Bisphosphonates use in Pachydermoperiostosis.

Pachydermoperiostosis is a rare genetic disorder which commonly presents with clubbing, bone pains and skin changes. The treatment is mostly unsatisfactory. We tried bisphosphonates in our case with encouraging results. We suggest that parenteral bisphosphonates should be tried early in treatment of Pachydermoperiostosis.

Genetic mutations associated with status epilepticus.

This paper reports the results of a preliminary search of the literature aimed at identifying the genetic mutations reported to be strongly associated with status epilepticus. Genetic mutations were selected for inclusion if status epilepticus was specifically mentioned as a consequence of the mutation in standard genetic databases or in a case report or review article. Mutations in 122 genes were identified. The genetic mutations identified were found in only rare conditions (sometimes vanishingly rare) and mostly in infants and young children with multiple other handicaps. Most of the genetic mutations can be subdivided into those associated with cortical dysplasias, inborn errors of metabolism, mitochondrial disease, or epileptic encephalopathies and childhood syndromes. There are no identified 'pure status epilepticus genes'. The range of genes underpinning status epilepticus differs in many ways from the range of genes underpinning epilepsy, which suggests that the processes underpinning status epilepticus differ from those underpinning epilepsy. It has been frequently postulated that status epilepticus is the result of a failure of 'seizure termination mechanisms', but the wide variety of genes affecting very diverse biochemical pathways identified in this survey makes any unitary cause unlikely. The genetic influences in status epilepticus are likely to involve a wide range of mechanisms, some related to development, some to cerebral energy production, some to diverse altered biochemical pathways, some to transmitter and membrane function, and some to defects in networks or systems. The fact that many of the identified genes are involved with cerebral development suggests that status epilepticus might often be a system or network phenomenon. To date, there are very few genes identified which are associated with adult-onset status epilepticus (except in those with preexisting neurological damage), and this is disappointing as the cause of many adult-onset status epilepticus cases remains obscure. It has been suggested that idiopathic adult-onset status epilepticus might often have an immunological cause but no gene mutations which relate to immunological mechanisms were identified. Overall, the clinical utility of what is currently known about the genetics of status epilepticus is slight and the findings have had little impact on clinical treatment despite what has been a very large investment in money and time. New genetic technologies may result in the identification of further genes, but if the identified genetic defects confer only minor susceptibility, this is unlikely to influence therapy. It is also important to recognize that genetics has social implications in a way that other areas of science do not. This article is part of a Special Issue entitled "Status Epilepticus".

Structural, optical and sensing properties of pure and Cu-doped SnO2 nanowires.

In present work, pure and copper (Cu) doped SnO2 nanowires have been synthesized by thermal evaporation process at ambient pressure. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) indicated the growth of wire-like pure and Cu-doped SnO2 nanostructures with their length of about 50 microm and 80 microm whereas transverse dimension of about 50-80 nm and 20-50 nm, respectively. The HRTEM and SAED pattern reveals the growth of single crystalline Cu-doped SnO2 nanowire. The EDX confirms that Cu has been doped in the SnO2 nanowires and atomic fraction of Cu in nanowires is about 2.5 at% when concentration of CuO in starting source powder is 50 wt%. X-ray diffraction showed that Cu gets incorporated into the SnO2 lattice and also confirms their tetragonal rutile structure. For comparative study of gas sensing properties of pure and Cu-doped SnO2 nanowire, isolated single nanowire based sensors have been fabricated for detection of ethanol gas. The doping of Cu was found to enhance the ethanol sensitivity of SnO2 nanowire based sensors and the sensor response improves with increase in ethanol concentration. This sensing behaviour offers a suitable application of the Cu-doped SnO2 nanowire sensor for detection of ethanol gas.

Overlapping drug-induced vasculitis, ANCA-associated vasculitis, and lupus nephritis caused by low-dose hydralazine.

