Phenolate-bonded bis(µ-oxido)-bis-copper(III) intermediates: hydroxylation and dehalogenation reactivities.

Exogenous phenolate ortho-hydroxylation by copper oxidants formed from dioxygen is generally thought to occur through one of two limiting mechanisms defined by the structure of the active oxidant: an electrophilic µ-η2:η2-peroxo-bis-copper(II) species as found in the oxygenated form of the binuclear copper enzyme tyrosinase (oxyTyr), or an isomeric bis(µ-oxido)-bis-copper(III) species (O) with ligated phenolate(s) as evidenced by most synthetic systems. The characterization of the latter is limited due to their limited thermal stability. This study expands the scope of an O species with ligated phenolate(s) using N,N'-di-tert-butyl-1,3-propanediamine (DBPD), a flexible secondary diamine ligand. Oxygenation of the [(DBPD)Cu(I)]1+ complex at low temperatures (e.g., 153 K) forms a spectroscopically and structurally faithful model to oxyTyr, a side-on peroxide intermediate, which reacts with added phenolates to form a bis(µ-oxido)-bis-copper(III) species with ligated phenolates, designated as an A species. The proposed stoichiometry of A is best understood as possessing 2 rather than 1 bonded phenolate. Thermal decomposition of A results in regiospecific phenolate ortho-hydroxylation with the ortho-substituent as either a C-H or C-X (Cl, Br) group, though the halogen displacement is significantly slower. DFT and experimental studies support an electrophilic attack of an oxide ligand into the π-system of a ligated phenolate. This study supports a hydroxylation mechanism in which O-O bond cleavage of the initially formed peroxide by phenolate ligation, which precedes phenolate aromatic hydroxylation.

Selective Oxidation of Exogenous Substrates by a Bis-Cu(III) Bis-Oxide Complex: Mechanism and Scope.

Cu(III)2(µ-O)2 bis-oxides (O) form spontaneously by direct oxygenation of nitrogen-chelated Cu(I) species and constitute a diverse class of versatile 2e-/2H+ oxidants, but while these species have attracted attention as biomimetic models for dinuclear Cu enzymes, reactivity is typically limited to intramolecular ligand oxidation, and systems exhibiting synthetically useful reactivity with exogenous substrates are limited. O tmpd (TMPD = N 1 , N 1 , N 3 , N 3 -tetramethylpropane-1,3-diamine) presents an exception, readily oxidizing a diverse array of exogenous substrates, including primary alcohols and amines selectively over their secondary counterparts in good yields. Mechanistic and DFT analyses suggest substrate oxidation proceeds through initial axial coordination, followed by rate limiting rotation to position the substrate in the Cu(III) equatorial plane, whereupon rapid deprotonation and oxidation by net hydride transfer occurs. Together, the results suggest the selectivity and broad substrate scope unique to O tmpd are best attributed to the combination of ligand flexibility, limited steric demands, and ligand oxidative stability. In keeping with the absence of rate limiting C-H scission, O tmpd exhibits a marked insensitivity to the strength of the substrate Cα-H bond, readily oxidizing benzyl alcohol and 1 octanol at near identical rates.

Exclusive imidazole ligation to CuIII2O2 and CuIIICuII2O2 cores.

We disclose herein the synthesis and characterization of L2Cu(iii)2O2 and L3Cu(iii)Cu(ii)2O2 complexes with nitrogen ligation exclusively from imidazoles for the first time. Their accessibility by direct oxygenation of a L-Cu(i) precursor and the resulting Cu(iii) formation inform on the kinetic accessibility and thermodynamic superiority of imidazole in stabilizing Cu(iii).

Development of Decreased-Gluten Wheat Enabled by Determination of the Genetic Basis of lys3a Barley.

Celiac disease is the most common food-induced enteropathy in humans, with a prevalence of approximately 1% worldwide. It is induced by digestion-resistant, proline- and glutamine-rich seed storage proteins, collectively referred to as gluten, found in wheat (Triticum aestivum). Related prolamins are present in barley (Hordeum vulgare) and rye (Secale cereale). The incidence of both celiac disease and a related condition called nonceliac gluten sensitivity is increasing. This has prompted efforts to identify methods of lowering gluten in wheat, one of the most important cereal crops. Here, we used bulked segregant RNA sequencing and map-based cloning to identify the genetic lesion underlying a recessive, low-prolamin mutation (lys3a) in diploid barley. We confirmed the mutant identity by complementing the lys3a mutant with a transgenic copy of the wild-type barley gene and then used targeting-induced local lesions in genomes to identify induced single-nucleotide polymorphisms in the three homeologs of the corresponding wheat gene. Combining inactivating mutations in the three subgenomes of hexaploid bread wheat in a single wheat line lowered gliadin and low-molecular-weight glutenin accumulation by 50% to 60% and increased free and protein-bound lysine by 33%.

