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Daniel Albo

Publications and source records attributed to Daniel Albo.

11 recordsLinked to original sources
PubMed2006

Epidemiology of exposure to blood borne pathogens on a surgical service.

BACKGROUND: The goal of this study was to analyze the type and mechanism of blood exposure injuries on the surgical service in order to develop appropriate preventative strategies. METHODS: A retrospective review of all exposure injuries affecting members of the operative care line at a single teaching institution between December 2002 and December 2005 was performed. RESULTS: Of 98 exposure injuries on the surgical service, only 17 (17%) were inflicted by hollow-bore needles. Seventy-four (76%) of these reported injuries occurred in the operating room (OR) and 24 (24%) occurred in other clinical areas. Sharps injuries accounted for 69 (93%) of OR injuries and were inflicted by suture needles (n = 37, 50%), hollow-bore needles (n = 7, 9%), and sharp instruments (n = 25, 34%). Mucocutaneous contamination accounted for 5 (7%) of the OR exposures. Professionals most frequently injured were residents (n = 43, 44%), followed by nurses (n = 28, 29%), students (n = 17, 17%) and other healthcare workers (n = 10, 10%). CONCLUSIONS: Blood exposure prevention strategies should be directed at safety within the surgical field and focused beyond hollow-bore needle stick injuries to include education, mentoring, and competency training.

Blood-Borne Pathogens↗
PubMed2006

Decellularized human cadaveric dermis provides a safe alternative for primary inguinal hernia repair in contaminated surgical fields.

BACKGROUND: Repair options for inguinal hernias in contaminated surgical fields include local tissue repair or mesh repair. The former is associated with higher hernia recurrence rates. The latter generally is avoided because of an unacceptably high infection rate. AlloDerm (Lifecell Corp., Branchburg, NJ) can potentially provide a strong repair resistant to infection. The aim of our study was to evaluate if AlloDerm provides a safe alternative for inguinal hernia repair in contaminated surgical fields. METHODS: We retrospectively reviewed the medical records of all patients who underwent inguinal hernia repair with AlloDerm from December 2004 to April 2006. Demographics, risk factors, perioperative data, and recurrence rates were evaluated. RESULTS: Twelve patients with contaminated surgical fields underwent inguinal hernia repair with AlloDerm. Serious perioperative complications occurred in only 1 patient. Two patients developed superficial wound infections (treated conservatively). There were no mortalities. No hernia recurrence has been documented with a follow-up period of 3 to 17 months (median, 9 mo). CONCLUSIONS: AlloDerm provides a safe alternative for inguinal hernia repair in contaminated surgical fields.

Aged↗
PubMed2005

Length of human immunodeficiency virus disease and not immune status is a risk factor for development of anal carcinoma.

BACKGROUND: The anal epithelium is subject to dysplastic change in patients with human immunodeficiency virus (HIV). We sought to determine if the duration of HIV disease or the patient's immune status were associated with the development of anal carcinoma. METHODS: HIV-positive patients diagnosed with anal neoplasms were reviewed. Statistical analysis was performed via an unpaired Student t test and the Fisher exact test. RESULTS: Fourteen patients were identified, 7 with anal intraepithelial neoplasms (group 1) and 7 with anal carcinoma (group 2). Human papillomavirus was detected in 100% of patients in group 1 and in 67% of patients in group 2. There was no significant difference in the level of immunosuppression as assessed by the CD4 counts (266.9 +/- 48.5 vs. 274.7 +/- 92.0 cell/c microl; P = .94) and viral loads (19,243 +/- 18,034 vs. 67,140 +/- 39,570 RNA/mL; P = .29) between groups 1 and 2, respectively. Group 2 had been HIV positive for a significantly longer period of time (12.6 +/- 2.3 y) compared with group 1 (5.9 +/- 2.0 y, P = .05). CONCLUSIONS: The most significant factor for the development of invasive anal carcinoma in patients with HIV is duration of disease. As a result of improved long-term survival secondary to new HIV therapy, anal invasive carcinoma will become an increasing problem.

Adult↗
PubMed2005

Bridging the communication gap in the operating room with medical team training.

