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Aims To map sensory and pelvic postganglionic neurons from three different regions of the female rat urethra. Methods The neuronal tracer True Blue (TB) was injected into the pre-pelvic, pelvic, and clitoral regions of the urethra from female Wistar rats. Seven days after TB injection, TB+ cells from the dorsal root ganglia (DRGs) and the major pelvic ganglion (MPG) were examined. The number and morphometry of TB+ cells were determined. Results TB+ cells were mainly distributed in lumbar 1 (L1), lumbar 2 (L2), lumbar 6 (L6), and sacral 1 (S1) DRGs, and in the MPG. The mean number of sensory neurons was 1200 ± 143. TB injection in pre-pelvic and pelvic urethra labeled neurons in L1, L2, L6, and S1 DRGs. TB injection in clitoral urethra labeled neurons in L6 and S1 DRGs. L6 DRG contained >50% of the total urethral TB+ neurons, and ~80% of the clitoral region. The mean value of the total number of MPG TB+ neurons was 1217 ± 72. DRG and MPG neurons projecting to the urethra presented a somatotopic distribution. Conclusions The results demonstrated that L6 DRG is the major supplier of afferent innervation to the urethra, and that the distal urethral region is exclusively innervated by lower lumbosacral DRGs. Considering that electrical stimulation of sensory pudendal nerve improves overactive bladder, and that most of the sensory neurons in the distal urethra are from L6 DRG, electrical stimulation of this ganglion may be an innovative and effective neuromodulation therapy for neurogenic urinary dysfunctions.

Cadmium (Cd) is a heavy metal classified as a carcinogen whose exposure could affect the function of the central nervous system. Studies suggest that Cd modifies neuronal morphology in the hippocampus and affects cognitive tasks. The oxidative stress pathway is proposed as a mechanism of toxicity. However, this mechanism is not precise yet. This study aimed to evaluate the effect of Cd administration on oxidative stress markers in the male rat's hippocampus. Male Wistar rats were divided into (1) control (drinking water) and (2) treatment with Cd (32.5 ppm of cadmium chloride (CdCl

Cadmium, one of the more hazardous environmental contaminants, has been proposed as a metabolic disruptor. Vanadium has emerged as a possible treatment for metabolic diseases. Both metals are important in public health. We aimed to investigate whether vanadium treatment is effective against metabolic disturbances caused by chronic exposure to the lowest-observable adverse effect level of cadmium. Male Wistar rats were exposed to cadmium (32.5 ppm) in drinking water for 3 months. Metabolic complications such as overweight, visceral adipose gain, hyperglycemia, impaired glucose tolerance, and dyslipidemia were detected, and low glycogen levels and steatosis were observed in the tissues. Then, the control and treated animals were subdivided and treated with a solution of 5 μM NaVO3/kg/twice a week for 2 months. The control-NaVO3 group did not show zoometric or metabolic changes. A strong interaction of NaVO3 treatment over cadmium metabolic disruption was observed. The vanadium accumulation diminished cadmium concentration in tissues. Also, vanadium interaction improved glucose homeostasis. The major effect was observed on glycogen synthesis, which was fully recovered in all tissues analyzed. Additionally, vanadium treatment prevented overweight and visceral fat accumulation, improving BMI and the percentage of fat. However, NaVO3 treatment did not have an effect on dyslipidemia or steatosis. In conclusion, this work shows that vanadium administration has a strong effect against metabolic disturbances caused by chronic cadmium exposure, observing powerful interaction on glucose homeostasis.

Metabolic syndrome (MetS) represents a cluster of related metabolic abnormalities, including central obesity, hypertension, dyslipidemia, hyperglycemia, and insulin resistance. These metabolic derangements present significant risk factors for chronic kidney disease that carries to loss of essential micronutrients, which accelerates comorbidity apparition. The work aimed was to evaluate the trace element homeostasis regarding morphological adaptations and renal function in MetS early-onset. Fifty male Wistar rats were divided into two groups: (a) control group and (b) hypercaloric diet group that developed MetS early-onset after 3 months. Classical zoometric parameters do not show changes; however, biochemical modifications were observed such as hyperglycemia, protein glycation, insulin resistance, dyslipidemia, hyperinsulinemia, and hypoadiponectinemia. MetS early-onset group observed renal structural modifications, but no functional changes. The structural modifications observed were minimal glomerular injury, glomerular basement membrane thickening, as well as mesangial and tubular cells that showed growth and proliferation. In serum and kidney (cortex and medulla), the concentrations of Zn, Fe, Cr, Mg, Mn, Cu, Co, and Ni were no differences between the experimental groups, but excretory fractions of these were lower in the hypercaloric diet group. In conclusion, MetS early-onset coexist renal structural modification and a hyperreabsorptive activity of essential trace elements that avoid its loss; thus, the excretory fraction of oligo-elements could be used a biomarker of early renal injury caused by metabolic diseases in the clinical practice.

This study presents a correlation between prenatal ultrasonographic images and neuropathologic findings of postmortem tissue samples from five confirmed cases of perinatal Zika virus (ZIKV) infection belonging to the cohort of the ZEN Initiative in Bucaramanga, Colombia. Deaths occurred between June 2016 and March 2017. Mothers consulted with ZIKV infection clinical manifestations or fetal central nervous system (CNS) abnormalities or both. A detailed ultrasound scan and neurosonographic protocol was performed by maternal fetal specialists. Perinatal autopsies were performed following the Colombian National Health Institute's ZIKV protocol. The autopsies were from two fetal deaths, and three early neonatal deaths. Gestational age was between 262/7 and 382/7 weeks. Two cases were classified as mild microcephaly. Few findings by ultrasound and pathology were found in case 1 because it was a late infection; the other cases presented findings corresponding to congenital Zika syndrome: craniofacial malformations, cerebellar hypoplasia, anomalies of the corpus callosum and ventriculomegaly, all confirmed in autopsy specimens. By ultrasonography, hyperechogenicities were seen in several brain structures, which correspond to cortical and periventricular calcifications, subependymal glial reactivity and perivascular rings. The ultrasound and pathological findings show a wide spectrum of CNS anomalies that confirm the neurotropic effect of the ZIKV, recognizing the neuroimaging findings of this disease (unilateral ventriculomegaly, alterations in the corpus callosum and cerebellum, and calcifications) are highly suggestive of ZIKV infection.

Metabolic syndrome (MetS) is a public health problem and a risk of developing cardiometabolic and neurodegenerative diseases. The biochemical-inflammatory impairment in brain areas related to learning and memory has not been differentiated between MetS models. We aimed to compare the effect of the MetS generated by consuming high-fat (HFD) or -carbohydrate diets (HCD) on the hippocampus and frontal cortex, related to astrocyte-neuron metabolism and neuroinflammation origin. Sixty male Wistar rats were separated into three groups: 1) control group, 2) HCD group, and 3) HFD group. After 3 months, we evaluated zoometry, a serum bioclinical profile, and in the hippocampus and frontal cortex, we performed biochemical assays (concentration of lactate, glutamate, fatty acids, and ASAT, ALAT, and LDH activity), immunoreactivity tests (GFAP, COX2, CD36, and BDNF), and immunoassays (TNF-α, IL-1β, IL-6, and PGE2). The bioclinical parameters showed that both diets induce MetS. At the brain level, it is noteworthy that the HCD group had an increase in lactate and glutamate concentration, reactive astrogliosis, immunoreactive COX2 neurons in the CA1 subfield hippocampus and frontal cortex, and high levels of PGE2, TNF-α, IL-1β, and IL-6, and low BDNF immunoreactivity. Meanwhile, the HFD is highlighted by increased fatty acid levels and CD36 expression in the hippocampus and frontal cortex, strong reactive astrogliosis and COX2 immunoreactivity, and the greatest inflammation with the lowest BDNF immunoreactivity. In conclusion, MetS induction by an HFD or HCD generates different biochemical, cellular, and inflammatory patterns in the hippocampus and frontal cortex.

