Knowledge of HPV/cervical cancer and acceptability of HPV self-sampling among women living with HIV: A scoping review.

Cervical cancer rates are disproportionately high among women living with the human immunodeficiency virus (wlhiv). Cervical cancer is preventable through hpv screening, regular Pap tests, and early cancer detection. Evidence indicates that hpv and cervical cancer screening are suboptimal among wlhiv, who face a myriad of access barriers. Considering that screening is an effective first-line defense to cervical cancer, we conducted a scoping review with the aim of gaining a better understanding about: (1) the knowledge and perceptions of hpv and cervical cancer screening among wlhiv; and (2) the acceptability of self-sampling for hpv among wlhiv. We searched five electronic databases for peer-reviewed articles that were published in English within the last ten years, reported on studies with hiv-positive women who were aged 16 or older, and satisfied the topics of the review. A total of 621 articles were found. After accounting for duplicates and unmet criteria, 17 articles and 1 abstract, reporting on studies in the United States and Africa, were included in this review. The review highlighted that most wlhiv had inadequate knowledge of hpv transmission and cervical cancer prevention, which influenced their perceptions of risk and susceptibility. Screening barriers included misconceptions about Pap tests, fear of diagnosis of serious illness, perceived pain, embarrassment, bodily modesty, and limited access to female health care providers. This review also affirms that self-sampling is an acceptable and promising screening option for wlhiv. Implications for policy, research, and practice are discussed.

HIV-positive MSM's knowledge of HPV and anal cancer self-sampling: A scoping review.

Human papillomavirus (hpv) infection is the cause of anal squamous cell cancer (ascc) in 80% of cases. Available research has also shown high prevalence of anal hpv infection among men who have sex with men (msm). However, hpv vaccination is low among msm in Canada. In light of this information, we conducted a scoping review with the aim of exploring (1) the knowledge of hpv and anal cancer among hiv-positive msm and (2) the acceptability of hpv and anal cancer self-sampling in this population. In conducting the review, we searched five electronic databases for peer-reviewed articles and abstracts published in English, between 2007 and 2017. A total of 803 articles were retrieved; after accounting for duplicates (n=40) and unmet criteria (n=754), a total of 794 articles were excluded. A final total of nine articles were used in this review. Results of this review show that hiv-positive msm have limited knowledge regarding the risks of anal cancer associated with hiv and hpv coinfection. Furthermore, there is limited research on hpv and anal cancer self-sampling in this population. However, the review of available studies suggested that hiv-positive msm were open to anal cancer self-sampling. It also identified potential barriers to self-sampling. In conclusion, we provide suggestions and future directions for policy-makers and educators to develop inclusive and accessible strategies to reach hiv-positive msm regarding anal cancer education and self-screening.

A characteristic pharmacological action of 'Yang-invigorating' Chinese tonifying herbs: enhancement of myocardial ATP-generation capacity.

In order to investigate the pharmacological basis of 'Yang-invigorating' action, the effect of oral treatment with the methanolic extract of 'Yang-invigorating' herbs on ATP-generation capacity was examined, using heart homogenates prepared from herb-pretreated mice. Tonifying (i.e., health-promoting) herbs of other functional categories were also included for comparison. The results indicated that 'Yang-invigorating' Chinese tonifying herbs could invariably enhance myocardial ATP-generation capacity, with the extent of stimulation varying among the herbs. In contrast, 'Yin-nourishing' herbs either did not stimulate or even decreased myocardial ATP-generation capacity. While 'Qi-invigorating' herbs produced variable effects on myocardial ATP-generation capacity, most of the 'blood-enriching' herbs did not cause any significant changes. The results obtained from studies using myocardial mitochondrial fractions isolated from herb-pretreated mice suggest that 'Yang-invigorating' herbs might speed up ATP generation by increasing mitochondrial electron transport. The ensemble of results has provided evidence for the first time to support the pharmacological basis of 'Yang invigoration' in Chinese medicine.

A yang-promoting Chinese herbal suppository preparation enhances the antioxidant status of red cells in male human subjects.