A realistic in silico model for structure/function studies of molybdenum-copper CO dehydrogenase.

CO dehydrogenase (CODH) is an environmentally crucial bacterial enzyme that oxidizes CO to CO2 at a Mo-Cu active site. Despite the close to atomic resolution structure (1.1 Å), significant uncertainties have remained with regard to the protonation state of the water-derived equatorial ligand coordinated at the Mo-center, as well as the nature of intermediates formed during the catalytic cycle. To address the protonation state of the equatorial ligand, we have developed a realistic in silico QM model (~179 atoms) containing structurally essential residues surrounding the active site. Using our QM model, we examined each plausible combination of redox states (Mo(VI)-Cu(I), Mo(V)-Cu(II), Mo(V)-Cu(I), and Mo(IV)-Cu(I)) and Mo-coordinated equatorial ligands (O(2-), OH(-), H2O), as well as the effects of second-sphere residues surrounding the active site. Herein, we present a refined computational model for the Mo(VI) state in which Glu763 acts as an active site base, leading to a MoO2-like core and a protonated Glu763. Calculated structural and spectroscopic data (hyperfine couplings) are in support of a MoO2-like core in agreement with XRD data. The calculated two-electron reduction potential (E = -467 mV vs. SHE) is in reasonable agreement with the experimental value (E = -558 mV vs. SHE) for the redox couple comprising an equatorial oxo ligand and protonated Glu763 in the Mo(VI)-Cu(I) state and an equatorial water in the Mo(IV)-Cu(I) state. We also suggest a potential role of second-sphere residues (e.g., Glu763, Phe390) based on geometric changes observed upon exclusion of these residues in the most plausible oxidized states.

Multi-charged heavy ion acceleration from the ultra-intense short pulse laser system interacting with the metal target.

Experimental demonstration of multi-charged heavy ion acceleration from the interaction between the ultra-intense short pulse laser system and the metal target is presented. Al ions are accelerated up to 12 MeV/u (324 MeV total energy). To our knowledge, this is far the highest energy ever reported for the case of acceleration of the heavy ions produced by the <10 J laser energy of 200 TW class Ti:sapphire laser system. Adding to that, thanks to the extraordinary high intensity laser field of ∼10(21) W cm(-2), the accelerated ions are almost fully stripped, having high charge to mass ratio (Q/M).

Autophagic program is regulated by miR-325.

Autophagy is required for the maintenance of cardiomyocytes homeostasis. However, the abnormal autophagy could lead to the development of heart failure. Autophagy is enhanced during myocardial ischemia/reperfusion; it remains to elucidate the molecular regulation of autophagy. We report here that miR-325, ARC and E2F1 constitute an axis that regulates autophagy. Our results showed that miR-325 expression is upregulated upon anoxia/reoxygenation and ischemia/reperfusion. Cardiomyocyte-specific overexpression of the miR-325 potentiates autophagic responses and myocardial infarct sizes, whereas knockdown of miR-325 inhibited autophagy and cell death. We searched for the downstream mediator of miR-325 and identified that ARC is a target of miR-325. ARC transgenic mice could attenuate autophagy and myocardial infarction sizes upon pressure-overload-induced heart failure, whereas ARC null mice exhibited an increased autophagic accumulation in the heart. The suppression of ARC by miR-325 led to its inability to repress autophagic program. In exploring the molecular mechanism by which miR-325 expression is regulated, our results revealed that the transcription factor E2F1 contributed to promote miR-325 expression. E2F1 null mice demonstrated reduced autophagy and myocardial infarction sizes upon ischemia/reperfusion. Our present study reveals a novel autophagic regulating model that is composed of E2F1, miR-325 and ARC. Modulation of their levels may provide a new approach for tackling cardiac failure.

Nicotine decreases ethanol-induced dopamine signaling and increases self-administration via stress hormones.

