Interactions of polynucleotides and their components. II. Interaction of uracil derivatives with alkali- and alkali earth chlorides.
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Calcium Chloride↗
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[Examination of the water supply with the alkali and alkali-earth supplement optimized DIN luminescent bacteria test, exemplified by the Saar river].
The light intensity emitted by luminescent bacteria is influenced by both the osmolarity and the ion composition of the test medium. The addition of potassium and calcium ions to a sodium chloride solution causes a considerable increase in the light intensity of bacteria. If these elements occur in the proper concentrations in the test material, the luminescence in the test sample will be higher than in the control sample containing only sodium chloride. This physiological dependence did not find the due consideration in the establishment of the German standard method for the luminescent bacteria test using Microtox bacteria (German Institute for Standardization DIN 38,412, Part 34--edition March 1991) where only the osmotic balancing by sodium chloride was taken into account. For testing chemicals, the luminescent bacteria test with Microtox reagent can be run without problems by the procedure that is recommended by Microbics Corporation and which became part of the DIN standard method. The situation is different when analyses of natural waters or effluents from wastewater plants are concerned, where matrix effects have to be expected. Stimulation of light intensity can be a reflection of a nonoptimized test medium and in the worst case may cause false negative results. The new ASW (artificial sea-water) luminescent bacteria medium according to Klein, which besides sodium contains potassium, magnesium, and calcium ions, brings stimulation to both samples and controls, effectively reducing enhancement and increasing the inhibitory effects of samples from the River Saar. However, high light stimulation rates measured in parallel tests with the DIN procedure could not be caused by the low concentrations of alkaline and alkaline-earth ions in the samples. The experiments indicate that there must be additional influencing substances which have not yet been identified. Furthermore, the experiments show that the matrix effects of unknown origin that will exert a positive influence on the light emission may be compensated by addition of alkaline and alkaline-earth ions.
Animals↗
[A case of the milk-alkali syndrome with a small amount of milk and magnesium oxide ingestion--the contribution of sustained metabolic alkalosis induced by hypertonic dehydration].
We described a patient with the milk-alkali syndrome induced by the ingestion of small amount of milk (200 ml/day) and ice cream (145 g/day) and the administration of small dose of absorbable alkali (magnesium oxide 2.0 g/day) for the treatment of chronic constipation. The present case shows not only triads, i.e., hypercalcemia (s-Ca 14.3 mg/dl), metabolic alkalosis (s-HCO3- 37.4 mEq/L), and renal insufficiency (s-Cre 2.3 mg/dl) but also hypernatremia (s-Na 161 mEq/L) and hypertonic dehydration after the frequent episodes of elevated body temperature. The milk-alkali syndrome has been defined as the hypercalcemia with a metabolic alkalosis from a high amount of calcium intake and long term administration of absorbable alkali in any form, usually as calcium carbonate for the treatment of peptic ulcer. As the present case could be distinguished from any other cases previously reported with regard to the amount of calcium (0.4 g/day) and alkali (36 mEq/day) intake and the clinical situations that induced the syndrome, we compared the present case with the previous reports, calculating the amount of calcium and alkali intake from milk and absorbable alkali. After the introduction of the H2 blockers for peptic ulceration, the most cases with milk-alkali syndrome had provoked by the smaller amount of calcium than previously reported, which were associated with the treatment of relatively large amount of alkali (50-150 mEq/day), suggesting the role of sustained metabolic alkalosis for the development. In the present case the metabolic alkalosis induced by hypertonic dehydration and enhanced by absorbable alkali intake also could cause an increase of renal tubular reabsorption of calcium and a decrease of ionized calcium which might produce increased secretion of parathyroid hormone followed by vitamin D3 activation and increased Ca absorption from the gut. The metabolic alkalosis might be essential to the development of the milk-alkali syndrome without a high calcium and absorbable alkali intake.
Aged↗
Expression of collagen I, smooth muscle alpha-actin, and vimentin during the healing of alkali-burned and lacerated corneas.
