Isolation and immunochemical characterization of the major allergen of birch pollen (Betula verrucosa)

The classification of some of the extractable birch pollen antigens as allergens was established by crossed radioimmunoelectrophoresis (CRIE). In CRIE the major allergen (antigen 23) exhibited the strongest “radiostaining” and only a few other components of birch pollen extract were visibly radiostained. The major allergen and a preparation containing mainly the minor allergens, antigens 25 and 19, were isolated from a crude aqueous birch pollen extract by a combination of anion-exchange, size-exclusion, and chelate chromatography. Antigen 23 was purified to near homogeneity. The molecular weights and the pIs of antigens 23, 25, and 19 were determined to be 17,000 daltons, pI 5.25 (5.5, 5.0); 25,000 daltons, pI 5.0 (4.9, 5.4); and 29,000 daltons, pI 6.2 (5.4), respectively. The classification of antigen 23 as the major allergen in birch pollen was supported by results of RAST inhibition experiments, RAST screening, and skin prick testing.     

The mechanisms of sodium current inhibition by benzocaine in the squid giant axon

(1) The effects of benzocaine on the ionic currents in the voltage-clamped squid giant axon have been examined under various conditions; intact axons internally perfused with CsF and axons dialysed with tetraethyl-ammonium ions were used. (2) Both the steady state outward (potassium) current and the early transient (sodium) current were reduced by ca. 50% by benzocaine (1 mM). (3) Plots of the changes produced by benzocaine (1 mM) in the Hodgkin-Huxley parameters for the steady state activation (m), the steady state inactivation (h) and the time constants (_m and _h) for activation and inactivation of the sodium current are shown. Them andh curves are shifted in positive and negative directions respectively on the voltage axis. The time constants are not greatly affected. (4) In axons in which the sodium current inactivation had been largely removed by treatment with chloramine T, the sodium current was still reduced by ca. 50% by 1 mM benzocaine and the positive shift in activation remained unchanged. (5) The dependence on benzocaine concentration (for2mM) of the peak sodium current reduction and the shift in steady state inactivation have been determined. (6) It is concluded that in the squid axon the effects on inactivation are not the main reason for the reduction of the sodium current by benzocaine and that, in common with many other neutral anaesthetics, there are at least two sites at which benzocaine acts.     

Effects of Na+, K+ and Mg2+ on45Ca2+ uptake by pancreatic islets

Microdissected pancreatic islets of noninbredob/ob-mice were used to study ionic effects on the lanthanum-nondisplaceable⁴⁵Ca²⁺ uptake by islet cells. Omission of Mg²⁺ from the incubation medium had no effect, but the⁴⁵Ca²⁺ uptake was increased by omission of Na⁺ and decreased by omission of K⁺. Excess Mg²⁺ (1.2–15 mM) inhibited and excess K⁺ (4.7–25 mM) stimulated the⁴⁵Ca²⁺ uptake in a concentration-dependent manner. Stimulation of⁴⁵Ca²⁺ uptake in Na⁺-deficient islets was associated with an enhancement of the basal insulin release. Total abolishment of glucose-stimulated⁴⁵Ca²⁺ uptake in K⁺-deficient islets did not preclude a significant secretory response to glucose. It is concluded that the lanthanum-nondisplaceable⁴⁵Ca²⁺ uptake shows a partial correlation to insulin release.     

阿魏酸钠对大鼠晶状体上皮细胞凋亡相关基因BCl-2和bax的调控

目的:本研究旨在探讨阿魏酸钠 (SF)对实验性氧化损伤大鼠晶状体上皮细胞 (LEC)凋亡相关基因BCl-2和bax的调控。方法:将SD大鼠双眼随机分成空白对照组、过氧化氢 (H₂O₂)组、吡诺克辛 (PS)组和SF组。无菌操作摘除眼球并在手术显微镜下分离晶状体,使晶状体孵育在 300μmol·L^-1H₂O₂ 培养液中复制LEC凋亡模型,同时加入终浓度为 5mmol·L^-1的SF,置二氧化碳培养箱共同孵育 2 4h。取晶状体前囊膜采用免疫组化法检测凋亡相关基因BCl-2和bax的蛋白表达并进行比较。结果:(1)正常SD大鼠LEC中BCl-2和Bax均有表达,BCl-2表达较Bax表达强。 (2)H₂O₂ 组BCl-2表达显著下调,Bax表达显著上调 (Ridit检验,P <0.01);BCl-2 /Bax比率下降。(3)与H₂O₂ 组比较,SF可明显上调BCl-2表达,下调Bax表达 (P <0.01),BCl-2 /Bax比率上升。 (4)PS与SF的调节作用相似,但SF的作用强于PS(P <0.05)。结论:本研究结果表明,SF调控凋亡相关基因BCl-2和bax的表达可能是SF抑制LEC凋亡的分子机制.     

