scholarly journals Color Detection of RGB Images Using Python and OpenCv

2021 ◽  
pp. 109-112
Author(s):  
P. Raguraman ◽  
A. Meghana ◽  
Y. Navya ◽  
Sk. Karishma ◽  
S. Iswarya
Keyword(s):  
Color Patterns ◽  
Color Detection ◽  
Normal Humans ◽  
Normal Human ◽  
Rgb Images

The main objective of this application is the methodology for identifying the shades of colors with an exact prediction with their names. A study says, a normal human can able to clearly identify nearly 1 million shades of colors. But in the case of human having “enchroma”, could be able to see only 1% (i.e.10,000 colors) from the normal humans. While painting pictures, a painter needs to identify the color patterns exactly or else the reality of image is not clear.

scholarly journals Color Detection of RGB Images Using Python and OPENCV

2021 ◽  
Vol 9 (8) ◽  
pp. 1957-1959
Author(s):  
Sai Praneeth Chapala
Keyword(s):  
Color Patterns ◽  
Healthy Human ◽  
Color Detection ◽  
Rgb Images ◽  
Different Color ◽  
Realistic Images

Abstract: This application intent is to accomplish the explicit strategy to recognize the miscellaneous shades of colors precisely. According to study of sciences, a normal healthy human can identify and differentiate nearly one million shades of color. But it is impossible for an individual having “enchroma”. It is indispensable for a painter to recognize different color patterns precisely to make realistic images Keywords: Enchroma, RGB value, OpenCv, pandas

Incorporation of the Non-Human Sialic Acid Neu5Gc into Human Leukemic Cells and Targeting by Natural Human Anti-Neu5Gc Antibodies.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3866-3866
Author(s):  
Dzung H. Nguyen ◽  
Pam Tangvoranuntakul ◽  
Ajit Varki
Keyword(s):  
Sialic Acid ◽  
Blood Cells ◽  
Leukemic Cells ◽  
Therapeutic Window ◽  
Last Common Ancestor ◽  
Activated T Cells ◽  
Human Sera ◽  
Normal Humans ◽  
Normal Human

Abstract Humans are incapable of synthesizing the common mammalian cell surface sialic acid N-glycolylneuraminic acid (Neu5Gc), due to an irreversible genetic mutation that occurred after our last common ancestor with great apes. Despite this, we found trace levels of Neu5Gc in certain normal human tissues, and higher levels in fetal and malignant tissues, apparently due to incorporation from dietary sources. Circulating anti-Neu5Gc antibodies also occur in most normal humans, with marked individual variations in levels. We now show that while normal human blood cells metabolically incorporate very little free Neu5Gc from the culture medium, human leukemic cell lines do so efficiently, displaying it on their cell surfaces, as detected by flow cytometry using a monospecific polyclonal chicken antibody, and confirmed chemically by HPLC. Specific deposition of IgG from Neu5Gc-reactive human sera onto Neu5Gc-expressing leukemic cells could be demonstrated. This was associated with lytic cell killing, apoptosis, and antibody-dependent cell-mediated cytotoxicity. Human sera with low levels of anti-Neu5Gc antibodies did not mediate such effects. These data show for the first time that the “natural” anti-Neu5Gc antibodies found in normal humans can be functionally active. The selective incorporation of Neu5Gc into leukemic cells could provide an approach for targeting leukemic cells in vivo, via naturally occurring Neu5Gc-specific antibodies. However, in contrast to unstimulated blood cells, activated human T-lymphocytes also incorporated some Neu5Gc, albeit to a lesser degree than leukemic cells, allowing IgG binding and complement deposition. Thus, exposure of rapidly dividing activated T cells to Neu5Gc could potentially affect ongoing immune responses. Since incorporation into leukemic cells was most efficient, it may still be possible to define a therapeutic window to selectively target malignant cells.

