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D A Brown

Publications and source records attributed to D A Brown.

At least 19 recordsLinked to original sources
PubMed2006

Orbital angular momentum contribution to the magneto-optical behavior of a binuclear cobalt(II) complex.

We report magnetic and magnetic circular dichroism investigations of a binuclear Co(II) compound. The Hamiltonian of the system involves an isotropic exchange interaction dealing with the real spins of cobalt(II) ions, spin-orbit coupling, and a low-symmetry crystal field acting within the (4)T(1g) ground manifold of each cobalt ion. It is shown that spin-orbit coupling between this ground term and the low-lying excited ones can be taken into consideration as an effective g factor in the Zeeman part of the Hamiltonian. The value of this g factor is estimated for the averaged experimental values of Racah and cubic ligand field parameters for high-spin cobalt(II). The treatment of the Hamiltonian is performed with the use of a irreducible tensor operator technique. The results of the calculation are in good agreement with experimental observations. Both a large effective g factor for the ground state and a large temperature-independent part of the magnetic susceptibility arise because of a strong orbital contribution to the magnetic behavior of the Co(II) dimer.

Circular Dichroism↗
PubMed2005

Upper limits on a stochastic background of gravitational waves.

The Laser Interferometer Gravitational-Wave Observatory has performed a third science run with much improved sensitivities of all three interferometers. We present an analysis of approximately 200 hours of data acquired during this run, used to search for a stochastic background of gravitational radiation. We place upper bounds on the energy density stored as gravitational radiation for three different spectral power laws. For the flat spectrum, our limit of omega0 < 8.4 x 10(-4) in the 69-156 Hz band is approximately 10(5) times lower than the previous result in this frequency range.

Journal Article↗
PubMed2005

Limits on gravitational-wave emission from selected pulsars using LIGO data.

We place direct upper limits on the amplitude of gravitational waves from 28 isolated radio pulsars by a coherent multidetector analysis of the data collected during the second science run of the LIGO interferometric detectors. These are the first direct upper limits for 26 of the 28 pulsars. We use coordinated radio observations for the first time to build radio-guided phase templates for the expected gravitational-wave signals. The unprecedented sensitivity of the detectors allows us to set strain upper limits as low as a few times 10(-24). These strain limits translate into limits on the equatorial ellipticities of the pulsars, which are smaller than 10(-5) for the four closest pulsars.

Journal Article↗
PubMed2004

Foot force direction control during leg pushes against fixed and moving pedals in persons post-stroke.

The component of foot force generated by muscle action (F(m)) during pedaling in healthy humans has a nearly constant direction with increasing force magnitude. The present study investigated the effect of stroke on the control of foot force. Ten individuals with hemiparesis secondary to a cerebral vascular accident performed pushing efforts against translationally fixed and moving pedals on a custom stationary cycle ergometer. We found that while F(m) direction remained constant with increasing effort in both the fixed- and moving-crank conditions for both limbs, the orientation of that force component differed between limbs. The non-paretic limb produced the same F(m) orientation as seen previously in healthy humans. However, relative to the non-paretic limb, the paretic limb force line-of-action was shifted away from the hip and closer to the knee in the sagittal-plane for both pedal motion conditions. In the frontal plane, the paretic limb force line-of-action was shifted laterally, closer to parallel to the midline, for both pedal motion conditions. These shifts were consistent with previously reported lower limb muscle weakness and alterations in muscle activation observed during pedaling tasks following stroke. The finding of similar orientations for static and dynamic pushing efforts suggests that limb posture could be a trigger for relative muscle activation levels. The preservation of a constant direction in F(m) with increasing force magnitude post-stroke, despite an orientation shift, suggests that control of lower limb force may be organized by magnitude and direction and that these two aspects are differentially affected by stroke.

Adult↗
PubMed2003

Modulation of the excitability of cholinergic basal forebrain neurones by KATP channels.

