Gallbladder injury

The Authors report on a rare case of blunt traumatic injury of the gallbladder. A careful clinical examination, an abdominal ultrasonography and a contrast material-enhanced computed tomography have a primary importance for a correct diagnosis. Laparoscopic surgery has an important diagnostic and, in selected cases, therapeutic role. In all traumatic gallbladder ruptures, after an accurate search of eventual associated injuries of other abdominal organs, cholecystectomy is considered the treatment of choice.     

Angiotensin II increases parathyroid hormone-related protein (PTHrP) and the type 1 PTH/PTHrP receptor in the kidney

Angiotensin II (AngII) participates in the pathogenesis of kidney damage. Parathyroid hormone (PTH)-related protein (PTHrP), a vasodilator and mitogenic agent, is upregulated during renal injury. The aim of this study was to investigate the potential relation between AngII and PTHrP system in the kidney. Different methods were used to find that both rat mesangial and mouse tubuloepithelial cells express PTHrP and the type 1 PTH/PTHrP receptor (PTH1R). In these cells, AngII increased PTHrP mRNA and protein production. In contrast, PTH1R mRNA was increased in mesangial cells and downregulated in tubular cells, but its protein levels were unmodified in both cells. AT(1) antagonist, but not AT(2), abolished AngII effects on PTHrP/PTH1R. The in vivo effect of AngII was further investigated by systemic infusion (a low dose of 50 ng/kg per min) into normal rats. In controls, PTHrP immunostaining was mainly detected in renal tubules. In AngII-infused rats, PTHrP staining increased in renal tubules and appeared in the glomerulus and the renal vessels. After AngII infusion, PTHR1 staining was markedly increased in all these renal structures at day 3 but remained elevated only in tubules at day 7. The AT(1) antagonist, but not the AT(2), significantly diminished AngII-induced PTHrP and PTHR1 overexpression in the renal tissue, associated with a decrease in tubular damage and fibrosis. The results indicate that AngII regulates renal PTHrP/PTH1R system via AT(1) receptors. These findings demonstrate that PTHrP upregulation occurs in association with the mechanisms of AngII-induced kidney injury.     

Prevention of bronchiolitis obliterans in rat lung allografts by type V collagen-induced oral tolerance

BACKGROUND: We have reported that feeding type V collagen (col(V)) to lung allograft recipients induces immune tolerance that prevents acute lung allograft rejection. Repeated acute rejection is a risk factor for or associated with chronic rejection, known as bronchiolitis obliterans (BO), the leading cause of death in lung allograft recipients. The current study examines if col(V)-induced oral tolerance prevents BO. METHODS: WKY rats (RT1l) were fed either col(V) or diluent before orthotopic transplantation of F344 (RT1lvl) lung allografts. No rats received any immunosuppression. At 10 weeks posttransplantation the time to onset of BO, delayed type hypersensitivity (DTH) responses to donor antigens, and col(V) were examined. In addition, proliferative responses of recipient T lymphocytes to donor antigens, and ability of recipient antigen presenting cells to present alloantigens in lung allografts were evaluated. RESULTS: The data show that recipient rats have sustained DTH responses to donor antigens and col(V). T lymphocytes from col(V)-fed lung allograft recipients were unable to proliferate in response to donor antigens, but feeding col(V) had no effect on the presentation of donor alloantigens by recipient antigen presenting cells. All diluent fed rats developed BO, but only mild acute rejection (grade 2) was present in all rats fed col(V). Transforming growth factor (TGF)-beta production was up-regulated systemically in col(V)-fed, but not diluent fed, lung allograft recipients, and neutralizing TGF-beta [corrected] recovered the DTH response to donor antigens in col(V)-fed rats. CONCLUSIONS: Collectively these data show that col(V)-induces oral tolerance that prevents BO, and that tolerance may be mediated by systemic production of TGF-beta [corrected].     

