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Biomedical subjects

M P Callery

Publications and source records attributed to M P Callery.

At least 37 records · Page 2Linked to original sources
PubMed2000

Hand-assisted laparoscopic surgery (HALS) with the HandPort system: initial experience with 68 patients.

OBJECTIVE: To evaluate the feasibility and potential benefits of hand-assisted laparoscopic surgery with the HandPort System, a new device. SUMMARY BACKGROUND DATA: In hand-assisted laparoscopic surgery, the surgeon inserts a hand into the abdomen while pneumoperitoneum is maintained. The hand assists laparoscopic instruments and is helpful in complex laparoscopic cases. METHODS: A prospective nonrandomized study was initiated with the participation of 10 laparoscopic surgical centers. Surgeons were free to test the device in any situation where they expected a potential advantage over conventional laparoscopy. RESULTS: Sixty-eight patients were entered in the study. Operations included colorectal procedures (sigmoidectomy, right colectomy, resection rectopexy), splenectomy for splenomegaly, living-related donor nephrectomy, gastric banding for morbid obesity, partial gastrectomy, and various other procedures. Mean incision size for the HandPort was 7.4 cm. Most surgeons (78%) preferred to insert their nondominant hand into the abdomen. Pneumoperitoneum was generally maintained at 14 mmHg, and only one patient required conversion to open surgery as a result of an unmanageable air leak. Hand fatigue during surgery was noted in 20.6%. CONCLUSIONS: The hand-assisted technique appeared to be useful in minimally invasive colorectal surgery, splenectomy for splenomegaly, living-related donor nephrectomy, and procedures considered too complex for a laparoscopic approach. This approach provides excellent means to explore, to retract safely, and to apply immediate hemostasis when needed. Although the data presented here reflect the authors' initial experience, they compare favorably with series of similar procedures performed purely laparoscopically.

Abdomen↗
PubMed1999

Biliary secretion of extracorporeal porcine livers with single and dual vessel perfusion.

BACKGROUND: Hepatic support systems that provide detoxification without biliary secretion (i.e., isolated hepatocyte systems) are sufficient to improve encephalopathy and bridge patients to transplantation. However, biliary secretion may be critical when hepatic support attempts to restore function and regeneration of the host liver. The purpose of these studies was to optimize the support liver secretory response to bile acid by either single-vessel (portal vein; PV) or dual-vessel (hepatic artery [HA] + PV) perfusions during extracorporeal porcine liver perfusion. METHODS: Extracorporeal porcine liver perfusion of anesthetized pigs was developed using support porcine livers perfused through the PV (n=4) alone and through the HA + PV (n=4) via a venovenous circuit. Support livers were provoked with taurocholate (TC) to enhance bile aqueous and hydrophobic outputs. RESULTS: After cold preservation and reperfusion, both PV and HA + PV livers had initial 1-hr bile aqueous outputs < 15% of in vivo flow, with cholesterol (C) and phospholipid (PC) outputs <25% of in vivo flow. Bile flow was significantly greater for recovered HA + PV livers (3.0+/-0.01 ml/15 min) than PV livers (1.9+/-0.01 ml/15 min). Despite this, PC output was significantly greater for PV than HA + PV livers. The C/PC ratio of PV livers was twice that of HA + PV livers. TC infusion (48 micromol/kg/15 min) of HA + PV livers demonstrated significantly greater increments in bile flow, PC output, and C output than PV livers. CONCLUSION: In the unstimulated state, porcine support livers with dual-vessel perfusion generated greater aqueous and C outputs despite diminished PC output than in those with single-vessel perfusion. TC stimulation increased bile flow, PC output, and C output in dual-perfused livers more than in PV livers. HA + PV perfusion of support livers is the preferred technique for removing hydrophobic compounds that require PC transport for excretion or exist in the aqueous phase.

Animals↗
PubMed1999

Sodium salicylate inhibits macrophage TNF-alpha production and alters MAPK activation.

