Traumatic avulsion of the eyeball: a case report

Ocular trauma is very common, but globe avulsion along with optic nerve avulsion is a rare clinical event. Blunt trauma during a road traffic accident can cause rupture or avulsion of the globe and the outcome can range from complete recovery on repositioning to visual loss because of globe perforation or optic nerve injury. Here, authors report a case of a 20-year-old male who presented with history of a road traffic accident causing severe facial injuries. The physical examination revealed oedema and ecchymoses over the right side of the face with avulsion of the right eyeball anteriorly outside the orbit along with avulsion of the optic nerve. The visual acuity in the injured eye was no perception of light and the direct pupillary response was absent. Computed tomography revealed fracture of the roof and lateral wall of the right orbit. As the eye was not salvageable, enucleation surgery was done. Insertion of an ocular prosthesis for rehabilitation was planned. The presentation, investigations, surgery and follow-ups are described

Dirhenium Carbonyl Complexes Bearing 2-Vinylpyridine, Morpholine and 1-Methylimidazole Ligands

Treatment of the labile compound [Re2(CO)8(MeCN)2] with 2-vinylpyridine in refluxing benzene affords exclusively the new compound [Re2(CO)8(μ-η1:η2-NC5H4CHCH2)] (1) in 39% yield in which the μ-η1:η2-vinylpyridine ligand is coordinated to one Re atom through the nitrogen and to the other Re atom via the olefinic double bond. Reaction of [Re2(CO)8(MeCN)2] with morpholine in refluxing benzene furnishes two compounds, [Re2(CO)9(η1-NC4H9O)] (2) and [Re2(CO)8(η1-NC4H9O)2] (3) in 5% and 29% yields, respectively. Reaction of [Re2(CO)8(MeCN)2] with 1-methylimidazole gives [Re2(CO)8{η1-NC3H3N(CH3)}2] (4) and the mononuclear compound fac-[ReCl(CO)3{η1-NC3H3N(CH3)}2] (5) in 18% and 26% yields, respectively. In the disubstituted compounds 2 and 4, the heterocyclic ligands occupy equatorial coordination sites. The mononuclear compound 5 consists of three CO groups, two N coordinated η1-1-methylimidazole ligands and a terminal Cl ligand. The XRD structures of complexes 1, 3 and 5 are reported

Reactivity of [Re\u3csub\u3e2\u3c/sub\u3e(CO)\u3csub\u3e8\u3c/sub\u3e(MeCN)\u3csub\u3e2\u3c/sub\u3e] with Thiazoles: Hydrido Bridged Dirhenium Compounds Bearing Thiazoles in Different Coordination Modes

Reactions of the labile compound [Re2(CO)8(MeCN)2] with thiazole and 4-methylthiazole in refluxing benzene afforded the new compounds [Re2(CO)7{μ-2,3-η2-C3H(R)NS}{η1-NC3H2(4-R)S}(μ-H)] (1, R = H; 2, R = CH3), [Re2(CO)6{μ-2,3-η2-C3H(R)NS}{η1-NC3H2(4-R)S}2(μ-H)] (3, R = H; 4, R = CH3) and fac-[Re(CO)3(Cl){η1-NC3H2(4-R)S}2] (5, R = H; 6, R = CH3). Compounds 1 and 2 contain two rhenium atoms, one bridging thiazolide ligand, coordinated through the C(2) and N atoms and a η1-thiazole ligand coordinated through the nitrogen atom to the same Re as the thiazolide nitrogen. Compounds 3 and 4 contain a Re2(CO)6 group with one bridging thiazolide ligand coordinated through the C(2) and N atoms and two N-coordinated η1-thiazole ligands, each coordinated to one Re atom. A hydride ligand, formed by oxidative-addition of C(2)–H bond of the ligand, bridges Re–Re bond opposite the thiazolide ligand in compounds 1–4. Compound 5 contains a single rhenium atom with three carbonyl ligands, two N-coordinated η1-thiazole ligands and a terminal Cl ligand. Treatment of both 1 and 2 with 5 equiv. of thiazole and 4-methylthiazole in the presence of Me3NO in refluxing benzene afforded 3 and 4, respectively. Further activation of the coordinated η1-thiazole ligands in 1–4 is, however, unsuccessful and results only nonspecific decomposition. The single-crystal XRD structures of 1–5 are reported

