The effectiveness of fascial closure with antimicrobial-coated sutures in preventing incisional surgical site infections in gastrointestinal surgery: a systematic review and meta-analysis.

The aim of this study was to conduct a systematic review and meta-analysis of the efficacy of fascial closure using antimicrobial-sutures specifically for the prevention of surgical site infections (SSIs) in gastrointestinal surgery, as part of the revision of the SSI prevention guidelines of the Japanese Society of Surgical Infectious Diseases (JSSI). We searched CENTRAL, PubMed and ICHUSHI-Web in May 2023, and included randomized controlled trials (RCTs) comparing antimicrobial-coated and non-coated sutures for fascial closure in gastrointestinal surgery (PROSPERO No. CRD42023430377). Three authors independently screened the RCTs. We assessed the risk of bias and the GRADE criteria for the extracted data. The primary outcome was incisional SSI and the secondary outcomes were abdominal wall dehiscence and the length of postoperative hospital stay. This study was supported partially by the JSSI. A total of 10 RCTs and 5396 patients were included. The use of antimicrobial-coated sutures significantly lowered the risk of incisional SSIs compared with non-coated suture (risk ratio: 0.79, 95% confidence intervals: 0.64-0.98). In subgroup analyses, antimicrobial-coated sutures reduced the risk of SSIs for open surgeries, and when monofilament sutures were used. Antimicrobial-coated sutures did not reduce the incidence of abdominal wall dehiscence and the length of hospital stay compared with non-coated sutures. The certainty of the evidence was rated as moderate according to the GRADE criteria, because of risk of bias. In conclusion, the use of antimicrobial-coated sutures for fascial closure in gastrointestinal surgery is associated with a significantly lower risk of SSI than non-coated sutures.

Association between skin suture devices and incidence of incisional surgical site infection after gastrointestinal surgery: systematic review and network meta-analysis.

BACKGROUND: Surgical site infections (SSIs) are common complications after abdominal surgery. AIM: To compare which suture devices could reduce the incidence of incisional surgical site infections (SSIs) after gastrointestinal surgery using a systematic review and network meta-analysis. METHODS: The CENTRAL, PubMed, and ICHUSHI-Web databases were searched from January 1st, 2000, to December 31st, 2022, for randomized clinical trials (RCTs) comparing the incidence of incisional SSI after gastrointestinal surgery among patients treated with different surgical suture devices, including non-absorbable sutures, absorbable sutures, skin staplers, and tissue adhesives (last searched in August 23th, 2023). The risk of bias was assessed using the criteria of the Cochrane Handbook for Systematic Reviews of Interventions. To estimate the pooled odds ratios (ORs) for each comparison, a fixed-effect inverse-variance model based on the Mantel-Haenszel approach was employed. FINDINGS: A total of 18 RCTs with 5496 patients were included in this study. The overall SSIs in absorbable sutures were significantly lower than those in skin staplers (OR: 0.77; 95% confidence intervals (CI): 0.63-0.95) and non-absorbable sutures (OR: 0.62; 95% CI: 0.39-0.99), whereas SSIs in absorbable sutures were not significantly different from the SSIs in tissue adhesive. The highest P-score was 0.91 for absorbable sutures. A funnel plot for estimating the heterogeneity of the studies revealed that a publication bias would be minimal (Egger test, P = 0.271). CONCLUSION: This study showed that absorbable sutures reduced incisional SSIs in gastrointestinal surgical operations compared to any other suture devices.

Influence of Carisolv on resin adhesion for two different adhesive systems to sound human primary dentin and young permanent dentin.

OBJECTIVE: This study evaluated the influence of Carisolv (Medi Team) for resin adhesion to sound human primary and young permanent dentin. METHODS: The buccal surfaces of 28 primary molars and 64 premolars were used. Two adhesive systems and resin composites were used; SE: Clearfil SE (Kuraray) and Clearfil APX (Kuraray), and SB: Single Bond (3M) and Z250 (3M). Six groups were prepared. Groups 1-2 were primary dentin and Groups 3-6 were permanent dentin. Groups 1 and 3: SE was used. Groups 2 and 4: treated with Carisolv and then primed, SE was used. Group 5: SB was used. Group 6: treated with Carisolv and then etched, SB was used. The microstructural effects of primer or etchant, and Carisolv plus primer or etchant applied to dentin were evaluated by SEM. In addition, the microstructure of the resin-dentin interfaces of each group was studied using SEM. Shear bond strengths (SBS) were tested, and the failed surfaces were observed using SEM. Data was statistically analyzed using ANOVA with subsequent application of Fisher's PLSD at p<0.05. RESULTS: The mean SBS (unit: MPa) of Groups 1-6 were: 27.8, 19.2, 21.3, 21.7, 6.7 and 7.6. The SBS of Group 2 was significantly lower than that of Group 1. There was no significant difference of the SBS among Groups 1 and 4, 2, 3 and 4, and 5 and 6. In SE groups, the hybrid layer for primary dentin was thicker than that for permanent dentin. CONCLUSIONS: Carisolv treatment before priming significantly decreased the SBS to primary dentin in SE groups, but did not influence the SBS to permanent dentin in both SE and SB groups.

