Accurate malaria diagnosis is crucial for effective case management, strong surveillance, and progress toward elimination. However, in highland regions, diagnostic tools are underutilized or yield suboptimal performance. While hematological alterations are frequently observed in malaria, their role remains largely supportive rather than diagnostic. This study aimed to evaluate diagnostic challenges by comparing the performance of HRP2-based rapid diagnostic tests, microscopy, and PCR at Bichena Primary Hospital, Northwest Ethiopia, with hematological profiles examined as supportive indicators to help contextualize diagnostic performance. A facility-based cross-sectional study was conducted between 31/12/2024 to 28/02/2025, with 274 participants enrolled through consecutive sampling. Socio-demographic data were collected using semi-structured questionnaires. The diagnostic evaluation used nested polymerase chain reaction (PCR) (from dried blood spots), microscopy (capillary and venous blood), histidine rich protein 2 (HRP2)-based rapid diagnostic tests (RDTs), and hematological profiling. Data analysis was carried out with Statistical Package for the Social Sciences (SPSS) version 25.0, assessing diagnostic accuracy through sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV), while inter-test agreement was measured using Cohen's Kappa coefficient. Results were summarized in text, figures, and tables. Higher prevalence of Plasmodium infections was detected in 23.4% of participants by PCR, 20.1% by microscopy and 19% by HRP2-antigen-based RDT. The HRP2-antigen based RDT showed lower sensitivity (79.1%), NPV (94.1%), and test accuracy (94.9%) compared to PCR. Similarly, microscopy exhibited high specificity and PPV (100%); however, the sensitivity was 85.9%, indicating that some true positives are missed compared to PCR. Moderate test agreement was observed between PCR and microscopy (κ=0.904; P=0.00) but weak agreement between PCR and RDTs (κ=0.847). Hematological analysis revealed a significantly lower platelet count among PCR-confirmed malaria cases (P<0.05), suggesting a supportive association rather than diagnostic utility. Both HRP2-antigen based RDTs and microscopy demonstrated lower sensitivity compared to PCR. RDTs showed the lowest diagnostic potential for P. falciparum, mixed and even P. vivax infections, this may be due to low parasitemia and possible pfhrp2 deletions. Hematological parameters, particularly platelet count, may serve as complementary indicators to support clinical suspicion but should not replace parasitological or molecular diagnosis. Further investigation of pfhrp2/pfhrp3 deletions is critical to inform the selection of appropriate diagnostic tools in the area.

Doxorubicin (DOX) is a common chemotherapy drug, which causes dose-dependent toxicity affecting multiple systems like heart, blood, liver, and kidneys. This study assessed the hematological and biochemical changes caused by DOX and explored the protective effects of Persea americana seed extract in an experimental animal model. Forty-two Wistar rats were divided into six groups: G1, control rats; G2, received 5mg/kg of DOX alone; G3, received 100mg/kg reference drug, vitamin C; G4, received 5mg/kg DOX + 500mg/kg extract; G5 received 5mg/kg DOX + 1000mg/kg extract; G6 received 5mg/kg DOX + 1500mg/kg extract. Dox (5 mg/kg) was given intraperitoneally, and treatments lasted four weeks. Blood parameters (RBC, Hb, PCV, WBC, platelets), liver function markers (ALT, AST, ALP, total protein, albumin, bilirubin), and kidney function markers (urea, creatinine, electrolytes) were evaluated using standard methods. DOX treatment led to significant reductions (p &lt; 0.05) in RBC, Hb, PCV, and platelets, along with an increase in WBC levels. It also raised liver enzymes and bilirubin while lowering total protein and albumin, indicating liver damage. Kidney impairment was shown by higher levels of urea and creatinine, as well as an electrolyte imbalance. Treatment with Persea americana seed extract significantly reduced these changes in a dose-dependent manner. The highest dose (1500 mg/kg) provided the most consistent improvement, similar to vitamin C. These results suggest that Persea americana seed extract may protect against DOX-related toxicity, likely through antioxidant effects. However, not all parameters completely normalized, showing partial recovery instead of full restoration. This study highlights the potential of Persea americana as a natural aid in reducing chemotherapy-induced toxicity and encourages more research into its therapeutic uses.

