Biomedical subjects

M E Anderson

Publications and source records attributed to M E Anderson.

At least 19 recordsLinked to original sources

PubMed2002

Digital vascular response to topical glyceryl trinitrate, as measured by laser Doppler imaging, in primary Raynaud's phenomenon and systemic sclerosis.

OBJECTIVE: To investigate digital microvascular responses to topical glyceryl trinitrate (GTN) in patients with primary Raynaud's phenomenon (PRP), limited cutaneous systemic sclerosis (LCSSc) and healthy control subjects, using laser Doppler imaging. METHODS: Ten patients with PRP, 13 with LCSSc and 10 control subjects were studied. Baseline skin microvascular blood flow of the dorsum of the index, middle and ring fingers of the non-dominant hand was measured using scanning laser Doppler imaging. After the initial image, 2% GTN ointment was rubbed on the dorsum of one finger for 1 min; placebo ointment was rubbed on the dorsum of a second finger for 1 min, and the third finger remained untreated. Further laser Doppler scanning of these three fingers was conducted immediately, 10 and 20 min after ointment application. RESULTS: There was increased blood flow response to placebo compared with no treatment (P<0.001) and to GTN compared with placebo (P=0.004). The change in blood flow over time differed significantly between placebo and GTN (P<0.001), but not between placebo and no ointment application: blood flow increased with GTN and decreased with placebo/no treatment at 10 and 20 min. There were no differences in initial baseline blood flow or response between the subject groups. CONCLUSIONS: An exogenous supply of nitric oxide by topical GTN ointment causes local endothelial-independent vasodilatory responses in PRP, LCSSc patients and control subjects. As well as demonstrating the effectiveness of topical GTN in patients with PRP and LCSSc, this study illustrates the ability of laser Doppler imaging to quantify local vasodilatory effects.

Administration, Topical↗

PubMed2001

Cooperative binding of gamma-glutamyl substrate to human glutathione synthetase.

Human glutathione synthetase is responsible for catalyzing the final step in glutathione biosynthesis. It is a homodimer with a monomer subunit MW of 52 kDa. Kinetic analysis reveals a departure from linearity of the Lineweaver-Burk double reciprocal plot for the binding of gamma-glutamyl substrate, indicating cooperative binding. The measured apparent K(m) values for gamma-glutamyl-alpha-aminobutyrate (an analog of gamma-glutamyl-alpha-aminobutyrate) are 63 and 164 microM, respectively. Neither ATP (K(m) of 248 microM) nor glycine (K(m) of 452 microM) exhibits such cooperative binding behavior. Although ATP is proposed to play a key role in the sequential binding of gamma-glutamyl substrate to the enzyme, the cooperative binding of the gamma-glutamyl substrate is not affected by alterations of ATP concentration. Quantitative analysis of the kinetic results for gamma-glutamyl substrate binding gives a Hill coefficient (h) of 0.75, indicating negative cooperativity. Our studies, for the first time, show that human glutathione synthetase is an allosteric enzyme with cooperative binding for gamma-glutamyl substrate.

Adenosine Triphosphate↗

PubMed2001

Calmodulin kinase and a calmodulin-binding 'IQ' domain facilitate L-type Ca2+ current in rabbit ventricular myocytes by a common mechanism.

1. Ca2+-calmodulin-dependent protein kinase II (CaMK) and a calmodulin (CaM)-binding 'IQ' domain (IQ) are both implicated in Ca2+-dependent regulation of L-type Ca2+ current (I(Ca)). We used an IQ-mimetic peptide (IQmp), under conditions in which CaMK activity was controlled, to test the relationship between these CaM-activated signalling elements in the regulation of L-type Ca2+ channels (LTCCs) and I(Ca) in rabbit ventricular myocytes. 2. A specific CaMK inhibitory peptide nearly abolished I(Ca) facilitation, but the facilitation was 'rescued' by cell dialysis with IQmp. 3. IQmp significantly enhanced I(Ca) facilitation and slowed the fast component of I(Ca) inactivation, compared with an inactive control peptide. Neither effect could be elicited by a more avid CaM-binding peptide, suggesting that generalized CaM buffering did not account for the effects of IQmp. 4. I(Ca) facilitation was abolished and the fast component of inactivation eliminated by ryanodine, caffeine or thapsigargin, suggesting that the sarcoplasmic reticulum (SR) is an important source of Ca2+ for I(Ca) facilitation and inactivation. IQmp did not restore I(Ca) facilitation under these conditions. 5. Engineered Ca2+-independent CaMK and IQmp each markedly increased LTCC open probability (P(o)) in excised cell membrane patches. The LTCC P(o) increases with CaMK and IQmp were non-additive, suggesting that CaMK and IQmp are components of a shared signalling pathway. 6. Both CaMK and IQmp induced a modal gating shift in LTCCs that favoured prolonged openings, indicating that CaMK and IQmp affect LTCCs through a common biophysical mechanism. 7. These findings support the hypothesis that CaMK is required for physiological I(Ca) facilitation in cardiac myocytes. Both CaMK and IQmp were able to induce a modal gating shift in LTCCs, suggesting that each of these signalling elements is important for Ca2+-CaM-dependent LTCC facilitation in cardiac myocytes.