In the 16-week pilot study, the effect of a Yang-promoting Chinese herbal suppository preparation (VI-28) on the red cell antioxidant status was examined in 31 healthy male subjects aged 41-66 years old. VI-28 treatment for 12 weeks (one suppository (0.3 g) daily for week 1-4; one every 2 days for week 5-8; one every 3 days for week 9-12) produced a time/dose-dependent alteration in red cell antioxidant status. The VI-28-induced change is characterized by a slight depletion in cellular reduced glutathione (GSH) level and a decrease in susceptibility to peroxide-induced lipid peroxidation as well as increases in catalase (CAT) and Cu-Zn-superoxide dismutase (SOD) activities. While a reversal trend of change was observed in cellular GSH level, the susceptibility to lipid peroxidation as well as the CAT activity after the cessation of treatment for 4 weeks, the SOD activity exhibited a protracted increase. The results indicate that VI-28 treatment enhances red cell antioxidant status in male subjects. The beneficial effect of VI-28 treatment on red cells may re fl ect a corresponding change in antioxidant status of peripheral tissues.

In vivo antioxidant action of a lignan-enriched extract of Schisandra fruit and an anthraquinone-containing extract of Polygonum root in comparison with schisandrin B and emodin.

The in vivo antioxidant action of a lignan-enriched extract of the fruit of Schisandra chinensis (FS) and an anthraquinone-containing extract of the root of Polygonum multiflorum (PME) was compared with their respective active constituents schisandrin B (Sch B) and emodin by examining their effect on hepatic mitochondrial glutathione antioxidant status in control and carbon tetrachloride (CCl 4 )-intoxicated mice. FS and PME pretreatments produced a dose-dependent protection against CCl 4 hepatotoxicity, with the effect of FS being more potent. Pretreatment with Sch B, emodin or alpha-tocopherol (alpha-Toc) also protected against CCl 4 hepatotoxicity, with the effect of Sch B being more potent. The extent of hepatoprotection afforded by FS/Sch B and PME/emodin pretreatment against CCl 4 toxicity was found to correlate well with the degree of enhancement in hepatic mitochondrial glutathione antioxidant status, as evidenced by increases in reduced glutathione level and activities of glutathione reductase, glutathione peroxidase as well as glutathione S-transferases, in both control and CCl 4 -intoxicated mice. alpha-Toc, which did not enhance mitochondrial glutathione antioxidant status, seemed to be less potent in protecting against CCl 4 hepatotoxicity. The ensemble of results indicates that FS/PME produced a more potent in vivo antioxidant action than alpha-Toc by virtue of their ability to enhance hepatic mitochondrial glutathione antioxidant status and that the differential potency of FS and PME can be attributed to the difference in in vivo antioxidant potential between Sch B and emodin. Abbreviations. ALT:alanine aminotransferases CCl 4 :carbon tetrachloride FS:lignan-enriched extract of Schisandra fruit GRD:glutathione reductase GSH:reduced glutathione GSH-Px: Se-glutathione peroxidase GST:glutathione S-transferases mt:mitochondrial MDA:malondialdehyde PME:anthraquinone-containing fraction of Polygonum root Sch B:schisandrin B SDH:sorbitol dehydrogenase alpha-Toc:alpha-tocopherol

Altered susceptibility to ischemia-reperfusion injury in isolated-perfused hearts of short-term diabetic rats associated with changes in non-enzymatic antioxidants.

The effects of short-term (2-week) diabetes on myocardial ischemia-reperfusion (I-R) injury and associated changes in myocardial non-enzymatic antioxidant level were examined. Isolated-perfused hearts prepared from control and diabetic rats were subjected to increasing periods of ischemia and reperfusion, and myocardial I-R injury was assessed by measuring the extent of lactate dehydrogenase (LDH) leakage and contractile force recovery. While a brief period (20 min) of post-ischemic reperfusion caused a smaller extent of LDH leakage, the prolonged period (40 min) of reperfusion produced a greater degree of I-R injury in diabetic hearts, as indicated by the impaired recovery of contractile force. The apparent protection against I-R injury in diabetic hearts during the early phase of post-ischemic reperfusion was associated with increases in myocardial reduced glutathione/ascorbic acid and a-tocopherol levels, with the effect on a-tocopherol being most prominent. Insulin treatment could reverse the diabetes-associated changes in susceptibility to myocardial I-R injury and antioxidant response. The ensemble of results indicates that the myocardium isolated from short-term diabetic rat can produce a beneficial antioxidant response to I-R challenge, which may, in turn, be attributable to the decreased susceptibility to I-R injury observable during the early phase of reperfusion.

