Effect of N-acetylcysteine on markers of skeletal muscle injury after fatiguing contractile activity

The effects of N-Acetylcysteine (NAC), an unspecific antioxidant, on fatiguing contractile activity-induced injury were investigated. Twenty-four male Wistar rats were randomly assigned to two groups. The placebo group (N=12) received one injection of phosphate buffer (PBS) 1 h prior to contractile activity induced by electrical stimulation. The NAC group (NAC; N=12) received electrical stimulation for the same time period and NAC (500 mg/kg, i.p.) dissolved in PBS 1 h prior to electrical stimulation. The contralateral hindlimb was used as a control, except in the analysis of plasma enzyme activities, when a control group (rats placebo group not electrically stimulated and not treated) was included. The following parameters were measured: tetanic force, muscle fatigue, plasma activities of creatine kinase (CK) and lactate dehydrogenase (LDH), changes in muscle vascular permeability using Evans blue dye (EBD), muscle content of reactive oxygen species (ROS) and thiobarbituric acid-reactive substances (TBARS) and myeloperoxidase (MPO) activity. Muscle fatigue was delayed and tetanic force was preserved in NAC-treated rats. NAC treatment decreased plasma CK and LDH activities. The content of muscle-derived ROS, TBARS, EBD and MPO activity in both gastrocnemius and soleus muscles were also decreased by NAC pre-treatment. Thus, NAC has a protective effect against injury induced by fatiguing contractile activity in skeletal muscle.

Effects of creatine supplementation on muscle wasting and glucose homeostasis in rats treated with dexamethasone

We aimed to investigate the possible role of creatine (CR) supplementation in counteracting dexamethasone-induced muscle wasting and insulin resistance in rats. Also, we examined whether CR intake would modulate molecular pathways involved in muscle remodeling and insulin signaling. Animals were randomly divided into four groups: (1) dexamethasone (DEX); (2) control pair-fed (CON-PF); (3) dexamethasone plus CR (DEX-CR); and (4) CR pair-fed (CR-PF). Dexamethasone (5 mg/kg/day) and CR (5 g/kg/day) were given via drinking water for 7 days. Plantaris and extensor digitorum longus (EDL) muscles were removed for analysis. Plantaris and EDL muscle mass were significantly reduced in the DEX-CR and DEX groups when compared with the CON-PF and CR-PF groups (P < 0.05). Dexamethasone significantly decreased phospho-Ser(473)-Akt protein levels compared to the CON-PF group (P < 0.05) and CR supplementation aggravated this response (P < 0.001). Serum glucose was significantly increased in the DEX group when compared with the CON-PF group (DEX 7.8 +/- A 0.6 vs. CON-PF 5.2 +/- A 0.5 mmol/l; P < 0.05). CR supplementation significantly exacerbated hyperglycemia in the dexamethasone-treated animals (DEX-CR 15.1 +/- A 2.4 mmol/l; P < 0.05 vs. others). Dexamethasone reduced GLUT-4 translocation when compared with the CON-PF and CR-PF (P < 0.05) groups and this response was aggravated by CR supplementation (P < 0.05 vs. others). In conclusion, supplementation with CR resulted in increased insulin resistance and did not attenuate muscle wasting in rats treated with dexamethasone. Given the contrast with the results of human studies that have shown benefits of CR supplementation on muscle atrophy and insulin sensitivity, we suggest caution when extrapolating this animal data to human subjects.

Distribuição do nervo ibular comum em fetos de equinos e descrição anatômica de pontos para bloqueio anestésico

Analisou-se a distribuição do nervo fibular comum em 30 fetos de equinos, sem raça definida, provenientes do acervo do Laboratório de Anatomia Animal da Faculdade de Medicina Veterinária da Universidade Federal de Uberlândia, que foram injetados e conservados em solução aquosa de formaldeído a 10%. Contatou-se que o referido nervo deriva do isquiático, divide-se em nervos fibulares superficial e profundo, distribuindo-se para os músculos extensores lateral e longo do dedo, fibular terceiro e tibial cranial. Traçando-se uma linha imaginária na região médio-lateral da tuberosidade do osso tíbia, o nervo fibular comum pode ser bloqueado em sua parte proximal, no terço caudal, entre o tendão de inserção do músculo bíceps femoral e a face lateral do músculo gastrocnêmio lateral (terço médio); e o nervo fibular profundo, na parte proximal da tíbia, crânio-distalmente ao fibular comum. O bloqueio do nervo fibular superficial pode ser realizado em duas regiões da tíbia: na proximal, considerando-se a linha imaginária, distalmente ao ponto citado para o fibular comum e caudalmente ao descrito para o fibular profundo; e na distal, na face lateral da articulação tíbio-társica, entre os tendões de inserção dos músculos extensores lateral e longo do dedo.

