University of Science, Art and Technology

The prevalence of diabetes, especially Type 2 diabetes or NIDDM is approaching epidemic proportions in much of Westernized society as the populations continue to age and as the prevalence of obesity, overweight conditions, and their common pathophysiologic sequelae emerge in parallel, while effective therapeutic options often place a strain on available resources. Applications of controlled UV irradiation however represent a novel potential approach in the treatment of a broad variety of metabolic conditions including NIDDM. The aim of the study is to examine the impact of Low Dose Biophotonic Treatment on Hematologic Parameters and Oxygen Saturation. The wide-ranging effects of healthful vs. damaging consequences of UV irradiation on key physiologic parameters are reviewed in this paper. The effects are largely dependent on the wavelengths encountered, the absolute intensity and duration of the exposure, the tissues exposed, and whether the UV effects were delivered via in vivo or as an extracorporeal exposure in vitro typically performed with freshly obtained heparinized aliquots of whole blood. The mechanism for the biophotonic-mediated alterations in hemoglobin glycation remain speculative however, and may be due to a pH induced reversal or limitation at the level of the committed step in the glycation process as depicted in Fig. 4 as a result of the biophotonic excitation. While damaging effects of high UV intensity may include irreversible irradiation damage to key cellular and molecular components, controlled low dosages of UV irradiation delivered via a conventional biophotonic apparatus at specific, controlled wavelengths can deliver beneficial effects on blood oxygenation, tissue repair, immune responses, glycemia, and glycated hemoglobin (HbA1c) concentrations. HbA1c is an important diagnostic marker for the effectiveness of diabetes management. Studies reviewed demonstrate increases in blood oxygenation and corresponding decreases in HbA1c concentrations following nominal low dose biophotonic treatment at selected wavelengths and indicate that the application of this therapy extends beyond its more commonly applied applications in the treatment and control of infectious illnesses. Oxygen availability in combination with ‘good’ ROS responses is a crucial component of a healthy wellbeing and immune responses and are important constituents of the broad spectrum of beneficial effects of UV- biophotonic therapy, and signal the reemergence of an old and reliable treatment for both old and emerging diseases.

The burgeoning prevalence of obesity and overweight conditions including NIDDM and dysregulation of energy balance are rapidly approaching epidemic proportions in much of Western society and imposing a significant burden on available health care resources. Once diagnosed, treatment is typically a life-long effort to attenuate the continued progression of pathophysiologic sequela of the disorders. Since the predominate proportion of macronutrient energy source in most Western diets is often carbohydrate, typically more than 50% by weight at ~4 kcals/gram, efforts to modulate the impact of dietary CHO on parameters of adiposity and weight gain were investigated. This study determined the effects of delayed carbohydrate digestion on energy intake and consequent weight gain groups of young adult, obese-NIDDM rats that were fed a USDA-formulated, hyperinsulinemic diet consisting of 54% sucrose plus essential fats, proteins, micronutrients and fiber for up to 8 weeks, or the same diet containing 150 mg/kg of (1,5 dideoxy-1,5-[(2-hydroxyethyl) imino]-D glucitol; generic miglitol). Measures of daily energy intake and weight gain were determined at weekly intervals. Adiposity was determined by dissecting major fat depots at the end of the study and determining adipose tissue mass and cellularity. Miglitol resulted in 20% less energy intake and weight gain, and corresponding decreases in adiposity after 8 weeks of study. The results of this study indicate that delayed carbohydrate digestion via the α-glucosidase inhibitor miglitol or other similar agents may be a useful adjunct in the regulation of food intake and in attenuating weight gain in man and animals in addition to their well-established effects as an adjunct in the treatment of impaired glycemic responses in obesity and NIDDM.