Effects of Schisandrin B and alpha-tocopherol on lipid peroxidation, in vitro and in vivo.

Effects of Schisandrin B (Sch B) and alpha-tocopherol (alpha-TOC) on ferric chloride (Fe3+) induced oxidation of erythrocyte membrane lipids in vitro and carbon tetrachloride (CCl4) induced lipid peroxidation in vivo were examined. While alpha-TOC could produce prooxidant and antioxidant effect on Fe(3+)-induced lipid peroxidation, Sch B only inhibited the peroxidation reaction. Pretreatment with alpha-TOC (3 mmol/kg/day x 3) did not protect against CCl4-induced lipid peroxidation and hepatocellular damage in mice, whereas Sch B pretreatment (0.3 mmol/3.0 mmol/kg/day x 3) produced a dose-dependent protective effect on the CCl4-induced hepatotoxicity. The ensemble of results suggests that the ability of Sch B to inhibit lipid peroxidation, while in the absence of pro-oxidant activity, may at least in part contribute to its hepatoprotective action.

Alterations in tissue glutathione antioxidant system in streptozotocin-induced diabetic rats.

Changes in tissue glutathione antioxidant system in streptozotocin-induced diabetic rats for a period of 15 weeks were examined. Total glutathione level was significantly increased in kidney tissue, but were slightly decreased and increased in liver and heart tissues, respectively. The small changes in total glutathione level in the liver and heart, though not statistically significant, were associated with reciprocal alterations in the activity of gamma-glutamylcysteine synthetase (GCS). While the GCS activity was not changed in kidney tissue, the activity of gamma-glutathione peroxidase was significantly increased in kidney tissue. Insulin treatment could completely or partly normalize almost all of these changes induced by diabetes. However, the decrease in hepatic glutathione S-transferases activity in diabetic rats was not reversed by the insulin treatment. The ensemble of results suggests that the diabetes-induced alterations in tissue glutathione antioxidant system may possibly reflect an inter-organ antioxidant response to a generalized increase in tissue oxidative stress associated with diabetes.

Effect of a lignan-enriched extract of Schisandra chinensis on aflatoxin B1 and cadmium chloride-induced hepatotoxicity in rats.

Treatment of rats with a lignan-enriched extract of the fruit of Schisandra chinensis could enhance hepatic antioxidant/detoxification system, as indicated by increases in hepatic reduced glutathione (GSH) level as well as hepatic glutathione reductase and glutathione S-transferase activities. The hepatoprotective action was evident after aflatoxin beta 1 or cadmium chloride (Cd) challenge. Schisandra chinensis pretreatment protected against aflatoxin B1-or Cd-induced hepatocellular damage in rats. However, pretreating rats with alpha-tocopherol acetate (vitamin E) did not protect against hepatic damage induced by both toxins. Results from the present as well as our previous studies demonstrate that the hepatoprotection afforded by Schisandra chinensis pretreatment is not hepatotoxin specific. Schisandra chinensis seems to be more effective than vitamin E in protecting against aflatoxin B1 and Cd toxicity. The mechanism of hepatoprotection afforded by Schisandra chinensis pretreatment may involve facilitation of both antioxidant and detoxification processes in the liver.

Schisandrin B protects against carbon tetrachloride toxicity by enhancing the mitochondrial glutathione redox status in mouse liver.