Background/objectives. Clostridioides difficile infection (CDI) remains a major cause of healthcare-associated infectious colitis, particularly among elderly and multimorbid patients. Disease severity and clinical evolution are influenced by the host’s systemic inflammatory response. This study aimed to evaluate the hematological and inflammatory profile of hospitalized CDI patients and to explore the prognostic value of routine laboratory parameters for prolonged hospitalization. Methods. A retrospective observational study was conducted on 50 adult patients hospitalized with laboratory-confirmed CDI (positive glutamate dehydrogenase, antigen and toxins A/B). Hematological parameters (WBC, hemoglobin, RDW) and inflammatory markers (CRP, fibrinogen) were analyzed at admission and discharge. Prolonged hospitalization was defined as length of stay (LOS) &gt; 8 days (cohort median). Multivariable logistic regression was performed to assess admission predictors of prolonged hospitalization, and model discrimination was evaluated using leave-one-out cross-validation (LOOCV). Results. At admission, patients exhibited marked inflammatory activation accompanied by reduced hemoglobin and elevated RDW. Significant correlations were observed between inflammatory markers. All inflammatory and hematologic parameters improved at discharge. In multivariable analysis, lower admission hemoglobin and higher log-transformed CRP showed exploratory associations with prolonged hospitalization. The internally validated model demonstrated moderate discriminative performance (AUC = 0.65). Conclusions. CDI is associated with substantial systemic inflammatory activation and hematologic alterations. While no individual predictor reached statistical significance, the observed effect sizes provide hypothesis-generating estimates to inform future prospective validation studies.

Purpose: This study aimed to investigate whether Prothrombin G20210A (Factor II) and PAI-1 4G/5G gene polymorphisms are associated with COVID-19 severity and clinical outcomes among patients admitted to the Emergency Department of Pamukkale University Hospital (Denizli, Türkiye) between June and December 2021.Materials and methods: In this prospective, cross-sectional, observational study, 150 PCR-confirmed COVID-19 patients and 300 healthy volunteers were genotyped for Prothrombin G20210A and PAI-1 4G/5G polymorphisms by PCR and DNA sequencing. Laboratory parameters, disease severity indices, intensive care unit (ICU) admission, and mortality were analyzed.Results: The genotype distribution among patients was GA 54.7% and GG 45.3% for Prothrombin G20210A, and 4G/4G 77.3% and 4G/5G 22.7% for PAI-1. There were no significant differences in Prothrombin G20210A variants except for lower lymphocyte counts in GA carriers (p=0.031). The PAI-1 4G/5G group showed a significantly higher monocyte count (p=0.012), while differences in urea and other biochemical parameters were not statistically significant (p&amp;gt;0.05). Patients carrying both PAI-1 and Prothrombin heterozygous variants (double heterozygotes, n=13) had lower hemoglobin (p=0.010) and lymphocyte counts (p=0.012), but higher monocyte (p=0.001) and ferritin levels (p=0.006). This subgroup also demonstrated lower oxygen saturation (p=0.049) and significantly higher intensive care unit admission (46.2% vs. 15.3%, p=0.005) and mortality (38.5% vs. 9.5%, p=0.002).Conclusion: Prothrombin G20210A and PAI-1 4G/5G polymorphisms particularly their coexistence were associated with hematologic and inflammatory alterations, as well as increased ICU admission and mortality rates. These variants may have potential value for risk stratification and should be evaluated in larger studies.

Circulating miR-146a-5p and miR-98-5p as Indicators of Inflammatory Response and Joint Pain in Chikungunya Fever.