Algorithms↗

PubMed2001

Regulation of neuronal traits by a novel transcriptional complex.

The transcriptional repressor, REST, helps restrict neuronal traits to neurons by blocking their expression in nonneuronal cells. To examine the repercussions of REST expression in neurons, we generated a neuronal cell line that expresses REST conditionally. REST expression inhibited differentiation by nerve growth factor, suppressing both sodium current and neurite growth. A novel corepressor complex, CoREST/HDAC2, was shown to be required for REST repression. In the presence of REST, the CoREST/HDAC2 complex occupied the native Nav1.2 sodium channel gene in chromatin. In neuronal cells that lack REST and express sodium channels, the corepressor complex was not present on the gene. Collectively, these studies define a novel HDAC complex that is recruited by the C-terminal repressor domain of REST to actively repress genes essential to the neuronal phenotype.

Animals↗

PubMed2001

Pause-dependent polymorphic ventricular tachycardia during long-term treatment with dofetilide: a placebo-controlled, implantable cardioverter-defibrillator-based evaluation.

OBJECTIVES: To compare the incidence of pause-dependent polymorphic ventricular tachycardia (PVT) in patients with implantable cardioverter-defibrillators (ICDs) randomly assigned to the QT-prolonging antiarrhythmic dofetilide or placebo. BACKGROUND: Drug-related torsade de pointes (TdP) is usually recognized within days of initiating therapy, but its incidence during long-term therapy is unknown. METHODS: We assessed the frequency of TdP and ICD electrograms compatible with TdP in a multicenter study that randomized ICD patients to placebo (n = 87) or dofetilide (n = 87). As reported elsewhere, the number of patients with a primary trial end point (ICD intervention for VT or ventricular fibrillation) was similar in the two groups. For this analysis, a qualifying event was TdP (on electrocardiogram) or an intracardiac electrogram showing pause-dependent PVT. RESULTS: A total of 620 electrograms obtained in 131 patients were analyzed blindly by prospectively defined criteria for episodes of pause-dependent polymorphic VT. These were identified in 15/87 (17%) patients receiving dofetilide and 5/87 (6%) patients on placebo (p < 0.05). Five of these episodes were early (<3 days), all of which were TdP on dofetilide. There were 15 late events, 10 on dofetilide and five on placebo (p = 0.29). The median time to a late event was 22 days (range 6 to 107 days) for dofetilide and 99 days (range 34 to 207 days) for placebo. CONCLUSIONS: Pause-dependent PVT was more common among patients receiving dofetilide, although total VT incidence was similar in the two groups. These data suggest that in ICD patients either long-term dofetilide therapy is associated with an increased risk of TdP or the drug alters VT morphology.

Anti-Arrhythmia Agents↗

PubMed2001

Calmodulin kinase is a molecular switch for cardiac excitation-contraction coupling.

