乙肝后肝硬化患者内源性-氧化氮产量及其与内毒素的关系

为了解乙肝后肝硬化患者内源性一氧化氮（ＮＯ）产量及其与内毒素的关系，对１１４例乙肝后肝硬化患者血浆ＮＯ２和内毒素水平进行了检测。结果显示，肝硬化患者ＮＯ２、内毒素水平明显升高。无腹水组、腹水组、腹水并肾衰组血浆ＮＯ２及内毒素水平依次升高。血浆ＮＯ２与内毒素呈显著相关（ｒ＝０．７４５２，Ｐ＜０．００１）。经治疗后，随内毒素水平的下降，ＮＯ２水平也下降。上述结果提示，肝硬化患者ＮＯ产量明显增多，内毒嵥匚渲饕找颉     

乙肝后肝硬化患者内源性一氧化氮产量及其与内毒素的关系

为了解乙肝后肝硬化患者内源性一化氮产量及其与内毒素的关系，对１１４例乙肝后肝硬化硬化患者血清ＮＯ＾－２和内毒素水平进行检测。结果显示，肝硬化患者ＮＯ＾－２，内毒素水平明显升高。无腹水组，腹水组，腹水并肾衰组血浆ＮＯ＾－２及内毒素水平依次升高。     

肝硬化患者血浆一氧化氮与GMP-140水平的变化

目的：观察肝硬化患者血浆一氧化氮（ＮＯ）与可溶性α－颗粒膜蛋白（ＧＭＰ－１４０）水平的变化。方法：分别采用硝酸还原酶法和酶联免疫分析法,测定２９例肝硬化（无腹水）、２３例肝硬化（有腹水）患者和３０例健康人的血浆ＮＯ２＾－／ＮＯ３＾－水平及ＧＭＰ－１４０含量。结果：肝硬化患者有腹水组和无腹水组较健康对照组血浆ＮＯ２＾－／ＮＯ３＾－水平均有显著性增高（Ｐ〈０．０１）;肝硬化有腹水组较健康对照组ＧＭＰ－１４０含量显著性增高（Ｐ〈０．０１）,无腹水且亦增高但无显著性意义。结论：提示ＮＯ和粘附分子可能参与肝硬化的发生发展过程。     

血浆内源性阿片肽升高与实验性肝硬化高动力循环状态及腹水形 …

目的：通过检测实验性肝经各阶段３种内源性阿片肽（ＥＯＰ）血浆浓度变化，探讨基佤肝硬化高动力循环状态及腹水形成的关系，方法；应用放射免疫法测定了卤氯化碳诱发大鼠肝硬化过程中血浆３种ＥＰＯ的含量变化。结果显示：肝硬化腹水组及肝经无腹水组血浆亮啡肽（Ｌ－ＥＮＫ）、强啡肽的含量均显著高于正常对照组，而且升高的水平与肝功能损害的程度呈显著正相关，但血浆β内啡肽的含量在３缚中无显著差异。提示肝脏灭活功能受损志     

肝硬化患者血浆内皮素和一氧化氮水平及与肾功能状态的关系

测定不同阶段肝硬化患者血浆的NO、ET水平，探索它们对肝硬化腹水形成和肾功能损害所起的作用及其相互关系。测血浆NO的代谢产物NO2^-浓度（Griess法），ET-1浓度（放免法）及肾功能。1.血浆NO浓度在肝硬化各组均明显高于正常对照组，在肾衰组明显高于有腹水、无肾衰组。血浆ET浓度在肝硬化各组均明显高于正常对照组，肾衰组明显高于有腹水、无肾衰组。2.肝硬化患者血浆ET浓度与血肌酐呈正相关，与肌酐清除率、血钠、尿钠呈负相关。3.肝硬化患者血浆NO与ET水平呈正相关。血浆NO和ET升高可能在肝硬化病程进展中起了重要作用，是形成腹水和引起肾功损害的重要因素，二者相互依赖、相互影响的协同作用是肝硬化进展及出现并发症的重要机制之一。     

