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Biomedical subjects

Kusal K Das

Publications and source records attributed to Kusal K Das.

8 recordsLinked to original sources

AI In Leukemia Diagnostics: Complementing the Pathologist's Role.

Artificial intelligence (AI) is reshaping every stage of leukemia diagnostics, from digital morphology and multiparameter flow cytometry to next-generation sequencing, multi-omics analysis, and emerging computational frontiers such as quantum-inspired feature selection. This review outlines how contemporary AI tools can automate labor-intensive quantitation, flag diagnostically salient patterns, and standardize interpretation, while the pathologist or hematologist retains authority over validation, context-specific integration, and clinical decision-making. We present an illustrative "human-in-the-loop" workflow that embeds AI modules within current laboratory information systems, emphasizing points where expert oversight mitigates algorithmic bias and resolves discordant findings. We further map the validator-integrator role across morphology, flow cytometry, and genomic/multi-omic interpretation and provide practical training competencies and use cases for AI-assisted hematopathology. Beyond technical deployment, the article addresses the educational transformation required for sustainable adoption. Drawing on international competency frameworks, including the Digital Health Competencies in Medical Education Framework and recently proposed AI-specific Entrustable Professional Activities, we map core skills that future hematopathologists must master: data-science literacy, critical appraisal of AI outputs, and ethical governance. We highlight evaluated training models such as the Pathology Informatics Essentials for Residents curriculum, Stanford Artificial Intelligence in Machine and Imaging workshops, and College of American Pathologists bootcamps and propose integration strategies adaptable across resource settings. By pairing rigorous validation with targeted education, AI can elevate rather than eclipse the diagnostic role of the leukemia specialist, enabling more timely, reproducible, and personalized patient care.

Humans↗

Protective role of L-ascorbic acid on antioxidant defense system in erythrocytes of albino rats exposed to nickel sulfate.

In this experimental study, we investigated whether L-ascorbic acid has any influence on the blood antioxidant defense system, lipid peroxidation and hematological parameters of the albino rats exposed to nickel sulfate(NiSO4). Twenty four adult rats were divided into four groups of six animals in each group. The control rats were untreated and comprised Group I. Group II rats were administered nickel sulfate (2.0 mg/100 g b.wt.; intraperitonially, i.p.). Group II rats were treated orally L-ascorbic acid (50 mg/100 g b.wt.) and Group IV rats were given both nickel sulfate and L-ascorbic acid simultaneously on alternate days until the tenth dose. The hematological parameters were assessed: red blood corpuscle counts, packed cell volume %, hemoglobin concentration, white blood corpuscle counts and platelets count decreased significantly and clotting time increased significantly in nickel treated rats. We also observed increase malondialdehyde (MDA) and decrease glutathione level (GSH) in erythrocytes of nickel treated rats. The activities of erythrocyte antioxidant enzymes like superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were significantly increased in rats treated with nickel sulfate. Simultaneously treatment of L-ascorbic acid exhibited a possible protective role on the toxic effect of nickel sulfate on the hematological values, erythrocyte MDA and GSH concentrations as well as antioxidant enzymatic defense system.

Animals↗

Effect of L-ascorbic acid on nickel-induced alterations in serum lipid profiles and liver histopathology in rats.

Nickel exposure greatly depletes intracellular ascorbate and alters ascorbate-cholesterol metabolism. We studied the effect of the simultaneous oral treatment with L-ascorbic acid (50 mg/100 g body weight (BW) and nickel sulfate (2.0 mg/100 g BW, i.p) on nickelinduced changes in serum lipid profiles and liver histopathology. Nickel-treated rats showed a significant increase in serum low-density lipoprotein-cholesterol, total cholesterol, triglycerides, and a significant decrease in serum high-density lipoprotein-cholesterol. In the liver, nickel sulfate caused a loss of normal architecture, fatty changes, extensive vacuolization in hepatocytes, eccentric nuclei, and Kupffer cell hypertrophy. Simultaneous administration of L-ascorbic acid with nickel sulfate improved both the lipid profile and liver impairments when compared with rats receiving nickel sulfate only. The results indicate that L-ascorbic acid is beneficial in preventing nickel-induced lipid alterations and hepatocellular damage.