Signaling between cell membrane-bound L-type Ca(2+) channels (LTCC) and ryanodine receptor Ca(2+) release channels (RyR) on sarcoplasmic reticulum (SR) stores grades excitation-contraction coupling (ECC) in striated muscle. A physical connection regulates LTCC and RyR in skeletal muscle, but the molecular mechanism for coordinating LTCC and RyR in cardiomyocytes, where this physical link is absent, is unknown. Calmodulin kinase (CaMK) has characteristics suitable for an ECC coordinating molecule: it is activated by Ca(2+)/calmodulin, it regulates LTCC and RyR, and it is enriched in the vicinity of LTCC and RyR. Intact cardiomyocytes were studied under conditions where CaMK activity could be controlled independently of intracellular Ca(2+) by using an engineered Ca(2+)-independent form of CaMK and a highly specific CaMK inhibitory peptide. CaMK reciprocally enhanced L-type Ca(2+) current and reduced release of Ca(2+) from the SR while increasing SR Ca(2+) content. These findings support the hypothesis that CaMK is required to functionally couple LTCC and RyR during cardiac ECC.

Amino Acid Sequence↗

PubMed2001

Minor role of oxidative stress during intermediate phase of acute pancreatitis in rats.

Reactive oxygen species have been implicated in the pathogenesis of acute pancreatitis. Few studies have focused on the loss of endogenous antioxidants and molecular oxidative damage. Two acute pancreatitis models in rats; taurocholate (3% intraductal infusion) and cerulein (10 microg/kg/h), were used to study markers of oxidative stress: Glutathione, ascorbic acid, and their oxidized forms (glutathione disulfide and dehydroascorbic acid), malondialdehyde, and 4-hydroxynoneal in plasma and pancreas, as well as 7-hydro-8-oxo-2'-deoxyguanosine in pancreas. In both models, pancreatic glutathione depleted by 36-46% and pancreatic ascorbic acid depleted by 36-40% (p <.05). In the taurocholate model, plasma glutathione was depleted by 34% (p <.05), but there were no significant changes in plasma ascorbic acid or in plasma and pancreas dehydroascorbic acid, malondialdehyde, and 4-hydroxynoneal, and no significant changes in the pancreas glutathione disulfide/glutathione ratio. While pancreas glutathione disulfide/glutathione ratio increased in the cerulein model, there were no significant changes in plasma glutathione, plasma, or pancreas ascorbic acid, dehydroascorbic acid, 4-hydroxynoneal, and malondialdehyde, or in pancreas 7-hydro-8-oxo-2'-deoxyguanosine. Reactive oxygen species have a minor role in the intermediate stages of pancreatitis models.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2001

Ca2+-dependent regulation of cardiac L-type Ca2+ channels: is a unifying mechanism at hand?

Ca2+ entry (I(Ca)) through cardiac L-type Ca2+ channels (LTCC) drives critical cellular processes ranging from contraction to gene expression, and, when disordered, is implicated in arrhythmias and hypertrophy. LTCC activation occurs by cell membrane depolarization, but LTCCs are also regulated by auxiliary proteins, phosphorylation, and intracellular CA2+([Ca2+]i). LTCC regulation by [Ca2+]i is especially intriguing because increased [Ca2+]i signals dual and conflicting commands for I(Ca)inactivation and facilitation. A recent explosion of work has shed new light on the mechanisms and molecular identity of domains necessary for [Ca2+]i-dependent regulation of LTCC.

Amino Acid Sequence↗

PubMed2001

In vivo breast tissue backscatter measurements with 7.5- and 10-MHz transducers.

Measurements of the ultrasound (US) backscatter coefficient (BSC) of fibroglandular and fatty breast tissues in vivo from 5.25 through 13 MHz, using the reference phantom method, are presented. Radiofrequency echo data were collected at a series of locations in the left breasts of 16 adults, age 46 to 84, and in a custom-built phantom calibrated for backscatter and attenuation. Matched regions of interest (ROIs) were then selected in these images, from which the backscatter coefficient and the backscatter frequency dependence were ratiometrically estimated, after compensation for attenuation. The mean results in fibroglandular tissues were 78.9 x 10(-3)/cm, sr at 7.2 MHz (n(ROI) = 43, n = 13) and 146 x 10(-3)/cm, sr at 10.3 MHz (n(ROI) = 19, n = 10) with frequency dependencies of f(2.28) and f(3.25). The corresponding results in subcutaneous fat were 2.59 x 10(-3)/cm, sr at 7.2 MHz (n(ROI) = 56, n = 16) and 7.08 x 10(-3)/cm, sr at 10.3 MHz (n(ROI) = 57, n = 16) with frequency dependencies of f(3.49) and f(3.43). These findings are discussed and compared to similar measurements in the literature.