Tobacco smoking is a well-known risk factor for subsequent alcohol abuse, but the neural events underlying this risk remain largely unknown. Alcohol and nicotine reinforcement involve common neural circuitry, including the mesolimbic dopamine system. We demonstrate in rodents that pre-exposure to nicotine increases alcohol self-administration and decreases alcohol-induced dopamine responses. The blunted dopamine response was due to increased inhibitory synaptic transmission onto dopamine neurons. Blocking stress hormone receptors prior to nicotine exposure prevented all interactions with alcohol that we measured, including the increased inhibition onto dopamine neurons, the decreased dopamine responses, and the increased alcohol self-administration. These results indicate that nicotine recruits neuroendocrine systems to influence neurotransmission and behavior associated with alcohol reinforcement.

Phosphatidylinositol(4,5)bisphosphate coordinates actin-mediated mobilization and translocation of secretory vesicles to the plasma membrane of chromaffin cells.

Neurosecretory vesicles undergo docking and priming before Ca(2+)-dependent fusion with the plasma membrane. Although de novo synthesis of phosphatidylinositol(4,5)bisphosphate (PtdIns(4,5)P(2)) is required for exocytosis, its precise contribution is still unclear. Here we show that inhibition of the p110δ isoform of PI3-kinase by IC87114 promotes a transient increase in PtdIns(4,5)P(2), leading to a potentiation of exocytosis in chromaffin cells. We then exploit this pathway to examine the effect of a transient PtdIns(4,5)P(2) increase on neurosecretory vesicles behaviour, outside the context of a secretagogue stimulation. Our results demonstrate that a rise in PtdIns(4,5)P(2) is sufficient to promote the mobilization and recruitment of secretory vesicles to the plasma membrane via Cdc42-mediated actin reorganization. PtdIns(4,5)P(2), therefore, orchestrates the actin-based conveyance of secretory vesicles to the plasma membrane.

In vitro identification and electrophysiological characterization of dopamine neurons in the ventral tegmental area.

Dopamine (DA) neurons in the ventral tegmental area (VTA) have been implicated in brain mechanisms related to motivation, reward, and drug addiction. Successful identification of these neurons in vitro has historically depended upon the expression of a hyperpolarization-activated current (I(h)) and immunohistochemical demonstration of the presence of tyrosine hydroxylase (TH), the rate-limiting enzyme for DA synthesis. Recent findings suggest that electrophysiological criteria may be insufficient for distinguishing DA neurons from non-DA neurons in the VTA. In this study, we sought to determine factors that could potentially account for the apparent discrepancies in the literature regarding DA neuron identification in the rodent brain slice preparation. We found that confirmed DA neurons from the lateral VTA generally displayed a larger amplitude I(h) relative to DA neurons located in the medial VTA. Measurement of a large amplitude I(h) (>100 pA) consistently indicated a dopaminergic phenotype, but non-dopamine neurons also can have I(h) current. The data also showed that immunohistochemical TH labeling of DA neurons can render false negative results after relatively long duration (>15 min) whole-cell patch clamp recordings. We conclude that whole-cell patch clamp recording in combination with immunohistochemical detection of TH expression can guarantee positive but not negative DA identification in the VTA.

Addictive nicotine alters local circuit inhibition during the induction of in vivo hippocampal synaptic potentiation.

The drug addiction process shares many commonalities with normal learning and memory. Addictive drugs subvert normal synaptic plasticity mechanisms, and the consequent synaptic changes underlie long-lasting modifications in behavior that accrue during the progression from drug use to addiction. Supporting this hypothesis, it was recently shown that nicotine administered to freely moving mice induces long-term synaptic potentiation of the perforant path connection to granule cells of the dentate gyrus. The perforant path carries place and spatial information that links the environment to drug taking. An example of that association is the nicotine-induced synaptic potentiation of the perforant path that was found to underlie nicotine-conditioned place preference. The present study examines the influence of nicotine over local GABAergic inhibition within the dentate gyrus during the drug-induced synaptic potentiation. In vivo recordings from freely moving mice suggested that both feedforward and feedback inhibition onto granules cells were diminished by nicotine during the induction of synaptic potentiation. In vitro brain slice studies indicated that nicotine altered local circuit inhibition within the dentate gyrus leading to disinhibition of granule cells. These changes in local inhibition contributed to nicotine-induced in vivo synaptic potentiation, thus, likely contributed to drug-associated memories. Through this learning process, environmental features become cues that motivate conditioned drug-seeking and drug-taking behaviors.

