Evaluación de la iluminación natural y de las protecciones solares en edificios de oficinas de la ciudad de S. M. de Tucumán

El trabajo muestra los resultados del estudio de la eficiencia de las protecciones solares y del comportamiento lumínico de aventanamientos en edificios de oficinas construidos en San Miguel de Tucumán. Se realizaron simulaciones con programas computacionales en 16 edificios. Así también se llevó a cabo la evaluación de las protecciones solares en 13 edificios, con el objeto de determinar la eficiencia de los mismos y su adecuación climática para localidad en estudio. Los resultados muestran que en la mayor parte de los locales de oficinas no se cumple con los valores mínimos de iluminación natural sobre el plano de trabajo requeridos para la tarea visual y que las protecciones solares no se comportan adecuadamente, produciendo deslumbramiento y un excesivo aporte de calor al ambiente, generando condiciones de inconfort y un incremento en los costos para el acondicionamiento artificial. Es así que el 61% de los edificios relevados no cuentan con protecciones solares en las ventanas y el tratamiento de sus frentes no difiere según sea la orientación de los mismos, con una elevada proporción de superficies vidriadas. Por otra parte, el 75% de los locales no cumplen con los valores de iluminación natural mínimos de normas, en el punto medio del local y el 94% en el punto más desfavorable.The work shows the results of the study of the efficiency of the solar protection and of the light behavior of windows in office buildings of San Miguel of Tucumán. In order to determining the light behavior of the windows, they were carried out simulations with software in 16 buildings. Likewise it was carried out the evaluation of the solar protection in 13 buildings, in order to determining the efficiency of them and their climatic adaptation for the town in study. The results show that in most of the offices it is not fulfilled the minimum values of natural illumination on the working plane, required for the visual tasks, and that the solar protection don't behave appropriately, producing dazzle and an excessive contribution of heat to the interior, generating conditions of lack of comfort and an increment in the energy costs.Asociación Argentina de Energías Renovables y Medio Ambiente (ASADES

Hypoglobulinemia and Nonsecretory Myeloma as a Rare Cause of Osteoporosis in a Young Man

A 27-year-old man was admitted to our hospital with the complaint of back pain. Bone mineral density evaluation revealed severe osteoporosis. The causes for secondary osteoporosis, such as thyrotoxicosis, glucocorticoid therapy, hypercortisolemia, hypercalciuria, and hyperparathyroidism were excluded. Laboratory examination revealed hypoglobulinemia. Further evaluation of the immunoglobulin levels was compatible with panhypoglobulinemia. The patient's vitamin D level was also low. The patient was first suspected of having a common variable immune deficiency, but he had not not experienced frequent infections. By carefully evaluating his chest x ray, a lytic lesion in his left humerus was observed. He did not have anemia and elevated sedimentation rate was not observed. Protein electrophoresis showed hypoglobulinemia. Haematology consultation was requested and a bone marrow aspiration was performed. Bone marrow examination revealed multiple myeloma with a myeloma cell increase of 70 to 80%. The patient was diagnosed as having nonsecretory myeloma which explained his hypoglobulinemia. Myeloma may cause severe osteoporosis, pain and hypercalcemia. A chemotherapy regimen (vincristine, adriablastina, dexamethasone) was initiated and further autologous stem cell transplantation was planned. The patient had also chromosome 13 abnormality. Osteoporosis at a young age especially in young men should always be extensively evaluated

Primary Hyperparathyroidism: A Rare Cause of Spinal Cord Compression: Differential Diagnosis