INTRODUCTION: Transcriptional activation of the TNF-alpha gene in LPS-stimulated macrophages is dependent upon nuclear factor kappa-B (NF-kappaB) activity. Salicylates may interfere with NF-kappaB activity through a MAPK (mitogen-activated protein kinase)-dependent process. These studies investigate the effects of sodium salicylate (NaSal) on TNF-alpha production and MAPK activation in macrophages. METHODS: Rat peritoneal macrophages were pretreated or not with sodium salicylate or ibuprofen for 1 h and then stimulated with 100 ng/ml LPS. Six hours following stimulation, cell viability was assessed by MTT assay. At specified time intervals after LPS stimulation, supernatant TNF-alpha was measured by ELISA. Western blots of cell lysates were performed for analysis of total and activated (phosphorylated) MAPKs. RESULTS: Salicylate and LPS, alone or combined, did not significantly alter macrophage viability. Salicylate, but not ibuprofen, significantly reduced TNF-alpha production in LPS-stimulated macrophages. LPS-stimulated activation of ERK and SAPK/JNK was inhibited by NaSal pretreatment. NaSal treatment of macrophages activated p38 MAPK independent of LPS stimulation. Pretreatment of samples with the specific p38 MAPK inhibitor, SB203580, did not significantly alter TNF-alpha production in either LPS or NaSal and LPS-treated samples. CONCLUSIONS: Salicylates alter MAPK signaling and suppress TNF-alpha production in LPS-stimulated macrophages. Salicylate-induced control of inflammatory mediator production in macrophages may, in part, underlie the clinically significant anti-inflammatory effects of these compounds.

Animals↗
PubMed1999

Salicylates inhibit NF-kappaB activation and enhance TNF-alpha-induced apoptosis in human pancreatic cancer cells.

INTRODUCTION: Tumor necrosis factor (TNF-alpha)-induced apoptosis is limited by its coactivation of nuclear factor kappa B (NF-kappaB)-dependent anti-apoptotic genes. Sodium salicylate (NaSal) inhibits NF-kappaB activation by limiting phosphorylation and degradation of its bound inhibitor protein, IkappaB-alpha. We examined whether NaSal enhances TNF-alpha-induced apoptosis in cultured human pancreatic cancer cell lines. METHODS: Two cultured human pancreatic cancer cell lines were studied. PANC-1 and BxPC-3 cells were serum-starved for 12 h, pretreated or not for 1 h with NaSal (5-20 mM), and then stimulated with recombinant human TNF-alpha (400 units/ml). Western blots of cytoplasmic lysates were performed to demonstrate IkappaB-alpha phosphorylation and degradation. Western blots of nuclear extracts were performed to assess nuclear translocation of NF-kappaB. In separate cultures, apoptosis was measured 4.5 h after TNF-alpha stimulation by both ELISA detection of interhistone DNA fragments and flow cytometry with propidium iodide staining. RESULTS: TNF-alpha induced IkappaB-alpha phosphorylation and degradation, which was inhibited by NaSal in both cell lines. TNF-alpha-induced apoptosis (DNA fragmentation) increased significantly when BxPC-3 cells were pretreated with NaSal. Flow cytometry confirmed this, demonstrating increases in apoptotic cell fractions: 8.5% (untreated), 9.3% (TNF-alpha alone), 14.9% (15 mM NaSal), and 22.9% (NaSal and TNF-alpha). In contrast, no increases in apoptosis were measured in the PANC-1 cell line among the various treatment groups. CONCLUSIONS: NaSal enhances TNF-alpha-induced apoptosis while inhibiting IkappaB-alpha phosphorylation and degradation in BxPC-3 human pancreatic cancer cells.

Adenocarcinoma↗
PubMed1999

Ubiquitin-proteasome inhibition enhances apoptosis of human pancreatic cancer cells.

BACKGROUND: Tumor necrosis factor (TNF-a)-induced apoptosis is limited by coactivation of nuclear factor kappa B (NF-kb)-dependent antiapoptotic genes. Nuclear translocation of NF-kB requires degradation of ubiquitinated phospho-IkB-a by the 26S proteasome. We examined whether inhibition of the ubiquitin-proteasome pathway enhances TNF-a-induced apoptosis in BxPC-3 human pancreatic cancer cells. METHODS: Serum-starved BxPC-3 cells (12 hours) were pretreated or not for 50 minutes with PSI (30 m mol/L), a peptide aldehyde known to inhibit specifically the chymotrypsin-like activity of the 26S proteasome. Cells were subsequently stimulated with recombinant human TNF-a (400 units/mL). Western blots were performed using antibodies to IkB-a and phospho-IkB-a. Level of apoptosis was determined by two methods: enzyme-linked immunosorbent assay detection of interhistone DNA fragments and flow cytometry with propidium iodide staining. RESULTS: TNF-a-induced degradation of IkB-a was inhibited by PSI. Phospho-IkB-a accumulation was observed 20 minutes after TNF-a stimulation. Apoptosis relative to constitutive levels was significantly increased after PSI pretreatment, as measured by DNA fragmentation (P < or = .05 by Student t test). Percent apoptosis by flow cytometry confirmed marked increases in apoptotic cell fractions from 5.9% (untreated) to 6.8% (TNF-a alone), 16.4% (PSI alone), and 18.9% (PSI and TNF-a). CONCLUSIONS: PSI enhances both constitutive and TNF-a-induced apoptosis through inhibition of IkB-a degradation in BxPC-3 human pancreatic cancer cells.