Nicotinic mechanisms influencing synaptic plasticity in the hippocampus.

Nicotinic acetylcholine receptors (nAChRs) are expressed throughout the hippocampus, and nicotinic signaling plays an important role in neuronal function. In the context of learning and memory related behaviors associated with hippocampal function, a potentially significant feature of nAChR activity is the impact it has on synaptic plasticity. Synaptic plasticity in hippocampal neurons has long been considered a contributing cellular mechanism of learning and memory. These same kinds of cellular mechanisms are a factor in the development of nicotine addiction. Nicotinic signaling has been demonstrated by in vitro studies to affect synaptic plasticity in hippocampal neurons via multiple steps, and the signaling has also been shown to evoke synaptic plasticity in vivo. This review focuses on the nAChRs subtypes that contribute to hippocampal synaptic plasticity at the cellular and circuit level. It also considers nicotinic influences over long-term changes in the hippocampus that may contribute to addiction.

Age dependent nicotinic influences over dopamine neuron synaptic plasticity.

The dopamine (DA) system of the ventral midbrain plays a critical role as mammals learn adaptive behaviors driven by environmental salience and reward. Addictive drugs, including nicotine, exert powerful influences over the mesolimbic DA system by activating and desensitizing nicotinic acetylcholine receptors (nAChRs) in a subtype-dependent manner. Nicotine induces synaptic plasticity at excitatory synapses onto DA neurons, thereby sending elevated DA signals that participate during the reinforcement of addictive behaviors. While humans and animals of any developmental age are potentially vulnerable to these drug-induced effects, evidence from clinical and epidemiological studies indicates that adolescents have an increased risk of addiction. Although this risk arises from a complex set of variables including societal and psychosocial influences, a contributing factor involves age dependent sensitivity to addictive drugs. One aspect of that sensitivity is drug-induced synaptic plasticity at excitatory synapses onto the dopamine neurons in the ventral midbrain. A single, acute exposure to addictive drugs, including nicotine, produces long-term potentiation (LTP) that can be quantified by measuring the shift in the subtypes of ionotropic glutamate receptors mediating evoked synaptic transmission. This change in glutamatergic transmission is expressed as an increased ratio of AMPA receptors to NMDA receptors at glutamatergic synapses. Age-related differences in the excitability and the nicotine sensitivity within the midbrain dopamine system may contribute to the greater risk of nicotine addiction in adolescent animals and humans.

Aberrant synaptic activation of N-methyl-D-aspartate receptors underlies ethanol withdrawal hyperexcitability.

Chronic ethanol exposure may induce neuroadaptive responses in N-methyl-d-aspartate (NMDA) receptors, which are thought to underlie a variety of alcohol-related brain disorders. Here, we demonstrate that hyperexcitability triggered by withdrawal from chronic ethanol exposure is associated with increases in both synaptic NMDA receptor expression and activation. Withdrawal from chronic ethanol exposure (75 mM ethanol, 5-9 days) elicited robust and prolonged epileptiform activity in CA1 pyramidal neurons from hippocampal explants, which was absolutely dependent upon NMDA receptor activation but independent of chronic inhibition of protein kinase A (PKA). Analysis of Sr(2+)-supported asynchronous NMDA receptor-mediated miniature excitatory postsynaptic currents (mEPSCs) was employed to assess changes in NMDA neurotransmission. After chronic exposure, ethanol withdrawal was associated with an increase in mEPSC amplitude 3.38-fold over that after withdrawal from acute ethanol exposure. Analysis of paired evoked alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid EPSCs and spontaneous mEPSCs indicated that withdrawal after chronic exposure was also associated with a selective increase in action potential evoked but not spontaneous transmitter release probability. Immunoblot analysis revealed significant increases in total NR1, NR2A, and NR2B subunit expression after chronic exposure and unaffected by PKA-inhibition manner. Confocal imaging studies indicate that increased NR1 subunit expression was associated with increased density of NR1 expression on dendrites in parallel with a selective increase in the size of NR1 puncta on dendritic spines. Therefore, neuroadaptation to chronic ethanol exposure in NMDA synaptic transmission is responsible for aberrant network excitability after withdrawal and results from changes in both postsynaptic function as well as presynaptic release.

