Assessment of Heavy Metal Contamination in Dust in Vilnius Schools: Source Identification, Pollution Levels, and Potential Health Risks for Children.

The main objective of this study is to thoroughly evaluate the diversity and sources of heavy metals in the school environment. Specifically, this study examines the presence of heavy metals in the dust found and collected from 24 schools in Vilnius. Employing hierarchical cluster analysis, principal component analysis, and positive matrix factorization, we identified combustion-related activities as primary contributors to elevated metal concentrations, notably zinc, scandium, and copper, with PM2.5/PM10 ratios indicating a combustion source. They reveal significant differences in the levels of elements such as arsenic (4.55-69.96 mg/kg), copper (51.28-395.37 mg/kg), zinc, and lead, which are affected by both local environmental factors and human activities. Elevated pollution levels were found in certain school environments, indicating environmental degradation. Pollution assessment and specific element pairings' strong positive correlations suggested shared origins or deposition processes. While this study primarily assesses non-carcinogenic risks to children based on a health risk assessment model, it acknowledges the well-documented carcinogenic potential of substances such as lead and arsenic. The research emphasizes the immediate necessity for efficient pollution management in educational environments, as indicated by the elevated hazard index for substances such as lead and arsenic, which present non-carcinogenic risks to children. This research offers important insights into the composition and origins of dust pollution in schools. It also promotes the need for broader geographic sampling and prolonged data collection to improve our understanding of pollution sources, alongside advocating for actionable strategies such as environmental management and policy reforms to effectively reduce exposure risks in educational settings. Furthermore, it aims to develop specific strategies to safeguard the health of students in Vilnius and similar urban areas.

Evaluation of histologic, antiapoptotic and antioxidant effects of melatonin against the acute ocular toxicity of Cisplatin.

This study aimed to investigate the protective effect of melatonin against the acute toxicity of cisplatin in ocular tissues. The eyes of 40 rats were divided into 4 groups: Control group (10 rats), Melatonin (Mel) group (10 rats), Cisplatin (Cis) group (10 rats), Melatonin (Mel) + Cisplatin (Cis) group (10 rats). Retina, cornea, and ciliary body tissues were examined after hematoxylin-eosin staining of sections obtained from the eyes and were scored for disorganization and degeneration. Apoptotic cells were counted for the retina, cornea, and ciliary body with the TUNEL (Terminal deoxynucleotidyl transferase dUTP nick end labeling) method. The total antioxidant status (TAS) / total oxidant status (TOS) of homogenized eye tissues were measured. While apoptotic cells were found to increase in the cornea of the Cisplatin (Cis) group, no difference was found regarding the retina and ciliary body cell count. An increased number of apoptotic cells in the cornea of the Cis group was found while there was a decrease in the group where Cisplatin and Melatonin were administered together (Mel+Cis group). There was no statistically significant difference amongst groups for TOS or TAS. Melatonin had a partial protective effect against histological damage.

L-Carnitine ameliorates the liver by regulating alpha-SMA, iNOS, HSP90, HIF-1alpha, and RIP1 expressions of CCL4-toxic rats.

OBJECTIVES: Carbon tetrachloride (CCL4) toxicity triggers fibrosis, activating various mechanisms within the cell. We aimed to create damage with CCL4 and investigate the effectiveness of L-carnitine on the mechanisms we identified. MATERIALS AND METHODS: Forty rats were divided into 5 groups with equal number of rats in each group. Group I: Control group, Group II: L-carnitine group, 200 mg/kg L-carnitine twice a week, Group III: CCL4 group, 0.2 ml/100 gr CCL4, IP, dissolved in olive oil 2 times a week during 6 weeks; Group IV: L-carnitine + CCL4 group, 200 mg/kg L-carnitine 24 hr before 0.2 ml/100 g CCL4 application twice a week; Group V: CCL4 + L-carnitine, 200 mg/kg L-carnitine half an hour after 0.2 ml/100 g CCL4 application. The liver was evaluated histologically. Immunohistochemically stained with α-SMA, iNOS, HSP90, HIF-1α, and RIP1. TNF-α, TGF-ß, AST, ALT, ALP, and GGT measurements were evaluated. RESULTS: In the classical lobule periphery, an increase in lipid accumulation and a decrease in glycogen accumulation were observed. After immunohistochemical measurements and biochemical analyzes, an increase in the expression density of all proteins was observed in group III. In group IV and V, an improvement in tissue and a decrease in protein expression densities were observed. CONCLUSION: iNOS serves as a free radical scavenger in response to damage caused by increased toxicity of α-SMA, HSP90, and HIF-1α. Especially, increased RIP1 level in the tissue indicates the presence of necrosis in the tissue after CCL4-toxicity. Supplementing the amount of endogenous L-carnitine with supplementation provides a significant improvement in the tissue.

