Environmental remediation of hazardous pollutants using MXene-perovskite-based photocatalysts: A review.

Photocatalysis utilizing semiconductors offer a cost-effective and promising solution for the removal of pollutants. MXene and perovskites, which possess desirable properties such as a suitable bandgap, stability, and affordability, have emerged as a highly promising material for photocatalytic activity. However, the efficiency of MXene and perovskites is limited by their fast recombination rates and inadequate light harvesting abilities. Nonetheless, several additional modifications have been shown to enhance their performance, thereby warranting further exploration. This study delves into the fundamental principles of reactive species for MXene-perovskites. Various methods of modification of MXene-perovskite-based photocatalysts, including Schottky junction, Z-scheme and S-scheme are analyzed with regard to their operation, differences, identification techniques and reusability. The assemblance of heterojunctions is demonstrated to enhance photocatalytic activity while also suppressing charge carrier recombination. Furthermore, the separation of photocatalysts through magnetic-based methods is also investigated. Consequently, MXene-perovskite-based photocatalysts are seen as an exciting emerging technology that necessitates further research and development.

Humoral response to SARS-CoV-2 vaccines among healthcare workers in a tertiary hospital in Malaysia.

INTRODUCTION: Healthcare workers (HCWs) were among the first to be fully vaccinated against SARS-CoV-2. However, the antibody responses to the vaccines and potential decline among Malaysian HCW are still unclear. The objective of this study is to follow-up anti-S antibody levels among HCW vaccinated with mRNA vaccine (BTN162b2) and inactivated vaccine (CoronaVac). MATERIALS AND METHODS: Plasma samples were collected prevaccination, 2 weeks and 6 months post-vaccination and tested for total immunoglobulin levels using ELISA method. RESULTS: A small percentage of HCW (2.2%, 15/677) had elevated anti-S antibody levels in their pre-vaccination plasma samples (median 20.4, IQR 5.8), indicating that they were exposed to SARS-CoV-2 infection prior to vaccination. The mRNA vaccine significantly increased anti-S levels of both previously infected and uninfected individuals to saturation levels (median 21.88, IQR.0.88) at 2 weeks postsecond dose of the vaccine. At 6 months post-vaccination, the antibody levels appeared to be maintained among the recipients of the mRNA vaccine. However, at this time point, anti-S antibody levels were lower in individuals given inactivated vaccine (median 20.39, IQR 7.31, n=28), and interestingly, their antibody levels were similar to anti-S levels in pre-vaccination exposed individuals. Antibody levels were not different between the sexes. CONCLUSION: Anti-S levels differ in individuals given the different vaccines. While further study is required to determine the threshold level for protection against SARSCoV- 2, individuals with low antibody levels may be considered for boosters.

Electron field emission from carbon nanotubes in air for excitation of atmospheric pressure microplasma.

Electron field emission (FE) from carbon nanotubes (CNTs) in air for excitation of atmospheric pressure microplasma was investigated in a scanning electron microscope (SEM). The results showed that, the FE properties of CNTs at 10 kPa and lower pressures were the same as those in vacuum. At pressures more than 10 kPa, the FE threshold voltages in air were higher than those in vacuum and increased with increasing air pressure. When the FE threshold voltage became higher than the gas breakdown voltage, microplasma was ignited before FE appearance. FE properties of CNTs were stable in air before appearing gas discharges.

Thiol proteinase inhibitor in the ascitic fluid of sarcoma 180 tumor-bearing mice.

A thiol proteinase inhibitor (TPI) has been purified from the ascitic fluid of Sarcoma 180 tumor-bearing mice. The molecular weight of the inhibitor was estimated to be 67,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the substance inhibited papain, cathepsins B and L, but not cathepsins H and D and trypsin. The inhibitor also liberated kinin upon treatment with trypsin or mouse glandular kallikrein, indicating that the inhibitor is a kininogen, and the kinin liberated upon trypsinization was identified as bradykinin. An immunoreactive TPI with a molecular weight indistinguishable from that of the ascites TPI was found in plasma of non-tumor-bearing mice as well as that of tumor bearers. Plasma levels of immunoreactivity were increased up to twice the normal levels in tumor bearers inoculated with Sarcoma 180 or 3LL tumor cells. Supplementation of the purified ascites TPI into Sarcoma 180 culture medium caused a significant suppression of cell growth as well as [3H]thymidine incorporation at a concentration below that normally present in plasma. In contrast, addition of ascites-TPI to cultured mouse embryonic cells caused enhancement of cell growth as well as [3H]thymidine incorporation. These results indicate that in mice responding to tumor growth, a TPI corresponding to a kininogen is induced which may regulate tumor growth by countering tumor-related proteolytic activity.