Phylogenetic analysis of mitochondrial DNA in Japanese pedigrees of sensorineural hearing loss associated with the A1555G mutation.

Thirteen Japanese families (ten of which were from the northern part of Japan), with sensorineural hearing loss associated with the 1555 A to G (A1555G) mitochondrial mutation, a known cause of non-syndromic hearing loss, were phylogenetically analysed using data obtained by restriction fragment length polymorphism (RFLP) and D-loop sequencing of mitochondrial DNA (mtDNA). Various types of mtDNA polymorphism were detected by restriction enzymes and D-loop sequence. No common polymorphic pattern throughout the 13 families was found, though three families exhibited the same restriction patterns and the same sequence substitution in the D-loop. To find where each of the 13 families are situated in the phylogenetic tree, the 482-bp of D-loop sequence were compared with those of 62 normal Japanese subjects. Despite the three families mentioned above appearing to be clustered, the remaining 10 families were scattered along the phylogenetic tree. This indicates that there was no common ancestor for the 13 Japanese families bearing the A1555G mutation except three families, and that the A1555G mutation occurred sporadically and multiplied through evolution of the mtDNA in Japan. The present results showed that the common pathogenicity (hearing loss associated with the A1555G mutation) can occur sporadically in families which have different genetic backgrounds, even in the Japanese population.

Identification of two polyketide synthase gene clusters on the linear plasmid pSLA2-L in Streptomyces rochei.

The 200kb linear plasmid pSLA2-L was suggested to be involved in the production of two macrolide antibiotics, lankamycin (Lm) and lankacidin (Lc), in Streptomyces rochei 7434AN4. Hybridization experiments with the polyketide synthase (PKS) genes for erythromycin and actinorhodin identified two eryAI-homologous regions and an actI-homologous region on pSLA2-L. The nucleotide sequence of a 3.6kb SacI fragment carrying one of the eryAI-homologs revealed that it codes for part of a large protein with four domains for ketoreductase, acyl carrier protein, ketosynthase, and acyltransferase. Gene disruption confirmed that the two eryAI-homologs are parts of a large type-I PKS gene cluster for Lm. A 4.8kb DNA carrying the actI-homologous region contains four open reading frames (ORF1-ORF4) as well as an additional ORF, i.e. ORF5, which might code for a thioesterase. Deletion of the ORF2-ORF4 region showed that it is not involved in the synthesis of Lm or Lc. Thus, it was confirmed that pSLA2-L contains two PKS gene clusters for Lm and an unknown type-II polyketide.

Molecular cloning and expression in Streptomyces lividans of a streptomycin 6-phosphotransferase gene from a streptomycin-producing microorganism.

The gene encoding streptomycin 6-kinase involved in the self-resistance of the streptomycin-producing Streptomyces griseus HUT 6037 was cloned in the plasmid vector pIJ703. The resulting plasmid, pSP6, contained 2.5 kb inserts of S. griseus DNA. When streptomycin-susceptible S. lividans 1326 was retransformed with pSP6, all transformants produced streptomycin 6-kinase. Addition of streptomycin to the culture medium of S. lividans carrying pSP6 plasmid brought about a remarkable increase in streptomycin 6-kinase activity in the cell extracts. It is suggested from the results that the production of streptomycin 6-kinase in streptomycin producer was induced by streptomycin accumulated during cultivation.

Discrete cellular and subcellular localization of glutamine synthetase and the glutamate transporter GLAST in the rat vestibular end organ.

Glial cells play an important role in the removal and metabolism of synaptically released glutamate in the central nervous system (CNS). It is not clear how glutamate is handled at peripheral glutamate synapses, which are not associated with glia. Glutamate is a likely transmitter in the synapse between the hair cells and afferent dendrites of the vestibular end organ. Immunocytochemistry was performed to investigate the distribution at this site of the high affinity glutamate transporter GLAST and glutamate metabolizing enzyme glutamine synthetase. Confocal microscopy revealed that GLAST and glutamine synthetase were co-localized in supporting cells apposed to the immunonegative hair cells. Postembedding immunoelectron microscopy revealed that GLAST was heterogeneously distributed along the plasma membranes of the supporting cells, with higher concentrations basally (at the level of the afferent synapses) than apically. Both immunoreactivities were also present in non-neuronal cells in the vestibular ganglion. The present findings suggest that glutamate released at the afferent synapse of vestibular hair cells may be taken up by adjacent supporting cells and converted into glutamine. Thus, at this peripheral synapse, the supporting cells may carry out functions similar to those of glial cells in the CNS.

