Loss Of Branches Research Articles

Calcium Influx and Release Cooperatively Regulate AChR Patterning and Motor Axon Outgrowth during Neuromuscular Junction Formation

Formation of synapses between motor neurons and muscles is initiated by clustering of acetylcholine receptors (AChRs) in the center of muscle fibers prior to nerve arrival. This AChR patterning is considered to be critically dependent on calcium influx through L-type channels (CaV1.1). Using a genetic approach in mice, we demonstrate here that either the L-type calcium currents (LTCCs) or sarcoplasmic reticulum (SR) calcium release is necessary and sufficient to regulate AChR clustering at the onset of neuromuscular junction (NMJ) development. The combined lack of both calcium signals results in loss of AChR patterning and excessive nerve branching. In the absence of SR calcium release, the severity of synapse formation defects inversely correlates with the magnitude of LTCCs. These findings highlight theimportance of activity-dependent calcium signaling in early neuromuscular junction formation and indicate that both LTCC and SR calcium release individually support proper innervation of muscle byregulating AChR patterning and motor axon outgrowth.

Branch Thinning and the Large-Scale, Self-Similar Structure of Trees.

Branch formation in trees has an inherent tendency toward exponential growth, but exponential growth in the number of branches cannot continue indefinitely. It has been suggested that trees balance this tendency toward expansion by also losing branches grown in previous growth cycles. Here, we present a model for branch formation and branch loss during ontogeny that builds on the phenomenological assumption of a branch carrying capacity. The model allows us to derive approximate analytical expressions for the number of tips on a branch, the distribution of growth modules within a branch, and the rate and size distribution of tree wood litter produced. Although limited availability of data makes empirical corroboration challenging, we show that our model can fit field observations of red maple (Acer rubrum) and note that the age distribution of discarded branches predicted by our model is qualitatively similar to an empirically observed distribution of dead and abscised branches of balsam poplar (Populus balsamifera). By showing how a simple phenomenological assumption-that the number of branches a tree can maintain is limited-leads directly to predictions on branching structure and the rate and size distribution of branch loss, these results potentially enable more explicit modeling of woody tissues in ecosystems worldwide, with implications for the buildup of flammable fuel, nutrient cycling, and understanding of plant growth.

Projecting the recovery of a long‐lived deep‐sea coral species after the Deepwater Horizon oil spill using state‐structured models

Abstract Deepwater coral communities are hotspots of diversity and biomass. Most deep‐sea coral species are long‐lived and slow‐growing and are, thus, expected to recover slowly after disturbance. A better understanding of the recovery potential of these organisms is necessary to make appropriate management decisions. We used data from high‐resolution monitoring of individual coral colonies that were impacted by the Deepwater Horizon oil spill (April 2010) to parameterize and validate an annual, impact‐dependent, state‐structured matrix model to estimate the time to recovery for each coral colony. We projected the dynamics of three branch states: visibly healthy, unhealthy and hydroid‐colonized. Although we implicitly included branch loss in the model, we focused on the short‐term return of extant, damaged branches to a visibly healthy state and did not consider the far longer term regrowth of lost branches. Our model estimates that, depending on the initial level of impact, corals impacted by the spill will take up to three decades to recover to a state where all remaining branches appear healthy, though the majority of corals are projected to reach that state within a decade. By that time, some of these colonies will have lost a significant number of branches, leading to approximately 10% reduction in total biomass at all impacted sites. Overall, our model overestimates recovery, but branch loss estimates were reliable. Thus, the available growth rate data suggest that hundreds of years may be necessary for impacted communities to grow back to their initial biomass. Policy implications. Our study quantifies the very slow recovery rate of deep‐sea corals impacted by the Deepwater Horizon oil spill and demonstrates the imperative of prioritizing a precautionary approach for deep‐sea ecosystems over restoration after the fact. As anthropogenic pressure on the deep sea is likely to increase, we suggest the establishment of coral monitoring sites implemented as part of Marine Protected Areas to limit and detect impact to deep‐sea corals. Furthermore, our model may be used to plan shorter‐ and longer‐term monitoring programmes after impact and to provide a timeline for policy.

