Comparative study of vitamin D3 levels in polycystic ovarian syndrome vs non-polycystic ovarian females

Background: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age and has a strong genetic component with a prevalence of 6–10% in the general population. Metabolic disturbances are common in women suffering from PCOS: 30–40% have impaired glucose tolerance and IR with compensatory hyperinsulinemia, and as many as 10% will have type 2 diabetes mellitus by their fourth decade. Recently, vitamin D deficiency has been proposed as the possible missing link between IR and PCOS. Polycystic ovarian syndrome (PCOS) and hypovitaminosis D are the two most common endocrine disorders in young women leading to many adverse metabolic consequences.  This study aims to estimate vitamin D3 levels in patients of polycystic ovarian disease and compare it with non PCOS females and to study correlation between Vitamin D3 levels and polycystic ovarian syndrome. Methods: The present patient population case control study was carried out in Department of Obstetrics and Gynaecology of Jaipur Golden Hospital diagnosed involving cases of PCOS and controls of non PCOS (48 each) by random sampling method from September 2019 to June 2021. History, general examination, systemic examination and Vitamin D levels was taken for each patient. Results: Mean vitamin D value of cases was 14.57±6.86 ng/ml and that in controls was 29.31±6.53 ng/ml. When we compared the mean vitamin D value of both the groups, there was statistically significant difference found between the two groups. . We found significant negative correlation found between vitamin D value with age and BMI. Conclusions: Hypovitaminosis D is very common in PCOS patients and exacerbates the metabolic abnormalities. It is essential to screen all the PCOS patients for 25OHD deficiency and institute appropriate replacement therapy to prevent the adverse consequences

Counterspeeches up my sleeve! Intent Distribution Learning and Persistent Fusion for Intent-Conditioned Counterspeech Generation

Counterspeech has been demonstrated to be an efficacious approach for combating hate speech. While various conventional and controlled approaches have been studied in recent years to generate counterspeech, a counterspeech with a certain intent may not be sufficient in every scenario. Due to the complex and multifaceted nature of hate speech, utilizing multiple forms of counter-narratives with varying intents may be advantageous in different circumstances. In this paper, we explore intent-conditioned counterspeech generation. At first, we develop IntentCONAN, a diversified intent-specific counterspeech dataset with 6831 counterspeeches conditioned on five intents, i.e., informative, denouncing, question, positive, and humour. Subsequently, we propose QUARC, a two-stage framework for intent-conditioned counterspeech generation. QUARC leverages vector-quantized representations learned for each intent category along with PerFuMe, a novel fusion module to incorporate intent-specific information into the model. Our evaluation demonstrates that QUARC outperforms several baselines by an average of 10% across evaluation metrics. An extensive human evaluation supplements our hypothesis of better and more appropriate responses than comparative systems.Comment: ACL 202

Resource discovery for distributed computing systems: A comprehensive survey

Large-scale distributed computing environments provide a vast amount of heterogeneous computing resources from different sources for resource sharing and distributed computing. Discovering appropriate resources in such environments is a challenge which involves several different subjects. In this paper, we provide an investigation on the current state of resource discovery protocols, mechanisms, and platforms for large-scale distributed environments, focusing on the design aspects. We classify all related aspects, general steps, and requirements to construct a novel resource discovery solution in three categories consisting of structures, methods, and issues. Accordingly, we review the literature, analyzing various aspects for each category

Multiple intra cardiac rhabdomyomas in neonate

An 18 day old neonate presented with tachypnea. Congenital heart disease was suspected and referred for Pediatric Cardiology opinion. 2D Echocardiography revealed multiple, intra cardiac, highly echogenic, well circumscribed, intramural and intra cavitary rhabdomyomas. There were no systemic manifestations of associated tuberous sclerosis. At present, surgical excision of rhabdomyoma was not indicated and hence child was advised regular follow up with echocardiography evaluation

Hammock mitral valve: A rare case report

Congenital mitral stenosis is a relatively rare disorder comprising 0.2% of all congenital heart defects. Hammock mitral valve producing severe mitral stenosis is a rare variant of congenital mitral stenosis. We report a 2-year-old boy who had hammock mitral valve producing severe mitral stenosis with severe pulmonary artery hypertension. He underwent successful surgical repair. Post-surgery, the mitral valve opening was adequate without residual stenosis or regurgitation. Pulmonary artery pressure had normalized. Follow-up data showed he had significant clinical and echocardiography improvement. This is the first reported case of successful surgical repair done for hammock mitral valve from our institute

Loss of photoreceptors results in upregulation of synaptic proteins in bipolar cells and amacrine cells.

