Laparoscopic Biopsies in Pancreas Transplantation.

As there is no precise laboratory test or imaging study for detection of pancreas allograft rejection, there is increasing interest in obtaining pancreas tissue for diagnosis. Pancreas allograft biopsies are most commonly performed percutaneously, transcystoscopically, or endoscopically, yet pancreas transplant surgeons often lack the skills to perform these types of biopsies. We have performed 160 laparoscopic pancreas biopsies in 95 patients. There were 146 simultaneous kidney-pancreas biopsies and 14 pancreas-only biopsies due to pancreas alone, kidney loss, or extraperitoneal kidney. Biopsies were performed for graft dysfunction (89) or per protocol (71). In 13 cases, an additional laparoscopic procedure was performed at the same operation. The pancreas diagnostic tissue yield was 91.2%; however, the pancreas could not be visualized in eight cases (5%) and in 6 cases the tissue sample was nondiagnostic (3.8%). The kidney tissue yield was 98.6%. There were four patients with intraoperative complications requiring laparotomy (2.5%) with two additional postoperative complications. Half of all these complications were kidney related. There were no episodes of pancreatic enzyme leak and there were no graft losses related to the procedure. We conclude that laparoscopic kidney and pancreas allograft biopsies can be safely performed with very high tissue yields.

Stress and musculoskeletal discomfort among hydrocarbon industry workers in Mexico.

This study of 114 workers in the hydrocarbon industry was conducted to identify the relationship between stress and musculoskeletal discomfort, and to view the roles played by such factors as age, schooling, obesity, workplace and job seniority. All factors except seniority were found to affect the presence of musculoskeletal discomfort in some area of the body.

Infección por parvovirus B19: diagnóstico y tratamiento en un paciente sometido a trasplante renal / No disponible

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Treating distal calciphylaxis with therapy associated with sevelamer and bisphosphonates

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Degenerative aneurysms of the superficial femoral artery.

PURPOSE: To review the pathogenesis, diagnosis, presentation, diagnosis, management and outcomes (morbidity and mortality) of superficial femoral artery aneurysms. METHODS: A comprehensive review of this entity was performed based on the available literature in all languages and a detailed discussion of our findings is also provided. RESULTS: Our review identified 61 cases of SFA aneurysms. They were most often seen in elderly men, predominately affected the right lower extremity, and were most often located in the middle-third of the artery. At the time of diagnosis, SFA aneurysms were frequently symptomatic because they reached a relative large diameter before the diagnosis was made. The most frequent presentation was localized pain in association with a pulsatile mass. In contrast to popliteal aneurysms, SFA aneurysms more frequently present with rupture than distal ischemia. Angiography was by far the most commonly utilized diagnostic tool. Treatment was primarily by means of an interposition graft, followed by exclusion and surgical bypass. Endovascular repair of SFA aneurysms has only been reported in three instances. SFA aneurysm repair was most often associated with favorable outcomes, with low reported rates of ischemia and limb loss.

Aortic paraprosthetic-colonic fistulae: a review of the literature.

BACKGROUND: Aortic graft-colonic fistulae are a rare complication of aortic reconstructive surgery. METHODS AND FINDINGS: A comprehensive review of this entity was performed based on the available literature from 1950 until 2006. Available reports were analyzed with respect to demographics, prior surgical intervention and its indication, prosthetic material used during the initial intervention, clinical presentation, the time interval in between the initial operation and symptoms, the method of treatment of the aortic graft-colonic fistula and its outcome.

Are your arteries older than your age?

