Microbiologic characteristics and in vitro susceptibility to antimicrobials in a large population of patients with cardiovascular implantable electronic device infection

Microbiologic Characteristics and In Vitro Susceptibility to Antimicrobials. Introduction: The incidence of cardiovascular implantable electronic device (CIED) infection is steadily increasing. However, no consensus has been reached with respect to the type and duration of antimicrobial therapy in this specific population of patients. The role played by new anti‐Staphylococcus agents has not been defined. The aims of this study were to describe the microbiological characteristics of a large population of patients with CIED infections and to test the in vitro susceptibility of the various strains to different antimicrobials. Methods: Two hundred eighty‐six patients with CIED infection were included. The minimal inhibitory concentrations of 9 antimicrobials, including linezolid, tigecycline, and daptomycin were measured against all strains of staphylococci isolated. Results: Microbiologic confirmation was obtained in 252 (88%) patients, the vast majority were from Staphylococcus species (86%), 90% of these were coagulase negative strains and 10% were Staphylococcus aureus; 30.5% were methicillin‐resistant. All strains were susceptible to vancomycin, nearly 15% of coagulase negative strains were nonsusceptible to teicoplanin, and nearly 100% of the strains were susceptible to the 3 new antimicrobials. Conclusions: In this large contemporary study, we show that Staphylococcus is by far the most common cause of CIED infections, with the majority due to coagulase negative strains. Methicillin‐resistance is common in this population. Currently, we would recommend vancomycin as first‐line empirical therapy. However, given that not all patients tolerate vancomycin, we believe that newer antimicrobial therapies should now be tested in clinical trials to establish their clinical effectiveness in treating patients with device infections.     

Pudendal Neurolysis by Laparoscopy

Study ObjectiveTo show how pudendal neurolysis can be managed safely with a laparoscopic approach.DesignStepwise demonstration of the technique with narrated video footage.SettingThe pudendal nerve is formed from spinal roots at levels S2, S3, and S4. It passes through the pelvis parallel to the pudendal vein and artery. This nerve exits the pelvis between the sacrospinous and sacrotuberous ligaments then passes through Alcock's canal. It can be compressed and responsible for pain in the gluteal and perineal regions.After confirmation of the diagnosis by positive analgesic block with computed tomography infiltration of the pudendal nerve, surgical decompression may be considered.The usual access procedures are the transglutal and transischiorectal ways.InterventionsThis video shows a total laparoscopic approach for a right pudendal neurolysis. It is a step-by-step didactic video.This technique of decompression of the right pudendal nerve by laparoscopy by means of dissection of the ischiorectal fossa along the right internal obturator muscle, after visualization of the obturator vessels and identification of the pudendal nerve, allowed the section of the right sacrospinous ligament and complete removal with repositioning of the nerve in its path. The nerve was followed until it passed freely through Alcock's canal. The procedure went well and without complications, with clinical improvement on waking up.ConclusionPudendal nerve neurolysis by laparoscopic technique is a reproducible and safe method for treating pudendal neuralgia, allowing good visualization and dissection of the entire pelvis toward the ischiorectal fossa.     

Pelvic cystic lymphangioma. Apropos of a case in an adult

The authors report about the observation of a subperitoneal pelvic cystic lymphangioma in an adult patient: ultrasound and CT dat had yet never been described for the rare pelvic form, and are the same as with the other locations of cystic lymphangioma in adults.     

Deficient nucleotide excision repair activity in protein extracts from normal human lymphocytes

DNA repair activity in human peripheral blood lymphocytes (PBL)has been investigated by various techniques. Here, we reportthe use of an in vitro assay in order to assess nucleotide excisionrepair activity (NER). The mechanism of this major repair processrelies on two broad steps: first, recognition, incision andexcision of the damaged DNA; second, repair synthesis on thegapped DNA. Briefly, damaged plasmids were incubated with wholecell extracts which allows one to quantify DNA repair synthesis.When NER was determined on plasmid DNA damaged with UV-lightor cisplatin, PBL extracts showed no repair synthesis for unstimulatedlymphocytes. Using a new in vitro assay measuring only the damage-specificDNA incision activity in cell extracts, we found that the incisionstep in the repair reaction was blocked in unstimulated PBL.By mixing PBL with XP (group A, B, C, D) extracts, no restorationof NER activity was observed. In addition, these lymphocytesalso lacked DNA replication activity as determined with pre-incisedplasmid substrate. However, a phytohemagglutinin treatment ofPBL led to an extent of repair synthesis similar to that observedwith extracts from lymphoblastoid cells. When lymphocytes wereincubated in 20% serum medium with and without phytohemagglutinin,the repair activity increased dramatically after 24 h. Duringthe activation of lymphocytes, the extent of repair synthesiswas proportional to the percentage of cells in S phase of thecell cycle. Our results suggest that the blockage of the cellcycle in G0/G1 in PBL may be responsible for their lack of NERactivity.     

Ontogenesis of peptidylglycyl alpha-amidation activity in the mouse hypothalamus in vivo and in serum-free medium cultures. Relation with thyroliberin (TRH) accumulation and release in vitro

The influence of peptidylglycine alpha-amidating monooxygenase (PAM) and of its co-factor, ascorbate, were studied in relation to thyroliberin (TRH) activity during mouse hypothalamus development. In vivo, PAM activity developed slowly at fetal stages, and exhibited a sharp rise around the 5th-8th postnatal day, the adult level being reached around day 15. The same developmental pattern was observed when studied in serum-free cultures initiated from fetal mouse hypothalamus. Using this in vitro model, we investigated the effects of ascorbate, a necessary co-factor of PAM, on TRH. Upon ascorbate supplementation of the culture medium, the TRH accumulation normally occurring in our cultures was further enhanced. The half maximum effect was attained with 20 microM, and the amplitude of the response to ascorbate was maximum around 9-13 days in vitro. Moreover, ascorbate increased to an even larger extent the amounts of TRH released upon chemical depolarization. These results are consistent with a direct role of ascorbate on PAM activity, but other more general effects on the maturation of the neuronal response to physiological stimuli cannot be excluded.