PURPOSES: Alkali-burned corneas can seldom heal properly to restore corneal transparency. To provide a better understanding of this devastating corneal injury, we compared the expression of collagen I, smooth muscle alpha-actin (alpha-SMA), and vimentin in lacerated and alkali-burned rabbit corneas. METHODS: A radiolabeled cDNA probe of alpha 1(I) chain was used in slot-blot hybridization to determine the levels of alpha 1(I) mRNA in alkali-burned corneas. In situ hybridization was used to identify the cell types that express the alpha 1(I) chain. Antibodies against collagen I, alpha-SMA, and vimentin were used in immunohistochemical studies to determine the tissue distribution of collagen I and to identify cells expressing alpha-SMA and vimentin. RESULTS: The levels of alpha 1(I) mRNA in alkali-burned corneas increased steadily after the alkali burn and reached a plateau within 2 weeks. One day after alkali burn, specific in situ hybridization signals were detected in stromal cells immediately surrounding the edge of the corneal injury. As the healing proceeded, the fibroblastic cells migrated into the injured stroma, and they showed positive reactions by in situ hybridization and by immunostaining with anti-collagen I probes. In alkali-burned corneas, retrocorneal membranes were formed 1 week after injury. This fibrillar membrane was stained by anti-collagen I antibody, and the fibroblastic cells in the membrane were hybridized by the 3H-labeled alpha 1(I) cDNA probe. No retrocorneal membrane was formed in the lacerated corneas, even after the injured corneas were allowed to heal for 3 weeks. The epithelial cells in the epithelial plug of lacerated corneas were positive by in situ hybridization, whereas the epithelial cells in the regenerated epithelium of alkali-burned cornea was not. Antibodies against alpha-SMA reacted with the migrating fibroblastic cells but did not react with epithelial cells or endothelial cells in the injured corneas. Anti-vimentin antibody reacted with fibroblastic cells, endothelial cells, and keratocytes in normal and injured corneas, and with the basal epithelial cells of injured corneas. CONCLUSIONS: During wound healing, the keratocytes that migrate to injured stroma transform into myofibroblasts. These myofibroblasts express high levels of alpha 1(I) mRNA, alpha-SMA, and vimentin. The healing of alkali-burned corneas differ from that of lacerated corneas in that the retrocorneal membranes are formed in the former but not in the latter. In addition, the epithelial cells of alkali-burned corneas lack alpha 1(I) mRNA, whereas it is found in the epithelium of lacerated corneas. These differences may result from the persistence of inflammatory cells in the alkali-burned corneas.
Actins↗
Mechanisms used to dispose of progressively increasing alkali load in rats.
Our objective was to describe the process of alkali disposal in rats. Balance studies were performed while incremental loads of alkali were given to rats fed a low-alkali diet or their usual alkaline ash diet. Control groups received equimolar NaCl or KCl. Virtually all of the alkali was eliminated within 24 h when the dose exceeded 750 micromol. The most sensitive response to alkali input was a decline in the excretion of NH(4)(+). The next level of response was to increase the excretion of unmeasured anions; this rise was quantitatively the most important process in eliminating alkali. The maximum excretion of citrate was approximately 70% of its filtered load. An even higher alkali load augmented the excretion of 2-oxoglutarate to >400% of its filtered load. Only with the largest alkali load did bicarbonaturia become quantitatively important. We conclude that renal mechanisms eliminate alkali while minimizing bicarbonaturia. This provides a way of limiting changes in urine pH without sacrificing acid-base balance, a process that might lessen the risk of kidney stone formation.
Acid-Base Equilibrium↗
Treatment of alkali-injured rabbit corneas with a synthetic inhibitor of matrix metalloproteinases.
