Diminished medial prefrontal cortex activation during the recollection of stressful events is an acquired characteristic of PTSD.

BACKGROUND: Previous research has shown relatively diminished medial prefrontal cortex activation and heightened psychophysiological responses during the recollection of personal events in post-traumatic stress disorder (PTSD), but the origin of these abnormalities is unknown. Twin studies provide the opportunity to determine whether such abnormalities reflect familial vulnerabilities, result from trauma exposure, or are acquired characteristics of PTSD. METHODS: In this case-control twin study, 26 male identical twin pairs (12 PTSD; 14 non-PTSD) discordant for PTSD and combat exposure recalled and imagined trauma-unrelated stressful and neutral life events using a standard script-driven imagery paradigm during functional magnetic resonance imaging and concurrent skin conductance measurement. RESULTS: Diminished activation in the medial prefrontal cortex during Stressful v. Neutral script-driven imagery was observed in the individuals with PTSD, relative to other groups. CONCLUSIONS: Diminished medial prefrontal cortex activation during Stressful v. Neutral script-driven imagery may be an acquired characteristic of PTSD. If replicated, this finding could be used prospectively to inform diagnosis and the assessment of treatment response.

Factors Associated With Need for Revascularisation in Non-coronary Arterial Occlusive Lesions Secondary to Takayasu's Arteritis.

OBJECTIVE/BACKGROUND: Takayasu's arteritis (TA) is rare inflammatory large vessel form of vasculitis. The objective of this study was to evaluate experience in the management of TA patients and to identify the influence of inflammatory markers and clinical variables associated with disease progression, worsening ischaemic symptoms, and the need for interventions. METHODS: Demographics, and laboratory and clinical variables in patients that required revascularisation procedures were compared with those who had adequate symptomatic control with medical management. Categorical data were analysed with Fisher's exact test, continuous variables with two-sample t test, and a life table analysis was used to study the recurrence of symptoms in intervened patients. RESULTS: From January 1995 to May 2016, 47 patients (mean age 30 years; range 14-59 years) were managed; 44 (94%) were female. During the mean follow-up period of 120 months, 21 (45%) underwent 23 procedures (17 of these [74%] open, six [26%] endovascular). From the intervened group, eight (38%) patients presented with transient ischaemic attacks, five (24%) with renovascular hypertension, and four (19%) with upper extremity and four (19%) lower extremity claudication. Comparative analysis demonstrated that elevation of erythrocyte sedimentation rate (ESR) at the time of the diagnosis (revascularisation group: median value 28 mm/hour; medical management group: median value 15 mm/hour) was associated with progression of the disease, worsening symptoms, and subsequent need for intervention (p = .04). Active smoking was a factor connected with the need for revascularisation (p = .05). Immediate symptomatic improvement occurred in 19 (90%) patients that underwent surgical or endovascular revascularisation. CONCLUSION: Patients with TA who underwent interventions had higher ESR at the time of diagnosis; this factor and active smoking were associated with progression of the disease and worsening ischaemic symptoms despite medical therapy. Revascularisation procedures are effective at relieving symptoms; lifelong surveillance is necessary.

Impact of optimal anticoagulation therapy on chronic venous ulcer healing in thrombophilic patients with post-thrombotic syndrome.

OBJECTIVE: Post-thrombotic syndrome (PTS) is the long-term sequelae of deep venous thrombosis (DVT). PTS clinical manifestations include chronic leg pain, oedema, lipodermatosclerosis and ulcers. The objective of this study is to determine in patients with documented history of thrombophilias and DVT whether the number of previous thrombotic events and optimal anticoagulation therapy are associated with the time to venous ulcer healing following the start of compression therapy. METHOD: Retrospective analysis performed in thrombophilic patients under the age of 50 years old with chronic venous ulcers secondary to DVT at the wound clinic in the National Institute of Medical Sciences and Nutrition 'Salvador Zubirán ' in Mexico City. Variables such as the number or episodes of thrombotic events, type of hypercoagulable disorder, optimal anticoagulation therapy with Warfarin monitored by therapeutic International Normalised Ratio (INR) (2-3) and compliance to compression therapy were examined. Patients that underwent superficial or perforator vein interruption or endovascular recanalisation of deep veins were excluded from the study. RESULTS: From a database of 29 patients with chronic venous ulcers followed in our clinic from January 1992 to September 2012, only 13 patients (61% female) met the inclusion criteria. Mean age±standard deviation (SD) was 32±12 years old. Of these, seven (54%) patients with suboptimal INR presented with an average of two previous thrombotic events and the remaining six (46%) patients with optimal INR only one event (p=0.28), the mean time to the clinical manifestation of a venous ulcer after the first episode of DVT was 39 months (range: 12-72) for patients with suboptimal INR and 82 months (range: 12-216) for those with optimal anticoagulation therapy (p=0.11). During the mean follow-up period of 52 months, all patients in optimal anticoagulation healed their ulcer; their mean time for wound healing was 44 months (range: 4-102). In the suboptimal INR group, only four healed the ulcers with an mean of 72 months (range: 2-204) (p=0.94). CONCLUSION: There seems to be an association between an optimal anticoagulation therapy with Warfarin monitored by INR and wound healing rates in thrombophilic patients with chronic venous ulcers. Further research is warranted. DECLARATION OF INTEREST: The authors have no conflict of interest.