Identification of Unique Biomarkers in Sepsis Associated Coagulopathy

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1237-1237
Author(s):  
Gautam Sharma ◽  
Rahul Bijlani ◽  
Evangelos Litinas ◽  
Debra Hoppensteadt ◽  
Josephine Cunanan ◽  
...  
Keyword(s):  
Conflicts Of Interest ◽  
Protein Chip ◽  
Plasma Samples ◽  
Molecular Weight Range ◽  
Array Technology ◽  
Surface Enhanced ◽  
Apparent Reduction ◽  
Normal Humans ◽  
Normal Human ◽  
Pathologic Processes

Abstract Abstract 1237 Introduction: Disseminated Intravascular Coagulation represents a complex multi-factorial pathophysiological process in which protease disregulation along with other pathologic processes play an important role. The uncontrolled protease activities result in generation of several mediators which are not fully characterized. Biomarker profiling using protein chip array technology has been used in the identification of unique mediators in various diseases. Surface Enhanced Laser Desorption Ionisation(SELDI) is an ionization method in mass spectrometry that is used for the analysis of protein mixtures and correspondingly in the profiling of biomarkers in various diseases. Purpose: The purpose of this study was to profile and identify unique biomarkers in hospitalized patients with sepsis associated coagulopathy. Study design: There were 385 plasma samples included in this study. Baseline protein chip array profile in Molecular weight range of 0–200 kDa was carried out using SELDI technique employing gold chips. Plasma samples from normal humans (n=100) and pooled preparation from both the normal (NHP) and suspect liver disease/coagulopathy were utilized as controls. Results: Of the 385 baseline samples analyzed 371 patients (96.86%) exhibited the presence of a unique biomarker at 11.6 kDa. In addition down regulation of a biomarker at 56.4 kDa was also noted in 218 of patients (56.74%) In the normal human pooled plasma the 11.6 kDa peak was nearly absent. However in Pathological pooled plasma a distinct biomarker at 11.6 kDa with a much lower intensity was noted. Additional markers in baseline samples in 1–10 kDa range were also noted. Conclusions: These observations suggest that sepsis associated coagulopathy results in the generation of specific unique biomarker at 11.6kDa which requires further characterization. The downregulation of biomarker at 56.4 kDa and the apparent reduction levels during hospitalization require further investigations. Disclosures: No relevant conflicts of interest to declare.

Extrageniculate Contributions to Reflex Visual Orienting in Normal Humans: A Temporal Hemifield Advantage

1991 ◽  
Vol 3 (4) ◽  
pp. 322-328 ◽  
Author(s):  
Robert Rafal ◽  
Avishai Henik ◽  
Jean Smith
Keyword(s):  
Reaction Time ◽  
Visual Attention ◽  
Choice Reaction Time ◽  
Human Subjects ◽  
Visually Guided ◽  
Manual Responses ◽  
Visual Orienting ◽  
Normal Humans ◽  
Normal Human ◽  
Benefits And Costs

Evidence is presented that the phylogenetically older retin-otectal pathway contributes to reflex orienting of visual attention in normal human subjects. The study exploited a lateralized neuroanatomic arrangement of retinotectal pathways that distinguishes them from those of the geniculostriate system; namely, more direct projections to the colliculus from the temporal hemifield. Subjects were tested under monocular viewing conditions and responded to the detection of a peripheral signal by making either a saccade to it or a choice reaction time manual keypress. Attention was summoned by noninformative peripheral precues, and the benefits and costs of attention were calculated relative to a central precue condition. Both the benefits and costs of orienting attention were greater when attention was summoned by signals in the temporal hemifield. This temporal hemifield advantage was present for both saccade and manual responses. These findings converge with observations in patients with occipital and midbrain lesions to show that the phylogenetically older retinotectal pathway retains an important role in controlling visually guided behavior; and they demonstrate the usefulness of temporal-nasal hemifield asymmetries as a marker for investigating extrageniculate vision in humans.

