The Burden of Surgical Site Infection at Hospital Universiti Sains Malaysia and Related Postoperative Outcomes: A Prospective Surveillance Study.

Surgical site infections (SSIs) are the most common healthcare-associated infections that occur among surgical patients. Surgical site infections result in longer hospital stays, hospital readmissions, and higher death and morbidity rates. The current study was designed to highlight the importance of such surveillance studies in a Malaysian surgical population with a motive to evaluate and revise concurrent infection control and prevention policies by exploring the burden of surgical site infection and identifying its associated risk factors for future considerations. In this prospective observational cohort study, a total of 216 patients admitted to a surgical ward were identified and studied. Of these 216 patients, 142 elective procedures and 74 emergency procedures were included in the study, of which 13 patients (9.2%) undergoing elective procedures and 15 (20.3%) patients undergoing emergency procedures were SSI positive (OR: 2.5, p = 0.02). Among surgical site infections, 21 were superficial and 7 were deep incisional SSI. No case of organ/space SSI was identified. The time taken for SSIs to develop ranged from 2-17 days with a median of 6 days. Risk factors such as presence of comorbidities (p = 0.011), major co-existing medical diagnosis ≥2 (p = 0.02), and pre-existing infection (p = 0.027) were statistically significant. SSI-positive patients experienced an increase in the post-operative length of hospital stay. In the current population, it was seen that identifying patients who were at high risk of malnutrition via MUST and the NNIS risk index will help clinicians in identifying high risk patients and in managing their patients appropriately. Identifying patients who were at high risk of malnutrition will also improve postoperative outcomes considerably.

Plant growth promoting and antifungal asset of indigenous rhizobacteria secluded from saffron (Crocus sativus L.) rhizosphere.

Saffron (Crocus sativus L.) is an important plant in medicine. The Kashmir Valley (J&K, India) is one of the world's largest and finest saffron producing regions. However, over the past decade, there has been a strong declining trend in saffron production in this area. Plant Growth Promoting Rhizobacteria (PGPR) are free living soil bacteria that have ability to colonize the surfaces of the roots and ability to boost plant growth and development either directly or indirectly. Using the efficient PGPR as a bio-inoculant is another sustainable agricultural practice to improve soil health, grain yield quality, and biodiversity conservation. In the present study, a total of 13 bacterial strains were isolated from rhizospheric soil of saffron during the flowering stage of the tubers and were evaluated for various plant growth promoting characteristics under in vitro conditions such as the solubilization of phosphate, production of indole acetic acid, siderophore, hydrocyanic acid, and ammonia production and antagonism by dual culture test against Sclerotium rolfsii and Fusarium oxysporum. All the isolates were further tested for the production of hydrolytic enzymes such as protease, lipase, amylase, cellulase, and chitinase. The maximum proportions of bacterial isolates were gram-negative bacilli. About 77% of the bacterial isolates showed IAA production, 46% exhibited phosphate solubilization, 46% siderophore, 61% HCN, 100% ammonia production, 69% isolates showed protease activity, 62% lipase, 46% amylase, 85% cellulase, and 39% showed chitinase activity. Three isolates viz., AIS-3, AIS-8 and AIS-10 were found to have the most plant growth properties and effectively control the growth of Sclerotium rolfsii and Fusarium oxysporum. The bacterial isolates were identified as Brevibacterium frigoritolerans (AIS-3), Alcaligenes faecalis subsp. Phenolicus (AIS-8) and Bacillus aryabhattai (AIS-10) respectively by 16S rRNA sequence analysis. Therefore, these isolated rhizobacterial strains could be a promising source of plant growth stimulants to increase cormlets growth and increase saffron production.

In vitro effects of cobalt nanoparticles on aspartate aminotransferase and alanine aminotransferase activities of wistar rats.

