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PubMed1982

Detection of Raji binding activity in hyperimmune allogeneic tumor bearing sera associated with anti-BSA activity.

Brown Norway (BN) rats were implanted twice with allogeneic (Lewis strain) Moloney sarcoma tumors (LM-2) and serum samples were assessed for Raji binding activity during primary and secondary tumor growth and rejection. Maximum Raji binding was observed 25 days after a primary tumor implant; thereafter, the binding activity decreased. Accelerated tumor rejection was observed after a second tumor implant and was associated with a 3-fold increase in serum Raji binding activity which remained elevated up to 40 days post-tumor implant. Raji binding activity in hyperimmune rats co-migrated with IgG in G-200 fractionated serum. Polyacrylamide gel electrophoresis (PAGE) revealed the presence of bovine serum albumin (BSA) on Raji cell membranes which reacted immunochemically with rabbit anti-BSA antiserum. Immunodiffusion studies revealed that sera from hyperimmune rats produced a precipitin band when reacted with Noniodet P-40 (NP-40) lysates of Raji cells and formed a line of identity with BSA.

Animals↗
PubMed2005

A murine model of dual infection with cytomegalovirus and Pneumocystis carinii: effects of virus-induced immunomodulation on disease progression.

Despite the use of antimicrobial prophylaxis, cytomegalovirus (CMV) and Pneumocystis carinii (PC) pneumonia (PCP) are both leading causes of morbidity and mortality in immunocompromised patients. It has previously been reported that CMV infection modulates host immune responses with a variety of mechanisms which include the suppression of helper T cell functions and antigen presenting cell (APC) functions, both of which are critical for PCP resolution. However, the mechanisms of these interactions and other possible immune regulatory effects are not clearly understood. In this study, we investigated the impact of murine CMV (MCMV) induced immunomodulation on the progression of PCP in a co-infection model. Initial results show that dually infected mice had evidence of more severe PC disease, which include a greater loss of body weight, an excess lung PC burden and delayed clearance of PC from lungs, compared to mice with PC infection alone. At day 7 post-infection, dually infected mice had reduced numbers of MHC-II expressing cells in the lung interstitium and lymph nodes and reduced migration of CD11c+ cells to both the tracheobronchial lymph nodes and alveolar spaces. Dual infected mice showed elevated numbers of specific CD8 responses concomitant with a decrease in activated CD4+ T cells in both the lymph nodes and in alveolar spaces when compared to mice infected with MCMV alone. These data suggest that MCMV infection inhibits the immune responses generated against PC which contribute to the delayed clearance of the organism.

Animals↗
PubMed1998

Endothelial cell integrin laminin receptor expression in multiple sclerosis lesions.

Laminin, a major glycoprotein component of vessel basement membranes, is recognized by beta1- and beta3-integrins expressed on endothelial cells. To determine how endothelial cell integrins might function in multiple sclerosis (MS) lesions, integrin laminin receptors and laminin were analyzed in central nervous system samples from MS patients and controls by immunohistochemistry. In active MS lesions, endothelial cell VLA-6 and beta1 subunits were decreased compared to controls whereas alpha(v) subunit and VLA-1 were increased. In chronic inactive lesions beta1, VLA-6 and alpha(v) were the same as controls but VLA-1 remained increased. Alpha3 subunit was constant in all samples. By immunoelectron microscopy VLA-1, VLA-6, beta1, and laminin were distributed throughout endothelial cells; alpha(v) was adjacent to and on luminal surfaces; alpha(v) and VLA-1 were on intercellular junctions. These results indicate distinct regulation and functions of these integrins in different lesion stages. In active lesions decreased endothelial cell beta1/VLA-6 could result in their detachment from laminin thereby facilitating leukocyte transvascular migration and blood-brain barrier breakdown. Alpha(v) and VLA-1 on intercellular junctions may participate in re-establishing vessel integrity after leukocyte migration. Luminal surface alpha(v) also likely binds intraluminal ligands and cells. In chronic inactive plaques persistently elevated endothelial cell VLA-1 correlates with long-standing endothelial cell and blood-brain barrier dysfunction.

Adolescent↗
PubMed2005

Electron trapping in polar-solvated zeolites.