Alpha-synuclein (α-syn), is a protein abundantly expressed in the central nervous system and in the erythrocytes, playing a pivotal role in the pathogenesis of Parkinson’s disease and other synucleinopathies. Among the GATA family transcription factors (TFs), GATA1 and GATA2 regulate the meg-erythrocytic differentiation starting from the hematopoietic stem cell. In erythropoiesis, the GATA1-2 switching, is known to regulate the α-syn gene (SNCA) expression, which is essential for iron metabolism and membrane stability. Abnormalities in α-syn regulation alter erythrocytic function, possibly contributing to pathological mechanisms of different synucleinopathies. Due to this potential role for GATA1 in synucleinopathies we aimed to underline the effects of GATA1 downregulation on aging and α-syn expression. To this aim we explored the contribution of hematological alteration in the development of neurodegenerative disorder by analyzing the different organs from the Gata1low mice, as model of aging and myelofibrosis. Bone marrow and brain section from young and aged Gata1low mice showed significant differences in the α-syn expression compared to their relative controls, suggesting a trend in α-syn aggregation that increases with aging. In the brain, the GATA1 expression was reduced in aged Gata1low mice and resulted in shrinker neurons with mitochondrial alterations. The bone marrow from aged Gata1low mice was characterized by increased level of inflammatory cytokine as TGF-α, that parallel the different expression and the aggregation of α-syn. Moreover, morphological determinations revealed that α-syn expression was related to cells resembling the most immature myeloid phenotype (ie. reticulocytes). These results suggest the pivotal role of GATA1 TF in the regulation of α-syn expression and aggregation, highlighting the potential role of GATA1 and bone marrow in the pathogenesis of synucleinopathies.

Background. Several hematological alterations involving cellular components of the blood have been reported in patients with type 2 diabetes mellitus (T2DM) and may contribute to the development of diabetes-related complications. Chronic hyperglycemia increases oxidative stress, which can affect red blood cells, white blood cells, and platelets. Glycated hemoglobin (HbA1c) reflects glycemic control over the preceding three months and is widely used to assess disease management. Objective. To evaluate the association between selected hematological parameters from the complete blood count (CBC), and glycemic control in patients with T2DM. Methods. This cross-sectional, exploratory study included 50 patients with T2DM, who were divided into two groups based on their HbA1c level into a good glycemic control group (n = 25, HbA1c &lt; 7%) and poor glycemic control (n = 25, HbA1c ≥ 7%). CBC parameters and HbA1c levels were measured. Group comparisons between groups were performed using the independent sample t-tests and Pearson’s correlation analysis was used to assess the relationship between hematological parameters and HbA1c. Results. Patients with poor glycemic control had significantly higher mean WBC count (7.90 ± 1.72 vs. 6.53 ± 0.89 × 109/L, p &lt; 0.001), neutrophil count (4.98 ± 1.57 vs. 3.91 ± 0.82 × 109/L, p &lt; 0.004), platelet count (286.88 ± 54.18 vs. 216.48 ± 39.33 × 109/L, p &lt; 0.001)), and mean platelet volume (10.44 ± 2.11 vs. 8.21 ± 0.86 fL, p &lt; 0.001) compared with the good control group. No significant differences were observed in RBC parameters. Platelet count showed a significant positive correlation with HbA1c (r = 0.516, p &lt; 0.001). In addition, WBC count (r = 0.485, p = 0.001), neutrophil count (r = 0.431, p = 0.002), and mean platelet volume (MPV) (r = 0.598, p &lt; 0.001) were also significantly positively correlated with HbA1c levels. Conclusion. Poor glycemic control in this cohort of patients with T2DM was associated with higher WBC, neutrophil, and platelet counts, as well as increased MPV. These results suggest a potential correlation between subclinical inflammation, platelet activation, and hyperglycemia. However, given the small sample size and the exploratory cross-sectional design of the study, the findings should be interpreted with caution and confirmed in larger prospective studies before any clinical utility can be established.

Antipyretic drugs are widely used to manage fever and pain and are generally regarded as safe when administered within recommended therapeutic ranges. Nevertheless, concerns remain regarding the potential biological effects associated with repeated or sub-chronic exposure. The present study evaluated the hematological, histopathological, and molecular effects of two commonly used antipyretics, paracetamol and ibuprofen, following repeated administration in male albino mice. Hematological analysis revealed drug-related alterations in selected blood parameters, with more pronounced changes observed in ibuprofen-treated groups, while paracetamol exposure was associated with comparatively milder effects. Qualitative histopathological examination demonstrated organ-specific structural alterations in the testes, liver, kidneys, and stomach, which were generally mild in nature and more frequently observed at higher experimental dose levels. No evidence of overt testicular failure or severe tissue damage was detected within the exposure period. At the molecular level, repeated exposure to paracetamol and ibuprofen was associated with downregulation of TNF-α and connexin 43 mRNA expression in peripheral blood, suggesting early systemic transcriptional responses accompanying the observed histological changes. However, molecular findings were limited to mRNA expression analysis and did not include protein-level or tissue-specific validation. Overall, the results indicate that repeated sub-chronic exposure to paracetamol and ibuprofen at therapeutic-equivalent dose ranges may be associated with early hematological, histological, and molecular alterations in mice. These findings highlight the importance of cautious and rational use of widely prescribed antipyretic drugs and underscore the need for further studies to elucidate long-term safety, underlying mechanisms, and tissue-specific functional outcomes.