INTRODUCTION: We present a case of drug-induced vasculitis secondary to low-dose hydralazine with overlapping features of antineutrophil cytoplasmic antibody-associated vasculitis and drug-induced lupus nephritis. CASE PRESENTATION: A 52-year-old Hispanic woman with a medical history of resistant hypertension treated with hydralazine 10 mg twice daily for 1 year presented with generalized weakness, dizziness, nausea, vomiting, and gross hematuria. There was fever, tachycardia, leukocytosis, lactic acidosis, hyperkalemia, renal failure, and anemia. Chest computed tomography and bronchoscopy revealed a left lower lobe infiltrate and diffuse alveolar hemorrhage. Serologic testing was positive for anti-double-stranded DNA, anti-Smith, lupus anticoagulant, anti-histone, anti-cardiolipin IgM antibodies, and antineutrophil cytoplasmic antibodies (myeloperoxidase and proteinase 3). A kidney biopsy revealed crescentic glomerulonephritis with an overlapping finding of membranous nephropathy. Broad-spectrum antibiotics, immunosuppressants, corticosteroids, and plasmapheresis were initiated. The patient survived but required continuous hemodialysis. CONCLUSIONS: Although a few cases of simultaneous antibody-associated vasculitis and drug-induced lupus nephritis secondary to hydralazine use have been reported, this case is singular. Similar findings were previously reported with doses of 50-100 mg two to three times daily over 1-5 years. In our patient, a dose of only 10 mg twice daily for a year caused a severe disease presentation. This brings to light the combination of different vasculitides that can coexist and the potentially life-threatening adverse effects of low-dose hydralazine that should be kept in mind.

Effect of substrates on structural and optical properties of tin oxide (SnO2) nanostructures.

We report on controlling the morphology of tin oxide (SnO2) nanostructures and the study of the effect of surface morphology on structural and optical properties of SnO2 nanostuctures. In present work, Tin oxide (SnO2) nanostructures such as nanowires and nanorods have been grown by thermal evaporation of SnO2 powder. To demonstrate the effect of different substrates on the morphology of grown SnO2 nanostructures, the thermal evaporation of SnO2 powder was carried out on Si and gold catalyzed Si (Au/Si) substrates. The scanning-electron-microscopic analysis shows the growth of SnO2 nanowires on Au/Si substrate and growth of SnO2 nanorods on Si substrate. The scanning-and transmission-electron-microscopic analysis shows that the diameter of SnO2 nanowires and nanorods are about 70 nm and 95 nm respectively and their length is about 80 microm and 30 microm respectively. The vapor-liquid-solid (VLS) growth of SnO2 nanowires and vapor-solid (VS) growth of SnO2 nanorods is also confirmed with the help of TEM and EDX spectra. The synthesized SnO2 nanowires show tetragonal rutile structure of SnO2, whereas SnO2 nanorods show tetragonal rutile as well as cassiterite structure of SnO2. UV-Vis absorption spectra showed the optical band gaps of 4.1 eV and 3.8 eV for the SnO2 nanowires and the nanorods, respectively. The SnO2 nanowires and nanorods show photoluminescence with broad emission peaks centred at around 600 nm and 580 nm respectively. Raman spectra of SnO2 nanowires shows three Raman shifts (478, 632, 773 cm(-1)) corresponding to Eg, A1g and B2g vibration modes, whereas in Raman spectra of SnO2 nanorods, A1g peak is dramatically reduced and the B2g mode is totally quenched.

The optical response of artificially twisted MoS[Formula: see text] bilayers.

Two-dimensional layered materials offer the possibility to create artificial vertically stacked structures possessing an additional degree of freedom-the interlayer twist. We present a comprehensive optical study of artificially stacked bilayers (BLs) MoS[Formula: see text] encapsulated in hexagonal BN with interlayer twist angle ranging from 0[Formula: see text] to 60[Formula: see text] using Raman scattering and photoluminescence spectroscopies. It is found that the strength of the interlayer coupling in the studied BLs can be estimated using the energy dependence of indirect emission versus the A[Formula: see text]-E[Formula: see text] energy separation. Due to the hybridization of electronic states in the valence band, the emission line related to the interlayer exciton is apparent in both the natural (2H) and artificial (62[Formula: see text]) MoS[Formula: see text] BLs, while it is absent in the structures with other twist angles. The interlayer coupling energy is estimated to be of about 50 meV. The effect of temperature on energies and intensities of the direct and indirect emission lines in MoS[Formula: see text] BLs is also quantified.

N-acetycysteine: A potential therapeutic agent in COVID-19 infection.

COVID-19 is an overwhelming pandemic which has shattered the whole world. Lung injury being the main clinical manifestation, it is likely to cause COPD (chronic obstructive pulmonary disease) and ARDS (acute respiratory distress syndrome). The possible cause behind this might be redox imbalance due to viral infection. Elevation in Glutathione (GSH) levels by administration of its promolecule might be effective. N-acetylcysteine is one such drug with potency to scavenge Reactive Oxygen Species, least side effects, and an effective precursor of glutathione. Consequently we hypothesize that N-acetylcysteine along with the conventional treatment may be treated as a potential therapeutic solution in cases of COVID-19 patients.