Localization of Melatonin Receptor 1 in Mouse Retina and Its Role in the Circadian Regulation of the Electroretinogram and Dopamine Levels

Melatonin modulates many important functions within the eye by interacting with a family of G-protein-coupled receptors that are negatively coupled with adenylate cyclase. In the mouse, Melatonin Receptors type 1 (MT1) mRNAs have been localized to photoreceptors, inner retinal neurons, and ganglion cells, thus suggesting that MT1 receptors may play an important role in retinal physiology. Indeed, we have recently reported that absence of the MT1 receptors has a dramatic effect on the regulation of the daily rhythm in visual processing, and on retinal cell viability during aging. We have also shown that removal of MT1 receptors leads to a small (3–4 mmHg) increase in the level of the intraocular pressure during the night and to a significant loss (25–30%) in the number of cells within the retinal ganglion cell layer during aging. In the present study we investigated the cellular distribution in the C3H/f+/+ mouse retina of MT1 receptors using a newly developed MT1 receptor antibody, and then we determined the role that MT1 signaling plays in the circadian regulation of the mouse electroretinogram, and in the retinal dopaminergic system. Our data indicate that MT1 receptor immunoreactivity is present in many retinal cell types, and in particular, on rod and cone photoreceptors and on intrinsically photosensitive ganglion cells (ipRGCs). MT1 signaling is necessary for the circadian rhythm in the photopic ERG, but not for the circadian rhythm in the retinal dopaminergic system. Finally our data suggest that the circadian regulation of dopamine turnover does not drive the photopic ERG rhythm

Potential benefits and therapeutic applications of "Panchgavya" therapy (Cowpathy) for human and animal health: Current scientific knowledge

Cow's milk, urine, dung, ghee, and curd (together known as "Panchgavya") have incomparable medicinal value in Ayurveda and ancient Indian clinical methods. Panchgavya is also known as Cowpathy in Ayurveda. In India, the cow is revered as a goddess known as "Gaumata" because of its nurturing qualities similar to those of a mother. Almost no adverse effects are associated with using Panchgavya, which is why it is recommended in Ayurveda for treating disorders affecting numerous body systems. Its possible antimicrobial effects have piqued the curiosity of medical researchers and practitioners. Cow milk is widely regarded as a nutritious diet and has been shown to effectively treat various medical conditions, including high body temperature, pain, cancer, diabetes, kidney diseases, and weakness. Milk can prevent the growth of microorganisms, has erotic qualities when combined with the leaves of medicinal herbs, and the fat in milk has anticancer characteristics. Toned and skim milk, lassi, yoghurt, cottage cheese, and khoa all come from milk and have important medicinal characteristics. Curd (dahi) is recommended as a blood purifier for conditions such as hemorrhoids, piles, and gastrointestinal issues. Ghee made from cows has been shown to boost immunity. It is important to highlight the use of cow dung as an antifungal and for treating malaria and tuberculosis. It has the potential to aid in the development of a populace free from disease, the creation of sustainable energy systems, the fulfilment of all nutritional needs, the elimination of poverty, the promotion of organic farming culture, and the like. Cow urine is a powerful remedy for numerous medical conditions, including but not limited to epileptic convulsions, diabetes, hepatitis, inflammation, fever, and anaemia. The current review article explores how the Panchgavya ingredients can be employed to safeguard human and animal health

Pleomorphic adenoma of minor salivary gland with therapeutic misadventure: a rare case report

