尿素对幽门螺杆菌生长的影响研究

目的 :研究尿素对幽门螺杆菌生长的影响。方法 :在幽门螺杆菌培养基中分别加入 3种浓度 (5 mmol/ L,10 mmol/ L和 2 0 m mol/ L )的尿素 ,然后将培养基 p H分别调至 3.5、4 .5、5 .5。将 10株 Hp分别接种于这 9种培养基中 ,以确定最佳条件组合。之后采用最佳条件进行胃黏膜活检标本 Hp的培养。结果 :10株 Hp在 9种含尿素培养基中以尿素浓度为 10 mmol/ L、p H为 4 .5时生长最好 ,其他 8种与之比较差异极为显著 (P<0 .0 1) ,5 7份胃镜活检标本分别接种于尿素浓度为 10 mm ol/ L、p H为 4 .5时生长最好 ,其他 8种与之比较差异极为显著 (P<0 .0 1) ,5 7份胃镜活检标本分别接种于尿素浓度为 10 mmol/、p H 4 .5培养基和 p H 7.0不含尿素的普通 Hp培养基中 ,32份标本 (5 6 .1% )在尿素培养基中培养阳性 ,其中 2 2份 (38.6 % )在普通培养基中培养阳性。结论 :含有适当浓度尿素的培养基可用于胃黏膜 Hp的分离培养。     

人工家蚕蛹巴西虫草的毒性研究

对人工家蚕蛹巴西虫草的毒性进行了研究。结果表明：小鼠和大鼠经口ＬＤ５０分别为＞４３．０ｇ／ｋｇ和＞５０ｇ／ｋｇ。３０天喂养试验中大鼠食欲下降，体重增长减慢；血清胆固醇和血清尿素氮浓度降低，血清总蛋白和血糖无改变；血尿常规无异常；心、肝、牌等脏器系数无改变；肝、肾组织病理学检查未发现明显改变。可认为该产品无明显急性和亚急性毒性。     

Mathematical model to analyse urea synthesis following alanine infusion in control subjects and in patients with liver cirrhosis

A three-compartment model was used to analyse the urea response to an alanine infusion in control subjects and patients with liver cirrhosis. Discriminant analysis showed a good separation between model coefficients of the two groups. A single parameter was derived, able to quantify the liver functional capacity. The method provides a useful diagnostic tool in patients with liver disease.     

Dialysate-side urea kinetics. Neural network predicts dialysis dose during dialysis

Determination of the adequacy of dialysis is a routine but crucial procedure in patient evaluation. The total dialysis dose, expressed as Kt/V, has been widely recognised to be a major determinant of morbidity and mortality in haemodialysed patients. Many different factors influence the correct determination of Kt/V, such as urea sequestration in different body compartments, access and cardiopulmonary recirculation. These factors are responsible for urea rebound after the end of the haemodialysis session, causing poor Kt/V estimation. There are many techniques that try to overcome this problem. Some of them use analysis of blood-side urea samples, and in recent years, on-line urea monitors have become available to calculate haemodialysis dose from dialysate-side urea kinetics. All these methods require waiting until the end of the session to calculate the Kt/V dose. In this work, a neural network (NN) method is presented for early prediction of the Kt/V dose. Two different portions of the dialysate urea concentration-time profile (provided by an on-line urea minitor) were analysed: the entire curve A and the first half B, using an NN to predict the Kt/V and compare this with that provided by the monitor. The NN was able to predict Kt/V is the middle of the 4h session (B data) without a significant increase in the percentage error (B data: 6.69%±2.46%; A data: 5.58%±8.77%, mean±SD) compared with the monitor Kt/V.     

Mitochondrial aspartate glutamate carrier (citrin) deficiency as the cause of adult-onset type II citrullinemia (CTLN2) and idiopathic neonatal hepatitis (NICCD)

