Management of penetrating pancreatic trauma: an 11-year experience of a level-1 trauma center

Introduction: We present our experience in the management of penetrating pancreatic injuries, focusing on factors related to complications and death.

Methods: Retrospective trauma registry-based analysis of 62 consecutive patients with penetrating pancreatic injuries during an 11-year period. Overall injury severity was assessed by the injury severity score (ISS) and the penetrating abdominal trauma index (PATI). Pancreatic injuries were graded according to the American Association for the Surgery of Trauma (AAST) Organ Injury Scaling (OIS). Complications were characterised using standardised definitions. Mortality was recorded as early (within 48 h after admission) and late (after 48 h).

Results: Thirty patients suffered gunshot wounds and 24 had grade I pancreatic injuries. Shotgun and gunshot wounds were more destructive than stab wounds (higher PATI, number of intraabdominal injuries and mortality). Seventeen patients died. Most deaths occurred within 1 h after admission due to massive bleeding and severe associated injuries. Only one death was potentially related to the pancreatic injury. Mortality rate also correlated with pancreatic injury grading. Sixty-one patients had associated intraabdominal injuries. Combined pancreaticoduodenal injuries were present in 13 patients, and five died. Simple drainage was the most common procedure performed. Pancreas-related complications were found in 12 out of 47 patients who survived more than 48 h; intraabdominal abscess (n=7) that was associated with colon injuries, and pancreatic fistula (n=5).

Conclusion: An approach based on injury grade and location is advised. Routine drainage is recommended; distal resection is indicated in the presence of main duct injury, and the management of severe injuries will be tailored according to the overall physiologic status, presence of associated injuries, and duodenal viability. Morbidity and mortality is mainly due to associated injuries.     

Neuronal uptake of [3H]GABA and [3H]glycine in laminae I-III (substantia gelatinosa Rolandi) of the rat spinal cord. An autoradiographic study

[3H]GABA or [3H]glycine were injected into the subarachnoidal space of adult rats at C4-C5 level. After 10-60 min, the animals were perfused with 4% paraformaldehyde-0.5% glutaraldehyde and thick sections of the cervical spinal cord were postosmicated and Epon embedded. Light microscope autoradiographs of transverse cord sections showed numerous silver grains over the dorsal column and laminae I-III, higher grain densities occurring over lamina I for GABA and lamina III for glycine. In [3H]GABA-injected animals nerve cell bodies in lamina I or at the transition to lamina II appeared strongly labeled in light and electron microscope autoradiographs. These cells were smaller and less rich in RER than marginal cells and poor in axosomatic synaptic contacts. High grain densities appeared over axon terminals synapsing with dendrites in laminae I-II and over the light peripheral axon endings of synaptic glomeruli of laminae II-III. After [3H]glycine treatment, a number of nerve cell bodies were labeled in lamina III. It is suggested that two types of inhibitory interneurons occur in the rat gelatinosa, one GABAergic with cell body in lamina I, and another glycinergic in lamina III.     

Effect of endogenous hydrogen sulfide inhibition on structural and functional renal disturbances induced by gentamicin

Animal models of gentamicin nephrotoxicity present acute tubular necrosis associated with inflammation, which can contribute to intensify the renal damage. Hydrogen sulfide (H₂S) is a signaling molecule involved in inflammation. We evaluated the effect of DL-propargylglycine (PAG), an inhibitor of endogenous H₂S formation, on the renal damage induced by gentamicin. Male Wistar rats (N = 8) were injected with 40 mg/kg gentamicin (im) twice a day for 9 days, some of them also received PAG (N = 8, 10 mg·kg⁻¹·day⁻¹, ip). Control rats (N = 6) were treated with saline or PAG only (N = 4). Twenty-four-hour urine samples were collected one day after the end of these treatments, blood samples were collected, the animals were sacrificed, and the kidneys were removed for quantification of H₂S formation and histological and immunohistochemical studies. Gentamicin-treated rats presented higher sodium and potassium fractional excretion, increased plasma creatinine [4.06 (3.00; 5.87) mg%] and urea levels, a greater number of macrophages/monocytes, and a higher score for tubular interstitial lesions [3.50 (3.00; 4.00)] in the renal cortex. These changes were associated with increased H₂S formation in the kidneys from gentamicin-treated rats (230.60 ± 38.62 µg·mg protein⁻¹·h⁻¹) compared to control (21.12 ± 1.63) and PAG (11.44 ± 3.08). Treatment with PAG reduced this increase (171.60 ± 18.34), the disturbances in plasma creatinine levels [2.20 (1.92; 4.60) mg%], macrophage infiltration, and score for tubular interstitial lesions [2.00 (2.00; 3.00)]. However, PAG did not interfere with the increase in fractional sodium excretion provoked by gentamicin. The protective effect of PAG on gentamicin nephrotoxicity was related, at least in part, to decreased H₂S formation.     