The Rate of Iron Accumulation in Iron Storage Disease

Blood ◽  
1963 ◽  
Vol 22 (4) ◽  
pp. 429-440 ◽  
Author(s):  
WILLIAM H. CROSBY ◽  
MARCEL E. CONRAD ◽  
MUNSEY S. WHEBY
Keyword(s):  
Iron Deficiency ◽  
Iron Accumulation ◽  
Deficiency Anemia ◽  
Iron Storage ◽  
Plasma Iron ◽  
Iron Deficient ◽  
Normal Humans ◽  
Normal Human ◽  
Hemoglobin Mass ◽  
Rate Of Accumulation

Abstract 1. By means of phlebotomy to recover and measure accumulated iron and by determining the rate of replenishment of hemoglobin after induction of iron-deficiency anemia, it is possible to compute the rate at which iron is accumulated by absorption from the diet. Normal humans are presumed to be in iron balance and absorb iron only to replace what is lost; under these conditions they accumulate none. During recovery from induced iron deficiency a normal human accumulated iron at the rate of 5 to 6 mg. per day. 2. Patients with hemochromatosis were found to accumulate iron at the rate of 1.5 to 5 mg. per day. With iron deficiency the rate increased to 8 to 10 mg. per day. Because of uncertainty concerning the manner of onset of iron accumulation in hemochromatosis, whether gradual or abrupt, it is not possible by extrapolation to establish the time of onset in these patients. However, at the rates of accumulation established in this study there was an insufficient excess of iron to permit a conclusion that such rates had existed throughout the patient’s life. If the disease began early, the initial or interim rates were less than those found. If the disease began and continued at the rate found, its onset was 10 to 17 years prior to this study. 3. In a patient with hypochromic iron-loading anemia the rate of accumulation was about 2.5 mg. per day. It was not appreciably increased by iron deficiency except when the deficiency was severe and the plasma iron was quite low. While this patient was iron deficient the plasma iron became abnormally high even before the hemoglobin mass was completely reconstituted. 4. A patient with transfusion siderosis who had recovered from his anemia was phlebotomized to remove the accumulated iron. When iron deficiency finally developed the total amount of iron which had been recovered was less than half of the 32.5 Gm. given in the transfusions some years before. It was computed that during those years the patient was losing iron at a rate of about 4.0 mg. per day. The rate of iron accumulation during his recovery from the induced iron deficiency was the same as the normal: 5 to 6 mg. per day. 5. The ability to lose iron which is in excess of requirement is implicit in the demonstration of iron-laden deciduous cells such as the glandular epithelium of the stomach and duodenum and macrophages in the intestinal villi. 6. In hemochromatosis there is a failure of the intestinal mucosal block to prevent absorption of unneeded iron. When absorption exceeds the capacity of the iron excretory mechanisms, iron accumulation occurs. In iron deficiency the excretory mechanisms become less active so that the rate of iron accumulation is further increased.

Complement fixation by antibodies to the alpha toxin of Staphylococcus aureus

1982 ◽  
Vol 28 (10) ◽  
pp. 1127-1132 ◽  
Author(s):  
Ching Y. Lo ◽  
Hugh B. Fackrell ◽  
Gary M. Barei
Keyword(s):  
Staphylococcus Aureus ◽  
Complement Fixation ◽  
Erythrocyte Membranes ◽  
Alpha Toxin ◽  
In Vivo Experiments ◽  
Carrier Erythrocytes ◽  
Human Sera ◽  
Normal Humans ◽  
Normal Human

When rabbits were injected with the heat-denatured alpha toxin (toxoid) of Staphylococcus aureus, the immune response was demonstrated by an increase in antitoxin that fixed complement. Such antitoxin was detected in 72% of normal human sera. After fractionation of the antitoxin into two types (the antibinding antibodies and the indirect hemagglutinating antibodies), both types of antibodies were found to fix complement in the standard serological complement fixation test. In addition, the indirect hemagglutinating antibodies were capable of fixing complement when the antigen (alpha toxin or toxoid) was covalently or noncovalently bound to erythrocyte membranes. The fixation of complement by membrane-bound immune complexes did not result in lysis of the carrier erythrocytes. The prevalence of complement-fixing antitoxin in normal humans and animals raised the concern that the outcome of in vivo experiments involving alpha toxin could be influenced by the immune status of the host.

