CD43 (human) _ Clone DFT_1
- Known as:
- CD43 (H. sapiens) _ Clone DFT_1
- Catalog number:
- T-1337.0200
- Product Quantity:
- 200ìg
- Category:
- -
- Supplier:
- New Immunology
- Gene target:
- CD43 (human) _ Clone DFT_1
Related genes to: CD43 (human) _ Clone DFT_1
- Gene:
- SPN NIH gene
- Name:
- sialophorin
- Previous symbol:
- -
- Synonyms:
- LSN, CD43, GPL115
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-31
- Date modifiied:
- 2016-07-19
Related products to: CD43 (human) _ Clone DFT_1
Related articles to: CD43 (human) _ Clone DFT_1
- This systematic literature review (SLR) evaluated the incidence and bacterial etiology of acute otitis media (AOM) in children. - Source: PubMed
Publication date: 2026/01/29
Bhuiyan Mejbah UddinHernandez-Suarez GustavoPilishvili TamaraMayer BenAbbing-Karahagopian Victoria - : Compression neuropathies such as Anterior Tarsal Tunnel Syndrome are usually associated with focal thickening at the compression site. This study aimed to determine the frequency and location of thickenings of dorsal foot nerves in asymptomatic, healthy volunteers. We hypothesized that focal nerve thickening of dorsal foot nerves is a frequent finding in asymptomatic individuals and occurs at anatomically plausible locations, potentially limiting the specificity of ultrasound in the diagnosis of anterior tarsal tunnel syndrome. : In this prospective study, the nerves at the dorsal foot were examined with ultrasound in 60 volunteers without clinical signs of neuropathy. Cross-sectional area (CSA) changes along the nerve course were assessed, their anatomical location recorded, and demographic data collected. : Focal deep peroneal nerve (DPN) thickening was observed in 45% of participants, with a median CSA of 2.14 mm (range: 0.84-5.16) and median length of 3.98 mm (range: 1.46-9.95). The most frequent site was the first tarsometatarsal joint (41%). Thickening occurred across all age groups. Superficial peroneal nerve (SPN) thickening was found in 13.3% of participants, primarily affecting the intermediate branch, with a median CSA of 1.82 mm and length of 3.02 mm. No thickening was observed in the sural nerve (SN). A strong correlation was found between CSA and length of DPN thickening (r = 0.67, < 0.001). : Asymptomatic, focal thickening of dorsal foot nerves, particularly the DPN, is a frequent sonographic finding in healthy volunteers. These findings highlight the potential for false-positive ultrasound results and the necessity of correlating imaging findings with clinical examination when evaluating for anterior tarsal tunnel syndrome and similar neuropathies. - Source: PubMed
Publication date: 2026/01/17
Vetchy VeronikaRossmann TobiasPruidze PaataGrisold WolfgangWeninger Wolfgang JMeng Stefan - Anticipatory EEG signals are characterized by the occurrence of negative slow cortical potentials. This negativity is posed to be enhanced when expecting highly emotional stimuli; however, the specific role attention plays in its generation is unclear, as emotional content is more salient and arousing, and thus recruits higher attentional resources. Here, affective anticipation signals were recorded in 35 participants with EEG, and their brain sources elucidated using multiple sparse priors algorithm. Using a cued-paradigm, the category of a sound being negatively valenced or neutral could be predicted with a 68.2% accuracy. To shift attentional resources away from the emotional content, participants were instructed to listen and respond to a burst of white noise that occurred on 9.1% of trials. Results showed slower reaction times following the aversive cue, yet no difference in EEG amplitude between aversive and neutral anticipation. Response times positively correlated with EEG amplitude-participants with stronger negativity were faster to respond. EEG source reconstruction demonstrated no differences between conditions, and showed activation of areas within the salience network including insula, somatosensory cortex, and thalamus. The current results suggest that anticipatory EEG negativity is an index of attentional resource-allocation during the anticipation period and does not reflect the emotional content of upcoming stimuli. - Source: PubMed
