Synthesis and Structural Studies of Nanocrystalline Cd0.3Zn0.7Fe2O4

The synthesis of Cd0.3Zn0.7Fe2O4 nanoparticles has been achieved by a simple thermal decomposition method from the inorganic precursor, Cdd0.3Zn0.7Fe2(cin)3(N2H4)2, which was obtained by a novel precipitation method from the corresponding metal salts, cinnamic acid and hydrazine hydrate. The precursor was characterized by hydrazine and metal analyses, infrared spectral analysis and thermogravimetric analysis. Under appropriate annealing conditions, Cd0.3Zn0.7Fe2(cin)3(N2H4)2 yielded Cd0.3Zn0.7Fe2O4 nanoparticles, which were characterized for their size and structure using X-Ray Diffraction (XRD), High  Resolution Transmission ElectronMicroscopic(HRTEM),SelectedArea ElectronDiffraction(SAED)andScanning ElectronMicroscopic(SEM)techniques.KEYWORDS: Cd0.3Zn0.7Fe2O4 nanoparticles, XRD, HRTEM, SAED, SEM

Study of Clinical Profile and outcome of Shock in Pediatric Intensive Care Unit of a Tertiary Referral Hospital

INTRODUCTION: Shock occurs in approximately 2% of all hospitalized children and adults in the united states 1. Majority of the childhood illness have the potential to lead to shock. Shock accounts for more morbidity and mortality in children world wide than any other diagnosis.2,3 Shock is one of the most dramatic, dynamic and life-threatening problems faced by the physician in critical care setting4. High index of suspicion is needed for early identification of shock. Early institution of treatment will definitely reduce the chances of progression of shock to end up in cardio respiratory failure. Rapid and focused cardiopulmonary assessment adds in the early recognition of shock state.5 Many studies have been done to classify shock at presentation and emphasize that there exists a wide range of etiologies for shock. The mortality rate of shock in pediatric patients has declined as a consequence of educational efforts (pediatric advance life support), which emphasize early recognition and intervention and rapid transfer of critically ill patients to a PICU via a transport service. AIM OF THE STUDY: To find the following in the paediatric intensive care unit: 1. Etiology and type of shock 2. Outcome of shock 3. Risk factors for mortality of shock in children admitted in PICU. DISCUSSION: In present study the frequency of shock was found to be 1.63%. According to Western data, shock occurs in approximately 2% of all hospitalized children and adults in united states1. In a study conducted by Daljit singh et al10 they found frequency of shock was 4.3%. The present study showed that maximum patients were observed in infancy, as is also reported by Daljit singh et al10. In our study, we found that fever was the common presentation in all age group followed by refusal of feeds in infant, breathlessness in other age groups. In our study fever was the common presentation in septic and hypovolemic shock.. Breathlessness was the common presentation in cardiogenic shock, in our study it was uniformly presenting all cases of cardiogenic shock convulsions were the most common presentation in distributive shock. In our study, we found that septic shock was the most common type of shock (47.4%), followed by distributive shock (19.5%), hypovolemic shock (17.4%), and cardiogenic shock (15.7%), This is contrary to the previous studies, where they found hypovolemic shock due to diarrhoea was the commonest cause of shock in children. This is because in our hospital children presenting with diarrhoea and shock, after the initial fluid resuscitation in the emergency room, will be admitted in separate diarrhoea ward, unless they have associated complications. As the present study is confined to children who present with shock to the PICU, the causes will be mostly diseases other than acute watery diarrhoea. A few cases of diarrhoea may get admitted in PICU, if they develop some complications. The incidence of septic shock is increasing world over with a 10 fold increase in the past 20 years, the reason being that more patients are surviving with the disease which were fatal previously and due to increase in invasive procedures which constitute risk factors for developing sepsis10. In our study culture proven sepsis were found in 36 cases (32.1%), and most of them were Gram negative organisms, which is similar to the previous studies1,15,16,17 . The other culture negative septic shock can be explained as majority of patients had received intravenous antibiotics as out patients before being referred to our hospital. Jacobs RF et al 15 in their study of septic shock in children found an incidence 25.2% of culture proven sepsis, of which H.Influenzae B, N.meningitidis and S.pneumoniae were the predominant organisms. In our study we found that infections were the common cause of shock in younger age group. DKA and status eplepticus/ seizure disorder were the common causes of shock in older age groups. SUMMARY AND CONCLUSION: 1. Shock is a common presentation of a critically ill child contributing about 1.63% of hospital admissions. 2. The etiology of shock varies with age groups with incidence decreasing as age advances. 3. Bronchopneumonia and other infections are the most common cause of shock in infants and younger children. 4. Seizure disorder / status epilepticus and diabetic keto acidosis are the common causes of shock in older children. 5. Septic shock is the most common type of shock in children admitted in PICU. 6. Under nutrition, Decompensated shock, inotrope requirement, MODS, leucopenia and ventilatory support are independently associated with poor outcome. 7. Diagnosis and management of shock in early compensated stage carries better prognosis than in decompensated shock irrespective of the age of the patien