Supplementation with beta-carotene in vivo and in vitro does not inhibit low density lipoprotein oxidation.

The inhibition of low density lipoprotein (LDL) oxidation has been postulated as one mechanism by which antioxidants may prevent the development of atherosclerosis. Available data on the ability of beta-carotene to inhibit LDL oxidation are conflicting. We examined the role of in vivo and in vitro supplementation with beta-carotene on metal ion-dependent (cupric ions, Cu2+) and metal ion-independent (2,2'-azobis[2-amidinopropane]dihydrochloride, AAPH) oxidation of LDL as measured by the formation of conjugated dienes (absorbance at 234 nm). Sixteen subjects were supplemented with 50-100 mg of beta-carotene on alternate days for 3 weeks following a week-long loading dose of 100 mg/day. Plasma beta-carotene levels rose 5.5-fold, while LDL beta-carotene levels rose 8.5-fold. Oxidation of LDL by Cu2+ or AAPH was not significantly delayed after in vivo supplementation with beta-carotene compared with baseline. For AAPH, the lag phase (in minutes) was 75 +/- 8 at baseline and 83 +/- 14 after supplementation (P = 0.07). For Cu2+, the lag phase was 172 +/- 41 at baseline and decreased to 130 +/- 24 after supplementation (P < 0.01). Similarly, no protective effect against Cu(2+)-induced oxidation was observed when beta-carotene was added to LDL in vitro. Supplementation of plasma with beta-carotene in vitro prior to LDL isolation also did not enhance LDL's resistance to Cu(2+)- or AAPH-induced oxidation, despite a 5-fold increase in LDL beta-carotene levels over vehicle control.(ABSTRACT TRUNCATED AT 250 WORDS)

Induction of c-fos and c-myc oncogene expression in the pyloric mucosa of rat stomach by N-methyl-N'-nitro-N-nitrosoguanidine and taurocholate.

The induction of c-fos and c-myc expression in the pyloric mucosa of 8-week-old F344 male rats after oral administration of the glandular stomach carcinogen, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), or the tumor-promoter, taurocholate, was examined by Northern blotting. MNNG at doses of 5-50 mg/kg body weight dose-dependently induced transient increase of up to 30-fold c-fos expression with a maximum after 30 min, and of 8-fold c-myc expression with a maximum after 3 h. It also induced up to 3-fold increase in S-phase cells in the proliferation zone of the pyloric mucosa after 16 h. Similar effects were observed with sodium taurocholate at doses of 200-800 mg/kg body weight. These results suggest that c-fos and c-myc oncogenes play a role in stomach carcinogenesis.

Acute phase responses of plasma angiotensinogen and T-kininogen in rats.

Acute phase responses of plasma angiotensinogen and kininogen were studied in rats. Plasma angiotensinogen levels increased about 3-fold during the first 8 hr, and returned to normal at 48 hr, following the induction of acute inflammation by lipopolysaccharide (LPS). Plasma kininogen reached maximum levels at 48 hr following LPS administration. In adrenalectomized rats, plasma angiotensinogen levels decreased significantly, and the administration of LPS did not elevate plasma angiotensinogen levels. In contrast, plasma kininogen levels were increased by adrenalectomy, as well as by sham-operation. Dexamethasone significantly increased plasma angiotensinogen levels in adrenalectomized rats as well as in normal rats, but aldosterone did not. Plasma kininogen levels of normal rats were not changed by the administration of dexamethasone or aldosterone. From these results, it was concluded that the acute phase response of plasma angiotensinogen is mediated by glucocorticoid, but that of plasma kininogen is not.

Alkaline elution of DNA from stomach pyloric mucosa of rats treated with glyoxal.

DNA damage in the pyloric mucosa of the stomach of male F344 rats was determined by the alkaline elution method after administration of glyoxal, a direct-acting mutagen present in various heated foods, by gastric intubation. Glyoxal at doses of 50-550 mg/kg body weight induced DNA damage in the pyloric mucosa of rat stomach, detected by a 5- to 12-fold increase in the elution rate constant 2 h after its administration. N-Methyl-N'-nitro-N-nitrosoguanidine, a glandular stomach carcinogen, used as a positive control at doses of 1-100 mg/kg body weight induced a 11- to 24-fold increase in the elution rate constant, while 2-acetylaminofluorene, which is not a gastric carcinogen, given as a negative control at doses of 200-400 mg/kg body weight did not increase the elution rate constant. Thus glyoxal, which was previously suggested to induce unscheduled DNA synthesis in the pyloric mucosa of rat stomach, was confirmed to be genotoxic in this region.