Apoptosis↗
PubMed1999

Endotoxin fails to stimulate inositol triphosphate production in macrophages.

UNLABELLED: Inositol Triphosphate (IP3) production is an early cell signaling event which leads to mobilization of intracellular calcium (Ca++). We examined whether bacterial endotoxin (lipopolysaccharide, LPS) stimulates IP3 production in macrophages pretreated with LPS (tolerant) or not. METHODS: RAW 264.7 macrophages were cultured at 5 x 10(6) cells in RPMI supplemented with 10% FCS. LPS tolerance was induced by pretreating macrophages (Tol) for 19 h with 10 ng/ml of LPS. Non-tolerant (Non-Tol) macrophages received no LPS pretreatment. Macrophages were next washed, repleted with fresh media, and stimulated with 100 ng/ml LPS. Paired cultures were stimulated with 1 microM platelet activating factor (PAF), a known stimulant of IP3 production. Following 1, 10, and 15-min stimulation intervals, IP3 was extracted with trichloroacetic acid and measured by receptor displacement assay. RESULTS: LPS did not stimulate IP3 production in either Non-Tol or Tol macrophages. In contrast, PAF stimulated significant increases in IP3 levels within 1 min in both Non-Tol (9.5 +/- 3.0 pmol/ml) and Tol (9.5 +/- 2.4 pmol/ml) macrophages. Non-Tol IP3 levels returned to baseline by 10 min, while Tol IP3 levels remained significantly elevated (8.2 +/- 1.7 pmol/ml). CONCLUSIONS: Unlike PAF, bacterial LPS fails to stimulate IP3 production in macrophages. Furthermore, IP3 production could not be elicited in cultured macrophages repetitively stimulated with LPS.

Cell Line↗
PubMed1998

Laparoscopic surgery and the systemic immune response.

OBJECTIVE: The authors review studies relating to the immune responses evoked by laparoscopic surgery. SUMMARY BACKGROUND DATA: Laparoscopic surgery has gained rapid acceptance based on clinical grounds. Patients benefit from faster recovery, decreased pain, and quicker return to normal activities. Only more recently have attempts been made to identify the metabolic and immune responses that may underlie this clinical success. The immune responses to laparoscopy are now being evaluated in relation to the present knowledge of immune responses to traditional laparotomy and surgery in general. METHODS: A review of the published literature of the immune and metabolic responses to laparoscopy was performed. Laparoscopic surgery is compared with the traditional laparotomy on the basis of local and systemic immune responses and patterns of tumor growth. The impact of pneumoperitoneum and insufflation gases on the immune response is also reviewed. CONCLUSIONS: The systemic immune responses for surgery in general may not apply to laparoscopic surgery. The body's response to laparoscopy is one of lesser immune activation as opposed to immunosuppression.

Carbon Dioxide↗
PubMed1998

The molecular and cellular biology of pancreatic cancer.

Adenocarcinoma of the pancreas carries a grave prognosis for affected patients. Certain oncogenes (K-ras and HER-2/neu) are mutated in a large proportion of these aggressive tumors. Adenocarcinoma of the pancreas has also been associated with loss of tumor suppressor genes (p53, DPC4, p16/MTS), either by deletion or by mutation and loss of function. Growth factors (EGF, TGF-alpha, HGF) and growth factor receptors (EGF-R, c-met, CCK) are expressed at levels not found in the normal pancreas. Finally, factors important for angiogenesis (FGF, integrins, selectins) are likely to play an important role in the growth and metastasis of clinically relevant tumors. This review attempts to summarize and assimilate current research into the molecular and cellular biology of pancreatic cancer.

Adenocarcinoma↗
PubMed1997

Radical resection of tumors of the inferior vena cava with vascular reconstruction and kidney autotransplantation.

