Nanowires of polyaniline festooned silver coated paper electrodes for efficient solid-state symmetrical supercapacitors

This paper demonstrates a facile strategy for the development of nanosilver decorated polyaniline coated (PAg) paper-based electrodes for the fabrication of solid-state symmetrical supercapacitors. PAg based printing paper was developed through a two-step process involving initial silver nucleation and growth on the paper followed by aniline polymerization. The developed electrically conductive paper exhibited a highly porous structure and excellent mechanical stability. Further symmetrical supercapacitors having the configuration PAg/electrolyte/PAg were fabricated and evaluated for electrochemical performance such as specific capacitance (483 F g⁻¹ and 613 F g⁻¹ in aqueous 1 M H₂SO₄ and PVA–H₂SO₄ gel electrolytes respectively), energy density (69.56 and 85.13 W h kg⁻¹), and power density (243.44 and 405.375 W kg⁻¹) and cycling stability (90% of its capacitance retention even after 2000 cycles), exhibiting excellent performance under various bending conditions. All these exciting results suggest that the developed paper-based flexible solid-state energy device can serve as an efficient, sustainable, and low-cost energy storage system for portable microelectronic devices which are expected to revolutionize the perception of energy-storage devices in the electronics industry.

This paper demonstrates a facile strategy for the development of nanosilver decorated polyaniline coated (PAg) paper-based electrodes for the fabrication of solid-state symmetrical supercapacitors.     

Lysosomal acid lipase deficiency – An under-recognized cause of dyslipidaemia and liver dysfunction

Lysosomal acid lipase deficiency (LAL-D) is a rare autosomal recessive lysosomal storage disease caused by deleterious mutations in the LIPA gene. The age at onset and rate of progression vary greatly and this may relate to the nature of the underlying mutations. Patients presenting in infancy have the most rapidly progressive disease, developing signs and symptoms in the first weeks of life and rarely surviving beyond 6 months of age. Children and adults typically present with some combination of dyslipidaemia, hepatomegaly, elevated transaminases, and microvesicular hepatosteatosis on biopsy. Liver damage with progression to fibrosis, cirrhosis and liver failure occurs in a large proportion of patients. Elevated low-density lipoprotein cholesterol levels and decreased high-density lipoprotein cholesterol levels are common features, and cardiovascular disease may manifest as early as childhood. Given that these clinical manifestations are shared with other cardiovascular, liver and metabolic diseases, it is not surprising that LAL-D is under-recognized in clinical practice. This article provides practical guidance to lipidologists, endocrinologists, cardiologists and hepatologists on how to recognize individuals with this life-limiting disease. A diagnostic algorithm is proposed with a view to achieving definitive diagnosis using a recently developed blood test for lysosomal acid lipase. Finally, current management options are reviewed in light of the ongoing development of enzyme replacement therapy with sebelipase alfa (Synageva BioPharma Corp., Lexington, MA, USA), a recombinant human lysosomal acid lipase enzyme.     

Biochemical changes on the cardioprotective effect of nicorandil and amlodipine during experimental myocardial infarction in rats

The synergistic protective effect of nicorandil (KATP channel opener) and amlodipine (calcium channel blocker) on mitochondrial respiration and mitochondrial lipid contents were examined on isoproterenol-induced myocardial infarction in rats. The rats given isoproterenol (150 mg kg(-1) daily, i.p.) for 2 days showed significant changes in mitochondrial respiration and mitochondrial lipid profile levels. Pretreatment with nicorandil (2.5 mg kg(-1) daily, p.o.) and amlodipine (5.0 mg kg(-1) daily, p.o.) for 3 days significantly prevented these alterations and restored the mitochondrial respiration and mitochondrial lipid contents to near normal. Histopathological observations were also in correlation with the biochemical parameters. These findings indicate the synergistic protective effect of nicorandil and amlodipine on mitochondrial respiration and its membrane integrity during isoproterenol-induced cardiac damage.     