Infrared absorption enhancement of C60 by overlaying thin silver island films.

Normal-incidence infrared absorption has been observed for silver overlaid C(60) thin films formed on surface-oxidized Si(111) substrates as a function of the silver or C(60) film thickness. The absorption spectra exhibit bands at 1429 and 1180 cm(-1) due, respectively, to the infrared active T(lu) (4) and T(lu) (3) modes of C(60) in multi-layers. Additionally, two bands appear at 1442 and 1370 cm(-1). The former band is caused by activation of the infrared inactive (Raman active) A(g) (2) mode via electron transfer from the silver to adsorbed C(60), and the latter is assigned to the T(1u) (4) mode red-shifted by the charge transfer. These bands are all enhanced in intensity dependent either upon the silver or C(60) thickness, i.e., the largest absorption enhancement is obtained for 25-monolayers-thick silver and 12-nm-thick C(60). Under atomic force microprobe inspection, the average size and height of the islands in the overlaid 25-monolayers-thick silver change with underlying C(60) film thickness. The influence of the C(60) film structure upon the silver film and in turn the absorption intensity is strongly suggested.

Frontal N30 potential following a sustained voluntary movement.

With 6 male subjects we investigated whether the decreased amplitude in the frontal N30 potential of Somatosensory Evoked Potentials is related to a sustained voluntary movement or not. We concluded that the diminution of frontal N30 was also closely related to the sustained voluntary movement.

Immunohistochemical study of p16 INK4A and survivin expressions in cervical squamous neoplasm.

INTRODUCTION: Cervical cancer is the second most common cancer affecting Malaysian women. Despite the implementation of pap smear screening, many women are still diagnosed only in the advanced stage of cervical cancer. This could partly be due to failure of detection of its precursor lesions; hence the need to search for novel biomarkers to assist in the screening and diagnosis of cervical neoplasia. This study aims to determine the expression of p16INK4A and survivin as possible predictive biomarkers in cervical squamous neoplasm. MATERIAL AND METHODS: This is a retrospective study on 201 cases of cervical neoplasm comprising of 129 cervical intraepithelial neoplasia (CIN) and 72 squamous cell carcinoma (SCC). All samples were evaluated by two independent observers using p16INK4A and survivin monoclonal antibodies. The p16 INK4A expression was graded as negative, focal and diffuse positivity. The intensity for survivin expression was graded as weak, moderate and intense. RESULTS: It is seen that p16 INK4A expression in CIN 1, CIN 2 and CIN 3 were 25.4%, 42.9% and 95.9% respectively. Majority of SCC (98.6%) showed p16 INK4A expression. Survivin expressions in CIN 1, CIN 2, CIN 3 and SCC were 56.7%, 33.4%, 87.5% and 98.6%. There was a linear relationship between increasing grade of CIN and p16 INK4A expressions. CONCLUSION: Our study showed that p16 INK4A expressions correlate well with the increasing grade of CIN. Although survivin does not correlate well to the increasing grade of CIN, it could be useful in differentiating CIN 3 from SCC.

Prevalence of human papillomavirus in abnormal cervical smears in Malaysian patients.

Cervical cancer is the second most common female malignancy in Malaysia. Despite advances in treatment, the overall survival for this disease has not changed in the last decade. Infection by certain types of HPV is recognized as a causal and necessary factor for its development. This study was carried out to determine the prevalence of HPV infection in abnormal cervical smears in Malaysian patients using archival cervical smears retrieved from the Cytopathology Unit, Universiti Kebangsaan Malaysia Medical Centre (UKMMC) between the years 1992-1995. DNA was extracted from 38 abnormal smears comprising 25 intraepithelial lesions and 13 cervical carcinomas and 10 normal smears. Amplification of HPV genes was carried out using the polymerase chain reaction (PCR) technique. HPV genotypes were determined using direct sequencing and the results were compared to the database from Genebank. DNA was successfully extracted from all 48 cervical smears. High-risk HPV (HR-HPV) genotypes were detected in 95% of the abnormal smears. Eight high-risk oncogenic types were identified: 16, 18, 31, 51, 52, 56, 58 and 66. All (100%) cervical cancer smears showed presence of HR-HPV compared to 92% of the cervical intraepithelial lesions. Among the eight HR-HPV genotypes identified, HPV 16 and 52 were the commonest (23.7% each) HPV genotypes encountered and among the CIN lesions, HPV 16 (28%) was the most frequent. We conclude that HPV 16 is the most prevalent HPV genotype present in abnormal cervical smears in Malaysian patients, and that the use of archival material to assess the presence of HPV is potentially worthwhile, and can be utilized for longitudinal studies of HPV presence and persistence.