Previous studies in our laboratory have demonstrated the effect of Schisandrin B (Sch B),an active ingredient of the fruit of Schisandra chinensis, on enhancing the hepatic glutathione antioxidant system in mice, as evidenced by the hepatoprotection against carbon tetrachloride (CCl4) toxicity. In the present study, the mechanism involved in the hepatoprotection afforded by Sch B treatment was investigated. Treating female Balb/c mice with 1, 3-bis(2-chloroethyl)-1-nitrosourea, an inhibitor of glutathione reductase (GRD), at a dose of 2 mmol/kg (i.p.) did not abrogate the hepatoprotective action of Sch B in CCl4-treated mice. The result indicates that the increased activity of hepatic GRD is not ascribable to the hepatoprotective action of Sch B. In control mice, the same Sch B treatment regimen caused an enhancement in hepatic mitochondrial glutathione redox status, as indicated by the significant increase and decrease in reduced and oxidized glutathione levels, respectively. While the CCl4 intoxication greatly impaired mitochondrial glutathione redox status, the beneficial effect of Sch B treatment became more evident after CCl4 challenge. Our results strongly suggest that the mechanism of hepatoprotection afforded by Sch B treatment may involve the enhancement of mitochondrial glutathione redox status.

Myocardial protective effect of Sheng Mai San (SMS) and a lignan-enriched extract of Fructus Schisandrae, in vivo and ex vivo.

Effects of Sheng Mai San (SMS), a traditional Chinese medicine used for the treatment of coronary heart disease, and the lignan-enriched extract of Fructus Schisandrae (FS), an antioxidant component of SMS, were examined in an in vivo model of myocardial infarction and an ex vivo model of myocardial ischemia-reperfusion injury in rats. Pretreatment with SMS (12 g/kg/day × 3, p. o.) or FS extract (0.8 g/kg/day × 3, p. o.) was found to protect against the isoproterenol-induced myocardial injury in rats and the ischemia-reperfusion injury in isolated perfused hearts prepared from the pretreated animals. Pretreatment with α-tocopherol (0.8 g/kg/day × 3, p. o.) produced similar beneficial effect on the myocardium. The myocardial protection afforded by SMS pretreatment is likely, at least in part, mediated by the FS-derived antioxidant activity.

Enhancement of hepatic glutathione regeneration capacity by a lignan-enriched extract of fructus schisandrae in rats.

Exposure of liver homogenates to an in vitro tert-butyl hydroperoxide challenge can be used as a means for measuring the reduced glutathione regeneration capacity (GRC) of hepatic tissues. Pretreatment of rats with a lignan-enriched extract of Fructus Schisandrae (FS) caused a moderate enhancement of hepatic GRC in control rats, but the GRC enhancing effect of FS pretreatment on hepatic tissues was greatly exaggerated after CCl4 challenge. This in vitro bioassay can be used for investigating the hepatic GRC promoting action of orally active agents.

Effect of schisandrin B on hepatic glutathione antioxidant system in mice: protection against carbon tetrachloride toxicity.

Pretreating female Balb/c mice with schisandrin B (Sch B) at increasing daily doses (1-4 mmol/kg) for 3 days caused dose-dependent increases in hepatic glutathione S-transferase (GST) and glutathione reductase (GRD) activities. However, the activities of glucose-6-phosphate dehydrogenase (G6PDH), Se-glutathione peroxidase (GPX), and gamma-glutamylcysteine synthetase (GCS) were down-regulated to varying degrees in a dose-dependent manner. While there were biphasic changes in hepatic reduced glutathione (GSH) level as well as susceptibility of hepatic tissue homogenates to in vitro peroxide-induced GSH depletion, a gradual decrease in hepatic malondialdehyde content was observed. The beneficial effect of Sch B on the hepatic GSH anti-oxidant system became more evident after CCl4 challenge. The same Sch B pretreatment regimen caused a dose-dependent protection against carbon tetrachloride (CCl4)-induced hepatotoxicity. The hepatoprotection was associated with significant enhancement in hepatic GSH status, as indicated by the substantial increase in tissue GSH levels and the corresponding decrease in susceptibility of tissue homogenates to GSH depletion. Where the activities of GST and GRD were increased linearly over non-CCl4 control values, there was also a gradual elevation in G6PDH activity upon administration of increasing doses of Sch B. In contrast, GPX activity was moderately down-regulated. The ensemble of results suggests that the hepatoprotection afforded by Sch B pretreatment may mainly be attributed to the enhancement in the functioning of the hepatic GSH anti-oxidant system, possibly through stimulating the activities of GSH related enzymes.

