Factors associated with Mortality in Adults admitted with Heart Failure at the University Teaching Hospital in Lusaka, Zambia

Background: Heart failure is a major public health problem and has been recognized as an important cause of morbidity and mortality for several years. It is one of the leading non-infectious causes of death among hospitalized patients at the University Teaching Hospital (UTH) in Lusaka, Zambia. This study aimed to investigate the predictors of 30-day mortality in heart failure patients admitted to the medical wards at the UTH using routinely obtained clinical data.Methods: We enrolled 390 heart failure patients and followed them up over a period of 30 days. Data collected included demographic characteristics (age, sex), medication use and co-morbidities (hypertension, diabetes  mellitus, Human Immunodeficiency Virus (HIV) infection). Clinical data included vital signs, blood urea, serum sodium, serum potassium, serum creatinine, and haemoglobin level. Trans-thoracic echocardiographs and electrocardiographs were also done to determine left ventricular ejection fraction (LVEF) and to check for the presence of arrhythmias. Patients were dichotomized into those with preserved (LVEF>=40 percent) and reduced (LVEF< 40 percent) systolic function. Recruited patients were then prospectively followed up to determine outcome by day 30 (i.e. dead or alive). Cox proportion Hazard regression analysis (on Epi Info software version 3.5.3) was used to analyse the effect of each of these parameters on outcome.Results: Of the recruited patients, 59% were female (95% CI 54-64). The median age was 50 years (IQR 33-68). 138 patients (35%, 95% CI 31-40) died within 30 days of admission. 94 (68%) of these deaths occurred  in-hospital. The factors shown to be independent predictors of death onmultivariate logistic regression analysis were LVEF<40 percent (OR=2.86, 95%CI 1.68- 4.87), NYHA class IV (OR=2.15, 95%CI 1.27- 3.64),serum urea above 15mmol/L (OR=2.48, 95%CI 1.07-5.70), and haemoglobin level below 12g/dL (OR=1.79, 95%CI 1.11- 2.89).The additional factor associated with increased risk of mortality on univariate analysis wassystolic blood pressure below 115mmHg (OR=1.63, 95%CI 1.05- 2.51). However, serum creatinine (OR=1.49, 95%CI  0.49-4.48) and HIV  seropositivity (OR=0.96, 95% CI 0.53-1.72)had no bearing on the risk of death in this patient population.Conclusions: Left ventricular ejection fraction <40 percent, New York Heart Association class IV, serum urea above 15mmol/L, haemoglobin level below 12g/dLand systolic blood pressure below 115mmHg are predictors of poor 30-day outcome in hospitalised heart failure patients

ROLE OF TESTOSTERONE IN THE TREATMENT OF ED

Hypogonadism may play a significant role in the pathophysiology of erectile dysfunction (ED). A threshold level of testosterone may be necessary for normal erectile function. Testosterone replacement therapy is indicated in hypogonadal patients and is beneficial in patients with ED and hypogonadism. Monotherapy with testosterone for ED is of limited effectiveness and may be most promising in young patients with hypogonadism and without vascular risk factors for ED. A number of laboratory and human studies have shown the combination of testosterone and other ED treatments, such as phosphodiesterase type 5 (PDE5) inhibitors, to be beneficial in patients with ED and hypogonadism, who fail PDE5 inhibitor therapy alone. There is increasing evidence that combination therapy is effective in treating the symptoms of ED in patients for whom treatment failed with testosterone or PDE5 inhibitors alone. Testosterone replacement therapy has potentially evolved from a monotherapy for ED in cases of low testosterone, to a combination therapy with PDE5 inhibitors. Screening for hypogonadism may be useful in men with ED who fail prior PDE5 inhibitors, especially in populations at risk for hypogonadism such as type 2 diabetes and the metabolic syndrome

Generation of GeV protons from 1 PW laser interaction with near critical density targets

The propagation of ultra intense laser pulses through matter is connected with the generation of strong moving magnetic fields in the propagation channel as well as the formation of a thin ion filament along the axis of the channel. Upon exiting the plasma the magnetic field displaces the electrons at the back of the target, generating a quasistatic electric field that accelerates and collimates ions from the filament. Two-dimensional Particle-in-Cell simulations show that a 1 PW laser pulse tightly focused on a near-critical density target is able to accelerate protons up to an energy of 1.3 GeV. Scaling laws and optimal conditions for proton acceleration are established considering the energy depletion of the laser pulse.Comment: 26 pages, 8 figure