Interaction of iNOS Gene (C150T) Polymorphism and Endothelial Dysfunction in Pathophysiology of Metabolic Syndrome.

OBJECTIVE: To study the endothelial dysfunction by measuring Nitric Oxide and Endothelin-1, and inter-genotypic variation of inducible Nitric Oxide Synthase gene (C150T) polymorphism among the study subjects. METHODS: 50 diagnosed cases of metabolic syndrome as per International Diabetes Federation (IDF) criteria and 50 healthy volunteers as control were enrolled. Nitric Oxide, Endothelin were measured and PCR-RFLP was done to identify the iNOS gene C150T polymorphism and its effect on serum nitric oxide levels. RESULTS: Subjects with metabolic syndrome had lower NO levels (16.3 ± 10.3 vs 20.9 ± 11 µM, p = 0.032) and higher endothelin (2.68 ± 1.73 vs 1.98 ± 0.82 fmol/ml, p = 0.011). The frequency of mutant T allele (10% vs 9%) was higher in cases. Serum nitric oxide levels were lower in cases expressing the Mutant T allele as compared to wild type C allele. However, the differences were not statistically significant. CONCLUSIONS: The present study demonstrated that iNOS C150T polymorphism did not show significant association with metabolic syndrome. Serum nitric oxide levels could be influenced by factors other than genetic polymorphism of iNOS gene (C150T) which cause endothelial dysfunction in metabolic syndrome and associated co-morbidities.

Plasma fireball: A unique tool to fabricate patterned nanodots.

A large plasma fireball is formed using a reverse biased planar sputter magnetron source. The magnetic field considerably reduces the contact area of the anode with the plasma and results in the formation of the fireball. Ions are extracted from the fireball using a large voltage cathode sheath of the grounded sample holder. The physical mechanism for the extraction of the ions from the fireball along with the effect of the sample holder on the fireball and the discharge current is discussed. The device is shown as a novel tool for developing nanodot patterns on a GaSb substrate without the use of additional ion source or power supplies. Variable nanodot patterns produced simply by the alteration of discharge conditions demonstrate unique surface wettability and reflection properties.

Raised TSH is associated with endothelial dysfunction in Metabolic Syndrome: A case control study.

INTRODUCTION: Endothelial dysfunction has been considered as one of the important factors in pathogenesis of Metabolic Syndrome (Met S). Subclinical hypothyroidism (SCH) has also been reported to be associated with Met S. The aim of our study is to evaluate the association of raised TSH with mediators of endothelial dysfunction in Met S with Subclinical hypothyroidism as compared to healthy controls. METHODS: Study population consisted of 100 subjects, out of which 50 were cases of Met S and 50 were healthy controls. Met S group were further divided into two, based on the presence & absence of SCH. Serum insulin, T3, T4, TSH were measured by chemiluminescence based immunoassay (CLIA). Serum nitric oxide (NO) levels were measured by Modified Griess's method and serum endothelin-1 (ET-1) levels were measured by ELISA. RESULTS: Out of 50 cases of Met S, SCH was diagnosed in 22. The mean serum TSH levels were significantly higher in Met S cases as compared to healthy controls (5.7 ± 1.2 µIU/mL vs. 2.3 ± 1.6 µIU/mL, P <0.0001). Mean serum NO levels were significantly lower in Met S cases as compared to healthy control (15.4 ± 10 µM vs. 21 ± 10 µM, p = 0.009). Mean serum ET-1 levels were significantly higher in Met S cases as compared to healthy controls (2.68 ± 1.7 fmol/mL vs. 2.1 ± 0.84 fmol/mL, p = 0.011). On Pearson's correlation analysis, TSH showed positive correlation with ET-1 (r = 0.341, p = 0.001) and negative correlation with NO (r = -0.331, p = 0.001). Binary logistic regression analysis showed that TSH, NO and ET-1 has significant odd's ratio for predicting Met S. CONCLUSION: Met S cases were screened for thyroid abnormalities and found to have 44% of SCH along with co-existing endothelial dysfunction. Raised TSH in SCH could cause endothelial dysfunction which may lead to Met S and associated co-morbidities. Present study gives new insight in linking endothelial dysfunction and raised TSH in Met S. Therefore, Met S cases should be screened for SCH and treated appropriately to attenuate endothelial dysfunction and associated comorbidities in Met S.