Sonographic visualization and ultrasound-guided blockade of the greater occipital nerve: a comparison of two selective techniques confirmed by anatomical dissection

BACKGROUND: Local anaesthetic blocks of the greater occipital nerve (GON) are frequently performed in different types of headache, but no selective approaches exist. Our cadaver study compares the sonographic visibility of the nerve and the accuracy and specificity of ultrasound-guided injections at two different sites. METHODS: After sonographic measurements in 10 embalmed cadavers, 20 ultrasound-guided injections of the GON were performed with 0.1 ml of dye at the classical site (superior nuchal line) followed by 20 at a newly described site more proximal (C2, superficial to the obliquus capitis inferior muscle). The spread of dye and coloration of nerve were evaluated by dissection. RESULTS: The median sonographic diameter of the GON was 4.2 x 1.4 mm at the classical and 4.0 x 1.8 mm at the new site. The nerves were found at a median depth of 8 and 17.5 mm, respectively. In 16 of 20 in the classical approach and 20 of 20 in the new approach, the nerve was successfully coloured with the dye. This corresponds to a block success rate of 80% (95% confidence interval: 58-93%) vs 100% (95% confidence interval: 86-100%), which is statistically significant (McNemar's test, P=0.002). CONCLUSIONS: Our findings confirm that the GON can be visualized using ultrasound both at the level of the superior nuchal line and C2. This newly described approach superficial to the obliquus capitis inferior muscle has a higher success rate and should allow a more precise blockade of the nerve.

AICAR and metformin, but not exercise, increase muscle glucose transport through AMPK-, ERK-, and PDK1-dependent activation of atypical PKC

Activators of 5'-AMP-activated protein kinase (AMPK) 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR), metformin, and exercise activate atypical protein kinase C (aPKC) and ERK and stimulate glucose transport in muscle by uncertain mechanisms. Here, in cultured L6 myotubes: AICAR- and metformin-induced activation of AMPK was required for activation of aPKC and ERK; aPKC activation involved and required phosphoinositide-dependent kinase 1 (PDK1) phosphorylation of Thr410-PKC-zeta; aPKC Thr410 phosphorylation and activation also required MEK1-dependent ERK; and glucose transport effects of AICAR and metformin were inhibited by expression of dominant-negative AMPK, kinase-inactive PDK1, MEK1 inhibitors, kinase-inactive PKC-zeta, and RNA interference (RNAi)-mediated knockdown of PKC-zeta. In mice, muscle-specific aPKC (PKC-lambda) depletion by conditional gene targeting impaired AICAR-stimulated glucose disposal and stimulatory effects of both AICAR and metformin on 2-deoxyglucose/glucose uptake in muscle in vivo and AICAR stimulation of 2-[(3)H]deoxyglucose uptake in isolated extensor digitorum longus muscle; however, AMPK activation was unimpaired. In marked contrast to AICAR and metformin, treadmill exercise-induced stimulation of 2-deoxyglucose/glucose uptake was not inhibited in aPKC-knockout mice. Finally, in intact rodents, AICAR and metformin activated aPKC in muscle, but not in liver, despite activating AMPK in both tissues. The findings demonstrate that in muscle AICAR and metformin activate aPKC via sequential activation of AMPK, ERK, and PDK1 and the AMPK/ERK/PDK1/aPKC pathway is required for metformin- and AICAR-stimulated increases in glucose transport. On the other hand, although aPKC is activated by treadmill exercise, this activation is not required for exercise-induced increases in glucose transport, and therefore may be a redundant mechanism.