Accelerating Protons to Therapeutic Energies with Ultra-Intense Ultra-Clean and Ultra-Short Laser Pulses

Proton acceleration by high-intensity laser pulses from ultra-thin foils for hadron therapy is discussed. With the improvement of the laser intensity contrast ratio to 10-11 achieved on Hercules laser at the University of Michigan, it became possible to attain laser-solid interactions at intensities up to 1022 W/cm2 that allows an efficient regime of laser-driven ion acceleration from submicron foils. Particle-In-Cell (PIC) computer simulations of proton acceleration in the Directed Coulomb explosion regime from ultra-thin double-layer (heavy ions / light ions) foils of different thicknesses were performed under the anticipated experimental conditions for Hercules laser with pulse energies from 3 to 15 J, pulse duration of 30 fs at full width half maximum (FWHM), focused to a spot size of 0.8 microns (FWHM). In this regime heavy ions expand predominantly in the direction of laser pulse propagation enhancing the longitudinal charge separation electric field that accelerates light ions. The dependence of the maximum proton energy on the foil thickness has been found and the laser pulse characteristics have been matched with the thickness of the target to ensure the most efficient acceleration. Moreover the proton spectrum demonstrates a peaked structure at high energies, which is required for radiation therapy. 2D PIC simulations show that a 150-500 TW laser pulse is able to accelerate protons up to 100-220 MeV energies.Comment: 26 pages, 6 figure

Energetic electron and ion generation from interactions of intense laser pulses with laser machined conical targets

The generation of energetic electron and proton beams was studied from the interaction of high intensity laser pulses with pre-drilled conical targets. These conical targets are laser machined onto flat targets using 7–180 µJ pulses whose axis of propagation is identical to that of the main high intensity pulse. This method significantly relaxes requirements for alignment of conical targets in systematic experimental investigations and also reduces the cost of target fabrication. These experiments showed that conical targets increase the electron beam charge by up to 44 ± 18% compared with flat targets. We also found greater electron beam divergence for conical targets than for flat targets, which was due to escaping electrons from the surface of the cone wall into the surrounding solid target region. In addition, the experiments showed similar maximum proton energies for both targets since the larger electron beam divergence balances the increase in electron beam charge for conical targets. 2D particle in cell simulations were consistent with the experimental results. Simulations for conical target without preplasma showed higher energy gain for heavy ions due to 'directed coulomb explosion'. This may be useful for medical applications or for ion beam fast ignition fusion.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/85411/1/nf10_5_055006.pd

Влияние ожирения и андрогенного дефицита на кровообращение в предстательной железе

In Study at 120 Diabetes Mellitus II type men the high frequency Obesity (71,7%) and Androgen Deficiency (52,8—64,5% of the patients depending on a degree of the indemnification) and them pathogenic authentic communications were shown. The blood level of total testosterone was represented by the critical factor of Prostatic arterial Blood Circulation. Obesity and Androgen Deficiency are seem as independent risk factors to development of ischemic prostatopathy, such as Prostatic blood circulation Disorders can develop earlier than other variants of the diabetic microangiophaty.При обследовании 120 мужчин с сахарным диабетом 2-го типа выявлена высокая частота ожирения (71,7%) и андрогенного дефицита (52,8—64,5% больных в зависимости от степени его компенсации), между которыми установлена достоверная связь. Уровень общего тестостерона крови представлялся критическим фактором, определявшим скорость артериального кровотока в простате. Ожирение и андрогенный дефицит являются факторам риска развития ишемической простатопатии, так как нарушения органного кровотока в предстательной железе могут возникать раньше других вариантов диабетической микроангиопатии

Новые системные механизмы патогенеза симптомов нижних мочевых путей у мужчин (литературный обзор)