Fluctuating sensorineural hearing loss associated with enlarged vestibular aqueduct maps to 7q31, the region containing the Pendred gene.

The most common form of inner ear abnormality, enlarged vestibular aqueduct (EVA), is of particular interest because it is associated with characteristic clinical findings, including fluctuating and sometimes progressive sensorineural hearing loss and disequilibrium symptoms. Although EVA has been reported to be inherited in a recessive manner, nothing else is known about the genetic basis of this hearing loss. Here we report on the localization of the gene responsible for sensorineural hearing loss associated with EVA to chromosomal region 7q31, with maximum multipoint LOD score of 3.647. The EVA candidate gene region lies in a 1.7-cM interval between the flanking markers D7S501 and D7S2425. Interestingly, this region overlaps the region containing the gene responsible for Pendred syndrome, called PDS, which was identified recently. However, the present subjects did not fulfill the criteria for Pendred syndrome. It is hypothesized that different mutations within the PDS gene may cause different phenotypes ranging from EVA to the Mondini deformity seen in Pendred syndrome.

Nucleotide sequence of a principal sigma factor gene (hrdB) of Streptomyces griseus.

The hrdB homologue was isolated from a streptomycin-producing Streptomyces griseus 2247 strain, which is independent of A-factor. The nucleotide sequence of the cloned DNA fragment revealed the presence of an open reading frame (ORF) of 1,542bp, which predicted a primary product of 514 amino acids and Mr 56,100. The N-terminal sequence of the purified HrdB protein of S. griseus was identical to the amino acid sequence deduced from the nucleotide sequence. The deduced amino acid sequence contains an "rpoD box" conserved in the principal sigma factors of eubacteria, and shows high similarity to the hrdB products of S. coelicolor A3(2)(89.9%) and S. aureofaciens (88.1%). The cloned gene encodes a principal sigma factor of S. griseus. The promoter region was identified by using a promoter-probe vector and by means of primer extensions experiments. The transcription start point is located 158-bp upstream of the initiation codon.

Purification and characterization of RNA polymerase holoenzyme (E sigma B) from vegetative-phase mycelia of Streptomyces griseus.

RNA polymerase was purified from vegetative-phase mycelia of Streptomyces griseus by a series of ion-exchange chromatographies. By western blot analysis using antiserum against S. coelicolor HrdB, which is a principal sigma factor (sigma(hrdB)), the purified holoenzyme was found to contain sigmaB (=sigma(hrdB)) of S. griseus. Significant amounts of HrdB protein were, however, eluted from the DEAE column at lower concentrations of KCl than that required for for elution of the holoenzyme containing sigmaB, suggesting that sigmaB is dissociated from the core enzyme, or an excess amount of sigmaB exists in S.griseus cells. The holoenzyme containing sigmaB (EsigmaB) transcribed in vitro the dagA promoter of S. coelicolor, and the hardB and hsp70 promoters of S. griseus, suggesting that it is involved in transcription of the essential genes. EsigmaB may be a major form of RNA polymerase holoenzyme in the growing phase of S. griseus.

NMDA (NMDAR1) and AMPA-type (GluR2/3) receptor subunits are expressed in the inner ear.

Using receptor subunit-specific antibodies, the cellular localization of NMDA and AMPA type glutamate receptor subunits was studied within the rodent (rat, guinea pig) and non-human primate (monkey) inner ear. In the spiral and vestibular ganglion, almost all cells were immunoreactive for the NMDAR1 subunit and the AMPA type receptor subunit GluR2/3. This indicates that both NMDA and non-NMDA type glutamate receptors may be co-distributed in the primary afferent neuronal components, and are possibly involved in neurotransmission in the primary auditory and vestibular systems. This study also indicated the possible localizations of glutamate receptors in the nonneuronal cells in the inner ear, suggesting that some nonneuronal cells may also have the ability to mediate glutamate signalling.

Expression of NMDA receptor subunit mRNA in the vestibular ganglion of the rat and guinea-pig.

The expression of NMDA R1 receptor mRNA in the rat and guinea-pig vestibular ganglion was examined using in situ hybridization histochemistry. Most of the ganglion cells of both species were strongly labelled, supporting the view that NMDA-type glutamate receptors may be involved in the vestibular afferent neurotransmission.

Various glutathione S-transferase isoforms in the rat cochlea.