Giulio Cesare Aranzio (Arantius) (1530-89) in the pageant of anatomy and surgery

Giulio Cesare Aranzio in Italian (Julius Caesar Arantius in Latin) has not received full acclaim for his achievements in the field of anatomy and surgery that remain unknown to most physicians. His anatomical books Observationes Anatomicas, and De Humano Foetu Opusculum and surgical books De Tumoribus Secundum Locos Affectos and Hippocratis librum de vulneribus capitis commentarius brevis printed in Latin and additional existing literature on Aranzio from medical history books and journals were analysed extensively. Aranzio became Professor of Anatomy and Surgery at the University of Bologna in 1556. He established anatomy as a distinguished branch of medicine for the first time in medical history. Aranzio combined anatomy with a description of pathological processes. He discovered the 'Nodules of Aranzio' in the semilunar valves of the heart. He gave the first description of the superior levator palpebral and the coracobrachialis muscles. Aranzio wrote on surgical techniques for a wide spectrum of conditions that range from hydrocephalus, nasal polyp, goitre and tumours to phimosis, ascites, haemorrhoids, anal abscess and fistulae, and much more. Aranzio had an extensive knowledge in surgery and anatomy based in part on the ancient Greek and his contemporaries in the 16th century but essentially on his personal experience and practice.

Excessive erythrocytosis in adult mice overexpressing erythropoietin leads to hepatic, renal, neuronal, and muscular degeneration

To investigate the consequences of inborn excessive erythrocytosis, we made use of our transgenic mouse line (tg6) that constitutively overexpresses erythropoietin (Epo) in a hypoxia-independent manner, thereby reaching hematocrit levels of up to 0.89. We detected expression of human Epo in the brain and, to a lesser extent, in the lung but not in the heart, kidney, or liver of tg6 mice. Although no acute cardiovascular complications are observed, tg6 animals have a reduced lifespan. Decreased swim performance was observed in 5-mo-old tg6 mice. At about 7 mo, several tg6 animals developed spastic contractions of the hindlimbs followed by paralysis. Morphological analysis by light and electron microscopy showed degenerative processes in liver and kidney characterized by increased vascular permeability, chronic progressive inflammation, hemosiderin deposition, and general vasodilatation. Moreover, most of the animals showed severe nerve fiber degeneration of the sciatic nerve, decreased number of neuromuscular junctions, and degeneration of skeletal muscle fibers. Most probably, the developing demyelinating neuropathy resulted in muscular degeneration demonstrated in the extensor digitorum longus muscle. Taken together, chronically increased Epo levels inducing excessive erythrocytosis leads to multiple organ degeneration and reduced life expectancy. This model allows investigation of the impact of excessive erythrocytosis in individuals suffering from polycythemia vera, chronic mountain sickness, or in subjects tempted to abuse Epo by means of gene doping.

Up-regulation of the peroxiredoxin-6 related metabolism of reactive oxygen species in skeletal muscle of mice lacking neuronal nitric oxide synthase

Although neuronal nitric oxide synthase (nNOS) plays a substantial role in skeletal muscle physiology, nNOS-knockout mice manifest an only mild phenotypic malfunction in this tissue. To identify proteins that might be involved in adaptive responses in skeletal muscle of knockout mice lacking nNOS, 2D-PAGE with silver-staining and subsequent tandem mass spectrometry (LC-MS/MS) was performed using extracts of extensor digitorum longus muscle (EDL) derived from nNOS-knockout mice in comparison to C57Bl/6 control mice. Six proteins were significantly (P < or = 0.05) more highly expressed in EDL of nNOS-knockout mice than in that of C57 control mice, all of which are involved in the metabolism of reactive oxygen species (ROS). These included prohibitin (2.0-fold increase), peroxiredoxin-3 (1.9-fold increase), Cu(2+)/Zn(2+)-dependent superoxide dismutase (SOD; 1.9-fold increase), heat shock protein beta-1 (HSP25; 1.7-fold increase) and nucleoside diphosphate kinase B (2.6-fold increase). A significantly higher expression (4.1-fold increase) and a pI shift from 6.5 to 5.9 of peroxiredoxin-6 in the EDL of nNOS-knockout mice were confirmed by quantitative immunoblotting. The concentrations of the mRNA encoding five of these proteins (the exception being prohibitin) were likewise significantly (P < or = 0.05) higher in the EDL of nNOS-knockout mice. A higher intrinsic hydrogen peroxidase activity (P < or = 0.05) was demonstrated in EDL of nNOS-knockout mice than C57 control mice, which was related to the presence of peroxiredoxin-6. The treatment of mice with the chemical NOS inhibitor L-NAME for 3 days induced a significant 3.4-fold up-regulation of peroxiredoxin-6 in the EDL of C57 control mice (P < or = 0.05), but did not alter its expression in EDL of nNOS-knockout mice. ESR spectrometry demonstrated the levels of superoxide to be 2.5-times higher (P < or = 0.05) in EDL of nNOS-knockout mice than in C57 control mice while an in vitro assay based on the emission of 2,7-dichlorofluorescein fluorescence disclosed the concentration of ROS to be similar in both strains of mice. We suggest that the up-regulation of proteins that are implicated in the metabolism of ROS, particularly of peroxiredoxin-6, within skeletal muscles of nNOS-knockout mice functionally compensates for the absence of nNOS in scavenging of superoxide.