Role of Sub Clinical Hypothyroidism in Association with Adiponectin Levels Causing Insulin Resistance in Metabolic Syndrome: A Case Control Study.

INTRODUCTION: Metabolic Syndrome (Met S) is reported to be associated with sub clinical hypothyroidism (SCH). The aim of our study is to evaluate the role of SCH in association with adiponectin levels causing insulin resistance in metabolic syndrome. MATERIALS AND METHOD: We recruited 100 study subjects; out of which 50 were cases of Met S, which were further divided into two groups based on presence and absence of SCH and 50 were healthy controls. Serum insulin, serum T3, T4, TSH were measured by chemiluminisence based immunoassay and serum adiponectin was measured by ELISA. RESULTS: Mean TSH levels were significantly higher in Met S cases as compare to control. Out of 50 cases of Met S, 22 (44 %) had SCH. Mean serum adiponectin were significantly lower in Met S cases as compare to control. On Pearson's correlation analysis, TSH showed significant positive correlation with HOMA-IR and negative correlation with adiponectin levels. Strong association was found on the likelihood of low levels of adiponectin in Met S cases. CONCLUSIONS: Met S cases showed insulin resistance and underlying SCH. SCH in Met S may cause altered adipocytes physiology which is associated with decreased release of insulin sensitising adiponectin which may lead to insulin resistance and future development of type II DM and associated co morbidities. Therefore, Met S cases should be screened for SCH and adiponectin levels thereafter. Also, our recommendation is SCH should be treated appropriately to attenuate insulin resistance and development of type II DM in Met S.

Association of prothrombotic adipokine (plasminogen activator inhibitor-1) with TSH in metabolic syndrome: a case control study.

Background Metabolic syndrome (MetS) involves a cluster of cardiovascular risk factors, including abnormal lipids, insulin resistance and hypertension. The aim of the present study is to investigate associations between thyroid profile and the pro-thrombotic mediator, plasminogen activator inhibitor-1 (PAI-1), in MetS and identify associated biochemical markers. Materials and methods The present study was a case control study and consisted of 50 diagnosed cases of MetS and 50 healthy volunteers as controls. MetS cases were further divided into two groups based on the presence and absence of subclinical hypothyroidism (SCH). Data collected included demographic profile, clinical history and routine lab investigation. Special investigations included the thyroid function test and serum PAI-1 levels. Results The mean serum thyroid-stimulating hormone (TSH) levels were significantly higher in MetS cases as compared to controls (5.7 ± 1.2 mIU/L vs. 2.3 ± 1.6 mIU/L, p < 0.0001), although the mean triiodothyronine (T3) and thyroxine (T4) levels were comparable in two groups. The mean levels of serum PAI-1 were significantly higher in MetS cases as compared to controls(231 ± 87 ng/mL vs. 185 ± 96 ng/mL, p = 0.013). TSH and PAI-1 levels were positively correlated with various markers of MetS and negatively correlated with high-density lipoprotein (HDL). Conclusion The present study points towards the presence of thyroid dysfunction, in the form of subclinical hypothyroidism (SCH), in cases of MetS. In the presence of thyroid dysfunction, abnormal adipocytes may release adipokines, such as PAI-1, which lead to increased risk of thrombotic episodes in these patients. Hence, SCH should be appropriately managed.

Obstetric history and reproductive tract infections among married female (15-44 yrs.) in rural area of district Meerut, U.P.

The prevalence of RTIs in 600 married females (15-44 yrs.) representing 12 subcentre villages of Daurala block of Meerut was 35.3%. The reproductive tract infections were significantly associated with place of last delivery (P< 0.001), person conducted the last delivery (P< 0.001) and in women had history of abortions (P< .005).

The study of markers of endothelial dysfunction in metabolic syndrome.