The wide-ranging effects of healthful vs. damaging consequences of UV irradiation on key physiologic parameters are reviewed in this paper. The effects are largely dependent on the wavelengths encountered, the absolute intensity and duration of the exposure, the tissues exposed, and whether the UV effects were delivered via in vivo or as an extracorporeal exposure in vitro typically performed with freshly obtained heparinized aliquots of whole blood. While damaging effects of high UV intensity may include irreversible irradiation damage to key cellular and molecular components, controlled low dosages of UV irradiation delivered via a conventional biophotonic apparatus at specific, controlled wavelengths can deliver beneficial effects on blood oxygenation, tissue repair, immune responses, glycemia, and glycated hemoglobin (HbA1c) concentrations. HbA1c is an important diagnostic marker for the effectiveness of diabetes management. Studies reviewed demonstrate increases in blood oxygenation and corresponding decreases in HbA1c concentrations following nominal biophotonic treatment and indicate that the application of this therapy extends beyond its more commonly applied applications in the treatment and control of infectious illnesses.

Human anatomy forms the foundation for clinical medicine: Thus its place in the medical school curriculum deserves careful attention. In an attempt to provide guidance to decision-makers involved in clinical anatomy curriculum development at the medical school level, the Educational Affairs Committee of the American Association of Clinical Anatomists (AACA) developed this document, which defines the contours of a gross anatomy curriculum leading to the M.D. or D.O. degree. The main body of the document sets forth the anatomical concepts as well as the subject matter a student should master prior to graduation from medical school. Gross anatomy dissection is still a crucial topic in graduate and medical school. The nature and content of gross anatomy, which was historically regarded as a core course in the first year of medical education in MBBS, MD, DO, and some PhD and Graduate curricula as well as in other disciplines of selective graduate education and non-allopathic medical programs, have been significantly impacted by emerging challenges in the pedagogy of delivering medical education in the past ten years. A seemingly ever-increasing emphasis on additional modules in molecular biology, emerging pharmacotherapeutics and pathophysiology content have resulted in a condensation and apparent erosion of previously allotted classroom and laboratory hours in the gross anatomy curriculum. In addition, an imposition of financial constraints and a decreasing availability of sufficient cadaver donations to support gross anatomy dissection labs has also occurred in some locations. An innovative clinically focused cadaveric anatomy program is described which has improved the delivery and content retention of medical and graduate students and has become one of the most sought-after modules in the revised clinically oriented curriculum and has been deemed highly relevant to current medical education and graduate studies.

This chapter determine the effect of obese phenotype and the carbohydrate type resulted in alterations in brain composition in the obese phenotype of the congenic LA/Ntul//-cp rat, groups (n= 8 rats/group) of male littermate lean and obese rats were fed standardized isocaloric diets containing 54% (w/w) cornstarch (ST diet) or 54% (w/w) sucrose (SUC diet) from 1 until 10.5 ± 0.5 months of age. Malnutrition is a pervasive global public health issue that contributes to several dietary-related non-communicable illnesses. In low-income nations, adult nutrition is frequently overlooked. In low- and middle-income nations, both dual malnutrition (over and undernutrition) and nutrition transition exist. The current popular emphasis on low fat diets has resulted in an upwards shift in dietary carbohydrate consumption. The strain's obese phenotype exhibits hypertrophic-hyperplastic obesity during early postweaning development and early onset chronic hyperinsulinemia without NIDDM. The total fat, protein, and DNA of typical aliquots of dissected brain tissues were analyzed. When fed the SUC food as opposed to the ST diet, body weights of obese >> lean animals were higher in both genotypes. In rats fed the SUC diet compared to the ST diet, brain mass was somewhat smaller in lean individuals compared to fat individuals. Brain total Protein and DNA content of lean rats were > obese rats and were modestly Lower in SUC than ST fed rats in both phenotypes, but the percent of lipid content was proportional to brain mass. The decreased brain mass was characterized by proportionate decreases in total lipid, brain protein and brain DNA content and were further impaired when fed the insulinogenic sucrose diet. Total body fat mass of obese was significantly greater than occurred in lean littermates and was only modestly greater in SUC than ST fed rats in both phenotypes. These results indicate that brain growth and cellular development is impaired in the aging, hyperinsulinemia-prone obese phenotype of this strain, were further impaired when fed SUC than ST diets, and the decreased brain parameters were likely associated with development of a chronic neuronal inflammatory syndrome common to excessive fat accretion and obesity, resulting in premature brain senescence.