Clinical and molecular features of methicillin-resistant, coagulase-negative staphylococci of pets and horses

OBJECTIVES To determine the antibiotic resistance and fingerprint profiles of methicillin-resistant coagulase-negative staphylococci (MRCoNS) from animal infections among different practices and examine the history of antibiotic treatment. METHODS Isolates were identified by mass spectrometry and tested for antimicrobial resistance by broth dilution, microarrays and sequence analysis of the topoisomerases. Diversity was assessed by PFGE, icaA PCR and staphylococcal cassette chromosome mec (SCCmec), arginine catabolic mobile element (ACME) and multilocus sequence typing. Clinical records were examined retrospectively. RESULTS MRCoNS were identified as Staphylococcus epidermidis (n=20), Staphylococcus haemolyticus (n=17), Staphylococcus hominis (n=3), Staphylococcus capitis (n=1), Staphylococcus cohnii (n=1) and Staphylococcus warneri (n=1). PFGE identified one clonal lineage in S. hominis isolates and several in S. haemolyticus and S. epidermidis. Fourteen sequence types were identified in S. epidermidis, with sequence type 2 (ST2) and ST5 being predominant. Ten isolates contained SCCmec IV, seven contained SCCmec V and the others were non-typeable. ACMEs were detected in 11 S. epidermidis isolates. One S. hominis and 10 S. epidermidis isolates were icaA positive. In addition to mecA-mediated β-lactam resistance, the most frequent resistance was to gentamicin/kanamycin [aac(6')-Ie-aph(2')-Ia, aph(3')-III] (n=34), macrolides/lincosamides [erm(C), erm(A), msr, lnu(A)] (n=31), tetracycline [tet(K)] (n=22), streptomycin [str, ant(6)-Ia] (n=20), trimethoprim [dfr(A), dfr(G)] (n=17), sulfamethoxazole (n = 34) and fluoroquinolones [amino acid substitutions in GyrA and GrlA] (n=30). Clinical data suggest selection through multiple antibiotic courses and emphasize the importance of accurate diagnosis and antibiograms. CONCLUSIONS MRCoNS from animal infection sites are genetically heterogeneous multidrug-resistant strains that represent a new challenge in the prevention and therapy of infections in veterinary clinics.

Phenotype of capillaries in skeletal muscle of nNOS-knockout mice

Because neuronal nitric oxide synthase (nNOS) has a well-known impact on arteriolar blood flow in skeletal muscle, we compared the ultrastructure and the hemodynamics of/in the ensuing capillaries in the extensor digitorum longus (EDL) muscle of male nNOS-knockout (KO) mice and wild-type (WT) littermates. The capillary-to-fiber (C/F) ratio (-9.1%) was lower (P ≤ 0.05) in the nNOS-KO mice than in the WT mice, whereas the mean cross-sectional fiber area (-7.8%) and the capillary density (-3.1%) varied only nonsignificantly (P > 0.05). Morphometrical estimation of the area occupied by the capillaries as well as the volume and surface densities of the subcellular compartments differed nonsignificantly (P > 0.05) between the two strains. Intravital microscopy revealed neither the capillary diameter (+3% in nNOS-KO mice vs. WT mice) nor the mean velocity of red blood cells in EDL muscle (+25% in nNOS-KO mice vs. WT mice) to significantly vary (P > 0.05) between the two strains. The calculated shear stress in the capillaries was likewise nonsignificantly different (3.8 ± 2.2 dyn/cm² in nNOS-KO mice and 2.1 ± 2.2 dyn/cm² in WT mice; P > 0.05). The mRNA levels of vascular endothelial growth factor (VEGF)-A were lower in the EDL muscle of nNOS-KO mice than in the WT littermates (-37%; P ≤ 0.05), whereas mRNA levels of VEGF receptor-2 (VEGFR-2) (-11%), hypoxia inducible factor-1α (+9%), fibroblast growth factor-2 (-14%), and thrombospondin-1 (-10%) differed nonsignificantly (P > 0.05). Our findings support the contention that VEGF-A mRNA expression and C/F-ratio but not the ultrastructure or the hemodynamics of/in capillaries in skeletal muscle at basal conditions depend on the expression of nNOS.