Cobalt nanoparticles (Co-NPs) have been extensively used in clinical practices and medical diagnosis. In this study, the potential toxicity effects of Co-NPs with special emphasis over the biochemical enzyme activities, such as aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) in serum, liver, and kidney of Wistar rats were investigated. This toxicity measurement of nanomaterials can support the toxicological data. The biochemical enzymatic variations are powerful tools for the assessment of toxicity. ASAT and ALAT enzymes have been widely used to predict tissue-specific toxicities associated with xenobiotic. The biochemical changes induced by Co-NPs have significance in their toxicological studies because the alterations in biochemical parameters before clinical symptoms indicate either their toxicant safety or detrimental effect. Herein, Co-NPs with particle size <50 nm significantly activated ASAT and ALAT enzymes in the serum, liver, and kidney of rats at concentration-dependent order.

Comparative study of toxicological assessment of yttrium oxide nano- and microparticles in Wistar rats after 28 days of repeated oral administration.

Despite their enormous advantages, nanoparticles (NPs) have elicited disquiet over their safety. Among the numerous NPs, yttrium oxide (Y2O3) NPs are utilised in many applications. However, knowledge about their toxicity is limited, and it is imperative to investigate their potential adverse effects. Therefore, this study explored the effect of 28 days of repeated oral exposure of Wistar rats to 30, 120 and 480 mg/kg body weight (bw) per day of Y2O3 NPs and microparticles (MPs). Before initiation of the study, characterisation of the particles by transmission electron microscopy, dynamic light scattering, Brunauer-Emmett-Teller and laser Doppler velocimetry was undertaken. Genotoxicity was evaluated using the comet and micronucleus (MN) assays. Biochemical markers aspartate transaminase, alanine transaminase, alkaline phosphatase, malondialdehyde, superoxide dismutase, reduced glutathione, catalase and lactate dehydrogenase in serum, liver and kidney were determined. Bioaccumulation of the particles was analysed by inductively coupled plasma optical emission spectrometry. The results of the comet and MN assays showed significant differences between the control and groups treated with 120 and 480 mg/kg bw/day Y2O3 NPs. Significant biochemical alterations were also observed at 120 and 480 mg/kg bw/day. Haematological and histopathological changes were documented. Yttrium (Y) biodistribution was detected in liver, kidney, blood, intestine, lungs, spleen, heart and brain in a dose- and the organ-dependent manner in both the particles. Further, the highest levels of Y were found in the liver and the lowest in the brain of the treated rats. More of the Y from NPs was excreted in the urine than in the faeces. Furthermore, NP-treated rats exhibited much higher absorption and tissue accumulation. These interpretations furnish rudimentary data of the apparent genotoxicity of NPs and MPs of Y2O3 as well as the biodistribution of Y. A no-observed adverse effect level of 30 mg/kg bw/day was found after oral exposure of rats to Y2O3 NPs.

Acute and subacute oral toxicity of copper oxide nanoparticles in female albino Wistar rats.

The extensive use of copper oxide nanoparticles (CuO-NPs) in various industries and their wide range of applications have led to their accumulation in different ecological niches of the environment. This excess exposure raises the concern about its potential toxic effects on various organisms including humans. However, the hazardous potential of CuO-NPs in the literature is elusive, and it is essential to study its toxicity in different biological models. Hence, we have conducted single acute dose (2000 mg/kg) and multiple dose subacute (30, 300 and 1000 mg/kg daily for 28 days) oral toxicity studies of CuO-NPs in female albino Wistar rats following OECD guidelines 420 and 407 respectively. Blood analysis, tissue aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and acetylcholinesterase, superoxide dismutase, catalase, lipid malondialdehyde and reduced glutathione assays, and histopathology of the tissues were carried out. The higher dose treatments of the acute and subacute study caused significant alterations in biochemical and antioxidant parameters of the liver, kidney and brain tissues of the rat. In addition, histopathological evaluation of these three organs of treated rats showed significantly high abnormalities in their histoarchitecture when compared to control rats. We infer from the results that the toxicity observed in the liver, kidney and brain of treated rats could be due to the increased generation of reactive oxygen species by CuO-NPs.

Toxicological assessment of tungsten oxide nanoparticles in rats after acute oral exposure.