Development and evaluation on a wireless multi-sensors system for fresh-cut branches of the North American holly cold chain

North American holly (Ilex Verticillata), deciduous shrub of the Aquifoliaceae genus, is commonly known as winterberry, having a high ornamental and medicinal value. The fresh-cut branches of North American holly are prone to rapid deterioration during the cold chain. The paper presents a wireless multi-sensors system to improve postharvest quality of the fresh-cut branches of North American holly in the cold chain. The system was evaluated and validated at a sampled chain from Weihai city to Beijing. The critical ambient parameters including temperature, relative humidity, CO2 and ethylene are real-time monitored and analyzed in fresh-cut branches of the North American holly cold chain. Results show that the system can monitor accurately and transfer steadily data on critical ambient parameters through the logistics process. The traceability system can improve the quality control by tracing the critical ambient parameters and provides an early warning. The quality loss of fresh-cut branches of North American holly decreased from 25% ∼ 30% to below 15%, and the market price increased from below 20yuan/bundle to above 50yuan/bundle, which heighten benefit of cold chain.

Vitamin D deficiency and periprocedural myocardial infarction in patients undergoing percutaneous coronary interventions.

Vitamin D deficiency has been implicated in the progression of atherosclerosis and acute thrombotic events. We aimed at evaluating the impact of vitamin D deficiency on periprocedural myocardial infarction (PMI) in patients undergoing percutaneous coronary interventions (PCI). We included 934 patients undergoing non-urgent PCI. Assessment of myocardial biomarkers was performed from 6 to 48 h after PCI. PMI was defined as Creatine Kinase-MB increase by 3 times the Upper Limit Normal or by 50% of an elevated baseline value, periprocedural myocardial damage as Troponin I increase by 3 × ULN or 50% of baseline. Patients were divided according to vitamin D tertiles values (<10.2 ng/ml; 10.2-18.7 ng/ml; ≥18.8 ng/ml). Lower tertiles values of vitamin D were associated with age (p = 0.04), female gender, (p = 0.001), and a higher cardiovascular risk profile. Lower vitamin D levels related with PCI of descending anterior coronary artery or bypass vein grafts (p = 0.03), treatment of bifurcations (p = 0.05) and side branch loss (p = 0.05) and inversely with direct stenting (p = 0.002). However, lower vitamin D levels did not influence the risk of PMI (adjusted OR [95% CI] = 0.81[0.65,1.18], p = 0.09) or periprocedural myocardial damage (adjusted OR [95% CI] = 0.93[0.77,1.13], p = 0.48). Similar results were achieved when considering the severity of vitamin D deficiency. Therefore, in patients undergoing PCI, no association was observed between vitamin D deficiency and the risk of periprocedural MI and myocardial damage.

Interactions between ectomycorrhizal fungi and chestnut blight (&lt;em&gt;Cryphonectria parasitica&lt;/em&gt;) on American chestnut (&lt;em&gt;Castanea dentata&lt;/em&gt;) used in coal mine restoration

Plant and fungal interactions drive successional trajectories within reforestation offering both mutualisms (ectomycorrhizal fungi [ECM]) and fungal pathogens. Appalachian forest and mine reclamation projects re-introducing American chestnut and chestnut hybrids will inevitably document the return of chestnut blight, resulting in cankers causing branch dieback and loss of photosynthetic tissue. Similar to herbivory, the loss of photosynthetic tissue may reduce ECM root colonization and cause changes in fungal species composition. To test this, 75 six-year-old established chestnut trees were selected to represent the following: (1) Healthy trees free of chestnut blight; (2) trees with cankers and 50% branch dieback; (3) trees that died prior to the fifth growing season. Each tree had a chestnut seed planted 24 cm from the base. ECM colonization of both the established parent trees (n = 50) and five-month-old seedlings (n = 64) were quantified and genera determined by fungal DNA sequencing of the internal transcribed (ITS) region. Healthier seven-year-old chestnuts trees had significantly more ECM roots than those trees infected with chestnut blight cankers. However, disease die-back on chestnut did not have an influence on community composition among the parent trees or the neighboring five month seedlings. Results also demonstrated that five-month-old seedlings neighboring healthy parent trees had greater ECM on roots (P = 0.002), were larger in size (P = 0.04), and had greater survival (P = 0.01). ECM genera such as Cortinarius, Russula and Scleroderma provided tree to seedling inoculation. ECM colonization by Cortinarius spp. resulted in larger chestnut plants and increased nitrogen foliar concentrations on the five month seedlings. It can be hypothesized that blight will aid in diversifying forest stand composition and these early ECM networks will help facilitate the survival of other native hardwoods that recruit into these sites over time.