Adipose Tissue↗

PubMed2001

Autoprotection in acetaminophen intoxication in rats: the role of liver regeneration.

Autoprotection by acetaminophen, i.e. increased resistance to toxic effects caused by pretreatment, is a well-known phenomenon. The purpose of the present work was to identify mechanisms for increased acetaminophen tolerance induced by pretreatment of rats. One group of female Wistar rats (pretreated rats) received acetaminophen orally in increasing doses (1 to 4.3 g/kg) twice a week for 3 weeks, one group (naïve rats) received the vehicle. At time zero pretreated rats received a toxic dose of 7.5 g/kg (100% lethal in naïve rats), and naïve rats received a toxic dose of 4.3 g/kg. Blood and liver tissue were collected before and 12, 24, 36, and 48 hr after the toxic dose and were analysed for hepatic glutathione and cysteine contents, hepatic glutathione-S-transferase and blood alanine aminotransferase activity, as well as acetaminophen concentration in plasma. Steady-state mRNA levels of proteins involved in acetaminophen detoxification, cell division and acute phase response were measured, liver tissue was examined for proliferating cell nuclear antigen and degree of hepatocyte necrosis. Six naïve rats not receiving acetaminophen served as controls. The mortality was the same in pre-treated and naïve rats (33 percent). Thus, pretreatment increased the tolerance twice. Before the toxic dose pretreated rats compared to control rats had higher activity of glutathione-S-transferase (liver) and alanine aminotransferase (serum), higher hepatic mRNA level of glutathione-S-transferase and gamma-glutamylcysteine synthetase heavy and light chain subunits, and lower hepatic concentration of glutathione, cysteine and mRNA of CYP1A2 than control rats. After the toxic dose, the mRNA levels of glutathione-S-transferase, gamma-glutamylcysteine synthetase heavy and light chain subunits, and CYP1A2 in naïve rats rose, approaching those of pretreated rats. Proliferating cell nuclear antigen labelling was high in pretreated rats, while only slightly increased in a few of the naïve rats. Necrotic hepatocytes were found at all time intervals in pretreated rats, and in naïve rats they appeared after 12 hr, peaking after 36 hr. Pretreatment increased the tolerance to acetaminophen toxicity twice, as estimated by mortality. The data indicate that pretreatment may reduce the relative production of toxic metabolites, but it primarily enhances the protection against these metabolites by regenerating hepatocytes.

Acetaminophen↗

PubMed2001

Germline mutations of the gene encoding bone morphogenetic protein receptor 1A in juvenile polyposis.

Juvenile polyposis (JP; OMIM 174900) is an autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for developing gastrointestinal cancers. Previous studies have demonstrated a locus for JP mapping to 18q21.1 (ref. 3) and germline mutations in the homolog of the gene for mothers against decapentaplegic, Drosophila, (MADH4, also known as SMAD4) in several JP families. However, mutations in MADH4 are only present in a subset of JP cases, and although mutations in the gene for phosphatase and tensin homolog (PTEN) have been described in a few families, undefined genetic heterogeneity remains. Using a genome-wide screen in four JP kindreds without germline mutations in MADH4 or PTEN, we identified linkage with markers from chromosome 10q22-23 (maximum lod score of 4.74, straight theta=0.00). We found no recombinants using markers developed from the vicinity of the gene for bone morphogenetic protein receptor 1A (BMPR1A), a serine-threonine kinase type I receptor involved in bone morphogenetic protein (BMP) signaling. Genomic sequencing of BMPR1A in each of these JP kindreds disclosed germline nonsense mutations in all affected kindred members but not in normal control individuals. These findings indicate involvement of an additional gene in the transforming growth factor-beta (TGF-beta) superfamily in the genesis of JP, and document an unanticipated function for BMP in colonic epithelial growth control.

Adenomatous Polyposis Coli↗

PubMed2001

Functional similarity between electrograms recorded from an implantable cardioverter defibrillator emulator and the surface electrocardiogram.