Advances in and the rapid growth of the nanotechnology sector have escalated manufacture of nanoparticles (NPs), resulting in a significant increase in the probability of exposure of humans and wildlife to these materials. Many NPs have been found to exert genotoxicity. Therefore, genotoxicity studies are mandatory to assess the toxicity of NPs as a concern of succumbing to genetic diseases and cancers are universal. Tungsten oxide (WO3) NPs are being explored extensively in various fields. However, the toxicological data of WO3 NPs by oral route in mammals is limited. Hence, the goal of the current investigation was to evaluate the acute toxicity of WO3 NPs and microparticles (MPs) after single oral administration with 100, 500 and 1000 mg/kg body weight doses in female Wistar rats. TEM, dynamic light scattering and laser Doppler velocimetry techniques were used to characterise the particles. The genotoxicity studies were conducted using comet, micronucleus and chromosomal aberration assays. Alterations in biochemical indices and metal distribution in various organs were also evaluated. The mean size of WO3 NPs and MPs by TEM was 53.2 ± 1.91 nm and 5.17 ± 3.18 µm, respectively. The results revealed a significant increase in DNA damage and micronuclei and chromosomal aberrations after exposure to 1000 mg/kg dose of WO3 NPs. Significant alterations in aspartate transaminase, alanine transaminase, reduced glutathione, catalase and malondialdehyde levels in serum and liver were found only at the higher dose of WO3 NPs. Tungsten (W) biodistribution was observed in all the tissues in a dose-, time- and organ-dependent manner. In addition, the maximum concentration of W was found in the liver and the least in the brain was observed. The test substances were found to have a relatively low acute toxicity hazard. The data obtained gives preliminary information on the potential toxicity of WO3 NPs and MPs.

Design, synthesis and immunological evaluation of 1,2,3-triazole-tethered carbohydrate-Pam3Cys conjugates as TLR2 agonists.

Novel triazolyl Pam3Cys conjugates encompassing various carbohydrate entities have been synthesized by copper mediated azide-alkyne click chemistry protocol with a view to probe the SAR pertaining to their adjuvant activity in conjunction with OVA as antigen. The preliminary ex vivo cytokine profiling revealed optimal Th1 activation and the in vivo adjuvant studies of ribose derived hybrid (6 e) revealed a marked improvement in the OVA specific antibody IgG response and Th1 cytokine expressions. The triazolyl Pam3Cys carbohydrate conjugates were found to be the hTLR2 agonists as revealed by their SEAP activity due to NFKB activation. The described protocol is the first successful attempt of the amalgamation of carbohydrate-Pam3Cys motifs tethered to a triazole linker as a peptide free adjuvant.

Assessment of genotoxic effects of lead in occupationally exposed workers.

The genotoxicological effects in 200 lead acid storage battery recycling and manufacturing industry workers in Hyderabad along with matched 200 controls were studied. The genetic damage was determined by comet, micronucleus (MN), and chromosomal aberration (CA) test in peripheral blood lymphocytes (PBL). The MN test was also carried out in buccal epithelial cells (BECs). Pb in ambient air, blood Pb (B-Pb) concentrations, and hematological parameters were measured. The superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx), and malondialdehyde (MDA) formed were also studied. The results of the present study showed that there was a statistically significant (P < 0.01) increase in mean percent tail DNA, frequency of CA, and MN in PBL as well as in BEC as compared to controls. Pb in ambient air and B-Pb concentrations were found to be significantly higher (P < 0.01). The hematocrit, hemoglobin, and red blood cell values were significantly lowered in Pb-exposed workers in comparison to controls. SOD, GPx, and CAT levels were significantly decreased while GSH and MDA levels increased in exposed group when compared to control group. The present study suggests that environmental health standards should be enforced to control Pb contamination from battery industries to reduce human health risk.

Toxicity study of cerium oxide nanoparticles in human neuroblastoma cells.