In the Modern Literary Review the newest pathogenic theories of interrelation between widespread somatic pathology — Metabolic Syndrome — and Androgen Deficiency and low urinary tract symptoms (LUTS) at men are considered. Metabolic Syndrome while is poorly familiar practical Urologists. However, they should be informed on an essential role of specified Hormonal and Metabolic factors in Pathogenesis of LUTS at men, as the new understanding of methodology of Urological diseases is possible today only on a joint of specialities.В литературном обзоре рассматриваются новейшие патогенетические теории взаимосвязи широко распространенной соматической патологии — метаболического синдрома — и андрогенного дефицита с симптомами нижних мочевых путей (СНМП) у мужчин. Метаболический синдром пока мало знаком практическим урологам. Однако они должны быть осведомлены о существенной роли указанных гормонально-метаболических факторов в патогенезе СНМП у мужчин, так как новое понимание методологии урологических заболеваний возможно сегодня только на стыке специальностей

A case of 17-beta-hydroxysteroid dehydrogenase deficiency type 3 in adult endocrinologist practice

17β-Hydroxysteroid dehydrogenase 3 deficiency (17HSD3) is a rare autosomal recessive cause of 46, XY disorders of sex development resulting from HSD17B3 gene mutations, in which conversion of androstenedione to testosterone is impared. The clinical signs of 17HSD3 deficiency depend on the residual activity of the enzyme. The diagnosis of 17HSD3 deficiency is based on reduced testosterone/androstenedione ratio (T/AD < 0.8). Patients are usually assigned at birth and raise as female. If the diagnosis is made before puberty, gonadectomy is recommended, taking into account the risk of masculinization during the puberty and estrogen therapy initiation in this period. If the diagnosis of 17HSD3 deficiency is established during puberty, when virilization manifests, the therapeutic strategy is based on the results of comprehensive psychological testing and gender identity of a patient. In patients with more pronounced masculinization or diagnosis established shortly after birth, who are assigned at birth and raise as male, testosterone therapy is used to achieve a male phenotype. The 17HSD3 deficiency and virilization often result in a change of gender identity during puberty. The article presents a clinical case of 17-βhydroxysteroid dehydrogenase type 3 deficiency with late diagnosis due to parental will. The diagnostic approaches and management of the disease are also described

Effect of 12 months of testosterone replacement therapy on metabolic syndrome components in hypogonadal men: data from the Testim Registry in the US (TRiUS)

<p>Abstract</p> <p>Background</p> <p>Recent evidence suggests that there may be a bidirectional, physiological link between hypogonadism and metabolic syndrome (MetS), and testosterone replacement therapy (TRT) has been shown to improve some symptoms of MetS in small patient populations. We examined the effect of 12 months of TRT on MetS components in a large cohort of hypogonadal men.</p> <p>Methods</p> <p>Data were obtained from TRiUS (Testim^®Registry in the United States), a 12-month, multicenter, prospective observational registry (N = 849) of hypogonadal men prescribed Testim 1% testosterone gel (5-10 g/day). Data analyzed included age, total testosterone (TT), free testosterone (FT), sex hormone-binding globulin (SHBG), and MetS components: waist circumference, blood pressure, fasting blood glucose, plasma triglycerides, and HDL cholesterol.</p> <p>Results</p> <p>Of evaluable patients (581/849) at baseline, 37% were MetS+ (n = 213) and 63% were MetS- (n = 368). MetS+ patients had significantly lower TT (p < 0.0001) and SHBG (p = 0.01) levels. Patients with the lowest quartile TT levels (<206 ng/dL [<7.1 nmol/L]) had a significantly increased risk of MetS+ classification vs those with highest quartile TT levels (≥331 ng/dL [≥11.5 nmol/L]) (odds ratio 2.66; 95% CI, 1.60 to 4.43). After 12 months of TRT, TT levels significantly increased in all patients (p < 0.005). Despite having similar TT levels after TRT, only MetS+ patients demonstrated significant decreases in waist circumference, fasting blood glucose levels, and blood pressure; lowest TT quartile patients demonstrated significant decreases in waist circumference and fasting blood glucose. Neither HDL cholesterol nor triglyceride levels changed significantly in either patient population.</p> <p>Conclusion</p> <p>Hypogonadal MetS+ patients were more likely than their MetS- counterparts to have lower baseline TT levels and present with more comorbid conditions. MetS+ patients and those in the lowest TT quartile showed improvement in some metabolic syndrome components after 12 months of TRT. While it is currently unclear if further cardiometabolic benefit can be seen with longer TRT use in this population, testing for low testosterone may be warranted in MetS+ men with hypogonadal symptoms.</p