Cellular mechanisms involved in the pathogenesis of airway remodeling in chronic lung disease.

Background: Airway epithelial cells and lung fibroblasts play an important role in the development of chronic lung disease, but the exact mechanisms responsible have not been clarified. Our objective was to investigate the involvement of these cells in the inflammatory response associated to chronic lung disease. Methods: Human lung fibroblasts and airway epithelial cells were challenged with Interleukin-1ß and hypoxia, and with inhibitory (simvastatin) stimuli of the inflammatory response. Expression of markers of local inflammation ((IL-8, monocyte chemoattractant protein-1 (MCP-1), factor-κB1 (NF-κB1)), systemic inflammation ((C-reactive protein (CRP) and serum amyloid A (SAA)) and proteases matrix metalloproteinase (MMP) 9 and 12 were assessed by PCR and ELISA. Apoptosis/necrosis was analyzed by flow cytometry. Results: Our results showed that the lung fibroblasts had a higher expression of local and systemic inflammation and protease activity markers when they were treated with IL-1ß compared to airway epithelial cells. Under hypoxic conditions, we observed a decrease in systemic inflammation in lung fibroblasts, which was further attenuated by simvastatin. Conclusion: The lung fibroblasts seem to be the main initially stimulated cells that could potentially trigger the inflammatory response, and be responsible for the eventual onset of chronic lung disease. The involvement of IL-1ß stimulation in systemic inflammatory and proteinase imbalance biomarkers is higher in lung fibroblasts. Apoptosis is not a predominant mechanism in these cells.

Contribution of vasopressin and the sympathetic nervous system in the early phase of high sodium one-kidney renal hypertension.

This study assessed the contributions of the sympathetic nervous system and arginine vasopressin to the onset of one-kidney, one-wrap (1K1W) renal hypertension in rats fed a high sodium diet. Two weeks before renal wrap or sham wrap, rats were given a high sodium diet and water ad libitum. At 3 days postwrap, resting mean arterial pressure (MAP) was significantly greater in renal-wrapped rats. The contributions of the sympathetic nervous system and vasopressin to blood pressure (BP) were assessed by ganglionic blockade and vascular vasopressin receptor antagonism, respectively. Depressor responses to ganglionic blockade were significantly greater in the normotensive rats as compared to the hypertensive rats. Administration of vasopressin antagonist caused a significant fall in pressure only in wrapped rats. In addition, enhanced pressor responses to bolus injections of vasopressin were observed in hypertensive rats. These results indicate that during this phase of the hypertension there is an activation of the vasopressin pressor system without an increase in neurogenic function. Equalization of arterial pressure occurred only when both systems were blocked, regardless of the order of blockade, which indicated that the sympathetic nervous system and vasopressin interact to maintain the hypertension. Comparison of depressor responses to the blocking agents revealed that the interaction is compensatory in nature since the contributions of the sympathetic nervous system and vasopressin to the maintenance of arterial pressure were greater when the other system was blocked.

Plasma vasopressin concentration in high sodium renal hypertension.

One-kidney, figure-8 renal wrapped and sham-operated rats maintained on high sodium intake were studied to determine plasma concentrations of vasopressin during the onset of hypertension. Animals were chronically prepared with femoral artery and vein catheters. Arterial blood samples were taken from conscious rats before and 3 days after renal wrap or sham operation while donor blood was simultaneously infused intravenously. Three days after surgery, arterial pressure, plasma osmolality and plasma vasopressin concentration increased significantly in the renal wrapped animals and remained unchanged in the sham-operated rats. Ganglionic blockade with hexamethonium and atropine produced equivalent decreases in arterial pressure and increases in plasma vasopressin concentration in the two groups of rats. Subsequent administration of the V1 vasopressin antagonist, d(CH2)5Tyr(Me)AVP, caused a significantly greater fall in arterial pressure in the hypertensive rats. These results provide further evidence for a contribution of vasopressin to sodium-dependent hypertension.