BACKGROUND: Tumors of the inferior vena cava (IVC) are rare tumors. Although often locally confined, juxtaposed vital structures usually limit the extent of resection. However, complete surgical resection has been shown to be the most important positive prognostic factor. METHODS: Four patients had resection of primary vena caval tumors. In two patients with locally extensive vena caval tumors the limits of conventional resection were extended by means of complete resection of the involved infrahepatic IVC, aorta, and both kidneys. The IVC and aorta were reconstructed with synthetic grafts, and the uninvolved kidney was autotransplanted for both patients. RESULTS: Of the two patients treated with more extensive resection, one patient had no evidence of disease 26 months after operation, and the second patient died of recurrent disease 23 months after operation. CONCLUSIONS: Primary tumors of the IVC may extend locally without distant metastasis. Radical surgical excision as the primary mode of treatment provides the best chance for prolonged survival in appropriately selected patients with tumors of the IVC. After surgical excision the patient with the leiomyosarcoma was treated with radiation therapy and the patient with rhabdomyosarcoma by chemotherapy. Although leiomyosarcomas of the IVC are rare tumors, the first patient is only the third reported case of the even rarer rhabdomyosarcoma of the IVC.

Adult↗
PubMed1997

The approach to the patient with single and multiple liver metastases, pulmonary metastases, and intra-abdominal metastases from colorectal carcinoma.

Recurrent colorectal carcinoma constitutes a major health care problem, with 90,000 patients diagnosed annually with metastatic disease. Recent advances have offered treatment to selected patients with liver, lung, and intra-abdominal metastases. Resection of liver secondary tumors improves 5-year survival from 0% to approximately 30% and offers the only possibility for cure. As experience mounts, hepatic surgery can be performed with quite acceptable morbidity and mortality. Adjuvant therapies are being developed that may improve results with surgery alone. Cryoablation is a new technique that appears to effectively eradicate liver tumors, but its role remains to be defined. In patients with unresectable disease, the benefit of hepatic artery infusion of chemotherapy is unproven. Resection of pulmonary metastases significantly improves survival in patients with solitary nodules. Consistent data regarding the benefit of pulmonary metastatectomy in patients with multiple nodules are not available. Combined cytoreductive surgery and intraperitoneal hyperthermic chemotherapy is being investigated as a treatment for peritoneal carcinomatosis from colorectal cancer. Although selected patients may benefit, this combined treatment modality appears to be less effective in patients with colorectal cancer than with other types of cancer.

Abdominal Neoplasms↗
PubMed1997

Staging laparoscopy with laparoscopic ultrasonography: optimizing resectability in hepatobiliary and pancreatic malignancy.

BACKGROUND: Open laparotomy has traditionally been required to stage hepatobiliary and pancreatic (HBP) cancers accurately. For unresectable patients, costs and morbidity have been high. Today, laparoscopy alone or combined with laparoscopic ultrasonography (LUS) is being examined for its value in defining the extent of malignancy. STUDY DESIGN: We have analyzed the effect of routine implementation of this new staging technique in our HBP center. Staging laparoscopy (SL) with LUS was performed in 50 consecutive patients with HBP malignancies. All patients were considered to have resectable tumors as determined by traditional preoperative staging modalities. Primary tumors were located in the liver (n = 7), biliary tract (n = 11), or pancreas (n = 32). An average of 2.7 preoperative studies per patient were performed prior to SL-LUS. RESULTS: Staging laparoscopy with laparoscopic ultrasonography predicted resectable tumors in 28 patients (56%). At laparotomy, 26 of 28 were actually resectable: the false-negative rate was 4%. Staging laparoscopy with laparoscopic ultrasonography indicated unresectability in 22 patients (44%). Staging laparoscopy alone demonstrated previously unrecognized occult metastases in 11 patients (22%). In 11 other patients (22%) in whom SL alone was negative, LUS established unresectability from vascular invasion (n = 5), lymph node metastases (n = 5), or intraparenchymal hepatic tumor (n = 1). All cases of unresectability due to vascular invasion were validated by laparotomy. Five of six lymph node or hepatic metastases were proved histologically by LUS-guided needle biopsy rather than laparotomy. CONCLUSIONS: Unnecessary laparotomy can be safely avoided by SL-LUS in many patients with HPB malignancies, reducing costs and morbidity.