The expression of ATP-sensitive K(+) (K(ATP)) channels by magnocellular cholinergic basal forebrain (BF) neurones was investigated in thin brain slice and dissociated cell culture preparations using a combination of whole-cell, perforated-patch and single-channel recording techniques. Greater than 95% of BF neurones expressed functional K(ATP) channels whose activation resulted in membrane hyperpolarization and a profound fall in excitability. The whole-cell K(ATP) conductance was 14.0 +/- 1.5 nS and had a reversal potential of -91.4 +/- 0.9 mV that shifted by 59.6 mV with a tenfold increase in [K(+)](o). I(KATP) was inhibited reversibly by tolbutamide (IC(50) of 34.1 microM) and irreversibly by glibenclamide (0.3-3 nM) and had a low affinity for [ATP](i) (67% reduction with 6 mm[MgATP](i)). Using perforated-patch recording, a small proportion of the conductance was found to be tonically active. This was weakly potentiated by diazoxide (0.1 mm extracellular glucose) but insensitive to pinacidil (< or =500 microM). Single-channel K(ATP) currents recorded in symmetrical 140 mm K(+)-containing solutions exhibited weak inward rectification with a mean conductance of 66.2 +/- 1.9 pS. Channel activity was inhibited by MgATP (>50 microM) and activated by MgADP (200 microM). The K(+) channels opener diazoxide (200-500 microM) increased channel opening probability (NP(o)) by 486 +/- 120% whereas pinacidil (500 microM) had no effect. In conclusion, the characteristics of the K(ATP) channels expressed by BF neurones are very similar to channels composed of SUR1 and Kir6.2 subunits. In the native cell, their affinity for ATP is close to the resting [ATP](i), potentially allowing them to be modulated by physiologically relevant changes in [ATP](i). The effect of these channels on the level of ascending cholinergic excitation of the cortex and hippocampus is discussed.

Action Potentials↗
PubMed2003

The plasma membrane calcium-ATPase as a major mechanism for intracellular calcium regulation in neurones from the rat superior cervical ganglion.

Patch-clamp recording combined with indo-l measurement of free intracellular calcium concentration ([Ca2+]i) was used to determine the homeostatic systems involved in the maintenance of resting [Ca2+]I and in the clearance of Ca2+ transients following activation of voltage-gated Ca2+ channels in neurones cultured from rat superior cervical ganglion (SCG). The Ca2+ binding ratio was estimated to be approximately 500 at 100 nM, decreasing to approximately 250 at [Ca2+]i approximately 1 pM, and to involve at least two buffering systems with different affinities for Ca2+. Removal of extracellular Ca2+ led to a decrease in[Ca2+]i that was mimicked by the addition of La3+, and was more pronounced after inhibition of the endoplasmic reticulum Ca2+ uptake system (SERCA). Inhibition of the plasma membrane Ca2+ pump (PMCA) by extracellular allkalinisation (pH 9) or intracellular carboxyeosin both increased resting [Ca2+]i and prolonged the recovery of Ca2+ transients at peak [Ca2+]i C 500 nM. For [Ca2+]i loads >500 nM, recovery showed an additional plateau phase that was abolished i nm-chlorophenylhydrazone (CCCP) or on omitting intracellular Na+. Inhibition of the plasma membrane Na+ -Ca2+ exchanger (NCX) and of SERCA had a small but significant additional effect on the rate of decay of these larger Ca2+ transients. In conclusion, resting [Ca2+]i is maintained by passive Ca2+ influx and regulated by a large Ca2+ buffering system, Ca2+ extrusion via a PMCA and Ca2+ transport from the intracellular stores. PMCA is also the principal Ca2+ extrusion system at low Ca2+ loads, with additional participation of the NCX and intracellular organelles at high [Ca2+]i.

Animals↗
PubMed2003

Effect of the KCNQ potassium channel opener retigabine on single KCNQ2/3 channels expressed in CHO cells.

KCNQ2/3 potassium channel subunits were co-expressed in Chinese hamster ovary (CHO) cells and currents through single channels recorded using cell-attached patches. Channels had a similar slope conductance in the presence (8.04 +/- 0.02 pS) and absence (7.6 +/- 0.01 pS) of 10 microM retigabine. The mean maximal open probability (Po) for single KCNQ2/3 channels was 0.13 +/- 0.02, with a half-maximal Po potential (Vo) of -28.7 +/- 1.4 mV for control recordings. Retigabine increased mean maximal Po to 0.38 +/- 0.04 and produced a hyperpolarising shift of Vo to -40.1 +/- 3.4 mV. Single KCNQ2/3 channels have multiple voltage-dependent kinetic components in their activity (CL-OS-CM-OL-CS; C = closed, O = open, L = long, S = short, M = medium), giving short, medium and long closed times (tauCS, tauCM, tauCL) and short and long open times (tauOS and tauOL). In the presence of retigabine at 0 mV the combined duration and contributions of the longest closed time tauCL decreased tenfold, while the short and long open times increased fourfold and twofold, respectively. Thus, steady-state kinetics were modified to favour the open channel configuration.