Healing of corneal alkali injuries remains a severe clinical challenge. The authors evaluated the effect of a new synthetic inhibitor of matrix metalloproteinases (GM6001 or N-[2(R)-2-(hydroxamido carbonylmethyl)-4-methylpentanoyl]-L-tryptophane methylamide) on preventing ulceration of rabbit corneas after alkali injury. Topical treatment of corneas with severe alkali injuries with 400 micrograms/ml or 40 micrograms/ml GM6001 alone prevented ulceration for 28 days, although 8 of 10 corneas treated with vehicle perforated. Corneas treated with 4 micrograms/ml GM6001 had midstromal depth ulcers. Corneas treated with 400 micrograms/ml of GM6001 contained very few inflammatory cells and had significantly reduced vessel ingrowth compared with vehicle-treated corneas. Epithelial regeneration after moderate alkali injuries also was investigated. Persistent epithelial defects developed 4 days after moderate alkali injury in rabbit corneas treated with vehicle and progressively increased to an average of 20% of the original 6 mm diameter wound by 27 days after moderate alkali injury. By contrast, epithelial regeneration was complete and persisted for 21 days for corneas treated with a formulation containing GM6001 (400 micrograms/ml), epidermal growth factor (10 micrograms/ml), fibronectin (500 micrograms/ml), and aprotinin (400 micrograms/ml). Sporadic punctate staining developed in 20% of the corneas treated with the combination of agents between days 21-28 after moderate alkali injury. These results demonstrate that topical application of GM6001 prevented corneal ulceration after severe alkali injury and that a combination containing GM6001, epidermal growth factor, fibronectin, and aprotinin promoted stable regeneration of corneal epithelium after moderate alkali injury.
Alkalies↗
Cellulose synthesis by extracts of Acanthamoeba castellanii during encystment. Stimulation of the incorporation of radioactivity from UDP-(14C)glucose into alkali-soluble and insoluble beta-glucans by glucose 6-phosphate and related compounds.
1. The activity of a particulate enzyme prepared from encysting cells of Acanthamoeba castellanii (Neff), previously shown to catalyze the incorporation of glucose from UDP-[14C]glucose into both alkali-soluble and alkali-insoluble beta-(1 leads to 4) glucans, was stimulated several fold by glucose-6-phosphate and several related compounds. 2. Incorporation was observed when [14C]glucose-6-P was incubated with the particles in the presence of UDP-glucose. The results of product analysis by partial acid hydrolysis indicated that glucose-6-P stimulates the formation of both alkali-soluble and alkali-insoluble beta-(1 leads to 4) glucans from UDP-[14C]glucose and was itself incorporated into an alkali-insoluble beta-(1 leads to 4)glucan. 3. When particles incubated with UDP-[14C]glucose and glucose-6-P were reisolated and then reincubated with unlabeled UDP-glucose and glucose-6-P, a loss of counts from the alkali-soluble fraction was detected along with a corresponding rise in the radioactivity of the alkali-insoluble fraction. This suggests that the alkali-soluble beta-glucan was converted to an alkali-insoluble product and possibly may be an intermediate stage in cellulose synthesis.
Amoeba↗
Milk-alkali syndrome is a major cause of hypercalcaemia among non-end-stage renal disease (non-ESRD) inpatients.
OBJECTIVE: Milk-alkali syndrome, once a common cause of hypercalcaemia, is now considered rare. Our aim was to estimate the prevalence of milk-alkali syndrome among hypercalcaemic, non-end-stage renal disease (non-ESRD) inpatients of a University Hospital and identify patients' and syndrome characteristics. DESIGN AND PATIENTS: In this retrospective chart review study, we identified patients hospitalized with possible hypercalcaemia between November 1998 and October 2003 by a computer search of admission, discharge and consultation diagnoses. Patients with renal transplantation, stage 5 chronic kidney disease (CKD-5) and those admitted for parathyroidectomy were excluded. The remaining patients' charts were reviewed for confirmation of hypercalcaemia and identification of the cause. In patients with milk-alkali syndrome, additional historical, clinical, laboratory and imaging data were collected. RESULTS: We identified 125 patients with hypercalcaemia, 11 (8.8%) of whom had milk-alkali syndrome, 42 (33.6%) had malignancy and 37 (29.6%) hyperparathyroidism. Thirty-five patients had severe hypercalcaemia, defined as corrected serum calcium 3.5 mmol/l. Malignancy accounted for 13 of those patients (37.1%) and milk-alkali for nine (25.7%). Conditions prevalent among the milk-alkali inpatients were female gender, hypertension, chronic kidney disease, osteoporosis, upper gastrointestinal diseases, diuretic treatment and vitamin D derivative supplementation. Five of the patients with milk-alkali syndrome were treated with bisphosphonates and all five developed hypocalcaemia, compared to one of the five who received conventional treatment (P = 0.047). CONCLUSION: Milk-alkali was the third leading cause of hypercalcaemia of any degree and the second cause of severe hypercalcaemia among inpatients without ESRD. In milk-alkali syndrome, treatment with bisphosphonates contributes to post-treatment hypocalcaemia.