Background: Chronic liver fibrosis is a progressive pathological condition characterized by excessive extracellular matrix deposition and architectural remodeling, which may ultimately lead to cirrhosis and liver failure. Although mesenchymal stem cells (MSCs) exhibit antifibrotic and immunomodulatory properties, their therapeutic effects in established chronic liver fibrosis remain incompletely defined. This study aimed to evaluate the biochemical, hematological, and histopathological effects of MSC therapy in a chronic thioacetamide-induced liver fibrosis model. Methods: A controlled preclinical experimental study was conducted using rats with liver fibrosis induced by intraperitoneal thioacetamide administration for 24 weeks. Animals were allocated into three groups: control, untreated fibrosis, and fibrosis treated with MSCs derived from human umbilical cord tissue after fibrosis establishment. Serum biochemical markers, hematological parameters, and liver histopathology were assessed. Fibrosis severity was evaluated using hematoxylin-eosin and Masson's trichrome staining and graded according to the METAVIR scoring system. Results: Thioacetamide exposure induced chronic liver injury characterized by marked elevations in serum transaminases, reduced albumin and total protein levels, hematological alterations, and early-to-intermediate fibrosis stages (METAVIR F1-F2). MSC-treated animals exhibited approximately 40-45% reductions in transaminase levels, partial recovery of hepatic synthetic function, and attenuation of hematological alterations. Histopathological analysis demonstrated a reduction in fibrotic burden and limitation of fibrogenic progression within METAVIR F1-F2 stages. Conclusions: MSC therapy partially mitigates biochemical, hematological, and histopathological alterations associated with chronic thioacetamide-induced liver fibrosis, supporting its potential as a modulatory strategy to attenuate fibrogenic progression and stabilize liver function rather than as a curative intervention.

Background: Repeated blood transfusion remains a cornerstone in the management of chronic hematological disorders but is associated with significant biochemical and hematological alterations, including iron overload, hepatic dysfunction, and electrolyte imbalance. Objective: To assess biochemical and hematological changes associated with repeated blood transfusion among patients attending a tertiary hospital. Methods: This hospital-based comparative cross-sectional study involved 120 participants comprising 80 patients who had received ≥3 blood transfusions in the preceding 12 months and 40 age- and sex-matched controls with ≤1 transfusion. Hematological parameters were analyzed using an automated hematology analyzer, while biochemical assays were performed using standard spectrophotometric methods. Data were analyzed using SPSS version 25. Independent t-test, Pearson correlation, and linear regression were applied. A p-value &lt;0.05 was considered statistically significant. Results: Repeatedly transfused patients had significantly higher mean serum ferritin (486.3 ± 162.5 ng/mL vs 168.4 ± 72.1 ng/mL; p&lt;0.001), ALT, AST, bilirubin, and potassium levels compared to controls. Serum calcium was significantly lower in transfused patients (p=0.02). Serum ferritin showed a strong positive correlation with transfusion frequency (r=0.64, p&lt;0.001). Conclusion: Repeated blood transfusion is associated with significant biochemical and hematological alterations, particularly iron overload and hepatic dysfunction. Routine laboratory monitoring is recommended for early detection and prevention of transfusion-related complications.