Animals↗
PubMed2003

Comparison of the neuropathological characteristics of bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) in mice.

Bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) belong to a group of diseases called the transmissible spongiform encephalopathies (TSEs). Transmission studies in inbred mice (strain typing) provided overwhelming evidence that vCJD arose from BSE. In this study, we compare the patterns of neuropathology in a panel of three inbred mouse strains (RIII, C57BL and VM) and one cross (C57BL x VM) infected with either vCJD or BSE. For each mouse strain, patterns of abnormal prion protein (PrPres) deposition, astrocytosis and vacuolation were similar in the vCJD- and BSE-challenged mice. Prion protein (PrP)-positive plaques were prominent in the VM and C57BL x VM mice in addition to diffuse PrPres accumulation, whereas only diffuse PrPres labelling was observed in the RIII and C57BL mice. The hippocampus was targeted in all mouse strains, as was the cochlear nucleus in the medulla, both showing consistent severe vacuolation and heavy PrPres deposition. Although the targeting of PrPres was similar in the BSE- and vCJD-infected brains, the amount and intensity of PrPres observed in the brains treated with formic acid during fixation was reduced considerably. The distribution of astrocytosis was similar to the targeting of PrPres deposition in the brain, although some differences were observed in the hippocampi of mice challenged with vCJD. We conclude that there are no significant differences in the targeting of neuropathological changes observed in the BSE- and vCJD-infected mice, consistent with the previous evidence of a link between BSE and vCJD.

Animals↗
PubMed2003

A comparison of patients who developed venous leg ulceration before and after their 50th birthday.

BACKGROUND: although chronic venous ulceration (CVU) is often viewed primarily as a disease of the elderly, recent epidemiological data suggest that a significant proportion of patients first develop CVU before middle age. Such patients may represent a distinct group in terms of aetiology, natural history, prognosis and therapeutic options. AIM: to compare patients who developed CVU before (Group 1) and after (Group 2) their 50th birthday. METHODS: one hundred and eighteen consecutive patients with "pure" CVU underwent history and examination, measurement of ankle-brachial pressure index (ABPI) and duplex ultrasound examination of the affected limb. Pure venous ulcers were defined as those of >4 weeks duration in the presence of venous reflux (>0.5) and in association with an ankle: brachial pressure index of >0.8. RESULTS: patients in Group 1 (n = 54, 46%) were more likely to be male (32/54 [59%] vs 14/64 [23%], p < 0.001 chi(2)), to have a higher median (interquartile [IQR]) body mass index (32 [27-39] vs 27 [23-34], p = 0.003, Mann-Whitney U [MWU]), to have a history of deep venous thrombosis (23/54 [43%] vs 16/64 [25%], p = 0.04 chi(2)) and of ipsilateral long bone fracture (13/54 [24%] vs 5/64 [8%], p = 0.01, chi(2)), to have previously undergone venous surgery (27/54 [50%] vs 19/64 [30%] a median (IQR) of 11.5 (6.5-19) and 10 (2-20) years earlier respectively, and to have worse disease in terms of the duration of present ulcer (12 (6-36) vs 8.5 [3-18] months, p = 0.035 MWU), the total duration of ulcer disease (216 [72-360] vs 48 [12-120] months, p < 0.001 MWU), and the number of episodes of ulceration (3 [2-7] vs 1 [1-3], p = 0.002 MWU). There was no significant difference between the two groups in the pattern and severity of venous reflux with 46/54 (85%) of Group 1 and 54/64 (84%) of Group 2 patients having surgically correctable superficial venous reflux. CONCLUSION: patients who develop CVU before their 50th birthday appear to represent a distinct group in terms of aetiology, natural history and prognosis. The importance of thrombo-embolic prophylaxis in the prevention, and the detection and correction of superficial venous reflux in the treatment, of such ulcers is re-emphasised.