The counterregulatory effects of glucocorticoids and insulin that commonly occur in obesity result in the development of insulin resistance and impaired glycemic responses to dietary carbohydrates. Both adipose tissue and skeletal muscle are dependent on insulin actions to bring about glucose uptake, and the combined hormonal effects contribute to disordered processes of energy metabolism in insulin dependent tissues that generally correspond to the magnitude of insulin resistance. To determine the effects of glucocorticoid inhibition on typical insulin-mediated glycemic processes in obese rats, groups (n=6 -12 rats/phenotype) of normally reared longevity-prone congenic lean and obese animals were fed a Purina chow diet from 6 to 9 weeks of age, and overfed with the Chow diet plus a highly palatable cafeteria diet from 9 to 12 weeks of age. The congenic LA/Ntul//-cp rat strain expresses the obese trait soon after weaning but remains glucose intolerant but non-diabetic thereafter. Subgroups of obese animals were subjected to bilateral adrenalectomy (ADX) at 6 weeks of age to remove glucocorticoid contributions to glycemic parameters. At 6, 9, and 12 weeks of age, each treatment group achieved weight gain (WG) and glucose tolerance (OGT). At 6 and 9 weeks of age on the chow diet, WG on ADX-obese rats was equivalent to that of their lean littermates, but was twice that of their lean littermates from 9 to 12 weeks of age. following 30 to 60 minutes, OGT responses and the area under the OGT curve were impaired but not diabetic in obese animals of all ages, and reverted to those of lean rats following ADX. At 12 weeks of age, the insulin to glucose ratio (I:G) was consistent with insulin resistance in obese rats but not in ADX-obesity or lean rats. At 9 and 12 weeks of age, ADX led to the normalization of OGT and glycemic indices in the obese phenotype. These findings support normalizationof typical insulin-mediated components of glycemic parameters and glucose uptake in peripheral tissues following glucocorticoid ablation of congenic obese rats, and suggest that the counterregulatory effects of insulin and glucocorticoid hormones may be contributory to the impaired glycemic responses in the obese phenotype of the LA/N//-cp (corpulent) rat and are consistent with a receptor-mediated element in the development of insulin resistance and glucose uptake in peripheral tissues commonly associated with the early development of obesity in this strain.