BackgroundSARS-CoV-2 infection is known to induce systemic biochemical and hematological alterations, particularly in hospitalized patients. However, data regarding subclinical changes in ambulatory, non-hospitalized individuals—especially in Latin American populations—remain limited.ObjectiveTo compare biochemical and hematological parameters between ambulatory adults with and without serological evidence of prior SARS-CoV-2 infection, in order to identify potential subclinical alterations associated with previous virus exposure.MethodsA cross-sectional study was conducted in 201 ambulatory adults from central-northern Mexico between August and December 2020. Anti–SARS-CoV-2 IgG and IgM antibodies were detected using two independent lateral flow immunochromatographic assays. Participants were classified as seropositive only when both assays showed concordant reactivity. Biochemical and hematological parameters were compared between seropositive and seronegative individuals using appropriate parametric or non-parametric tests.ResultsOverall seroprevalence of anti–SARS-CoV-2 antibodies was 22.3%. No significant differences were observed in hematological parameters between seropositive and seronegative participants. In contrast, seropositive individuals exhibited significantly lower high-density lipoprotein cholesterol (HDL-C) levels compared to seronegatives (median: 40.5 vs. 45.3 mg/dL; p = 0.009), with significance maintained in females. Liver enzymes were significantly higher among seropositive subjects, including aspartate aminotransferase (AST) (median: 30 vs. 24 U/L; p = 0.007) and alanine aminotransferase (ALT) (median: 32.5 vs. 20 U/L; p = 0.001). These differences were more pronounced in males. No significant differences were found in glucose, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), alkaline phosphatase (ALP), or total bilirubin (TB).ConclusionEven mild or asymptomatic SARS-CoV-2 infection is associated with subtle but consistent alterations in lipid metabolism and liver enzymes in ambulatory, unvaccinated individuals. These findings support the need for biochemical monitoring after SARS-CoV-2 infection, particularly in populations with high baseline cardiometabolic risk.

Dicroceliosis is an important parasitic disease of small ruminants that can cause significant physiological disturbances and economic losses. The present study investigated the pathophysiological mechanisms, clinical outcomes, and hematobiochemical alterations in sheep naturally infected with Dicrocoelium lanceatum, including cases with concurrent babesiosis. A total of 120 sheep were examined, of which 39 animals were infected with D. lanceatum. Hematological analysis in mono-infected sheep revealed slight reductions in hemoglobin (53.69 ± 5.75 g/dl) compared with healthy animals (56.81 ± 11.34 g/dl), as well as decreases in packed cell volume (34.62 ± 5.01% vs 38.52 ± 7.75%) and mean corpuscular volume (65.51 ± 8.11 vs 69.71 ± 11.92 fL). White blood cell counts showed only minor variation (12.31 ± 1.94 ×10³/µl in infected sheep vs 12.15 ± 1.88 ×10³/µl in healthy animals). In contrast, sheep with concurrent infection of D. lanceatum and Babesia ovis exhibited more pronounced hematological and biochemical disturbances. In co-infected animals, white blood cell counts increased markedly (16.8–28.2 ×10³/µl) compared with healthy sheep (8.4–14.6 ×10³/µl), while hemoglobin levels decreased to 3.8–5.6 g/dl. Biochemical analysis revealed elevated liver enzyme activities, including AST (116–309 U/L) and ALP (136–454 U/L), along with increased total bilirubin levels (0.1–1.1 mg/dl) and decreased albumin concentrations (1.9–2.5 g/dl). These findings indicate that while mono-infection with D. lanceatum induces moderate hematological alterations, concurrent infection with babesiosis leads to severe systemic disturbances characterized by anemia, leukocytosis, and hepatic dysfunction. Early diagnosis and integrated parasite control strategies are therefore essential to reduce disease severity and associated economic losses in sheep production.

