Surgical site infection in spinal surgery: a comparative study between 2-octyl-cyanoacrylate and staples for wound closure

Background

Surgical site infection (SSI) after spinal surgery is a devastating complication. Various methods of skin closure are used in spinal surgery, but the optimal skin-closure method remains unclear. A recent report recommended against the use of metal staples for skin closure in orthopedic surgery. 2-Octyl-cyanoacrylate (Dermabond; Ethicon, NJ, USA) has been widely applied for wound closure in various surgeries. In this cohort study, we assessed the rate of SSI in spinal surgery using metal staples and 2-octyl-cyanoacrylate for wound closure.

Methods

This study enrolled 609 consecutive patients undergoing spinal surgery in our hospital. From April 2007 to March 2010 surgical wounds were closed with metal staples (group 1, n = 294). From April 2010 to February 2012 skin closure was performed using 2-octyl-cyanoacrylate (group 2, n = 315). We assessed the rate of SSI using these two different methods of wound closure. Prospective study of the time and cost evaluation of wound closure was performed between two groups.

Results

Patients in the 2-octyl-cyanoacrylate group had more risk factors for SSI than those in the metal-staple group. Nonetheless, eight patients in the metal-staple group compared with none in the 2-octyl-cyanoacrylate group acquired SSIs (p < 0.01). The closure of the wound in length of 10 cm with 2-octyl-cyanoacrylate could save 28 s and $13.5.

Conclusions

This study reveals that in spinal surgery, wound closure using 2-octyl-cyanoacrylate was associated with a lower rate of SSI than wound closure with staples. Moreover, the use of 2-octyl-cyanoacrylate has a more time saving effect and cost-effectiveness than the use of staples in wound closure of 10 cm in length.     

Effects of tank color on melanin-concentrating hormone levels in the brain, pituitary gland, and plasma of the barfin flounder as revealed by a newly developed time-resolved fluoroimmunoassay

A pleuronectiform fish, the barfin flounder Verasper moseri, reared in a white tank had a smaller ratio of pigmented area of the skin on non-eyed side, grew faster, and had greater melanin-concentrating hormone (MCH)-immunoreactive cell bodies and MCH gene expression in the brain than in the black tank, indicating that synthesis and release of MCH are higher in fish from a white tank. In the present study, a time-resolved fluoroimmunoassay for MCH was developed. MCH levels were assessed in the brain, pituitary gland, and plasma of barfin flounders reared in a white or black tank. A competitive assay using two antibodies was performed among secondary antibodies in the solid phase, MCH antibodies, samples, and europium-labeled MCH. Displacement curves of serially diluted extracts (brain, pituitary gland, and plasma) of the barfin flounder paralleled that of the MCH standard. MCH levels in the brain and plasma were higher in fish reared in the white tank for 5 months than in the black tank. These results suggest that synthesis and secretion of MCH are enhanced with the white background and that MCH is involved in both somatic growth and the skin pigmentation in the barfin flounder.     

P66shc regulates endothelial NO production and endothelium-dependent vasorelaxation: implications for age-associated vascular dysfunction

The p66shc adaptor protein mediates age-associated oxidative stress. We examined the role of p66shc in endothelial nitric oxide synthase (eNOS) signaling. Overexpression of p66shc inhibited eNOS-dependent NO production. RNAi-mediated down-regulation of endogenous p66shc led to activation of the proto-oncogene ras, and Akt kinase, with a corresponding increase in phosphorylation of eNOS at S1177 (S1179 on bovine eNOS). In rat aortic rings, down-regulation of p66shc suppressed the vasoconstrictor response to phenyephrine that was abrogated by treatment with the NOS inhibitor l-NAME, and enhanced vasodilation induced by sub-maximal doses of acetylcholine. These findings highlight a pivotal role for p66shc in inhibiting endothelial NO production, and endothelium-dependent vasorelaxation, that may provide important mechanistic information about endothelial dysfunction seen with aging.     

Hepatitis C virus JFH-1 strain infection in chimpanzees is associated with low pathogenicity and emergence of an adaptive mutation

The identification of the hepatitis C virus (HCV) strain JFH-1 enabled the successful development of infectious cell culture systems. Although this strain replicates efficiently and produces infectious virus in cell culture, the replication capacity and pathogenesis in vivo are still undefined. To assess the in vivo phenotype of the JFH-1 virus, cell culture-generated JFH-1 virus (JFH-1cc) and patient serum from which JFH-1 was isolated were inoculated into chimpanzees. Both animals became HCV RNA-positive 3 days after inoculation but showed low-level viremia and no evidence of hepatitis. HCV viremia persisted 8 and 34 weeks in JFH-1cc and patient serum-infected chimpanzees, respectively. Immunological analysis revealed that HCV-specific immune responses were similarly induced in both animals. Sequencing of HCV at various times of infection indicated more substitutions in the patient serum-inoculated chimpanzee, and the higher level of sequence variations seemed to be associated with a prolonged infection in this animal. A common mutation G838R in the NS2 region emerged early in both chimpanzees. This mutation enhances viral assembly, leading to an increase in viral production in transfected or infected cells. CONCLUSION: Our study shows that the HCV JFH-1 strain causes attenuated infection and low pathogenicity in chimpanzees and is capable of adapting in vivo with a unique mutation conferring an enhanced replicative phenotype.     