The global prevalence of obesity and metabolic syndrome and its pathophysiologic sequela are currently approaching epidemic proportions, with unacceptable levels in much of Westernized and economically developed society. The clinical stigmata of metabolic syndrome typically include the comorbidities of obesity, hypertension, non-insulin dependent diabetes, and hyperlipidemia with decreased plasma high density lipoprotein concentrations. In addition, a common finding of hyperinsulinemia and insulin resistance typical of high carbohydrate diets often accompanies the syndrome. The incorporation of the insulin sparing ketogenic diet as a dietary strategy for the treatment of metabolic syndrome may bring about improvements in insulin action and substrate utilization in peripheral tissues with at least a partial if not significant resolution of the syndrome. Thus, the ketogenic diet in addition to adaptations toward a healthy lifestyle and pharmacologic therapies have been explored as potential mechanisms to resolve the pathophysiologic sequela of obesity and metabolic syndrome and their impact on the delivery of healthcare. Metabolic syndrome (MetS) is a condition defined as a clustering of risk factors that is strongly associated with obesity, heart disease, and diabetes [22]. It has recently been estimated that the global prevalence of MetS has reached epidemic levels including the U.S.A., where it has been estimated that 20% to 25% of the adult global population meets the diagnostic criterion for MetS [3], which may be established when at least three of the five primary risk factors are present. The risk factors include a large waistline (abdominal or visceral obesity), high plasma triglyceride levels, low plasma HDL cholesterol concentrations, elevated blood pressure, and fasting hyperglycemia. The standard and most effective treatments for MetS to date have been incorporation of lifestyle changes, with dietary interventions being one of the major effective lifestyle modifications utilized to treat both obesity and MetS [14];[41]. The Ketogenic Diet (KD) is one dietary intervention that may have the potential to improve MetS risk factors. Historically, one of the primary uses of the KD has been to treat epilepsy, however, there is substantial evidence that it may also help to improve other conditions and illnesses, including obesity and MetS [30]; [48]; [35]. Despite this potential, certain dietary misconceptions may have prevented or slowed further research on the KD applications to weight control and use of the KD, particularly the emergence of the national dietary guidelines that have now promoted a low-fat, high-carbohydrate diet for several decades [18]; [51]; [52]. The purpose of this paper is to conduct a review of the literature regarding MetS, the KD, and the implications of the KD as a treatment for obesity and MetS. Existing research is systematically reviewed regarding the KD’s potential to address MetS and MetS risk factors. The results of the review indicate the validity of the diet and the need for further research on the KD and its potential to address the benefits, potential risks and clinical efficacy of the KD on reducing the pathophysiologic sequalae of obesity and MetS. MetS = Metabolic Syndrome, KD = ketogenic diet, KB = ketone bodies, including metabolic remnants acetoacetate (AcAc),3-beta-hydroxybutyrate (3HB), and acetone, PSMF = Protein Sparing Modified Fast, HDL, HDL-C= plasma high density cholesterol lipoprotein, LDL, LDL-C = low density cholesterol lipoprotein, TG, TRIG = plasma triglycerides, CRP = C-reactive protein, GLUT4 = Glucose Transporter 4, and insulin-linked cellular entity, ATP = Adenosine tri-phosphate, a high energy phosphate, CCK = cholecystokinin, CR = calorie restricted diet, LFD = low fat diet, LCKD = low calorie ketogenic diet, BP = blood pressure; SBP = systolic blood pressure; DBP = diastolic blood pressure, A(1c) = glycosylated hemoglobin fraction, NHLBI = National Heart, Lung and Blood Institute of the National Institutes of Health

The prevalence of obesity and overweight conditions has now reached epidemic proportions in much of the Western world, and is generally assumed to be due to a metabolic imbalance between energy intake and energy expenditure. Animal models represent the preferred experimental tools to investigate mechanisms of energy metabolism in an attempt to discover a pharmacotherapeutic or other clinical approach to treat the disordered metabolism. The role of impaired thermogenesis contributes to an economy of energy metabolism that persists throughout the lifespan in the obese phenotype of the corpulent rat. Obesity and mild to moderate impaired carbohydrate tolerance develops in the obese phenotype of the LA/Ntul//-cp (corpulent) rat strain by 6 weeks of age. Groups (n=12-20 rats/phenotype] of female congenic lean and obese LA/Ntul//-cp (corpulent) rats were fed ad libitum standardized Purina #5012 diet ad house water for 4, 14, or 24 months of age. Measures of Body weight (BW) and of resting oxygen consumption (RMR; VO2) at thermal neutrality and for up to 45 minutes of (4°C) spontaneous cold exposure, and norepinephrine-stimulated thermogenesis (100 ug. s.c.) were determined at each age. Body weights of lean rats increased only gradually during the study (p=n.s.), but weights of obese phenotype were ~2-fold greater at 4 months (p=<0.05), 14 months (p-<0.01), and ~3.5 to 4-fold greater at 24 months of age (p=<0.01). Resting metabolic rates in the lean phenotype decreased modestly after 24 months (p=<0.05), and they were higher than resting metabolic rates in the obese phenotype at all ages studied (p=<0.05). In 4-month-old rats, cold exposure at 4°C caused a dramatic 5-fold increase in oxygen consumption after 5 minutes, which decreased to 2x resting metabolic rate within 15 minutes and stayed unchanged thereafter in the lean phenotype. In lean 14-month-old rats, the increase in oxygen consumption at 5 minutes was on average ~4-fold higher than resting levels, and it decreased to two times resting levels from 15 to 45 minutes of exposure to 4°C. In 24-month-old lean rats however, the cold induced increases in metabolism were markedly diminished to only ~3x resting metabolic rates at 5 minutes cold exposure but remained similar to the other lean age groups thereafter. In the obese phenotype, the peak responses at 5 minutes were lower than those of lean rats at 5 minutes in 4- and 14-month-old rats and were significantly impaired in 24-month-old rats at all times measured. Norepinephrine resulted in a >1.5-fold increase in oxygen consumption in the lean phenotype at all ages studied, while in obese rats norepinephrine resulted in a~1.4-fold increase in oxygen consumption at 4 months of age with non-significant ~1.1 to 1.2-fold increases at the two older ages. In both phenotypes, the resting and the norepinephrine-stimulated oxygen consumption responses tended to decrease with increasing age. The findings from this research indicate that the obese phenotype has significantly higher body weights than their lean littermates across the age spectrum studied, and that both resting metabolic rates, 4°C cold exposure, and norepinephrine-stimulated thermogenesis are lower in the obese phenotype compared to the lean phenotype and become lower with age. Thus, the economy of energy metabolism is deemed a significant contributory factor in the epigenetic expression of adipogenesis and fat accretion in the obese phenotype of this strain.