Feed-borne Salmonella enterica contamination remains a major challenge in commercial poultry production, adversely affecting bird health, growth performance, and food safety. Intestinal colonization by Salmonella can impair nutrient absorption, induce systemic stress, and compromise productivity in broilers. The current study was conducted to evaluate the dose-dependent potential of dietary Salmonella enterica serovar Typhimurium contamination on growth performance, hematological and serum biochemical parameters, intestinal histomorphometry, and histopathological alterations in broiler chickens. A total of 120 one-day-old Cobb 500 broiler chicks were randomly allocated into four groups (n = 30). The control group received a non-contaminated basal diet, while treatment groups were fed diets contaminated with Salmonella at 0.5 × 10⁶, 1.0 × 10⁶, and 1.5 × 10⁶ CFU/L of feed for 42 days. Growth performance indices were recorded weekly. At day 42, blood samples were collected for hematological and biochemical analyses. Intestinal tissues were processed for histomorphometric measurements and histopathological scoring. Data were analyzed using one-way ANOVA, with significance declared at P &lt; 0.05. Salmonella contamination significantly reduced final body weight, average daily gain, and villus height, while increasing feed conversion ratio, mortality, crypt depth, and histopathological scores (P &lt; 0.05). Hemoglobin, packed cell volume (PCV), total erythrocyte count (TEC), total protein, albumin, sodium, and chloride levels decreased significantly, whereas total leukocyte count, heterophil-to-lymphocyte ratio, glucose, and potassium levels increased in a dose-dependent manner (P &lt; 0.05). Dietary Salmonella enterica contamination induced significant growth suppression, metabolic disturbances, hematological alterations, and intestinal damage in broilers in a dose-dependent manner. Strict feed hygiene, routine microbial monitoring, and enhanced biosecurity practices are strongly recommended to minimize feed-borne Salmonella contamination in commercial poultry operations.

The emergence of Plasmodium falciparum strains with reduced susceptibility to the artemisinin component of artemisinin combination therapies poses a serious threat to the treatment and control of malaria in sub-Saharan Africa. Regimens consisting of combinations of three or more conventional antimalarials have been proposed as a new treatment paradigm to overcome the impending problem of drug-resistant malaria. It was the aim of the MultiMal study to assess the safety, tolerability, and efficacy of the two novel multidrug antimalarial combination therapies, artesunate-pyronaridine-atovaquone-proguanil (APAP) and artesunate-fosmidomycin-clindamycin (AFC), in comparison with standard artesunate-pyronaridine (AP). This open-label, randomised, controlled, clinical, phase 2 trial was done in Lambaréné, Gabon, and Kumasi, Ghana. Patients with uncomplicated malaria who had fever or a history of fever in the preceding 24 h and a parasitaemia in the range of 1000-100 000 per μL of blood were enrolled. Random permuted blocks of variable block sizes stratified by country were computed to generate a treatment allocation sequence. Recruitment was done across three age groups: children aged 6 months to 10 years, adolescents aged 11-17 years, and adults aged 18-65 years. Weight-adjusted oral, once-daily therapy was administered for 3 consecutive days for AP and APAP regimens dosed according to the recommendations of the manufacturer and twice daily for AFC (dose: artesunate 2 mg/kg, fosmidomycin 30 mg/kg, and clindamycin 10 mg/kg). Participants were followed up over a 42-day period. The primary endpoints of the trial, related to pharmacokinetic analyses, are being reported elsewhere; this Article reports the secondary endpoints-safety, tolerability, and efficacy of the treatment regimens (defined as adequate clinical and parasitological response [ACPR]) at days 28 and 42 after treatment initiation. ACPRs were calculated in the intention-to-treat and PCR-corrected per-protocol populations at these timepoints, whereas safety and tolerability outcomes were assessed continuously over the 42-day follow-up period in the safety population. This trial is registered with pactr.samrc.ac.za, PACTR202008909968293 and is complete. Recruitment and follow-up took place between Jan 5 and Nov 5, 2021. Of 309 screened individuals, 100 patients with uncomplicated malaria were recruited into this clinical trial: 20 semi-immune patients aged 18-65 years, 40 adolescents aged between 11 and 17 years, and finally 40 patients aged 6 months to 10 years. PCR-corrected ACPR in the per-protocol set was 100% (95% CI 80-100) for AP, 100% (90-100) for APAP, and 97% (86-100) for AFC for day 28, and 87·5% (62-98) for AP, 85·3% (69-95) for APAP, and 94·4% (81-99) for AFC on day 42. Uncorrected ACPR in the intention-to-treat set was 85% (95% CI 62-97%) for AP, 87·5% (73-96) for APAP, and 82·5% (67-93) for AFC on day 28, and 70% (46-88) for AP, 75% (59-87) for APAP, and 75% (59-87) for AFC on day 42. There was no evidence for a differential efficacy across AP, APAP, and AFC. The proportion of patients with treatment-emergent adverse events (TEAEs) did not differ across study groups (p=0·37) and all treatment regimens were safe. Three (7%) of 46 TEAEs in the APAP group were severe compared with two (10%) of 20 in the AP control group and zero of 56 in the AFC group; all severe TEAEs were haematological alterations. The other TEAEs were mild or moderate. Moreover, there were two serious adverse events (SAEs) in the APAP group (peptic ulcer disease and chest contusion) and none in the other groups; these SAEs were rated as not related to the study medication. Antimalarial regimens of APAP and AFC have unique characteristics to tackle the development and spread of drug-resistant P falciparum malaria. Given that APAP and AFC were safe, well tolerated, and highly efficacious in this clinical phase 2 study, they constitute promising multidrug combination regimens for further clinical development. German Center for Infection Research.

