The organization of colposcopy services in Ontario: recommended framework.

OBJECTIVE: The purpose of this guideline is to help ensure the provision of high-quality colposcopy practices in the province of Ontario, including those conducted as diagnostic procedures in follow-up to an abnormal cervical screening test. METHODS: This document updates the recommendations published in the 2008 colposcopy guideline from Cancer Care Ontario, The Optimum Organization for the Delivery of Colposcopy Service in Ontario. A systematic review of guidelines was conducted to evaluate the existing evidence and recommendations concerning these key aspects of colposcopy: □ Training, qualification, accreditation, and maintenance of competence□ Practice setting requirements□ Operational practice□ Quality indicators and outcomes. RESULTS: This guideline provides recommendations on training and maintenance of competence for colposcopists in the practice settings in which colposcopic evaluation and treatments are conducted. It also provides recommendations on operational issues and quality indicators for colposcopy. CONCLUSIONS: This updated guideline is intended to support quality improvement for colposcopy for all indications, including the follow-up of an abnormal cervical screening test and work-up for lower genital tract lesions that are not clearly malignant. The recommendations contained in this document are intended for clinicians and institutions performing colposcopy in Ontario, and for policymakers and program planners involved in the delivery of colposcopy services.

Limb regeneration in salamanders and digital tip regeneration in experimental mice: implications for the hand surgeon.

UNLABELLED: Several lessons and observations from limb regeneration in animals could open new insights to direct related research in the field of hand surgery. This article briefly reviews the biology of limb regeneration in salamanders and experimental mice, with special emphasis on implications for hand surgery. LEVEL OF EVIDENCE: 5.

Correlation of TGF beta 1 overexpression with down-regulation of proliferation-inducing molecules in HPV-11 transformed human tissue xenografts.

The epidemiologic association of human papillomavirus (HPV) infection with dysplasia and cervical cancer is well established. Transforming growth factor beta 1 (TGF beta 1) has regulatory effects on a broad spectrum of cell types and is a growth inhibitory protein for epithelial cells. To examine the phenotype of experimentally generated, HPV-11 transformed human tissues, we looked at expression of TGF beta 1 and a number of proliferation-enhancing molecules which are known to be regulated by TGF beta 1, including bcl-2, c-myc, c-Ha-ras, c-jun and NFkB. HPV-11 transformed xenografts showed up-regulation of TGF beta 1 expression and down-regulation of the expression levels of bcl-2, c-myc, c-Ha-ras, c-jun and NFkB. These results suggest that TGF beta 1 may exert antiproliferative effects on HPV-11 transformed papillomas by down-regulating different proliferation-enhancing molecules.

Transforming growth factor beta 1 (TGF beta 1) down-regulates expression and function of proliferation-inducing molecules in HPV-transformed cells.

The epidemiologic association of human papillomavirus (HPV) infection with dysplasia and cervical cancer is well established. Transforming growth factor beta 1 (TGF beta 1) is a growth inhibitory protein for epithelial cells. To examine the phenotype of HPV-transformed cells, we examined expression of TGF beta 1 and a number of cellular proliferation-enhancing molecules which are known to be regulated by TGF beta 1, including bcl-2, c-jun and NFkB. Previous studies had identified significant induction of TGF beta 1 and concomitant down-regulation of other growth stimulatory molecules in experimental papillomas. We used HPV-16 and -18 transformed cell lines. The HPV-16 transformed cells showed down-regulation of bcl-2 and NFkB as well as NFkB function upon TGF beta 1 treatment. The results suggest that TGF beta 1 may exert antiproliferative effects on some HPV-transformed cells by down-regulating expression and function of different proliferation-enhancing molecules. It is uncertain if this function is virus type specific and/or related to state of tumor cell progression.

Fat embolism syndrome: traumatic coagulopathy with respiratory distress.

Fractures and other types of trauma can cause severe metabolic, platelet, coagulative, and pulmonary changes. These changes are variable but tend to increase with the severity of the trauma and may result in the clinical findings often referred to as the fat embolism syndrome. The role in pathogenesis of increased liberation of lipids into the bloodstream, either from the marrow at the fracture site or because of physiochemical changes in the blood and mobilization of fat stores, has received a great deal of attention. These changes, however, may not be as important as the platelet activation and intravascular coagulation that occurs simultaneously. All of these phenomena appear to impair pulmonary function and cause hypoxemia. The results of treatment of the fat embolism syndrome should improve if there is a realization that even relatively uncomplicated fractures of the extremities cause significant metabolic, platelet, coagulation and pulmonary changes. These asymptomatic or subclinical forms of fat embolism are far more frequent than generally appreciated. Evidence of increasing platelet, coagulation or blood gas changes should alert the physician to begin aggressive therapy. Particular emphasis must be placed on maintaining optimal ventilation, using ventilatory assistance early if needed. Aspirin or massive steroids may also be quite helpful, particularly if they are given before the fat embolism syndrome has become fully established.