Of current interest in our laboratory is the nature of photoinduced processes in the cavities of zeolites completely submerged in polar solvents, or polar-solvated zeolites (PSZ). The present study addresses the nature of electron trapping in PSZ with emphasis on the zeolites NaX and NaY. Free electrons were generated by two-photon, pulsed-laser excitation of either pyrene or naphthalene included in zeolite cavities. Trapped electrons were monitored by diffuse transmittance, transient absorption spectroscopy at visible wavelengths. In anhydrous alcohols, electron trapping by Na(4)(4+) ion clusters was observed in both NaX and NaY. The resulting trapped electrons decayed over the course of tens of milliseconds. No evidence for alcohol-solvated electrons was found. More varied results were observed in solvents containing water. In NaX submerged in CH(3)OH containing 5% or higher water, species having microsecond lifetimes characteristic of solvated electrons were observed. By contrast, a 2 h exposure of NaY to 95/5 CH(3)OH/H(2)O had no effect on electron trapping relative to anhydrous CH(3)OH. The difference between NaX and NaY was explained by how fast water migrates into the sodalite cage. Prolonged exposure to water at room temperature or exposure to water at elevated temperatures was necessary to place water in the sodalite cages of NaY and deactivate Na(4)(4+) as an electron trap. Additional studies in NaY revealed that solvent clusters eventually become lower energy traps than Na(4)(4+) as the water content in methanol increases. In acetonitrile-water mixtures, electron trapping by Na(4)(4+) was eliminated and no equivalent species characteristic of solvated electrons in methanol-water mixtures was observed. This result was explained by the formation of low energy solvated electrons which cannot be observed in the visible region of the spectrum. Measurements of the rate of O(2) quenching in anhydrous solvents revealed rate constants for the quenching of ion cluster trapped electrons that were 2-4 times higher than that for pyrene triplets. In NaX, the rate constant in methanol was 10(4) times smaller than that in cyclohexane, showing greater inhibition of O(2) reactivity in the medium of PSZ. The results of this study point out the conditions under which Na(4)(4+) is active as an electron trap in PSZ and that water must be present in the sodalite cage to produce solvated electrons in the supercage.

Journal Article↗
PubMed1996

Hb Montefiore (126(H9)Asp-->Tyr). High oxygen affinity and loss of cooperativity secondary to C-terminal disruption.

Hb Montefiore was found, in the heterozygous state, in a Puerto Rican female who had a slightly elevated total Hb level. Structural analysis revealed that Asp-alpha126 was replaced by Tyr. Hb Montefiore migrates close to HbF (at pH 8.6) and accounts for 20.3% of the hemolysate. Oxygen binding of red blood cells revealed a 40% decrease in the P50 (pH 7.4) and a low n value of 1.6 (normal: 2.6). Depletion of red blood cell 2,3-DPG did not change the results. Stripped Hb Montefiore at pH 7.2 showed an 8-fold reduction in P50 (0.6 versus 4.6 mm Hg) and very low cooperativity (n = 1.2 versus 2.9 for the control). Heterotopic effectors, as 2,3-diphosphoglycerate and inositol hexaphosphate had a normal effect and in addition, they increased cooperativity. The chloride ion effect and the Bohr effect were moderately reduced. A bezafibrate derivative (L345), known to bind alpha126, increases the P50 of HbA by 9-fold, but only by 1. 5-fold that of Hb Montefiore. Combining these functional studies with intrinsic fluorescence and Resonance Raman spectroscopy, we interpret the very low n value and the high oxygen affinity for Hb Montefiore as a result of both a destabilized T state that switches to R upon ligand binding and a deoxy T state that binds ligands with higher affinity than that of deoxy HbA. Hb Montefiore still binds ligands cooperatively, but the difference in ligand binding properties of the two quaternary states has been drastically reduced.

Allosteric Regulation↗
PubMed2026

Comprehensive analysis suggests CRIF1 is a potential target in breast cancer associated with prognosis and immune infiltration.

BACKGROUND: CRIF1 is a multifunctional factor that regulates cell biological processes such as the cell cycle, cell proliferation, and energy metabolism, and it is a new molecule that contributes to the poor prognosis of many malignancies. However, its involvement in breast cancer development is not fully known. MATERIALS AND METHODS: To investigate the relationship between CRIF1 expression, prognosis, and clinical characteristics using The Cancer Genome Atlas (TCGA-BRCA). The relationship between CRIF1 expression and the immunological microenvironment was investigated using CIBERSORT, ESTIMATE. Breast tissue and CRIF1 expression were validated by IHC. A tiny interfering plasmid was designed to transiently transfect breast cancer cell lines, and proliferation-related functional tests were carried out. The effect of sh CRIF1 on tumor formation was confirmed using a subcutaneous tumor experiment in naked mice. RESULTS: We discovered that CRIF1 was highly elevated in breast cancer tissues and associated with a poor prognosis. CRIF1 stimulates breast cancer cell proliferation, migration, and invasion. Knockdown decreased PI3K/AKT/mTOR signaling, which boosted autophagy activity. Immune infiltration research revealed that patients with high CRIF1 expression had higher CD8+ T cell expression but reduced macrophage M2 expression. CONCLUSION: Upregulation of CRIF1 in breast cancer cells enhances malignant behavior, which may be mediated by PI3K/AKT/mTOR signaling and is linked to cellular autophagy.

