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870 records · Page 49Linked to original sources
PubMed2003

[Reconstruction of big rotator cuff ruptures. A new technique of tendon refixation with the corkscrew suture anchor system].

Tendon retraction and fatty degeneration is a major problem in repair of massive rotator cuff tears. Especially in the transosseous refixation technique, a tension-free refixation cannot be obtained in all cases. The purpose of this prospective study was to evaluate the postoperative results using a new tension-free reinsertion technique with a Corkscrew suture anchor system. Thirty patients (25 males, 5 females) with complete one and two tendon tears underwent open rotator cuff repair (rupture of one tendon: n=14, 47%). The torn tendons were mobilized and reinserted medially to reduce tension. Medialization was achieved by inserting tendon near the osteochondral border in a bony trough. The number of implanted suture anchors ranged from 2 to 6 (mean: 3.56). The mean age was 56 years (39-68 years) with a follow-up of 24 months (17-33 months). In one patient physical and sonographic examination showed a complete and in two patients a partial rerupture. A temporarily frozen shoulder occurred in two cases. No infection or rejection response was seen. In no case was revision surgery necessary. No displacement or loosening of the Corkscrew anchors was noticed. The constant score improved from 45 points preoperatively to 85 points at the time of follow-up (mean). The Corkscrew suture anchor system in combination with the new suture technique offers the possibility of a stable reinsertion even in reduced calcified bone structure. This facilitates good conditions for stable fibroblastic healing. Our midterm results show good osseous union combined with a low rerupture rate.

Adult↗
PubMed1994

[Technique of intraoperative treatment of a retro-mandibular defect after parotidectomy. Use of a blot clot].

As noticed in our experience, cosmetic results, after total parotidectomy, were better if the patient presented an hematoma. The author got the idea to fill the retro-mandibular defect with a clot. The technique is presented in detail. Fifty four patients had a total parotidectomy between January 1992 and May 1993. A clot was used in 39 of these 54 cases. Were excluded malignant tumors, superficial parotidectomies or the presence of a general pathology (diabetes, cirrhosis). The result was excellent in 31 cases even if a local treatment was necessary due to a secondary hematoma. There was no infectious complication. The follow-up of this series is insufficient, but by analogy with spontaneous hematoma, the results should be persistent. This technique is simple, does not increased the time of the surgical procedure and does not induced injury on any donor site.

Clot Retraction↗
PubMed2001

Dopamine receptors in human platelets.

The expression of dopamine receptors by human platelets was investigated by Western blot analysis and immunocytochemical techniques using antibodies raised against dopamine D1-D5 receptor protein. The influence of dopamine D1-like and D2-like receptor agonists on adrenaline-induced platelet aggregation was also investigated. Western blot analysis revealed that platelet membranes bind anti-dopamine D3 or D5 receptor protein antibodies, but not anti-D1, D2 or D4 receptor protein antibodies. Cytospin centrifuged human platelets exposed to anti-dopamine D3 or D5 receptor protein antibodies developed a specific immune staining, whereas no positive staining was noticeable in platelets exposed to other antibodies tested. Both the D1-like receptor agonist 1-phenyl2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol hydrochloride (SKF 38393) and the D2-like receptor agonist 7-hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OH-DPAT) dose-dependently inhibited adrenaline-induced platelet aggregation. These effects were decreased respectively by the D-like and D2-like receptor antagonists R(+)-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepin-7-ol hydrochloride (SCH 23390) and (-)sulpiride. The above findings indicate that human platelets express dopamine D3 and D5 receptors probably involved in the regulation of platelet function.

Adult↗
PubMed2004

Quinoxaline 1,4-dioxides induce G2/M cell cycle arrest and apoptosis in human colon cancer cells.

We have recently shown that quinoxaline 1,4-dioxide (QdNO) derivatives, namely 2-benzoyl-3-phenyl-6,7-dichloroquinoxaline 1,4-dioxide (DCQ), 2-benzoyl-3-phenyl-quinoxaline 1,4-dioxide (BPQ) and 2-acetyl-3-methyl-quinoxaline 1,4-dioxide (AMQ), suppress the growth of T-84 human colon cancer cells. Here we show that the growth-suppressive effects of QdNOs are due to their ability to induce cell cycle arrest and/or apoptosis. While AMQ blocked more than 60% of cells at the G2/M phase without inducing apoptosis, DCQ caused a significant increase in apoptotic cells with no noticeable effects on the cycling of cells. Treatment with BPQ resulted in G2/M cell cycle arrest and induction of apoptosis. With regard to the effects of QdNOs on molecules that regulate apoptosis and the G2 to M transition, both BPQ and AMQ inhibited the expression of cyclin B, while DCQ significantly decreased the levels of Bcl-2 and increased Bax expression. Next, we investigated whether transforming growth factor-beta1 (TGF-beta1) and/or extracellular signal-regulated kinase (ERK) mediate the antiproliferative and apoptotic effects of QdNOs in colon cancer cells. Interestingly, the above QdNOs increased differentially total TGF beta1 mRNA expression and decreased TGF alpha mRNA and ERK phosphorylation. None of these QdNOs induced changes in TGF beta-2 mRNA expression. The addition of a specific inhibitor of MEK greatly enhanced apoptosis in cells treated with DCQ, suggesting that the inhibition of ERK phosphorylation may explain, to an extent, the apoptogenic effects of this compound. Taken together, these findings provide insights into possible molecular mechanisms of growth inhibition by QdNOs that could aid in their evaluation for anticancer therapy.