Synthesis and characterization of photocrosslinked biobased polyester membrane

A series of bio-based photocrosslinked polyester membranes, poly(1,8-octanediol-itaconate-citrate-dodecandioate), (POSCI) were synthesized through polycondensation followed by photocrosslinking under UV irradiation in the presence of 2,2-dimethoxy-2-phenylacetophenone (DMPA) as photoinitiator (PI). Upon varied UV exposure time and DMPA content, the corresponding changes in chemical, structural, and mechanical properties of the polymer were studied. The transmission peak of FTIR spectrum centred at 1725 cm-1 indicates the formation of ester structure. Contact angle results suggested all of the synthesized POSCI membranes had hydrophilic properties as their contact angle is less than 90 °. Sol-gel analysis shows that the swelling ratio of POSCI decreases while the gel fraction increases with increasing in photocrosslinking time. The tensile strength of POSCI, thus, increased correspondingly with longer UV exposure. Excess DMPA, however, proved otherwise

Occurrence and growth of the commercially important red algae in fish culture pond at Mandapam

The red algae Gracilaria edulis, Hypnea valenliae, Acanthophora spicifera ard Sarconema irdica have been observed to occur arrl grow in a culture pard. Ove- a period of eight month s, the algae grew to lJ4 kg in the pard of 800 sq m. The hyd rological cordilions in the porn are compared to those in the sea containing natursl beds of these algae during the periro of observations. This occurrence ard growth may open up the ,,4. possibility of growing these algae in culture pards providing the requisite hyd rological ard nutrient corditions

Nrf2 deficiency influences susceptibility to steroid resistance via HDAC2 reduction

Abnormal lung inflammation and oxidant burden are associated with a significant reduction in histone deacetylase 2 (HDAC2) abundance and steroid resistance. We hypothesized that Nrf2 regulates steroid sensitivity via HDAC2 in response to inflammation in mouse lung. Furthermore, HDAC2 deficiency leads to steroid resistance in attenuating lung inflammatory response, which may be due to oxidant/antioxidant imbalance. Loss of antioxidant transcription factor Nrf2 resulted in decreased HDAC2 in lung, and increased inflammatory lung response which was not reversed by steroid. Thus, steroid resistance or inability of steroids to control lung inflammatory response is dependent on Nrf2-HDAC2 axis. These findings have implications in steroid resistance, particularly during the conditions of oxidative stress when the lungs are more susceptible to inflammatory response, which is seen in patients with chronic obstructive pulmonary disease, asthma, rheumatoid arthritis, and inflammatory bowel disease

Selective Disruption Of Tlr2-Myd88 Interaction Inhibits Inflammation And Attenuates Alzheimer\u27S Pathology

Induction of TLR2 activation depends on its association with the adapter protein MyD88. We have found that TLR2 and MyD88 levels are elevated in the hippocampus and cortex of patients with Alzheimer\u27s disease (AD) and in a 5XFAD mouse model of AD. Since there is no specific inhibitor of TLR2, to target induced TLR2 from a therapeutic angle, we engineered a peptide corresponding to the TLR2-interacting domain of MyD88 (TIDM) that binds to the BB loop of only TLR2, and not other TLRs. Interestingly, WT TIDM peptide inhibited microglial activation induced by fibrillar Aβ1-42 and lipoteichoic acid, but not 1-methyl-4-phenylpyridinium, dsRNA, bacterial lipopolysaccharide, flagellin, or CpG DNA. After intranasal administration, WT TIDM peptide reached the hippocampus, reduced hippocampal glial activation, lowered Aβ burden, attenuated neuronal apoptosis, and improved memory and learning in 5XFAD mice. However, WT TIDM peptide was not effective in 5XFAD mice lacking TLR2. In addition to its effects in 5XFAD mice, WT TIDM peptide also suppressed the disease process in mice with experimental allergic encephalomyelitis and collagen-induced arthritis. Therefore, selective targeting of the activated status of 1 component of the innate immune system by WT TIDM peptide may be beneficial in AD as well as other disorders in which TLR2/MyD88 signaling plays a role in disease pathogenesis

Amino Acid Compositions of 27 Food Fishes and Their Importance in Clinical Nutrition

Proteins and amino acids are important biomolecules which regulate key metabolic pathways and serve as precursors for synthesis of biologically important substances; moreover, amino acids are building blocks of proteins. Fish is an important dietary source of quality animal proteins and amino acids and play important role in human nutrition. In the present investigation, crude protein content and amino acid compositions of important food fishes from different habitats have been studied. Crude protein content was determined by Kjeldahl method and amino acid composition was analyzed by high performance liquid chromatography and information on 27 food fishes was generated. The analysis showed that the cold water species are rich in lysine and aspartic acid, marine fishes in leucine, small indigenous fishes in histidine, and the carps and catfishes in glutamic acid and glycine. The enriched nutrition knowledge base would enhance the utility of fish as a source of quality animal proteins and amino acids and aid in their inclusion in dietary counseling and patient guidance for specific nutritional needs

Disruption of Nrf2, a Key Inducer of Antioxidant Defenses, Attenuates ApoE-Mediated Atherosclerosis in Mice