Cadmium is a nonessential transition metal considered one of the more hazardous environmental contaminants. The population is chronically exposed to this metal at low concentrations, designated as the LOAEL (lowest observable adverse effect level) dose. We aimed to investigate whether oral subacute exposure to cadmium LOAEL disrupts hormonal and metabolic effects of the liver-adipose axis in Wistar rats. Fifty male Wistar rats were separated into two groups: control (standard normocalorie diet + water free of cadmium) and cadmium (standard normocalorie diet + drinking water with 32.5 ppm CdCl2). After 1 month, zoometry, a serum lipid panel, adipokines, and proinflammatory cytokines were evaluated. Tests of glucose and insulin tolerance (ITT) and insulin resistance were performed. Histological studies on structure, triglyceride distribution, and protein expression of the insulin pathway were performed in the liver and retroperitoneal adipose tissue. In both tissues, the cadmium, triglyceride, glycogen, and proinflammatory cytokine contents were also quantified. The cadmium group developed dyslipidemia, glucose intolerance, hyperinsulinemia, hyperleptinemia, inflammation, and selective insulin resistance in the liver and adipose tissue. In the liver, glycogen synthesis was diminished, while de novo lipogenesis increased, which was associated with low GSK3β-pS9 and strong expression of SREBP-1c. Dysfunctional adipose tissue was observed with hypertrophy and lipolysis, without changes in SREBP-1c expression and low glycogen synthesis. Both tissues accumulated cadmium and developed inflammation. In conclusion, oral subacute cadmium LOAEL dose exposure induces inflammation, insulin signaling modifications, an early insulin resistance stage (insensibility), and impairment of the hormonal and metabolic liver-adipose axis in Wistar rats.

Autism spectrum disorder (ASD) is a range of neurodevelopmental disorders characterized by movement and social deficits with rapidly increasing incidence worldwide. Propionic acid (PPA) is a histone deacetylase inhibitor that regulates neuronal plasticity in the brain. Evaluation of the behavioral and cellular consequences of PPA exposure during a critical neurodevelopmental window is required. Therefore, in the present study we aimed to evaluate the effects of prenatal PPA exposure on locomotor behavior and astrocyte number, as well as on levels of nitric oxide (NO), synaptophysin (SYP; a marker of synaptic plasticity), and metallothionein 3 (MT-III; a marker of reactive oxygen species and zinc metabolism), in the prefrontal cortex (PFC) of male rats. All parameters were evaluated at three critical ages of development: postnatal days (PD) 21 (weaning age), PD35 (pre-pubertal age) and PD70 (post-pubertal age). Prenatal PPA exposure induced hypolocomotion and decreased rearing events at weaning age. Moreover, astrogliosis in the PFC was observed in PPA-treated rats at pre- and post-pubertal age. SYP levels were dramatically decreased in PPA-treated rats with simultaneous astrogliosis, suggesting reduced synaptic plasticity. MT-III expression was deregulated in PPA-treated rats. Finally, the expression of NO in the PFC remained unaltered in PPA-treated rats. These results mimic behavioral, neuronal and astrocytic characteristics observed in ASD patients.

Cadmium (Cd) is a toxic metal and classified as a carcinogen whose exposure could affect the function of the central nervous system. There are studies that suggest that Cd promotes neurodegeneration in different regions of the brain, particularly in the hippocampus. It is proposed that its mechanism of toxicity maybe by an oxidative stress pathway, which modifies neuronal morphology and causes the death of neurons and consequently affecting cognitive tasks. However, this mechanism is not yet clear. The aim of the present work was to study the effect of Cd administration on recognition memory for 2, 3 and 4 months, neuronal morphology and immunoreactivity for caspase-3 and 9 in rat hippocampi. The results show that the administration of Cd decreased recognition memory. Likewise, it caused the dendritic morphology of the CA1, CA3 and dentate gyrus regions of the hippocampus to decrease with respect to the time of administration of this heavy metal. In addition, we observed a reduction in the density of dendritic spines as well as an increase in the immunoreactivity of caspase-3 and 9 in the same hippocampal regions of the animals treated with Cd. These results suggest that Cd affects the structure and function of the neurons of the hippocampus, which contribute to the deterioration of recognition memory. Our results suggest that the exposure to Cd represents a critical health problem, which if not addressed quickly, could cause much more serious problems in the quality of life of the human population, as well as in the environment in which they develop.

The consumption of foods rich in carbohydrates, saturated fat, and sodium, accompanied by a sedentary routine, are factors that contribute to the progress of metabolic syndrome (MS). In this way, they cause the accumulation of body fat, hypertension, dyslipidemia, and hyperglycemia. Additionally, MS has been shown to cause oxidative stress, inflammation, and death of neurons in the hippocampus. Consequently, spatial and recognition memory is affected. It has recently been proposed that metformin decavanadate (MetfDeca) exerts insulin mimetic effects that enhance metabolism in MS animals; however, what effects it can cause on the hippocampal neurons of rats with MS are unknown. The objective of the work was to evaluate the effect of MetfDeca on hippocampal neurodegeneration and recognition memory in rats with MS. Administration of MetfDeca for 60 days in MS rats improved object recognition memory (NORt). In addition, MetfDeca reduced markers of oxidative stress and hippocampal neuroinflammation. Accompanied by an increase in the density and length of the dendritic spines of the hippocampus of rats with MS. We conclude that MetfDeca represents an important therapeutic agent to treat MS and induce neuronal and cognitive restoration mechanisms.

Context: The chronic exposure to Cadmium (Cd) constitute an risk to develop hypertension and cardiovascular diseases associated with the increase of oxidative stress.Objective: In this study, we investigate the role of metabolic changes produced by exposure to Cd on the endothelial dysfunction via oxidative stress.Methods: Male Wistar rats were exposed to Cd (32.5-ppm) for 2-months. The zoometry and blood pressure were evaluated, also glucose and lipids profiles in serum and vascular reactivity evaluated in isolated aorta rings.Results: Rats exposed to Cd showed an increase of blood pressure and biochemical parameters similar to metabolic syndrome. Additionally, rats exposed to Cd showed a reduced relaxation in aortic rings, which was reversed after the addition of SOD and apocynin an inhibitor of NADPH.Conclusion: The Cd-exposition induced hypertension and endothelial injury by that modifying the vascular relaxation and develop oxidative stress via NADPH oxidase, superoxide and loss nitric oxide bioavailability.

Metabolic syndrome (MS) is a health problem that is characterized by body fat accumulation, hypertension, dyslipidemia, and hyperglycemia; recently, it has been demonstrated that MS also damages memory processes. The first-line drug in the treatment of MS and type 2 diabetes mellitus is metformin, which is an antihyperglycemic agent. This drug has been shown to produce neuroprotection and to improve memory processes. However, the mechanism involved in this neuroprotection is unknown. A 90-day administration of metformin improved the cognitive processes of rats with MS as evaluated by the novel object recognition test, and this finding could be explained by an increase in the neuronal spine density and spine length. We also found that metformin increased the immunoreactivity of synaptophysin, sirtuin-1, AMP-activated protein kinase, and brain-derived neuronal factor, which are important plasticity markers. We conclude that metformin is an important therapeutic agent that increases neural plasticity and protects cognitive processes. The use of this drug is important in the minimization of the damage caused by MS.

An important worldwide health problem as the result of current lifestyle is metabolic syndrome (MS). It has been shown that MS induced by a high-calorie diet (HCD) in rats produces cognitive deterioration in the novel object recognition test (NORt) and decreases synaptic connections and dendritic order in the hippocampus and temporal cortex. However, it is unknown whether MS induced by an HCD participates in the cognitive process observed with the injection of Aβ1–42 into the hippocampus of rats as a model of Alzheimer disease (AD). The induction of MS in rats produces a deterioration in NORt; however, rats with MS injected with Aβ1–42 show a major deterioration in the cognitive process. This event could be explained by the increment in the oxidative stress in both cases studied (MS and Aβ1–42): together, the hippocampus and temporal cortex produce an enhancer effect. In the same way, we observed an increment in interleukin-1β, TNF-α, and GFAP, indicative of exacerbated inflammatory processes by the combination of MS and Aβ1–42. We can conclude that MS might play a key role in the apparition and development of cognitive disorders, including AD. We propose that metabolic theory is important to explain the apparition of cognitive diseases.

Pentraxin-3 has been reported as a promising biomarker of pre-eclampsia and its severity; however, available studies have small sample sizes, and analyses are not always adjusted for confounders. The aim of this study is to establish the strength of the association between maternal Pentraxin-3 level and pre-eclampsia or HELLP syndrome. It was a case-control study. Women with pre-eclampsia or HELLP syndrome were defined as cases, and women with healthy pregnancies at term (37 weeks) were classified as controls. Plasma concentrations of Pentraxin-3 were determined at the time of delivery by quantitative enzyme immunoassay. Associations between Pentraxin-3 and pre-eclampsia and HELLP syndrome were assessed by multinomial logistic regression. Subsidiary analysis for the time of disease onset was also carried out. Odds ratios and 95% confidence intervals are reported. A total of 1024 pregnant women were included (461 controls, 368 pre-eclampsia, 195 HELLP). A positive log-linear relationship was found between the top pentraxin-3 quintile and HELLP syndrome. After adjustment for confounders (maternal age, ethnicity, socioeconomic position, date and place of recruitment, family history of pre-eclampsia, smoking, body mass index at beginning of pregnancy, gestational age and multiple pregnancy), the strength of the association was higher for HELLP syndrome [OR 1.13 (95% CI 1.08; 1.18)] than for pre-eclampsia [OR 1.03 (95% CI 1.03; 1.10)]. No difference according to time of onset or pentraxin-3 level was found. In summary, pentraxin-3 level was associated with pre-eclampsia, but it was more strongly associated with HELLP syndrome. Longitudinal studies with a lower probability of residual confounding are necessary to improve our knowledge about the role of pentraxin-3 in pre-eclampsia.