Small-diameter mesocaval shunts: a 10-year evaluation.

The use of small-diameter portosystemic shunts for the treatment of bleeding esophageal varices caused by portal hypertension has emerged as an outgrowth of the development of polytetrafluoroethylene vascular grafts, which allow the use of a narrow lumen. We report our experience with this type of graft over a 10-year period. Thirty-three patients with good liver function (Child-Pugh class A) were electively operated. The average age of these patients was 45 years (range 17 to 71 years). Twenty-nine patients had liver cirrhosis, one had portal fibrosis, and three had idiopathic portal hypertension. Operative mortality was 3%, and the rebleeding rate was 15%. Postoperative encephalopathy was observed in 14 patients (11%), three of whom had grade III to IV encephalopathy. The remaining 11 patients, had mild encephalopathy that was easily controlled. Postoperative angiography showed shunt patency in 81% of the patients, reduction in portal vein diameter in 33% of the patients, and portal vein thrombosis in 6%. Good postoperative quality of life was observed in 63% of the patients. Survival according to the Kaplan-Meier actuarial method was 81% at 12 months, 56% at 60 months, and 36% at 10 years. These shunts are a good alternative for patients being considered for surgery in whom other portal blood flow preserving procedures (i.e., elective shunts, devascularization with esophageal transection) are not feasible.

Diminished morbidity and mortality in portal hypertension surgery: relocation in the therapeutic armamentarium.

Although several effective therapeutic options are available for bleeding from portal hypertension, surgery has a well-defined role in the management of patients with good liver function who are electively operated. The aim of this investigation was to evaluate the operative mortality and morbidity of portal blood flow-preserving procedures in a highly select patient population. The records of 148 patients operated on between 1996 and 2000 using one of two techniques (selective shunts or a Sugiura-Futagawa operation [complete portoazygos disconnection]) were analyzed with particular attention to operative mortality, postoperative rebleeding, and encephalopathy. Survival was calculated according to the Kaplan-Meier method. Sixty-one patients had distal splenorenal shunts placed, and 87 patients had a devascularization procedure. Operative mortality for the group as a whole was 1.2%. In the group with selective shunts, the rebleeding rate was 4.9%, the encephalopathy rate was 9.8%, and the shunt obstruction rate was 1.6%. Survival at 24 months was 94% and at 48 months was 92%. In those undergoing devascularization, the encephalopathy rate was 5% and the rebleeding rate was 14%. Survival at 24 months was 90% and at 48 months was 86%. Portal blood flow-preserving procedures have very low morbidity and mortality rates at specialized centers. In addition, a low rebleeding rate is associated with a good quality of life. Low-risk patients with bleeding portal hypertension should be considered for surgical treatment.

Acute bile duct injury. The need for a high repair.

BACKGROUND: An immediate repair is considered optimal in acute biliary duct injuries; however, it may prove to be a challenge, because such repairs are usually performed on small ducts whose viability cannot always be determined. METHODS: We performed a retrospective review of the charts of patients with acute bile duct injury who underwent repair at a tertiary care academic university hospital. A total of 204 patients with acute bile duct injury were seen between 1989 and 2002. Of these, 30 were repaired within minutes to hours after the injury. These patients were divided into two groups. Group I patients had a Roux-en-Y hepatojejunostomy below the hepatic junction; Group II patients had a Roux-en-Y hepatojejunostomy at the junction level. We then performed a long-term evaluation of anastomosis function in these patients, using clinical, radiological, and laboratory. RESULTS: Twenty-eight injuries were secondary to a laparoscopy; the other two resulted from open cholecystectomies. All of the patients suffered complex injuries with complete section of the duct and substance loss (Strasberg E). There were 12 patients in group I and 18 in group II. Three cases in group I (25%) and one in group II (5%) developed anastomosis dysfunction. Mean follow-up was 56 months (range, 12-80) in group I and 52 months (range, 10-76) in group II. Two cases in group I (16%) and none in group II (0) required reoperation (p < 0.05). CONCLUSIONS: In the acute setting, complex lesions should be treated with a high bilioenteric anastomosis (at the junction level) in the first attempt at repair. Lower-level anastomoses are associated with a higher dysfunction rate and the need for radiological manipulation and reoperation. Also, stenosis of the anastomosis secondary to undetected duct ischemia in the acute repair is more frequent in low bilioenteric anastomoses.

Biomedical imaging modalities: a tutorial.