Historically many patients may present with symptoms suggestive of hypothyroidism or disordered thyroidal parameters, but when the usual labs come back, they often fail to identify any obvious failings in their hypothalamic-thyroidal axis. However, when we turn to the findings in lab rats we may discern the real culprit in the patients’ apparent symptomology. Patients often experiment with any number of a broad assortment of dietary and exercise approaches to resolve their body weight and other issues with little success. Indeed, Laurberg et al. noted that small differences in thyroid function alone have been associated with up to 5 kg difference in body weight.1 Some patients may also experience symptoms of being overly sensitive to dietary carbohydrates, but even after careful monitoring of the types and amounts of carbohydrates consumed, may still often harbor lingering weight control issues but which fall well short of that required for a diagnosis of metabolic syndrome

The prevalence of child abuse and human trafficking in human existence has occurred in various forms for many centuries and now appears to be approaching epidemic proportions in many societies where borders are insecure and enforcement resources are inadequate. The emergence of child abuse and human trafficking in their different forms is a serious crime that affects virtually every country in the world, where they not only represent a violation of the basic human rights and dignity of those impacted, but also have an impact on their families and loved ones who may be inadvertently left behind. While the majority of cases of human trafficking have traditionally involved humans being coercively forced to engage in sex and labor violations, an emerging area of illegal organ trafficking to support an increasing need for organ transplantation procedures can now be included. While children and young adults are the most frequently affected segments of the population for some types of trafficking, human trafficking can affect victims of any age, gender, race, ethnicity, culture, or persuasion, and they can reveal in the clinic accompanied or unaccompanied for urgent care. When presenting, a patient may display cardinal signs, symptoms, and clinical stigmata that are of a suspicious nature and suggest further investigation, including reporting the issues to competent authorities, especially if the victim is an infant or regarded a minor, less than 18 years of age in most countries. Since health care professionals are frequently the first point of contact when symptoms and stigmata of human trafficking, child abuse, and other signs of abuse are evident, additional modules in health care forensics would be a welcome addition to medical curricula and public health perspectives for physicians and other members of the healthcare team. Thus, the goal of this paper was to review the characteristics of human trafficking and abuse, to summarize key areas of legal, medical, and administrative responsibility in order to ensure the availability of optimal and appropriate patient-centered care for victims, and to emphasize the significance of including modules in forensic medical education in medical curricula.