Adult↗
PubMed2003

Macrophage inhibitory cytokine-1 in gestational tissues and maternal serum in normal and pre-eclamptic pregnancy.

Macrophage inhibitory cytokine-1 (MIC-1), a divergent member of transforming growth factor-beta superfamily, has been recently shown to be produced by the human placenta with detectable levels in maternal serum. In this study, using immunohistochemistry, we have localized MIC-1 in placenta, decidua and foetal membranes across pregnancy and, using an enzyme-linked immunoassay, measured MIC-1 in maternal serum in normal pregnancy, in association with labour and pre-eclampsia. In the placenta MIC-1 was principally localized to the syncytiotrophoblast while in the foetal membranes MIC-1 was present in the amniotic epithelium, chorionic trophoblasts and adherent decidual cells. There were no differences in MIC-1 staining distribution or intensity in the placentae between women in labour and not in labour, or between healthy and pre-eclamptic pregnancies. MIC-1 staining in the foetal membranes was slightly stronger after a labour and delivery compared to those delivered by elective Caesarean section. MIC-1 levels in the maternal serum increased with advancing gestation but there were no significant differences in maternal serum levels associated with either labour or pre-eclampsia.These observations would be consistent with MIC-1 having roles at the maternal-foetal interface, perhaps in the establishment and/or maintenance of pregnancy. Our data argue against MIC-1 having a significant role in the regulation of labour or in the pathophysiology of pre-eclampsia.

Adult↗
PubMed2002

Molecular correlates of the M-current in cultured rat hippocampal neurons.

M-type K(+) currents (I(K(M))) play a key role in regulating neuronal excitability. In sympathetic neurons, M-channels are thought to be composed of a heteromeric assembly of KCNQ2 and KCNQ3 K(+) channel subunits. Here, we have tried to identify the KCNQ subunits that are involved in the generation of I(K(M)) in hippocampal pyramidal neurons cultured from 5- to 7-day-old rats. RT-PCR of either CA1 or CA3 regions revealed the presence of KCNQ2, KCNQ3, KCNQ4 and KCNQ5 subunits. Single-cell PCR of dissociated hippocampal pyramidal neurons gave detectable signals for only KCNQ2, KCNQ3 and KCNQ5; where tested, most also expressed mRNA for the vesicular glutamate transporter VGLUT1. Staining for KCNQ2 and KCNQ5 protein showed punctate fluorescence on both the somata and dendrites of hippocampal neurons. Staining for KCNQ3 was diffusely distributed whereas KCNQ4 was undetectable. In perforated patch recordings, linopirdine, a specific M-channel blocker, fully inhibited I(K(M)) with an IC(50) of 3.6 +/- 1.5 microM. In 70 % of these cells, TEA fully suppressed I(K(M)) with an IC(50) of 0.7 +/- 0.1 mM. In the remaining cells, TEA maximally reduced I(K(M)) by only 59.7 +/- 5.2 % with an IC(50) of 1.4 +/- 0.3 mM; residual I(K(M)) was abolished by linopirdine. Our data suggest that KCNQ2, KCNQ3 and KCNQ5 subunits contribute to I(K(M)) in these neurons and that the variations in TEA sensitivity may reflect differential expression of KCNQ2, KCNQ3 and KCNQ5 subunits.

Animals↗
PubMed2002

Dominant-negative subunits reveal potassium channel families that contribute to M-like potassium currents.

M-currents are K+ currents generated by members of the KCNQ family of K+ channels (Wang et al., 1998). However, in some cells, M-like currents may be contaminated by members of other K+ channel gene families, such as the erg family (Meves et al., 1999; Selyanko et al., 1999). In the present experiments, we have used the acute expression of pore-defective mutants of KCNQ3 (DN-KCNQ3) and Merg1a (DN-Merg1a) as dominant negatives to separate the contributions of these two families to M-like currents in NG108-15 neuroblastoma hybrid cells and rat sympathetic neurons. Two kinetically and pharmacologically separable components of M-like current could be recorded from NG108-15 cells that were individually suppressed by DN-Merg1a and DN-KCNQ3, respectively. In contrast, only DN-KCNQ3, and not DN-Merg1a, reduced currents recorded from sympathetic neurons. Pharmacological tests suggested that the residual current in DN-KCNQ3-treated sympathetic neurons was carried by residual KCNQ channels. Ineffectiveness of DN-Merg1a in sympathetic neurons was not caused by lack of expression, as judged by confocal microscopy of Flag-tagged DN-Merg1a. These results accord with previous inferences regarding the roles of erg and KCNQ channels in generating M-like currents. This experimental approach should therefore be useful in delineating the contributions of members of these two gene families to K+ currents in other cells.