Adult↗
Attainment and maintenance of normal stature with alkali therapy in infants and children with classic renal tubular acidosis.
Growth was evaluated in a group of 10 infants and children with familial or idiopathic classic renal tubular acidosis in whom alkali therapy was initiated at ages ranging from 8 days to 9.5 yr and administered at dosage schedules documented to sustain correction of acidosis in at least four prolonged observation periods on the Pediatric Clinical Research Ward. When alkali therapy was begun, six patients (four infants and two children) were stunted (height <2.5 SD below mean). Of the four who were not, two infants were too young (<2 wk of age) to have become stunted, and two children had been documented earlier to be nonacidotic. At the start of alkali therapy, the heights of the patients correlated inversely with the maximal possible duration of prior acidosis. WITH SUSTAINED ALKALI THERAPY: (a) each patient attained and maintained normal stature; (b) the mean height of the 10 patients increased from the 1.4+/-4 to the 37.0+/-33 percentile (of a normal age- and sex-matched population); (c) the mean height reached the 69th percentile in the eight patients whose heights could be analyzed according to parental prediction (Tanner technique); (d) the rate of growth increased two- to threefold, and normal heights were attained within 6 mo of initiating alkali therapy in the stunted infants and within 3 yr in the stunted children; (e) the height attained correlated inversely with the maximal possible duration of acidosis (before alkali therapy) only in those patients in whom alkali therapy was started after 6 mo of age, and not in those treated earlier. The amount of alkali required to sustain correction of acidosis increased substantially during the course of treatment in each patient. The maximal alkali requirement ranged from 4.8 to 14.1 meq/kg per day, and in each patient its amount was determined principally by the magnitude of renal bicarbonate wasting.
Acidosis, Renal Tubular↗
A neutrophil chemoattractant is released from cellular and extracellular components of the alkali-degraded cornea and blood.
PURPOSE: A tripeptide chemoattractant(s) for neutrophils has been shown to release from alkali-degraded cornea. This study is designed to determine the source of the chemoattractant(s). METHODS: Whole corneas were degraded in 1 N NaOH for 10 minutes, 30 minutes, 1 hour, 4, 8, 24, and 48 hours to determine an optimal duration of alkali exposure for production of the chemoattractant. Whole cornea, cornea minus epithelium, cornea minus endothelium, and stroma alone were degraded in 1 N NaOH for 4 hours to determine the relative contribution of each corneal layer. In a separate experiment, epithelium alone, endothelium alone, cultured keratocytes alone, or bovine corneal collagen were treated separately in 1 N NaOH for 4 hours. Finally, human plasma, platelets, polymorphonuclear leukocytes (PMNL), and red blood cells were treated separately in 1 N NaOH for 4 hours to determine if a similar chemoattractant was released from alkali-treated noncorneal tissue. Neutralized suspensions of all samples were ultrafiltered and dialyzed. The chemotactic potential of each sample was determined in the polarization assay. RESULTS: Activation of the PMNL polarization response increased with the duration of exposure of corneal tissue to alkali, peaking at 6 hours. Release of the chemoattractant from alkali-degraded corneal tissue showed a significant decrease when the epithelium was removed from the stroma. All tissue layers showed a PMNL polarization response when treated with alkali. The response decreased from epithelium > endothelium > cultured keratocytes > collagen. Alkali degradation of human blood components, including plasma, showed significant polarization responses ranked in the following order: plasma > PMNL > tendon collagen > platelets = red blood cells. CONCLUSIONS: This study demonstrates that the tripeptide chemoattractant(s) is released from all layers of the cornea after alkali injury. The substance released from blood components is of similar size and biologic activity as that found in the cornea, but its exact molecular composition is yet to be determined. Timed response of alkali degradation determined the optimal conditions for generation of the chemoattractant(s) including clinically relevant time intervals.
Acetylation↗
Alkali absorption and citrate excretion in calcium nephrolithiasis.