scholarly journals Colony Growth of Human Peripheral White Blood Cells In Vitro

Blood ◽  
1971 ◽  
Vol 37 (2) ◽  
pp. 136-141 ◽  
Author(s):  
JOHN E. KURNICK ◽  
WILLIAM A. ROBINSON
Keyword(s):  
Peripheral Blood ◽  
Blood Cells ◽  
Mononuclear Cells ◽  
White Blood Cells ◽  
Colony Growth ◽  
Lymphocytic Leukemia ◽  
Normal Humans ◽  
Normal Human ◽  
Peripheral White Blood Cells

Abstract Peripheral blood from normal humans and patients with circulating atypical mononuclear cells have been studied for their ability to form granulocytic colonies in vitro in the agar-gel method of hematopoietic cell culture. WBC from patients with chronic lymphocytic leukemia failed to proliferate. Normal human white blood cells gave rise to 0.5-8 colonies per 1 x 106 cells plated, while peripheral blood containing large mononuclear cells gave rise to 15 to 120 colonies per 1 x 106 cells plated, depending upon the number of such cells plated. Colonies averaged 500 cells in size by day 20 of culture and appeared to be granulocytic.

Use of a leucine clamp to demonstrate that IGF-I actively stimulates protein synthesis in normal humans

1994 ◽  
Vol 267 (4) ◽  
pp. E591-E598 ◽  
Author(s):  
D. L. Russell-Jones ◽  
A. M. Umpleby ◽  
T. R. Hennessy ◽  
S. B. Bowes ◽  
F. Shojaee-Moradie ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Insulin Infusion ◽  
Whole Body ◽  
Insulin Levels ◽  
Factor I ◽  
Anabolic Action ◽  
Human Volunteers ◽  
Igf I ◽  
Normal Humans ◽  
Normal Human

Insulin-like growth factor I (IGF-I) is thought to mediate the anabolic action of growth hormone. A glucose and amino acid clamp technique was used to investigate the effects of a 3-h intravenous infusion of either 43.7 pmol.kg-1.min-1 (20 micrograms.kg-1.h-1) IGF-I or 3.4 pmol.kg-1.min-1 (0.5 mU.kg-1.min-1) insulin on whole body leucine turnover in five normal human volunteers. During the IGF-I infusion, IGF-I levels increased (P < 0.01; 26.6 +/- 2.8 to 88.9 +/- 14.2 nmol/l) and insulin levels fell (P < 0.05; 0.096 +/- 0.018 to 0.043 +/- 0.009 nmol/l). During the insulin infusion, insulin levels increased (P < 0.01; 0.057 +/- 0.013 to 0.340 +/- 0.099 nmol/l), and there was no change in IGF-I. There was no significant change in leucine production rate (Ra; a measure of protein degradation) during the IGF-I infusion (2.23 +/- 0.17 to 2.13 +/- 0.2 mumol.kg-1.min-1), but there was an increase (P < 0.03) in nonoxidative leucine disposal rate (Rd; a measure of protein synthesis; 1.83 +/- 0.15 to 2.05 +/- 0.21 mumol.kg-1.min-1). In contrast, insulin reduced (P < 0.02) leucine Ra (1.81 +/- 0.24 to 1.47 +/- 0.24 mumol.kg-1.min-1) and had no effect on nonoxidative leucine Rd (1.44 +/- 0.25 to 1.41 +/- 0.22 mumol.kg-1.min-1). We conclude that IGF-I, under conditions of adequate substrate supply, directly increases protein synthesis in contrast to insulin, which exerts its anabolic action by reducing proteolysis.

