Prospective study on Role of Early Enteral Feeding in Gastric / Duodenal Perforation

INTRODUCTION: Perforation of gut is one of a common surgical emergency encountered in clinical practice. Patients with gastric / duodenal perforations presents with severe peritonitis and septicemia. Upper GI perforations need immediate repair mostly by Omental patch closure. Following surgical repair of the perforation patients will be observed postoperatively regarding the improvement of vitals and return of normal bowel movements and improvements in biochemical parameters for planning of introduction of oral feeds. OBJECTIVES: To derive conclusions about efficacy of EARLY ENTERAL FEEDING IN PATIENTS WITH GASTRIC/ DUODENAL PERFORATION and its impact on recovery of patients after surgery. PATIENTS AND METHODS: This prospective study was conducted in patients who got admitted with Gastric/Duodenal Perforation at Government Rajaji Hospital, Department of General Surgery, Madurai medical college, Madurai. All patients were evaluated with history, clinical examination and relevant laboratory and radiological investigations including X-ray chest and abdomen, ultrasound abdomen. Statistical analysis was performed with IBM SPSS version 16 (SPSS Inc., Chicago, IL). RESULTS: During study period, 50 patients with Gastric/Duodenal Perforation were selected randomly into two groups. Study group of 25 patients were randomly selected for starting Early Enteral Feeding (EEF) via Intra operatively inserted NasoJejunal (NJ) Tube from POD-1. Control group of 25 patients were started oral feeds post operatively after appearance of bowel sounds and passage of stools (POD 5-7). There is no statistically significant difference between the study and the control groups (p>0.05) regarding mean age, duration of Perforation, Manheim Peritonitis Index Score. Among the study group on an average, shifting out of ICU (on POD-2), appearance of bowel sounds (on POD 3), passage of flatus (on POD-4), removal of Ryle’s tube (on POD-5) happened one day prior to the control group. The clinical and biochemical parameters showed statistically significant improvement (p<0.05) in study group than the control group on POD-3. But there was no significant difference in clinical and biochemical parameters on POD-7 among both the groups. 60% of patients among the study group were without any major postoperative complications compared to only 12% among the control group. There is no significant difference (p>0.05) in mortality rate among the study group (8%) and the control group (12%). On an average patients under the study group got discharged from the hospital about 3 days prior to the control group which is statistically significant (p<0.05). CONCLUSION: Early Enteral Feeding in postoperative period is beneficial to patients with Gastric/ Duodenal perforation both in recovery evidenced by reducing the duration of stay and also in preventing major postoperative complications. There is no significant decrease in postoperative mortality among the Early Enteral fed patients

Single-Echelon Supply Chain Two Stage Distribution Inventory Optimization Model for the Confectionery Industry

Abstract In this paper, a supply chain two stage distribution inventory optimization model with interactive-lateral transshipment among retailers in a particular period is considered. Interactive-lateral transshipment among retailers means that once the stocks are allocated to retailers from ware houses, we allow lateral stocks transfer among retailers if the further optimization is possible which will enable us to further minimize overall cost in the supply chain. The proposed model is formulated as a linear programming model which is validated with help of a confectionary industry data. This model is to provide an optimal inventory level for the warehouses and retailers and also, minimizing the total cost of the entire supply chain for a finite planning horizon. Mathematics Subject Classification: 90B05, 90B06, 90B50, 90C05, 62P3

Rapid intraoperative histology of unprocessed surgical specimens via fibre-laser-based stimulated Raman scattering microscopy

Conventional methods for intraoperative histopathologic diagnosis are labor- and time-intensive and may delay decision-making during brain tumor surgery. Stimulated Raman scattering (SRS) microscopy, a label-free optical process, has been shown to rapidly detect brain tumor infiltration in fresh, unprocessed human tissues. Previously, the execution of SRS microscopy in a clinical setting has not been possible. We report the first demonstration of SRS microscopy in an operating room using a portable fiber-laser-based microscope in unprocessed specimens from 101 neurosurgical patients. Additionally, we introduce an image-processing method, stimulated Raman histology (SRH), which leverages SRS images to create virtual hematoxylin and eosin- stained slides, revealing essential diagnostic features. In a simulation of intraoperative pathologic consultation in 30 patients, the concordance of SRH and conventional histology for predicting diagnosis was nearly perfect (κ>0.89) and accuracy exceeded 92%. We also built and validated a multilayer perceptron based on quantified SRH image attributes that predicts brain tumor subtype with 90% accuracy. This study provides insight into how SRH can now be used to improve the surgical care of brain tumor patients.Chemistry and Chemical Biolog