In preterm newborn, problems with the interpretation of 17-OHP may occur.Evaluate 17-OHP values in healthy preterm newborns until they reach the corrected gestational age.Longitudinal study of 36 preterm infants with 17-OHP evaluation using ELISA from heel blood from 3 to 5 days and thereafter every 2 weeks until the corrected gestational age. Values adjusting multiple variables such as gestational age, birth weight and sex, among others were compared. The results were analyzed against 82 healthy full-term infants.In the first week of life, early term infants born within less than 34 months of gestational age show 17-OHP values that are much higher than the full term neonates. After a week, the values decrease and stabilize, but are still higher than those of full term neonates and remain so even at the corrected gestational age. (average difference of 63.0%, CI 95%: 11.8%-115.5%). 33.6% (41 samples) of a total of 122 samples taken from preterm infants were higher than 30 ng/mL.17-OHP values in early term infants are higher than those in full term neonates and can be related to postnatal adaptive processes. It is suggested that a second screening at the 37th week of corrected age be performed.En recién nacidos pretérmino se presentan problemas para interpretar la 17-OHP.Evaluar los valores de 17-OHP en recién nacidos sanos pretérmino hasta cuando alcanzan el término de edad gestacional corregida.Estudio longitudinal de 36 prematuros con evaluación de la 17-OHP por ELISA en sangre de talón desde los 3-5 días de vida y luego cada dos semanas hasta la edad gestacional de término corregida. Se comparó los valores ajustando múltiples variables como edad gestacional, peso al nacer y sexo, entre otras. Se analizaron los resultados frente a los de 82 recién nacidos a término sanos.En la primera semana de vida, los prematuros menores de 34 semanas de edad gestacional tienen valores de 17-OHP muy superiores a los neonatos de término. Al alcanzar la semana 34 de edad gestacional corregida, los valores descienden y se mantienen estables, siempre mayores a los de término, incluso al llegar a edad a término corregida (diferencia promedio de 63.0%, IC 95%: 11.8%-115.5%). El 33.6% (41 muestras) de un total de 122 muestras hechas en los prematuros eran mayores de 30 ng/mL.Los valores de 17-OHP en recién nacidos pretérmino son más altos que en neonatos a término, pudiendo ser relacionado con los procesos adaptativos postnatales. Se sugiere realizar un segundo tamizaje al llegar a la semana 37 de edad corregida.

Aggregation of the amyloid beta (Aβ) peptide and hyperphosphorylation of tau protein, which are markers of Alzheimer's disease (AD), have been reported also in diabetes mellitus (DM). One regulator of tau phosphorylation is O-GlcNAcylation, whereas for hyperphosphorylation it could be GSK3beta, which is activated in hyperglycemic conditions. With this in mind, both O-GlcNAcylation and phosphorylation of tau protein were evaluated in the brain of rats with streptozotocin (STZ)-induced hyperglycemia and hyperinsulinemia and treated with the As25-35 peptide in the hippocampal region CA1. Weight, glycated hemoglobin, glucose, and insulin were determined. Male Wistar rats were divided in groups (N=20): a) control, b) treated only with the Aβ25-35 peptide, c) treated with Aβ25-35 and STZ, and d) treated only with STZ. Results showed statistically significant differences in the mean weight, glucose levels, insulin concentration, and HbA1c percentage, between C- and D-treated groups and not STZ-treated A and B (P

Amphetamines (AMPH) are psychostimulants widely used for therapy as well as for recreational purposes. Previous results of our group showed that AMPH exposure in pregnant rats induces physiological and behavioral changes in the offspring at prepubertal and postpubertal ages. In addition, several reports have shown that AMPH are capable of modifying the morphology of neurons in some regions of the limbic system. These modifications can cause some psychiatric conditions. However, it is still unclear if there are changes to behavioral and morphological levels when low doses of AMPH are administered at a juvenile age. The aim of this study was to assess the effect of AMPH administration (1mg/kg) in Sprague-Dawley rats (postnatal day, PD21-PD35) on locomotor activity in a novel environment and compare the neuronal morphology of limbic system areas at three different ages: prepubertal (PD 36), pubertal (PD50) and postpubertal (PD 62). We found that AMPH altered locomotor activity in the prepubertal group, but did not have an effect on the other two age groups. The Golgi-Cox staining method was used to describe the neural morphology of five limbic regions: (Layers 3 and 5) the medial prefrontal cortex (mPFC), the dorsal and ventral hippocampus, the nucleus accumbens and the amygdala, showing that AMPH induced changes at pubertal ages in arborization and spine density of these neurons, but interestingly these changes did not persist at postpubertal ages. Our findings suggest that even early-life AMPH exposure does not induce long-term behavioral and morphological changes, however it causes alterations at pubertal ages in the limbic system networks, a stage of life strongly associated with the development of substance abuse behaviors.

BACKGROUND Over the years, many materials have been used in orbital reconstruction and cranioplasty. Among the materials in current use, polymethyl methacrylate (PMMA) offers a high degree of compatibility with human tissue. OBJECTIVE This work describes a new, custom-made, 3D printing-aided, prosthetic fabrication process for orbital and/or cranial reconstruction using PMMA. METHODS On the basis of information obtained from computerized tomography scanning processed in Digital Imaging and Communication in Medicine format and exported to treatment planning software, a 3D prosthesis master model was designed and digitally printed. This was then used to create an injection mold from which the prosthesis was cast in PMMA and implanted in the patient. Five patients with cranial and/or orbital defects of tumoral or traumatic etiology were treated by this method. After 5 to 7 years follow-up, no complications occurred to cause the removal of the prostheses. CONCLUSION This novel method makes it possible to produce customized PMMA prostheses to treat orbital and/or cranial defects that are cost-effective and individualized to each case.

Background: Gastrectomy is the main treatment for gastric and Siewert type II-III esophagogastric junction (EGJ) cancer. This surgery is associated with significant morbidity. Total morbidity rates vary across different studies and few have evaluated postoperative morbidity according to complication severity. Aim: To identify the predictors of severe postoperative morbidity. Methods: This was a retrospective cohort study from a prospective database. We included patients treated with gastrectomy for gastric or EGJ cancers between January 2012 and December 2016 at a single center. Severe morbidity was defined as Clavien-Dindo score ≥3. A multivariate analysis was performed to identify predictors of severe morbidity. Results: Two hundred and eighty-nine gastrectomies were performed (67% males, median age: 65 years). Tumor location was EGJ in 14%, upper third of the stomach in 30%, middle third in 26%, and lower third in 28%. In 196 (67%), a total gastrectomy was performed with a D2 lymph node dissection in 85%. Two hundred and eleven patients (79%) underwent an open gastrectomy. T status was T1 in 23% and T3/T4 in 68%. Postoperative mortality was 2.4% and morbidity rate was 41%. Severe morbidity was 11% and was mainly represented by esophagojejunostomy leak (2.4%), duodenal stump leak (2.1%), and respiratory complications (2%). On multivariate analysis, EGJ location and T3/T4 tumors were associated with a higher rate of severe postoperative morbidity. Conclusion: Severe postoperative morbidity after gastrectomy was 11%. Esophagogastric junction tumor location and T3/T4 status are risk factors for severe postoperative morbidity.

The main characteristic of brain aging is an exacerbated inflammatory and oxidative response that affects dendritic morphology and the function of the neurons of the prefrontal cortex (PFC) and the hippocampus. This consequently causes memory loss. Recently, the use of the Goji berry (Lycium barbarum) as an antioxidant extract has provided neuroprotection and neuroplasticity, however, its therapeutic potential has not been demonstrated in aging conditions. The objective of this study was to evaluate the effect of Goji administration on memory recognition, as well as the changes in the dendritic morphology of the PFC and Hippocampus pyramidal neurons in old rats. Goji (3 g/kg) was administrated for 60 days in 18-month-old rats. After the treatment, recognition memory was evaluated using the new object recognition task (NORt). The changes in the neuron morphology of the PFC and hippocampus pyramidal neurons in old rats were evaluated by Golgi-cox stain and immunoreactivity for synaptophysin, glial fibrillary acidic protein (GFAP), caspase-3, 3-nitrotyrosine (3-NT) and nuclear factor erythroid 2-related factor 2 (Nrf2). The rats treated with Goji showed a significant increase in dendritic morphology in the PFC and hippocampus neurons, a greater immunoreactivity to synaptophysin and a decrease in reactive astrogliosis and also in caspase-3, in 3-NT and in Nrf2 in these brain regions was also observed. Goji administration promotes the plasticity processes in the PFC and in the hippocampus of old rats, critical structures in the brain aging process.