PURPOSE: To determine the effect of age and atherosclerotic risk factors on the carotid intima-media layer thickness and morphology characteristics. PATIENTS AND METHODS: Three groups of subjects were included in the study: Individuals with atherosclerotic risk factors including a family history of CHD, hypertension, hyperlipidemia, diabetes, and/or smoking (group A, n=180), age- and sex-matched healthy subjects without risk factors (group B, n=60) and a group of significantly younger volunteers (group C, n=25). The carotid artery was imaged longitudinally with B-mode ultrasound. Intima media thickness (IMT) was measured in the common (CCA) and internal carotid (ICA) arteries. Surface irregularity and continuity of the intima-media layer (IML) were assessed by high definition imaging. Echogenicity of the wall was quantified using Adobe Photoshop. The presence of calcium deposits was recorded. The double line wall pattern seen in young healthy people was used as a control to assess patterns and texture of the carotid IML. Fifteen subjects had their measurements repeated for intraobserver variability. RESULTS: IMT measurements were reproducible in both the CCA and ICA (coefficient of variation 6% and 9%). IMT increased linearly with age (adjusted R(2)=0.72, p<0.0001), which was also an independent risk factor for increased IMT. All the risk factors had a significant association with increased IMT. In the lowest (third) decade the wall/blood interface was smooth and the double line was visualized with an echolucent center. With increased age and number of risk factors present, the wall/blood interface became more irregular (p<0.01), the double line was distorted (p<0.01) and the IML was more echogenic (p<0.01). The increase in IMT and the changes in the echogenicity of the IML were more pronounced in the ICA. CONCLUSIONS: Age is an independent risk factor for increased IMT. Atherosclerotic risk factors are associated with the age-related changes seen in the IML. Such changes are also seen in younger asymptomatic volunteers with risk factors indicating that their arteries are older than their age.

Anthropometric study of Mexican primary school children.

This paper presents the results of an anthropometric survey conducted on male and female Mexican primary school children age 6-11 years in the metropolitan area of the city of Guadalajara. A set of 50 body dimensions was taken based on international standards. The sample consisted of 4758 children (boys and girls). The anthropometric measurements were compared to those of American, Cuban and Mexican children. The results indicate that the body dimensions of Mexican children from this study are different from those of American, Cuban, and other Mexican children, probably due to ethnic differences and the time lapse between the different studies. It is considered that the 50 parameters are necessary for the design of school furniture, fittings and equipment in order to minimize musculoskeletal, visual, and circulatory problems resulting from using those badly designed elements.

Effect of interleukin-11 on body temperature in afebrile and febrile rats.

Interleukin (IL)-11 is a member of the gp130 family of cytokines. In contrast to IL-6 (another gp130 cytokine), IL-11 does not induce fever in humans. In the present study, the effect of recombinant human IL-11 (hrIL-11) injected intracerebroventricularly on body temperature of afebrile and febrile rats was studied. Results showed that: (i) hrIL-11 in doses of 5, 50 and 500 ng injected into the cerebral ventricles does not alter body temperature in rats; (ii) febrile response induced by intraperitoneal injection of E. coli endotoxin (50 microg/kg) was initiated more rapidly in rats injected with 500 ng of hrIL-11 in the cerebral ventricles, and (iii) the enhancement of the initial phase of fever induced by hrIL-11 was not accompanied by changes in plasma concentrations of IL-6 and tumor necrosis factor (TNF). These results indicate that hrIL-11 is not pyrogenic when administered into the brain ventricles. The data obtained also demonstrate that central application of hrIL-11 alters body temperature in conditions of pyrogenic stimulation, but that this effect is not due to the alterations in plasma concentrations of IL-6 or TNF. These data suggest that during the development of the systemic inflammatory response, activation of gp130 subunit becomes effective in altering body temperature.

Lack of obesity and normal response to fasting and thyroid hormone in mice lacking uncoupling protein-3.

Uncoupling protein-3 (UCP3) is a mitochondrial protein that can diminish the mitochondrial membrane potential. Levels of muscle Ucp3 mRNA are increased by thyroid hormone and fasting. Ucp3 has been proposed to influence metabolic efficiency and is a candidate obesity gene. We have produced a Ucp3 knockout mouse to test these hypotheses. The Ucp3 (-/-) mice had no detectable immunoreactive UCP3 by Western blotting. In mitochondria from the knockout mice, proton leak was greatly reduced in muscle, minimally reduced in brown fat, and not reduced at all in liver. These data suggest that UCP3 accounts for much of the proton leak in skeletal muscle. Despite the lack of UCP3, no consistent phenotypic abnormality was observed. The knockout mice were not obese and had normal serum insulin, triglyceride, and leptin levels, with a tendency toward reduced free fatty acids and glucose. Knockout mice showed a normal circadian rhythm in body temperature and motor activity and had normal body temperature responses to fasting, stress, thyroid hormone, and cold exposure. The base-line metabolic rate and respiratory exchange ratio were the same in knockout and control mice, as were the effects of fasting, a beta3-adrenergic agonist (CL316243), and thyroid hormone on these parameters. The phenotype of Ucp1/Ucp3 double knockout mice was indistinguishable from Ucp1 single knockout mice. These data suggest that Ucp3 is not a major determinant of metabolic rate but, rather, has other functions.

