Anti-Human CD68 FITC 25 tests
- Known as:
- Antibody toHuman CD68 fluorecein 25 tests
- Catalog number:
- 11-0689-71
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD68 FITC 25 tests
Related genes to: Anti-Human CD68 FITC 25 tests
- Gene:
- CD68 NIH gene
- Name:
- CD68 molecule
- Previous symbol:
- -
- Synonyms:
- SCARD1, macrosialin, GP110, DKFZp686M18236, LAMP4
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-11
- Date modifiied:
- 2016-10-05
Related products to: Anti-Human CD68 FITC 25 tests
Related articles to: Anti-Human CD68 FITC 25 tests
- Fine particulate matter (PM) from wildfire smoke is a major air pollutant in dairy-producing regions of the United States. However, knowledge of direct causative effects of wildfire-derived pollutants on calf health is lacking because of a reliance on observational studies from natural wildfire smoke exposures. Calves represent an important population in a dairy herd and improving their health is especially critical during the vulnerable pre-weaning window, as respiratory diseases during this period can affect performance later in life. The objective of this study was to evaluate the acute effects of controlled short-term wood smoke exposure on respiratory function, immune responses, and clinical health measures in pre-weaned dairy calves using novel smoke enclosures we developed. Intact male Holstein calves (n = 24; 37 ± 2 d of age [mean ± SD]) were randomly assigned to control (CON; n = 12) or wood smoke (WS; n = 12) treatments. Calves were kept for 6 h in the experimental smoke enclosures where they were either exposed to wood combustion smoke (WS; smoke inlet open) or not exposed (CON; smoke inlet closed). Environmental conditions within the enclosures including PM, carbon dioxide, carbon monoxide, ambient air temperature, and relative humidity were recorded during the experiment trials. Fine particulate matter concentrations (mean ± SD) were 9.94 ± 4.50 µg/m for CON and 238.44 ± 62.97 µg/m for WS. All other environmental conditions were similar between CON and WS groups. Immediately after treatment, pulmonary function and health scores were evaluated, and blood samples were collected. Calves were humanely euthanized, and bronchoalveolar lavage was performed. Wood smoke exposure altered pulmonary function, as WS calves had a lower respiratory rate (17.50 vs. 21.52 breaths/min) and higher tidal volume (0.90 vs. 0.75 L) compared with CON calves, while minute ventilation did not differ between groups. Bronchoalveolar lavage fluid (BALF) immunophenotyping revealed increased proportions of granulocytes, CD68-positive macrophages, and natural killer cells in WS compared with CON calves, suggesting activation of pulmonary innate immune responses. Circulating neutrophil counts were reduced in WS calves, whereas total white blood cell counts, and other hematological variables did not differ between groups. Plasma concentrations of acute phase proteins, including serum amyloid A, haptoglobin, and albumin, did not differ statistically between treatments. Phagocytosing granulocytes (%) in whole blood was greater in the WS group compared with CON (97.03 vs. 93.89%). Oxidative stress, assessed by concentrations of thiobarbituric acid reactive substances (TBARS) in BALF and plasma, was not affected by treatment. These findings demonstrate that short-term wood smoke exposure at concentrations reflective of natural wildfire conditions induces an acute pulmonary inflammatory response and alters respiratory physiology in pre-weaned dairy calves. A systemic inflammatory response and oxidative stress were not detected, which could be attributed to the timing of sample collection immediately after exposure. This novel controlled exposure model provides a foundation for future studies investigating the progression of air pollution-induced health effects in dairy cattle and other large animals. - Source: PubMed
Publication date: 2026/09/28
Kamyabi MPace AKok J RSmith A M SSarantopulos DChristensen LMarquez-Acevedo A SPereira L De MouraLarson MAhmadzadeh AKonetchy DRezamand PSkibiel A L - Imaging tumor-associated macrophages (TAMs) may reflect prognosis, therapeutic response and radiotheranostic potential. We report the discovery and development of a synthetic human Fab as the first immunoPET tracer targeting human CD68 (huCD68), the gold standard histopathological biomarker of pan-macrophages. - Source: PubMed
Publication date: 2026/09/28
