A pre-experimental study to assess the effectiveness of stretching exercises on joint pain among obese women in selected area at Vellore.

A pre - experimental study to assess the effectiveness of stretching exercises on joint pain among obese women in selected area at Vellore. The objectives of the study were, 1. To assess the pre test and post test level of joint pain among obese women, 2. To evaluate the effectiveness of stretching exercise on joint pain among obese women. 3. To find the association between the pre test and post test level of joint pain among obese women in selected demographic variables. 4. To find the association between the pre test and post test level of joint pain among obese women in selected clinical variables. The research approach was evaluative and Research deaign used was pre - experimental involving only one group pre test and posttest design.Purposive sampling technique was adopted to choose. Joint pain was assessed by Lysholm Knee Scoring scale. Stretching exercise was done daily 8 minutes. Major findings of the study are Demographic variables showed that 11 (36.7%) of obese women participated in the study were in the age group of above 59 years. Majority 16 (53.7%) of obese women were Hindus. One third 13(43.3%) of obese women were illiterate. More than of 20(66.7%) obese women were non-vegetarian. Majority of 13 (43.3%) of obese women participated in the study were married. More than half 17 (56.7%) obese women were implemented family planning method. Clinical variables showed the majority 12 (40%) whose BMI is 30.0-39.9 waist circumstances is extremely high 10 (33%) of obese women. All obese women do not have maximum resistance 8(27%). Majority of obese women were partly depended 11(37%). Majority of obese women have duration of joint pain less than 1 to 5 years 14 (47%). Majority of obese women are using comfort devices as pillows 26 (90%) and some are using back rest 3(7%) and sand bag 1 (3%). Before stretching exercises out of 30 obese student none of them had mild joint pain. 7% had moderate joint pain 93% had sever joint pain. But after stretching exercises 10% have moderate pain and none of them had sever joint pain. The comparison using paired t-test is 25.90*** which proved highly significant of p<001.Hence H01 stated earlier there is significant difference between the level of Joint pain among obese. The study revealed that there is significant association between the selected demographic variable and their post test level of joint pain among elderly. Statistical significance was calculated using chi square test hence H02 stated significant association between the post test level of joint pain among elderl.y There is significant association between the selected clinical variable and their post test level of joint pain. Statistical significance was calculated by using chi - square test. Hence H03 is state earlier - There is no significant association between the post test level of joint pain among obese women and selected clinical variable is accepted

Disparities and Microbiome Affecting Liver Disease Progression

Non-alcoholic fatty liver disease (NAFLD) is a metabolic illness that encompasses a wide range of pathological states, from simple steatosis to steatohepatitis (NASH) to cirrhosis and hepatocellular carcinoma. NAFLD is the most prevalent liver disease in the world, accounting for 25% of all liver diseases cases. A high-fat diet, smoking, and alcohol consumption have all been proven to disrupt the balance of beneficial and possibly pathogenic bacterial species, resulting in intestinal dysbiosis. The prevalence of liver cancer (LC) among Latinos in South Texas remains greater than elsewhere in the United States, necessitating further research on population-specific risk factors and aggressive mortality. Incidence rates among Hispanics are three to four times greater than among non-Hispanic whites. There are no precise molecular markers or imaging modalities that have the sensitivity or specificity to identify NAFLD patients at an early stage of illness or at a high risk of developing NASH/Cirrhosis or HCC and consider them candidates for early surgical intervention. Therefore, there is a need for the creation of non-invasive, selective molecular markers for detecting precursor lesions with dysplasia that advance to HCC. The makeup of the human gut microbiota, which is made up of hundreds of microbial species, can change with chronic illnesses that underpin health inequities that disproportionately afflict ethnic minorities. In this study, we explored the incidence and mortality rates of liver cancer in different ethnicities, Hispanics, African Americans, and non-Hispanic whites (NHW). Hispanics have the highest microbial richness and evenness in both study groups, followed by Non-Hispanic whites and Asian Pacific Islanders. Obesity, diabetes, and lifestyle changes, among other factors, have contributed to an increase in the number of instances of NAFLD in Hispanics. An increase in the number of Enterobacteriaceae, Veillonellaceae, and Streptococcaceae, as well as a reduction in the abundance of Lachnospiracea is witnessed in cirrhosis patients. There are different microbial fingerprints and interspecies interactions in several liver disorders that are susceptible to develop in HCC across ethnicities. Future studies are warranted to investigate the role of microbiota in conversion of NAFLD patients, role of microbiota in mediating HC