 By using homozygosity mapping and positional cloning, we have shown that adult-onset type II citrullinemia (CTLN2) is caused by mutations of the SLC25A13 gene, which is localized on chromosome 7q21.3 and encodes a mitochondrial solute carrier protein named citrin. So far, we have reported nine mutations, most of which cause loss of citrin, and we have established several methods for DNA diagnosis. These methods have shown that more than 90% of the patients diagnosed as suffering from CTLN2 by enzymatic analysis carry SLC25A13 mutations in both alleles, indicating that CTLN2 is caused by citrin deficiency. Furthermore, by using the same DNA diagnosis methods, we discovered that 70 neonates or infants suffering from a particular type of neonatal hepatitis carry the same SLC25A13 mutations. Since the symptoms of the neonates are different from those of the more severe CTLN2 and usually ameliorate without special treatment, we designated the neonatal disease neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD). We conclude that citrin deficiency causes NICCD in neonates and CTLN2 in adults through the additional effects of genetic or environmental modifiers. Since the function of citrin, together with that of an isoform, aralar, was found to be as a mitochondrial aspartate glutamate carrier, the various symptoms of NICCD and CTLN2 may be understood as caused by defective aspartate export from the mitochondria to the cytosol and defects in the malate aspartate shuttle. It is, however, still difficult to understand the cause of the hepatic deficiency of argininosuccinate synthetase protein in CTLN2. Received: March 20, 2002 / Accepted: March 28, 2002     

Effect of atrial natriuretic factor and cyclic guanosine monophosphate on water and urea transport in the inner medullary collecting duct

We examined the action of high (2×10^–8M) and low (6×10^–9M) concentrations of atrial natriuretic factor (ANF) on water and urea transport in the rat inner medullary collecting duct (IMCD) using the in vitro microperfusion technique. We measured the hydraulic conductivity (Lp ×10^–6 cm/atm per second) and both lumen-to-bath (P _u(lb)) and bath-to-lumen (P _u(bl)) ¹⁴C-urea permeabilities (P _u× 10^–5 cm/s) in the absence and in the presence of vasopressin (VP). High concentrations of ANF were able to inhibit the maximum activity of (50 U/ml) VP-stimulated L _p but physiological concentration of ANF inhibit only submaximum activity (10 U/ml) of VP-stimulated L _p. The hydrosmotic effect of dibutyryl-cyclic 3,5 adenosine monophosphate (cAMP) (10^–4M) was unchanged by high concentrations of ANF (2×10^–8M). Also we found that high (10^–4M) and low (10^–6M) concentrations of exogenous cyclic 3,5-guanosine monophosphate (GMP) while unable to change the Lp in the absence of VP, decreased the maximum activity of VP-stimulated Lp significantly. We also found that ANF inhibits partially and in a reversible manner the VP-stimulated P _u(lb) but not the VP-stimulated P _u(bl). These results demonstrated that plasma concentrations of ANF observed during volume expansion (10^–10M) are able to inhibit submaximum activity of VP-stimulated (10 U/ml) L _p in the rat IMCD, this effect seems to occur before cAMP formation and it appears to be mediated by cGMP. ANF (6× 10^–9M) also reduced the VP-stimulated urea outflux. Therefore, the increase in water excretion produced by ANF could be explained, at least in part, by the inhibition by ANF of vasopressin effects on water and urea transport in the IMCD.This study was presented in part at the VI Latin American Congress of Nephrology, Brazil, October 1985 and at the X^th International Congress of Nephrology, London, July 1987.     

Sites of arginine synthesis and urea production along the nephron of a desert rodent species,Meriones shawi

The distribution of arginine synthase and arginase activities along the successive nephron segments ofMeriones kidney was measured in vitro with single tubule enzymatic microtechniques making use of eitherl-[ureido-¹⁴C] Citrulline (0.108 mM) orl-[guanidion-¹⁴C]arginine (0.2 mM) as the respective substrates. Arginase activity (fmol urea formed per min per mm of tubule) was very low (5–25 fmol.min^–1.mm^–1) in most nephron segments including the early portions of proximal convoluted tubules (early PCT). It increased progressively after 3 mm of the PCT to reach a value of 200 fmol.min^–1.mm^–1 in the cortical portion of the straight proximal tubule (CPST), with a further increase, along the pars recta, of up to 250 fmol.min^–1.mm^–1 in the outer medullary portion (OSPST). In addition, arginase activity in OSPST and the adjacent descending thin limb (DTL) was higher in juxtamedullary nephrons (JN) than in the corresponding portions of superficial nephrons (SN). Arginine synthase activity (fmol arginine formed per mm of tubule per min) was present in proximal tubules exclusively, with a gradient decreasing along the PCT (about 600 fmol.min^–1.mm^–1 in the 1st mm, 65 fmol.min^–1.mm^–1 in CPST and 30 fmol. min^–1. mm^–1 in OSPST). It has been checked that CPST and OSPST (where the two enzyme systems are present) are able to convert citrulline directly into urea with a yield of 65%. It is suggested that: (1) in early PCT cells, arginine synthase activity permits the conversion of the reabsorbed citrulline into arginine (which then diffuses towards blood vessels); and (2) in pars recta cells, arginase activity results in a net entry of arginine across the basolateral membranes and in a net exit of the formed urea into the tubular fluid, if the permeability to urea of luminal membranes is greater than that of basolateral membranes. Such a mechanism of urea secretion might contribute to the maintenance of urea recycling in the medulla and, thereby, participate in the process of concentrating the urine.     