The role of net gastrointestinal (GI) alkali absorption in the development of hypocitraturia was investigated. The net GI absorption of alkali was estimated from the difference between simple urinary cations (Ca, Mg, Na, and K) and anions (Cl and P). In 131 normal subjects, the 24 h urinary citrate was positively correlated with the net GI absorption of alkali (r = 0.49, p < 0.001). In 11 patients with distal renal tubular acidosis (RTA), urinary citrate excretion was subnormal relative to net GI alkali absorption, with data from most patients residing outside the 95% confidence ellipse described for normal subjects. However, the normal relationship between urinary citrate and net absorbed alkali was maintained in 11 patients with chronic diarrheal syndrome (CDS) and in 124 stone-forming patients devoid of RTA or CDS, half of whom had "idiopathic" hypocitraturia. The 18 stone-forming patients without RTA or CDS received potassium citrate (30-60 mEq/day). Both urinary citrate and net GI alkali absorption increased, yielding a significantly positive correlation (r = 0.62, p < 0.0001), with the slope indistinguishable from that of normal subjects. Thus, urinary citrate was normally dependent on the net GI absorption of alkali. This dependence was less marked in RTA, confirming the renal origin of hypocitraturia. However, the normal dependence was maintained in CDS and in idiopathic hypocitraturia, suggesting that reduced citrate excretion was largely dietary in origin as a result of low net alkali absorption (from a probable relative deficiency of vegetables and fruits or a relative excess of animal proteins).
Acidosis, Renal Tubular↗
The effect of heat treatment on bone-bonding ability of alkali-treated titanium.
The purpose of this study was to evaluate the bone-bonding ability of alkali-treated titanium with and without heat treatment. Three groups of smooth titanium plate were prepared: control, or pure titanium, alkali-treated titanium, and alkali- and heat-treated titanium. The plates were inserted transcortically into the proximal metaphyses of bilateral rabbit tibiae. The tensile failure loads between implants and bones were measured at two time intervals using a detaching test. The tensile failure loads of the alkali- and heat-treated titanium group were 2.71 and 4.13 kgf, at 8 and 16 weeks, respectively, and significantly higher than those of the other titanium groups. Histological examination revealed that alkali- and heat-treated titanium was in direct contact with bone, but the other titanium groups had a thin intervening fibrous tissue. This result indicated that the alkali-treated titanium without heat treatment had no bone-bonding ability due to the unstable reactive surface layer of alkali-treated titanium. In conclusion, both alkali and heat treatment are essential for preparing bioactive titanium and this bioactive titanium is thought to be useful for orthopedic implants with cementless fixation.
Alkalies↗
Simultaneous measurement of gastric acid and duodenal alkali secretion by in situ titration in health and disease.
We have devised a technique for simultaneously measuring the acid secretion into the stomach and alkali into the duodenum by in situ titration using a modification of the technique of Fordtran and Walsh. Using this technique, the results of acid and alkali secretion measured simultaneously were identical with those obtained using the conventional aspiration method on separate days. In response to stimulation with pentagastrin acid output was 17.2 +/- 1.4 vs 15.4 +/- 1.9 mmol/h and alkali response with secretin was 16.0 +/- 0.8 vs 14.4 +/- 1.5 mmol/h. The response to food was measured in 10 control subjects, 10 patients with duodenal ulcer, and 10 patients with pancreatitis. In controls, the acid and alkaline secretion were similar (15.8 +/- 1.7 vs 18.2 +/- 1.3 mmol/h), in patients with duodenal ulcer acid secretion was significantly greater than alkaline secretion (31.9 +/- 2.2 vs 21.9 +/- 1.7 mmol/h), and in patients with pancreatitis the alkali secretion was significantly less than acid (19.8 +/- 1.9 mmol/h acid vs 11.4 +/- 0.6 mmol/h alkali). It can, therefore, be concluded that in response to food the patients with duodenal ulcer are significant hypersecretors of acid (DU acid greater than DU alkali output) and patients with pancreatitis are significant hyposecretors of alkali (pancreatitis-alkaline output less than acid output) and normal subjects secrete equal amounts of acid and alkali.
Alkalies↗
DNA alkali-labile sites induced by incorporation of 5-aza-2'-deoxycytidine into DNA of mouse leukemia L1210 cells.