Coincident signaling in mesolimbic structures underlying alcohol reinforcement.

The medium spiny neurons (MSNs) of the nucleus accumbens function in a critical regard to examine and integrate information in the processing of rewarding behaviors. These neurons are aberrantly affected by drugs of abuse, including alcohol. However, ethanol is unlike any other common drug of abuse, due to its pleiotropic actions on intracellular and intercellular signaling processes. Intracellular biochemical pathways appear to critically contribute to long-term changes in the level of synaptic activation of these neurons, which have been implicated in ethanol dependence. Additionally, these neurons also display a fascinating pattern of up/down activity, which appears to be, at least in part, regulated by convergent activation of dopaminergic and glutamatergic (NMDA) inputs. Thus, dopaminergic and NMDA receptor-mediated synaptic transmission onto these neurons may constitute a critical site of ethanol action in mesolimbic structures. For instance, dopaminergic inputs alter the ability of ethanol to regulate NMDA receptor-mediated synaptic transmission onto accumbal MSNs. Prior activation of D1-signaling cascade through the cAMP-regulated phosphoprotein-32kD (DARPP-32) and protein phosphatase-1 (PP-1) pathway significantly attenuates ethanol inhibition of NMDA receptor function. Therefore, the interaction of D1-signaling and NMDA receptor signaling may alter NMDA receptor-dependent long-term synaptic plasticity, contributing to the development of ethanol-induced neuroadaptation of the reward pathway.

Actions of acute and chronic ethanol on presynaptic terminals.

This article presents the proceedings of a symposium entitled "The Tipsy Terminal: Presynaptic Effects of Ethanol" (held at the annual meeting of the Research Society on Alcoholism, in Santa Barbara, CA, June 27, 2005). The objective of this symposium was to focus on a cellular site of ethanol action underrepresented in the alcohol literature, but quickly becoming a "hot" topic. The chairs of the session were Marisa Roberto and George Robert Siggins. Our speakers were chosen on the basis of the diverse electrophysiological and other methods used to discern the effects of acute and chronic ethanol on presynaptic terminals and on the basis of significant insights that their data provide for understanding ethanol actions on neurons in general, as mechanisms underlying problematic behavioral effects of alcohol. The 5 presenters drew from their recent studies examining the effects of acute and chronic ethanol using a range of sophisticated methods from electrophysiological analysis of paired-pulse facilitation and spontaneous and miniature synaptic currents (Drs. Weiner, Valenzuela, Zhu, and Morrisett), to direct recording of ion channel activity and peptide release from acutely isolated synaptic terminals (Dr. Treistman), to direct microscopic observation of vesicular release (Dr. Morrisett). They showed that ethanol administration could both increase and decrease the probability of release of different transmitters from synaptic terminals. The effects of ethanol on synaptic terminals could often be correlated with important behavioral or developmental actions of alcohol. These and other novel findings suggest that future analyses of synaptic effects of ethanol should attempt to ascertain, in multiple brain regions, the role of presynaptic terminals, relevant presynaptic receptors and signal transduction linkages, exocytotic mechanisms, and their involvement in alcohol's behavioral actions. Such studies could lead to new treatment strategies for alcohol intoxication, alcohol abuse, and alcoholism.

Dual synaptic sites of D(1)-dopaminergic regulation of ethanol sensitivity of NMDA receptors in nucleus accumbens.

Regulation of NMDAreceptor-mediated synaptic transmission onto accumbal medium spiny neurons (MSN) may constitute an important site in drug reward and reinforcement in mesolimbic structures. Previously, we reported that D(1)-like dopamine receptors activate a postsynaptic cAMP/PKA/DARPP-32 signaling cascade culminating in phosphorylation of SER897-NR1 subunits and a reduction in the sensitivity to ethanol of NMDA receptor-mediated synaptic transmission. Here, we use a detailed electrophysiological analysis of D(1)-like receptor regulation of the ethanol sensitivity of accumbal NMDA receptors (NMDARs) through recordings of quantal Sr(2+)-supported NMDA miniature synaptic currents (mEPSCs) in reduced Mg(2+) (0.6 mM) and report dual presynaptic and postsynaptic components of D(1)-like regulation of ethanol sensitivity of NMDARs. Ethanol inhibited NMDA mEPSC amplitude and frequency in a dose-dependent manner (25-75 mM), indicating inhibitory effects on presynaptic and postsynaptic components NMDA receptor-mediated synaptic transmission. The presynaptic inhibitory effect was corroborated by analysing the ratio of paired-pulse facilitation (PPF) of Ca(2+)-supported NMDA EPSCs. Activation of D(1) receptors with the agonist, SKF 38393 (25 microM), reversed ethanol suppression of NMDA mEPSC frequency and amplitude. Furthermore, the Mg(2+)-dependent decay off-rate of NMDA mEPSCs was substantially reduced by ethanol in a manner strongly reversed by the D(1) agonist. D(1) receptor-mediated attenuation of both the presynaptic and postsynaptic actions of ethanol was completely blocked by a D(1) selective antagonist (SCH 23390). These data suggest that D(1)-like receptors modulate both the presynaptic and postsynaptic effects of ethanol on NMDA receptor-mediated synaptic transmission in nucleus accumbens (NAc) and that these interactions may contribute to ethanol-induced neuroadaptation of the reward pathway.