Background: Laparoscopic gastrectomy has numerous perioperative advantages, but the long-term survival of patients after this procedure has been less studied. Aim: To compare survival, oncologic and perioperative outcomes between completely laparoscopic vs. open gastrectomy for early gastric cancer. Methods: This study was retrospective, and our main outcomes were the overall and disease-specific 5-year survival, lymph node count and R0 resection rate. Our secondary outcome was postoperative morbidity. Results: Were included 116 patients (59% men, age 68 years, comorbidities 73%, BMI 25) who underwent 50 laparoscopic gastrectomies and 66 open gastrectomies. The demographic characteristics, tumour location, type of surgery, extent of lymph node dissection and stage did not significantly differ between groups. The overall complication rate was similar in both groups (40% vs. 28%, p=ns), and complications graded at least Clavien 2 (36% vs. 18%, p=0.03), respiratory (9% vs. 0%, p=0.03) and wound-abdominal wall complications (12% vs. 0%, p=0.009) were significantly lower after laparoscopic gastrectomy. The lymph node count (21 vs. 23 nodes; p=ns) and R0 resection rate (100% vs. 96%; p=ns) did not significantly differ between groups. The 5-year overall survival (84% vs. 87%, p=0.31) and disease-specific survival (93% vs. 98%, p=0.20) did not significantly differ between the laparoscopic and open gastrectomy groups. Conclusion: The results of this study support similar oncologic outcome and long-term survival for patients with early gastric cancer after laparoscopic gastrectomy and open gastrectomy. In addition, the laparoscopic approach is associated with less severe morbidity and a lower occurrence of respiratory and wound-abdominal wall complications.

Conventional serum tumor markers (CSTM) are widely used for monitoring patients with cancer. However, their usefulness as a diagnostic tool is controversial in primary or metastatic liver cancer (PMLC).To evaluate the diagnostic performance of the most commonly requested CSTM in the diagnostic approach of PMLC.Review of medical records of patients aged over 18 years with a liver biopsy, attended from 2005 to 2017 in a tertiary hospital and a regional cancer center in Colombia. The results of liver biopsies were compared with tumor markers such as carcinoembryonic antigen (CEA), alpha-fetoprotein (AFP), CA 19-9, CA 125 and prostate specific antigen (PSA) using a receiver operating characteristic (ROC) curve analysis.We reviewed 2063 medical records and retrieved 118 eligible patients (59 cases and 59 controls, 70% males). Thirty percent had obstructive jaundice. There was heterogeneity in the amount of tumor markers requested according to medical criteria. Only CA 19-9 showed discriminative capacity (17.6 U/m), with a cut-off point lower than that reported in the literature and a sensitivity of 69.5%, specificity of 91.6%, a positive likelihood ratio (LR) of 8.32, and a negative LR of 0.33.Except for CA 19-9, tumor markers were not useful for the initial diagnostic approach in patients with suspected primary or metastatic malignant liver tumors.

Amyloid-β (Aβ) plays a relevant role in the neurodegenerative process of Alzheimer's disease (AD). The 25-35 peptide of amyloid-β (Aβ25-35) induces the inflammatory response in brain experimental models. Mucin-type O-glycosylation has been associated with inflammation of brain tissues in AD, thus in this work, we aimed at identifying changes in the glycosylation profile generated by the injection of Aβ25-35 into the CA1 of the hippocampus of rats, using histochemistry with lectins. Our results indicate that 100μM Aβ25-35 induce increased recognition of the Amaranthus leucocarpus lectin (ALL) (specific for Galβ1,3-GalNAcα1,0-Ser/Thr); whereas concanavalin A (Con A) (specific for α-Man) showed no differences among treated and control groups of rats. Jacalin and peanut agglutinin (Galβ1,3GalNAcα1,0-Ser/Thr) showed no recognition of brain cells of control or treated rats. After 6-h treatment of the tissue with trypsin or with 200mM GalNAc, the interaction with ALL was inhibited. Immunohistochemistry showed positive anti-NeuN and ALL-recognition of neurons; however, anti-GFAP and anti-CD11b showed no co-localization with ALL. The ALL+ neurons revealed the presence of cytochrome C in the cytosol and active caspase 3 in the cytosol and nucleus. Administration of the interleukin-1 receptor antagonist (IL-1RA) to Aβ25-35-treated rats diminished neuroinflammation and ALL recognition. These results suggest a close relationship among over-expression of mucin-type O-glycosylation, the neuroinflammatory process, and neuronal death.

Apomorphine is a dopamine receptor agonist that activates D1-D5 dopamine receptors and that is used to treat Parkinson's disease (PD). However, the effect of apomorphine on non-motor activity has been poorly studied, and likewise, the effects of dopaminergic activation in brain areas that do not fulfill motor functions are unclear. The aim of this study was to determine how dopamine receptor activation affects behavior, as well as plasticity, morphology, and oxidative stress in the hippocampus. Adult mice were chronically administered apomorphine (1 mg/kg for 15 days), and the effects on memory and learning, synaptic plasticity, dendritic length, inflammatory responses, and oxidative stress were evaluated. Apomorphine impaired learning and long-term memory in mice, as evaluated in the Morris water maze test. In addition, electrophysiological recording of field excitatory postsynaptic potentials (fEPSP) indicated that the long-term potentiation (LTP) of synaptic transmission in the CA1 region of the hippocampus was fully impaired by apomorphine. In addition, a Sholl analysis of Golgi-Cox stained neurons showed that apomorphine reduced the total length of dendrites in the CA1 region of the hippocampus. Finally, there were more reactive astrocytes and oxidative stress biomarkers in mice administered apomorphine, as measured by GFAP immunohistochemistry and markers of redox balance, respectively. Hence, the non-selective activation of dopaminergic receptors in the hippocampus by apomorphine triggers deficiencies in learning and memory, it prevents LTP, reduces dendritic length, and provokes neuronal damage.

CASE A 21-year-old woman in her second pregnancy was referred to our Maternal-Fetal Unit for abnormal fetal growth detected during a 23-week routine scan. Her husband was 29 years old and this baby was his first. There was neither consanguinity nor any family history of congenital anomalies. Fetal detailed ultrasound findings (Accuvix V10, Medison, Seoul, Korea) were cranial suture diastasis (Figure 1a), nasal bone hypoplasia (Figure 1b), cranial bones and clavicles hypomineralization (Figures 1b and c), maxillary hypoplasia (Figure 1d), cerebellar vermis hypoplasia (Figure 2a) and low-set ears (Figure 2b). With this prenatal information the first diagnosis proposal was cleidocranial dysplasia. Karyotype analysis was suggested but impossible to realize due to administrative red tape. In prenatal ultrasound follow-up an intrauterine growth restriction was identified. At 32 weeks new central nervous system findings were detected: hypoechoic frontal cortex images suggestive of bilateral porencephalic cysts (Figure 2c) and first cervical vertebra dysraphism with dura mater bulging (Figure 2d). At 35 weeks intrauterine growth restriction and Doppler evaluation defined cesarean section. A male baby of 1410 g and 44 cm height was born. Apgar score was 8 at 1min and 9 at 5min. Minor respiratory distress was solved with cephalic oxygen chamber. Anthropometric measurements were cephalic perimeter 29 cm (Po5), 44 cm height (P 10 to 25), inner canthal distance 1.6 cm (P 3), interpupillary distance 3 cm (Po3), outer canthal distance 4.6 cm (P 3 to 50), palpebral fissures 1.2 cm (Po3), labial intercommissure 1.8 cm (Po3), total ear length 2.4 cm (Po3), total hand length 6 cm (P 50 to 97) and middle finger length 2.5 cm (P 50 to 97); lower segment length 19.6 cm, upper segment length 24.4 cm and upper/lower segments ratio 1.24 (normal range 1.65 to 1.70); feet length 7 cm (P 50 to 75) and penis length 1.6 cm (Po3). Physical examination showed pseudohydrocephalus, hypotricosis, scalp collateral venous system visible, triangular face (Figure 3a), widened fontanelles, biparietal prominence, low-set ears, upper oblique palpebral fissure, depressed nasal bridge with beaked nose profile (Figure 3b). Labial commissures had a downward orientation; two central natal teeth were visible, micrognathia and thin neck were evident. The cardiac evaluation demonstrated a systolic murmur grade II/IV. External genitalia agreed with male condition except for bilateral criptorquidia. Limbs presented general hypotrophy and with imitated articular movements (Figure 3c). Hands and feet were longer than normal (Figure 3d and e). Reduced subcutaneous fat was evident. Neurological examination reported general hypertonic condition and poor suction. Echocardiogram showed persistent ductus arteriosus 2.4 mm with mild pulmonary hypertension, without cardiac structural anomalies. Transfontanellar scan demonstrated hypoechoic collection associated with bilateral frontal porencephalic cysts and a wider cisterna magna and a dysraphism of the first cervical vertebra with dura mater bulging. Axial computerized tomography reported hypodense lines suggestive of bilateral frontal porencephalic cysts. All these findings permite to conclude that this case correspond to the Wiedemann–Rautenstrauch syndrome (WRS; online mendelian inheritance in man: 264090) or neonatal progeroid syndrome. Neonatal respiratory distress was successfully resolved after 24 h. Indirect hiperbilirrubinemia was treated with phototherapy. The baby was discharged once adecuate suction level was reached 40 days after birth weighing 1925 g. At 3 weeks buttocks upper fat was evident.