Progressive loss of retinal blood vessels in a live model of retinitis pigmentosa

ObjectiveTo assess retinal blood vessels in a live retinitis pigmentosa (RP) model with rd1 mutation and green fluorescent protein (GFP) expressed in vascular endothelium. MethodsHomozygous (hm) Tie2-GFP mice with rd1 mutation and known retinal degeneration were crossed with wild-type CD1 mice to generate control heterozygous (ht) Tie2-GFP mice. The retinas of 16 live hm mice were evaluated at 2 weeks and 3, 5, and 8 months of age, and compared with age-matched control ht and CD1 mice by optical coherence tomography (OCT) and confocal scanning laser ophthalmoscopy (cSLO). Fluorescence intensity was measured and compared between strains at 3, 5, and 8 months. In vivo findings were validated by immunostaining with collagen IV and isolectin histopathology. ResultsAll hm Tie2-GFP mice showed progressive outer retinal degeneration by OCT. Loss of small branches of blood vessels and then larger main vessels was seen by cSLO. Retinal tissue and vessels were preserved in control ht mice. At all ages, measurements of fluorescence intensity were reduced in hm compared with ht mice (p < 0.001). In all strains, intensity at 8 months was reduced compared with 3 months (p < 0.001) and 5 months (p = 0.021). Histopathological studies confirmed in vivo findings and revealed a pattern of blood vessel regression in the deep plexus, followed by intermediate and superficial retinal plexuses. ConclusionsThis is the first evidence of progressive loss of retinal blood vessels in a live mouse model of RP. These findings may be highly relevant to understanding retinal degeneration in RP to prevent blindness.

Crown reaction and acclimation to cyclical V-trimming of city trees: An analysis using terrestrial laser scanning

Trimming is an important practice for reducing potential contact between trees and power lines. V-trimming occurs when a tree is located directly under the electrical wires and results in the formation of a bilateral crown, but not much is known about a tree’s reaction and acclimation to such a repeated stress in an urban context.Using Terrestrial Laser Scanning (TLS), we present a study that focuses on documenting (i) short term effect of V-trimming on the tree structure, through the quantification and analysis of the dispersion of trimming induced branch loss and subsequent growth reaction, and, (ii) long term acclimation (i.e. changes in biomass location) of tree structure to repeated unidirectional trimming. A voxelisation method was used to derive space exploration metrics from TLS data based on explored volume quantification and voxels dispersion within the tree crown.Our results show that V-trimming induces a significant decrease in explored crown space volume (12.8% on average) but that this loss is regained by trimmed trees within only 1year following trimming thanks to a rapid regrowth rate. This was supported by an analysis of radial growth that showed that the growth of trimmed trees was greater than non-trimmed trees although this tendency was not statistically significant. In our study this regrowth was achieved without suckering; instead the regrowth mainly occurred within the crown periphery. We also observed that trimming had a significant influence on the way trees explore space with their crowns. While non-trimmed trees explored space preferentially toward a South direction, trimmed trees explored space in directions perpendicular to the wires (East and West). We also observed that crown biomass was located more in the extreme crown periphery in trimmed trees compared to non-trimmed trees.

Pericytes regulate VEGF-induced endothelial sprouting through VEGFR1

Pericytes adhere to the abluminal surface of endothelial tubules and are required for the formation of stable vascular networks. Defective endothelial cell-pericyte interactions are frequently observed in diseases characterized by compromised vascular integrity such as diabetic retinopathy. Many functional properties of pericytes and their exact role in the regulation of angiogenic blood vessel growth remain elusive. Here we show that pericytes promote endothelial sprouting in the postnatal retinal vasculature. Using genetic and pharmacological approaches, we show that the expression of vascular endothelial growth factor receptor 1 (VEGFR1) by pericytes spatially restricts VEGF signalling. Angiogenic defects caused by pericyte depletion are phenocopied by intraocular injection of VEGF-A or pericyte-specific inactivation of the murine gene encoding VEGFR1. Our findings establish that pericytes promote endothelial sprouting, which results in the loss of side branches and the enlargement of vessels when pericyte function is impaired or lost.

NLRP3/IL-1β mediates denervation during bladder outlet obstruction in rats.