Global, regional, and national incidence and mortality for HIV, tuberculosis, and malaria during 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013

BACKGROUND: The Millennium Declaration in 2000 brought special global attention to HIV, tuberculosis, and malaria through the formulation of Millennium Development Goal (MDG) 6. The Global Burden of Disease 2013 study provides a consistent and comprehensive approach to disease estimation for between 1990 and 2013, and an opportunity to assess whether accelerated progress has occured since the Millennium Declaration. METHODS: To estimate incidence and mortality for HIV, we used the UNAIDS Spectrum model appropriately modified based on a systematic review of available studies of mortality with and without antiretroviral therapy (ART). For concentrated epidemics, we calibrated Spectrum models to fit vital registration data corrected for misclassification of HIV deaths. In generalised epidemics, we minimised a loss function to select epidemic curves most consistent with prevalence data and demographic data for all-cause mortality. We analysed counterfactual scenarios for HIV to assess years of life saved through prevention of mother-to-child transmission (PMTCT) and ART. For tuberculosis, we analysed vital registration and verbal autopsy data to estimate mortality using cause of death ensemble modelling. We analysed data for corrected case-notifications, expert opinions on the case-detection rate, prevalence surveys, and estimated cause-specific mortality using Bayesian meta-regression to generate consistent trends in all parameters. We analysed malaria mortality and incidence using an updated cause of death database, a systematic analysis of verbal autopsy validation studies for malaria, and recent studies (2010-13) of incidence, drug resistance, and coverage of insecticide-treated bednets. FINDINGS: Globally in 2013, there were 1·8 million new HIV infections (95% uncertainty interval 1·7 million to 2·1 million), 29·2 million prevalent HIV cases (28·1 to 31·7), and 1·3 million HIV deaths (1·3 to 1·5). At the peak of the epidemic in 2005, HIV caused 1·7 million deaths (1·6 million to 1·9 million). Concentrated epidemics in Latin America and eastern Europe are substantially smaller than previously estimated. Through interventions including PMTCT and ART, 19·1 million life-years (16·6 million to 21·5 million) have been saved, 70·3% (65·4 to 76·1) in developing countries. From 2000 to 2011, the ratio of development assistance for health for HIV to years of life saved through intervention was US$4498 in developing countries. Including in HIV-positive individuals, all-form tuberculosis incidence was 7·5 million (7·4 million to 7·7 million), prevalence was 11·9 million (11·6 million to 12·2 million), and number of deaths was 1·4 million (1·3 million to 1·5 million) in 2013. In the same year and in only individuals who were HIV-negative, all-form tuberculosis incidence was 7·1 million (6·9 million to 7·3 million), prevalence was 11·2 million (10·8 million to 11·6 million), and number of deaths was 1·3 million (1·2 million to 1·4 million). Annualised rates of change (ARC) for incidence, prevalence, and death became negative after 2000. Tuberculosis in HIV-negative individuals disproportionately occurs in men and boys (versus women and girls); 64·0% of cases (63·6 to 64·3) and 64·7% of deaths (60·8 to 70·3). Globally, malaria cases and deaths grew rapidly from 1990 reaching a peak of 232 million cases (143 million to 387 million) in 2003 and 1·2 million deaths (1·1 million to 1·4 million) in 2004. Since 2004, child deaths from malaria in sub-Saharan Africa have decreased by 31·5% (15·7 to 44·1). Outside of Africa, malaria mortality has been steadily decreasing since 1990. INTERPRETATION: Our estimates of the number of people living with HIV are 18·7% smaller than UNAIDS's estimates in 2012. The number of people living with malaria is larger than estimated by WHO. The number of people living with HIV, tuberculosis, or malaria have all decreased since 2000. At the global level, upward trends for malaria and HIV deaths have been reversed and declines in tuberculosis deaths have accelerated. 101 countries (74 of which are developing) still have increasing HIV incidence. Substantial progress since the Millennium Declaration is an encouraging sign of the effect of global action. FUNDING: Bill & Melinda Gates Foundation

Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013

Background: The Global Burden of Disease, Injuries, and Risk Factor study 2013 (GBD 2013) is the first of a series of annual updates of the GBD. Risk factor quantification, particularly of modifiable risk factors, can help to identify emerging threats to population health and opportunities for prevention. The GBD 2013 provides a timely opportunity to update the comparative risk assessment with new data for exposure, relative risks, and evidence on the appropriate counterfactual risk distribution. Methods: Attributable deaths, years of life lost, years lived with disability, and disability-adjusted life-years (DALYs) have been estimated for 79 risks or clusters of risks using the GBD 2010 methods. Risk-outcome pairs meeting explicit evidence criteria were assessed for 188 countries for the period 1990-2013 by age and sex using three inputs: risk exposure, relative risks, and the theoretical minimum risk exposure level (TMREL). Risks are organised into a hierarchy with blocks of behavioural, environmental and occupational, and metabolic risks at the first level of the hierarchy. The next level in the hierarchy includes nine clusters of related risks and two individual risks, with more detail provided at levels 3 and 4 of the hierarchy. Compared with GBD 2010, six new risk factors have been added: handwashing practices, occupational exposure to trichloroethylene, childhood wasting, childhood stunting, unsafe sex, and low glomerular filtration rate. For most risks, data for exposure were synthesised with a Bayesian metaregression method, DisMod-MR 2.0, or spatial-temporal Gaussian process regression. Relative risks were based on meta-regressions of published cohort and intervention studies. Attributable burden for clusters of risks and all risks combined took into account evidence on the mediation of some risks such as high body-mass index (BMI) through other risks such as high systolic blood pressure and high cholesterol. Findings: All risks combined account for 57·2% (95% uncertainty interval [UI] 55·8-58·5) of deaths and 41·6% (40·1-43·0) of DALYs. Risks quantified account for 87·9% (86·5-89·3) of cardiovascular disease DALYs, ranging to a low of 0% for neonatal disorders and neglected tropical diseases and malaria. In terms of global DALYs in 2013, six risks or clusters of risks each caused more than 5% of DALYs: dietary risks accounting for 11·3 million deaths and 241·4 million DALYs, high systolic blood pressure for 10·4 million deaths and 208·1 million DALYs, child and maternal malnutrition for 1·7 million deaths and 176·9 million DALYs, tobacco smoke for 6·1 million deaths and 143·5 million DALYs, air pollution for 5·5 million deaths and 141·5 million DALYs, and high BMI for 4·4 million deaths and 134·0 million DALYs. Risk factor patterns vary across regions and countries and with time. In sub-Saharan Africa, the leading risk factors are child and maternal malnutrition, unsafe sex, and unsafe water, sanitation, and handwashing. In women, in nearly all countries in the Americas, north Africa, and the Middle East, and in many other high-income countries, high BMI is the leading risk factor, with high systolic blood pressure as the leading risk in most of Central and Eastern Europe and south and east Asia. For men, high systolic blood pressure or tobacco use are the leading risks in nearly all high-income countries, in north Africa and the Middle East, Europe, and Asia. For men and women, unsafe sex is the leading risk in a corridor from Kenya to South Africa. Interpretation: Behavioural, environmental and occupational, and metabolic risks can explain half of global mortality and more than one-third of global DALYs providing many opportunities for prevention. Of the larger risks, the attributable burden of high BMI has increased in the past 23 years. In view of the prominence of behavioural risk factors, behavioural and social science research on interventions for these risks should be strengthened. Many prevention and primary care policy options are available now to act on key risks

Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013

Background Up-to-date evidence on levels and trends for age-sex-specific all-cause and cause-specific mortality is essential for the formation of global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013) we estimated yearly deaths for 188 countries between 1990, and 2013. We used the results to assess whether there is epidemiological convergence across countries. Methods We estimated age-sex-specific all-cause mortality using the GBD 2010 methods with some refinements to improve accuracy applied to an updated database of vital registration, survey, and census data. We generally estimated cause of death as in the GBD 2010. Key improvements included the addition of more recent vital registration data for 72 countries, an updated verbal autopsy literature review, two new and detailed data systems for China, and more detail for Mexico, UK, Turkey, and Russia. We improved statistical models for garbage code redistribution. We used six different modelling strategies across the 240 causes; cause of death ensemble modelling (CODEm) was the dominant strategy for causes with sufficient information. Trends for Alzheimer's disease and other dementias were informed by meta-regression of prevalence studies. For pathogen-specific causes of diarrhoea and lower respiratory infections we used a counterfactual approach. We computed two measures of convergence (inequality) across countries: the average relative difference across all pairs of countries (Gini coefficient) and the average absolute difference across countries. To summarise broad findings, we used multiple decrement life-tables to decompose probabilities of death from birth to exact age 15 years, from exact age 15 years to exact age 50 years, and from exact age 50 years to exact age 75 years, and life expectancy at birth into major causes. For all quantities reported, we computed 95% uncertainty intervals (UIs). We constrained cause-specific fractions within each age-sex-country-year group to sum to all-cause mortality based on draws from the uncertainty distributions. Findings Global life expectancy for both sexes increased from 65·3 years (UI 65·0-65·6) in 1990, to 71·5 years (UI 71·0-71·9) in 2013, while the number of deaths increased from 47·5 million (UI 46·8-48·2) to 54·9 million (UI 53·6-56·3) over the same interval. Global progress masked variation by age and sex: for children, average absolute differences between countries decreased but relative differences increased. For women aged 25-39 years and older than 75 years and for men aged 20-49 years and 65 years and older, both absolute and relative differences increased. Decomposition of global and regional life expectancy showed the prominent role of reductions in age-standardised death rates for cardiovascular diseases and cancers in high-income regions, and reductions in child deaths from diarrhoea, lower respiratory infections, and neonatal causes in low-income regions. HIV/AIDS reduced life expectancy in southern sub-Saharan Africa. For most communicable causes of death both numbers of deaths and age-standardised death rates fell whereas for most non-communicable causes, demographic shifts have increased numbers of deaths but decreased age-standardised death rates. Global deaths from injury increased by 10·7%, from 4·3 million deaths in 1990 to 4·8 million in 2013; but age-standardised rates declined over the same period by 21%. For some causes of more than 100 000 deaths per year in 2013, age-standardised death rates increased between 1990 and 2013, including HIV/AIDS, pancreatic cancer, atrial fibrillation and flutter, drug use disorders, diabetes, chronic kidney disease, and sickle-cell anaemias. Diarrhoeal diseases, lower respiratory infections, neonatal causes, and malaria are still in the top five causes of death in children younger than 5 years. The most important pathogens are rotavirus for diarrhoea and pneumococcus for lower respiratory infections. Country-specific probabilities of death over three phases of life were substantially varied between and within regions. Interpretation For most countries, the general pattern of reductions in age-sex specific mortality has been associated with a progressive shift towards a larger share of the remaining deaths caused by non-communicable disease and injuries. Assessing epidemiological convergence across countries depends on whether an absolute or relative measure of inequality is used. Nevertheless, age-standardised death rates for seven substantial causes are increasing, suggesting the potential for reversals in some countries. Important gaps exist in the empirical data for cause of death estimates for some countries; for example, no national data for India are available for the past decade. Funding Bill &amp; Melinda Gates Foundation

Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: A systematic analysis for the Global Burden of Disease Study 2015

Background: The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. Methods: We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors—the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). Findings: Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6–58·8) of global deaths and 41·2% (39·8–42·8) of DALYs. In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]). From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines. Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use. Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI. In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015. Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa. Interpretation: Declines in some key environmental risks have contributed to declines in critical infectious diseases. Some risks appear to be invariant to SDI. Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention. Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining. Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden. Funding: Bill & Melinda Gates Foundation

Assessment of Left Atrial Functional Index (LAFI) by Transthoracic Echocardiogram in patients with Atrial Fibrillation and Diastolic dysfunction.

In the past, left atrium was thought of as a chamber that passively transports blood from the pulmonary circulation to the left ventricle. But it is not so. During the later half of the last century, multiple studies were conducted to obtain normal values for left atrium. S o far several echocardiographic variables have been developed for the evaluation of the function of left atrium. The size of the left atrium in M mode, trans mitral flow velocities, (E & A ) tissue Doppler estimation of myocardial relaxation ( e’ & a’) are the ones useful in the evaluation of the left atrial function. Another important parameter, Left atrial funtional index1,3 (LAFI) is a ratio that involves the analogues of left ventricular stroke volume, reservoir function of left atrium and the size of the left atrium. LAFI adjusts for extremes of body weight and extremes of heart rate. In otherwords it is rhythm independent3 . In patients with AF and normal sized left atrium ( good emptying during diastole) the LAFI should be normal. AIMS AND OBJECTIVES: To evaluate Left Atrial Functional Index (LAFI) using Transthoracic Echocardiogram in persons suffering from atrial fibrillation and also in patients with diastolic dysfunction and the comparison of this left atrial functional index to the conventional echocardiogrophic parameters of left atrial function. CONCLUSION: For the evaluation of left atrium no single parameter is sufficient. Several traditional parameters like LAOT A wave peak velocity, LAOT A VTI and fraction of atrial contribution to ventricular filling, are dependent on the rhythm as well as the Systolic function of the LV. L e ft atrial volume indexed to body surface area was higher in persons with abnormal transmitral filling patterns as well as in patients with chronic atrial fibrillation. Left atrial volume is increased in patients with left atrial dysfunction. Several studies have confirmed that measurement of left atrial volume is an independent predictor of cardiovascular events in patients with HFpEF. Our study demonstrates clear association between left atrial volume and left atrial dysfunction. W e found that the Left Atrial Functional Index as measured by echocardiogram, is decreased in patients with abnormal myocardial relaxation and also in persons with chronic atrial fibrillation. Since this parameter incorporates cardiac output and body surface area in addition to left atrial end systolic volume, it is rhythm independent marker for left atrial function. T he predictors of the left atrial functional index are the baseline left atrial dimension by M mode Echo and the rhythm at the time of evaluation. These factors remain independent predictors of LAFI even after correction for other parameters. Thus baseline LA dimension has got negative association with LAFI and sinus rhythm has got positive association with LAFI. LAFI can be used in the prognostication of heart failure with normal ejection fraction group of patients. The prognostic value of LAFI can be increased, when it is used in association with Other clinical risk factors and NT-proBNP. Because LAFI is a rhythm independent marker of left atrial function, it can be used as a marker of left atrial dysfunction in patients with atrial fibrillation. In the future, the LAFI may be used as a potential target for therapeutic maneuvers