Metabolic syndrome (MS) is a serious public health problem, which can promote neuronal alterations in cognitive regions related to learning and memory processes, such as the hippocampus. However, up to now there has been information of a regional segregation of this damage. In this study, we evaluate the MS effect on the neuronal morphology of the hippocampus. Our results demonstrate that 90days of a high-calorie diet alters the metabolic energy markers causing the MS and causes memory impairments, evaluated by the recognition of novel objects test (NORT). In addition, MS animals showed significant differences in dendritic order, total dendritic length and density of dendritic spines in CA1, CA3 and the dentate gyrus (DG) of the hippocampal area, compared with rats fed with a normocaloric diet (vehicle group). Furthermore, the immunoreactivity to synaptophysin (Syp) decreased in the hippocampus of the MS animals compared to the vehicle group. These results indicate that metabolic alterations induced by the MS affect hippocampal plasticity and hippocampal dependent memory processes.

Gastrectomy represents the main treatment for gastric adenocarcinoma. This procedure is associated with substantial morbidity and mortality. The aim of this study was to evaluate the postoperative mortality changes across the study period and to identify predictive factors of 30-day mortality after elective gastrectomy for gastric cancer.This was a retrospective cohort study of a prospective database from a single centre. Patients treated with an elective gastrectomy from 1996 to 2014 for gastric adenocarcinoma were included. We compared postoperative mortality between four time periods: 1996-2000, 2001-2005, 2006-2010, and 2011-2014. Univariate and multivariate analyses were applied to identify predictors of 30-day postoperative mortality.We included 1066 patients (median age 65 years; 67% male). The 30-day mortality rate was 4.7%. Mortality decreased across the four time periods; from 6.5% to 1.8% (P = 0.022). In the univariate analysis, age, ASA score, albumin3.5, multivisceral resection, splenectomy, intrathoracic esophagojejunal anastomosis, R status, and T status were significantly associated with postoperative mortality. In the multivariate analysis, ASA class 3 (OR 10.06; CI 1.97-51.3; P = 0.005) and multivisceral resection (OR 1.6; CI 1.09-2.36; P = 0.016) were associated with higher postoperative 30-day mortality; surgery between 2011 and 2014 was associated with lower postoperative 30-day mortality (OR 0.55; CI 0.33-0.15; P = 0.030).There was a decrease in postoperative 30-day mortality during this 18-year period at our institution. We have identified ASA score and multivisceral resection as predictors of 30-day mortality for elective gastrectomy for cancer.

Introduction Worldwide, burns are responsible for more than 300,000 deaths annually; infection is a major cause of morbidity and mortality in these patients. Early identification and treatment of infection improves outcome. Toward this end it's necessary to identify the institutions flora and organisms that most frequently produces infection. Objectives To characterize infections developed by burn patients hospitalized at the University Hospital of Santander (HUS). Methodology Burn patients hospitalized in the HUS from January 1 to December 2014 were followed. Medical information regarding infections, laboratory and pathology reports were obtained. Statistical analysis with measures of central tendency, proportions, global and specific incidence density plus overall and specific incidence was obtained. For the microbiological profile proportions were established. Results 402 burn patients were included, 234 (58.2%) men and 168 (41.8%) women, aged between 6 days and 83 years, median 12.5 years. The burn agents include scald (52.5%), fire (10.0%), gasoline (9.2%), electricity (7.5%), among others. Burn area ranged from 1% to 80% TBS. Cumulative mortality was 1.5%. 27.8% of burned patients had one or more infections. Identified infections include folliculitis (27.0%), urinary tract infection (19.0%), infection of the burn wound (10.4%), pneumonia (8.6%), Central venous catheter (7.4%), bloodstream infection (7.4%) and skin grafts infection (4.3%) among others. Bacteria were responsible for 88.5% of the cases and fungi 11.5%. The most frequently isolated germs were P. aeruginosa, A. baumannii, E. coli, S. aureus and K. pneumoniae. Most gram-negative bacteria were sensitive to Amikacin, gram positive bacteria were sensitive to multiple antibiotics. Conclusion Burns is a severe trauma that occurs in adult and pediatric patients, has several causative agents and can compromise the patient's life. The burned patient is at risk for a variety of infections. According to the type of infection it is possible to infer the most common causative organisms and their antibiotic sensitivity/resistance which allow a directed early empiric treatment.

Energy drinks (EDs) are often consumed in combination with alcohol because they reduce the depressant effects of alcohol. However, different researches suggest that chronic use of these psychoactive substances in combination with alcohol can trigger an oxidative and inflammatory response. These processes are regulated by both a reactive astrogliosis and an increase of proinflammatory cytokines such as IL-1β, TNF-α, and iNOS, causing cell death (apoptosis) at the central and peripheral nervous systems. Currently, mechanisms of toxicity caused by mixing alcohol and ED in the brain are not well known. In this study, we evaluated the effect of chronic alcohol consumption in combination with ED on inflammatory response and oxidative stress in the temporal cortex (TCx) and hippocampus (Hp) of adult rats (90 days old). Our results demonstrated that consuming a mixture of alcohol and ED for 60 days induced an increase in reactive gliosis, IL-1β, TNF-α, iNOS, reactive oxygen species, lipid peroxidation, and nitric oxide, in the TCx and Hp. We also found immunoreactivity to caspase-3 and a decrease of synaptophysin in the same brain regions. The results suggested that chronic consumption of alcohol in combination with ED causes an inflammatory response and oxidative stress, which induced cell death via apoptosis in the TCx and Hp of the adult rats.

Amyloid-β (Aβ)25-35 is able to cause memory impairment and neurodegenerative events. Recent evidence has shown that the injection of Aβ25-35 into the temporal cortex (TCx) of rats increases the inflammatory response; however, it is unclear how the inflammatory process could be involved in the progression of Aβ25-35 toxicity. In this study we investigated the role of inflammation in the neuronal damage and spatial memory impairment generated by Aβ25-35 in rat TCx using immunohistochemistry, ELISA, and a behavioral test in the radial maze. Our findings show that Aβ25-35 -injection into the TCx induced a reactive gliosis (GFAP and CD11b-reactivity) and an increase of pro-inflammatory cytokines (IL-1β, IL-6, IL-17, and TNF-α) in the TCx and the hippocampus at 5, 15, and 30 days after injection. Thirty days after Aβ25-35 injection, we observed that the inflammatory reaction probably contributed to increase the immunoreactivity of inducible nitric oxide synthase and nitrite levels, as well as to the loss of neurons in TCx and hippocampus. Behavioral performance showed that the neurodegeneration evoked by Aβ25-35 delayed acquisition of learning and impaired spatial memory, because the Aβ25-35-treated animals showed a greater number of errors during the task than the control group. Previous administration of an interleukin receptor antagonist (IL-1ra) (10 and 20 μg/μL, into TCx), an anti-inflammatory agent, suppressed the Aβ25-35-induced inflammatory response and neurodegeneration, as well as memory dysfunction. This study suggests that the chronic inflammatory reaction could contribute to the progression of Aβ25-35 toxicity and cause cognitive impairment.

