Evaluating the effect of polytetrafluoroethylene and extractum cepae-heparin-allantoin gel in peripheral nerve injuries in a rat model

BACKGROUND:Peripheral nerves can be injured by congenital, mechanical, thermal or chemical causes. Peripheral nerve injuries are increasing in frequency, particularly in countries that are becoming more industrialized. Nerve and extremity injuries result in work loss and high treatment costs, and can lead to separation of patients from their social environment. Failure of nerve repair causes muscle functional losses, sensory losses and painful neuropathies.OBJECTIVES:To compare the effects of condensed polytetrafluoroethylene (cPTFE) and cPTFE-extractum cepae-heparin-allantoin (cPTFE-EHA) gel compound on nerve and functional recovery, and the prevention of adhesion and scar tissue formation after total peripheral nerve injury repaired by primary suture in a rat model.RESULTS:cPTFE alone and cPTFE-EHA gel was found to provide better functional recovery and nerve regeneration compared with primary repair only. In the macroscopic evaluation, the cPTFE-EHA gel was found to have no negative effect on wound healing and, despite increasing extra-neural scar tissue and adhesions, it had no negative effect on nerve function; in addition, it facilitated functional recovery.CONCLUSIONS:Compared with the cPTFE application alone, the application of perineural cPTFE-EHA gel during peripheral nerve surgery appeared to provide better functional recovery without causing any significant changes in epineural and extraneural scar tissue formation.     

Human Herpesvirus 8–Related Primary Effusion Lymphoma After Liver Transplantation

Primary effusion lymphoma is a rare subclass of non‐Hodgkin lymphoma associated with human herpesvirus 8 infection and principally seen in human immunodeficiency virus–positive patients. We report on the case of a 72‐year‐old human immunodeficiency virus–negative male with a hepatic transplant 10 years prior, who presented with a symptomatic right‐sided pleural effusion and was found to have primary effusion lymphoma by flow cytometric and cytopathologic examination. Immunohistochemistry of his lymphoma cells was positive for human herpesvirus 8. Both he and his donor had no identifiable risk factors for human herpesvirus 8 infection. The patient was intolerant of antiviral therapy and chemotherapy, dying 7 months after diagnosis. Posttransplant primary effusion lymphoma is exceedingly rare and carries a very poor prognosis. Individualized treatment strategies are necessary given the scant body of published literature with guidance based solely on case reports.     

Intrarenal Surgery vs Percutaneous Nephrolithotomy in the Management of Lower Pole Stones Greater than 2 cm

Purpose

To compare the efficacy of RIRS and PNL in lower pole stones ≥2 cm. Materials and and Methods: A total of 109 patients who underwent PNL or RIRS for solitary lower pole stone between April 2009 and December 2012, were retrospectively analyzed. Lower pole stone was diagnosed with CT scan. Stone size was assessed as the longest axis of the stone. All patients were informed about the advantages, disadvantages and probable complications of both PNL and RIRS before the selection of the procedure. Patients decided the surgery type by themselves without being under any influences and written informed consent was obtained from all patients prior to the surgery. Patients were divided into two groups according to the patients’ preference of surgery type. Group 1 consisted of 77 patients who underwent PNL and Group 2 consisted of 32 patients treated with RIRS. Stone free statuses, postoperative complications, operative time and hospitalization time were compared in both groups.

Results

There was no statistical significance between the two groups in mean age, stone size, stone laterality, mean follow-up periods and mean operative times. In PNL group, stone-free rate was 96.1% at first session and 100% after the additional procedure. In Group 2, stone-free rate was 90.6% at the first procedure and 100% after the additional procedure. The final stone-free rates and operative times were similar in both groups.

Conclusions

RIRS should be an effective treatment alternative to PNL in lower pole stones larger than 2 cm, especially in selected patients.     

Migration of endotacker into the bladder 7 years after laparoscopic retroperitoneal burch application

Laparoscopy began to be used widely since the second half of 1990s as an alternative to laparotomy or vaginal approaches in incontinence and pelvic diseases in women, based on its claimed better success rates. Injuries were reported in the bladder, gastrointestinal system and the entry of the Verress cannula in early and late laparoscopic applications. De-novo urging, voiding dysfunctions, marked recurrences and surgical inefficiencies were observed in 5-year follow-ups after laparoscopic incontinence surgery. Although tension-free midurethral sling operations replaced open laparoscopic colposuspensions nowadays, laparoscopic colposuspension is still preferred in cases where simultaneous laparoscopic paravaginal repair or sacrocolpopexy is considered or where synthetic graft implantation is contraindicated. Moreover, meshes and endotackers are still frequently used in many laparoscopic applications in various clinics. The migration of the tacker used in mesh fixation in a patient where retroperitoneal laparoscopic Burch was performed 7 years ago due to stress urinary incontinence and the extraction of the ossified tacker from the bladder will be presented.     