Roohani BornaVaughn Embs AylaKumar RobinLee SupumKatz Samantha RLa Prairie ChloeNash DajahDangarwala MannKluger Harriet MKlein Daryl EZhang PingLarimer Benjamin MNelson BryceMarquez-Nostra Bernadette - Erdheim-Chester disease (ECD) is a rare clonal non-Langerhans cell histiocytosis characterized by the infiltration of foamy, CD68-positive/CD1a-negative histiocytes into multiple organ systems. Activating MAPK/ERK pathway mutations, most commonly BRAF V600E, represent common targets for ECD therapies. Although vemurafenib has been approved for BRAF V600E-mutant ECD, data regarding dual BRAF and MEK inhibition remain scarce. - Source: PubMed
Publication date: 2026/09/27
Kurihara YuyaHonda AkiraMatsumoto ShuheiYamaguchi TeruakiTakano HirofumiYuasa MitsuhiroTsujimoto TakayukiHinata MunetoshiTanaka MarikoKurokawa Mineo - Pyroptosis is a form of programmed cell inflammatory death. Macrophage pyroptosis has been implicated in the development of various immune diseases, yet its role in lupus nephritis (LN) remains poorly understood. This study examined macrophage pyroptosis in LN and its clinical correlations. This was a cross-sectional observational study. Renal tissues and clinical data were collected from 49 LN patients and 20 minimal change disease (MCD) patients. Macrophage pyroptosis was detected using immunofluorescence (cluster of differentiation 68 [CD68]/gasdermin D [GSDMD] co-staining), and serum inflammatory markers were analyzed via ELISA. Hierarchical regression analyses were performed to identify clinical parameters significantly associated with macrophage pyroptosis. A comparative analysis between the LN cohort (41 females, 8 males; mean age 32.6 ± 12.1 years) and MCD controls revealed significantly elevated levels of blood urea nitrogen, C-reactive protein, uric acid, and anti-double-stranded DNA antibodies (P < .05), accompanied by decreased complement component 3 (C3), complement component 4 (C4), estimated glomerular filtration rate (eGFR), and total cholesterol. Immunofluorescence demonstrated a marked increase in CD68/Cleaved GSDMD double-positive cells within both glomerular and interstitial compartments of LN patients (P < .001). LN patients with chronic kidney disease (CKD) stages 5 exhibited significantly interstitial macrophage pyroptosis (P < .05). This study is the first to report the presence of macrophage pyroptosis in LN renal tissues, with the extent of interstitial pyroptosis showing a significant cross-sectional association with CKD stage (by eGFR). This observation suggests a potential link between macrophage pyroptosis and disease severity in LN, meriting further investigation. - Source: PubMed
Ye KunYang QianJiang TingtingChen RunhangHuang YunfengHuang YiyunLan JiaoMeng Lingzhang - Obesity is a major public health problem and a risk factor for numerous diseases. Furthermore, the high prevalence of 25-hydroxyvitamin D (25(OH)D) deficiency in obese individuals promotes a state of persistent inflammation and contributes to the development of hard-to-heal skin wounds. Although calcifediol is effective in correcting this deficiency, its effect on cutaneous wound healing in obesity has not been fully established. Thus, the objective of this work has been to evaluate the impact of calcifediol treatment on wound healing in an animal model of obesity with vitamin D deficiency. Wistar rats fed a high-fat, vitamin D-deficient diet were subjected to dorsal skin wounds. One group received calcifediol treatment for 14 days. Serum 25(OH)D levels, wound closure rate, histological parameters, and molecular markers related to inflammation were analyzed. Calcifediol significantly increased serum 25(OH)D levels and accelerated wound closure compared to untreated animals. It also improved re-epithelialization, reduced the depth and extent of the lesions, and promoted collagen deposition. Furthermore, it increased the expression of anti-inflammatory markers (IL-10 and CD163) and decreased the infiltration of CD68+ macrophages, indicating a more efficient resolution of the inflammatory response. Calcifediol supplementation improves cutaneous wound healing in obesity with 25(OH)D deficiency by accelerating wound closure, promoting extracellular matrix remodeling, and modulating the inflammatory response, supporting its use as a complementary strategy to enhance tissue repair in conditions of obesity and vitamin D deficiency. - Source: PubMed
Publication date: 2026/09/17
Torrecillas-Baena BárbaraPulido-Escribano VictoriaCamacho-Cardenosa MartaCarmona-Luque María DoloresCastillo-Peinado Laura De Los SantosPriego-Capote FelicianoQuesada-Gómez José ManuelDorado GabrielGálvez-Moreno María ÁngelesCasado-Díaz Antonio