Conservative management of iatrogenic oesophageal perforations--a viable option.

OBJECTIVE: Iatrogenic Oesophageal perforations are a dreaded complication and there is no consensus as to their best management. The aim of our study was to assess the results of conservative management in these cases. METHODS: Twenty-six patients with iatrogenic perforations of the oesophagus treated over a 10-year period were reviewed retrospectively. They were managed conservatively by keeping them nil by mouth on intravenous fluids and intravenous antibiotics. Out of these 26, nine were patients of carcinoma of the oesophagus while the remaining 17 had benign pathologies. Twenty-two were diagnosed within 6h, while the remaining four were diagnosed over 24h after perforation. Twenty-three of the 26 were caused by oesophageal dilatations. RESULTS: Twenty-two (84.6%) of the 26 survived on this regimen. Out of the four that died, two had advanced carcinomas and died of chest complications, one died of a myocardial infarction and the fourth was an old debilitated man who died of renal failure. All four who died had extension of the leak into the pleural cavity. Early diagnosis and treatment is of critical importance and is only possible by maintaining a high index of suspicion. CONCLUSIONS: Conservative management when applied to cases of iatrogenic oesophageal perforations gives results comparable to or better that those reported in series where early surgical intervention was practised. Extension of the leak into the pleura carries a worse prognosis.     

Interventions to Increase Multivitamin Use Among Women in the Interconception Period: An IMPLICIT Network Study

Maternal and Child Health Journal - Each year, 3% of infants in the Unites States (US) are born with congenital anomalies, including 3000 with neural tube defects. Multivitamins (MVIs) including...     

Predicting emergency interventions in patients with acute ureteral colic using acute renal colic scoring system in a Pakistani cohort

International Urology and Nephrology - To evaluate the acute renal colic score (ARC) in predicting the need of emergency intervention (EI) in patients with ureteric colic secondary to a ureteral...     

Age-dependent rate of anaplastic transformation in low-grade astrocytoma

Age and histologic grade are interrelated characteristics of diffuse fibrillary astrocytomas, because the peak age incidence rises with increasing grade. The relationship between age and grade may be explained if age determines the rate of anaplastic progression in astrocytomas. The authors tested this hypothesis by determining the interval between diagnosis of low-grade astrocytoma and progression to high-grade astrocytoma in patients of various ages. A two-way scatterplot of age at initial diagnosis versus interval to anaplastic progression demonstrated a strong negative correlation (n = 24; Pearson correlation coefficient = -0.83; Spearman correlation coefficient = -0.79; p < 0.001 for both values). It was concluded that the rate of anaplastic progression in low-grade astrocytoma is directly correlated with patient age.     

In vivo chondroprotection and metabolic synergy of glucosamine and chondroitin sulfate

Supplements of glucosamine hydrochloride, low molecular weight chondroitin sulfate, and manganese ascorbate were tested separately and in combination for their ability to retard progression of cartilage degeneration in a rabbit instability model of osteoarthrosis. Computerized quantitative histologic evaluation of safranin O stained sections of the medial femoral condyles measured the grade and extent of tissue involvement of lesions. Severe lesions (Mankin grade greater than 7) were absent in all animals supplemented with a dietary mixture of glucosamine, chondroitin sulfate, and manganese ascorbate. Total linear involvement (mm of lesioned surface) and total grade (mean grade x number of lesions per animal) were reduced significantly in animals given the combination compared with controls (59% and 74% respectively). Animals supplemented with glucosamine, chondroitin sulfate, or manganese ascorbate alone had less moderate and severe tissue involvement than controls but not to the extent of the combined group. In vitro, a combination of glucosamine hydrochloride and chondroitin sulfate acted synergistically in stimulating glycosaminoglycan synthesis (96.6%). Chondroitin sulfate and manganese ascorbate but not glucosamine were effective in inhibiting degradative enzyme activity. These data suggest that the disease modifying effect (the ability to retard progression of cartilage degeneration) of a mixture of glucosamine, chondroitin sulfate, and manganese ascorbate is more efficacious than either agent alone.     