Humans↗
PubMed2005

Innate immune responses to adenoviral vector-mediated acute pancreatitis.

OBJECTIVES: The role of innate immunity in the development of acute viral pancreatitis is not well understood. The aim of the study was to characterize the role of the innate immune system, especially macrophages, natural killer (NK), and NK T (NKT) cells, in the generation of immune responses to intrapancreatic delivery of recombinant adenoviral vector. METHODS: Adenoviral vectors expressing beta-galactosidase or green fluorescent protein genes with viral capsid conjugated covalently with carbocyanine dye were directly injected into the pancreas of C57Bl/6 mice. RESULTS: Fluorescent microscopy of the pancreas showed that 30 minutes after vector administration, adenoviral particles localized to cell membranes, internalized, and localized to the nucleus by 4 hours, and transgene expression began at 24 hours. Immunohistochemical staining showed macrophages entering the pancreas shortly after vector administration, with maximal infiltration at day 4, and then disappearing as antigen-expressing cells were eliminated. Intrapancreatic macrophages appeared to deliver viral capsid proteins to the spleen. Flow cytometry showed that NK and NKT cells migrate to the pancreas and persist. Serum cytokines IL-6, IL-10, and IL-12 were all elevated. CONCLUSION: Macrophages and NK and NKT cells play a major role in the development of acute adenovirus-mediated pancreatitis.

Acute Disease↗
PubMed2026

DPM2 promotes melanoma progression and serves as a prognostic factor.

Recently, dolichol phosphate mannose synthase (DPMS) has emerged as a promising new target for treatment in various cancers. Nonetheless, DPM2, a crucial element of the DPMS family, remains unexplored in melanoma research. This study aims to explore the predictive significance and biological role of DPM2, utilizing extensive databases and functional tests conducted in vitro. We conducted an in-depth examination of the DPM2 expression feature within The Cancer Genome Atlas database. Group differences were evaluated using Student's t-test, one-way analysis of variance, and long-rank test, while survival distributions were estimated using the Kaplan-Meier method. Functional experiments were conducted in multiple melanoma cell lines to evaluate the effects of altered DPM2 expression. Our research indicated a direct correlation between the expression levels of DPM2 and the severity of melanoma. In addition, an elevated level of DPM2 expression was significantly linked to unfavorable prognoses. Suppression of DPM2 inhibits the proliferation, migration, and invasion of melanoma cells and induces their apoptosis. These findings suggest that DPM2 plays a pivotal role in melanoma progression and may serve as an independent prognostic biomarker for the disease.

DPM2↗
PubMed1994

The Bristol prostate cancer pilot screening study--a 3-year follow-up.

OBJECTIVE: To undertake a follow-up study of 472 men who were screened 3 years previously, in general practice, for prostate cancer, and to investigate the efficacy and patient acceptability of a 3-year screening interval. SUBJECTS AND METHODS: Eligible men (n = 472) were sent postal invitations to attend their Health Centre in North Bristol. Serum prostate-specific antigen (PSA) was the initial screening test. Men with PSA > 4 ng/ml (Hybritech) were referred to the Department of Urology for digital rectal examination and transrectal ultrasound +/- biopsy. RESULTS: A total of 132 (28%) men were excluded because of intercurrent illness, death and migration. Two hundred of 340 (59%) men were re-screened. Thirty-seven men had an elevated PSA and were referred as above. Seventeen men had prostatic biopsies, resulting in the diagnosis of six carcinomas; five were localized to the prostate and one was metastatic. In the latter patient, the PSA had risen from 2 to 120 ng/ml over 3 years. CONCLUSION: Serum PSA alone can be used as an acceptable repeat screening test to detect prostate cancer in general practice, but 3-year repeat screening will not always protect the individual against the interval development of metastatic disease.

Aged↗
PubMed2004

Differential regulation of urokinase-type plasminogen activator expression by fluid shear stress in human coronary artery endothelial cells.