Denervation of the bladder is a detrimental consequence of bladder outlet obstruction (BOO). We have previously shown that, during BOO, inflammation triggered by the NLRP3 inflammasome in the urothelia mediates physiological bladder dysfunction and downstream fibrosis in rats. The aim of this study was to assess the effect of NLRP3-mediated inflammation on bladder denervation during BOO. There were five groups of rats: (i) Control (no surgery); (ii) Sham-operated; (iii) BOO rats given vehicle; (iv) BOO rats given the NLRP3 inhibitor glyburide; and (v) BOO rats given the IL-1 receptor antagonist anakinra. BOO was constructed by ligating the urethra over a 1 mm catheter and removing the catheter. Medications were given prior to surgery and once daily for 12 days. Bladder sections were stained for PGP9.5, a pan-neuronal marker. Whole transverse sections were used to identify and count nerves while assessing cross-sectional area. For in vitro studies, pelvic ganglion neurons were isolated and treated with IL-1β. After a 48 h incubation apoptosis, neurite length and branching were assessed. In obstructed bladders, the number of nerves decreased while total area increased, indicating a loss of cell number and/or branching. The decrease in nerve density was blocked by glyburide or anakinra, clearly implicating the NLRP3 pathway in denervation. In vitro analysis demonstrated that IL-1β, a product of the inflammasome, induced apoptosis in pelvic ganglion neurons, suggesting one mechanism of BOO-induced denervation is NLRP3/IL-1β triggered apoptosis. The NLRP3/IL-1β-mediated inflammation pathway plays a significant role in denervation during BOO.

Identification of saponins from Panax notoginseng in metabolites of rats

UPLC-QTOF-MS/MS was used to identify metabolites in rat blood, urine and feces after the administration of n-butanol extract derived from steamed notoginseng. The metabolic process of saponins came from steamed notoginseng was analyzed. The metabolites were processed by PeakView software, and identified according to the structural characteristics of prototype compounds and the accurate qualitative and quantitative changes of common metabolic pathways. Four saponins metabolites were identified based on MS/MS information of metabolites, namely ginsenoside Rh₄, Rk₃, Rk₁, Rg₅,and their 15 metabolites were verified. The metabolic pathways of the four ginsenosides in n-butanol extract included glucuronidation, desugar, sulfation, dehydromethylation, and branch loss. The metabolites of main active saponin components derived from steamed Panax notoginseng were analyzed from the perspective of qualitative analysis. And the material basis for the efficacy of steamed notoginseng was further clarified.

Current and future patterns of fire-induced forest degradation in Amazonia

Amazon droughts directly increase forest flammability by reducing forest understory air and fuel moisture. Droughts also increase forest flammability indirectly by decreasing soil moisture, triggering leaf shedding, branch loss, and tree mortality—all of which contribute to increased fuel loads. These direct and indirect effects can cause widespread forest fires that reduce forest carbon stocks in the Amazon, with potentially important consequences for the global carbon cycle. These processes are expected to become more widespread, common, and intense as global climate changes, yet the mechanisms linking droughts, wildfires, and associated changes in carbon stocks remain poorly understood. Here, we expanded the capabilities of a dynamic forest carbon model to better represent (1) drought effects on carbon and fuel dynamics and (2) understory fire behavior and severity. We used the refined model to quantify changes in Pan-Amazon live carbon stocks as a function of the maximum climatological water deficit (MCWD) and fire intensity, under both historical and future climate conditions. We found that the 2005 and 2010 droughts increased potential fire intensity by 226 kW m−1 and 494 kW m−1, respectively. These increases were due primarily to increased understory dryness (109 kW m−1 in 2005; 124 kW m−1 in 2010) and altered forest structure (117 kW m−1 in 2005; 370 kW m−1 in 2010) effects. Combined, these historic droughts drove total simulated reductions in live carbon stocks of 0.016 (2005) and 0.027 (2010) PgC across the Amazon Basin. Projected increases in future fire intensity increased simulated carbon losses by up to 90% per unit area burned, compared with modern climate. Increased air temperature was the primary driver of changes in simulated future fire intensity, while reduced precipitation was secondary, particularly in the eastern portion of the Basin. Our results show that fire-drought interactions strongly affect live carbon stocks and that future climate change, combined with the synergistic effects of drought on forest flammability, may strongly influence the stability of tropical forests in the future.

Etiolated Stem Branching Is a Result of Systemic Signaling Associated with Sucrose Level.