Predicting Compressive and Splitting Tensile Strengths of Silica Fume Concrete Using M5P Model Tree Algorithm

Compressive strength (CS) and splitting tensile strength (STS) are paramount parameters in the design of reinforced concrete structures and are required by pertinent standard provisions. Robust prediction models for these properties can save time and cost by reducing the number of laboratory trial batches and experiments needed to generate suitable design data. Silica fume (SF) is often used in concrete owing to its substantial enhancements of the engineering properties of concrete and its environmental benefits. In the present study, the M5P model tree algorithm was used to develop models for the prediction of the CS and STS of concrete incorporating SF. Accordingly, large databases comprising 796 data points for CS and 156 data records for STS were compiled from peer-reviewed published literature. The predictions of the M5P models were compared with linear regression analysis and gene expression programming. Different statistical metrics, including the coefficient of determination, correlation coefficient, root mean squared error, mean absolute error, relative squared error, and discrepancy ratio, were deployed to appraise the performance of the developed models. Moreover, parametric analysis was carried out to investigate the influence of different input parameters, such as the SF content, water-to-binder ratio, and age of the specimen, on the CS and STS. The trained models offer a rapid and accurate tool that can assist the designer in the effective proportioning of silica fume concrete.     

Effect of maxillary and mandibular extrusion arches on dentoskeletal changes in adults with anterior open bite: a quantitative analysis

ObjectiveTo quantify dentoskeletal changes accompanying the use of extrusion arches during the treatment of anterior open bite (AOB) in adults.Materials and MethodsA total of 23 adult patients with an AOB of −3.05 mm ± 1.27 mm were treated with upper and lower extrusion arches after the alignment phase. Lateral cephalograms were taken before placement of the extrusion arch, immediately after closure of the open bite (T2), and at the end of orthodontic treatment (T3). Data were statistically analyzed using repeated-measures analysis of variance and the Bonferroni post hoc test for pairwise comparisons (α = 0.05).ResultsSuccessful closure of AOB, with an overall change in overbite of 4.73 ± 1.93 mm, was achieved in an average of 3.8 months and remained stable at T3. Upper and lower incisors were significantly extruded by 2.05 mm ± 0.72 mm and 2.54 mm ± 1.63 mm, respectively, and significantly retroclined by 6.36° ± 1.63° and 8.45° ± 3.83°, respectively, with a resultant increase in the interincisal angle of 12.80° ± 2.09°. Statistically significant intrusion and mesial tipping (P < .001) of the maxillary and mandibular first molars were observed at T2. Dentoskeletal changes remained stable at T3, except for a significant reduction of the mesial tipping of the maxillary and mandibular first molars.ConclusionsThe combined use of maxillary and mandibular extrusion arches resulted in significant favorable dentoskeletal changes that led to the successful closure of AOB during a short duration of treatment.     

The Achilles’ heel of cancer survivors: fundamentals of accelerated cellular senescence

Recent improvements in cancer treatment have increased the lifespan of pediatric and adult cancer survivors. However, cancer treatments accelerate aging in survivors, which manifests clinically as the premature onset of chronic diseases, such as endocrinopathies, osteoporosis, cardiac dysfunction, subsequent cancers, and geriatric syndromes of frailty, among others. Therefore, cancer treatment–induced early aging accounts for significant morbidity, mortality, and health expenditures among cancer survivors. One major mechanism driving this accelerated aging is cellular senescence; cancer treatments induce cellular senescence in tumor cells and in normal, nontumor tissue, thereby helping mediate the onset of several chronic diseases. Studies on clinical monitoring and therapeutic targeting of cellular senescence have made considerable progress in recent years. Large-scale clinical trials are currently evaluating senotherapeutic drugs, which inhibit or eliminate senescent cells to ameliorate cancer treatment–related aging. In this article, we survey the recent literature on phenotypes and mechanisms of aging in cancer survivors and provide an up-to-date review of the major preclinical and translational evidence on cellular senescence as a mechanism of accelerated aging in cancer survivors, as well as insight into the potential of senotherapeutic drugs. However, only with time will the clinical effect of senotherapies on cancer survivors be visible.

Cancer survival times have increased annually owing to advances in early detection and treatment that prolong patient survival. However, increasing survivorship has underscored the observation that cancer survivors develop age-related diseases prematurely, which cause significant morbidity, health expenditures, and mortality. Many cancer survivors have been exposed to chemotherapy, radiotherapy, or both; despite eradicating cancer cells, these therapies also damage normal cells to accelerate biologic aging, such that a discrepancy exists between their biologic and chronologic age (1). Considerable data exist regarding the phenotypes of accelerated aging. However, mechanical and molecular uncertainties have limited the study of these manifestations in a clinical context. Our Review discusses accelerated aging phenotypes in cancer survivors and the cellular mechanisms underpinning these phenomena. We then discuss the translational evidence on how accelerated aging phenotypes, mainly related to senescence, are being targeted while highlighting areas of uncertainty for future research to address.