Alzheimer's disease (AD) is a neurodegenerative disorder caused by the aggregation of the amyloid-beta peptide (Aβ) in senile plaques and cerebral vasculature. The Aβ

Sialic acid in glycoconjugates participates in important cellular functions associated with normal development, growth, and communication. Therefore we evaluated the sialylation pattern and memory deficits caused by the injection of Aβ((25-35)) into the hippocampus (Hp) of rats. The eight-arm maze spatial-learning and memory test indicated that the injection of Aβ((25-35)) into subfield CA1 of the Hp impaired both learning and memory. The sialylation pattern was examined using sialic acid-specific lectins. Our results showed that Maackia amurensis agglutinin (MAA, specific for Neu5Acα2,3Gal) showed reactivity in the CA1 and dentate gyrus (DG) subfields of the Hp mainly in the group injected with vehicle, whereas Macrobrachium rosenbergii lectin (MRL, specific for Neu5,9,7Ac) and Sambucus nigra agglutinin (SNA, specific for Neu5Acα2,6Gal-GalNAc) had increased reactivity in the CA1 and DG subfields of the Hp in the Aβ((25-35))-injected group. The staining pattern of the antibody specific for polysialic acid (a linear homopolymer of α-2,8-linked sialic acid) increased in the CA1 and DG subfields of the Hp of the Aβ((25-35)) group compared to the control group. Our results suggest that injection of Aβ((25-35)) causes impairment in spatial memory and alters the sialylation pattern in response to compensatory reorganization and-or sprouting of dendrites and axons of the surviving neurons.

The Aβ(25-35) fraction mimics the toxic effects of the complete peptide Aβ(1-42) because this decapeptide is able to cause memory impairment and neurodegenerative events. Recent evidence has shown that the injection of Aβ(25-35) into the temporal cortex (TCx) of the rat increases the nitric oxide (NO) pathways with several consequences, such as neuronal loss in rats. Our aim was to investigate the effects of each NOS isoform by the prior injection of NOS inhibitors before the injection of the Aβ(25-35). One month after the treatment, the animals were tested for their spatial memory in the radial maze. The hippocampus (Hp) and TCx were assessed for NO production, nitration of proteins (3-NT), astrocytosis (GFAP), and neuronal loss. Our findings show a significant impairment in the memory caused by Aβ25-35 injection. In contrast NOS inhibitors plus Aβ25-35 cause a protection yielding a high performance in the memory test and reduction of cell damage in the TCx and the Hp. Particularly, iNOS is the major source of NO and related to the inflammatory response leading to the memory deficits. The inhibition of iNOS is an important target for neuronal protection against the toxicity of the Aβ25-35 over the long term.

Aging is a stage of life where cognitive and motor functions are impaired. This is because oxidative and inflammatory processes exacerbate neurodegeneration, which affects dendritic morphology and neuronal communication of limbic regions with memory loss. Recently, the use of trophic substances has been proposed to prevent neuronal deterioration. The neuropeptide-12 (N-PEP-12) has been evaluated in elderly patients with dementia, showing improvements in cognitive tasks due to acts as a neurotrophic factor. In the present work, we evaluated the effect of N-PEP-12 on motor activity and recognition memory, as well as its effects on dendritic morphology and the immunoreactivity of GFAP, Synaptophysin (SYP), and BDNF in neurons of the prefrontal cortex (PFC), dorsal hippocampus (DH) and nucleus accumbens (NAcc) of aged rats. The results show that N-PEP-12 improved the recognition memory, but the motor activity was not modified compared to the control animals. N-PEP-12 increases the density of dendritic spines and the total dendritic length in neurons of the PFC (layers 3 and 5) and in DH (CA1 and CA3). Interestingly NAcc neurons showed a reduction in the number of dendritic spines. In the N-PEP-12 animals, when evaluating the immunoreactivity for SYP and BDNF, there was an increase in the three brain regions, while the mark for GFAP decreased significantly. Our results suggest that N-PEP-12 promotes neuronal plasticity in the limbic system of aged animals, which contributes to improving recognition memory. In this sense, N-PEP-12 can be considered as a pharmacological alternative to prevent or delay brain aging and control senile dementias.

Amyloid-beta is involved in neurodegeneration in Alzheimer's disease. The Amyloid-beta fraction 25-35 (Amyloid-beta 25-35) is believed to cause neurotoxicity through oxidative stress. We evaluated the antioxidant effects of Epicatechin on the Abeta25-35-caused hippocampal toxicity in vivo. Biochemical and histological evaluations, and learning and memory tasks, were assessed. Amyloid-beta 25-35 (100 microM/microL) or vehicle was injected into the CA1 hippocampal region of the rat 5 h after a single oral dose of Epicatechin (30 mg/kg). Lipid peroxidation and reactive oxygen species formation were measured in Amyloid-beta- and Amyloid-beta-Epicatechin-treated groups at 2 h and 24 h after dosing and formation of the lesion. There was an increase in lipid peroxidation and reactive oxygen species formation at 2-h and 24-h postlesion. Learning and memory tests were made 27-30 days after surgery in independent groups under the same experimental conditions. Immunohistochemical detection of glial-fibrilar acidic protein (GFAP) was evaluated in hippocampal tissues from the animals 30-days postsurgery. Amyloid-beta 25-35 caused a significant increase in lipid peroxidation and reactive oxygen species and a decrease in memory skills. In addition, hippocampal tissues from Amyloid-beta 25-35-treated animals showed an increased immunoreactivity against GFAP. In contrast, animals pretreated with Epicatechin had a significant decrease in lipid peroxidation and reactive oxygen species and an improvement in memory skills. GFAP immunoreactivity was also decreased. Our results showed that Amyloid-beta 25-35-caused oxidative damage of the hippocampus was blocked by the administration of Epicatechin.

The chemical alpha-asarone is an important active substance of the Acori graminei rhizome (AGR). It has pharmacological effects that include antihyperlipidemic, antiinflammatory, and antioxidant activity. Our aim was to study the effects alpha-asarone on nitric oxide (NO) levels in the hippocampus and temporal cortex of the rat after injection of the fraction 25-35 from amyloid-beta (Abeta((25-35))). In addition we examined the working spatial memory in an eight-arm radial maze. Our results showed a significant increase of nitrites in the hippocampus and temporal cortex of Abeta((25-35))-treated rats. Other evidence of neuronal damage was the expression of a glial-fibrillar-acid protein and a silver staining. There were impairments in the spatial memory evaluated in the eight-arm radial maze. We wanted to determine whether alpha-asarone improves the memory correlated with NO overproduction and neuronal damage caused by the injection of Abeta((25-35)) into rats. Then animals received a 16-day treatment of alpha-asarone before the Abeta((25-35)) injection. Our results show a significant decrease of nitrite levels in the hippocampus and temporal cortex, without astrocytosis and silver-staining cells, which correlates with memory improvement in the alpha-asarone-treated group. Our results suggest that alpha-asarone may protect neurons against Abeta((25-35))-caused neurotoxicity by inhibiting the effects of NO overproduction in the hippocampus and temporal cortex.

This study aimed to establish the prevalence of daily cigarette smoking (DCS) and its gender correlated factors in high-school attending adolescents from Bucaramanga, Colombia. A random cluster sample was surveyed (N = 2291). The previous month DCS prevalence was 11.6% (95% CI 9.7-13.5) in boys and 4.4% (95% CI 3.3-5.5) in girls. In girls, DCS was associated with previous month illegal substance use (OR 8.13, 95%CI 3.52-18.87), abusive alcohol consumption (OR 5.88, 95% CI 2.54-13.70), being the best friend of a smoker (OR 3.25, 95% CI 1.38-7.63), and poor or mediocre academic achievement (OR 2.46, 95% CI 1.25-4.85). In boys, DCS was related to previous month substance use (OR 6.23, 95% CI 3.62-10.71), being the best friend of a smoker (OR 5.87, 95% CI 2.93-11.76), poor or mediocre academic achievement (OR 2.09, 95% CI 1.34-3.24), and being older than non-smokers (OR 1.48, 95% CI 1.21-1.81). DCS presents associated factors very similar for girls and boys. Thus, more research is needed.