Torpor in mice is induced by both leptin-dependent and -independent mechanisms.

We tested the effect of chronic leptin treatment on fasting-induced torpor in leptin-deficient A-ZIP/F-1 and ob/ob mice. A-ZIP/F-1 mice have virtually no white adipose tissue and low leptin levels, whereas ob/ob mice have an abundance of fat but no leptin. These two models allowed us to examine the roles of adipose tissue and leptin in the regulation of entry into torpor. Torpor is a short-term hibernation-like state that allows conservation of metabolic fuels. We first characterized the A-ZIP/F-1 animals, which have a 10-fold reduction in total body triglyceride stores. Upon fasting, A-ZIP/F-1 mice develop a lower metabolic rate and decreased plasma glucose, insulin, and triglyceride levels, with no increase in free fatty acids or beta-hydroxybutyrate. Unlike control mice, by 24 hr of fasting, they have nearly exhausted their triglycerides and are catabolizing protein. To conserve energy supplies during fasting, A-ZIP/F-1 (but not control) mice entered deep torpor, with a minimum core body temperature of 24 degrees C, 2 degrees C above ambient. In ob/ob mice, fasting-induced torpor was completely reversed by leptin treatment. In contrast, neither leptin nor thyroid hormone prevented torpor in A-ZIP/F-1 mice. These data suggest that there are at least two signals for entry into torpor in mice, a low leptin level and another signal that is independent of leptin and thyroid hormone levels. Studying rodent torpor provides insight into human torpor-like states such as near drowning in cold water and induced hypothermia for surgery.

An antipyretic role for interleukin-10 in LPS fever in mice.

Interleukin (IL)-10 inhibits the synthesis of proinflammatory cytokines implicated in fever, including IL-1beta, IL-6, and tumor necrosis factor (TNF)-alpha. We hypothesized that IL-10 functions as an antipyretic in the regulation of fevers to lipopolysaccharide (LPS) and turpentine. Body temperature was measured by biotelemetry. Swiss Webster (SW) mice treated with recombinant murine IL-10 were resistant to fever induced by a low dose of LPS (100 microgram/kg ip) and to the hypothermic and febrile effects of a high (septiclike) dose of LPS (2.5 mg/kg ip). IL-10 knockout mice developed an exacerbated and prolonged fever in response to a low dose of LPS (50 microgram/kg ip) compared with their wild-type counterparts. At 4 h after injection of the low dose of LPS, plasma levels of IL-6, but not TNF-alpha, were significantly elevated in the IL-10 knockout mice compared with their wild-type controls (ANOVA, P < 0.05). After injection of the same high dose of LPS injected into SW mice, wild-type mice developed a fever at 24 h whereas IL-10 knockout mice immediately developed a profound hypothermia that lasted through 41 h (ANOVA, P < 0.05). Body weight and food intake were more significantly depressed in response to the high dose of LPS in the knockout mice compared with their wild-type controls. Only 30% of the IL-10 knockout mice survived compared with 100% of the wild-type mice (Fisher's exact test, P < 0.05). Fever in response to the injection of turpentine (100 microliter/mouse sc) did not differ between wild-type and IL-10 knockout mice. These data support the hypotheses that 1) IL-10 functions as an endogenous antipyretic following exposure to LPS, 2) a putative mechanism of the early antipyretic action of IL-10 is through the inhibition of plasma levels of IL-6, 3) IL-10 has a protective role in the lethal effects of exposure to high levels of LPS, and 4) endogenous IL-10 does not have a role in fever induced by turpentine.

Intestinal amoebiasis: antibody-secreting cells and humoral antibodies.