Quantitation of infectious myonecrosis virus in different tissues of naturally infected Pacific white shrimp, Litopenaeus vannamei, using real-time PCR with SYBR Green chemistry

The Pacific white shrimp, Litopenaeus vannamei, is the most important shrimp species in volume in world aquaculture. However, in recent decades, outbreaks of diseases, especially viral diseases, have led to significant economic losses, threatening the sustainability of shrimp farming worldwide. In 2004, Brazilian shrimp farming was seriously affected by a new disease caused by the Infectious myonecrosis virus (IMNV). Thus, disease control based on rapid and sensitive pathogen detection methods has become a priority. In this study, a specific quantitation method for IMNV was developed using real-time PCR with SYBR Green chemistry and viral load of the principal target tissues of chronically infected animals was quantified. The quantitative analysis revealed that mean viral load ranged from 5.08 × 10⁸ to 1.33 × 10⁶ copies/μg of total RNA in the hemolymph, 5.096 × 10⁵ to 1.26 × 10³ copies/μg in the pleopods, 6.85 × 10⁸ to 3.09 × 10⁴ copies/μg in muscle and 8.15 × 10⁶ to 3.90 × 10³ copies/μg in gills. Different viral loads of IMNV were found with greater values in the hemolymph and muscle, followed by the pleopods and gills.     

Importance of the cutoff ratio for detecting antibodies against hepatitis A virus in oral fluids by enzyme immunoassay

Multiple studies have examined the use of oral fluids in modified serum-based assays aiming to replace serum in antibody detection for hepatitis A. However, the reliable detection of HAV immunity in oral fluid requires an extremely sensitive assay; most immunoassays designed for serum antibody determination lack sufficient sensitivity for this purpose. Consequently, an “in-house” competitive enzyme immunoassay (EIA) designed specifically for use with oral samples collected using a ChemBio^® device was developed to detect total anti-HAV antibodies (IgG and IgM). This system was compared to an in-house competitive EIA and a commercial EIA considered to be the “gold standard” using corresponding serum samples (n = 225) to determine the accuracy of the assay and to evaluate the importance of the cutoff ratio for the detection of anti-HAV antibodies in oral fluids. When the median serum cutoff and the optimal oral fluid cutoff (ROC analysis) obtained from the in-house competitive EIA were compared, the oral fluid cutoff was found to be 28.8% higher than the serum cutoff. When different oral fluid cutoff values were compared, a reduction of about 17% was shown to be essential to increase test accuracy. At an oral fluid cutoff value of 0.351, sensitivity and specificity were higher, reaching 91.7% and 86.2% (p < 0.001, AUROC = 0.915), respectively. The convenience, accuracy and non-invasive nature of the developed method make it a useful alternative to serum-based assays for discriminating between HAV-immune and non-immune individuals.     

Pectus deformities: tomographic analysis and clinical correlation

Objective  

To assess, with computed tomography (CT) studies, features of anterior chest wall development that can be related to different types of pectus deformities.     