<p>Abstract</p> <p>Background</p> <p>The benign tumors of nasopharynx are least encountered tumors in otolaryngology, as nasopharynx is considered one of notorious anatomical site for the malignant tumors. Pleomorphic adenoma of the minor salivary gland of nasopharynx and parapharyngeal space is rare. We present a pleomorphic adenoma of minor salivary gland which was mismanaged.</p> <p>Case presentation</p> <p>An adult male presented with left nostril obstruction for five months. The examination found big mass extending from nasopharynx to oropharynx. On CT scan, this tumor was quite big and extending to the parapharyngeal space. The FNAB found it a carcinoma but it did not respond to radiotherapy. The excision biopsy of tumor revealed it as pleomorphic adenoma. We found only five published reports on this tumor arising from nasopharynx.</p> <p>Discussion and conclusion</p> <p>Although, in this case report exact origin of the tumor could not be ascertained as it also appeared to be a parapharyngeal tumor but we kept the possibility of a nasopharyngeal tumor on the basis of clinical features. The pleomorphic adenoma of nasopharynx is rare. It can be misdiagnosed as malignant epithelial tumor on histopathology. The differentiation from its malignant variant is also difficult. A possibility of benign tumor should always be kept in nasopharyngeal growth with no evidence of metastasis, and histopathological diagnosis of growth should be available before any definitive treatment.</p

Transcriptional regulation of Satb1 in mouse trophoblast stem cells

SATB homeobox proteins are important regulators of developmental gene expression. Among the stem cell lineages that emerge during early embryonic development, trophoblast stem (TS) cells exhibit robust SATB expression. Both SATB1 and SATB2 act to maintain the trophoblast stem-state. However, the molecular mechanisms that regulate TS-specific Satb expression are not yet known. We identified Satb1 variant 2 as the predominant transcript in trophoblasts. Histone marks, and RNA polymerase II occupancy in TS cells indicated an active state of the promoter. A novel cis-regulatory region with active histone marks was identified ∼21 kbp upstream of the variant 2 promoter. CRISPR/Cas9 mediated disruption of this sequence decreased Satb1 expression in TS cells and chromosome conformation capture analysis confirmed looping of this distant regulatory region into the proximal promoter. Scanning position weight matrices across the enhancer predicted two ELF5 binding sites in close proximity to SATB1 sites, which were confirmed by chromatin immunoprecipitation. Knockdown of ELF5 downregulated Satb1 expression in TS cells and overexpression of ELF5 increased the enhancer-reporter activity. Interestingly, ELF5 interacts with SATB1 in TS cells, and the enhancer activity was upregulated following SATB overexpression. Our findings indicate that trophoblast-specific Satb1 expression is regulated by long-range chromatin looping of an enhancer that interacts with ELF5 and SATB proteins

Expression of Human Frataxin Is Regulated by Transcription Factors SRF and TFAP2

Friedreich ataxia is an autosomal recessive neurodegenerative disease caused by reduced expression levels of the frataxin gene (FXN) due to expansion of triplet nucleotide GAA repeats in the first intron of FXN. Augmentation of frataxin expression levels in affected Friedreich ataxia patient tissues might substantially slow disease progression.We utilized bioinformatic tools in conjunction with chromatin immunoprecipitation and electrophoretic mobility shift assays to identify transcription factors that influence transcription of the FXN gene. We found that the transcription factors SRF and TFAP2 bind directly to FXN promoter sequences. SRF and TFAP2 binding sequences in the FXN promoter enhanced transcription from luciferase constructs, while mutagenesis of the predicted SRF or TFAP2 binding sites significantly decreased FXN promoter activity. Further analysis demonstrated that robust SRF- and TFAP2-mediated transcriptional activity was dependent on a regulatory element, located immediately downstream of the first FXN exon. Finally, over-expression of either SRF or TFAP2 significantly increased frataxin mRNA and protein levels in HEK293 cells, and frataxin mRNA levels were also elevated in SH-SY5Y cells and in Friedreich ataxia patient lymphoblasts transfected with SRF or TFAP2.We identified two transcription factors, SRF and TFAP2, as well as an intronic element encompassing EGR3-like sequence, that work together to regulate expression of the FXN gene. By providing new mechanistic insights into the molecular factors influencing frataxin expression, our results should aid in the discovery of new therapeutic targets for the treatment of Friedreich ataxia

Mapping of variations in child stunting, wasting and underweight within the states of India: the Global Burden of Disease Study 2000–2017