The potato (Solanum tuberosum) tuber is a swollen stem. Sprouts growing from the tuber nodes represent loss of apical dominance and branching. Long cold storage induces loss of tuber apical dominance and results in secondary branching. Here, we show that a similar branching pattern can be induced by short heat treatment of the tubers. Detached sprouts were induced to branch by the heat treatment only when attached to a parenchyma cylinder. Grafting experiments showed that the scion branches only when grafted onto heat- or cold-treated tuber parenchyma, suggesting that the branching signal is transmitted systemically from the bud-base parenchyma to the grafted stem. Exogenous supply of sucrose (Suc), glucose, or fructose solution to detached sprouts induced branching in a dose-responsive manner, and an increase in Suc level was observed in tuber parenchyma upon branching induction, suggesting a role for elevated parenchyma sugars in the regulation of branching. However, sugar analysis of the apex and node after grafting showed no distinct differences in sugar levels between branching and nonbranching stems. Vacuolar invertase is a key enzyme in determining the level of Suc and its cleavage products, glucose and fructose, in potato parenchyma. Silencing of the vacuolar invertase-encoding gene led to increased tuber branching in combination with branching-inducing treatments. These results suggest that Suc in the parenchyma induces branching through signaling and not by excess mobilization from the parenchyma to the stem.

Dysregulation of chromatin remodelling complexes in amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis is a fatal neurodegenerative disease with paralysis resulting from dysfunction and loss of motor neurons. A common neuropathological finding is attrition of motor neuron dendrites, which make central connections vital to motor control. The chromatin remodelling complex, neuronal Brahma-related gene 1 (Brg1)-associated factor complex (nBAF), is critical for neuronal differentiation, dendritic extension and synaptic function. We have identified loss of the crucial nBAF subunits Brg1, Brg1-associated factor 53b and calcium responsive transactivator in cultured motor neurons expressing FUS or TAR-DNA Binding Protein 43 (TDP-43) mutants linked to familial ALS. When plasmids encoding wild-type or mutant human FUS or TDP-43 were expressed in motor neurons of dissociated spinal cord cultures prepared from E13 mice, mutant proteins in particular accumulated in the cytoplasm. Immunolabelling of nBAF subunits was reduced in proportion to loss of nuclear FUS or TDP-43 and depletion of Brg1 was associated with nuclear retention of Brg1 mRNA. Dendritic attrition (loss of intermediate and terminal dendritic branches) occurred in motor neurons expressing mutant, but not wild-type, FUS or TDP-43. This attrition was delayed by ectopic over-expression of Brg1 and was reproduced by inhibiting Brg1 activity either through genetic manipulation or treatment with the chemical inhibitor, (E)-1-(2-Hydroxyphenyl)-3-((1R, 4R)-5-(pyridin-2-yl)-2, 5-diazabicyclo[2.2.1]heptan-2-yl)prop-2-en-1-one, demonstrating the importance of Brg1 to maintenance of dendritic architecture. Loss of nBAF subunits was also documented in spinal motor neurons in autopsy tissue from familial amyotrophic sclerosis (chromosome 9 open reading frame 72 with G4C2 nucleotide expansion) and from sporadic cases with no identified mutation, pointing to dysfunction of nBAF chromatin remodelling in multiple forms of ALS.

Fast Decoupled State Estimation for Distribution Networks Considering Branch Ampere Measurements

Fast decoupled state estimation (FDSE) is proposed for distribution networks, with fast convergence and high efficiency. Conventionally, branch current magnitude measurements cannot be incorporated into FDSE models; however, in this paper, branch ampere measurements are reformulated as active and reactive branch loss measurements and directly formulated in the proposed FDSE model. Using the complex per unit normalization technique and special chosen state variables, the performance of this FDSE can be guaranteed when it is applied to distribution networks. Numerical tests on seven different distribution networks show that this method outperforms Newton type solutions and is a promising method for practical application.

Wind effects and regeneration in broadleaf and pine stands after hurricane Felix (2007) in Northern Nicaragua

Large-scale wind disturbances shape forest structure and composition and leave long lasting legacies. Adequate understanding of the role of disturbances in tropical stand dynamics is necessary to guide management efforts. In this study, we used field data to characterize the effects of a major hurricane in broadleaf and pine stands in Northern Nicaragua. First, we described tree and stand attributes associated with observed structural effects: branch loss, snapping and uprooting. Secondly, to assess the potential influence of hurricane Felix on stand composition, we characterized two key life-history traits: regeneration through resprouting and shade tolerance. Findings indicated that tree attributes such as diameter at breast height (dbh) and height to diameter ratio (hdr), were strongly associated with the type and magnitude of wind effects. All trees >70cmdbh exhibited visible effects and trees taller than 14m were more likely to be uprooted (7.3% vs. 0.8% of total). Results confirmed that Felix caused significant structural effects in broadleaf stands and mild effects in pine stands. Abundant post-hurricane resprouting was observed in both shade-tolerant and shade-intolerant species but was absent in pines. Among canopy trees we found eleven shade-intolerant species that exhibited abundant resprouting. These species could become dominant in the next decade. Our findings illustrate the role of wind disturbances on tropical stand dynamics at different spatial and temporal scales.