Tumor necrosis factor alpha (TNF-alpha) receptor-II is required for TNF-alpha-induced leukocyte-endothelial interaction in vivo.

Tumor necrosis factor-alpha (TNF-alpha) binds to 2 distinct cell-surface receptors: TNF-alpha receptor-I (TNFR-I: p55) and TNF-alpha receptor-II (TNFR-II: p75). TNF-alpha induces leukocyte adhesion molecules on endothelial cells (ECs), which mediate 3 defined steps of the inflammatory response; namely, leukocyte rolling, firm adhesion, and transmigration. In this study, we have investigated the role of p75 in TNF-alpha-induced leukocyte adhesion molecules using cultured ECs derived from wild-type (WT), p75-null (p75-/-), or p55-null (p55-/-) mice. We observed that p75 was essential for TNF-alpha-induced E-selectin, vascular cell adhesion molecule 1 (VCAM-1), and intercellular adhesion molecule 1 (ICAM-1) expression. We also investigated the putative role of p75 in inflammation in vivo using an intravital microscopic approach with a mouse cremaster muscle model. TNF-alpha-stimulated leukocyte rolling, firm adhesion to ECs, and transmigration were dramatically reduced in p75-/- mice. Transplanted WT cremaster in p75-/- mice showed a robust leukocyte rolling and firm adhesion upon TNF-alpha activation, suggesting that the impairment in EC-leukocyte interaction in p75-/- mice is due to EC dysfunction. These results demonstrate, for the first time, that endothelial p75 is essential for TNF-alpha-induced leukocyte-endothelial-cell interaction. Our findings may contribute to the identification of novel p75-targeted therapeutic approaches for inflammatory diseases.

Extension of composite tissue allograft survival across major histocompatibility barrier under short course of anti-lymphocyte serum and cyclosporine a therapy.

In this study, the authors investigated the effects of combined use of cyclosporine A (CsA) and anti-lymphocyte serum (ALS) on the survival of rat hindlimb allografts across a fully allogeneic major histocompatibility complex (MHC) barrier between Brown-Norway rats (BN, RT1 n) and Lewis rats (LEW, RT1 l). Thirty transplantations were performed in five groups of six rats each: Group 1 was the isograft control; Group 2 was the allograft control; Group 3 received ALS, Group 4 received CsA, and Group 5 received CsA and ALS. Treatment was started 2 hr before surgery and was then given for 21 days. Donor-derived chimerism was monitored by FACS analysis. Survival time was calculated as the number of post-transplant days until the first signs of rejection. The allografts in Group 2, Group 3, and Group 4 survived a mean of 5, 6, and 33 days, respectively. The longest mean survival time-51 days-was noted in Group 5 (p<0.05). Donor- derived chimerism peaked at 17 percent and fell to 0 percent at the time of rejection. A combined protocol of ALS/CsA extended survival of rat hindlimb allografts across a fully allogeneic MHC barrier.

[The injection of acrylic bone cement prevents bone collapse in the intercalar bones lacking bony support: an experimental sheep semilunar bone model]. / Akrilik kemik çimentosu enjeksiyonu kemik doku destegini yitirmis interkalar kemiklerde olusan çökmeyi önleyebilir.

OBJECTIVES: In a sheep semilunar bone model, we investigated whether collapse in the intercalar bones lacking bony support could be prevented by the injection of acrylic bone cement. METHODS: The study included 16 limbs of eight sheep. Preoperatively, anteroposterior and lateral views of the carpal joints in the fore limbs were obtained. The animals were divided into four groups. In group 1 (n=3) no surgical procedure was performed in the right semilunar bones, whereas the periosteum on the contralateral side was elevated (group 2; n=3). The first two groups were left as controls. In Group 3 (n=5) the left semilunar bones were filled with acrylic bone cement following decancellation of the bone, while the right semilunar bones were left decancellated (group 4; n=5). The sheep were monitored for three months. Radiographs of the carpal joints were obtained to evaluate collapse occurrence in the semilunar bones. Thereafter, the animals were sacrificed and the semilunar bones were excised for biomechanical and histological examinations. Osteonecrosis and cartilage damage were sought and resistance to compressive forces was investigated. RESULTS: Radiologically, the extent of collapse was statistically significant in the semilunar bones in group 4 (p<0.05). The use of acrylic bone cement was found to prevent collapse in group 3, with no significant difference being noted between preoperative and postoperative semilunar bone heights (p>0.05). Biomechanically, the least resistance to compressive forces was measured in group 4 (p<0.05). Histologically, cartilage damage and osteonecrosis were only seen in group 4. CONCLUSION: Our data suggest that the use of acrylic bone cement prevents collapse in the semilunar bones, without inducing any cartilage damage or osteonecrosis.