Clinical use of stored electrogram (EGM) configurations currently used in ICDs is limited. The hypothesis that EGMs recorded from electrodes on the ICD surface may improve diagnostic capabilities of the device was tested in the present study. The Buttons on Active Can Emulator (BACE), an ICD-sized device containing four button electrodes, was temporarily placed into a subcutaneous or submuscular left pectoral pocket in 16 patients during ICD implantation. Simultaneous recordings were obtained from the ECG lead II, bipolar EGMs using BACE electrodes, and a bipolar atrial EGM during sinus rhythm (SR), ventricular pacing (VP) at cycle lengths of 500 and 400 ms, and VT. Visible P waves were present in all patients during SR (n = 15), in 5 (33%) of 15 patients during VP, and none of the patients during VT (n = 4) using BACE EGMs and lead II. P and QRS amplitudes and the P:QRS ratio during SR in BACE EGMs were significantly lower than those in lead II. BACE EGMs showed prominent changes in QRS morphology and duration during VP and VT compared to SR, and the magnitude of QRS prolongation during VP was similar to that in lead II. Measurements of PR, QRS, and QT duration during SR showed good agreement between BACE EGMs and lead II. In conclusion, EGMs recorded from electrodes embedded on the ICD housing may potentially improve visual discrimination between supraventricular and ventricular arrhythmias. They also may be useful as a surrogate of the ECG for analysis and monitoring of different components of P-QRS-T complex.

Defibrillators, Implantable↗

PubMed2001

2-D motion estimation using two parallel receive beams.

We describe a method for estimating 2-D target motion using ultrasound. The method is based on previous ensemble tracking techniques, which required at least four parallel receive beams and 2-D pattern matching. In contrast, the method described requires only two parallel receive beams and 1-D pattern matching. Two 1-D searches are performed, one in each lateral direction. The direction yielding the best match indicates the lateral direction of motion. Interpolation provides sub-pixel magnitude resolution. We compared the two beam method with the four beam method using a translating speckle target at three different parallel beam steering angles and transducer angles of 0, 45, and 90 degrees. The largest differences were found at 90 degrees, where the two beam method was generally more accurate and precise than the four beam method and also less prone to directional errors at small translations. We also examined the performance of both methods in a laminar flow phantom. Results indicated that the two beam method was more accurate in measuring the flow angle when the flow velocity was small. Computer simulations supported the experimental findings. The poorer performance of the four beam method was attributed to differences in correlation among the parallel beams. Specifically, center beams 2 and 3 correlated better with each other than with the outer beams. Because the four beam method used a comparison of a kernel region in beam pair 2-3 with two different beam pairs 1-2 and 3-4, the 2-to-1 and 3-to-4 components of this comparison increased the incidence of directional errors, especially at small translations. The two beam method used a comparison between only two beams and so was not subject to this source of error. Finally, the two beam method did not require amplitude normalization, as was necessary for the four beam method, when the two beams were chosen symmetric to the transmit axis. We conclude that two beam ensemble tracking can accurately estimate motion using only two parallel receive beams.

Biomedical Engineering↗

PubMed2001

A role for physician assistants in organ procurement.

Healthcare in the United States, as well as the environment in which physician assistants work, is rapidly changing. Consequently, the role of a physician assistant is expanding to meet the needs of patients and physicians of all specialties of medicine and surgery. In organ procurement, physician assistants can be a valuable asset to an organ procurement organization because of their medical education, versatility, and commitment to personalized care to organ donors and their families. Physician assistants are healthcare professionals who are uniquely qualified for a variety of roles within the organization: clinician, educator, consultant, donor and family liaison, and researcher.

Adult↗

PubMed2001

Potassium current antagonist properties and proarrhythmic consequences of quinolone antibiotics.

Quinolones are clinically important antibiotic drugs. One quinolone antibiotic, sparfloxacin (SPX), has been recently reported to increase the QT interval, and another quinolone, grepafloxacin (GRX), was withdrawn because it induced torsade de pointes (TdP), a polymorphic ventricular tachycardia (VT) linked to excessive QT interval prolongation. To determine whether SPX, GRX, and other recently developed quinolones, gatifloxacin (GAT) and moxifloxacin (MOX), have similar, potentially deleterious, properties we compared these agents in two ways. First, we measured their relative antagonist potency against the rapid component of the delayed rectifier K(+) current (I(Kr)), and second we determined the QT interval prolongation and inducibility of VT and TdP using a well established in vivo rabbit arrhythmia model. All of these agents are I(Kr) antagonists with the following IC(50) values (mean +/- S.E.) for I(Kr) block: SPX, 0.23 +/- 0.07 microM; MOX, 0.75 +/- 0.31 microM; GAT, 26.5 +/- 13.4 microM; and GRX, 27.2 +/- 11.6 microM. All agents also increased the maximum QT interval (mean +/- S.E.) from baseline (241 +/- 10 ms): SPX, 370 +/- 30 ms; MOX, 270 +/- 30 ms; GRX, 280 +/- 25 ms; and GAT, 255 +/- 23 ms. No agents caused TdP during a standard 30-min observation period, but SPX-treated animals developed nonsustained VT (three of six) and TdP (one of six) during an extended 60-min observation period. These findings show that I(Kr) block may be a common feature of many quinolone antibiotics, and that the proarrhythmic consequences vary according to I(Kr) antagonist potency, but are also influenced by additional, unidentified factors.