Adult↗
PubMed1996

Listeria monocytogenes induces apoptosis of infected hepatocytes.

Infection with blood-borne Listeria monocytogenes results in their early uptake by the liver. Foci of hepatocytes become heavily infected and develop into microabscesses. Infection results in apoptosis of the hepatocytes. This is particularly evident in the edge of the microabscess, where hepatocytes are not yet destroyed by the neutrophil. It is also apparent when neutrophils are depleted from the circulation. Infection of hepatocytes in culture induces their death by apoptosis with the release of neutrophil chemoattractants. Cytokines do not reduce the multiplication of Listeria in cultured hepatocytes. This study calls attention to an early program of inflammation induced in infected cells that are unresponsive to cytokines.

Animals↗
PubMed1996

Inhibition of phosphatidylinositol-3'-kinase prevents induction of endotoxin tolerance in vitro.

Previous studies have shown an increase in the expression of phosphatidylinositol-3'-kinase (PI-3'-K) in macrophages from endotoxin tolerant (ET) rats. This implicates PI-3'-K cell signaling in attenuated macrophage responsiveness to lipopolysaccharide (LPS). These experiments examined the effects of selective pharmacologic inhibition of PI-3'-K in an in vitro model of ET. To induce ET, RAW 264.7 macrophages cultured in RPMI 1640 with 10% fetal calf serum were initially exposed to 10 ng/ml LPS (E. coli 0111:B4) for 19 hr. Non-tolerant cells received an equal volume of phosphate buffered saline. Some cultures were also incubated with the specific PI-3'-K inhibitor wortmannin (10 nM) during this tolerizing period. Cells were then washed and re-challenged with 100 ng/ml LPS for 24 hr. Next, macrophage tumor necrosis factor-alpha (TNF-alpha) and nitrite production were measured as indicators of ET induction. Macrophage TNF-alpha production decreased significantly while nitrite production increased significantly following ET induction. Specific inhibition of PI-3'-K prevented this decrease in TNF-alpha and increase in nitrite production in ET macrophages. Production of each mediator returned to levels not different than in non-tolerant macrophages. In this in vitro model of macrophage ET, pharmacologic inhibition of the PI-3'-K signaling pathway prevented the induction of LPS tolerance as measured by the production of two inflammatory mediators.

Androstadienes↗
PubMed1996

Complications of laparoscopic general surgery.

With the growth of laparoscopic general surgery, both minor and major complications are being encountered. This article discusses complications related to operative laparoscopy, including those associated with access techniques and the pneumoperitoneum. Complications specific to certain procedures, including laparoscopic cholecystectomy, appendectomy, colon resection, anti-reflux surgery, and herniorrhaphy, are also discussed in detail.

Anesthesia, General↗
PubMed1996

Strangulated incisional hernia at trocar site.

An incisional hernia at a trocar site after laparoscopy may arise from infection, premature suture disruption, or failure to adequately reapproximate fascial wound edges. The condition is accurately diagnosed postoperatively on physical examination, and a bulge at a previous port site should immediately raise suspicion. A case is reported in which an incisional hernia strangulated soon after an elective laparoscopic inguinal herniorrhaphy in which, the fascia of the 10-mm trocar site was not closed. This report underscores the importance of meticulous closure of all abdominal port sites > 5 mm. Furthermore, early diagnosis of an incarcerated hernia may avoid the morbidity of an extensive intestinal resection.

Hernia, Inguinal↗
PubMed1996

Laparoscopic management of complicated biliary tract disease in children.

Laparoscopic cholecystectomy is a safe and feasible surgical treatment for children with symptomatic cholelithiasis. We describe the laparoscopic management of choledocholithiasis and biliary pancreatitis, two unusual but complicated pediatric biliary tract diseases. The operative techniques described were safe and effective and permitted early discharge with rapid return to diet, school, and full activity.

Adolescent↗
PubMed1996

Laparoscopic surgery of the bile ducts.

Laparoscopic surgery of the bile ducts is evolving rapidly. Laparoscopic bile duct exploration is reaching wide application and is competitive with postoperative ERCP for treatment of choledocholithiasis. Staging laparoscopy is an important laparoscopic advance that is increasing resectability rates for pancreatic and hepatic tumors through laparoscopic detection of unresectable tumors. Bile duct injury is an important problem in laparoscopic cholecystectomy. Classification, avoidance, and management are discussed.

Biliary Tract↗