Effect of a lignan-enriched fructus schisandrae extract on hepatic glutathione status in rats: protection against carbon tetrachloride toxicity.

The effect of a lignan-enriched extract of the fruits of Schisandra chinensis (FS) on hepatic glutathione (GSH) status was examined in both control and carbon tetrachloride (CCl4)-treated rats. FS treatment caused a dose-dependent enhancement in hepatic GSH status, as evidenced by significant increases in hepatic GSH level and activities of hepatic glucose-6-phosphate and glutathione reductase (GRD), as well as a decreased susceptibility of hepatic tissue homogenates to in vitro peroxide-induced GSH depletion. The beneficial effect of FS treatment on hepatic GSH status became more evident after CCl4 challenge. Pretreating rats with FS extract at increasing daily doses ranged from 0.2 to 3.2 g/kg for 3 days caused a dose-dependent protection against the CCl4-induced impairment in hepatic GSH status. The enhancement in hepatic GSH status was associated with corresponding decreases in tissue malondialdehyde levels and plasma alanine aminotransferases activities, indicating a significant reduction in the extent of oxidative hepatocellular damage. Our results indicate that the molecular mechanism of hepatoprotection afforded by FS pretreatment may involve the facilitation of GSH regeneration via the GRD-catalyzed and NADPH-mediated reaction.

Prooxidant and antioxidant effects of Trolox on ferric ion-induced oxidation of erythrocyte membrane lipids.

The prooxidant and antioxidant actions of Trolox were examined in an in vitro system measuring ferric ion-induced oxidation of erythrocyte membrane lipids. Trolox was found to produce a concentration-dependent biphasic effect on the ferric ion-stimulated lipid peroxidation, with the mode of action being similar to those produced by reducing-agent antioxidants, such as ascorbic acid and reduced glutathione, and iron chelator, such as desferrioxamine. Phytic acid, a potent iron chelator, could suppress the prooxidant actions of Trolox and desferrioxamine, but not those of ascorbic acid and reduced glutathione. The ability of Trolox to stimulate ferric ion-catalyzed ascorbate oxidation, as similar to the action produced by ethylenediaminetetraacetic acid, indicates the presence of iron-chelating activity. The ensemble of results suggests the possible involvement of iron chelation in the prooxidant action of Trolox in ferric ion-stimulated lipid peroxidation reactions.

Thin-layer chromatographic and column liquid chromatographic analyses of morphine in urine via dabsylation.

A semiquantitative screening method for morphine in urine and a quantitative assay method for the drug were developed. In the semiquantitative method, morphine in urine was directly reacted with 4-dimethylaminoazobenzene-4'-sulphonyl chloride (dabsyl chloride) in a slightly alkaline medium. The orange-coloured dabsyl morphine was separated by silica gel thin-layer chromatography and the spot intensity was visually compared with that of the standards. The limit of detection is 0.075 microgram/ml. In the quantitative method, morphine was extracted from urine before dabsylation. The dabsylation reaction is very fast and is complete within 5-10 min at room temperature. Dabsylation yield is maximum at a dabsyl chloride concentration of 6.2 mM. Total recovery of morphine using the extraction and dabsylation procedures described is 66%. Dabsyl morphine, thus formed, was analysed using high-performance liquid chromatography by monitoring its absorbance at 436 nm on a normal-phase mu Porasil column. The limit of quantitation using high-performance liquid chromatography is 0.26 microM (0.075 microgram/ml), which corresponds to 10.5 pmol of injected dabsyl morphine. Quantitative assay was also carried out by thin-layer chromatography on silica gel followed by densitometry. The limit of quantitation is 1.3 microM (0.375 microgram/ml).