A 66-year-old woman was admitted to our hospital with difficulty in walking. Magnetic resonance imaging revealed mass lesions at T2- T3 vertebrae causing deviation of the spinal cord. The positron emission tomography (PET) scan of the body showed a hypermetabolic state in the right maxillary sinus and multiple metastatic lesions in the skeletal system indicating a metastatic tumor of unidentified origin. The patient was operated immediately for cord compression that could lead to a neurological problem. Pathological examination of the operation specimen was consistent with a giant cell tumor. The patient's serum calcium level was elevated (11.6 mg/dL; reference limits: 8.5-10.5) and phosphorus level was below the normal ranges. Parathyroid hormone was extremely high; 2097 pg/mL (reference limits: 15-65 pg/mL). Sonographic examination of the neck revealed multinodular goiter and a lesion at the inferior region of the right thyroid lobe suggesting a parathyroid adenoma. Skeletal X-rays suggested Brown tumors of long bones. The case was diagnosed as primary hyperparathyroidism and was referred for parathyroidectomy

Common variants of genes encoding TLR4 and TLR4 pathway members TIRAP and IRAK1 are effective on MCP1, IL6, IL1 beta, and TNF alpha levels in type 2 diabetes and insulin resistance

Objective and designType 2 diabetes is a pandemic disease characterized by hyperglycemia, ineffective insulin use, and insulin resistance and affecting 1 in 11 people worldwide. Inflammation-related insulin resistance is thought to play an important role in the etiology of the disease. TLR4 is the central receptor of the natural immune system and has an important role as a trigger of the inflammatory response. The IRAK1 and TIRAP are members of the TLR4 pathway and involved in the TLR4-mediated inflammatory response. Genetic variants in the TLR4 gene or in the IRAK1 and TIRAP genes may have an important role in the development of insulin resistance and type 2 diabetes by disrupting the inflammatory response. In this direction, we aimed to investigate the relationship among TLR4 and IRAK1, TIRAP gene variants, and type 2 diabetes and insulin resistance, and investigate how these variants affect inflammatory factors (TNF-alpha, IL-6, MCP-1, and IL-1 beta).Subjects and methodsIn our study, a total of seven variations on the genes of TLR4 (rs4986790, rs4986791), IRAK1 (rs1059703, rs3027898, rs7061789), and TIRAP (rs8177374, rs8177400) were genotyped by the MassARRAY((R)) Iplex GOLD SNP genotyping in 100 type 2 diabetic patients and 100 non-diabetic individual. The TLR4 rs4986790 and rs4986791 variation was confirmed by PCR-RFLP method also. The serum IL1-beta, IL6, MCP-1, and TNF-alpha levels were measured using enzyme-linked immunosorbent assay kits.Results and conclusionAs a result of our study, no correlation was found among TLR4, IRAK1, and TIRAP gene variants and the risk of type 2 diabetes and insulin resistance. However, TNF-alpha, IL-6, MCP-1, and IL-1 beta levels were also associated with diabetes and insulin resistance (p>0.05). Although the gene variants were not significant in type 2 diabetes and insulin resistance groups, IRAK1, TLR4, and TIRAP gene variants were found to be associated with TNF-alpha, IL-6, MCP-1, and IL-1 beta levels

The genetic variants of solute carrier family 11 member 2 gene and risk of developing type-2 diabetes

Type-2 diabetes (T2DM) is a metabolic disorder characterized by long-term insulin resistance, impaired insulin secretion from -cells, and loss of beta cell mass and function. Inflammation and oxidative stress play a key role in the development of diabetes and are associated with insulin resistance. Notably, recent studies have demonstrated an association between body iron stores, insulin resistance and T2DM. Free iron, a powerful pro-oxidant molecule, is involved in oxidative stress, lipid peroxidation and endothelial dysfunction via its ability to generate free radicals. Specifically, the accumulation of iron in beta cells triggers oxidative stress and DNA damage, which have been reported to be associated with -cell death and apoptosis. Solute carrier family-11 member-2 (SLC11A2) functions to transport ferrous iron and some divalent metal ions throughout the plasma membrane and across endosomal membranes. Functional polymorphisms in the SLC11A2 gene have been reported to cause excess storage of iron, resulting in iron overload. In this study, we evaluated the association between T2DM and SLC11A2 gene variants IVS4+44C/A, 1303C/A and 1254T/C by performing PCR-RFLP analysis on 100 T2DM patients and 100 healthy subjects. PCR products were digested with MnlI, MboI and SfanI restriction endonucleases and the products were then separated by 3% agarose gel electrophoresis. The genotype frequencies of the 1254T/C and 1303C/A SLC11A2 gene variants did not differ between healthy controls and T2DM patients (P>0.05). But, in recessive model (P=0.037) and homozygous CC genotype (P=0.030) for IVS4+44C/A showed significant correlation with T2DM risk. It is thought that presence of C allele of IVS4+44C/A plays pathological roles