BACKGROUND: In the operating room (OR), poor communication among the surgeons, anesthesiologists, and nurses may lead to adverse events that can compromise patient safety. A survey performed at our institution showed low communication ratings from surgeons, anesthesiologists, and OR nursing staff. Our objective was to determine if communication in the operating room could be improved through medical team training (MTT). METHODS: A dedicated training session (didactic instruction, interactive participation, role-play, training films, and clinical vignettes) was offered to the entire surgical service using crew resource management principles. Attendees also were instructed in the principles of change management. A change team was formed to drive the implementation of the principles reviewed through a preoperative briefing conducted among the surgeon, anesthesiologist, and OR nurse. A validated Likert scale survey with questions specific to effective communication was administered to the nurses, anesthesiologists, and surgeons 2 months after the MTT to determine the impact on communication. Data are presented as mean +/- SEM. RESULTS: There was a significant increase in the anesthesiologist and surgeon communication composite score after medical team training (anesthesia pre-MTT = 2.0 +/- .3, anesthesia post-MTT = 4.5 +/- .6, P <.0008; surgeons pre-MTT = 5.2 +/- .2, surgeons post-MTT = 6.6+/-.3, P <.0004; nurses pre-MTT = 4.3 +/- .3, nurses post-MTT = 4.2 +/- .4, P = .7). CONCLUSIONS: Medical team training using crew resource management principles can improve communication in the OR, ensuring a safer environment that leads to decreased adverse events.

Anesthesiology↗
PubMed2005

Macrophage inflammatory protein-3alpha promotes pancreatic cancer cell invasion.

BACKGROUND: Human CC chemokine Macrophage Inflammatory Protein-3alpha (MIP-3alpha) directs inflammatory cell migration through its binding to the transmembrane receptor CCR6. MIP-3alpha has recently been shown to promote tumor cell migration in pancreatic adenocarcinoma by up-regulation of matrix metalloproteinases (MMPs). We hypothesized that MIP-3alpha promotes pancreatic cancer invasion through the up-regulation of MMP-9, a Type 4 collagenase. MATERIALS, METHODS, AND RESULTS: Immunohistochemistry and RT-PCR confirmed the presence of MIP-3alpha in PANC-1 cells, a human pancreatic adenocarcinoma cell line. MIP-3alpha stimulated the production of both latent and active forms of MMP-9 in PANC-1 by Western analysis. Tumor cell invasion was then evaluated using a modified Boyden chamber invasion assay. MIP-3alpha promoted a dose-dependent increase in pancreatic cancer cell invasion (P < 0.05) at 100 ng/ml. The activity at the putative MIP-3alpha receptor, CCR6, was demonstrated by receptor blockade. Anti-CCR6 antibody and anti-MMP-9 antibody inhibited MIP-3alpha-stimulated PANC-1 cell invasion of collagen to 37% and 35% of control, respectively (P < 0.05). CONCLUSIONS: MIP-3alpha, through its CCR6 receptor, promotes tumor cell invasion by the up-regulation of MMP-9. Molecular based therapy aimed at the inhibition of MIP-3alpha activity through the CCR6 receptor may serve as a future target to prevent tumor cell invasion in pancreatic adenocarcinoma.

Cell Line, Tumor↗
PubMed2004

Antiangiogenic therapy.

Angiogenesis, the formation of blood vessels from preexisting ones, plays a crucial role in tumor progression. Activation of an "angiogenic switch" allows tumor cells to invade and metastasize. The growing interest in the use of antiangiogenic agents in the treatment and prevention of cancer lies in the theoretical advantages of this molecularly targeted modality of chemotherapy. Delivery of antiangiogenic agents are not complicated by having to penetrate large bulky masses but, instead, have easy access to tumoral endothelial cells. Antiangiogenic drugs may not cause cytopenias and thus will avoid many of the unwarranted toxicities of standard chemotherapeutic agents. Because they act directly on nascent endothelial cells, antiangiogenic agents may avoid tumor resistance mechanisms. If antiangiogenic agents are successful, they might be applicable to many tumor types and not be dependent on cell type or growth fraction of cells within a tumor. However, several important obstacles remain with regards to using antiangiogenic drugs in clinical trials with which we must contend in order to determine accurately the efficacy of these agents. In this article, we review the different classes of antiangiogenic agents available, ongoing clinical trials, as well as potential pitfalls and future directions in this exciting field.