The renal factor in the post-traumatic "fluid overload" syndrome.

Hypervolemia with hypertension often occurs 36-72 hours following massive blood and fluid replacement for hypovolemic shock. This syndrome of "fluid overload" has been attributed to the rapid intravascular flux of previously sequestered fluid in patients with impaired diuresis. This hypothesis was tested in 35 injured patients who received a mean of 9.3 L of blood and 17.4 L of salt during resucitation. The renal parameters measured soon after resuscitation included: 1) renal clearance of inulin (GFR), para-amino hippurate (ERPF), milliosmoles, sodium, and free water; 2) inulin space, renal vascular resistance (RVR), O2 consumption, renin, renal blood flow (RBF), and response to furosemide. Eighteen patients developed hypertension, hypervolemia, and respiratory insufficiency. When compared to the 17 normovolemic, non-hypertensive patients, the 18 hypervolemic patients had significantly increased RVR, with a significant decrease in RBF despite an increase in plasma volume and cardiac output. Furosemide produced less diuresis and natriuresis in the hypertensive patients. The balance between hypovolemia and "fluid overload" seemed percarious in the hypertensive patients. Peripheral renin and catecholamine levels were normal in both groups. Patients with post-traumatic "fluid overload" appear to have a combination of hypervolemia, respiratory insufficiency, hypertension, increased cardiac output, decreased extracellular fluid space, and decreased renal perfusion. These findings suggest that decreased interstitial fluid space compliance rather than "fluid overload" is the underlying factor leading to respiratory insufficiency. The therapeutic aspects of these findings are discussed.

Fat embolism prophylaxis: a study of four treatment modalities.

Significant coagulation and blood gas changes may occur with uncomplicated extremity fractures. To more accurately define the effect of therapy on these changes, a prospective study of 58 patients with uncomplicated fractures was undertaken. An initial group of 10 selected patients was studied to determine the changes with "standard therapy." The remaining 48 patients were then randomized into five groups: control, increased fluid intake, increased glucose intake, aspirin, and massive steroids. The patients were studied on 5 consecutive days. Treatment of patients in the latter four groups with aspirin or steroids resulted in significant normalization of blood gases, coagulation proteins, and platelet numbers when compared to controls. These measurements in patients treated with fluid loading or increased glucose intake were not significantly different from controls.

Renal hemodynamic response to furosemide in septic and injured patients.

Furosemide frequently is advocated as a prophylaxis against renal failure in septic and injured patients; this effect is thought to be secondary to an increase in renal blood flow. This postulate was tested within 72 hours of admission in 22 previously healthy patients with acute pancreatitis (two), massive trauma (ten), or severe sepsis (ten). Renal clearances of inulin (GFR), para-amino hippurate (ERPF), sodium (CNA), osmoles (COsm), and free water (CH2O) were measured in milliliters per minute before and after the intravenous infusion of furosemide (0.5 mg. per kilogram of body weight). Renal vein PAH levels (EPAH) in eight patients were used to calculate true renal plasma flow (TRPF), true renal blood flow (TRBF), and renal vascular resistance (RVR). Furosemide caused a significant increase in urine volume, CNa, and COsm; there were no significant changes in GFR, ERPF, RVR, TRBF, and EPAH. These findings also were observed when the patients were subgrouped according to elevated, normal, or low renal plasma flow and elevated renal vascular resistance. No significant changes were seen in EPAH, thus making a redistribution of renal blood flow unlikely. These studies indicate that furosemide has only a diuretic effect and no hemodynamic effect in the kidney; it has the potential of seriously reducing the circulatory volume and causing renal failure in critical patients.

Electrocoagulation of bleeding in the upper part of the gastrointestinal tract: a preliminary experimental clinical report.

Electrocoagulation of gastric or esophageal bleeding sites was evaluated in dogs using a flexible suction coagulator electrode passed through the endoscope using an electrocautery unit (Cameron-Miller model 80-7910). Acute and chronic coagulation studies in 25 dogs showed that electrocoagulation of both the esophageal and gastric mucosa was safe at an electrocautery unit setting of 5 for three to five seconds. This level of coagulation was successful in stopping bleeding created from actively bleeding esophageal and gastric mucosal defects by taking multiple large biopsy specimens. Based on these data, six patients with active bleeding gastric lesions have undergone mucosal coagulation. This successfully stopped the bleeding initially in all six patients; two patients rebled and required operative intervention within 48 hours. Further clinical evaluation is being implemented to determine its clinical role in the treatment of bleeding in the upper part of the gastrointestinal tract.