Mutations and polymorphisms in the human ornithine transcarbamylase gene

Deletions of variable size involving one or more exons, 29 different missense, nonsense, or frameshift mutations, and three polymorphisms have been found in patients with ornithine transcarbamylase (OTC) deficiency. Most of the deletions and mutations were found in patients with severe disease manifested clinically as acute neonatal hyperammonemia. A small number of mutations or somatic mosaicism for deletions were found in males with “late onset” disease and in heterozygous females who were symptomatic. Approximately 10–15% of all molecular alterations associated with OTC defi ciency are large deletions involving all or part of the OTC gene with or without contiguous genes on the short arm of the X chromosome. Approximately 10% of all point mutations involve the CpG dinucleotide of codon 141 with a CGA→CAA transition producing a deleterious Arg→Gln substitu tion in position 109 of the mature enzyme and causing the elimination of a TaqI recognition site. The majority of the remaining mutations in the OTC gene are unique to the affected family and are usually not found in unrelated patients. To date, two mutations have been described in the sequence of the “leader” peptide, 23 mutations have been found in the coding sequence of the “mature” enzyme, and four mutations have been discovered in splicing recognition sites. Approximately 20 single base polymorphisms have been postulated to exist by comparing two reported OTC gene sequences; six of these substitutions cause amino acid changes of which three have been confirmed in patients. Of the known point mutations, 27 are single base substitutions: 17 missense, 6 nonsense, 4 splice site, and the remaining 2 are single base deletions. © 1993 Wiley-Liss, Inc.     

The mechanisms of fast renal compensation

Summary The changes in blood concentration which result in the adjustment of excretion when renal functioning mass is acutely reduced have been investigated by means of paired experiments on isolated dog kidneys. One kidney was perfused with undiluted blood; the other kidney was perfused with blood supplemented with an amount of water and solutes corresponding to the amount retained after the suppression of the contralateral kidney in situ; the response was evaluated from the difference in excretion between the two organs. The results may be summarized as follows: a) the adjustment of the excretion of water, sodium, potassium and urea results from small changes in blood concentration (haematocrit, plasma proteins and solutes), in the absence of specific stimuli of extrarenal origin; b) increased urea concentration is not the major determinant of the readjustment of sodium and water excretion; c) the response is potentiated by high arterial blood pressure; d) if the load of water exceeds the load of sodium, this ion is retained by the kidney even in the presence of an osmotic load of urea; e) the changes in the blood concentrations do not provide an adequate adjustment of the excretion of phosphate; f) increased excretion per nephron results from decreased fractional reabsorption without significant change in glomerular filtration rate.     

Monitoring exercise stress by changes in metabolic and hormonal responses over a 24-h period

Summary Metabolic and endocrine responses of 14 subjects of varying levels of fitness to an intensive anaerobic interval training session were assessed before exercise and at 2 h, 4 h, 8 h and 24 h postexercise. The endocrine response of the same subjects to a control day, where they were required not to exercise, was also assessed and compared with the values obtained on the interval training day. Uric acid, urea, and creatine phosphokinase concentrations still remained elevated above pre-exercise values 24 h postexercise. Lactate, creatinine, testosterone and cortisol concentrations were significantly elevated above pre-exercise values immediately postexercise but these had reversed by 2 h postexercise. Over the remainder of the recovery period testosterone concentrations remained significantly lower than values measured at similar times on the control day. This was shown to be due directly to a change in testosterone as sex hormone binding globulin concentration remained constant throughout the recovery period. The data indicate that when comparisons of data were made to control (rest) days, imbalances in homeostasis, due to intensive training, are not totally reversed within the next 24-h. The data also demonstrate that the parameters measured undergo the same variations in subjects with a wide range of physical fitness, indicating that these parameters could be used to monitor exercise stress and recovery in athletes of a wide range of abilities. The more acute responses to exercise could be mistaken for overtraining if insufficient recovery time were not permitted between the final exercise session and taking blood samples, further emphasising the need to be able to recognise the difference between the fatigue associated with acute exercise and a state of chronic fatigue that may result from too little regeneration time within the training programme.