Deafferentation is known to cause significant changes in the postsynaptic neurons in the central nervous system. Loss of photoreceptors, for instance, results in remarkable morphological and physiological changes in bipolar cells and horizontal cells. Retinal ganglion cells (RGCs), which send visual information to the brain, are relatively preserved, but show aberrant firing patterns, including spontaneous bursts of spikes in the absence of photoreceptors. To understand how loss of photoreceptors affects the circuitry presynaptic to the ganglion cells, we measured specific synaptic proteins in two mouse models of retinal degeneration. We found that despite the nearly total loss of photoreceptors, the synaptophysin protein and mRNA levels in retina were largely unaltered. Interestingly, the levels of synaptophysin in the inner plexiform layer (IPL) were higher, implying that photoreceptor loss results in increased synaptophysin in bipolar and/or amacrine cells. The levels of SV2B, a synaptic protein expressed by photoreceptors and bipolar cells, were reduced in whole retina, but increased in the IPL of rd1 mouse. Similarly, the levels of syntaxin-I and synapsin-I, synaptic proteins expressed selectively by amacrine cells, were higher after loss of photoreceptors. The upregulation of syntaxin-I was evident as early as one day after the onset of photoreceptor loss, suggesting that it did not require any massive or structural remodeling, and therefore is possibly reversible. Together, these data show that loss of photoreceptors results in increased synaptic protein levels in bipolar and amacrine cells. Combined with previous reports of increased excitatory and inhibitory synaptic currents in RGCs, these results provide clues to understand the mechanism underlying the aberrant spiking in RGCs

Classical Photoreceptors Are Primarily Responsible for the Pupillary Light Reflex in Mouse.

Pupillary light reflex (PLR) is an important clinical tool to assess the integrity of visual pathways. The available evidence suggests that melanopsin-expressing retinal ganglion cells (mRGCs) mediate PLR-driven by the classical photoreceptors (rods and cones) at low irradiances and by melanopsin activation at high irradiances. However, genetic or pharmacological elimination of melanopsin does not completely abolish PLR at high irradiances, raising the possibility that classical photoreceptors may have a role even at high irradiances. Using an inducible mouse model of photoreceptor degeneration, we asked whether classical photoreceptors are responsible for PLR at all irradiances, and found that the PLR was severely attenuated at all irradiances. Using multiple approaches, we show that the residual PLR at high irradiances in this mouse was primarily from the remnant rods and cones, with a minor contribution from melanopsin activation. In contrast, in rd1 mouse where classical photoreceptor degeneration occurs during development, the PLR was absent at low irradiances but intact at high irradiances, as reported previously. Since mRGCs receive inputs from classical photoreceptors, we also asked whether developmental loss of classical photoreceptors as in rd1 mouse leads to compensatory takeover of the high-irradiance PLR by mRGCs. Specifically, we looked at a distinct subpopulation of mRGCs that express Brn3b transcription factor, which has been shown to mediate PLR. We found that rd1 mouse had a significantly higher proportion of Brn3b-expressing M1 type of mRGCs than in the inducible model. Interestingly, inducing classical photoreceptor degeneration during development also resulted in a higher proportion of Brn3b-expressing M1 cells and partially rescued PLR at high irradiances. These results suggest that classical photoreceptors are primarily responsible for PLR at all irradiances, while melanopsin activation makes a minor contribution at very high irradiances

Retinal levels of synaptophysin protein and mRNA were largely unaltered following photoreceptor loss.

<p>A) Representative blots of synaptophysin and β-tubulin in whole retinas of wild-type and rd1 mice at different developmental stages (“A” is for “Adult”). B) Ratio of synaptophysin to β-tubulin for several animals (Mean ± SE). The ratio in rd1 mouse was not statistically different from that in wild-type mouse at any stage (n = 6, 8, 9, 9 and 7 for 7, 14, 21, 28 days old and adult animals respectively). C) Synaptophysin mRNA levels normalized to 18S rRNA (Mean ± SE) were also similar in adult rd1 and wild-type mice (n = 6). D) Representative blots of synaptophysin and β-tubulin in whole retinas of sham-injected control and at various days after MNU injection. E) Ratio of synaptophysin to β-tubulin for several animals (Mean ± SE). Similar to rd1 mouse, the levels of synaptophysin in MNU-injected animals were not significantly different from the control for up to at least 28 days after the injection, except at 7 days (p>0.1, except for PID-7 where p = 0.044; n = 6 for all stages). *p<0.05</p

Synaptophysin in the IPL of rd1 mouse was upregulated.

<p>A, B) Representative images of vertical sections of adult wild-type (A) and rd1 (B) mouse retinas immunostained for synaptophysin. Scale bar: 50 µm. C) Representative profile of staining intensity through retinal depth covering both plexiform layers of the images shown in A and B. After background subtraction, a line moving vertically from top to bottom across the images measured the signal intensity using Plot Profile function in ImageJ, which is shown here from left to right. Synaptophysin staining is nearly absent in OPL of rd1 mouse retina, whereas that in IPL is higher than in wild-type, particularly in the Off sublamina. D) Levels of synaptophysin in IPL (mean ± SE), measured with quantitative immunohistochemistry were significantly higher in adult rd1 mouse retina than in wild-type (p = 0.018; n = 6). Within IPL, the levels were significantly higher in Off sublamina (p = 0.01), but not in On sublamina (p = 0.068). The data shown here are essentially the area under the curve for On (60% of IPL) and Off (40%) sublaminas shown in 2C. *<i>p</i><0.05.</p