Screening of Banana Hybrids for Resistance to Pratylenchus coffeae

The reaction of twenty-four new synthetic banana hybrids to Pratylenchus coffeae was studied under artificially inoculated pot conditions. Two banana hybrids, H-04-05 and H-04-06 were found to be resistant and ten hybrids, H-04-01, H-04-03, H-04-04, H-04-07, H-04-09, H-04-11, H-04-16, H-04-19, H-04-21 and H-04-24 were found to be tolerant to the lesion nematode, Pratylenchus coffeae and the remaining were rated as susceptible

Novel therapy targeting Mutant-KRASG12D and Galectin-1 in Pancreatic Cancer

Introduction: Although, surgical resection and chemotherapy are the gold standard for treating Pancreatic Ductal Adenocarcinoma (PDAC), low patient survival rate remains the problem. The activating point mutation of the KRAS on codon-12 is present in 70–95% of PDAC cases and so far, no success has been achieved to inhibit KRAS. KRASG12D regulates cell proliferation, differentiation, apoptosis. Recent preliminary and published studies show high Galectin-1 (Gal-1) levels in both pancreatic cancer and stromal cells, which modulate tumor microenvironment and metastasis. Additionally, genetic deletion of gal1 inhibits metastasis and improves survival in KRAS mouse model of PDAC (1). Therefore, our objective is to develop a novel combination therapy for PDAC by targeting mutated KRASG12D point mutation and Gal1. This includes the delivery of KRASG12D inhibiting siRNA (siKRASG12D) using a superparamagnetic iron oxide nanoparticle (SPION) and a galectin inhibitor. Methods: ASPC1/Panc-1 (human), KPC (mouse) cells were used. Our patented SPION nano-formulation (2) has been used to deliver siKRASG12D and investigated in conjunction with Gal-1 for its anticancer efficacy. Particles were investigated for size, physico-chemical characterization (Dynamic light scattering), hemocompatibility (hemolysis assay) and the complexation of siKRAS (gel retardation assay). Cellular internalization and uptake of the particles were investigated using FAM labelled siRNA and Prussian blue assay. KRASG12D silencing was confirmed at both mRNA and protein levels. Anti-cancer efficacy of the formulation was determined using in vitro functional assays for cell viability (MTT), migration (Boyden chambers), invasion (Matrigel), clonogenicity, tumor spheroid formation, and in nude mice. Results: Our results demonstrate optimal particle size and zeta potential of SP-siKRAS formulation. SPsiKRAS efficiently internalized in PDAC cells and suppressed KRASG12D as well as its downstream targets, YAP and PDL-1. Combined targeting of siKRAS and Gal-1 inhibited cell proliferation. The formulation inhibited chemoresistance, cell proliferation, clonogenicity, migration, and invasion of pancreatic cancer cells. This resulted in activation of death related mechanisms, such as Bax, bcl-2, PARP cleavage in KRASG12D cells. Interestingly, the formulation was highly effective in inhibiting KRASG12D and growth of tumor spheroid in 3D cell models, which recapitulate the heterogeneity and pathophysiology of PDAC. This further provides a clinical validation demonstrating potential of SP-siKRAS particles to efficiently silence KRAS expression. SP-siKRAS also exhibited hemocompatibility, suggesting its potential of silencing KRAS without being toxic to the body. Additionally, the formulation was efficiently delivered in nude mice to exhibit KRasG12D silencing and inhibit tumor growth. Conclusion: This gene therapy targeting KRAS G12D mutation with a Gal-1 inhibition has a potential to modulate the oncogenic network and tumor microenvironment resulting in the repression of growth, metastasis, chemoresistance, and improvement in patient survival. This study will develop a novel sustainable therapeutic approach to target pancreatic cancer growth and improve patient survivability