NCOA2 is a candidate target gene of 8q gain associated with clinically aggressive prostate cancer

Prostate carcinomas harboring 8q gains are associated with poor clinical outcome, but the target genes of this genomic alteration remain to be unveiled. In this study, we aimed to identify potential 8q target genes associated with clinically aggressive prostate cancer (PCa) using fluorescence in situ hybridization (FISH), genome‐wide mRNA expression, and protein expression analyses. Using FISH, we first characterized the relative copy number of 8q (assessed with MYC flanking probes) of a series of 50 radical prostatectomy specimens, with available global gene expression data and typed for E26 transformation specific (ETS) rearrangements, and then compared the gene expression profile of PCa subsets with and without 8q24 gain using Significance Analysis of Microarrays. In the subset of tumors with ERG fusion genes (ERG+), five genes were identified as significantly overexpressed (false discovery rate [FDR], ≤5%) in tumors with relative 8q24 gain, namely VN1R1, ZNF417, CDON, IKZF2, and NCOA2. Of these, only NCOA2 is located in 8q (8q13.3), showing a statistically higher mRNA expression in the subgroup with relative 8q gain, both in the ERG+ subgroup and in the whole series (P = 0.000152 and P = 0.008, respectively). Combining all the cases with NCOA2 overexpression, either at the mRNA or at the protein level, we identified a group of tumors with NCOA2 copy‐number increase, independently of ETS status and relative 8q24 gain. Furthermore, for the first time, we detected a structural rearrangement involving NCOA2 in PCa. These findings warrant further studies with larger series to evaluate if NCOA2 relative copy‐number gain presents prognostic value independently of the well‐established poor prognosis associated with MYC relative copy‐number gain. © 2016 Wiley Periodicals, Inc.     

Long-term evolution of the acute tubular necrosis (ATN) induced by glycerol: role of myofibroblasts and macrophages

Late structural changes such as interstitial fibrosis in the renal cortex and tubular atrophy have been detected after severe acute tubular necrosis (ATN). The aim of this study was to investigate the expression of fibronectin, alpha-smooth muscle actin and macrophages during the evolution of the ATN induced by glycerol and their relationship with the late structural changes observed in the kidneys of these animals. Forty-nine male Wistar rats were injected with a 50% glycerol solution, 8 mL/kg (4 mL/kg applied i.m. to each hind leg) and 14 with 0.15 m NaCl solution. Before glycerol injection on day 1, water was removed for 17 h. Blood and urine samples were collected 1 day after the injection to quantify sodium and creatinine. The animals were killed 5, 30 and 60 days after the injections and the kidneys removed for histological and immunohistochemical studies. The results of the histological and immunohistochemical studies were scored according to the extent of lesion or staining in the cortical tubulointerstitium, respectively. The percentage of tubulointerstitial lesions was determined by morphometry. Glycerol-injected rats presented a transitory increase in plasma creatinine levels and in fractional sodium excretion. The immunohistochemical studies showed increased fibronectin, alpha-smooth muscle actin (alpha-SM-actin), TGF-beta and ED-1 (macrophages) staining in the renal cortex from rats killed 5, 30 and 60 days after glycerol injection (P < 0.05) compared to control. The animals killed on day 30 and 60 also presented chronic lesions (fibrosis, tubular dilatation and atrophy) in the renal cortex, despite the recovery of renal function. Macrophages, TGF-beta and myofibroblasts may have contributed to the development of renal fibrosis in these rats.     

Carboxymethylation of ulvan and chitosan and their use as polymeric components of bone cements

Ulvan, extracted from the green algae Ulva lactuca, and chitosan, extracted from Loligo forbesis squid-pen, were carboxymethylated, yielding polysaccharides with an average degree of substitution of ～98% (carboxymethyl ulvan, CMU) and ～87% (carboxymethyl chitosan, N,O-CMC). The carboxymethylation was confirmed by Fourier transform infrared spectroscopy and quantified by conductimetric titration and ¹H nuclear magnetic resonance. The average molecular weight increased with the carboxymethylation (chitosan, M_n 145→296 kDa and M_w 227→416 kDa; ulvan, M_n 139→261 kDa and M_w 368→640 kDa), indicating successful chemical modifications. Mixtures of the modified polysaccharides were tested in the formulation of polyacrylic acid-free glass-ionomer bone cements. Mechanical and in vitro bioactivity tests indicate that the inclusion of CMU in the cement formulation, i.e. 0.50:0.50 N,O-CMC:CMU, enhances its mechanical performance (compressive strength 52.4 ± 8.0 MPa and modulus 2.3 ± 0.3 GPa), generates non-cytotoxic cements and induces the diffusion of Ca and/or P-based moieties from the surface to the bulk of the cements.