Low-pressure laparoscopy may ameliorate intracranial hypertension and renal hypoperfusion

BACKGROUND: Increased abdominal pressure is associated with elevations in the intracranial pressure (ICP) and impaired renal function. These adverse effects are potentially important in clinical situations such as severe abdominal trauma and laparoscopic donor nephrectomy. It was hypothesized that the secondary elevation of ICP leads to release of vasoconstrictors, which may affect renal function by decreasing the renal blood flow (RBF). We investigated the effect of laparoscopy on ICP and renal blood flow in a porcine model. MATERIALS AND METHODS: The abdominal pressure of swine (N = 5; 20-25 kg) was gradually increased from baseline to 5, 15, and 25 mm Hg by insufflation of nitrogen into the abdominal cavity. The ICP was measured using a Camino monitor, and RBF was simultaneously measured using a Transonic Doppler probe placed on the renal artery. Results were analyzed using repeated measures ANOVA and the paired t-test. RESULTS: No significant change from baseline was observed in ICP and RBF when the abdominal pressure was 5 mm Hg. However, both ICP and RBF were affected by increasing the abdominal pressure to 15 and 25 mm Hg (P = 0.035 and 0.04 for ICP and P = 0.074 and 0.034 for RBF, respectively). CONCLUSIONS: Low-pressure laparoscopy may reduce the adverse effects of pneumoperitoneum on ICP and RBF. It may be advisable to use low pressures in laparoscopic surgery, especially when changes in ICP or renal perfusion may have significant clinical implications.     

Chemokines and diabetic wound healing

Chemokines are critical for white blood cell recruitment to injured tissues and play an important role in normal wound healing processes. In contrast, impaired wound healing in diabetic patients is accompanied by decreased early inflammatory cell infiltration but persistence of neutrophils and macrophages in the chronic, nonhealing wounds. These changes in inflammatory cell recruitment occur in conjunction with alterations in chemokine and growth factor expression. In addition to leukocyte trafficking, many different cell types, including endothelial cells, fibroblasts, and keratinocytes, produce and respond to chemokines, and these interactions are altered in diabetic wounds. Thus, the chemokine system may have both direct and inflammatory-mediated effects on many different aspects of diabetic wound healing. The potential roles of chemokines and inflammatory or immune cells in nonhealing diabetic wounds, including impairments in growth factor expression, angiogenesis, extracellular matrix formation, and reepithelialization, are examined.     

The extended brow lift: the toucan technique

Brow ptosis is the main consequence of aging in the upper third of the face. Many methods have been described to correct it: skin excisions of the brow hairline, skin excisions of the forehead natural creases, skin trimmings of the temporal, coronal, or forehead hairline flaps, and endoscopic methods [1,15,17,18,24,26,27]. The authors created a procedure which is based on a forehead-temporal subcutaneous flap and a muscular relocation. It treats the brow ptosis and its surrounding area—temporal ptosis, upper and lower lateral eyelid ptosis, crow's feet—and at the same time improves the sclera show or ectropion. The method preserves the sideburn and the temporal hairline and can reduce the width between the temporal hairline and the lateral end of the eyebrow. The method produces maximum improvement, with high-quality scars and minimal evidence of surgery. The procedure is called "The Toucan Technique," due to the shape of the skin resection which looks like a toucan bird [11,13,14].     

The Impact of Financial Conflict of Interest on Surgical Research: An Observational Study of Published Manuscripts

Background

Substantial discrepancies exist between industry-reported and self-reported conflicts of interest (COI). Although authors with relevant, self-reported financial COI are more likely to write studies favorable to industry sponsors, it is unknown whether undisclosed COI have the same effect. We hypothesized that surgeons who fail to disclose COI are more likely to publish findings that are favorable to industry than surgeons with no COI.

Methods

PubMed was searched for articles in multiple surgical specialties. Financial COI reported by surgeons and industry were compared. COI were considered to be relevant if they were associated with the product(s) mentioned by an article. Primary outcome was favorability, which was defined as an impression favorable to the product(s) discussed by an article and was determined by 3 independent, blinded clinicians for each article. Primary analysis compared incomplete self-disclosure to no COI. Ordered logistic multivariable regression modeling was used to assess factors associated with favorability.

Results

Overall, 337 articles were reviewed. There was a high rate of discordance in the reporting of COI (70.3%). When surgeons failed to disclose COI, their conclusions were significantly more likely to favor industry than surgeons without COI (RR 1.2, 95% CI 1.1–1.4, p < 0.001). On multivariable analysis, any COI (regardless of relevance, disclosure, or monetary amount) were significantly associated with favorability.

Conclusions

Any financial COI (disclosed or undisclosed, relevant or not relevant) significantly influence whether studies report findings favorable to industry. More attention must be paid to improving research design, maximizing transparency in medical research, and insisting that surgeons disclose all COI, regardless of perceived relevance.

     

Mechanisms of vascular dysfunction in the interleukin-10–deficient murine model of preeclampsia indicate nitric oxide dysregulation

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