Novel therapy targeting Mutant-KRASG12D and Galectin-1 in Pancreatic Cancer

Introduction: Although, surgical resection and chemotherapy are the gold standard for treating Pancreatic Ductal Adenocarcinoma (PDAC), low patient survival rate remains the problem. The activating point mutation of the KRAS on codon-12 is present in 70–95% of PDAC cases and so far, no success has been achieved to inhibit KRAS. KRASG12D regulates cell proliferation, differentiation, apoptosis. Recent preliminary and published studies show high Galectin-1 (Gal-1) levels in both pancreatic cancer and stromal cells, which modulate tumor microenvironment and metastasis. Additionally, genetic deletion of gal1 inhibits metastasis and improves survival in KRAS mouse model of PDAC (1). Therefore, our objective is to develop a novel combination therapy for PDAC by targeting mutated KRASG12D point mutation and Gal1. This includes the delivery of KRASG12D inhibiting siRNA (siKRASG12D) using a superparamagnetic iron oxide nanoparticle (SPION) and a galectin inhibitor. Methods: ASPC1/Panc-1 (human), KPC (mouse) cells were used. Our patented SPION nano-formulation (2) has been used to deliver siKRASG12D and investigated in conjunction with Gal-1 for its anticancer efficacy. Particles were investigated for size, physico-chemical characterization (Dynamic light scattering), hemocompatibility (hemolysis assay) and the complexation of siKRAS (gel retardation assay). Cellular internalization and uptake of the particles were investigated using FAM labelled siRNA and Prussian blue assay. KRASG12D silencing was confirmed at both mRNA and protein levels. Anti-cancer efficacy of the formulation was determined using in vitro functional assays for cell viability (MTT), migration (Boyden chambers), invasion (Matrigel), clonogenicity, tumor spheroid formation, and in nude mice. Results: Our results demonstrate optimal particle size and zeta potential of SP-siKRAS formulation. SPsiKRAS efficiently internalized in PDAC cells and suppressed KRASG12D as well as its downstream targets, YAP and PDL-1. Combined targeting of siKRAS and Gal-1 inhibited cell proliferation. The formulation inhibited chemoresistance, cell proliferation, clonogenicity, migration, and invasion of pancreatic cancer cells. This resulted in activation of death related mechanisms, such as Bax, bcl-2, PARP cleavage in KRASG12D cells. Interestingly, the formulation was highly effective in inhibiting KRASG12D and growth of tumor spheroid in 3D cell models, which recapitulate the heterogeneity and pathophysiology of PDAC. This further provides a clinical validation demonstrating potential of SP-siKRAS particles to efficiently silence KRAS expression. SP-siKRAS also exhibited hemocompatibility, suggesting its potential of silencing KRAS without being toxic to the body. Additionally, the formulation was efficiently delivered in nude mice to exhibit KRasG12D silencing and inhibit tumor growth. Conclusion: This gene therapy targeting KRAS G12D mutation with a Gal-1 inhibition has a potential to modulate the oncogenic network and tumor microenvironment resulting in the repression of growth, metastasis, chemoresistance, and improvement in patient survival. This study will develop a novel sustainable therapeutic approach to target pancreatic cancer growth and improve patient survivability

Bilateral supernumerary cusps on deciduous and permanent molars: A case report with a short review

Extra cusps or the central cusps have been recognized as supernumerary cusps by many authors. Extra cusps are usually seen on premolars. Central cusps are of clinical importance as it could be associated with some anomalies that can lead to clinical complications. Extra or accessory cusps rarely pose any problem to the dentist. Even though, it may not cause an emergency in the clinic fracture of this cusp may lead to clinical problems. We present this rare case with bilateral central cusps both on permanent and deciduous molars. Review regarding central cusp, need for continuous follow‑up are also been included

The impact of individual health education on health literacy: Evaluation of the translated version (sinhala) of health education impact questionnaire in type 2 diabetes

INTRODUCTION: The prevalence of Type 2 diabetes is globally on the rise, in both developed and developing countries. Type 2 diabetes is a major public health issue in Sri Lanka. This study aims to investigate the effect of structured self-management health education intervention based on ‘PITS model’ (Pathophysiology, Indications, Treatment and Specifics) would result in a clinically significant improvement in glycaemic control of type 2 Diabetes Mellitus (T2DM) patients. METHODS: Patients who were diagnosed with T2DM at two tertiary care hospitals in Sri Lanka, comply with the selection criteria were enrolled to the study. The intervention consisted with two repeated one to one education sessions followed up in six and twelve months. HbA1c, lipid profiles, waist circumference, BMI and other biomedical measurements were done in both groups. Analysis of covariance between groups were conducted to determine the effectiveness of the intervention. RESULTS: Mean HbA1c level in both intervention and usual care group was 8.6% with deviation from their target glycaemic level (6.5%,48 mmol/mol) at baseline. At six months, there was a significant reduction (p < 0.001; size of effect = 0.69) in HbA1c between the intervention and the usual care group controlling the baseline values. CONCLUSION: The results demonstrate the effectiveness of one to one diabetes self-management intervention among the adults with T2DM

Lasers in pediatric dentistry: A review

In ancient Greece, the sun was used in heliotherapy, or the exposure of the body to the sun for the restoration of health. The Chinese used the sun to treat such conditions as rickets, skin cancer and even psychosis. This use of light for treatment of various pathologies is referred to as phototherapy. In 1903, a Danish physician named Niels Finsen developed a technique known as carbon arc phototherapy for the treatment of lupus vulgaris that employed the use of ultraviolet rays