The rs1043994 and rs3815188 genetic variations of the NOTCH3 gene and risk of type 2 diabetes mellitus

NOTCH pathways are important regulators at the beginning of the genetic mechanisms controlling the embryonic development and cell differentiation required for normal pancreatic development during the embryonic period. Disruption of the NOTCH pathway induces apoptosis in pancreatic cells or corrupted pancreatic development that can lead to diabetes. Genetic mutations affecting the NOTCH pathway have been extensively studied in certain types of cancer, including solid tumours, but its metabolic functions are not well known. The objective of our study was to explore the relationship between NOTCH3 gene variants and the risk of developing type 2 diabetes mellitus in 100 patients and 100 healthy control subjects. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was carried out to identify the genotypes in 100 patients with diabetes and 100 control individuals. DNA extracted from peripheral blood samples was amplified and the rs1043994 variant was digested with MwoI, while the rs3815188 variant was digested with AciI. The products were evaluated by 3% agarose gel electrophoresis. The obtained results suggested that the rs1043994 variant was associated with the development of type 2 diabetes due to a significant ratio with the presence of the A allele. Similarly, the presence of the CC genotype and the absence of the T allele were determined to be associated with a notable risk of developing type 2 diabetes for individuals with the rs3815188 variant. In conclusion, we found a significant association between the rs1043994 and rs3815188 variants of the NOTCH3 gene and the risk of developing type 2 diabetes mellitus

Lack of Association Between Type 2 Diabetes and the 3673G/A and 9041G/A Gene Variants of Vitamin K Epoxide Reductase Complex Subunit 1 (VKORC1)

The vitamin K epoxide reductase complex subunit 1 (VKORC1) gene is expressed in many tissue types, and encodes the VKORC1 protein, which is a key enzyme in the vitamin K cycle. Although researchers have focused on the effects of vitamin K on glucose metabolism, and on its role in the development of type 2 diabetes (T2DM), no consensus has yet been reached. Therefore, here we aimed to investigate the association between VKORC1 variants and the risk of T2DM. The 3673G/A (rs9923231) and 9041G/A (rs7294) VKORC1 variants were investigated by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 100 control individuals and 100 patients with T2DM. The genomic regions were amplified by PCR; amplicons were digested using the AciI and NciI enzymes and visualized by agarose gel electrophoresis. The genotype frequencies of the 3673G/A variants were GG (22%), GA (56%), and AA (22%) in the control group and GG (19%), GA (52%), and AA (29%) in patients with T2DM (p > 0.05). The genotype frequencies of the 9041G/A variants were GG (37%), GA (53%), and AA (10%) in the control group and GG (46%), GA (45%), and AA (9%) in patients with T2DM (p > 0.05). In conclusion, we found no significant correlation between the control group and patients with T2DM, with regard to the different genetic models of the 3673G/A and 9041G/A variants. These data suggest that these VKORC1 gene variants may not be linked to T2DM

Utilization of statins and LDL-cholesterol target attainment in Turkish patients with type 2 diabetes-a nationwide cross-sectional study (TEMD dyslipidemia study)