The localization of three glutathione S-transferase (GST) isoforms in the rat cochlea was examined using specific antibodies against each isoform. GST immunoreactivities were found in particular parts of the cochlea, including the intermediate cells and the basal cells of the stria vascularis and various types of fibrocytes in the spiral ligament. The different cell types showed varying combinations of GST isoforms. The GST immunopositive cells identified in the present study may play a central role in the metabolism and inactivation of endogenous and exogenous ototoxic compounds. The specific arrangements also indicated a possible contribution to the detoxification process in the form of a blood-labyrinth barrier.

Cell death in the inner ear associated with aging is apoptosis?

Programmed cell death (apoptosis) in the inner ear of senescence-accelerated mouse was identified using specific labeling of fragmented DNA (the TUNEL method). In spite of some inter-individual differences, the apoptotic cells were predominantly found in the phylogenetically newer part of the inner ear, the cochlea and the saccules. In the saccules, sensory hair cells as well as supporting cells were positively labeled. In the cochlea, positive staining was detected in inner and outer hair cells, pillar cells, Deiters' cells, interdental cells, the stria vascularis (marginal cells, intermediate cells, basal cells), and cells in Reissner's membrane. The present results suggest that age-related cell death, which may cause hearing impairment and dysequilibrium, is due to apoptosis occurring in the inner ear.

Immunoelectron microscopy of AMPA receptor subunits reveals three types of putative glutamatergic synapse in the rat vestibular end organs.

To characterize the synapses between hair cells and afferent nerve endings in the rat vestibular end organs, the ultrastructural localization of AMPA receptor subunits (GluR1-4) was examined by postembedding immunogold cytochemistry. Immunoreactivities for GluR2/3 and GluR4 were associated with the synapses between type I hair cells and the surrounding chaliceal nerve endings and with the bouton type nerve endings contacting type II hair cells. There was no detectable immunoreactivity for GluR1. A third type of immunoreactive synapse was found between the outer face of chalices and type II hair cells. While the linear densities of gold particles (particles per micrometer postsynaptic specialization) of bouton type endings and chaliceal nerve endings were the same, the former type of ending showed larger postsynaptic specializations and, hence, a higher number of receptor molecules. These data indicate that there are three types of putative glutamatergic synapse in the vestibular end organ.

Genetic and clinical features of sensorineural hearing loss associated with the 1555 mitochondrial mutation.

Five Japanese families showing aminoglycoside-induced hearing loss were genetically as well as clinically investigated. A mitochondrial mutation at nucleotide 1555 was found in 28 out of 32 subjects. One hundred American control subjects did not show any evidence of the mutation at nucleotide 1555, suggesting that the 1555 A-->G (A1555G) mitochondrial mutation may be found more frequently among populations in the Asian continent. Many subjects who harbor this mitochondrial mutation exhibit a mild, high-frequency, progressive hearing loss even without aminoglycoside injection. The results presented here appear to support the hypothesis that the A1555G mutation may play a more general role in causing hearing loss.

Bone destruction due to the rupture of a cholesteatoma sac: a pathogenesis of bone destruction in aural-cholesteatoma.

Severe bone destruction in a cholesteatoma is one of the characteristic clinical features. To clarify the mechanism of bone destruction in cholesteatoma, the matrix of cholesteatoma and the attached bone, obtained during middle ear surgery, was observed by light microscope. Rupture of the epithelial lining in a cholesteatoma and the escaping contents (keratin), which gave rise to intense characteristic granulations in subepithelial tissue, were found. Furthermore bone destruction was always found at the site of subepithelial tissue of cholesteatoma. From these facts, the escape of contents from the sac of cholesteatoma into the subepithelial layer is considered to be an important factor in the mechanism of bone destruction.

Histopathology of the inner ear in Usher's syndrome as observed by light and electron microscopy.

A case of Usher's syndrome, type 3, is described. Histologic study of the inner ear of the patient demonstrated hair cell loss in the basal turn, severe loss of spiral ganglion cells, widespread neural degeneration in the cochlea, and discrete collections of degenerating supporting cells in the organ of Corti. The pattern of neural degeneration bore some similarity to abnormalities in the retina in retinitis pigmentosa. However, the findings in the supporting cells had no obvious parallel to the findings in the retina in this disorder. The histopathology of Usher's syndrome has been equated with the Scheibe, or cochleosaccular, pattern of degeneration. However, the findings in the present case and a critical analysis of published data did not support this concept.

Three familial cases of hearing loss associated with enlargement of the vestibular aqueduct.

The present report describes three familial cases of recessive hearing loss associated with enlargement of the vestibular aqueduct (EVA). Six siblings from three families showed EVA. The common characteristic of these patients was the presence of congenital, high-frequency, fluctuating sensorineural hearing loss. These cases suggest that EVA may be a useful discriminator between different types of recessive hearing loss.