Novel therapy targeting mutant-KRASG12D and galectin-1 in pancreatic cancer

Introduction: In pancreatic ductal adenocarcinoma (PDAC), low patient survival rate remains a problem. The activating point mutation of KRAS on codon-12 is present in 70–95% of PDAC cases and so far, no success has been achieved to inhibit KRAS. KRASG12D regulates cell proliferation, differentiation, apoptosis; recent preliminary and published studies show high Galectin-1 (Gal-1) levels in both PDAC and stromal cells, which modulate tumor microenvironment and metastasis. Therefore, we have developed a novel combination therapy for PDAC by targeting mutated KRASG12D and Gal-1 to target both proliferation and metastasis in PDAC. This includes the delivery of KRASG12D inhibiting siRNA (siKRASG12D) using a superparamagnetic iron oxide nanoparticle (SPION) and a galectin inhibitor. Methods: Our patented SPION nano-formulation was used to deliver siKRASG12D and investigated in conjunction with Gal-1 inhibitor for its anticancer efficacy. Particles were investigated for size, physico-chemical characterization (Dynamic light scattering), hemocompatibility (hemolysis assay) and the complexation of siKRAS (gel retardation assay). Cellular internalization and uptake of the particles were investigated. Anti-cancer efficacy was determined using in vitro functional assays for cell viability (MTT), migration (Boyden chambers), invasion (Matrigel), clonogenicity, tumor spheroid formation, and in a mouse model. Results: Our results demonstrate optimal particle size/zeta potential of SP-siKRAS formulation. SP-siKRAS efficiently internalized in PDAC cells and suppressed KRASG12D as well as its downstream targets, YAP and PDL-1. Combined targeting of siKRAS and Gal-1 inhibited cell proliferation. It inhibited cell proliferation, clonogenicity, migration, and invasion of PDAC cells. This resulted in activation of death related mechanisms, such as Bax, bcl-2, PARP cleavage in KRASG12D cells. Interestingly, the formulation was highly effective in inhibiting KRASG12D and growth of tumor spheroid in 3D cell models, which recapitulate the heterogeneity and pathophysiology of PDAC. This further provides a clinical validation demonstrating potential of SP-siKRAS particles to efficiently silence KRAS expression. SP-siKRAS also exhibited hemocompatibility and stability suggesting its potential of silencing KRAS without being toxic to the body. The formulation efficiently exhibited KRasG12D silencing and inhibited tumor growth and metastasis in nude mice. Conclusion: This gene therapy targeting KRAS G12D mutation with a Gal-1 inhibition has a potential to modulate the oncogenic network and tumor microenvironment resulting in the repression of growth, metastasis, chemoresistance, and improvement in patient survival. This study will develop a novel sustainable therapeutic approach to target PDAC growth and improve patient survivability

Exenatide Improves Glucose Homeostasis and Prolongs Survival in a Murine Model of Dilated Cardiomyopathy

There is growing awareness of secondary insulin resistance and alterations in myocardial glucose utilization in congestive heart failure. Whether therapies that directly target these changes would be beneficial is unclear. We previously demonstrated that acute blockade of the insulin responsive facilitative glucose transporter GLUT4 precipitates acute decompensated heart failure in mice with advanced dilated cardiomyopathy. Our current objective was to determine whether pharmacologic enhancement of insulin sensitivity and myocardial glucose uptake preserves cardiac function and survival in the setting of primary heart failure.The GLP-1 agonist exenatide was administered twice daily to a murine model of dilated cardiomyopathy (TG9) starting at 56 days of life. TG9 mice develop congestive heart failure and secondary insulin resistance in a highly predictable manner with death by 12 weeks of age. Glucose homeostasis was assessed by measuring glucose tolerance at 8 and 10 weeks and tissue 2-deoxyglucose uptake at 75 days. Exenatide treatment improved glucose tolerance, myocardial GLUT4 expression and 2-deoxyglucose uptake, cardiac contractility, and survival over control vehicle-treated TG9 mice. Phosphorylation of AMP kinase and AKT was also increased in exenatide-treated animals. Total myocardial GLUT1 levels were not different between groups. Exenatide also abrogated the detrimental effect of the GLUT4 antagonist ritonavir on survival in TG9 mice.In heart failure secondary insulin resistance is maladaptive and myocardial glucose uptake is suboptimal. An incretin-based therapy, which addresses these changes, appears beneficial