Angiogenesis Inhibitors↗
PubMed2003

Evaluation of lymph node status in male breast cancer patients: a role for sentinel lymph node biopsy.

Sentinel lymph node (SLN) biopsy is rapidly emerging as an alternative to axillary lymph node dissection (ALND) for many female breast cancer patients. In contrast, ALND remains the standard of care for male breast cancer patients with similar tumors. We evaluated the results of SLN biopsy in male breast cancer patients with clinically negative axillae. This study included all male breast cancer patients who underwent SLN biopsy at our institution between October 1999 and 2000. All patients had negative axillae on clinical examination and sonography. All patients underwent preoperative lymphoscintigraphy followed by SLN biopsy performed using a combination of isosulfan blue dye and technetium Tc 99m sulfur colloid. Tc 99m sulfur colloid was injected at a dose of 2.5 mCi 24 h before surgery (four patients) or 0.5 mCi 2-4 h before surgery (three patients). Intraoperatively, 5 ml of 1% isosulfan blue was injected adjacent to the breast tumor or biopsy cavity prior to SLN biopsy. A gamma probe was used intraoperatively in order to localize SLNs. Any node that was blue or associated with ex vivo radioactivity counts at least 10 times higher than the axillary background counts was defined as a SLN. SLNs were assessed intraoperatively using touch preparation cytologic examination. Completion ALND was performed if nodal metastases were identified. Seven patients, 44-76 years of age, were included in the study. Preoperative lymphoscintigraphy identified SLNs in five patients. Intraoperatively, SLNs were identified in all seven patients. SLNs were identified in six patients using the gamma probe and in all seven patients using blue dye. The mean number of SLNs encountered was 2.9. Findings on touch preparation cytology correlated with findings on the final pathological analysis examination in all patients. One patient had a positive SLN, this patient had three additional positive nodes identified in his completion ALND specimen. Three patients with negative SLNs had been elected preoperatively to undergo ALND regardless of findings on SLN biopsy, no positive lymph nodes were identified in the ALND specimens from these patients. These findings compare favorably with findings reported in the literature regarding SLN biopsy in female breast cancer patients. Blue dye injection and radioisotope injection were complementary. SLN biopsy should be considered for axillary staging in male breast cancer patients with clinically negative axillae.

Adult↗
PubMed2003

Intestinal transformation results in transforming growth factor-beta-dependent alteration in tumor cell-cell matrix interactions.

BACKGROUND: An alteration in the expression of and response to transforming growth factor-beta 1 (TGF-beta 1) appears to be an important event during colorectal carcinogenesis. However, the precise role of TGF-beta 1 in colorectal carcinogenesis is not clear. We have previously described in detail the changes in cell proliferation and differentiation caused by chronic exposure to TGF-beta 1. In this study we sought to better characterize the changes in tumor cell-cell matrix interactions seen during TGF-beta 1-mediated intestinal transformation. METHODS: Rat intestinal epithelial cells (RIE) and RIE cells transformed by chronic exposure to TGF-beta 1 (RIE-Tr) were treated with TGF-beta 1 and production of components of the plasmin/plasminogen system measured by ELISA and Western blotting. TGF-beta 1 effects on invasion and adhesion were determined in vitro. The role of urokinase on TGF-beta 1-mediated invasion and adhesion were determined using immunoneutralization. The role of COX-2 was determined using a specific COS-2 inhibitor. RESULTS: TGF-beta 1 had no effect on RIE-1 adhesion to collagen types I and IV, fibronectin, and laminin, or invasion through collagen types I and IV. However, 5 ng/mL TGF-beta 1 significantly increased the invasiveness and decreased the adhesiveness of RIE-Tr. This effect of TGF-beta 1 on RIE-Tr was associated with a significant increase in plasmin activity secondary to increased expression of uPA. TGF-beta 1 had no effect on either uPA receptor or PAI-1 in this system. Antibodies to uPA completely blocked the TGF-beta 1-mediated invasiveness of the RIE-Tr cells and returned their adhesiveness to basement membrane proteins to baseline. Addition of the selective Cox-2 inhibitor SC-58125 resulted in a dose-dependent decrease in TGF-beta 1-mediated invasion and uPA expression. CONCLUSION: This study provides additional evidence for TGF-beta 1 as a tumor promoter during intestinal carcinogenesis and a possible new mechanism for Cox-2-related colon carcinogenesis.