Animals↗
PubMed2002

Adenovirus-mediated G(alpha)(q)-protein antisense transfer in neurons replicates G(alpha)(q) gene knockout strategies.

Antisense approaches are increasingly used to dissect signaling pathways linking cell surface receptors to intracellular effectors. Here we used a recombinant adenovirus to deliver G-protein alpha(q) antisense into rat superior cervical ganglion (SCG) neurons and neuronal cell lines to dissect G(alpha)(q)-mediated signaling pathways in these cells. This approach was compared with other G(alpha)(q) gene knockdown strategies, namely, antisense plasmid and knockout mice. Infection with adenovirus expressing G(alpha)(q) antisense (G(alpha)(q)AS AdV) selectively decreased immunoreactivity for the G(alpha)(q) protein. Expression of other G(alpha) protein subunits, such as G(alpha)(oA/B,) was unaltered. Consistent with this, modulation of Ca(2+) currents by the G(alpha)(q)-coupled M(1) muscarinic receptor was severely impaired in neurons infected with G(alpha)(q)AS AdV whereas modulation via the G(alpha)(oA)-coupled M(4) muscarinic receptor was unchanged. In agreement, activation of phospholipase C and consequent mobilization of intracellular Ca(2+) by UTP receptors was lost in NG108-15 cells infected with G(alpha)(q)AS AdV but not in cells infected with the control GFP-expressing adenovirus. Results obtained with this recombinant AdV strategy qualitatively and quantitatively replicated results obtained using SCG neurons microinjected with G(alpha)(q) antisense plasmids or SCG neurons from G(alpha)(q) knockout mice. This combined antisense/recombinant adenoviral approach can therefore be useful for dissecting signal transduction mechanisms in SCG and other neurons.

Adenoviridae↗
PubMed2002

Mutability of bifunctional thigh muscle activity in pedaling due to contralateral leg force generation.

Locomotion requires uninterrupted transitions between limb extension and flexion. The role of contralateral sensorimotor signals in executing smooth transitions is little understood even though their participation is crucial to bipedal walking. However, elucidating neural interlimb coordinating mechanisms in human walking is difficult because changes to contralateral sensorimotor activity also affect the ipsilateral mechanics. Pedaling, conversely, is ideal for studying bilateral coordination because ipsilateral mechanics can be independently controlled. In pedaling, the anterior and posterior bifunctional thigh muscles develop needed anterior and posterior crank forces, respectively, to dominate the flexion-to-extension and extension-to-flexion transitions. We hypothesized that contralateral sensorimotor activity substantially contributes to the appropriate activation of these bifunctional muscles during the limb transitions. Bilateral pedal forces and surface electromyograms (EMGs) from four thigh muscles were collected from 15 subjects who pedaled with their right leg against a right-crank servomotor, which emulated the mechanical load experienced in conventional two-legged coupled-crank pedaling. In one pedaling session, the contralateral (left) leg pseudo-pedaled (i.e., EMG activity and pedal forces were pedaling-like, but pedal force was not allowed to affect crank rotation). In other sessions, the mechanically decoupled contralateral leg was first relaxed and then produced rhythmic isometric force trajectories during either leg flexion or one of the two limb transitions of the pedaling leg. With contralateral force production in the extension-to-flexion transition (predominantly by the hamstrings), rectus femoris activity and work output increased in the pedaling leg during its flexion-to-extension transition, which occurs simultaneously with contralateral extension-to-flexion in conventional pedaling. Similarly, with contralateral force production in the other transition (i.e., flexion-to-extension; predominantly by rectus femoris), hamstrings activity and work output increased in the pedaling leg during its extension-to-flexion transition. Therefore rhythmic isometric force generation in the contralateral leg supported the ongoing bifunctional muscle activity and resulting work output in the pedaling leg. The results suggest that neural interlimb coordinating mechanisms fine-tune bifunctional muscle activity in rhythmic lower-limb tasks to ensure limb flexion/extension transitions are executed successfully.