A novel technique for peripheral nerve repair.

OBJECTIVE: To evaluate a novel technique for the repair of neural deficits using a single fascicle to bridge an injury in the rat sciatic nerve. STUDY DESIGN: Twenty-four male Lewis rats were divided into four groups as follows: group 1 (control group), 1.5-cm deficit without repair; group 2, conventional epineural repair with autografts (100% diameter); group 3, nerve repair with large single autograft fascicle (50% diameter); and group 4, nerve repair with small single autograft fascicle (25% diameter). METHODS: Nerve regeneration was evaluated at 3, 6, and 12 weeks by somatosensory evoked potential (SSEP) evaluation and standardized pin-prick and toe-spread tests. Nerve samples were harvested at 12 weeks and stained with toluidine blue to assess the total number of myelinated axons, axon area, and myelin sheath thickness. RESULTS: In group I, the pin-prick and toe-spread tests showed no response at 3, 6, and 12 weeks. Rats in groups 3 and 4 demonstrated significantly better pin-prick test results and a trend toward better toe-spread test responses compared with conventional-repair animals. The SSEP evaluations displayed nondiagnostic waves in rats in group 1 rats. There was no evidence that the other surgery groups differed significantly in median SSEP latencies. Histological evaluation revealed fibrosis in rats in group 1 rats and a significantly higher median number of axons and myelin thickness in the small single fascicle (1296 axons and 4.22 microm, respectively) and large fascicle (2682 axons and 4.62 microm, respectively) groups compared with the conventional autograft group (630 axons and 2.93 microm, respectively). The small fascicle group had a significantly greater mean axon area (58.59 micro m2) than the large fascicle (29.66 micro m2) and conventional autograft (25.35 micro m2) groups. CONCLUSIONS: Peripheral nerve repair using a single fascicle graft resulted in better functional recovery and morphometric outcome without a significant difference in electrophysiological status compared with conventional nerve repair. This technique may provide expanded sources of nerve autografts and alleviate the morbidity of harvesting peripheral nerves from multiple sites for individuals with extensive peripheral nerve injuries.

Development of mouse cremaster transplantation model for intravital microscopic evaluation.

OBJECTIVE: In this study, we investigated the possibility of transplanting cremaster muscle in mice. After transplantation, we measured the microcirculatory parameters and compared with the cremaster-control values with no transplantation. METHODS: In group 1 (n = 10, C57BL/6N), normal cremaster microcirculation parameters were measured without transplantation. In group 2 (n = 6), isograft transplantations were performed between C57BL/6N mice. After transplantation, standard microcirculatory parameters were measured for 3 hours in both groups. RESULTS: The procedure was performed with a 95% success rate and 75 minutes of ischemia time. Functional capillary perfusion, diameters, and red blood cell velocities of the first-, second-, and third-order arterioles and veins showed significant decreases in the isograft group within the first 2 hours (p < 0.05) but returned to normal values at the third hour. The number of rolling, adhering, and transmigrating leukocytes and lymphocytes also showed an increase in the isograft group within the first and second hours (p < 0.05, compared to cremaster control). CONCLUSIONS: Leukocyte/endothelial interaction and hemodynamic parameters of muscle flap circulation displayed the effects of ischemia in the isograft group. The cremaster muscle transplantation in mice was found to be a reliable and reproducible model offering the unique possibility of observing and studying the leukocyte-endothelial interaction during ischemia/reperfusion injury and allograft rejection using intravital microscopy.

Effect of chronic cyclosporine administration on peripheral nerve regeneration: a dose-response study.