Anatomic foveal reconstruction of the triangular fibrocartilage complex with a tendon graft

An acute injury to the triangular fibrocartilage complex (TFCC) with avulsion of the foveal attachment can produce distal radioulnar joint (DRUJ) instability. The avulsed TFCC is translated distally so the footprint will be bathed in synovial fluid from the DRUJ and will become covered in synovitis. If the TFCC fails to heal to the footprint, then persistent instability can occur. The authors describe a surgical technique indicated for the treatment of persistent instability of the DRUJ due to foveal detachment of the TFCC. The procedure utilizes a loop of palmaris longus tendon graft passed through the ulnar aspect of the TFCC and into an osseous tunnel in the distal ulna to reconstruct the foveal attachment. This technique provides stability of the distal ulna to the radius and carpus. We recommend this procedure for chronic instability of the DRUJ due to TFCC avulsion, but recommend that suture repair remain the treatment of choice for acute instability. An arthroscopic assessment includes the trampoline test, hook test, and reverse hook test. DRUJ ballottement under arthroscopic vision details the direction of instability, the functional tear pattern, and unmasks concealed tears. If the reverse hook test demonstrates a functional instability between the TFCC and the radius, then a foveal reconstruction is contraindicated, and a reconstruction that stabilizes the radial and ulnar aspects of the TFCC is required. The foveal reconstruction technique has the advantage of providing a robust anatomically based reconstruction of the TFCC to the fovea, which stabilizes the DRUJ and the ulnocarpal sag.

Twelve percent of hips with a primary cam deformity exhibit a slip-like morphology resembling sequelae of slipped capital femoral epiphysis

BACKGROUND In some hips with cam-type femoroacetabular impingement (FAI), we observed a morphology resembling a more subtle form of slipped capital femoral epiphysis (SCFE). Theoretically, the morphology in these hips should differ from hips with a primary cam-type deformity. QUESTIONS/PURPOSES We asked if (1) head-neck offset; (2) epiphyseal angle; and (3) tilt angle differ among hips with a slip-like morphology, idiopathic cam, hips after in situ pinning of SCFE, and normal hips; and (4) what is the prevalence of a slip-like morphology among cam-type hips? METHODS We retrospectively compared the three-dimensional anatomy of hips with a slip-like morphology (29 hips), in situ pinning for SCFE (eight hips), idiopathic cam deformity (171 hips), and 30 normal hips using radial MRI arthrography. Normal hips were derived from 17 asymptomatic volunteers. All other hips were recruited from a series of 277 hips (243 patients) seen at a specialized academic hip center between 2006 and 2010. Forty-one hips with isolated pincer deformity were excluded. Thirty-six of 236 hips had a known cause of cam impingement (secondary cam), including eight hips after in situ pinning of SCFE (postslip group). The 200 hips with a primary cam were separated in hips with a slip-like morphology (combination of positive fovea sign [if the neck axis did not intersect with the fovea capitis] and a tilt angle [between the neck axis and perpendicular to the basis of the epiphysis] exceeding 4°) and hips with an idiopathic cam. We evaluated offset ratio, epiphyseal angle (angle between the neck axis and line connecting the center of the femoral head and the point where the physis meets the articular surface), and tilt angle circumferentially around the femoral head-neck axis. Prevalence of slip-like morphology was determined based on the total of 236 hips with cam deformities. RESULTS Offset ratio was decreased anterosuperiorly in idiopathic cam, slip-like, and postslip (eg, 1 o'clock position with a mean offset ranging from 0.00 to 0.14; p < 0.001 for all groups) compared with normal hips (0.25 ± 0.06 [95% confidence interval, 0.13-0.37]) and increased posteroinferiorly in slip-like (eg, 8 o'clock position, 0.5 ± 0.09 [0.32-0.68]; p < 0.001) and postslip groups (0.55 ± 0.12 [0.32-0.78]; p < 0.001) and did not differ in idiopathic cam (0.32 ± 0.09 [0.15-0.49]; p = 0.323) compared with normal (0.31 ± 0.07 [0.18-0.44]) groups. Epiphyseal angle was increased anterosuperiorly in the slip-like (eg, 1 o'clock position, 70° ± 9° [51°-88°]; p < 0.001) and postslip groups (75° ± 13° [49°-100°]; p = 0.008) and decreased in idiopathic cam (50° ± 8° [35°-65°]; p < 0.001) compared with normal hips (58° ± 8° [43°-74°]). Posteroinferiorly, epiphyseal angle was decreased in slip-like (eg, 8 o'clock position, 54° ± 10° [34°-74°]; p < 0.001) and postslip (44° ± 11° [23°-65°]; p < 0.001) groups and did not differ in idiopathic cam (76° ± 8° [61°-91°]; p = 0.099) compared with normal (73° ± 7° [59°-88°]) groups. Tilt angle increased in slip-like (eg, 2/8 o'clock position, 14° ± 8° [-1° to 30°]; p < 0.001) and postslip hips (29° ± 10° [9°-48°]; p < 0.001) and decreased in hips with idiopathic cam (-7° ± 5° [-17° to 4°]; p < 0.001) compared with normal (-1° ± 5° [-10° to 8°]) hips. The prevalence of a slip-like morphology was 12%. CONCLUSIONS The slip-like morphology is the second most frequent pathomorphology in hips with primary cam deformity. MRI arthrography of the hip allows identifying a slip-like morphology, which resembles hips after in situ pinning of SCFE and distinctly differs from hips with idiopathic cam. These results support previous studies reporting that SCFE might be a risk factor for cam-type FAI.