Glucose counterregulation during prolonged hypoglycemia in normal humans

1984 ◽  
Vol 247 (2) ◽  
pp. E206-E214 ◽  
Author(s):  
G. B. Bolli ◽  
I. S. Gottesman ◽  
P. E. Cryer ◽  
J. E. Gerich
Keyword(s):  
Insulin Secretion ◽  
Glucose Utilization ◽  
Glucose Production ◽  
Regular Insulin ◽  
Glucose Turnover ◽  
Temporal Relationships ◽  
Human Volunteers ◽  
Clinical Disorders ◽  
Normal Humans ◽  
Normal Human

To study glucose counterregulation under conditions approximating those of clinical disorders in which hypoglycemia develops gradually and is reversed over a prolonged period, we injected regular insulin subcutaneously, in a dose (0.15 U/kg) selected to produce two- to threefold increases in plasma insulin, in 11 normal human volunteers and measured plasma glucose, insulin, C-peptide, and counterregulatory hormone concentrations as well as rates of glucose production, glucose utilization, and insulin secretion over 12 h. The data suggest that the mechanisms of gradual recovery from prolonged hypoglycemia may differ from those of rapid recovery from short-term hypoglycemia produced by intravenous injection of insulin in that 1) both stimulation of glucose production and limitation of glucose utilization contribute to recovery from prolonged hypoglycemia; 2) increases in glucagon, epinephrine, growth hormone, and cortisol secretion as well as a decrease in insulin secretion may all participate in glucose counterregulation during prolonged hypoglycemia; 3) epinephrine may play a more important role than glucagon during prolonged hypoglycemia. The latter two conclusions are based primarily on the temporal relationships between changes in the rates of glucose turnover and changes in plasma hormone concentrations and should not be considered proved. However, they provide the basis for testable hypotheses concerning the physiology of gradual recovery from prolonged hypoglycemia that can be expected to be relevant to the pathophysiology of clinical hypoglycemia.

Hyperoxia and moderate hypoxia fail to affect inspiratory muscle fatigue in humans

1989 ◽  
Vol 66 (2) ◽  
pp. 894-900 ◽  
Author(s):  
B. T. Ameredes ◽  
T. L. Clanton
Keyword(s):  
Human Subjects ◽  
Initial Pressure ◽  
Inspiratory Muscles ◽  
Mouth Pressure ◽  
Rate Of Decay ◽  
Normal Humans ◽  
Normal Human ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Inspiratory Muscle Fatigue

Normal human subjects (n = 7) breathing 21% O2 (normoxia), 13% O2 (hypoxia), or 100% O2 (hyperoxia) performed repeated maximal inspiratory maneuvers (inspiratory duration = 1.5 s, total breath duration = 3.5 s) on an “isoflow” system, which delivered a constant mouth flow (1.25 or 1 l/s) while maintaining normocapnia (5.5% end-tidal CO2). Respective mean arterial O2 saturation values (ear lobe oximetry) were 98 +/- 1, 91 +/- 4 (P less than or equal to 0.01), and 99 +/- 1% (NS). Maximal mouth pressure (Pm) was measured during inspirations at rest and during a 10-min fatigue trial, and the Pm measurements obtained during the fatigue trials were fit to an exponential equation. The parameters of the equation included the time constant (tau), which describes the rate of decay of Pm from the initial pressure (Pi) to the asymptote, or “sustainable” pressure (Ps). The mean fraction of Pm remaining at the end of the fatigue trials (Ps/Pi) was 63 +/- 5%. No significant differences in Pi, Ps, or tau were observed between O2 treatments. This suggests that fatigue of the inspiratory muscles in normal humans occurs by a mechanism that is insensitive to changes in blood O2 content that occur during inspiration of O2 in the range of 13–100%.

Sign in / Sign up

Export Citation Format

Share Document