BACKGROUND: Metabolic syndrome (MetS) consists of a constellation of metabolic abnormalities that confer increased risk of cardiovascular disease (CVD) and diabetes mellitus (DM). Endothelial dysfunction is one of the key components of MetS which is caused by imbalance between vasodilatory substances like nitric oxide (NO) and vaso-constrictive substances like endothelin and prothrombotic factors like plasminogen activator inhibitor-1 (PAI-1). OBJECTIVE: To study the markers of endothelial dysfunction (NO and endothelin) and prothrombotic markers (PAI-1) among the study subjects. MATERIALS AND METHODS: We enrolled 50 diagnosed cases of MetS as per International Diabetes Federation (IDF) criteria and 50 healthy volunteers as controls. Clinical evaluation included anthropometric, routine biochemical, hematological, serum insulin, NO, endothelin and PAI-1 measurements. RESULTS: Subjects with MetS had higher insulin, endothelin and PAI-1 levels and low NO levels as compared to controls and the difference was found to be significant. The serum insulin levels were positively correlated with PAI-1 and endothelin, and negatively correlated with NO. CONCLUSION: Endothelial functional status as reflected by decreased NO and increased serum endothelin levels along with insulin resistance is seen in MetS. Moreover, higher serum level of PAI-1 also tilts towards a more prothrombotic milieu in the vascular endothelium. Hence endothelial dysfunction and prothrombotic markers may be used to guide for early diagnosis of cardiovascular disease and type 2 diabetes in patients with MetS.

Neurochemical changes in the hippocampus of the brown Norway rat during aging.

Microdensitometrical and stereological techniques were applied to study the effects of aging on the hippocampus of 3-, 6-, 12-, 18-, 24-, 30-, and 36-month-old male Brown Norway rats. Stereological analysis of basic fibroblast growth factor (bFGF) immunoreactive glial cells in the CA1 area showed an age-dependent decrease in the number of cells, starting at 18 months of age. Specific mean gray values of the immunoreactivity for bFGF were reduced in the CA3 area, in the dentate gyrus, and in fields of the CA1 area, starting at 24 months of age. There were no differences between the age groups in the number of glial fibrillary acidic protein or glucocorticoid receptor (GR) immunoreactive cells of the CA1-CA2 areas. However, the intensity of the GR immunoreactivity was decreased in the 18-month-old and older rats. No changes in the immunoreactivity for the mineralocorticoid receptor were observed in the CA1-CA2 areas of any of the age groups. Spontaneous alternation test and reactivity in an open field did not reveal marked differences between the age groups. These findings give evidence that there is a loss of neural GR immunoreactivity, but no loss of GR immunoreactive neurons, in the CA1-CA2 areas of the aged Brown Norway rat. Aging may also be characterized by substantial deficits of glially derived growth factors, such as bFGF in the hippocampus. The changes in immunoreactivities were not correlated to alterations in selected behaviors dependent on normal hippocampal function.

Enhancement of reactive oxygen-dependent mitochondrial membrane lipid peroxidation by the anticancer drug adriamycin.

Mitochondrial degeneration is a consistently prominent morphological alteration associated with adriamycin toxicity which may be the consequence of adriamycin-enhanced peroxidative damage to unsaturated mitochondrial membrane lipids. Using isolated rat liver mitochondria as an in vitro model system to study the effects of the anticancer drug adriamycin on lipid peroxidation, we found that NADH-dependent mitochondrial peroxidation--measured by the 2-thiobarbituric acid method--was stimulated by adriamycin as much as 4-fold. Marker enzyme analysis indicated that the mitochondria were substantially free of contaminating microsomes (less than 5%). Lipid peroxidation in mitochondria incubated in KCl-Tris-HCl buffer (pH 7.4) under an oxygen atmosphere was optimal at 1-2 mg of mitochondrial protein/ml and with NADH at 2.5 mM. Malonaldehyde production was linear with time to beyond 60 min, and the maximum enhancement of peroxidation was observed with adriamycin at 50-100 microM. Interestingly, in contrast to its stimulatory effect on NADH-supported mitochondrial peroxidation, adriamycin markedly diminished ascorbate-promoted lipid peroxidation in mitochondria. Superoxide dismutase, catalase, 1,3-dimethylurea, reduced glutathione, alpha-tocopherol and EDTA added to incubation mixtures inhibited endogenous and adriamycin-augmented NADH-dependent peroxidation of mitochondrial lipids, indicating that multiple species of reactive oxygen (superoxide anion radical, hydrogen peroxide and hydroxyl radical) and possibly trace amounts of endogenous ferric iron participated in the peroxidation reactions. In submitochondrial particles freed of endogenous defenses against oxyradicals, lipid peroxidation was increased 7-fold by adriamycin. These observations suggest that some of the effects of adriamycin on mitochondrial morphology and biochemical function may be mediated by adriamycin-enhanced reactive oxygen-dependent mitochondrial lipid peroxidation.