实验性肝硬化血浆内源性阿片肽含量的变化及其意义

目的：通过检测实验性肝硬化变各阶段三种内源性阿片肽（ＥＯＰ）血浆浓度变化，探讨其与肝硬化高动力循环状态及腹水形成的关系，方法：应用放射免疫法测定了四氯化碳（ＣＣｌ４）诱发大鼠肝硬化过程中血浆三种ＥＯＰ的含量变化。结果：结果显示肝硬化腹水组及肝硬化无腹水线血浆亮啡肽（Ｌ－ＥＮＫ）强啡肽（ＤｙｎＡｌ－１３）含量均显著高于正常对照组（Ｐ〈０．０１，Ｐ〈０．０５），而且升高的水平与肝功能损害的程度呈显著正     

肝硬化患者血浆、腹水中ANP、ALD水平分析

本文应用放射免疫测定法检测了36例肝硬化患者血浆心钠素(ANP),醛固酮(ALD)及腹水中ANP、ALD含量,并设ANP正常人对照组。结果表明:肝硬化患者血浆ANP含量明显高于正常对照组(P均<0.001)。其中肝硬化无腹水组明显高于腹水组(P均<0.01)。肝硬化腹水组血浆ANP、ALD含量均明显高于腹水中ANP、ALD含量(P均<0.01)。本文结果提示:肝硬化腹水形成与ANP、ALD有一定关系,推测ANP可用于治疗肝硬化腹水。根据腹水中测到一定浓度ANP、ALD推测:肝性腹水,不仅口服抗醛固酮药物,应注意静脉及腹腔内抗醛固酮治疗。     

实验性肝硬化血浆内毒素、一氧化氮与内皮素的含量变化及其意义

目的：通过观察实验性肝硬化形成过程内毒素,一氧化氮（ＮＯ）与内皮素（ＥＴ）与内皮素（ＥＴ）的动态变化,探讨其与肝硬化高动力循环状态的关系。方法：采用鲎试剂基质显色法,镉还原比色法和放射免疫分析法测定了四氯化碳（ＣＣＩ＾４）诱发大鼠肝硬变形过程中血浆内毒素,ＮＯ,ＥＴ含量变化。结果：在肝硬化进程中血浆内毒素,ＮＯ含量呈上升趋势且明显高于正常对照组（Ｐ〈０．０１）,血浆ＥＴ含量呈下降趋势且明显低于正常     

肝硬化患者血浆和腹水内毒素检测的临床意义

内毒素是固紫阴性杆菌细胞壁的组成部分,在正常情况下,内毒素经胃肠道吸收进入门脉血后,被肝脏的网状内皮细胞清除。当肝脏严重损害或显著门脉高压时,虽无感染存在,内毒素可以在腹水或体循环中发现。作者对46例证明有食管静脉曲张的肝硬化,采用鲎测定法(LimuIus assay)检测血浆和腹水的内毒素。分成两组:腹水组29例,无腹水组17例。另外,慢性进行性肝炎12例作为对照。血浆内毒素阳性在腹水组有22例(75.9％),无腹水组4例(23.5％),两组差异非常显著(P<0.01)。腹水组中,腹水内毒素阳性23例(79.3％),其中17例内毒素滴度≥10~(-3)     

肝硬化患者血浆亮啡肽,神经肽Y含量的变化及临床意义

目的　探讨肝硬化患者血浆亮啡肽（ＬＥＮＫ）、神经肽Ｙ（ＮＰＹ）含量的变化规律及其临床意义。方法用放射免疫法检测４９例肝硬化患者血浆ＬＥＮＫ、 ＮＰＹ含量，并以１８例慢性肝炎、１４例急性肝炎和１０名健康者作对照。结果　肝硬化患者血浆ＬＥＮＫ含量显著高于正常人和急、慢性肝炎（Ｐ＜０．０５），有腹水、肝性脑病者分别显著高于无腹水和无肝性脑病者（Ｐ＜０．０５）；而血浆ＮＰＹ水平肝硬化患者明显下降（Ｐ＜０．０５），有腹水或肝性脑病者下降更明显（Ｐ＜０．０５）。结论肝硬化患者血浆ＬＥＮＫ、ＮＰＹ等内源性神经肽水平明显变化，且以有腹水、肝性脑病等严重并发症者更为明显，提示这些神经肽可能参与了肝硬化患者的高动力状态循环异常，并与腹水及肝性脑病形成有关。     

Micronutrients and infection: interactions and implications with enteric and other infections and future priorities