Background To inform actions at the district level under the National Nutrition Mission (NNM), we assessed the prevalence trends of child growth failure (CGF) indicators for all districts in India and inequality between districts within the states. Methods We assessed the trends of CGF indicators (stunting, wasting and underweight) from 2000 to 2017 across the districts of India, aggregated from 5 × 5 km grid estimates, using all accessible data from various surveys with subnational geographical information. The states were categorised into three groups using their Socio-demographic Index (SDI) levels calculated as part of the Global Burden of Disease Study based on per capita income, mean education and fertility rate in women younger than 25 years. Inequality between districts within the states was assessed using coefficient of variation (CV). We projected the prevalence of CGF indicators for the districts up to 2030 based on the trends from 2000 to 2017 to compare with the NNM 2022 targets for stunting and underweight, and the WHO/UNICEF 2030 targets for stunting and wasting. We assessed Pearson correlation coefficient between two major national surveys for district-level estimates of CGF indicators in the states. Findings The prevalence of stunting ranged 3.8-fold from 16.4% (95% UI 15.2–17.8) to 62.8% (95% UI 61.5–64.0) among the 723 districts of India in 2017, wasting ranged 5.4-fold from 5.5% (95% UI 5.1–6.1) to 30.0% (95% UI 28.2–31.8), and underweight ranged 4.6-fold from 11.0% (95% UI 10.5–11.9) to 51.0% (95% UI 49.9–52.1). 36.1% of the districts in India had stunting prevalence 40% or more, with 67.0% districts in the low SDI states group and only 1.1% districts in the high SDI states with this level of stunting. The prevalence of stunting declined significantly from 2010 to 2017 in 98.5% of the districts with a maximum decline of 41.2% (95% UI 40.3–42.5), wasting in 61.3% with a maximum decline of 44.0% (95% UI 42.3–46.7), and underweight in 95.0% with a maximum decline of 53.9% (95% UI 52.8–55.4). The CV varied 7.4-fold for stunting, 12.2-fold for wasting, and 8.6-fold for underweight between the states in 2017; the CV increased for stunting in 28 out of 31 states, for wasting in 16 states, and for underweight in 20 states from 2000 to 2017. In order to reach the NNM 2022 targets for stunting and underweight individually, 82.6% and 98.5% of the districts in India would need a rate of improvement higher than they had up to 2017, respectively. To achieve the WHO/UNICEF 2030 target for wasting, all districts in India would need a rate of improvement higher than they had up to 2017. The correlation between the two national surveys for district-level estimates was poor, with Pearson correlation coefficient of 0.7 only in Odisha and four small north-eastern states out of the 27 states covered by these surveys. Interpretation CGF indicators have improved in India, but there are substantial variations between the districts in their magnitude and rate of decline, and the inequality between districts has increased in a large proportion of the states. The poor correlation between the national surveys for CGF estimates highlights the need to standardise collection of anthropometric data in India. The district-level trends in this report provide a useful reference for targeting the efforts under NNM to reduce CGF across India and meet the Indian and global targets. Keywords Child growth failureDistrict-levelGeospatial mappingInequalityNational Nutrition MissionPrevalenceStuntingTime trendsUnder-fiveUndernutritionUnderweightWastingWHO/UNICEF target

The role of acyl-coenzyme A carboxylase complex in lipstatin biosynthesis of Streptomyces toxytricini

Streptomyces toxytricini produces lipstatin, a specific inhibitor of pancreatic lipase, which is derived from two fatty acid moieties with eight and 14 carbon atoms. The pccB gene locus in 10.6 kb fragment of S. toxytricini chromosomal DNA contains three genes for acyl-coenzyme A carboxylase (ACCase) complex accA3, pccB, and pccE that are presumed to be involved in secondary metabolism. The pccB gene encoding a β subunit of ACCase [carboxyltransferase (CT)] was identified upstream of pccE gene for a small protein of ε subunit. The accA3 encoding the α subunit of ACCase [biotin carboxylase (BC)] was also identified downstream of pccB gene. When the pccB and pccE genes were inactivated by homologous recombination, the lipstatin production was reduced as much as 80%. In contrast, the accumulation of another compound, tetradeca-5.8-dienoic acid (the major lipstatin precursor), was 4.5-fold increased in disruptant compared with wild-type. It implies that PccB of S. toxytricini is involved in the activation of octanoic acid to hexylmalonic acid for lipstatin biosynthesis