Benzaquén EsterGriffiths Timothy DKumar Sukhbinder - Striatal spiny-projection neurons (SPNs) integrate glutamatergic inputs from the motor cortex and thalamus with neuromodulatory signals to regulate motor output. In vivo Ca imaging has demonstrated that spatially overlapping ensembles of direct and indirect pathway SPNs (dSPNs, iSPNs) are co-active during spontaneous movement. This co-activity is statistically greater among nearby neurons, correlates with behavioral state, and changes in an SPN-type-specific manner under pathological conditions. How this co-activity arises and whether it is important for movement are not well understood. Co-activity likely arises from shared excitatory inputs, the strength of which are scaled by well-characterized mechanisms of synaptic plasticity. Here, we show that the Group I metabotropic glutamate receptor 5 (mGluR5), which regulates the strength of corticostriatal synapses, is a key mediator of behaviorally relevant SPN co-activity. Pharmacological modulation of mGluR5 signaling bidirectionally altered movement and co-activity, but not the absolute level of activity in dSPNs. Targeted deletion of mGluR5 in dSPNs recapitulated the effects on spatiotemporal neural dynamics and movement, consistent with a striatum-specific effect of mGluR5 modulation. Targeted deletion of mGluR5 also produced changes in the synaptic properties of dSPNs. Separate from any effects on overall activity, our results show that excitatory synaptic modulation influences motor function by coordinating the spatial co-activation of dSPNs in vivo. - Source: PubMed
Publication date: 2026/01/27
Marshall John JXu JianYeh Nai-HsingYun SeongsikNomura ToshihroArmstrong John NParker JonesContractor Anis - (Spn) is typically an asymptomatic colonizer of the nasopharynx, but it also causes pneumonia and disseminated disease affecting various host anatomical sites. To delineate host-pathogen transcriptional interactions during pneumococcal (EF3030) and influenza A (pH1N1) coinfection, we used primary differentiated human bronchial epithelial cells (HBEC-three human donors) in a transwell monolayer model at an air-liquid interface, and a mouse pneumonia model, profiled with multispecies deep RNA-seq and NanoString nCounter as complementary models. Distinct pneumococcal gene expression profiles were observed in the presence and absence of influenza in HBEC infection. Influenza coinfection enabled significantly greater pneumococcal growth and triggered the differential expression of bacterial genes corresponding to multiple metabolic pathways. Notably, a fundamentally altered bacterial metabolic state and a greater nutrient availability were observed when coinfecting with influenza. Downregulation/deletion of sialic acid utilization genes promoted EF3030 proliferation during mono/coinfection with pH1N1 on HBEC. Surprisingly, HBEC transcriptomes were only modestly perturbed by infection with EF3030 alone relative to changes resulting from influenza A infection or coinfection. Influenza-infected HBEC transcriptomes showed significant loss of ciliary function, with changes in host defense, microtubules, and extracellular matrix (ECM). Some of these findings were confirmed in the murine lung infection model. Influenza-mediated changes in the host epithelium transcriptome also contribute to bacterial invasiveness. This included downregulation of genes involved in expressing cilia and increased ECM degradation. Ultimately, we identified novel genes and pathways involved in the dynamics of epithelium-influenza-pneumococcus coinfection, such as EF3030 metabolic regulons (NanR, LacR, etc.) and epithelial protein families (keratins and matrix metalloproteases). We conclude that influenza infection promotes a pneumococcal metabolic shift, allowing for transition from colonization to disseminated disease and an exacerbated breakdown in the epithelium, potentially permitting enhanced EF3030 infection and dissemination.IMPORTANCETransition from pneumococcal colonization to invasive disease is not well understood. Studies have shown that such a transition can occur as a result of influenza A virus (IAV) coinfection. We investigated the pneumococcal (serotype 19F, strain EF3030, and isogenic mutants) and airway epithelial transcriptomes with and without IAV (A/California/07 2009 pH1N1) infection. Pneumococcus and influenza coinfection leads to enhanced bacterial transcriptional programs related to growth, nutrient availability, and energy biosynthesis, suggesting conversion to an invasive phenotype. Influenza-induced secondary EF3030 infection influences human bronchial epithelial cell (HBEC) microtubules and extracellular matrix. Notably, sialic acid (NanR) utilization is a central regulon in EF3030 mono/coinfection with pH1N1 on HBEC. Downregulation of sialic acid utilization during influenza coinfection improved Spn pathogenicity but did not alter disease suggesting other metabolic cues are also important. This study uncovers critical metabolic features of the EF3030-pH1N1 interface to inform how Spn proliferates during IAV coinfection. - Source: PubMed
Publication date: 2026/01/26
D'Mello AdonisEarnhardt Erin YLane Jessica RTipper Jennifer LMartínez ErielProkopczuk Federico IIm HansolRoussey Holly NHarrod Kevin SOrihuela Carlos JTettelin Hervé