Symposium presentations have focused on the elegant molecular science and the biologic mechanisms by which micronutrients play critical roles in cellular and humoral immune responses, cellular signaling and function, and even in the evolution of microbial virulence. The concluding session examined the practical issues of how best to evaluate the nutritionally at-risk host, especially in the areas of greatest need-an analytical model of nutrient-immune interactions, implications of nutritional modulation of the immune response for disease, and the implications for international research and child health. This overview illustrated how malnutrition may be a major consequence of early childhood diarrhea and enteric infections, as enteric infections may critically impair intestinal absorptive function with potential long-term consequences for growth and development. The potentially huge, largely undefined DALY (disability-adjusted life years) impact of early childhood diarrheal illnesses demonstrates the importance of quantifying the long-term functional impact of largely preventable nutritional and infectious diseases, especially in children in developing areas.     

Convection and permeation and albumin between plasma and interstitium.

Nonequilibrium thermodynamics is combined with compartmental analysis to interpret albumin sieving and tracer experiments in terms of a permeability-surface product PS (permeation) and a solvent drag reflection coefficient σ_f (convection) for various blood-tissue barriers. The human whole-body albumin data of Lassen, Parving, and Rossing (Lassen, Parving, and Rossing, Microvasc. Res.7, i–iv (1974)), modified for nonliver tissues by Johnson and Levitt (Johnson &; Levitt, Microvasc. Res.9, 141 (1975)) lead to P ～ 1.8 × 10^?8 cm sec^?1 (based on a surface area per unit plasma volume of 700 cm^?1) and to σ_f ～ 0.9, which imply, in agreement with Johnson and Levitt, that permeation is the dominant nonliver blood-tissue transport mechanism for albumin in the normal resting human. Similar values are derived from the dog paw muscle data of Garlick and Renkin (Garlick and Renkin, Amer. J. Physiol.219, 1595–1605 (1970)). The Casley-Smith (Casley-Smith, Microvasc. Res.9, 43–48 (1975)) mechanism of uphill albumin transport is verified as possible. It is tentatively inferred that lymph formation in resting tissue does not result from a small difference between a large fluid (volumetric) filtration and an almost equally large fluid reabsorption, either in the same capillary (Starling) or between different capillaries (Zweifach) (Zweifach, Circ. Res.34, 858–866 (1974)). Rather, reabsorption is negligibly small relative to filtration, and lymph flow is comparable to volumetric filtration.     

Renal markers and predictors, and renal and cardiovascular risk factors

An important task of the nephrologists during the last century, it has been the search of elements and means that allow us, with the adequate precision, to correlate the functional deterioration of the kidney, and the patient's clinical reality. And the continuous searching of factors and markers that injure them, the prognosis, and early diagnosis, to be able to predict the degree of the organs and patient's survival. Almost parallel survival presage in the natural history of the illness, almost one century ago. In the second half of the XX century, in the developed countries, appear modifications of the social, cultural, and sanitary conditions, that make appear some very different partner-sanitary and epidemic circumstances, and take place like they are, among others: 1. An increase of per cápita private rents, what takes place to increase of the level of social life and the population's health. With increment of the longevity, and smaller incidence and prevalence of classic process, as malnutrition, infections, infantile mortality, so increasing the weight of the cardiovascular diseases and death. This is potentiated for the increment and the incidence of environmental cardiovascular risk's factors (like high caloric and fatty-rich diets, smoke, alcohol, disappearance of the physical work, inactivity, etc). And that situations are also product of the change of the outline of human and social values and guides. 2. Access of the whole population to a sanitary attention of more quality and effectiveness. It allows the biggest survival of patients that suffer vascular crisis, (as angina, miocardial infarction or cerebrovascular accident), that few years ago they have had a higher morbimortality and an inferior survival (2). 3. The execution of big epidemic studies has been able to, not only characterize and test with scientific evidence to numerous factors and markers, that induce renal and cardiovascular prejudicial changes, but risk and death probability prediction. And also, its possible association nexuses, its injuring mechanisms, and the characterization of the new "emergent" renal and cardiovascular risk's markers and factors. 4. The impact on the possibility to treat the end stage renal disease with effective and prolonged procedures, by hemodialisis or kidney transplantation, has been occurred. The affected population's survival with the adequacy renal-sustitution treatment, and the possibility of indefinite duration of its treatment, has also impacted on the public health, and its resources, in an evident way. Simultaneously to increase of the incidence in the population, the electivity for the treatment has been enlarged and extended increasing it exponentially. These facts are documented here, and are defined the characteristics of the factors and markers of risk, of renal and cardiovascular diseases. The defined factors are valued to mark, so far as with the well-known evidence is possible, the prediction and the progression of the renal and cardiovascular functional deterioration: The hypertension, cardiovascular remodeling, the arterial stiffness, the heart rate, the sympathetic activation, the modification of the physiological response of the target organ to the overcharge, the metabolic syndrome, the obesity, the insulin resistance, the altered lipid profile, and metabolism of the fatty acids, the salt-sensibility, the decrease of the renal functional reserve, the glomerular hyperfiltration, the absence of the arterial pressure nocturnal descent, the abnormal excretion of proteins for the urine, the phenomenon induced by dysfunctions of the clotting, superoxide production, growth factors, the production of chronic inflammation and its markers, the factors of the glomerulosclerosis progression, the hyperuricemic status, the endothelial dysfunction and others, are evaluated. As well as their association among them and with other factors of risk not changeable like the age, and in turn, with other acquired voluntarily factors of risk, as the smoking habit and the alcohol. These facts are now impacting on the population's sanity. And also in the professional nephrologic exercise, so much for the cardiovascular and renal morbimortality increased, as for the increase of the incidence of end-stage renal disease susceptible to treat with of substitutive procedures. They try to justify the sentence of Alan Weder of the heading, and other concepts like "epidemic factors of the XXI century", and intuitive expressions like "predialitic endothelial disruption or ruin".     