Serum leptin levels in gastric cancer patients and the relationship with insulin resistance

Introduction

Serum leptin levels have been examined in various cancers, with conflicting results. However, there is limited information regarding serum leptin levels and insulin resistance in gastric cancer patients. Therefore, we aimed to investigate serum leptin levels, performance status, insulin levels and insulin resistance in patients with gastric cancer. In addition, we examined the relationship between these measurements and leptin levels.

Material and methods

Thirty-nine patients with gastric cancer and 30 control subjects were enrolled in the study. Serum leptin, total protein, albumin, growth hormone, insulin and glucose levels were measured. The homeostasis model assessment (HOMA) was used to assess insulin resistance.

Results

Serum levels of insulin, glucose and growth hormone and insulin resistance were significantly lower in gastric cancer patients than controls (p < 0.05 for all). In the Pearson correlation analysis, insulin resistance was found to be significantly correlated with serum leptin levels in gastric cancer patients (r = 0.320, p = 0.047). We observed a significant negative correlation between performance status and insulin resistance in patients with cachexia (r = –0.512, p = 0.030), while no association was found in non-cachectic patients.

Conclusions

We concluded that serum leptin levels are significantly lower in gastric cancer patients. In addition, gastric cancer patients have decreases in insulin levels, insulin resistance and growth hormone levels. This study found a positive association between serum leptin levels and insulin resistance. Moreover, there is a negative association between serum leptin levels and growth hormone levels. Thus, low insulin and growth hormone levels may suppress the production of leptin in gastric cancer patients.     

Effects of intra-abdominal pressure on adrenal gland function and morphology in rats

Intra-abdominal hypertension and abdominal compartment syndrome (IAH/ACS) are life-threatening conditions and caused by several clinical status. Although there is insufficient data regarding its effects on adrenal glands. This study aimed to identify whether elevated intra-abdominal pressure (IAP) caused any alteration on the morphology and function of adrenal glands in a rat model. Twenty four Sprague-Dawley male rats were included in the study. Animals were allocated into 4 groups. IAP was elevated to 15 mmHg for one hour and four hours in group 2 and 4. Group 1 and 3 were sham groups. Blood samples were taken for the assessment of plasma adrenaline, noradrenaline, and corticosterone levels and adrenalectomies were performed to evaluate apoptosis. Blood adrenaline, noradrenaline and corticosterone levels were significantly higher in the study groups compared with the sham groups. However, there were no significant changes in apoptotic index scores in the study groups as compared to sham groups. These results support that increased IAH leads to discharge of catecholamine and corticosterone from the adrenal glands. Failure to demonstrate similar changes in apoptotic index score may be concluded as apoptosis is not a leading pathway for impairment of adrenal glands during IAH period.     

Prepubertal Unilateral Gynecomastia: Report of 2 Cases

Prepubertal unilateral gynecomastia is an extremely rare condition. At present, its etiology and management strategy are not well known. Two unrelated prepubertal boys of ages 8 and 9 who presented with complaints of unilateral enlargement of breast tissue are reported. Physical examination, biochemical, hormonal and oncologic work-up findings were normal. Both patients were treated with peripheral liposuction successfully. Histopathological and immunohistochemical examinations showed benign fibroglandular gynecomastia and intensive (3+) estrogen receptor expression in 100% of periductal epithelial cells. Although an extremely rare and generally benign condition, patients with prepubertal unilateral gynecomastia should have a full endocrine and oncologic work-up.     

Delta MELD as a predictor of early outcome in adult-to-adult living donor liver transplantation

Background/AimsAn increased post-operative mortality risk has been reported among patients who undergo living donor liver transplantation (LDLT) with higher model for end-stage liver disease (MELD) scores. In this study, we investigated the effect of MELD score reduction on post-operative outcomes in patients with a high MELD (≥20) score by pre-transplant management.Materials and MethodsWe retrospectively analyzed 386 LDLT cases, and patients were divided into low-MELD (<20, n=293) vs. high-MELD (≥20, n=93) groups according to their MELD score at the time of index hospitalization. Patients in the high-MELD group were managed specifically according to a treatment algorithm in an effort to decrease the MELD score. Patients in the high-MELD group were further divided into 2 subgroups: (1) responders (n=34) to pre-transplant treatment with subsequent reduction of the MELD score by a minimum of 1 point vs. (2) non-responders (n=59), whose MELD score remained unchanged or further increased on the day of LDLT. Responders vs. non-responders were compared according to etiology, demographics, and survival.     

