; Acehan, D; Frey, AB; Miller, G
BACKGROUND & AIMS: Immune cells of the liver must be able to recognize and react to pathogens yet remain tolerant to food molecules and other nonpathogens. Dendritic cells (DCs) are believed to contribute to hepatic tolerance. Lipids have been implicated in dysfunction of DCs in cancer. Therefore, we investigated whether high lipid content in liver DCs affects induction of tolerance. METHODS: Mouse and human hepatic nonparenchymal cells were isolated by mechanical and enzymatic digestion. DCs were purified by fluorescence-activated cell sorting or with immunomagnetic beads. DC lipid content was assessed by flow cytometry, immune fluorescence, and electron microscopy and by measuring intracellular component lipids. DC activation was determined from surface phenotype and cytokine profile. DC function was assessed in T-cell, natural killer (NK) cell, and NKT cell coculture assays as well as in vivo. RESULTS: We observed 2 distinct populations of hepatic DCs in mice and humans based on their lipid content and expression of markers associated with adipogenesis and lipid metabolism. This lipid-based dichotomy in DCs was unique to the liver and specific to DCs compared with other hepatic immune cells. However, rather than mediate tolerance, the liver DC population with high concentrations of lipid was immunogenic in multiple models; they activated T cells, NK cells, and NKT cells. Conversely, liver DCs with low levels of lipid induced regulatory T cells, anergy to cancer, and oral tolerance. The immunogenicity of lipid-rich liver DCs required their secretion of tumor necrosis factor alpha and was directly related to their high lipid content; blocking DC synthesis of fatty acids or inhibiting adipogenesis (by reducing endoplasmic reticular stress) reduced DC immunogenicity. CONCLUSIONS: Human and mouse hepatic DCs are composed of distinct populations that contain different concentrations of lipid, which regulates immunogenic versus tolerogenic responses in the liver.
PMCID:3459067
PMID: 22705178
ISSN: 0016-5085
CID: 172916

Dendritic cells regulate fibro-inflammation but exacerbate steatosis in non-alcoholic steatohepatitis [Meeting Abstract]

Henning, J R; Graffeo, C S; Deutsch, M; Fallon, N; Rehman, A; Barilla, R; Medina-Zea, M; Zambirinis, C; Miller, G
INTRODUCTION: Non-alcoholic steatohepatitis (NASH) is the most common cause of chronic liver dysfunction in theUnited States and can lead to cirrhosis, liver failure, and the need for liver transplantation. Dendritic cells (DC) are antigen presenting cells with an emerging role in hepatic inflammation. However, the role of DC in the progression of NASH is unknown. METHODS: NASH was induced in C57BL/6 mice by feeding a methionine-choline deficient diet. NASH progression was assessed by changes in liver inflammation, steatosis, and fibrosis. DC recruitment and activation was assessed by flow cytometry. DC depletion using diphtheria toxin (4ng/g/day) was achieved in C57BL/6 mice made chimeric with CD11c. DTR bone marrow. RESULTS: DC expand in NASH 4-5 fold (Table) and upregulate their expression of MHCII, CD40, ICAM-1, B7-1, and B7-2. DC also accumulate intracellular lipid in NASH (Table) and are primary in the clearance of necrotic hepatocytes, thereby limiting byproducts of sterile inflammation. Conversely, DC depletion in NASH (NASH-DC) markedly exacerbated intrahepatic inflammation, evidenced by increased liver cytokines, markedly increased CD45+ inflammatory infiltrate (Table), and activation of Kupffer cells (KC) and neutrophils with concomitant decrease in regulatory T cells. In NASH-DC, KC, inflammatory monocytes, and neutrophils underwent lower rates of apoptosis and produced increased TNF-alpha, IL-6 and pro IL-1beta. Further, end-organ fibrosis was significantly higher in NASH-DC mice (Table). (Table presented) CONCLUSIONS: DC become activated in NASH and contribute to steatosis by accumulating lipids. However, DC protect against intrahepatic fibro-inflammation by clearance of necrotic debris, thus limiting KC, monocyte, and neutrophil activation. Targeting DC may hold promise for NASH treatment
EMBASE:70864249
ISSN: 1072-7515
CID: 178255