Oxidative modification and antioxidant protection of human low density lipoprotein at high and low oxygen partial pressures.

Oxidative modification of low density lipoprotein (LDL) in the subendothelial space of the arterial wall has been implicated as an initial process in atherosclerosis. In vitro studies of LDL oxidation are usually done at ambient oxygen partial pressure (pO2; approximately 160 torr, or 21% O2), which is considerably higher than arterial tissue pO2 (30-70 torr, and as low as 20 torr, or 2.5% O2, in atherosclerotic lesions). In addition, beta-carotene acts as an efficient free radical scavenger only at low pO2. Therefore, we investigated the effects of high (20%) and low (2%) pO2 on the kinetics of LDL oxidation, and the effectiveness of beta-carotene compared to other physiological antioxidants in preventing LDL oxidation. At low pO2, the rate of Cu(2+)-induced oxidative modification of LDL was lower than at high pO2. Furthermore, at high pO2 there was a distinct lag phase preceding the propagation phase of lipid peroxidation in Cu(2+)-exposed LDL, as measured by cholesteryl ester hydroperoxide formation; in contrast, there appeared to be no distinct lipid peroxidation lag phase in LDL incubated with Cu2+ at low pO2. Elevating alpha-tocopherol levels in LDL about 5-fold resulted in significant antioxidant protection: the lipid peroxidation lag phase at high pO2 increased by 45% (from 58 +/- 11 to 84 +/- 3 min, P < 0.05), and the initial rate (0-1 h) of lipid hydroperoxide formation at low pO2 was reduced by 52% (from 11.6 +/- 1.9 to 5.6 +/- 1.0 nmol/mg LDL protein/h, P < 0.01). In contrast, increasing LDL beta-carotene levels about 6-fold did not inhibit LDL oxidation at either pO2. Most remarkably, low concentrations of ascorbic acid (30 microM) drastically reduced LDL oxidation, regardless of pO2: the lipid peroxidation lag phase at high pO2 increased more than 7-fold (from 46 +/- 11 min to > 360 min, P < 0.001), and at low pO2 no lipid hydroperoxides could be detected for at least 6 h of incubation. These results show that at low physiological pO2, Cu(2+)-induced LDL oxidation occurs at a significantly lower rate than at ambient pO2. At both high and low pO2, beta-carotene cannot inhibit LDL oxidation, whereas alpha-tocopherol has a moderate protective effect, and low physiological concentrations of ascorbic acid very strongly suppress LDL oxidation.

Inductions of ornithine decarboxylase and replicative DNA synthesis but not DNA single strand scission or unscheduled DNA synthesis in the pyloric mucosa of rat stomach by catechol.

The possible tumor-promoting and genotoxic activities of catechol were examined. Administration of catechol by gastric intubation at doses of 10 to 90 mg/kg body weight to male F344 rats induced up to 19-fold increase in ornithine decarboxylase activity with a maximum after 8 h and up to 8-fold increase in replicative DNA synthesis with a maximum after 24 h in the pyloric mucosa of the stomach. These results suggest that catechol has tumor-promoting activity in the pyloric mucosa of rat stomach. However, its administration at doses of 37.5 to 90 mg/kg body weight did not induce DNA single strand scission in the pyloric mucosa as determined by the alkaline elution method after 2 and 6 h or unscheduled DNA synthesis examined after 2 and 12 h.

A preliminary study of the reliability of immediate vs. delayed interviews of cardiac arrest witnesses.