Age and sex specific biomarker profiling of malaria infection in Ghana: Implications for demographic-tailored clinical management

Hookworm infections remain a major public health concern in endemic areas, modulating both the adaptive and innate immune systems. While the type 2 response is well-characterised, the roles of T follicular helper (Tfh), Th17, and IL-9-producing lymphocytes remain poorly defined. Here, we characterised these T cell subsets in individuals naturally infected with hookworms. From 1500 faecal samples screened, 60 were positive for hookworms, and peripheral blood was collected from 10 uninfected controls from endemic (NEG END) and non-endemic (NEG NE) areas, as well as from 7 infected individuals before (HKW BT) and after (HKW PT) treatment. Infected individuals displayed haematological alterations, including anaemia (n = 2), eosinophilia (n = 1), monocytosis (n = 4), and lymphocytosis (n = 3), along with an expansion of PBMCs, particularly Tfh cells, during infection. Expression of IL-9 and IL-10 by Tfh cells was markedly elevated after treatment. In contrast, individuals from non-endemic areas displayed a distinct baseline profile with higher Tfh activation (CD69) expression, suggesting immune adaptation in endemic settings. While IL-10-producing Tfh expanded during infection, IL-9-producing cells and Th17 cells expanded mainly after treatment. These findings suggest that individuals living in endemic areas, regardless of infection status, exhibit signs of persistent antigenic stimulation that promote a more tolerogenic and regulated immune profile. Moreover, hookworm infection and subsequent treatment reshape the immune landscape, highlighting the contribution of Tfh- and Th17-associated pathways, as well as IL-9 and IL-10 production, in modulating host-parasite interactions.

Quantum dots (QDs), especially metal oxide QDs, possess properties such as size-tunable band gaps and a high surface-to-volume ratio that are exceptionally advantageous in biomedical applications. In this study, we synthesized zinc oxide quantum dots (ZnO-QDs) and polyethylene glycol (PEG) functionalized ZnO-QDs (PFQD) and characterized them using transmission electron microscopy, UV-vis absorption spectroscopy, Fourier-transform infrared spectroscopy, and X-ray diffraction. An in vivo acute toxicity analysis of ZnO-QD and PFQD was conducted over 96h. The LD50 values for both the ZnO-QD and PFQD were 144.082 and 225.246µg/g b.w., respectively. Following the acute toxicity assessment, a sub-acute toxicity test was conducted to assess the effects on bioaccumulation, as well as hematological, histological, and enzymatic parameters, oxidative responses, and genotoxicity in fish. This was achieved by administering 1/50 of the LD50 values of the acute dose to fish, alongside a control group, over 14days. PFQD relative to the ZnO-QD nanoparticles showed significantly lower bioaccumulation of Zn levels (ppm/g) in both liver and head kidney tissues (p < 0.05). ZnO-QD exposure reduced erythrocyte count, hemoglobin levels, and hematocrit, with increased leukocyte and platelet counts, while PFQD caused fewer hematological alterations. According to serum biochemical indicators, ZnO-QD exposure caused hepatic and renal damage, inflammation, histopathological changes, and an apoptotic assay (as determined from DNA laddering and DAPI Annexin V-FITC staining), contrasting with PFQD. In the liver and kidney, macrophages (Kupffer and mesangial cells) showed that ZnO-QDs enhanced lipid peroxidation and significantly lowered antioxidant defenses. In contrast, PFQD decreased LPO and increased antioxidant enzyme activity. In conclusion, this study suggests that PFQD exhibits superior radical scavenging capabilities, positioning it as a potential antioxidant and a better biocompatible agent.