Genetic Control of Floral Architecture: Insights into Improving Crop Yield

Selection of plants with traits that are beneficial for cultivation and consumption has been a common practice for thousands of years; however, combination of these traits can be detrimental too, for instance by leading to undesirable branching and yield loss in tomato. The findings from Soyk etal. in this issue of Cell help understand how to bypass such negative effects and improve crop productivity.

N-glycan branching inhibits pro-inflammatory B cell activity by controlling TLR4 and BCR signaling.

Abstract N-glycosylation is a critical regulator of T cell function. The branching and number of N-glycans on cell surface glycoproteins drive binding to galectins, forming a galectin-glycoprotein lattice that controls T cell growth, differentiation and development by regulating receptor clustering, distribution and endocytosis. N-glycan branching is ~1.5–2 fold higher in B cells compared to T cells, yet effects on B cell function are unknown. Here we report that branching regulates pro-inflammatory signaling via Toll Like Receptor – 4 (TLR4) and the B cell receptor (BCR). Mechanisms controlling pro-inflammatory (cell surface) versus anti-inflammatory (endosomal) TLR4 signaling in B cells is poorly understood. Loss of branching in B cells de-couples LPS induced proliferative from pro-inflammatory responses by inhibiting TLR4 endocytosis. Similar de-coupling is observed with BCR signaling, where loss of branching inhibits BCR driven proliferation and Lyn/Syk/PLCγ2/Ca2+ signaling via reduced CD19 surface expression while concurrently driving pro-inflammatory effector functions and PI3K/Akt/mTOR activation. Together, these data reveal N-glycan branching as a critical negative regulator of TLR4 and BCR triggered pro-inflammatory B cell responses.

A Method of Experimental Determination of Parameters of Equivalent Circuits of Induction Motors

A method is presented for determining parameters of an equivalent circuit of an induction motor with a squirrel-cage rotor according to data from digital recording of instantaneous values of currents and stator voltage and slip, obtained from usual operational modes of start-up and work under load. Parameters of the stator, magnetization branch, and core loss contour are determined by data of measurements from two or more modes of load conditions with various slips, and the dependence of current displacement coefficients for active and inductive rotor resistances on the slip, from startup mode. Parameters of an equivalent circuit are derived from the iterative-method solution of equations containing the design and measured mode parameters. Examples confirming the efficacy of the developed method are presented.

Ab initio study of laser cooling of AlF+ and AlCl+ molecular ions

A theoretical investigation on the suitability of laser cooling AlF+ and AlCl+ molecular ions is performed by employing ab initio calculations. Four low-lying electronic states are determined using the multi-reference configuration interaction method plus Davidson correction. The calculated spectroscopic constants are in good agreement with the available theoretical and experimental data. The Franck–Condon factors (FCFs) and radiative lifetimes are verified by calculating the potential energy curves (PECs) and transition dipole moments for the C 2Π (v′) → X 2Σ+ (v), C 2Π (v′) → A 2Π (v) and C 2Π (v′) → B 2Σ+ (v) transitions. Our calculation indicates that the C 2Π (v′) → X 2Σ+ (v) transition is provided with sufficiently diagonally distributed FCFs and the radiative lifetimes for the C 2Π (v′) vibrational state are short enough for rapid laser cooling for both AlF+ and AlCl+ molecular ions. However, our calculation also indicates that the AlF+ radical is not suitable for laser cooling due to the predissociation of the C 2Π state. The calculation and analysis of the electronic states demonstrate the possibility of AlCl+ for laser cooling, and give more insight into the behavior of these four low-lying electronic states for further experimental and theoretical study. Its laser-cooling scheme requires one main pumping laser (λ00 = 268 nm) and three repumping lasers (λ10 = 272 nm, λ21 = 273 nm and λ31 = 278 nm). Moreover, the low mass, short radiative lifetime and small vibrational branching loss ratios to the intervening states make the AlCl+ radical suitable for laser cooling in theory.