Apoptosis↗
PubMed2001

The significance of cystic duct stones encountered during laparoscopic cholecystectomy.

BACKGROUND: Cystic duct stones (CDS) are occasionally encountered during laparoscopic cholecystectomy (LC). They may be noticed during the dissection of the cystic pedicle or seen to extrude from the cystic duct (CD) when it is divided or opened to perform the intraoperative cholangiogram (IOC). The procedures for dealing with CDS range from the simple removal of stones that fall out when the duct is opened to incising the duct over an impacted stone to facilitate its removal or converting to open surgery due to a large stone in a CD adherent to the bile duct (e.g., Mirizzi syndrome). Therefore, we set out to establish criteria that might be predictive of CDS, to examine the technical problems caused by them, to look for the most effective ways of avoiding adverse consequences, especially the risk of missing bile duct stones. METHODS: We performed a review and analysis of a database that included preoperative, operative, and postoperative data for all patients treated at our hospital who were found to have CDS. RESULTS: In a series of 520 LC performed over a period of 5 years, 64 cases of CDS were documented (12.3%). The preoperative risk factors in 45 of these cases (70.3%) were recent sever acute pain with or without liver function test (LFT) derangement (34.3%), jaundice (14%), pancreatitis (14%), and previous acute cholecystitis (7.8%). At operation, a single stone was found in the CD in 64% of the cases; multiple stones were found in 36%. Dissection of the pedicle was difficult in 21 cases and had to be carried out fundus-first in four cases. The CD was reported to be wide in 18 cases; five of them eventually needed to be closed with endoloops. Operative difficulty was reported in three of 19 cases where there were no preoperative risk factors. Simple removal of the stones was possible in most cases. CDS needed be crushed, the CD incised, or the procedure converted to open in only five cases (7.8%). IOC was attempted in all cases; it was normal in 39 (61%) and failed in two cases (3%). Eighteen patients (28%) were found to have bile duct stones; another five (7.8%) had CBD dilation or debris indicating possible recent passage of stones. Fourteen transcystic and nine direct bile duct explorations were performed. CONCLUSION: Some CDS may slip from the gallbladder into the CD or the CBD during dissection. Careful retraction and manipulation should therefore be done to minimize this risk. Most CDS are easy to deal with, but some of them can result in increased operative difficulty. If IOC is not carried out on a routine basis, it becomes mandatory if CDS are encountered because 35% of them may be associated with bile duct stones.

Adolescent↗
PubMed2001

Pro-survival function of Akt/protein kinase B in prostate cancer cells. Relationship with TRAIL resistance.

Tumor necrosis factor superfamily member TRAIL/Apo-2L has recently been shown to induce apoptosis in transformed and cancer cells. Some prostate cancer cells express constitutively active Akt/protein kinase B due to a complete loss of lipid phosphatase PTEN gene, a negative regulator of phosphatidylinositol 3-kinase pathway. Constitutively active Akt promotes cellular survival and resistance to chemotherapy and radiation. We have recently noticed that some human prostate cancer cells are resistant to TRAIL. We therefore examined the intracellular mechanisms of cellular resistance to TRAIL. The cell lines expressing the highest level of constitutively active Akt were more resistant to undergo apoptosis by TRAIL than those expressing the lowest level. Down-regulation of constitutively active Akt by phosphatidylinositol 3-kinase inhibitors, wortmannin and LY294002, reversed cellular resistance to TRAIL. Treatment of resistant cells with cycloheximide (a protein synthesis inhibitor) rendered cells sensitive to TRAIL. Transfecting dominant negative Akt decreased Akt activity and increased TRAIL-induced apoptosis in cells with high Akt activity. Conversely, transfecting constitutively active Akt into cells with low Akt activity increased Akt activity and attenuated TRAIL-induced apoptosis. Inhibition of TRAIL sensitivity occurs at the level of BID cleavage, as caspase-8 activity was not affected. Enforced expression of anti-apoptotic protein Bcl-2 or Bcl-X(L) inhibited TRAIL-induced mitochondrial dysfunction and apoptosis. We therefore identify Akt as a constitutively active kinase that promotes survival of prostate cancer cells and demonstrate that modulation of Akt activity, by pharmacological or genetic approaches, alters the cellular responsiveness to TRAIL. Thus, TRAIL in combination with agents that down-regulate Akt activity can be used to treat prostate cancer.

Androstadienes↗