Ovarian stimulation by clomiphene citrate and hMG in combination with cetrorelix acetate for ICSI cycles

BACKGROUND: The introduction of GnRH antagonists such as cetrorelix acetate has made possible the simplification of ovarian stimulation. However, the most effective protocol for their administration has not yet been clearly defined. METHODS: Forty women with male-factor infertility undergoing 40 ICSI cycles were included in the study. Clomiphene citrate at 100 mg a day was given from cycle day 3 through day 7. hMG at 150 IU was given on cycle days 4, 6 and 8, and was adjusted from day 9 according to the follicular and hormone responses. Cetrorelix acetate at 2.5 mg was administered when the leading follicle reached 14 mm. The remaining 0.5 mg was divided into two 0.25 mg injections for possible later use. Serum FSH, LH, estradiol and progesterone levels were measured daily from the day of cetrorelix acetate injection until hCG was given. RESULTS: Serum LH level was suppressed effectively for 4 days. Four patients (10%) needed one or two additional injections of 0.25 mg cetrorelix acetate. No premature LH surge was detected in any of the women treated. Sixteen women became pregnant (40%), of which 14 pregnancies (35%) were ongoing at the time of writing. CONCLUSIONS: This study demonstrates that this new protocol is feasible for couples with male-factor infertility undergoing ICSI.     

Effects of enclomiphene and zuclomiphene on basal and gonadotrophin-stimulated progesterone secretion by isolated subpopulations of small and large ovine luteal cells

We examined the effects of enclomiphene and zuclomiphene, aloneand in combination with oestradiol, on basal and gonadotrophin-stimulatedprogesterone secretion by isolated subpopulations of both large(granulosa-lutein) and small (theca-lutein) ovine luteal cells.Isolated large and small luteal cells derived from intact, enucleatedovine corpora lutea were incubated for 48–120 h with orwithout 22R-hydroxycholesterol or pregnenolone (2.5 µM)and a range of enclomiphene, zuclomiphene, and/or oestradiolconcentrations (3–100 µM), both with and withoutovine Iuteinizing hormone (100 ng/ml). Spent media were assayedin duplicate for progesterone content by radioimmunoassay. Enclomiphene,zuclomiphene, and oestradiol exhibited equivalent dose-dependentinhibitory effects on basal and gonadotrophin-stimulated smalland large ovine luteal cell progesterone secretion under allsubstrate conditions. Both cell types became more sensitiveto clomiphene inhibition with increasing time in culture. Incombined treatments, the effects of oestradiol and either enclomipheneor zuclomiphene became additive in longer-term cultures andwere never antagonistic In this model system, (i) clomiphene,like oestradiol, appears to inhibit 3-hydroxysteroid dehy-drogenaseactivity, (ii) both stereoisomers act as oestrogen agonists,(iii) neither demonstrates any anti-oestrogenic properties,and (iv) both large and small luteal cells become more sensitiveto clomiphene inhibition with increasing duration of exposure.     

Effect of extracellular volume expansion on renal cortical and medullary Na+−K+-ATPase

Summary The role of renal Na⁺–K⁺-ATPase in the acute changes in sodium reabsorption caused by isotonic volume expansion was evaluatedin vivo andin vitro in the rat and the dog. Duringin vivo volume expansion with isotonic saline in the rat, renal medullary Na⁺–K⁺-ATPase specific activity increased, while the simultaneously determined cortical Na⁺–K⁺-ATPase specific activity and kinetics remained unchanged. Furthermore, experimentsin vitro failed to demonstrate a circulating inhibitor of renal Na⁺–K⁺-ATPase both in plasma dialysates from volume-expanded rats and in plasma dialysates concentrated 20-fold by ultrafiltration from volume-expanded dogs. These results suggest that the decreased proximal tubular reabsorption of sodium during volume expansion is not mediated by inhibition of renal cortical Na⁺–K⁺-ATPase. The acute increment in medullary Na⁺–K⁺-ATPase observed could represent an adaptive response to increased sodium reabsorption by the loops of Henle, and raises the possibility that this enzyme may participate in relatively rapid adjustments in the transport of sodium by the renal tubule.     

The concentrative nucleoside transporter family,SLC28

The SLC28 family consists of three subtypes of sodium-dependent, concentrative nucleoside transporters, CNT1, CNT2, and CNT3 (SLC28A1, SLC28A2, and SLC28A3, respectively), that transport both naturally occurring nucleosides and synthetic nucleoside analogs used in the treatment of various diseases. These subtypes differ in their substrate specificities: CNT1 is pyrimidine-nucleoside preferring, CNT2 is purine-nucleoside preferring, and CNT3 transports both pyrimidine and purine nucleosides. Recent studies have identified key amino acid residues that are determinants of pyrimidine and purine specificity of CNT1 and CNT2. The tissue distributions of the CNTs vary: CNT1 is localized primarily in epithelia, whereas CNT2 and CNT3 have more generalized distributions. Nucleoside transporters in the SLC28 and SLC29 families play critical roles in nucleoside salvage pathways where they mediate the first step of nucleotide biosynthesis. In addition, these transporters work in concert to terminate adenosine signaling. SLC28 family members are crucial determinants of response to a variety of anticancer and antiviral nucleoside analogs, as they modulate the entry of these analogs into target tissues. Further, this family is involved in the absorption and disposition of many nucleoside analogs. Several CNT single nucleoside polymorphisms (SNPs) have been identified, but have yet to be characterized.     