Background: Oxidative stress and inflammation are two critical factors that drive the formation of plaques in atherosclerosis. Nrf2 is a redox-sensitive transcription factor that upregulates a battery of antioxidative genes and cytoprotective enzymes that constitute the cellular response to oxidative stress. Our previous studies have shown that disruption of Nrf2 in mice (Nrf2-/-) causes increased susceptibility to pulmonary emphysema, asthma and sepsis due to increased oxidative stress and inflammation. Here we have tested the hypothesis that disruption of Nrf2 in mice causes increased atherosclerosis. Principal Findings: To investigate the role of Nrf2 in the development of atherosclerosis, we crossed Nrf2-/- mice with apoliporotein E-deficient (ApoE-/- mice. ApoE-/- and ApoE-/- Nrf2-/- mice were fed an atherogenic diet for 20 weeks, and plaque area was assessed in the aortas. Surprisingly, ApoE-/- Nrf2-/- mice exhibited significantly smaller plaque area than ApoE-/- controls (11.5% vs 29.5%). This decrease in plaque area observed in ApoE-/- Nrf2-/- mice was associated with a significant decrease in uptake of modified low density lipoproteins (AcLDL) by isolated macrophages from ApoE-/- Nrf2-/- mice. Furthermore, atherosclerotic plaques and isolated macrophages from ApoE-/- Nrf2-/- mice exhibited decreased expression of the scavenger receptor CD36. Conclusions: Nrf2 is pro-atherogenic in mice, despite its antioxidative function. The net pro-atherogenic effect of Nrf2 may be mediated via positive regulation of CD36. Our data demonstrates that the potential effects of Nrf2-targeted therapies on cardiovascular disease need to be investigated.9 page(s

Nrf2 protects against pulmonary fibrosis by regulating the lung oxidant level and Th1/Th2 balance

<p>Abstract</p> <p>Background</p> <p>Pulmonary fibrosis is a progressive and lethal disorder. Although the precise mechanisms of pulmonary fibrosis are not fully understood, oxidant/antioxidant and Th1/Th2 balances may play an important role in many of the processes of inflammation and fibrosis. The transcription factor Nrf2 acts as a critical regulator for various inflammatory and immune responses by controlling oxidative stress. We therefore investigated the protective role of Nrf2 against the development of pulmonary fibrosis.</p> <p>Methods</p> <p>To generate pulmonary fibrosis, both wild-type C57BL/6 mice and Nrf2-deficient mice of the same background were administered bleomycin intratracheally.</p> <p>Results</p> <p>The survival of Nrf2-deficient mice after bleomycin administration was significantly lower than that of wild-type mice. The degree of bleomycin-induced initial pulmonary inflammation and pulmonary fibrosis was much more severe in Nrf2-deficient mice than in wild-type mice. The expression of antioxidant enzymes and phase II detoxifying enzymes was significantly reduced in the lungs of Nrf2-deficient mice, concomitant with an elevation of lung 8-isoprostane level, compared with wild-type mice. The expression of Th2 cytokines, such as interleukin-4 and interleukin-13, was significantly elevated in the lungs of Nrf2-deficient mice with an increase in the number of Th2 cells that express GATA-binding protein 3.</p> <p>Conclusions</p> <p>The results indicated that Nrf2 protects against the development of pulmonary fibrosis by regulating the cellular redox level and lung Th1/Th2 balance. Thus, Nrf2 might be an important genetic factor in the determination of susceptibility to pulmonary fibrosis.</p

Mechanism of Chemical Activation of Nrf2

NF-E2 related factor-2 (Nrf2) promotes the transcription of many cytoprotective genes and is a major drug target for prevention of cancer and other diseases. Indeed, the cancer-preventive activities of several well-known chemical agents were shown to depend on Nrf2 activation. It is well known that chemopreventive Nrf2 activators stabilize Nrf2 by blocking its ubiquitination, but previous studies have indicated that this process occurs exclusively in the cytoplasm. Kelch-like ECH-associated protein 1 (Keap1) binds to Nrf2 and orchestrates Nrf2 ubiquitination, and it has been a widely-held view that inhibition of Nrf2 ubiquitination by chemopreventive agents results from the dissociation of Nrf2 from its repressor Keap1. Here, we show that while the activation of Nrf2 by prototypical chemical activators, including 5,6-dihydrocyclopenta-1,2-dithiole-3-thione (CPDT) and sulforaphane (SF), results solely from inhibition of its ubiquitination, such inhibition occurs predominantly in the nucleus. Moreover, the Nrf2 activators promote Nrf2 association with Keap1, rather than disassociation, which appears to result from inhibition of Nrf2 phosphorylation at Ser40. Available evidence suggests the Nrf2 activators may block Nrf2 ubiquitination by altering Keap1 conformation via reaction with the thiols of specific Keap1 cysteines. We further show that while the inhibitory effects of CPDT and SF on Nrf2 ubiquitination depend entirely on Keap1, Nrf2 is also degraded by a Keap1-independent mechanism. These findings provide significant new insight about Nrf2 activation and suggest that exogenous chemical activators of Nrf2 enter the nucleus to exert most of their inhibitory impact on Nrf2 ubiquitination and degradation