4-Quinolones↗

PubMed2000

Determinants for calmodulin binding on voltage-dependent Ca2+ channels.

Calmodulin, bound to the alpha(1) subunit of the cardiac L-type calcium channel, is required for calcium-dependent inactivation of this channel. Several laboratories have suggested that the site of interaction of calmodulin with the channel is an IQ-like motif in the carboxyl-terminal region of the alpha(1) subunit. Mutations in this IQ motif are linked to L-type Ca(2+) current (I(Ca)) facilitation and inactivation. IQ peptides from L, P/Q, N, and R channels all bind Ca(2+)calmodulin but not Ca(2+)-free calmodulin. Another peptide representing a carboxyl-terminal sequence found only in L-type channels (designated the CB domain) binds Ca(2+)calmodulin and enhances Ca(2+)-dependent I(Ca) facilitation in cardiac myocytes, suggesting the CB domain is functionally important. Calmodulin blocks the binding of an antibody specific for the CB sequence to the skeletal muscle L-type Ca(2+) channel, suggesting that this is a calmodulin binding site on the intact protein. The binding of the IQ and CB peptides to calmodulin appears to be competitive, signifying that the two sequences represent either independent or alternative binding sites for calmodulin rather than both sequences contributing to a single binding site.

Amino Acid Sequence↗

PubMed2000

Novel kinetics of mammalian glutathione synthetase: characterization of gamma-glutamyl substrate cooperative binding.

Glutathione (GSH) synthetase [L-gamma-glutamyl-L-cysteinyl:glycine ligase (ADP-forming), EC 6.3.2.3] catalyzes the final step in GSH biosynthesis. Mammalian glutathione synthetase is a homodimer with each subunit containing an active site. We report the detailed kinetic data for purified recombinant rat glutathione synthetase. It has the highest specific activity (11 micromol/min/mg) reported for any mammalian glutathione synthetase. The apparent K(m) values for ATP and glycine are 37 and 913 microM, respectively. The Lineweaver-Burk double reciprocal plot for gamma-glutamyl substrate binding revealed a departure from linearity indicating cooperative binding. Quantitative analysis of the kinetic results for gamma-glutamyl substrate binding gives a Hill coefficient (h) of 0. 576, which shows the negative cooperativity. Neither ATP, the other substrate involved in forming the enzyme-bound gamma-glutamyl phosphate intermediate, nor glycine, which attacks this intermediate to form GSH, exhibit any cooperativity. The cooperative binding of gamma-glutamyl substrate is not affected by ATP concentration. Thus, mammalian glutathione synthetase is an allosteric enzyme.

Animals↗

PubMed2000

Binding of octa-plus porphyrazines to DNA.

We present a preliminary report of the interaction of octacationic N-methyl-pyridyl metalloporphyrazines, M=Cu(II) (Cupz+8) and Zn(II) (Znpz+8), with calf thymus DNA. These were monitored by electronic absorption spectroscopy, and in the case of Znpz+8, also by emission spectroscopy. These studies show that both the Cupz+8 and Znpz+8 interact strongly with DNA, and at sufficient concentrations induce a highly colored precipitate. The spectrum of Cupz+8 red-shifts as DNA is added, which is interpreted as indicative of pi stacking of the charged macrocycle as it binds electrostatically to the outside of the DNA duplex. The spectrum of Znpz+8 does not shift, indicative of simple electrostatic surface binding. The absence of stacking may be related to the presence of an axial metal-ion ligand for Znpz+8, presumably 1120, while the metal ion of Cupz+8 is four-coordinate.

Animals↗