An experimental study was conducted to investigate the effect of chronic cyclosporine A (CsA) administration with different doses on peripheral nerve regeneration. Forty adult male Lewis rats weighing 150 to 200 g were used. The right sciatic nerve was transected 1 cm distal to the sciatic notch, and a conventional end-to-end nerve coaptation was performed. According to the daily dose of subcutaneous CsA injections, animals were randomized into one control group and four experimental groups of 8 animals each (group I, control with no treatment; group II, 2 mg per kilogram CsA; group III, 4 mg per kilogram CsA; group IV, 8 mg per kilogram CsA; and group V, 16 mg per kilogram CsA). Daily injections of CsA were administered for 12 weeks by an investigator blinded to the different treatment groups. At 3, 6, and 12 weeks after nerve repair, motor recovery was evaluated by the toe spread test, and sensory recovery was measured using the pin-prick test and somatosensory evoked potentials (SEPs). Evaluations were performed by an investigator who was blinded to the treatment groups. At 12 weeks, sciatic nerve samples were harvested for histomorphometric analysis. Motor recovery was retarded regardless of CsA dose at each time point of evaluation. Sensory recovery was only delayed in the 16-mg-per-kilogram CsA treatment group at the 3 week follow-up. SEP results revealed significantly prolonged N2 and P1 latencies in all CsA treatments regardless of dose and time frame of evaluation compared with the control group (p < 0.05). Histomorphometric analysis demonstrated significantly reduced numbers of myelinated axons, reduced myelin sheath thickness, and reduced diameters in all CsA treatment groups compared with the control group (p < 0.05). Based on these findings in this experimental model of sciatic nerve, the authors conclude that CsA overall had direct deleterious effects on peripheral nerve regeneration as demonstrated by SEP, pin-prick test, toe spread test, and histomorphometric nerve analysis. These adverse effects seemed to be dose related for sensory recovery only at 3 and 6 weeks of CsA exposure after nerve repair. Motor recovery was affected negatively by short- and long-term CsA administration regardless of dose.

Effect of long-term cyclosporine administration on muscle flap hemodynamics.

Long-term use of cyclosporine A (CsA) is associated with deleterious effects such as nephrotoxicity and hypertension as a result of its toxicity on microvasculature. These effects raise the possibility that long-term CsA use harms the microvasculature of the skeletal muscle tissue. An experimental study was conducted to investigate the effect of chronic systemic cyclosporine administration on the microvasculature of the cremaster flap model in the rat. Thirty male Sprague-Dawley rats were divided into five groups of 6 animals each. The control group received no treatment. The four CsA treatment groups received a daily subcutaneous injection of 2 mg per kilogram, 4 mg per kilogram, 8 mg per kilogram, and 16 mg per kilogram of cyclosporine for 6 weeks before surgery. The effect of long-term CsA administration on cremaster flap microcirculation was evaluated in vivo using an intravital microscopy system. Hemodynamic parameters of the cremaster muscle flap such as vessel diameter, red blood cell velocity, capillary density, leukocyte-endothelial interaction, and microvascular permeability were measured. There was no significant (p > 0.05) difference in vessel diameter in all groups. There was a significant increase in the number of adherent leukocytes in the 8-mg and 16-mg CsA group compared with the control (12 +/- 4.8 leukocytes per 100 microm and 12 +/- 4.5 leukocytes per 100 microm vs. 6 +/- 4.3 leukocytes per 100 microm; p < 0.05). Microvascular permeability indices increased significantly at 0 and 30 minutes after fluorescent isothiocyanate-albumin injection in the 8-mg and 16-mg CsA groups compared with the control (0 minutes: 0.6 +/- 0.2% and 0.5 +/- 0.1% vs. 0.4 +/- 0.05%; 30 minutes: 0.8 +/- 0.2% and 0.7 +/- 0.1% vs. 0.5 +/- 0.04%; p < 0.05). Histologically, the cremaster muscle flaps in all cyclosporine groups showed evidence of interstitial inflammation and venous vasculitis. In the 8-mg and 16-mg CsA groups there was also focal muscle injury. The toxic effect of CsA on the microvascular tree of a muscle flap was demonstrated by the increased permeability index in vivo, and the moderate venulitis and focal muscle injury histologically. Systemic CsA administration seems to have minimal impact on the viability of the muscle flaps, which was confirmed by preserved capillary function and muscle flap perfusion. These data suggest that there is a minimal risk in undertaking a pedicled muscle flap transfer procedure using a CsA immunosuppressive protocol.