Atherosclerotic plaques preferentially localize at arterial regions exposed to turbulent low-shear flow. Urokinase-type plasminogen activator (uPA) plays a role in vascular remodeling by facilitating smooth muscle cell migration and proliferation in addition to the proteolysis of extracellular matrix, and the expression of uPA is elevated in atherosclerotic lesions. In this study, we analyzed the effects of laminar and turbulent shear stress on uPA expression in cultured human coronary artery endothelial cells. The application of laminar shear stress (1.5 or 15 dyn/cm2) significantly decreased the amount of uPA mRNA as well as the secretion of uPA protein. In contrast, turbulent shear stress (average intensity, 1.5 dyn/cm2) markedly increased uPA gene expression and protein secretion. Laminar shear stress downregulated uPA gene expression transcriptionally and posttranscriptionally; laminar shear stress activated transcription factor GATA6, which binds to a GATA consensus element located between -692 and -687 bp in the uPA promoter, thereby inhibiting uPA gene transcription. Laminar shear stress also accelerated the degradation of uPA mRNA; the half-life of uPA mRNA decreased to about half of the static control's half-life. Although turbulent shear stress had no effect on the transcription of uPA, it significantly increased uPA mRNA stability; the half-life of uPA mRNA increased by about two times the static control's half-life. Our results suggest that endothelial uPA expression is flow sensitive and differentially regulated by laminar and turbulent shear stress in vitro. We speculate that this effect may contribute to the local nature of atherosclerosis.

Arteries↗
PubMed2006

Proteases in helminth- and allergen- induced inflammatory responses.

Proteolytic activity is a central biochemical property that endows molecules with intrinsic allergenicity. Thus, the cysteine protease of dust mite, Der p1, the aspartic protease of cockroach, Bla g 2, the serine protease of Aspergillus fumigatus and the bacterial subtilisins are all major allergenic molecules responsible for the increase in asthma and atopic conditions worldwide. These proteases induce Th2-driven inflammatory responses in the airways by disrupting the epithelial cell junctions so that these, and other molecules, gain access to, and alter the function of, underlying cells of the innate immune system (dendritic cells, mast cells, basophils and macrophages) and B and T cells. Helminth parasites secrete proteases to gain entry into their hosts, and to feed on and migrate through tissues. Their action leads to tissue damage and the activation of inflammatory responses dominated by elevated IgE, eosinophilia and Th2 cells, much like allergenic responses. In certain situations, such as in acute infections (especially with zoonotic helminths), proteases secreted by helminths may sensitise individuals to allergens. However, the anti-inflammatory responses observed in chronic helminthiases, involving IL-10 and TGFBeta, that are primarily responsible for controlling immune-mediated damage to the host that is initiated by secreted proteases, coincidentally protects against similar inflammatory damage by allergens.

Allergens↗
PubMed2000

Autocrine stimulation of VEGFR-2 activates human leukemic cell growth and migration.

Emerging data suggest that VEGF receptors are expressed by endothelial cells as well as hematopoietic stem cells. Therefore, we hypothesized that functional VEGF receptors may also be expressed in malignant counterparts of hematopoietic stem cells such as leukemias. We demonstrate that certain leukemias not only produce VEGF but also express functional VEGFR-2 in vivo and in vitro, resulting in the generation of an autocrine loop that may support leukemic cell survival and proliferation. Approximately 50% of freshly isolated leukemias expressed mRNA and protein for VEGFR-2. VEGF(165) induced phosphorylation of VEGFR-2 and increased proliferation of leukemic cells, demonstrating these receptors were functional. VEGF(165) also induced the expression of MMP-9 by leukemic cells and promoted their migration through reconstituted basement membrane. The neutralizing mAb IMC-1C11, specific to human VEGFR-2, inhibited leukemic cell survival in vitro and blocked VEGF(165)-mediated proliferation of leukemic cells and VEGF-induced leukemic cell migration. Xenotransplantation of primary leukemias and leukemic cell lines into immunocompromised nonobese diabetic mice resulted in significant elevation of human, but not murine, VEGF in plasma and death of inoculated mice within 3 weeks. Injection of IMC-1C11 inhibited proliferation of xenotransplanted human leukemias and significantly increased the survival of inoculated mice. Interruption of signaling by VEGFRs, particularly VEGFR-2, may provide a novel strategy for inhibiting leukemic cell proliferation.