Background Attaining acceptable levels of LDL Cholesterol (LDL-C) significantly improves cardiovascular (CV) outcomes in patients with type 2 diabetes mellitus (T2DM). The LDL-C target attainment and the characteristics of patients attaining these targets were investigated in this study. Furthermore, the reasons for not choosing statins and the physicians' attitudes on the treatment of diabetic dyslipidemia were also examined. Methods A nationwide, cross-sectional survey was conducted in tertiary centers for diabetes management. Adult patients with T2DM, who were under follow-up for at least a year in outpatient clinics, were consecutively enrolled for the study. LDL-C goals were defined as below 70 mg/dL for patients with macrovascular complications or diabetic nephropathy, and below 100 mg/dL for other patients. Data about lipid-lowering medications were self-reported. Results A total of 4504 patients (female: 58.6%) were enrolled for the study. The mean HbA1c and diabetes duration was 7.73 +/- 1.74% and 10.9 +/- 7.5 years, respectively. The need for statin treatment was 94.9% (n = 4262); however, only 42.4% (n = 1807) of these patients were under treatment, and only 24.8% (n = 448) of these patients achieved LDL-C targets. The main reason for statin discontinuation was negative media coverage (87.5%), while only a minority of patients (12.5%) mentioned side effects. Physicians initiated lipid-lowering therapy in only 20.3% of patients with high LDL-C levels. It was observed that the female gender was a significant independent predictor of not attaining LDL-C goals (OR: 0.70, 95% CI: 0.59-0.83). Conclusions Less than 50 % of patients with T2DM who need statins were under treatment, and only a quarter of them attained their LDL-C targets. There exists a significant gap between the guideline recommendations and the real-world evidence in the treatment of dyslipidemia in T2DM

Landscape of congenital adrenal hyperplasia cases in adult endocrinology clinics of Türkiye-a nation-wide multicentre study

Background and aimsCongenital adrenal hyperplasia (CAH) is a group of disorders that affect the production of steroids in the adrenal gland and are inherited in an autosomal recessive pattern. The clinical and biochemical manifestations of the disorder are diverse, ranging from varying degrees of anomalies of the external genitalia to life-threatening adrenal insufficiency. This multicenter study aimed to determine the demographics, biochemical, clinical, and genetic characteristics besides the current status of adult patients with CAH nationwide.MethodsThe medical records of 223 patients with all forms of CAH were evaluated in the study, which included 19 adult endocrinology clinics. A form inquiring about demographical, etiological, and genetic (where available) data of all forms of CAH patients was filled out and returned by the centers.ResultsAmong 223 cases 181 (81.16%) patients had 21-hydroxylase deficiency (21OHD), 27 (12.10%) had 11-beta-hydroxylase deficiency (110HD), 13 (5.82%) had 17-hydroxylase deficiency (17OHD) and 2 (0.89%) had 3-beta-hydroxysteroid-dehydrogenase deficiency. 21OHD was the most prevalent CAH form in our national series. There were 102 (56.4%) classical and 79 (43.6%) non-classical 210HD cases in our cohort. The age of the patients was 24.9 +/- 6.1 (minimum-maximum: 17-44) for classical CAH patients and 30.2 +/- 11.2 (minimum-maximum: 17-67). More patients in the nonclassical CAH group were married and had children. Reconstructive genital surgery was performed in 54 (78.3%) of classical CAH females and 42 (77.8%) of them had no children. Thirty-two (50.8%) NCAH cases had homogenous and 31 (49.2%) had heterogeneous CYP21A2 gene mutations. V281L pathological variation was the most prevalent mutation, it was detected in 35 (55.6%) of 21OHD NCAH patients.ConclusionOur findings are compatible with the current literature except for the higher frequency of 110HD and 17OHD, which may be attributed to unidentified genetic causes. A new classification for CAH cases rather than classical and non-classical may be helpful as the disease exhibits a large clinical and biochemical continuum. Affected cases should be informed of the possible complications they may face. The study concludes that a better understanding of the clinical characteristics of patients with CAH can improve the management of the disorder in daily practice