Anticholinergic drugs reduce the efficacy of acetylcholinesterase inhibitors (AChEI) and are inappropriate in elderly patients. The aim of this study is to determine the prevalence rate of prescription AChEI drugs and anticholinergics in a Healthcare Area, to identify the affected patients, and to inform the attending physicians, in order to evaluate the suitability of treatments.A descriptive cross-sectional observational study of prevalence. Patients on treatment with AChEI and any anticholinergic drug in the first quarter of 2015 were selected. The review of Duran et al. was used as reference to identify anticholinergics, assigning a score to each drug according to its anticholinergic potency. Physicians were provided with a report about the interaction, the list of affected patients, and recommendations.A total of 486 patients were included in the study, representing 59.0% of total patients with Alzheimer's disease in the Area. There were 66.0% women, and 86.8% of the patients were older than 75 years, and with a mean of 9.2 drugs per patient. The mean number of anticholinergic drugs was 1.6, and 38.3% of patients were prescribed various anticholinergic drugs, with 23.9% on high potency anticholinergic drugs. A statistically significant association was found between taking an anticholinergic and AChEI concomitantly (P=.000; OR: 3.9).The prevalence of interactions between AChEI and anticholinergic drugs is relevant, considering that it affects vulnerable members of the population. Providing physicians with information about the interaction could help them make clinical decisions, and could improve patient safety, as well as health outcomes.

Resveratrol may induce its neuroprotective effects by reducing oxidative damage and chronic inflammation apart from improving vascular function and activating longevity genes, it also has the ability to promote the activity of neurotrophic factors. Morphological changes in dendrites of the pyramidal neurons of the prefrontal cortex (PFC) and hippocampus have been reported in the brain of aging humans, or in humans with neurodegenerative diseases such as Alzheimer's disease. These changes are reflected particularly in the decrement of both the dendritic tree and spine density. Here we evaluated the effect of resveratrol on the dendrites of pyramidal neurons of the PFC (Layers 3 and 5), CA1- and CA3-dorsal hippocampus (DH) as well as CA1-ventral hippocampus, dentate gyrus (DG), and medium spiny neurons of the nucleus accumbens of aged rats. 18-month-old rats were administered resveratrol (20 mg/kg, orally) daily for 60 days. Dendritic morphology was studied by the Golgi-Cox stain procedure, followed by Sholl analysis on 20-month-old rats. In all resveratrol-treated rats, a significant increase in dendritic length and spine density in pyramidal neurons of the PFC, CA1, and CA3 of DH was observed. Interestingly, the enhancement in dendritic length was close to the soma in pyramidal neurons of the PFC, whereas in neurons of the DH and DG, the increase in dendritic length was further from the soma. Our results suggest that resveratrol induces modifications of dendritic morphology in the PFC, DH, and DG. These changes may explain the therapeutic effect of resveratrol in aging and in Alzheimer's disease.

The benefits of adjuvant treatment in the context of a D2 lymph node dissection are controversial. The aim was to investigate the effects of postoperative adjuvant treatment on the survival of patients with a curative resection for gastric cancer and a D2 lymph node dissection.We performed a retrospective cohort study. Patients operated from 1996 to 2013 were selected. We compared long term survival of patients treated with surgery alone and those with surgery plus postoperative adjuvant treatment. A multivariate analysis for survival was applied in every stage.The study included 580 patients. Two-hundred and four patients received postoperative adjuvant treatment (AD) and 376 patients were treated only with surgery (SU). Patients in the AD group were younger (60 versus 68, p 0.001), had a lower rate of multiple organ resection (21% versus 39%, p 0.001) and had less postoperative complications (14% versus 32%, p 0.001). In the AD group, patients had more advanced disease (stage III; 77% versus 66%, p 0.001). No difference was found in lymph nodes resected (31 versus 30, p = ns). The median survival with adjuvant treatment was 33 months (39% 5 year survival) and 22 months (31% 5 year survival) for patients without adjuvant treatment (p = 0.003). On multivariate analysis, patients with stage IIIB and IIIC had significantly better overall and disease specific long-term survival with adjuvant treatment.These results suggest that there is a long-term survival benefit for patients treated with postoperative adjuvant treatment for stages IIIB and IIIC gastric cancer after D2 lymph node dissection.

Human immunodeficiency virus (HIV) infection was the second most common cause of death, after injuries of external causes, among young adults from Bucaramanga in 2013.To establish the extent of knowledge on HIV mechanisms of transmission prevention strategies among schoolchildren in the age range of 13 to 20 years old from poor districts of Bucaramanga.Cross-sectional study among randomly selected schoolchildren using a self-administered anonymous survey. For analysis, each outcome measure and binomial models for the association of answers by age, gender, education level and past sexual experience were described.A survey was administered to 729 students (57% were girls); 50.6% of boys and 31.1% of girls reported having had sexual intercourse. Also, 58.6% stated that a healthy-looking person can have HIV. Besides, 69.1% indicated that HIV can be transmitted during pregnancy; 39.2%, during delivery; 37.7%, through breastfeeding; 79.7%, through needle sharing; 29.5%, by sharing food with someone who has HIV; and 31.7%, by mosquito bites. In addition, 70.6% considered that they could prevent HIV by abstaining from having sexual relationships; 67.5%, by having a single partner; and 80.0%, by wearing condoms correctly. The proportion of adequate answers was not related to a higher education level, age, gender or sexual experience.The quality of knowledge regarding HIV mechanisms of transmission and prevention is very poor, in spite of curricular contents providing sex education. It was observed that knowledge was not greater among those with higher education levels.La infección por el virus de la inmunodeficiencia humana (VIH) fue la segunda causa de mortalidad en adultos jóvenes residentes en Bucaramanga en 2013, después de las lesiones de causa externa.Establecer el grado de conocimiento sobre mecanismos de transmisión y estrategias de prevención del VIH en estudiantes de 13 a 20 anos de colegios de las comunas pobres de Bucaramanga.Establecer el grado de conocimiento sobre mecanismos de transmisión y estrategias de prevención del VIH en estudiantes de 13 a 20 anos de colegios de las comunas pobres de Bucaramanga.Se encuestaron 729 estudiantes (57% mujeres); el 50,6% de los varones afirmaron haber tenido relaciones sexuales, así como el 31,1% de las mujeres. El 58,6% aseguraron que una persona que se veía saludable podía estar infectada. El 69,1% respondieron que podía transmitirse durante el embarazo; el 39,2%, durante el parto; el 37,7%, con la lactancia; el 79,7%, por medio de jeringas usadas por otros; el 29,5%, por compartir alimentos con personas infectadas; y el 31,7%, por mosquitos. El 70,6% consideraron que podía prevenir el VIH evitando relaciones sexuales; el 67,5%, si eran monógamos; y el 80,0%, usando correctamente condón. La proporción de respuestas adecuadas no estuvo relacionada con mayor nivel académico, edad, género o experiencia sexual.La calidad del conocimiento sobre mecanismos de transmisión y prevención de la infección por VIH es muy deficiente, a pesar del currículo de educación sexual. El conocimiento no fue mejor en los grados académicos más altos.

When comparing current smoking in schizophrenia patients versus the general population, the average odds ratio (OR) was 5.3 in a meta-analysis of 42 studies from 20 nations. Limited tobacco access can eliminate this strong association in some nations. Out of the 42 ORs, 37 were significantly higher than 1. Of the 5 non-significant ORs, three came from Colombian studies comparing current smoking prevalences in schizophrenia versus those in the general population (18%). However, the 3 ORs were not adjusted for confounders. We hypothesized that the association between schizophrenia and smoking is so strong that it can be detected in populations with limited access to smoking after carefully controlling for confounders. Of the three Colombian studies, one included 73 schizophrenia patients (DSM-IV schizophrenia or schizoaffective disorder) and 111 patients with mood disorders (DSM-IV bipolar or major depressive disorders). The current study matched each of these patients with 2 controls from the general population and performed more sophisticated statistical analyses. Prevalences of current smoking were 26% for schizophrenia patients and 10% for their matched controls (adjusted Mantel-Haenszel OR=3.1, 95% CI, 1.4-6.8), and 7% for patients with mood disorders and 12% for their matched controls (adjusted Mantel-Haenszel OR=0.62; CI, 0.28-1.4). The previously observed lack of association between schizophrenia and current smoking was due to lack of control of important confounding variables because of the absence of a control group. This re-analysis, which used a careful matching that controlled for confounders, suggests that the association between schizophrenia and smoking behaviors can stand in populations with low monetary income and low smoking rates. This study also suggests that the association between severe mood disorders (bipolar and major depression) and smoking is not as strong as that observed between schizophrenia and smoking, and may not be observable in countries where people have limited economic resources.