Animals↗

L-ascorbic acid protects the antioxidant defense system in nickel-exposed albino rat lung tissue.

We studied the effect of oral supplementation with L-ascorbic acid (50 mg /100 g body weight (BW) on nickel sulfate (2.0 mg/ 100 g BW, i.p)-induced lipid peroxidation and histopathology in the lung of Wister strain male albino rats. Lipid peroxide and glutathione levels and the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), were estimated. Nickel sulfate administration significantly increased the level of lipid peroxides and decreased all antioxidant enzyme activities. Nickel sulfate treatment also induced (a) loss of normal characteristics and architectural organization, (b) inflammation in bronchioles, (c) alveolar congestion, (d) alveolar cell hyperplasia, and (e) congestion in the lumen. The simultaneous administration of L-ascorbic acid and nickel sulfate improved both lipid peroxidation and the histopathology of lung when compared with rats receiving nickel sulfate alone. The results indicate that L-ascorbic acid prevents nickel-induced alteration of antioxidant defense mechanisms and histopathology of lung tissue.

Animals↗

Effect of lead (Pb) exposure on the activity of superoxide dismutase and catalase in battery manufacturing workers (BMW) of Western Maharashtra (India) with reference to heme biosynthesis.

The aim of this study was to estimate the activity of superoxide dismutase (SOD) and catalase in erythrocytes and malondialdehyde (MDA) in plasma of battery manufacturing workers (BMW) of Western Maharashtra (India) who were occupationally exposed to lead (Pb) over a long period of time (about 15 years). This study was also aimed to determine the Pb intoxication resulted in a disturbance of heme biosynthesis in BMW group. The blood Pb level of BMW group (n = 28) was found to be in the range of 25.8 - 78.0 microg/dL (mean + SD, 53.63 + 16.98) whereas in Pb unexposed control group (n = 35) the range was 2.8 - 22.0 microg/dL (mean + SD, 12.52 + 4.08). The blood level (Pb-B) and urinary lead level (Pb-U) were significantly increased in BMW group as compared to unexposed control. Though activated d- aminolevulinic acid dehydratase (ALAD) activities in BMW group did not show any significant change when compared to control group but activated / non activated erythrocyte - ALAD activities in BMW group showed a significant increase. Erythrocyte- zinc protoporphyrin (ZPP), urinary daminolevulinic acid (ALA-U) and porphobilinogen (PBG-U) of BMW groups elevated significantly as compared to control. A positive correlation (r = 0.66, p < 0.001) between Pb-B and ALA-U were found in BMW group but no such significant correlation (r = 0.02, p> 1.0) were observed in control group. Hematological study revealed a significant decrease of hemoglobin concentration, packed cell volume (%) and other blood indices and a significant increase of total leucocytes count in BMW group in comparison to control group. The serum MDA content was significantly increased (p < 0.001) and the activities of antioxidant enzymes such as erythrocyte- SOD (p < 0.001) and erythrocytecatalase (p < 0.001) were significantly reduced in BMW group as compared to control group. A positive correlation (r = 0.45, p < 0.02) between Pb-B and serum MDA level was observed in BMW group (Pb-B range 25.8 - 78.0 microg / dL) but such significant correlation did not notice in control group (Pb-B range 2.8 - 22.0 microg / dL). The study clearly showed an adverse effect of heme biosynthesis and imbalance of pro-oxidant / antioxidant status in lead exposed battery manufacturing workers resulting in increase in lipid peroxidation associated with decrease in erythrocyte-SOD and erythrocyte-catalase activities.

Adult↗

Studies on the role of ascorbic acid on nickel induced hepatic nucleic acid concentrations in rats.