Animals↗
PubMed2002

Up-regulation of matrix metalloproteinase 9 by thrombospondin 1 in gastric cancer.

BACKGROUND: Matrix metalloproteinase 9 (MMP-9) plays a key role in tumor cell invasion. It was recently reported that plasma levels of MMP-9 in patients with gastric cancer correlate with the tumors' metastatic potential. We previously demonstrated that thrombospondin 1 (TSP-1) up-regulates MMP-9 expression by endothelial cells and promotes tumor cell invasion. We hypothesized that TSP-1 plays a role in the up-regulation of MMP-9 in gastric cancer. METHODS: MMP-9, TSP-1, and CSVTCG-specific TSP-1 receptor expression were measured by immunohistochemical staining in 31 consecutive gastric adenocarcinomas from patients who did not undergo neoadjuvant chemotherapy or radiation therapy. Additionally, we measured TSP-1, CSVTCG-specific TSP-1 receptor, and MMP-9 expression by Western blotting, zymography, and immunohistochemical staining in AGS gastric adenocarcinoma cells. We also investigated the effect of TSP-1 on MMP-9 expression by AGS cells. RESULTS: TSP-1 localized to the tumor-associated extracellular matrix. CSVTCG-specific TSP-1 receptor and MMP-9 colocalized to tumor cells, fibroblasts, and tumor-associated microvessels. Intense staining for TSP-1, CSVTCG-specific TSP-1 receptor, and MMP-9 correlated with markers of aggressive tumor behavior. AGS gastric adenocarcinoma cells expressed high levels of CSVTCG-specific TSP-1 receptor but not TSP-1. TSP-1 up-regulated MMP-9 expression by AGS cells. CONCLUSIONS: We conclude that TSP-1 plays a role in the up-regulation of MMP-9 expression in gastric cancer. Our data also suggest a correlation between expression of TSP-1, CSVTCG-specific TSP-1 receptor, and MMP-9 and the acquisition of an aggressive tumor phenotype.

Adenocarcinoma↗
PubMed2002

Fibroblasts promote breast cancer cell invasion by upregulating tumor matrix metalloproteinase-9 production.

BACKGROUND: Thrombospondin-1 (TSP-1) promotes breast cancer cell invasion of collagen by upregulating matrix metalloproteinase-9 (MMP-9) production. Stromal TSP-1 may play a role in regulating tumor cell invasion. We hypothesize that fibroblasts promote breast cancer cell invasion by upregulating the production of MMP-9 through TSP-1. METHODS: MDA-MB-231 human breast carcinoma cells were grown alone or in coculture with human fibroblasts. Gelatin zymography and Western immunoblot analysis for MMP-9 were performed on the coculture cell media and the single cell media. Inhibition of fibroblast-mediated breast tumor cell invasion by an anti-TSP-1 or an anti-MMP-9 antibody was evaluated using a modified Boyden chamber. RESULTS: Coculture experiments showed an increased production of MMP-9 when compared with breast cancer single cell culture or fibroblast single cell culture experiments as demonstrated by zymography and Western immunoblot analysis. Fibroblast-stimulated MMP-9 production was comparable with TSP-1-stimulated MMP-9 production. Anti-TSP-1 antibody and anti-MMP-9 antibody inhibited fibroblast-stimulated tumor cell invasion to 30% and 26% of controls, respectively (P <.05). CONCLUSIONS: Fibroblasts may regulate breast cancer cell invasion by promoting tumor MMP-9 production through TSP-1. Inhibition of stromal TSP-1 stimulation of MMP-9 synthesis may prevent matrix degradation necessary for tumor invasion and metastasis.

Antibodies↗