Evidence that Meningeal Mast Cells Can Worsen Stroke Pathology in Mice

Stroke is the leading cause of adult disability and the fourth most common cause of death in the United States. Inflammation is thought to play an important role in stroke pathology, but the factors that promote inflammation in this setting remain to be fully defined. An understudied but important factor is the role of meningeal-located immune cells in modulating brain pathology. Although different immune cells traffic through meningeal vessels en route to the brain, mature mast cells do not circulate but are resident in the meninges. With the use of genetic and cell transfer approaches in mice, we identified evidence that meningeal mast cells can importantly contribute to the key features of stroke pathology, including infiltration of granulocytes and activated macrophages, brain swelling, and infarct size. We also obtained evidence that two mast cell-derived products, interleukin-6 and, to a lesser extent, chemokine (C-C motif) ligand 7, can contribute to stroke pathology. These findings indicate a novel role for mast cells in the meninges, the membranes that envelop the brain, as potential gatekeepers for modulating brain inflammation and pathology after stroke.Stroke, the leading cause of adult disability and the fourth most common cause of death in the Unites States,^1,2 occurs when there is insufficient blood flow to the brain, and the resultant injury initiates a cascade of inflammatory events, including immune cell infiltration into the brain.^3–5 This post-stroke inflammation is a critical determinant of damage and recovery after stroke; understanding the interplay between the immune system and the brain after stroke holds much promise for therapeutic intervention.^4–7 However, successfully exploiting this therapeutic potential requires a detailed understanding of the interplay between the immune system and the brain after stroke.⁴An understudied but important aspect of this interplay is the role of meningeal-located immune cells in modulating brain pathology. The meninges have long been recognized as an anatomical barrier that protects the central nervous system (CNS). However, accumulating evidence suggests that the meninges are important for communication between the CNS and immune system during health and disease.^8–10 All blood vessels pass through the meningeal subarachnoid space before entering the brain, and this vascular connection and the close proximity of the meninges to the underlying parenchymal nervous tissue make them ideally located to act as a gatekeeper to modulate immune cell trafficking to the CNS. To support this gatekeeper function is evidence that the meninges modulate brain infiltration of T cells, neutrophils, and monocytes during meningitis and autoimmune conditions,^11–14 with immune cells observed in some instances accumulating in the meninges before they infiltrate into the parenchyma.^11,13Emerging evidence suggests that the actions of immune cells resident in the meninges are important for this gatekeeper function.^11,12,15 Mast cells (MCs), best known as proinflammatory effector cells, can play critical roles in the development of inflammation in many disease settings.^16–18 MCs reside in high numbers within the meninges, but their function in this site has not been fully investigated in stroke pathology. Unlike most immune cells, mature MCs do not circulate in the blood but are long-term residents of tissues, often in perivascular locations, and can rapidly perform their functions in situ. CNS MCs are found in the brain parenchyma and the meninges of rodents and humans.¹⁸ It has been proposed that brain parenchymal MCs can enhance brain neutrophil numbers after stroke and can exacerbate stroke pathology.^19–24 However, much of the evidence to support such conclusions is indirect. For example, some of the studies that implicate MCs in stroke pathology used pharmacologic approaches to interfere with MC activation,^19,20,22 but such drugs can have effects on other cell types.²⁵ Moreover, the role of the meningeal MCs in modulating post-stroke inflammation and pathology is unknown. Finally, little is understood about which among the many MC-derived mediators may be important in stroke pathology.^17,26To address these questions, we used genetic and cell transfer approaches to study the role of MCs in the pathology of ischemic stroke in mice. Specifically, we tested a c-kit–mutant mouse model (ie, WBB6F₁-Kit^W/W-v mice) which is profoundly MC deficient and can be repaired of this deficiency by engraftment of in vitro-derived MCs from wild-type (WT) mice. This MC knock-in approach enables the MC-dependent effects in the mutant mice to be separated from effects due to other abnormalities associated with their mutation,^11,17,26,27 because only the MC deficiency is repaired by MC engraftment. Furthermore, one can investigate the mechanisms by which MCs influence stroke pathology by engrafting MCs from transgenic mice that lack specific MC-associated products. We also tested our newly described Cpa3-Cre; Mcl-1^fl/fl mice, in which MC (and basophil) numbers are reduced constitutively via Cre-mediated depletion of the anti-apoptotic factor, myeloid cell leukemia sequence 1 (Mcl-1), in the affected lineages.²⁸ Cpa3-Cre; Mcl-1^fl/fl mice lack the other abnormalities associated with the c-kit mutations in WBB6F₁-Kit^W/W-v mice.²⁸With the use of these in vivo models, we identified meningeal MCs as important contributors to key features of stroke pathology, including increased numbers of brain granulocytes and activated macrophages, brain swelling, and infarct size. We also obtained evidence that two potentially proinflammatory MC-derived products, IL-6 and, to a lesser extent, chemokine (C-C motif) ligand 7 (CCL7), can contribute to pathology in this setting.