We studied the effect of oral treatment with ascorbic acid (50 mg/100 g body weight) on nickel sulfate-induced (2.0 mg/100 g body weight, i.p.) alteration of nucleic acids and total protein concentration in the liver of Wistar strain male albino rats. Nucleic acids and total protein concentrations in treated rats decreased significantly when compared with untreated controls. The simultaneous administration of ascorbic acid with nickel sulfate resulted in a remarkable improvement of nucleic acids and total protein concentrations in liver in comparison with rats treated with nickel sulfate only. The results indicate that nickel influences the expression of genetic information by reducing hepatic DNA, RNA, and protein concentration in animals. Simultaneous treatment with ascorbic acid was beneficial for fighting against nickel-induced hepatoxicity.

Administration, Oral↗

Effect of nickel sulfate on testicular steroidogenesis in rats during protein restriction.

Nickel, a widely used heavy metal, exerts potent toxic effects on peripheral tissues as well as on the reproductive system. Low dietary protein coupled with exposure to this metal induces more severe changes, including biochemical defects, structural disorders, and altered physiologic functions. This study was designed to assess the effects of nickel sulfate on testicular steroidogenesis and to ascertain whether such alterations are reversible with normal protein and protein-restricted dietary regime. Nickel sulfate [2 mg/100 g body weight (bw)] dissolved in double-distilled water was administered on alternate days for 10 doses in a normal protein diet (18% casein) and a protein-restricted diet (5% casein) to Wistar male albino rats (bw 160 +/- 5 g). Two groups, one with a normal protein diet and the other with a protein-restricted diet, served as controls. Twenty-four hours after the last treatment, all the animals except those in withdrawal groups were sacrificed by decapitation. We observed a significant reduction in the activities of the testicular steroidogenic enzymes and plasma testosterone concentration accompanied by a significant elevation in cholesterol and ascorbic acid level in both dietary groups. After 15 days of withdrawal from the nickel sulfate treatment, the testicular steroidogenic enzymes, along with plasma testosterone level, improved significantly in both normal protein-fed and protein-restricted dietary groups. The effects of nickel on testicular cholesterol and ascorbic acid concentration were also reduced after withdrawal. Our results indicate that nickel sulfate affects the steroidogenic enzymes, causing alteration in the formation of testosterone in both dietary groups, which was manifested in the elevated cholesterol and ascorbic acid level with decreased activities of steroidogenic enzymes in adult rats testes. However, these alterations were reversible in both groups of animals fed normal protein diets and protein-restricted diets.

Administration, Oral↗

A study on predictors of Peak Expiratory Flow Rate in Muslim subjects (aged 18 to 20 years) of Karnataka.

This study aims to develop Peak Expiratory Flow Rate (PEFR) predictors for Karnataka Muslim male and female subjects of aged 18 to 20 years. PEFR was recorded in a standing position using mini Wright Peak Flow Meter on one hundred and four (104) healthy male and sixty one (61) healthy female subjects. Anthropometrical measurements i.e. height, weight, body surface area and body mass index were calculated. Statistically significant correlation were found in both sexes between PEFR and standing height (male, r = 0.94, P < 0.001; female, r = 0.95, P < 0.001), weight (male, r = 0.56, P < 0.001; female, r = 0.70, P < 0.001) and body surface area (male, r = 0.68, P < 0.001; female, r = 0.57, P < 0.001). The correlation between PEFR and body mass index were not found statistically significant in both sexes (male, r = 0.081; female, r = 0.17). The prediction equation for Karnataka male and female Muslim subjects (aged 18 to 20 years) based on height, weight and body surface area and multiple regression equation based on all those physical parameters have been developed (PEFR (l/m) (male) = 1.7304 x height + 0.155 x weight + 140.45 x BSA + 5.02; PEFR (l/m) (female) = 2.0448 x height--16.08 weight + 664.697 x BSA--101.24).

Adolescent↗