Curcuma is a natural compound that has shown neuroprotective properties, and has been reported to prevent aging and improve memory. While the mechanism(s) underlying these effects are unclear, they may be related to increases in neural plasticity. Morphological changes have been reported in neuronal dendrites in the limbic system in animals and elderly humans with cognitive impairment. In this regard, there is a need to use alternative therapies that delay the onset of morphologies and behavioral characteristics of aging. Therefore, the objective of this study was to evaluate the effect of curcuma on cognitive processes and dendritic morphology of neurons in the prefrontal cortex (PFC), the CA1 and CA3 regions of the dorsal hippocampus, the dentate gyrus, and the basolateral amygdala (BLA) of aged rats. 18-month-old rats were administered curcuma (100 mg/kg) daily for 60 days. After treatment, recognition memory was assessed using the novel object recognition test. Curcuma-treated rats showed a significant increase in the exploration quotient. Dendritic morphology was assessed by Golgi-Cox staining and followed by Sholl analysis. Curcuma-treated rats showed a significant increase in dendritic spine density and dendritic length in pyramidal neurons of the PFC, the CA1 and CA3, and the BLA. The preservation of dendritic morphology was positively correlated with cognitive improvements. Our results suggest that curcuma induces modification of dendritic morphology in the aforementioned regions. These changes may explain how curcuma slows the aging process that has already begun in these animals, preventing deterioration in neuronal morphology of the limbic system and recognition memory.

The laparoscopic approach for the treatment of gastric tumors has many advantages.To evaluate the results of a laparoscopic gastrectomy program developed in a public hospital.Retrospective review of epidemiological, perioperative and follow-up data of patients who were treated with a laparoscopic gastrectomy due to gastric tumors between 2006 and 2013. A totally laparoscopic technique was used for all cases. Complications were evaluated according to the Clavien-Dindo classification.Fifty one patients, aged 65 (36-85) years, underwent a laparoscopic gastrectomy. In 22 patients a total gastrectomy was performed. Conversion rate to open surgery was 8%. Operative time was 330 (90-500) min and bleeding was 200 (20-500) ml. Median hospital stay was 7 (3-37) days. Postoperative morbidity was present in 17 (33%) patients, 3 (6%) patients had complications grade 3 or higher and one patient died (1.9%). Tumor pathology was adenocarcinoma in 39 patients. A complete resection was achieved in 97%. Twenty nine patients (74%) with gastric adenocarcinoma had early gastric cancer and 84% of patients were in stage one. Median lymph node count was 24. Median follow-up was 26 (1-91) months. There was no cancer related mortality among patients subjected to a curative resection. Overall survival for patients with adenocarcinoma was 92% at 3 years.This study supports the feasibility and safety of a laparoscopic gastrectomy program in a public hospital; with low morbidity, adequate lymph node dissection and long-term survival. This approach must be considered an option for selected patients with gastric cancer.

Alzheimer disease (AD) is a neurodegenerative disorder caused by accumulation of the amyloid-beta peptide (Aβ) in neuritic plaques. Its neurotoxic mechanisms are associated with inflammatory responses and nitrosative stress generation that promote expression of inducible nitric oxide synthase (iNOS) and increased nitric oxide causing neuronal death and memory impairment. Studies suggest that treatment with anti-inflammatory and anti-oxidant agents decreases the risk of developing AD. Aminoguanidine (AG) is an iNOS inhibitor with anti-inflammatory and anti-oxidant effects. In this study, we evaluated the effects of systemic administration of AG (100 mg/kg/day for 4 days) on spatial memory and inflammatory responses induced by an injection of Aβ(25-35) [100 μM] into the temporal cortex (TCx) of rats. A significant improvement of spatial memory was evident in the Aβ(25-35)-treated group at day 30 post-injection subjected to AG treatment; this effect was correlated with decreases in reactive gliosis, IL-1β, TNF-α, and nitrite levels, as well as a reduction in neurodegeneration in the TCx and hippocampus (Hp). These results suggest that AG treatment inhibited glia activation and cytokine release, which may help to counteract neurodegenerative events induced by the toxicity of Aβ.

Continuous positive airway pressure (CPAP) is useful in low birth weight infants with respiratory distress, but it is not known if it is a better alternative to mechanical ventilation after early pulmonary surfactant administration.To compare the incidence of adverse events in 28 to 32-week newborns with respiratory distress managed with mechanical ventilation or CPAP after early surfactant administration.In total, 176 newborns were treated with CPAP and 147 with mechanical ventilation, all with Apgar scores3 at five minutes and without apnea.The incidence of CPAP failure was 6.5% (95% CI: 11.3-22.8%); 29 patients died: 7 with CPAP (4.0%) and 22 with mechanical ventilation (15.0%, p0.001). The relative risk of dying with CPAP versus mechanical ventilation was 0.27 (95% CI: 0.12-0.61), but after adjusting for confounding factors, CPAP use did not imply a higher risk of dying (RR=0.60; 95% CI: 0.29-1.24). Mechanical ventilation fatality rate was 5.70 (95% CI: 3.75-8.66) deaths/1,000 days-patient, while with CPAP it was 1.37 (95% CI: 0.65-2.88, p0.001). Chronic lung disease incidence was lower with CPAP than with mechanical ventilation (RR=0.71; 95% CI: 0.54-0.96), as were intracranial hemorrhage (RR=0.28, 95% CI: 0.09-0.84) and sepsis (RR=0.67; 95%CI: 0.52-0.86), and it was similar for air leaks (RR=2.51; 95% CI: 0.83-7.61) and necrotizing enterocolitis (RR=1.68, 95% CI: 0.59-4.81).CPAP exposure of premature infants with respiratory distress syndrome is protective against chronic lung disease, intraventricular hemorrhage and sepsis compared to mechanical ventilation. No differences were observed regarding air leak syndrome or death.

Gastric lipoma is a rare benign gastric tumor. We report a 62-year-old man, who presented with abdominal pain, vomiting and weight loss. An upper gastrointestinal endoscopy showed a gastric antral, submucosal tumor. Abdominal ultrasound and computed tomography revealed a large antral lesion with content of high echogenicity and fat density, measuring 11 x 6 cm. The patient was treated with a laparoscopic distal subtotal gastrectomy, and a Roux-en-Y reconstruction. The patient had no postoperative morbidity, was started on a liquid diet on the third postoperative day and was discharged on the third postoperative day. The pathological study revealed a gastric lipoma with clear margins. This laparoscopic procedure represents a good alternative in the treatment of this benign gastric tumor.

Alzheimer's disease (AD) is a neurodegenerative disorder caused by the deposition of the amyloid-beta peptide (Aβ) in senile plaques and cerebral vasculature. Its neurotoxic mechanisms are associated with the generation of oxidative stress and reactive astrogliosis that cause neuronal death and memory impairment. Estrogens reduce the rate of Azheimer's disease because of their antioxidant activity. Prolame (N-(3-hydroxy-1,3,5(10)-estratrien-17β-yl)-3-hydroxypropylamine) is an aminoestrogen with estrogenic and antithrombotic effects. In our study we evaluated the role of prolame on Aβ(25-35)-caused oxidative stress, reactive astrogliosis, and impairment of spatial memory(.) The Aβ(25-35) (100 μM/μl) or vehicle was injected into the CA1 subfield of the hippocampus of the rat. The subcutaneous injection of prolame (400 μl, 50 nM) or sesame oil (400 μl) started 1 day before the Aβ(25-35) injection and was continued for another 29 days. The results showed a significant impairment of spatial memory evident 30 days after the Aβ(25-35) injection. The prolame treatment significantly reduced spatial-memory impairment and decreased lipid peroxidation, reactive oxygen species, and reactive gliosis. It also restored the eNOS and nNOS expression to normal levels. In conclusion the aminoestrogen prolame should be considered as an alternative in the treatment of Alzheimer's disease.

The diagnosis and treatment of periampullary tumors represents a challenge for current medicine.To review the results of pancreaticoduodenectomy (PDD) in the treatment of periampullary tumors and to identify risk factors that impact the long-term survival.We performed a retrospective study of patients who underwent a PDD for periampullary tumors between 1993 and 2009. We reviewed perioperative results and long term survival. We performed a multivariate analysis for long-term survival.A PDD was performed in 181 patients aged 58 ± 12 years (98 females). Pyloric preservation was done in 53% and a pancreatogastric anastomosis was used in 94% of cases. Morbidity was 62% and postoperative mortality was 5.5%. Pancreatic cancer was the most frequent pathological finding in 41%, followed by ampullary cancer in 28% and distal bile duct cancer in 16%. Median survival was 17 months, with a five years survival of 24%. Survival for ampullary tumors was 28 months with a five years survival of 32%. The median and five years survival were 14 months and 16% for bile duct cancer and 11 months and 14% for pancreatic cancer. Multivariate analysis identified tumor type (pancreas /bile duct) and lymph node dissemination as independent predictors of mortality.One quarter of patients experienced long term survival. Mortality predictors were tumor type and lymph node dissemination.