Cell cavities increase tortuosity in brain extracellular space.

Brain extracellular space (ECS) forms hindered pathways for molecular diffusion in chemical signaling and drug delivery. Hindrance is quantified by the tortuosity lambda; the tortuosity obtained from simulations using uniformly spaced convex cells is significantly lower than that measured experimentally. To attempt to account for the difference in results, this study employed a variety of ECS models based on an array of cubic cells containing open rectangular cavities that provided the ECS with dead-space microdomains. Monte Carlo simulations demonstrated that, in such ECS models, lambda can equal or exceed the typical experimental value of about 1.6. The simulations further revealed that lambda is relatively independent of cavity shape and the number of cavities per cell. It mainly depends on the total ECS volume fraction alpha, the cavity volume fraction alpha(c), and whether the cavity is located at the center of a cell face or formed at the junction of multiple cells. To describe the results from the different ECS models, an expression was obtained that related lambda to alpha, alpha(c), and an empirical exit factor beta that correlated with the ease with which a molecule could leave a cavity and its vicinity.

Ethanol selectively inhibits enhanced vesicular release at excitatory synapses: real-time visualization in intact hippocampal slices.

BACKGROUND: Conflicting information exists concerning the actions of ethanol on vesicular release at excitatory synapses. Because long-term alterations in synaptic transmission are thought to underlie neuroadaptive responses to ethanol, we have directly measured the actions of ethanol on release dynamics at an intact central synapse. METHODS: Here we investigated the effects of ethanol on release dynamics in hippocampal slices using confocal microscopy with the lipophilic dye, FM1-43, complemented by a patch clamp analysis of AMPA miniature excitatory postsynaptic currents (mEPSCs). After a pretreatment/loading paradigm with sulforhodamine (S-Rhd) and FM1-43, stable, dense punctate FM1-43 staining in the CA1 stratum radiatum was evident. RESULTS: FM1-43 fluorescence destaining was dose-dependently induced by perfusion with elevated K+ (20-60 mM). Cadmium inhibited K+-induced destaining, whereas nifedipine had no significant effect. Ethanol (25-75 mM) inhibited K+-induced destaining with high efficacy and had no effect on basal destaining. Both omega-Conotoxin GVIA and omega-Agatoxin IVA inhibited K+-induced destaining with high efficacy. The combination of omega-Conotoxin GVIA and omega-Agatoxin IVA occluded the inhibitory effect of ethanol, indicating that ethanol inhibition of release was dependent on inhibition of N/P/Q-voltage-gated calcium channels (VGCCs). Patch clamp studies of AMPA mEPSCs revealed similar findings in that vesicular release was enhanced with K+ depolarization in an ethanol-sensitive manner. CONCLUSIONS: These findings indicate that the FM1-43/S-Rhd method is a stable and powerful approach for direct real-time measurement of vesicular release kinetics in intact brain slice preparations and that ethanol inhibits vesicular release induced by depolarization via inhibition of N/P/Q-VGCCs.

Scintigraphic findings of Mycobacterium avium complex tenosynovitis of the index finger in a patient with systemic lupus erythematosus.

The presented case is a 36-year-old woman with a history of systemic lupus erythematosus for 10 years. She had progressively painful swelling of the right index finger that later proved to be a rare case of tenosynovitis caused by Mycobacterium avium complex. Serial images of 3-phase bone scans, gallium scan, and magnetic resonance imaging demonstrate the area of involvement.