ERCP and MRCP--when and why

Since the introduction of endoscopic retrograde cholangiopancreatography (ERCP) in the 1970s, gastroenterologists have a wide spectrum of diagnostic and therapeutic options in the biliopancreatic ductal system at their disposal. With its arrival in the 1990s, magnetic resonance cholangiopancreatography (MRCP) developed as a potent diagnostic tool in biliopancreatic pathology. Currently, MRCP is widely replacing diagnostic ERCP and thereby avoiding complications related to endoscopic technique.We summarize evidence-based data and demonstrate indications and differential indications for MRCP and ERCP in pancreatic disease. Complications related to the procedures and possible medical prevention are discussed. The feasibility of interventional endoscopy in pancreatic disease is reported in detail. The role of gastroenterologists in performing MRCP is outlined on the basis of practical examples.     

Diaphragmatic and paradiaphragmatic tumors and pseudotumors

Primary lesions of the diaphragm are rare and are often difficult to distinguish from a host of other entities. Primary tumors include lipomas, cysts, and sarcomas, while secondary lesions, which can mimic them, include direct extensions from neighboring organs or metastatic implants and adenopathy. In addition, one must exclude a variety of pseudotumors, such as eventrations, diaphragmatic invaginations, and crural thickening. Examples of such primary and nonprimary diaphragmatic lesions are discussed.     

Urbanization and tropical health--then and now

Since the launch of the Annals of Tropical Medicine and Parasitology 100 years ago, the percentage of the world's population living in urban settings has more than tripled and is now approaching 50%. Urbanization will continue at a high pace, particularly in the less developed regions of Africa and Asia. The profound demographic, ecological and socio-economic transformations that accompany the process of urbanization have important impacts on health and well-being. In industrialized countries, urbanization led to the so-called 'epidemiological transition', from acute infectious and deficiency diseases to chronic non-communicable diseases, many decades ago. In the developing world, surprisingly little research has been carried out on the health-related aspects of urbanization. In a temporal analysis of publications in the Annals of Tropical Medicine and Parasitology, for example, in which the first volume in every decade from 1907 was examined, only 16 (2.6%) of the 604 articles investigated focused on epidemiological and/or public-health issues in urban tropical settings. This review begins with the question 'what is urban?' and then provides a summary of the trends seen in urbanization, and its impacts on human health, over the past century, on both a global and regional scale. For the main tropical diseases, estimates of the at-risk populations and the numbers of cases are updated and then split into urban and non-urban categories. The inhabitants of urban slums are particularly vulnerable to many of these diseases and require special attention if internationally-set targets for development are to be met. Heterogeneity, a major feature of urban settings in the tropics that complicates all efforts at health improvement, is demonstrated in an exploration of a densely populated municipality of a large West African town. Urban planners, public-health experts and other relevant stakeholders clearly need to make much more progress in alleviating poverty and enhancing the health and well-being of urban residents, in an equity-effective and sustainable manner.     