The effects of 5-aza-2'-deoxycytidine on DNA in mouse L1210 leukemia cells were investigated using the alkaline elution technique. By comparing the DNA elution rate at pH 12.1 and 12.6, it was found that the drug produced DNA alkali-labile lesions. Alkali-labile sites were present only in DNA strands that were synthesized in the presence of the drug. They persisted for at least 48 h after drug treatment, and only after 72 h did the number of alkali-labile sites decline, thus suggesting a slow repair process. The production of alkali-labile sites was found to be concentration dependent and observable at concentrations which were effective in inhibiting the clonogenic viability of L1210 cells and which are attainable in vivo. 5-Aza-2'-deoxycytidine did not cause other DNA lesions such as DNA double-strand breaks or DNA-protein cross-links. Two hypotheses were considered to explain the origin of alkali-labile lesions in DNA that has incorporated 5-aza-2'-deoxycytidine: (a) the production of apyrimidinic sites by a glycosylase that recognizes and removes aza-cytosine from DNA and (b) the alkali-catalyzed decomposition of azacytosine residues to ring-opened products which could lead to alkali-induced DNA strand scission through a beta-elimination mechanism. The second hypothesis was considered to be the more probable and suggests that the alkali lability may be a means by which one could determine the extent of substitution and precise location of azacytosine residues or their ring-opened products in DNA.
Alkalies↗
Alkali burn causes aldehyde dehydrogenase 3A1 (ALDH3A1) decrease in mouse cornea.
PURPOSE: Aldehyde dehydrogenase 3A1 (ALDH3A1) is the most abundant soluble protein component in the mouse cornea, produced mainly by corneal epithelial cells. High levels of ALDH3A1 in cornea contribute to maintenance of a stable an d transparent corneal structure. Alkali burn is a common damage to the corneal surface, which produces an alkaline hydrolysis of matrix proteins and induces an inflammatory reaction. Our study was intended to detect changes in ALDH3A1 expression after corneal alkaline burn. METHODS: To address this issue we employed RTQ-PCR to monitor the transcriptional change of ALDH3A1 after alkali burn. We used zymography to test enzyme activity changes of ALDH3A1 in the alkali burn cornea; And SDS-PAGE and mass spectrometry technology were used to verify protein content changes and to identify ALDH3A1 protein. RESULTS: Using zymography, ALDH3A1 enzymic activity was observed to decrease immediately after corneal alkali burn and the levels recovered following healing. Proteins extracted from alkali burned corneas, when run on SDS-PAGE, showed the same sized band (about 54 kDa, which is the molecular weight of ALDH3A1) but in much smaller quantity, compared to normal corneas. This result was further verified by mass spectrometry fingerprinting of the in-gel lysis product. An immediate decrease of ALDH3A1 transcription after alkali burning of the cornea was also found using RTQ-PCR. This level of transcription was gradually restored during healing. CONCLUSIONS: Alkali burn of the corneal surface caused a rapid decrease of ALDH3A1 in the corneal at both the RNA and protein levels, which leads to the loses of the protective component of the corneal surface and makes it vulnerable to further damage. The ALDH3A1 level in the cornea gradually recovered during the healing process. Use of an anti-oxidation reagent as a treatment ingredient for alkali burn of the corneal surface could compensate for the decrease of anti-oxidation protection potential caused by ALDH3A1 loss.
Aldehyde Dehydrogenase↗
Physiological and transcriptomic responses of sunflower to combined saline-alkali stress.