Animals↗
PubMed2004

Insulin-like growth factor-I receptor signalling and acquired resistance to gefitinib (ZD1839; Iressa) in human breast and prostate cancer cells.

De novo and acquired resistance to the anti-tumour drug gefitinib (ZD1839; Iressa), a specific epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) has been reported. We have determined whether signalling through the IGF-I receptor (IGF-1R) pathway plays a role in the gefitinib-acquired resistance phenotype. Continuous exposure of EGFR-positive MCF-7-derived tamoxifen resistant breast cancer cells (TAM-R) to 1 microM gefitinib resulted in a sustained growth inhibition (90%) for 4 months before the surviving cells resumed proliferation. A stable gefitinib-resistant subline (TAM/TKI-R) was established after a further 2 months and this showed no detectable basal phosphorylated EGFR activity. Compared with the parental TAM-R cells, the TAM/ TKI-R cells demonstrated (a) elevated levels of activated IGF-1R, AKT and protein kinase C (PKC)delta, (b) an increased sensitivity to growth inhibition by the IGF-1R TKI AG1024 and (c) an increased migratory capacity that was reduced by AG1024 treatment. Similarly, the EGFR-positive androgen-independent human prostate cancer cell line DU145 was also continuously challenged with 1 microM gefitinib and, although substantial growth inhibition (60%) was seen initially, a gefitinib-resistant variant (DU145/TKI-R) developed after 3 months. Like their breast cancer counterparts, the DU145/TKI-R cells showed increases in the levels of components of the IGF-1R signalling pathway and an elevated sensitivity to growth inhibition by AG1024 compared with the parent DU145 cell line. Additionally, DU145/TKI-R cell migration was also decreased by this inhibitor. We have therefore concluded that in breast and prostate cancer cells acquired resistance to gefitinib is associated with increased signalling via the IGF-1R pathway, which also plays a role in the invasive capacity of the gefitinib-resistant phenotype.

Antineoplastic Agents↗
PubMed2026

Pathomics-based machine learning models for predicting METTL5 expression and prognosis in lung adenocarcinoma.

BACKGROUND: METTL5, an N6-methyladenosine (m6A) RNA methyltransferase, has been implicated in tumor progression, but its prognostic value and non-invasive prediction in lung adenocarcinoma (LUAD) remain unclear. This study aimed to develop a pathomics-based machine learning model to predict METTL5 expression from histopathological images and evaluate its prognostic significance in LUAD. METHODS: A total of 327 LUAD patients from The Cancer Genome Atlas (TCGA) with matched hematoxylin and eosin (H&E) slides, transcriptomic, and clinical data were included and randomly divided into training and validation sets (7:3). Quantitative histopathological features were extracted using PyRadiomics. Feature selection was performed via maximum relevance minimum redundancy (mRMR) and recursive feature elimination (RFE), followed by construction of a Gradient Boosting Machine (GBM) model. A pathomics score (PS) was generated to assess prognostic relevance. Survival analyses, gene set variation analysis (GSVA), tumor mutational burden (TMB), immune infiltration analysis, and in vitro functional assays were conducted. RESULTS: METTL5 overexpression was independently associated with poor overall survival [hazard ratio (HR) =1.637, P=0.007]. The model achieved good predictive performance [area under the curve (AUC) =0.847 in the training set and 0.752 in the validation set]. High PS was significantly associated with worse survival and remained an independent prognostic factor (HR =1.563, P=0.03). Elevated PS correlated with altered metabolic pathways, increased TMB, and immune microenvironment changes. METTL5 knockdown reduced proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in A549 cells. CONCLUSIONS: The pathomics-based model accurately predicts METTL5 expression and provides prognostic stratification in LUAD, supporting its potential as a practical imaging-derived biomarker.

Methyltransferase-like 5↗
PubMed2003

Activation of cutaneous protein kinase C alpha induces keratinocyte apoptosis and intraepidermal inflammation by independent signaling pathways.