The present study consisted of cytotoxic, genotoxic, and oxidative stress responses of human neuroblastoma cell line (IMR32) following exposure to different doses of cerium oxide nanoparticles (CeO2 NPs; nanoceria) and its microparticles (MPs) for 24 hours. Cytotoxicity was evaluated by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide and lactate dehydrogenase assays whereas genotoxicity was assessed using the cytokinesis-block micronucleus and comet assays. A battery of assays including lipid peroxidation, reactive oxygen species (ROS), hydrogen peroxide, reduced glutathione, nitric oxide, glutathione reductase, glutathione peroxidase, superoxide dismutase, catalase, and glutathione S-transferase were performed to test the hypothesis that ROS was responsible for the toxicity of nanoceria. The results showed that nanosized CeO2 was more toxic than cerium oxide MPs. Hence, further study on safety evaluation of CeO2 NPs on other models is recommended.

Biochemical alterations induced by acute oral doses of iron oxide nanoparticles in Wistar rats.

Magnetic iron oxide nanoparticles with appropriate surface chemistry have been widely used with potential new applications in biomedical industry. Therefore, the aim of this study was to assess the size-, dose-, and time-dependent effects, after acute oral exposure to iron oxide-30 NP (Fe(2)O(3)-30), on various biochemical enzyme activities of clinical significances in a female Wistar rat model. Rats were exposed to three different doses (500, 1,000, and 2,000 mg/kg) of Fe(2)O(3)-30 and Fe(2)O(3)-Bulk along with control. Fe(2)O(3)-30 had no effect on growth, behavior, and nutritional performance of animals. Fe(2)O(3)-30 caused significant inhibition of acetylcholinestrase in red blood cells as well as in brains of treated rats. Further, more than 50% inhibition of total, Na(+)-K(+), Mg(2+), and Ca(2+)-ATPases activities, as observed in brains of exposed female rats, may be the result of disturbances in cellular physiology and the iono-regulatory process. Activation of the hepatotoxicity marker enzymes, aspartate aminotransferase and alanine aminotransferase, was recorded in serum and liver, whereas inhibition was observed in kidney. Similarly, enhancement of lactate dehydrogenase activity was observed in serum and liver; however, a decrease in enzyme levels was observed in kidneys of Fe(2)O(3)-30-treated rats. On the other hand, Fe(2)O(3)-Bulk did not depict any significant changes in these biochemical parameters, and alterations were near to control. Therefore, this study suggests that exposure to nanosize particles at acute doses may cause adverse changes in animal biochemical profiles. The use of the rat model signifies the correlation with the human system.

Repeated oral dose toxicity of iron oxide nanoparticles: biochemical and histopathological alterations in different tissues of rats.

Iron oxide (Fe2O3) nanoparticles are widely used in different fields of nanotechnology. However, studies on its toxicological effects in humans and the environment are scarce. Therefore in this investigation 28 days repeated dose oral toxicity studies were conducted on Fe2O3-30 nanoparticles and its counterpart Fe2O3-Bulk with special reference to target biochemical enzymes and histopathological changes in different tissues of female albino Wistar rats. The alterations observed after Fe2O3-30 treatment in various tissues of exposed rats were dose dependent. Low dose was less effective than medium and high doses with low dose demonstrating "no observed adverse effect" (NOAEL). Further, high dose treated rats showed toxic sign and symptoms but no mortality. Due to the repeated doses of Fe2O3-30 nanoparticles, significant inhibition was observed in total, Na(+)-K+, Mg2+ and Ca(2+)-ATPases in brain of exposed rats. Similarly, significant inhibition was recorded in RBC and brain acetylcholinesterase indicating that both synaptic transmission and nerve conduction were affected by this compound. Fe2O3-30 significantly increased aspartate amino transferase, alanine amino transferase and lactate dehydrogenase in serum and liver, whereas, these enzymes were significantly decreased in kidney indicating tissue necrosis and possible leakage of these enzymes into the blood stream. Increased levels of these enzymes in liver as well as in serum might be an adaptive mechanism due to the stress of iron nanoparticles. High dose treated rats of Fe2O3-30 showed dilated central vein, perivascular round cell collections in liver along with focal areas of necrosis, whereas kidney showed focal tubular damage and red pulp congestion, whereas prominent white pulp indices were observed in spleen. However, histopathological analysis of heart and brain tissues failed to show any adverse changes in their architecture exposed to repeated doses of Fe2O3-30 when compared with controls. Fe2O3-Bulk did not induce any adverse effects in either biochemical parameters or histopathology in the treated rats and the changes observed were near to controls and mostly insignificant, indicating that the counter part of nanoparticles i.e., bulk material is less potent than the nanoparticles in causing toxicity in the exposed animals. These results suggested that as particle size decreases, this iron nanoparticle showed increased toxicity, even though the same material is relatively inert in bulk form. The changes observed in these target enzyme activities could be useful as biomarkers of exposure to nanoparticles.