Splenic plasma cell response and systemic antibody response to intestinal amoebiasis were studied in C3H/HeJ mice from 5 to 60 days post-inoculation with Entamoeba histolytica. At various time intervals specific antibody-secreting cells (ASC) in the spleen were measured in infected mice and non-infected control mice by enzyme-linked immunospot (ELISPOT) assay. Serum antibodies were measured by enzyme-linked immunosorbent assay (ELISA). The infected animals showed high IgA ASC from 30 to 50 days post-inoculation as compared to IgM and IgG ASC. However, class-specific serum antibody showed high IgG titre from 30 to 60 days post-inoculation as compared to IgM and IgA serum titres. Our results suggest that E. histolytica trophozoites can induce a plasma cell response in the spleen that is different from anti-amoebic antibody response in serum.

Role of IL-6 and TNF in thermoregulation and survival during sepsis in mice.

Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) have been implicated as key mediators in inflammation, morbidity, and mortality associated with sepsis. We examined the role of IL-6 and TNF-alpha signaling on hypothermia, fever, cachexia, anorexia, and survival during sepsis induced by cecal ligation and puncture (CLP) in male and female gene knockout mice. Male wild-type mice developed an initial hypothermia and subsequent fever during sepsis. Male IL-6 knockout mice did not develop fever; rather, they maintained a profound hypothermia during sepsis. Male TNF p55/p75 receptor (TNFR) knockout mice had attenuated hypothermia, but developed a virtually identical fever as wild-type mice. Cachexia did not differ between male wild-type and IL-6 or TNFR knockout mice, whereas anorexia was prolonged in IL-6 knockout mice. Due to the rapid lethality of sepsis in female mice, survival was the only variable we were able to statistically compare among female genotypes. Female wild-type mice had significantly decreased survival compared with male wild-type mice. Survival was significantly enhanced in male and female TNFR knockout mice compared with their wild-type controls. Lack of IL-6 did not affect male or female lethality. These data support the hypothesis that IL-6 is a key mediator of fever and food intake, whereas TNF is responsible for the initial hypothermia and lethality of sepsis in both sexes of mice. The enhanced lethality of CLP-treated female mice supports a role for sex steroids during sepsis.

The use of knockout mice to understand the role of cytokines in fever.

1. In most instances, data obtained using knockout mice to dissect the role of cytokines in fever are similar to data obtained by other, more traditional experimental techniques. 2. Interleukin (IL)-1beta appears to be critically involved in fever caused by some routes of infection/inflammation (e.g. localized inflammation with turpentine). This cytokine has only a small role in fevers caused by i.p. injection of lipopolysaccharide (LPS). These IL-1beta-induced fevers in knockout mice appear to be via the induction of IL-6, similar to LPS-induced fevers in rats. Interleukin-6 also appears to be critically involved in turpentine-induced fever. 3. The precise role of tumour necrosis factor (TNF) in fever is controversial. Data obtained from knockout mice lacking both TNF receptors do not support a pyrogenic role for TNF in fever either to i.p. injection of LPS, s.c. injection of turpentine or following caecal ligation and puncture. 4. The roles of these cytokines in fevers induced by injection of LPS, IL-1beta, turpentine and caecal ligation and puncture are summarized. The data show the complexity of the febrile response. Depending on the types of inflammatory/infectious stimuli, different cytokines play important roles. Because other cytokines are thought to be involved in fever (e.g. macrophage inflammatory protein, interferons), considerable work is still needed to dissect the precise roles of cytokines in fever.

Effect of heat stress on LPS-induced fever and tumor necrosis factor.

Exposure to heat stress leads to both short-term and long-term effects on morbidity. Male rats were exposed to a high ambient temperature of 40 degrees C, which resulted in biotelemetered core body temperature rising to approximately 42 degrees C. This treatment led to a marked enhancement in lipopolysaccharide (LPS)-induced fever at 24 h after exposure to heat stress. The increase in fever was accompanied by a significant suppression in the circulating concentration of tumor necrosis factor. Heat-shock protein-70 measured in liver was elevated by the heat exposure (but not further elevated by the injection of LPS). An enhanced fever to LPS and other inflammatory stimuli found in heat-stressed human subjects could explain the apparent increase in susceptibility to disease.