A case of invasive hemolymphangioma of the pancreas

Hemolymphangioma of the pancreas is a very rare benign tumor. There were only five reports of this disease until March 2008. Herein, we report a case of hemolymphangioma of the pancreas with gastrointestinal bleeding due to duodenal invasion. A 53-year-old man had been admitted a referral hospital because of severe anemia due to gastrointestinal bleeding in December 2005. He was then transferred to our institute with a diagnosis of a tumor of the head of the pancreas with duodenal invasion in January 2006. No abnormalities were revealed except for anemia in laboratory data including CEA and CA19-9. Gastrointestinal endoscopy revealed bleeding at the duodenum. Computed tomography also demonstrated a heterogenous mass at the pancreatic head and suspected invasion to the duodenal wall. Ultrasonography showed a huge mass at the pancreatic head with a mixture of high and low echoic areas. Pylorous-preserving pancreatoduodenectomy was performed. The pancreatic tumor was soft and had invaded to the duodenum. The pathological diagnosis was a hemolymphangioma of the pancreas invaded to the duodenum. His postoperative course was uneventful and he was discharged on the 26th d after surgery. Hemolymphangioma of the pancreas is a very rare benign tumor. In a literature review until March 2008, we found five case reports. Major symptoms are abdominal pain and distension due to the enlarged tumor. However, we experienced a case of hemolymphangioma of the pancreas with gastrointestinal bleeding due to invasion to the duodenum. This disease is a very rare entity, but should be considered when patients have gastrointestinal bleeding.     

Common variants at 1p36 are associated with superior frontal gyrus volume

The superior frontal gyrus (SFG), an area of the brain frequently found to have reduced gray matter in patients with schizophrenia, is involved in self-awareness and emotion, which are impaired in schizophrenia. However, no genome-wide association studies of SFG volume have investigated in patients with schizophrenia. To identify single-nucleotide polymorphisms (SNPs) associated with SFG volumes, we demonstrated a genome-wide association study (GWAS) of gray matter volumes in the right or left SFG of 158 patients with schizophrenia and 378 healthy subjects. We attempted to bioinformatically ascertain the potential effects of the top hit polymorphism on the expression levels of genes at the genome-wide region. We found associations between five variants on 1p36.12 and the right SFG volume at a widely used benchmark for genome-wide significance (P<5.0 × 10⁻⁸). The strongest association was observed at rs4654899, an intronic SNP in the eukaryotic translation initiation factor 4 gamma, 3 (EIF4G3) gene on 1p36.12 (P=7.5 × 10⁻⁹). No SNP with genome-wide significance was found in the volume of the left SFG (P>5.0 × 10⁻⁸); however, the rs4654899 polymorphism was identified as the locus with the second strongest association with the volume of the left SFG (P=1.5 × 10⁻⁶). In silico analyses revealed a proxy SNP of rs4654899 had effect on gene expression of two genes, HP1BP3 lying 3′ to EIF4G3 (P=7.8 × 10⁻⁶) and CAPN14 at 2p (P=6.3 × 10⁻⁶), which are expressed in moderate-to-high levels throughout the adult human SFG. These results contribute to understand genetic architecture of a brain structure possibly linked to the pathophysiology of schizophrenia.     

Enzyme replacement therapy on hypophosphatasia mouse model

Hypophosphatasia (HPP) is an inborn error of metabolism caused by deficiency of the tissue-nonspecific alkaline phosphatase (TNSALP), resulting in a defect of bone mineralization. Natural substrates for this ectoenzyme accumulate extracellulary including inorganic pyrophosphate (PPi), an inhibitor of mineralization, and pyridoxal 5-phosphate (PLP), a co-factor form of vitamin B6. Enzyme replacement therapy (ERT) for HPP by functional TNSALP is one of the therapeutic options. The C-terminal-anchorless human recombinant TNSALP derived from Chinese hamster ovary cell lines was purified. TNSALP-null mice (Akp2 ^-/- ), an infantile model of HPP, were treated from birth using TNSALP and vitamin B6 diet. Long-term efficacy studies of ERT consisted of every 3 days subcutaneous or intravenous injections till 28 days old (dose 20 U/g) and subsequently every 3 days intravenous injections for 6 months (dose 10 U/g). We assessed therapeutic effect by growth and survival rates, fertility, skeletal manifestations, and radiographic and pathological finding. Treated Akp2 ^-/- mice grew normally till 4 weeks and appeared well with a minimum skeletal abnormality as well as absence of epilepsy, compared with untreated mice which died by 3 weeks old. The prognosis of TNSALP-treated Akp2 ^-/- mice was improved substantially: 1) prolonged life span over 6 months, 2) improvement of the growth, and 3) normal fertility. After 6 months of treatment, we found moderate hypomineralization with abnormal proliferative chondrocytes in growth plate and articular cartilage. In conclusion, ERT with human native TNSALP improves substantial clinical manifestations in Akp2 ^-/- mice, suggesting that ERT with anchorless TNSALP is also a potential therapy for HPP.