Adult↗
PubMed2002

Antibody-based approach to high-volume genotyping for MIC-1 polymorphism.

Macrophage inhibitory cytokine-1 (MIC-1) is a divergent member of the TGF-beta superfamily. There are at least two known alleles of MIC-1 that are due to a G-->C point substitution at position 6 of the mature protein, which alters a histidine to an aspartic acid (MIC-1 H and MIC-1 D). We have determined the phenotype of MIC-1 circulating in serum by exploiting the differences in the affinity of the two monoclonal antibodies to the H and D alleles of MIC-1. A PCR-RFLP-based method for genotyping MIC-1 is also described. We validate these two assays using DNA sequencing of 19 subjects as the standard. We then used the validated assay to determine the frequency of the two MIC-1 alleles in a population of 261 adult blood donors. Inter-assay and sequencing concordance was 100%. The frequency of the three common MIC-1 genotypes was homozygous (HH), 54%; heterozygous (HD), 39%; and homozygous (DD), 7%. This novel antibody-based assay confidently determines the genotype of MIC-1. It offers the advantages of an ELISA-ease of automation, high-volume throughput of samples, and ease of use in a routine, clinical laboratory.

Adolescent↗
PubMed2001

Magnetic, spectroscopic, and structural studies of dicobalt hydroxamates and model hydrolases.

The cobalt(II) urease model complex [Co(2)(mu-OAc)(3)(urea)(tmen)(2)][OTf] (2) prepared from the cobalt model hydrolase [Co(2)(mu-H(2)O)(mu-OAc)(2)(OAc)(2)(tmen)(2)] (1) undergoes facile reaction with acetohydroxamic acid (AHA) to give the monobridged hydroxamate complex [Co(2)(mu-OAc)(2)(mu-AA)(urea)(tmen)(2)][OTf]( )()(3) while 1 gives the dibridged hydroxamate complex [Co(2)(mu-OAc)(mu-AA)(2)(tmen)(2)][OTf] (4). The structures and Co-Co distances of the hydroxamate derivatives of 1 and 2 are very close to those of their nickel analogues and suggest that hydroxamic acids can also inhibit cobalt-based hydrolases as well as inhibiting urease. 1 also reacts with glutarodihydroxamic acid (gluH(2)A(2)) to eliminate hydroxylamine with formation of [Co(2)(mu-OAc)(2)[mu-O(N) (OC)(2)(CH(2))(3)](tmen)(2)][OTf] (5), the structure of which is very close to that of its nickel analogue. Both 1 and 3 show weak antiferromagnetic coupling. Oxidation of 1 with H(2)O(2) gives three dicobalt(III) hydroxy complexes (7-9), the first of which [Co(2)(mu-OAc)(2)(OAc)(2)(mu-OH)(tmen)(2)][OTf] (7) contains a bridging hydroxyl and the second [Co(2)(mu-OAc)(2)(OAc)(mu-OH)(OH)(tmen)(2)][OTf] (8) containing both a bridging and terminal hydroxyl, while the third [Co(2)(mu-OAc) (OAc)(2)(mu-OH)(2)(tmen)(2)][OTf] (9) contains two bridging OH groups with mixed-valence Co(II)/(Co(III) intermediates.

Algorithms↗
PubMed2001

GABA(B2) is essential for g-protein coupling of the GABA(B) receptor heterodimer.

GABA(B) receptors are unique among G-protein-coupled receptors (GPCRs) in their requirement for heterodimerization between two homologous subunits, GABA(B1) and GABA(B2), for functional expression. Whereas GABA(B1) is capable of binding receptor agonists and antagonists, the role of each GABA(B) subunit in receptor signaling is unknown. Here we identified amino acid residues within the second intracellular domain of GABA(B2) that are critical for the coupling of GABA(B) receptor heterodimers to their downstream effector systems. Our results provide strong evidence for a functional role of the GABA(B2) subunit in G-protein coupling of the GABA(B) receptor heterodimer. In addition, they provide evidence for a novel "sequential" GPCR signaling mechanism in which ligand binding to one heterodimer subunit can induce signal transduction through the second partner of a heteromeric complex.

Amino Acids↗