Skin keratinocytes are major mediators of host immune responses. The skin is also a target for immunologically based inflammation in many pathological states. Activation of protein kinase C (PKC) can induce cutaneous inflammation, but the precise role of each of six cutaneous PKC isoforms (alpha, delta, epsilon, eta, zeta, mu) that regulate normal skin homeostasis or contribute to skin pathology has not been clarified. We generated transgenic mice that overexpress PKCalpha in the basal layer of the epidermis and the outer root sheath of hair follicles under the regulation of the bovine keratin 5 promoter. K5-PKCalpha transgenic mice exhibit severe intraepidermal neutrophilic inflammation and disruption of the epidermis and upper hair follicles when treated topically with 12-O-tetradecanoylphorbol-13-acetate (TPA). Both TPA and UVB cause apoptosis in transgenic skin, but only TPA evokes intraepidermal inflammation. TPA also induces apoptosis in cultured transgenic keratinocytes, and this is prevented by an AP-1 dominant-negative construct. However, inhibiting AP-1 in vivo does not abrogate intraepidermal inflammation. Transcripts for specific cytokines and chemokines are elevated in TPA-treated cultured transgenic keratinocytes, and conditioned culture medium from these cells promotes neutrophil migration in vitro. Chemokine expression and neutrophil migration are not diminished by inhibiting AP-1. Thus, PKCalpha activation induces keratinocyte apoptosis via an AP-1-dependent pathway and mediates chemokine induction and intraepidermal inflammation independently. This model system will be useful to define specific chemokines regulated by PKCalpha that promote intraepidermal neutrophilic inflammation, a condition that characterizes several human cutaneous diseases such as pustular psoriasis and acute generalized exanthematous pustulosis.

Animals↗
PubMed1985

Immunological responses to monoassociated Bifidobacterium longum and their relation to prevention of bacterial invasion.

After monoassociation of Bifidobacterium longum with germ-free BALB/c mice (nu/+, heterozygous to nu gene), B. longum was recovered (10(2)-10(4) viable units per organ) from the mesenteric lymph nodes, liver and kidneys for 2 weeks post intragastric inoculation, but not after 4 weeks and later. Cessation of bacterial translocation was not observed in monoassociated nude (nu/nu) mice. Anti-B. longum IgA antibody was detected by ELISA using B. longum cell wall antigen in bile from Week 1 and in ileac wall extract from Week 8 post-association in both nu/+ and nu/nu mice. Total IgA levels in bile, ileac wall extract and caecal contents were also elevated in both mice after monoassociation. Cell-mediated immunity measured by the footpad test and macrophage migration inhibition test using B. longum protein fraction was detected in nu/+ mice in Week 4 and later, but not in nu/nu mice. Nu/nu mice reconstituted 4 weeks prior to monoassociation with lymphocytes from flora bearing nu/+ mice developed delayed footpad reactivity and bacterial translocation stopped after 4 weeks. Cell-mediated immunity rather than IgA antibody correlated well with the cessation of translocation.

Actinomycetales Infections↗
PubMedDate not supplied

[Clinical, structural and functional studies of HbG Philadelphia detected in a Moroccan newborn].

Hb G Philadelphia (alpha68 Asn leads to Lys) is widely distributed in black people but is uncommon in North-Africa. Only one case has been previously described in an Arab immigrant. The latter and our propositus originated from North-East morocco. Hb G alpha Philadelphia is stable. The abnormal hemoglobin represented 28% of total hemoglobin in the hemolysate of the propositus, a 7 month old child. At birth, 4 fractions were detected on electrophoresis: Hb A, Hb F, Hb G Philadelphia, which migrated like Hb S, and a mutant alpha2Ggamma2. The oxygen affinity of Hb G Philadelphia was slightly elevated. Cooperativity and Bohr effect were normal. The abnormal hemoglobin was also detected in the father of the propositus in the heterozygote state: its clinical and hematological data were normal. No evidence of thalassemia trait was found in the family. The percentage of abnormal hemoglobin obtained in the propositus and his father is in accordance with the presence of two loci for the alpha chain on the homologous chromosome.

Electrophoresis, Cellulose Acetate↗
PubMed1983

Splenic accumulation of stromal progenitor cells in response to bacterial lipopolysaccharides.

An analysis was made of fibroblastoid colony-forming units (CFUF) in spleens of mice treated with bacterial lipopolysaccharide (LPS). Increased CFUF numbers were observed on days 2, 3 and 4 after treatment with 10, 30 and 100 micrograms of LPS. The splenic CFUF accumulation occurred at the same time as spleen hemopoiesis increased, however, the CFUF returned to normal and subnormal numbers on day 5, while the spleen cellularity was still elevated on day 21 after LPS treatment. The mechanism of splenic CFUF accumulation appeared to involve CFUF migration via the blood from other sites of hemopoiesis rather than increased CFUF plating efficiency in vitro or enhanced CFUF proliferation. The results suggest a relationship between the LPS-induced fibroblastoid progenitor cell increase and a requirement for splenic microenvironments to support LPS-induced hemopoiesis.

Animals↗