The introduction of advanced imaging technologies has improved significantly the quality of medical care available to patients. Non-invasive imaging modalities allow a physician to make increasingly accurate diagnoses and render precise and measured modes of treatment. Current uses of imaging technologies include laboratory medicine, surgery, radiation therapy, nuclear medicine, and diagnostic radiology. This paper provides an overview of most of the popular imaging modalities currently in clinical use. It is hoped that a general understanding of the modality from which an image is derived will help researchers in the subsequent analysis of the image data.

[Evaluation of 20 years of experience and quality of life in patients surgically treated for liver cystic disease]. / Evaluación de 20 años de experiencia y calidad de vida en pacientes con tratamiento quirúrgico para la enfermedad quística del hígado.

UNLABELLED: Surgical treatment of liver cystic disease is reserved for symptomatic patients. The surgical approach is chosen according to the size and distribution of the cysts. In patients with massive hepatomegaly secondary to polycystic liver disease, liver transplantation is indicated with excellent results and quality of life. OBJECTIVE: To evaluate over 20-year period, the results in terms of clinical outcome of three groups of patients with cystic liver disease (EQ) who received surgical treatment and to determine postoperative quality of life. MATERIALS AND METHODS: In a 20-year period, 44 patients were operated on; 24 had simple liver cyst, 13 had polycystic liver disease, and seven cystadenomas. Using the SF36 questionnaire, self-perception of quality of life was evaluated using eight scales in two major categories: Physical component summary (PCS) and mental component summary (MCS). RESULTS: Upper abdominal pain was the main clinical symptom. Fenestration was the most frequent procedure performed. No differences in quality of life were observed in all, while good quality of life was recorded in all groups at a median follow-up of 39 months. CONCLUSIONS: Surgical treatment of cystic liver disease is reserved for symptomatic patients or complications such as rupture, infection, and hemorrhage. Therapeutic alternatives should been chosen on an individual basis. Good quality of life is obtained after surgery in these patients.

[Granulosa cell tumor with liver metastasis treated with partial hepatectomy and chemotherapy. Report of a case]. / Tumor de células de la granulosa metastásico a hígado tratado con hepatectomía parcial y quimioterapia. Reporte de un caso.

A patient with granulosa cell tumor recurrence 14 years after primary resection, was treated with partial hepatectomy and adjuvant chemotherapy (vinblastine, cisplatin and bleomycin). She achieved complete remission and is free of disease 18 months after treatment.

Development of high sodium renal hypertension during chronic blockade of the vascular effects of vasopressin.

Studies in sodium-dependent models of hypertension have shown that arginine-vasopressin (AVP) plays an important role in the maintenance of blood pressure, predominantly through its vasoconstrictor action. In addition to AVP, the sympathetic nervous system (SNS) also acts to maintain blood pressure in high sodium one-kidney, figure-8 renal wrap hypertension. The purpose of this study was to determine if chronic blockade of vascular AVP (V1) receptors affected the induction of high sodium renal hypertension and the contribution of the SNS to the maintenance of blood pressure. Rats receiving chronic s.c. administration of a V1 antagonist, d(CH2)5Tyr(Me)AVP, or vehicle were subjected to renal wrapping or sham surgery, V1 receptor blockade was confirmed periodically by an 80 +/- 3% reduction of the pressor response to a bolus injection of 10 mU/kg of AVP. d(CH2)5Tyr(Me)AVP did not affect the development of hypertension or the associated changes in plasma sodium, potassium, osmolality and hematocrit. In renal-wrapped rats, ganglionic blockade caused a greater fall in blood pressure in animals treated with d(CH2)5Tyr(Me)AVP than in vehicle-treated animals. However, this apparent increase in SNS function was not responsible for the hypertension in d(CH2)5Tyr(Me)AVP-treated, renal-wrapped rats, inasmuch as ganglionic blockade lowered blood pressure a similar amount in normotensive d(CH2)5Tyr(Me)AVP-treated, sham-operated rats and blood pressure remained elevated after combined blockade of the SNS, AVP and the renin-angiotensin systems. These results indicated that chronic blockade of V1 receptors did not alter the induction of high sodium renal hypertension and the mechanism of the elevated blood pressure was not through an activation of the SNS or other neurohumoral mechanisms.

Hemodynamic changes during onset of high-sodium one-kidney figure-8 renal hypertension.