BACKGROUND: Sunflower (Helianthus annuus L.), an important oilseed crop, is often used as a pioneer species for improving saline-alkali soils. However, the molecular mechanisms underlying sunflower seedling responses to combined saline-alkali stress remain unclear. This study aimed to elucidate the molecular basis of saline-alkali tolerance at the seedling stage by comparing physiological and transcriptomic responses between tolerant and sensitive sunflower hybrids. The saline-alkali tolerant hybrid K-27 and the sensitive hybrid K-7 were used as experimental materials. Root samples were collected at 0, 3, 12, 24, 48, and 96 h after exposure to combined saline-alkali stress (0.5% NaCl + Na2CO3, adjusted to pH 9.0). Physiological parameters, including antioxidant enzyme activities, osmolyte contents, ion concentrations, membrane damage levels, and cell wall components, were measured, followed by transcriptome sequencing analysis. RESULTS: Phenotypic analysis showed that the root length inhibition rate and fresh weight loss rate of K-27 were significantly lower than those of K-7, indicating stronger tolerance. Physiological analysis revealed that K-27 exhibited an inducible antioxidant enzyme response pattern. In addition, K-27 achieved osmotic adjustment through sustained proline accumulation (peaking at 12 h and remaining significantly higher than that of K-7 at 96 h) and exhibited higher basal levels of lignin and hemicellulose. Transcriptome analysis showed that the number of upregulated genes in K-27 was consistently higher than in K-7 at all time points, with 5,283 genes upregulated as early as 3 h after stress exposure. Venn analysis identified 44 core differentially expressed genes (cDEGs) shared between the two genotypes, which were mainly enriched in auxin biosynthesis regulation, phenylpropanoid biosynthesis, and glutathione metabolism. Among them, the benzoic acid carboxyl methyltransferase gene (BAMT) was continuously upregulated in K-27 but persistently downregulated in K-7. In addition, five other genes (encoding fatty aldehyde dehydrogenase, pectin methylesterase inhibitor, glutathione S-transferase, INPP5E, and HXXXD-type acyltransferase) exhibited significantly higher expression levels in K-27. CONCLUSION: K-27 tolerates combined saline-alkali stress through coordinated multi-layered response mechanisms, including inducible antioxidant defense, maintenance of ion homeostasis, sustained osmotic adjustment, and activation of the phenylpropanoid metabolic pathway. Candidate genes such as BAMT may provide potential targets for molecular breeding of saline-alkali tolerant sunflower, although their functions require further experimental validation.
Helianthus↗
Effect of alkali metal hydroxides on the enantioseparation of amines using di-O-isopropylidene-keto-L-gulonic acid as the selector in NACE.
The present work demonstrates the importance of the ionic composition in the BGE for enantioseparation. (-)-2,3:4,6-di-O-Isopropylidene-2-keto-L-gulonic acid ((-)-DIKGA) has been used as the chiral selector in methanolic and ethanolic BGEs. The influence of added alkali metal hydroxides on the EOF and the chiral separation of amines (atenolol, isoprenaline, pindolol and propranolol) have been studied. The ion-pair formation constants in ethanol were determined by precision conductometry for the enantiomers of pindolol with (-)-DIKGA, for Li(+), Na(+) and Cs(+) with (-)-DIKGA, and also for the corresponding alkali metal hydroxides. The effective mobilities and the enantiomeric mobility differences were affected by the type of alkali metal hydroxide (LiOH, NaOH, KOH, RbOH or CsOH) added to the BGE. The effective mobility and mobility difference were increased with decrease in solvated radius of the alkali metal cation. These differences could partly be correlated to the ion-pair formation constants of the alkali metal cations with the chiral selector, affecting the equilibrium concentration of the free selector. The electroosmosis was also affected by the alkali metal hydroxide added to the BGE. The cathodic electroosmosis decreased with decreasing solvated radius of the alkali metal cation added to the BGE. Interestingly, the cathodic EOF was even reversed, i.e. became anodic in the ethanolic BGEs containing KOH, RbOH or CsOH and the methanolic ones with RbOH and CsOH.
Amines↗
High energy collision-induced dissociation of alkali-metal ion adducts of crown ethers and acyclic analogs.
High energy collision-induced dissociation (CID) techniques were applied for structural elucidation of alkali-metal ion adducts of crown ethers. The CID of alkali-metal adducts of tetraglyme and hexaethylene glycol were also evaluated to contrast the fragmentation pathways of the cyclic ethers with those of acyclic analogs. A common fragmentation channel for alkali-metal ion adducts of all the ethers, which results in distonic radical cations, is the homolytic cleavage of carbon-carbon bonds. Additionally, dissociation by carbon-oxygen bond cleavages occurs, and these processes are analogous to the fragmentation pathways observed for simple protonated ethers. The proposed fragmentation pathways for alkali-metal ion adducts of crown ethers result mostly in odd-electron, acyclic product ions. Dissociation of the alkali-metal ion adducts of the acyclic ethers is dominated by losses of various neutral species after an initial hydride or proton transfer. The CID processes for all ethers are independent of the alkali-metal ion sizes; however, the extent of dissociation of the complexes to bare alkali-metal ions increases with the size of the metal.
Chemical Phenomena↗