Mitigating role of baicalein on lysosomal enzymes and xenobiotic metabolizing enzyme status during lung carcinogenesis of Swiss albino mice induced by benzo(a)pyrene

The lungs mainly serve as a primary site for xenobiotic metabolism and constitute an important defense mechanism against inhalation of carcinogens. Our current study aimed to evaluate the chemotherapeutic efficacy of baicalein (BE) in Swiss albino mice exposed to tobacco‐specific carcinogen benzo(a)pyrene [B(a)P] for its ability to mitigate pulmonary carcinogenesis. Here, we report that altered activities/levels of lysosomal enzymes (cathepsin‐D, cathepsin‐B, acid phosphatase, β‐D‐galactosidase, β‐D‐glucuronidase, and β‐D‐N‐acetyl glucosaminidase), phase I biotransformation enzymes (cytochrome P450, cytochrome b5, NADPH‐cytochrome P450 reductase, and NADH‐cytochrome b5 reductase), and phase II enzymes (glutathione S‐transferase, UDP‐glucuronyl transferase, and DT‐diaphorase) were observed in the B(a)P‐induced mice. Treatment with BE significantly restored back the activities/levels of lysosomal enzymes, phase I and phase II biotransformation enzymes. Moreover, assessment of lysosomal abnormalities by transmission electron microscopic examination revealed that BE treatment effectively counteract B(a)P‐induced oxidative damages. Protein expression levels studied by immunohistochemistry, immunofluorescence, and immunoblot analysis of CYP1A1 revealed that BE treatment effectively negate B(a)P‐induced upregulated expression of CYP1A1. Further analysis of scanning electron microscopic studies in lung was carried out to substantiate the anticarcinogenic effect of BE. The overall data suggest that BE treatment significantly inhibits lysosomal and microsomal dysfunction, thus revealing its potent anticarcinogenic effect.     

Silymarin attenuated mast cell recruitment thereby decreased the expressions of matrix metalloproteinases-2 and 9 in rat liver carcinogenesis

Summary  Liver cancer is the sixth most common cancer worldwide but because of very poor prognosis, it is the third most common cause of death from cancer. There are currently limited therapeutic regimens available for effective treatment of this cancer. Silymarin is a naturally derived polyphenolic antioxidant, is the active constituent in a widely consumed dietary supplement milk thistle (Silybum marianum) extract. Mast cells play an important role in the inflammatory component of a developing neoplasm; they are also a major source for matrix metalloproteinases (MMPs), which are involved in invasion and angiogenesis. In the present study, we investigated whether dietary supplementation of silymarin has any role in mast cell density (MCD) and in the expressions of MMP-2 and MMP-9 in N-nitrosodiethylamine induced (NDEA) liver cancer in Wistar albino male rats. NDEA administered rats showed increased MCD as revealed by toluidine blue staining along with upregulated expressions of MMP-2 and MMP-9. Silymarin treatment inhibited this increase in MCD and downregulated the expressions of MMP-2 and MMP-9 as revealed by Western blotting and immunohistochemistry. In conclusion, silymarin exerted beneficial effects on liver carcinogenesis by attenuating the recruitment of mast cells and thereby decreased the expressions of MMP-2 and MMP-9.     

Clozapine induced myopericarditis: early recognition improves clinical outcome

Clozapine is an atypical dibenzodiazepine antipsychotic used for resistant schizophrenia. Uncommonly, it is associated with myocarditis. We report a case of myopericarditis masquerading as an acute myocardial infarction based on presenting electrocardiogram and cardiac markers. Emergent coronary angiography confirmed the absence of epicardial coronary occlusion and revealed severe left ventricular systolic dysfunction. Immediate discontinuation of the clozapine, along with aggressive supportive care resulted in complete recovery to baseline. Cardiovascular health professionals should be aware of this uncommon but serious side effect of clozapine since failure to recognize the association may result in adverse clinical outcome and inappropriate therapy.     

The premaxillary triangle: clue to the diagnosis of cleft lip and palate.

OBJECTIVE: The prenatal detection rate of cleft lip and palate is low, especially in low-risk patients who undergo targeted sonography. The reason is that evaluating surface anatomy is relatively difficult and requires operator expertise. Our purpose was to describe a technique to improve the diagnostic accuracy of facial clefts (lip and palate) and to assess the feasibility of including this technique as part of standard protocol during targeted imaging. METHODS: A prospective study was done during 2000 through 2002 to evaluate the accuracy of the "premaxillary triangle (PMT) sign": a new sign to diagnose unilateral cleft lip and palate in women referred for prenatal sonography at our center. Patients with only isolated unilateral cleft lip and palate and cleft lip were included in this study. Before this, all examiners were trained to image the PMT. The images were reviewed by a senior consultant. It was later decided to include this sign as part of the protocol of targeted sonography done between 18 and 22 weeks in our institution. However, depending on the fetal position, the PMT was documented even in patients referred for the first time in late second and third trimesters. RESULTS: Twenty-nine cases of isolated facial clefts were diagnosed during the study period, of which 2 had unilateral cleft lip and 27 had unilateral cleft lip and palate. The PMT sign was absent in all cases of unilateral cleft lip and palate but was present in 2 cases of isolated cleft lip without cleft palate. CONCLUSIONS: The PMT sign can be easily incorporated into targeted sonography at 18 to 22 weeks' gestation. Its inclusion would help in increasing the detection rate of unilateral cleft lip and palate. It may also be potentially used for differentiating between isolated cleft lip and cleft lip and palate, which helps in better prenatal counseling.     