Oxidative stress induced by aluminum oxide nanomaterials after acute oral treatment in Wistar rats.

This study investigated the oxidative stress induced after acute oral treatment with 500, 1000 and 2000 mg kg⁻¹ doses of Al2O3 -30 and -40 nm and bulk Al2O3 in Wistar rats. Both the nanomaterials induced significant oxidative stress in a dose-dependent manner in comparison to the bulk. There was no significant difference between the two nanomaterials. However, the effect decreased with increase with time after treatment. The histopathological examination showed lesions only in liver with Al2O3 nanomaterials at 2000 mg kg⁻¹.

Genotoxicity in filling station attendants exposed to petroleum hydrocarbons.

OBJECTIVES: Biomonitoring of exposure in workplaces has gained importance in evaluation of human health hazards. Since occupational exposure to petroleum hydrocarbons may have deleterious effects, genotoxicity risk among 200 fuel filling station attendants (FFSAs) and 200 matched controls was investigated. METHODS: The probable genetic damage was determined by comet assay and micronucleus test in peripheral blood lymphocytes (PBL) of study subjects. Air and blood sample analysis was done to estimate the benzene, toluene, and xylene (BTX) concentrations using gas chromatography-mass spectrometry. The effect of exposure on antioxidant enzymes was also studied by determining the levels of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), and rate of lipid peroxidation measured as concentration of malondialdehyde (MDA) formed. RESULTS: The results of the present study suggest that there was a statistically significant increase in mean comet tail length (25.09 versus 10.27 µm) and frequency of micronuclei in PBL (11.83 versus 5.83 per thousand; P < 0.05) of FFSAs as compared to controls. BTX concentrations were found to be significantly higher in ambient air of petrol pumps and FFSAs showed elevated levels of these compounds in their breathing zone in comparison to controls (P < 0.05). Blood BTX levels were found to be significantly enhanced in FFSAs. SOD and GPx were significantly decreased with an increased rate of CAT and MDA in FFSAs as compared to controls. CONCLUSIONS: The results of our study suggest that exposure to BTX has the potential to cause genetic changes in the exposed subjects. The data highlight the need to maintain safety measures and intervention to minimize exposure.

Effects of a novel organophosphorus pesticide (RPR-V) on extra hepatic detoxifying enzymes after repeated oral doses in rats.

The effects of a novel organophosphorous pesticide, 2-butenoic acid-3-(diethoxy phosphinothionyl) ethyl ester (RPR-V) on glutathione S-transferases (GST), UDP-glucuronyl transferases (UDPGT) and the level of glutathione (GSH) were evaluated in rats after repeated oral administration at 33 microg kg(-1)day(-1) (low), 66 microg kg(-1)day(-1) (mid) and 99 microg kg(-1)day(-1) (high) for 90 days and at 28 days (withdrawal) post-treatment. GSH level and GST in kidney; GSH level in brain decreased significantly at mid and high doses on 45th and 90th day (P < 0.05). However, UDPGT activity in brain and kidney increased significantly at mid and high doses on 45th and 90th day (P < 0.05). Interestingly, the withdrawal study revealed that the effect was reversible 28 days after the treatment when all the enzymes reverted to levels close to those of controls. These results suggest that RPR-V has the potential to modulate the extrahepatic detoxifying enzymes and thereby interact with other physiological processes in the exposed organisms.