Reconstruction of Chronic Foveal TFCC Tears with an Autologous Tendon Graft

Background A triangular fibrocartilage complex (TFCC) injury can produce distal radioulnar joint (DRUJ) instability. If the foveal attachment is avulsed, it translates distally. The footprint is separated from its origin and will become covered in synovitis, preventing healing. The authors describe a surgical technique for the treatment of instability of the DRUJ due to chronic foveal detachment of the TFCC. Technique The procedure utilizes a loop of autologous palmaris longus tendon graft passed through the ulnar aspect of the TFCC and through an osseous tunnel in the distal ulna to reconstruct the fovel attachment. Patients and Methods We report on nine patients with a mean age of 42. Median follow-up was 13 months. Results The median pain scores measured were reduced from 8 to 3 postoperatively, and all had a stable DRUJ. Conclusions This technique provides stability of the distal ulna to the radius and carpus, with potential for biologic healing through osseous integration. It is a robust, anatomically based reconstruction of the TFCC to the fovea that stabilizes the DRUJ and the ulnar-carpal sag.

Commentarius De Re Rustica Veterum Hebraeorum

Vorlage d. Digitalisats aus d. Besitz d. Theol. Hochschule St. Georgen

BIOCHEMICAL CHARACTERIZATION AND CLINICAL SIGNIFICANCE OF COAGULASE-NEGATIVE STAPHYLOCOCCI

Although coagulase-negative staphylococci (C-NS) have been implicated in certain human infections, they are generally regarded as contaminants and their clinical significance is questioned. To assess their role as pathogens, 205 isolates of C-NS from wounds, and body fluids (blood, urine, pleural and peritoneal fluids, etc.) were studied. Patient's charts were reviewed and using strict criteria a determination was made regarding the clinical significance of these isolates. The organisms were then identified using the scheme of Kloos and Schleifer to determine if certain species of C-NS were associated with specific infections. S. epidermidis sensu stricto accounted for 81% of the C-NS isolated; the frequency of other species was S. haemolyticus (6%), S. hominis (5%), S. capitis (4%), S. warneri (3%), and others (1%). Only two isolates were novobiocin resistant; neither was identified as S. saprophyticus. Using these criteria, 22% of C-NS were considered to be clinically significant and the majority of these (93%) were due to S. epidermidis. The most common source of the clinically relevant C-NS isolates was from wounds. These data suggest that identifying C-NS species other than S. epidermidis may be of limited value in predicting clinical significance.^ In addition, selected pathogenic and non-pathogenic strains of C-NS were compared for their ability to adhere to human cells in vitro. Although the results were not conclusive, it appeared that pathogenic C-NS adhered more avidly than non-pathogenic C-NS to buccal cells. Experiments with HeLa cells showed no difference between pathogenic and non-pathogenic C-NS in adherence abilities. ^