Defensive nature of Sargassum polycystum (Brown alga) against acetaminophen-induced toxic hepatitis in rats: Role of drug metabolizing microsomal enzyme system, tumor necrosis factor-a and fate of liver cell structural integrity

AIM: To assess the defensive nature of Sargassum polycystum (S. polycystum) (Brown alga) against acetaminophen (AAP)-induced changes in drug metabolizing mi crosomal enzyme system, tumor necrosis factor (TNF-α) and fine structural features of the liver during toxic hepatitis in rats. METHODS: Male albino Wistar strain rats used for the study were randomly categorized into 4 groups. GroupⅠconsisted of normal control rats fed with standard diet. GroupⅡrats were administered with acetaminophen (800 mg/kg body weight, intraperitoneally). GroupⅢrats were pre-treated with 5. polycystum extract alone. GroupⅣrats were orally pre-treated with S. polycystum extract (200 mg/kg body weight for 21 d) prior to acetaminophen induction (800 mg/kg body weight, intraperitoneally). Serum separated and liver was excised and microsomal fraction was isolated for assaying cytochrome P450, NADPH Cyt P450 reductase and bs. Serum TNF-αwas detected using ELISA. Fine structural features of liver were examined by transmission electron microscopy. RESULTS: Rats intoxicated with acetaminophen showed considerable impairment in the activities of drug metabolizing microsomal enzymes, such as cytochrome P450, NADPH Cyt P450 reductase and bs when compared with the control rats. The rats intoxicated with acetaminophen also significantly triggered serum TNF-αwhen compared with the control rats. These severe alterations in the drug metabolizing enzymes were appreciably prevented in the rats pretreated with 5. polycystum. The rats pretreated with S. polycystum showed considerable inhibition in the elevation of TNF-αcompared to the rats intoxicated with acetaminophen. The electron microscopic observation showed considerable loss of structural integrity of the endoplasmic reticulum, lipid infiltration and ballooning of mitochondria in the acetaminophen-intoxicated rats, whereas the rats treated with S. polycystum showed considerable protection against acetaminophen-induced alterations in structural integrity. CONCLUSION: These observations suggest that the animals treated with 5. polycystum extract may have the ability to protect the drug metabolizing enzyme system and mitochondrial functional status from free radical attack, thereby showing its defense mechanism in protecting hepatic cells from acetaminophen toxic metabolite N-acetyl-para-benzoquinone-imine (NAPQI).     

Effect of Aqueous Extract of Passiflora edulis on Biochemical and Hematological Parameters of Wistar Albino Rats

Passiflora edulis is traditionally used in folk lore medicine for the treatment of various ailments. To validate its use in traditional medicine, it is important to evaluate its toxicity in the animal system. Therefore, this study aimed to evaluate the toxicological effects of oral administration of aqueous leaf extract of P. edulis in Wistar albino rats. Acute toxicity tests were conducted by the oral administration of 200, 500, 1000 and 2000 mg/kg body weight of the animal. In subacute study, they were administered with various doses of aqueous extract of P. edulis (100, 200, 300, and 400 mg/kg body weight) to evaluate its toxicity for a period of 7 days. The effect of aqueous extract of P. edulis on organ weight, hematological, renal, and hepatic markers were analyzed. In acute toxicity study, no mortality was seen with in 24 h of the administration of P. edulis extract. No signs of neurological and behavioral changes were noticed with in 72 h. In the subacute study, the extract intake has not changed the hematological parameters such as RBC, WBC, and platelets and it was also found that the plasma level of amino transferases, ALP, urea, uric acid and, creatinine were also not altered by the administration of P. edulis extract throughout the study. The weight of organ was found to be unaltered in all the doses selected. The acute toxicity study reveals that the oral administration of the extract was found to be safe up to the dose level of 2000 mg/kg. The subacute study indicates that the extract is safe on the bone marrow function and it is neither hepatotoxic nor nephrotoxic. This supports the safety use of the aqueous extract of P. edulis in pharmacological studies.