Physiological, genetic and genomic analyses of herbicide resistance in grain sorghum (Sorghum bicolor)

Doctor of PhilosophyDepartment of AgronomyMithila JugulamP. V. Vara PagadalaGrain sorghum [Sorghum bicolor (L.) Moench ssp. bicolor] is a versatile crop with multiple uses, including for food, feed, and fuel. Postemergence (POST) grass weed control continues to be a major challenge in grain sorghum, primarily due to a lack of herbicide options registered for POST use. The 4- hydroxyphenylpyruvate dioxygenase (HPPD)- (e.g., mesotrione or tembotrione) and acetolactate synthase (ALS)- inhibitor (e.g., chlorsulfuron) herbicides are used for POST control of a broad-spectrum of weeds including grasses in corn and wheat but not in sorghum, due to crop injury. The development of herbicide-resistant sorghum technology to facilitate broad-spectrum POST weed control can be an economical and viable solution. Previously we have identified four sorghum genotypes, two each resistant to mesotrione (G-1 and G-10), tembotrione (G-200 and G-350) and, one susceptible genotype (S-1) from the sorghum association panel. Further, we found that the genotype S-1 is highly resistant to chlorsulfuron. The objectives of this dissertation were to 1) investigate the inheritance, mechanism, and identify genetic loci conferring resistance to mesotrione and tembotrione, 2) characterize, and investigate the inheritance and mechanism of resistance to chlorsulfuron in grain sorghum. To understand the inheritance of the mesotrione and tembotrione resistance, F₁ and F₂ progeny were generated by performing crosses using S-1 and G-1, G-10, G-200, or G-350. The F₁ and F₂ progeny were evaluated for their response to various doses of mesotrione and tembotrione treatment. Likewise, chlorsulfuron dose-response experiments were conducted using S-1 along with BTx623, a susceptible check and also F₁ and F₂ progeny were generated by crossing S-1 and BTx623. The results of genetic analyses of the F₁ and F₂ progeny demonstrated that the mesotrione resistance in G-1 and G-10 is a single dominant trait, and while the tembotrione resistance in G-200 and G-350 is a partially dominant polygenic trait. Further, sequencing of HPPD gene, the molecular target of mesotrione and tembotrione in the resistant genotypes, revealed no mutations known to bestow resistance. Additionally, the role of cytochrome P450 (CYP) in metabolizing mesotrione and tembotrione, using CYP-inhibitors, malathion and piperonyl butoxide (PBO) was also assessed. The results indicated a significant reduction in biomass accumulation in sorghum plants pre-treated with malathion or PBO, suggesting the involvement of CYPs in the metabolism of mesotrione and tembotrione. Bulk segregation analysis combined with RNA-Seq (BSR-seq) was used to identify the genomic region associated with mesotrione resistance; however, the sequence analyses was unable to map the resistance gene within a smaller interval. Genotype-by-sequencing (GBS) based quantitative trait loci (QTL) mapping revealed three QTLs associated with tembotrione resistance in G-200. The results of the chlorsulfuron dose-response assay indicated that S-1 and F₁ progeny were ~20-fold, more resistant to chlorsulfuron relative to BTx623. Segregation of F₂ progeny into 3:1 (resistance: susceptibility), suggested that chlorsulfuron resistance in S-1 is a single dominant trait. Sequence analysis of the ALS gene, the molecular target of chlorsulfuron from S-1 revealed no mutations that confer resistance to chlorsulfuron; however, a significant reduction in biomass accumulation was found in plants pre-treated with malathion, indicating that the metabolism of chlorsulfuron contributes to resistance in S-1. Overall, the results of this dissertation provide opportunities to develop herbicide-resistant sorghum hybrids via introgression, which can help effective, POST weed management