INTRODUCTION: Methods to characterize the interval between a collapse from cardiac arrest until a 911 call is made have not yet been developed. OBJECTIVE: To determine the concordance of cardiac arrest data obtained by two methods: an immediate nurse interview of out-of-hospital cardiac arrest (OHCA) witnesses, and a follow-up phone interview performed two weeks later. METHODS: This was a prospective study of OHCA witnesses dating from January 1997 to May 1998. Witnesses were briefly interviewed at the time of emergency department presentation, and two weeks later a more lengthy structured phone interview was performed. The authors identified key data elements: 1) was the arrest witnessed? (Wit); 2) was CPR administered prior to EMS arrival? (BCPR); 3) was the first call placed to 911? (c911); and 4) was the estimated collapse to call interval <4 minutes? (ECCI). The analysis utilized Cohen's kappa statistic and Spearman's correlation coefficient. RESULTS: A convenience sample of 42 matched pairs of OHCA cases was analyzed. Kappa statistics for agreement between methods were: 1) Wit(kappa = 0.750), 2) BCPR(kappa = 0.892), 3) c911 (kappa = 0.892), and 4) ECCI(kappa = 0.571, Spearman's 0.528). CONCLUSION: There is good to excellent agreement between immediate and phone interview data retrieval methods. Phone interviews appear to yield data comparable to that with the more difficult and expensive, direct interview method.

Influences of maternal ethanol intake on maternal and perinatal hepatic heme and drug metabolizing enzymes in rats.

The effect of ethanol on maternal and neonatal hepatic heme and drug metabolizing systems was determined. Ethanol (16%, w/v) was administered orally as drinking solution to pregnant or lactating rats at different pre- and post-natal stages. The dams and pups were sacrificed on days 7, 14 and 21 after parturition, respectively. Ethanol administration to lactating rats from just after birth caused an appreciable decrease in the maternal and neonatal body and liver weights. In addition, the activities of nicotinamide adenine dinucleotide phosphate-cytochrome c reductase, nicotinamide adenine dinucleotide-cytochrome b5 reductase and heme oxygenase were significantly enhanced in the livers of neonates whose mothers were exposed to the ethanol during only first week of lactation, but those activities were not altered in the maternal livers. However, no remarkable alterations were observed in the contents of cytochrome P-450 and b5, and the activities of aminopyrine demethylase, aniline hydroxylase and delta-aminolevulinic acid synthetase in the livers of neonates from mothers who had received ethanol during lactation period or last week of gestation, although the activities of aminopyrine demethylase and aniline hydroxylase were enhanced significantly in lactating dams by ethanol consumption for 14 d after parturition.

Effects of maternal ethanol intake during pregnancy on fetal and maternal liver enzyme systems in Wistar rats.

In the present study, the effects of maternal ethanol intake during pregnancy on microsomal cytochrome contents and on enzyme activities in the developing fetus were investigated. Ethanol intake to pregnant females did not affect the maternal body weight or number of fetuses, but tended to reduce the mean fetal body weight, especially the fetuses from a litter of mother who were treated with ethanol during day zero to 20 of gestation showed significant decreases in the body and liver weights. No significant changes were observed in the contents of cytochrome P-450 and b5 and the activities of NADPH-cytochrome c reductase and heme oxygenase in the livers of fetuses whose mothers were exposed to ethanol during pregnancy when compared with that of untreated pregnant rats. However, NADH-cytochrome b5 reductase activity in the fetal livers was found to significantly decrease by maternal ethanol intake during pregnancy.

Protective role of renal metallothionein against Cd nephropathy in rats.

Rats were treated with four types of Cd compound: CdCl2, Cd bound (Cd-peptide), and Cd bound to metallothionein (Cd-MT). This treatment caused no nephropathy. Subsequently, toxic doses of Cd compounds were administered to these pretreated rats and their effects on renal function were examined. When 1.4 mg Cd/kg as Cd-Cys was administered, marked increases in urinary protein, glucose, and amino acid were observed. However, when the animals were pretreated with 1 mg Cd/kg/day as CdCl2 for 3 days, and 1.4 mg Cd/kg as Cd-Cys was administered 24 hr later, no renal damage was observed. Such a protective effect against the nephrotoxic action of Cd-Cys was also shown by pretreatment with Cd-Cys, Cd-peptide, or Cd-MT. Furthermore such a phenomenon was also observed when the nephropathy was caused by Cd-peptide or Cd-MT. The efficacy of pretreatment depended on the time before subsequent administration of Cd and the dose used for pretreatment. Incorporation of Cd into the liver and the kidney was not altered by the pretreatment. No matter in which form the nephrotoxic dose of Cd was administered, the incorporated Cd was distributed between particulates and cytosol; 3 hr after administration, cytosolic Cd was present in almost equal amounts in the high-molecular-weight and the MT fractions in the nonpretreated rats. However, after pretreatment, more of the Cd subsequently administered was found in the MT fraction. These results suggest that MT participates in the detoxication mechanism against Cd in the kidney, as it does in the liver.