Leucine and alpha-ketoisocaproate metabolism and interconversions in fed and fasted sheep

Fed and three-day-fasted sheep were infused with [1-14C] alpha-ketoisocaproate (KIC), L-[1-14C] leucine, and [14C] bicarbonate for determination of their whole-body turnovers, interconversions, and oxidation. Protein synthesis (PS), protein degradation (PD), net tissue metabolism, unidirectional utilization, and production rates also were estimated for the portal-drained viscera, liver, and hindquarters. KIC and leucine arterial concentrations (6.5 and 95 mumol X L-1) both increased with fasting. KIC turnover (9 mumol X min-1) also increased but leucine turnover (108 mumol X min-1) decreased. About 40% of KIC and 15% of leucine were oxidized, but they contributed less than 1% of whole-body CO2 production. The portal-drained viscera released KIC and leucine into the blood only in fed sheep. Hepatic net utilization of KIC and leucine (approximately 2 and 12 mumol X min-1) changed only little with fasting; thus, total splanchnic tissues utilized both in fasted sheep. Net metabolism by the hindquarters (representative of skeletal muscle) was always opposite to splanchnic metabolism. Thus, muscle must produce both KIC and leucine during fasting. In fed sheep whole-body PS, expressed as mumol X min-1 of leucine, was 92 +/- 6 and PD was 71 +/- 5. After fasting, PS decreased by 27%. Calculated liver protein metabolism was unaffected by the fast; PS (fixed and plasma) remained at about 25 and PD at about 15 mumol X min-1. However, protein metabolism by the hindquarters was sensitive to fasting; PS decreased from 30 +/- 4 in fed sheep to 20 +/- 3 mumol X min-1 after fasting and PD increased from 27 +/- 2 to 35 +/- 6 mumol X min-1. Thus, hepatic PS was maintained at the expense of muscle. If the total muscle mass of the body is considered, muscle PS contributed more than one half of whole-body PS.     

Hyponatremia and heart failure--pathophysiology and implications

Fluid and electrolyte disturbances are a common feature of heart failure. Among the electrolyte disturbances that occur in heart failure, disorders of potassium and magnesium have traditionally received the most attention. Abnormalities involving either of these actions serve as risk factors for sudden cardiac death/arrhythmias. More recently, a growing appreciation has emerged for the importance of hyponatremia in the heart failure patient. Hyponatremia is multifactorial in origin, and its presence correlates with disease severity and outcome. There are few effective therapies for hyponatremia, and those that are available are not viewed as offering specific survival benefits per se. The recent availability of vasopressin receptor antagonists, however, offers a different approach to the management of this complex electrolyte disturbance, but one that is still evolving as to the scope of its clinical benefits.     

Sex and Gender and Allostatic Mechanisms of Cardiovascular Risk and Disease

Cardiovascular diseases are leading causes of mortality and morbidity in adults worldwide. Multiple studies suggest that there are clinically relevant sex differences in cardiovascular disease. Women and men differ substantially in terms of prevalence, presentation, management, and outcomes of cardiovascular disease. To date, however, little is known about why cardiovascular disease affects women and men differently. Because many studies do not differentiate the concept of sex and gender, it is sometimes difficult to discriminate sociocultural vs biological contributors that drive observed clinical differences. Female sex has some biological advantages in relation to cardiovascular disease, but many of these advantages seem to disappear as soon as women develop cardiovascular risk factors (eg, type 2 diabetes, hypertension, dyslipidemia). Furthermore, stress and allostatic load could play an important role in the relationship between sex/gender and cardiovascular diseases. In this narrative review, we argue that chronic stress and psychosocial factors might better encompass the patterns of allostatic load increases seen in women, while biological risk factors and unhealthy behaviours might be more important mechanisms that drive increased allostatic load in men. Indeed, men show allostatic load patterns that are more associated with impaired anthropometric, metabolic, and cardiovascular functioning and women have greater dysregulation in neuroendocrine and immune functioning. Thus gender-related factors might contribute to the pathogenesis of cardiovascular disease especially through stress mechanisms. It is important to continue to study the mechanisms by which gender influences chronic stress, because chronic stress could influence modifiable gendered factors to promote cardiovascular disease prevention.