The hemodynamic changes associated with the onset of one-kidney, figure-8, renal-wrap hypertension were monitored in rats fed a high-sodium diet. In addition, the hemodynamic contributions of the sympathetic nervous system (SNS) and arginine vasopressin (AVP) were assessed during the 1st week of hypertension. Renal wrapping caused mean arterial pressure (MAP) to increase significantly from 108 +/- 4 to 140 +/- 4 mmHg on day 5 after renal surgery. The hypertension was associated with a significant bradycardia and no significant change in cardiac output (CO), as measured with an electromagnetic flow probe. Total peripheral resistance (TPR) was significantly elevated to 140% above control value on day 5 after renal surgery. Ganglionic blockade caused similar decreases in MAP and TPR in normotensive and hypertensive animals. Sympathetic blockade after pretreatment with a specific vascular antagonist of AVP, [1-beta-mercapto-beta, beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine]Arg8-vasopressin ([d(CH2)5Tyr(Me)]AVP), caused a greater depressor response in the renal-wrapped animals as compared with the effect of ganglionic blockade alone in these animals. The effect of [d(CH2)5Tyr(Me)]AVP alone on the hemodynamics was not different between the two groups of rats. After ganglionic blockade pretreatment, [d(CH2)5Tyr(Me)]AVP caused a significant decrease in MAP and TPR in the renal-wrapped animals. In addition, the difference in MAP and TPR between the two groups of rats was eliminated after combined blockade of AVP and the SNS. The results of this study indicated that the onset of hypertension was a result of an activation of neurohumoral mechanisms to increase TPR.(ABSTRACT TRUNCATED AT 250 WORDS)

Neurohumoral mechanisms of sodium-dependent hypertension.

The contribution of neurohumoral factors to arterial pressure has been studied in several models of sodium-dependent hypertension including the deoxycorticosterone-saline, Dahl salt-sensitive rats, and reduced renal mass-saline. Observations from these animals have largely pointed to the sympathetic nervous system and arginine vasopressin (AVP) as the critical factors responsible for mediating the increased arterial pressure. Our work has indicated that the one-kidney, figure-8 renal wrap model of experimental hypertension is also sodium dependent. In these rats, prior sodium depletion prevented the development of hypertension whereas high sodium intake exacerbated the increase in arterial pressure. An activation of the sympathetic nervous system and increased AVP activity appeared to be responsible for the hypertension in rats maintained on normal and high sodium intake. Stimulation of the AVP and sympathetic nervous systems in sodium-dependent hypertension may be associated with a suppression of cardiovascular gamma-aminobutyric acid (GABA)-ergic function in the central nervous system. The inhibitory neurotransmitter, GABA, and an inhibitor of GABA uptake, nipecotic acid, lowered arterial pressure in a sodium-stimulated model of hypertension.

Usefulness of magnetic resonance spectroscopy for diagnosis of hepatic encephalopathy in a patient with relapsing confusional syndrome.

Magnetic resonance spectroscopy allows the assessment of several metabolites in brain tissue. In patients with hepatic encephalopathy, this technique shows a rise in glutamine and a decrease in myoinositol in brain tissue. However, the role of magnetic resonance spectroscopy in the diagnosis of hepatic encephalopathy is not known. We report the case of a patient with a relapsing confusional syndrome who underwent magnetic resonance spectroscopy. Previously, hepatic encephalopathy was ruled out because of the negative results of a transjugular liver biopsy and normal hepatic venous pressure gradient. The results of magnetic resonance were characteristic of hepatic encephalopathy. Abdominal computed tomography demonstrated large portosystemic shunts associated with cirrhosis of the liver. This case shows that magnetic resonance spectroscopy is an useful technique for the diagnosis of hepatic encephalopathy in selected cases, such as those without clinical signs of cirrhosis and/or large portosystemic shunts.

Oxido nitrico de ilustre desconocido a motor fisiologico / Nitric oxide: a review

En las últimad décadas el óxido nítrico ha pasado de ser un contaminante ambiental a una mólecula implicada en múltiples funciones fisiológicas, actualmente se han multiplicado las investigaciones en torno a sus funciones. El óxido nítrico juega un papel imortnate en la regulación de una serie de procesos fisiológicos como ser: el tono vasomotor, la motilidad intestinal, actúa como un neurotransmisor central y periférico, desemeña un papel fundamental en la funciones del sistema inmune y la fisiologia del os procesos de agregación plaquetaria y leucocitaria. Sus acciones fisioatológiocas incluyen un rol determinante en la génesis del Shock séptico, en el daño tisular resultado de la inflamación, en el envejecimiento motocondrial, en el desarrollo dela rtrosis y la artritis reumatoidea, enfermedades degenerativas dels istema nervioso central y en el daño producido por la isquemia miocárdica y cerebral. Demostrando múltiples aplicaciones terapéuticas en el tratamiento de varias patologías.