The effects of anesthesia on the excretion of an isotonic saline load in the rat

The ability to excrete a volume of isotonic saline equal to 10% of body weight infused over 60 min, was examined in awake rats and in rats anesthetized with 1 of the 2 agents most commonly used in renal clearance studies, Inactin or Nembutal. Rats anesthetized with Inactin excreted significantly less of the infused sodium during the period of infusion and in the 120-min post-infusion periods as compared to Nembutal-anesthetized rats or awake rats. Following saline infusion, there was a significantly greater decrease in serum protein concentration (25.5±4.7%) in rats anesthetized with Inactin, compared to that observed in the awake or Nembutal-treated rats. In a separate group of saline-infused awake rats, induction of anesthesia with Inactin resulted in a significant increase in hematocrit and a decrease in serum protein concentration. These studies suggest that Inactin anesthesia decreases the ability of the kidney to excrete a saline load and that, in studies of sodium excretion in the rat, especially if volume expansion is to be part of the experimental protocol, Nembutal rather than Inactin may be the anesthetic of choice.These studies were performed while Drs. Knight and Frankfurt were Fellows in Nephrology of Baylor College of Medicine, and were supported in part by a Clinical Investigatorship award to Dr. Weinman and an Associate Investigatorship award to Dr. Frankfurt from the Veterans Administration. This work was presented in part at the Combined Session, Southern Section, American Federation for Clinical Research and the Southern Society for Clinical Investigation, New Orleans, Louisiana, January 27–29, 1977, and has appeared in abstract form in Clin. Res.25, 61 A (1977)     

Effekte einer Captopriltherapie auf die Natrium- und Wasserausscheidung bei Patienten mit Leberzirrhose und Aszites

Summary Ascites in patients with cirrhosis of the liver frequently is refractory to diuretic treatment. It was postulated that vasoconstriction of the renal cortex, mediated by activation of the renin-angiotensin-aldosterone-system (RAAS), may be one course of the disturbed sodium- and water-excretion in these patients. We therefore investigated in 14 cirrhotic patients with ascites under constant diuretic treatment the effects of low-dose captopril therapy on urinary sodium- and potassium-excretion, body weight, abdominal girth, serum-sodium,-potassium, creatinine-clearance, plasma-renin-activity (PRA), plasma-aldosterone (PA) and mean arterial pressure (MAP). After a control period of 4 days the patients received 2 × 6.25 mg/d captopril for 5 days and 4 × 6.25 mg/d for further 5 days. Treatment was followed by a second control period without captopril.PRA increased significantly after 2 days of captopril treatment. 2 × 6.25 mg/d captopril induced a significant increase in sodium excretion and a significant decrease of body weight. MAP decreased slightly but significantly without clinical signs of hypotension. 4 × 6.25 mg/d captopril resulted in a further reduction of body weight and a further enhancement of sodium excretion. Three days after withdrawal of captopril sodium output was significantly reduced again. Conclusion: In cirrhotic patients low-dose captopril seems to be efficient in the treatment of ascites resistant to diuretics without causing major side effects.

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Abkürzungen ACE Angiotensin-Converting-Enzym - A-II Angiotensin II - C_{H 2 O} Frei-Wasser-Clearance - C_Krea Kreatinin-Clearance - C_Osmo Osmolale Clearance - g Gramm - h Stunde - kg Kilogramm - l/d Liter pro Tag - MAP Mittlerer arterieller Blutdruck - mg Milligramm - mg/d Milligramm pro Tag - ml/min Milliliter pro Minute - mmHg Millimeter Quecksilbersäule (Torr) - mmol/d Millimol pro Tag - NaCl Natriumchlorid - ng/ml/h Nanogramm pro Milliliter und Stunde - PA Plasma-Aldosteron - pg/ml Picogramm pro Milliliter - PRA Plasma-Renin-Aktivität - RAAS Renin-Angiotensin-Aldosteron-System - SEM Standardfehler des Mittelwertes - S_Krea Kreatininkonzentration im Serum - S_Osm Serum-Osmolalität - U_Krea Kreatininkonzentration im Urin - U_Osm Urin-Osmolalität - V Urinminutenvolumen - vgl. vergleiche - µmol/l Micromol pro Liter