HIV infection profoundly impacts both the immune and hematologic systems. This retrospective study aimed to assess the effect of CD4+ T-cell depletion on peripheral immune and hematologic cell populations in 1293 people living with HIV (PLWH). Patients with CD4+ counts < 200 cells/µL exhibited significant reductions in neutrophils (4000 ± 1200 cells/µL), eosinophils (150 ± 50 cells/µL), basophils (30 ± 10 cells/µL), monocytes (300 ± 100 cells/µL), erythrocytes (4.3 ± 0.6 × 106/µL), and platelets (268 ± 78 × 103/µL). As evaluated in 93 PLWH cases, B cells showed a similar trend (150 ± 50 cells/µL), while the decrease of NK cells was not significant (200 ± 70 cells/µL),. In parallel, we observed a compensatory increase in CD8+ T lymphocytes (850 ± 300 cells/µL). These findings highlight the complex interplay between CD4+ T-cell depletion and both immune and hematologic cells in the context of HIV infection, which emphasizes the need for integrated monitoring to inform targeted interventions and optimize clinical outcomes.

Background: Acute leukemia is a malignant hematological disorder characterized by abnormal proliferation of immature cells in the bone marrow, leading to impaired hematopoiesis. Histological evaluation of bone marrow combined with hematological analysis is essential for differentiating acute myeloid leukemia (AML) from acute lymphoblastic leukemia (ALL). Methods: This study included 50 adult patients (16–78 years) diagnosed with acute leukemia between September 2023 and January 2024 at the Hematology Unit, Baghdad Teaching Hospital, Medical City, Baghdad. Diagnosis was confirmed using flow cytometry. Hematological parameters, including white blood cells (WBCs), red blood cells (RBCs), hemoglobin (HB), and platelets (PLTs), were assessed. Bone marrow aspirates and biopsy samples were obtained and examined histologically using routine and special staining techniques to compare findings between AML and ALL. Results: Statistical analysis showed a significant difference in platelet counts between AML and ALL patients (P &lt; 0.05), while no significant differences were observed for WBCs, RBCs, or HB. Fever and pallor were the most common clinical manifestations, followed by bleeding and generalized pain in both leukemia types. Histological examination revealed marked bone marrow abnormalities, including hypercellularity, increased fatty infiltration, fibrosis, and replacement of normal hematopoietic tissue. Conclusion: Acute leukemia is associated with significant hematological and histopathological alterations in the bone marrow. Platelet count may serve as a useful parameter for differentiating AML from ALL, while histological findings highlight severe disruption of normal marrow architecture in both conditions.

Chronic exposure to cement dust is an occupational hazard associated with systemic inflammation, oxidative stress, and haematological dysfunction. Cement dust contains silica and heavy metals, which can trigger immune activation, oxidative damage, and alterations in trace element homeostasis, particularly among workers in developing countries. This study assessed the impact of chronic cement dust exposure on haematological indices, inflammatory response, oxidative balance, and trace element status among industrial and non-industrial block molders in Benin City, Nigeria. A cross-sectional study was conducted involving 205 participants: 80 industrial block molders, 80 non-industrial block molders, and 45 unexposed controls. Blood parameters measured included red blood cell count (RBC), haemoglobin, white blood cell count (WBC), erythrocyte sedimentation rate (ESR), interleukin-10 (IL-10), total antioxidant status (TAS), calcium, and zinc levels, using automated analyzers and immunoassays. Data were analyzed using ANOVA, with significance set at p&lt;0.05. Compared to controls, exposed workers exhibited significant reductions in RBC count and haemoglobin levels, indicating anaemia (p=0.001). Inflammatory markers ESR and IL-10 were significantly elevated in both exposed groups (p=0.001), suggesting persistent systemic inflammation. Total antioxidant status was reduced (p=0.001), reflecting oxidative stress. Trace element analysis showed zinc depletion and calcium elevation (p=0.001). The industrial block molders demonstrated more pronounced hematological and biochemical alterations than non-industrial molders. Chronic cement dust exposure impairs haematological function through mechanisms involving inflammation and oxidative stress and disrupts trace element balance. These findings highlight the need for occupational health interventions, including dust control, consistent use of personal protective equipment, and routine health monitoring of exposed workers.