Endoscopic Anterior Transposition of Ulnar Nerve (EATUN) for Treatment of Tardy Ulnar Nerve Palsy

BackgroundTardy ulnar nerve palsy is the development of late onset ulnar nerve dysfunction and is usually treated by open anterior transposition of ulnar nerve. Open technique is done using a longitudinal incision about 6–8 inch. in length with chances of development of medial antebrachial cutaneous nerve neuromas.PurposeIn this study, we describe the technique of Endoscopic Anterior Transposition of Ulnar Nerve (EATUN procedure) to treat tardy ulnar nerve palsy and analyze the results.MethodsSeven patients diagnosed to have tardy ulnar nerve palsy was treated by EATUN. The humerus-elbow-wrist angle (HEW), pre- and post-operative intrinsic muscle power and sensory assessment, Dellon scores, and the Q-DASH was analyzed.ResultsThe minimum follow-up was 12 months (Mean 27.4 months, Range 12–36 months). Improvement in Dellon and Q-DASH scores following EATUN procedure was statistically significant. There was objective improvement of intrinsic muscle power and sensation on follow-up, though not statistically significant. No instance of neuroma of the medial cutaneous nerve of forearm was noted.ConclusionsThe endoscopic anterior transposition of the ulnar nerve is a good option in surgical management of tardy ulnar nerve palsy.Level of evidenceTherapeutic Level IV.Supplementary InformationThe online version contains supplementary material available at 10.1007/s43465-021-00366-w.     

Prognostic importance of DNA repair gene polymorphisms of <Emphasis Type="Italic">XRCC1</Emphasis> Arg399Gln and <Emphasis Type="Italic">XPD</Emphasis> Lys751Gln in lung cancer patients from India

Purpose Inter individual variation in lung cancer susceptibility may be modulated in part through genetic polymorphisms in the DNA repair genes, especially the genes involved in the Base Excision Repair (BER) and nucleotide excision repair (NER) pathway. Two of the genetic polymorphisms, XRCC1Arg399Gln and XPD Lys751Gln have been extensively studied in the association with lung cancer risk, although published studies have been inconclusive. Methods In order to verify the role of the common variant alleles in the XPD gene, we have genotyped 211 lung cancer patients and 211 healthy controls using PCR-RFLP assays in a hospital based, case-control study in an Indian population. Logistic regression models were fit to examine the relationship between the log odds of lung cancer and each covariate. Overall Survival in relation to various genotypes and clinicopathological factors were analyzed using Kaplan Meier estimates and hazard ratios were calculated using Cox Regression analysis. Results The carriers of XRCC1 399 AA genotypes were at higher risk of lung cancer (OR = 2.1, 95% CI:1.224–3.669, P = 0.007) than carriers of GG genotype. Subjects carrying 751 AC genotype were at an increased risk of carcinoma of the lung (OR = 1.8; 95% CI:1.233–2.807, P = 0.003) than subjects with AA genotypes. Compared to the XRCC1 399 GG/ XPD 751 AA reference genotype, the combined variants, XRCC1 399 GG/ XPD 751 AC+CC (OR = 1.9, 95% CI: 1.037–3.481), P = 0.03), XRCC1 399 GA+AA/ XPD 751 AA (OR = 1.7, 95% CI: 1.020–2.833, P = 0.04), XRCC1 399 GA+AA/XPD 751 AC+CC (OR = 2.7, 95% CI: 1.582–4.864, P = 0.01), had significantly higher odds ratios. Increasing numbers of either XPD or XRCC1 variant alleles were associated with shorter overall survival, the risk being significant for the XRCC1 gene polymorphism (P = 0.01 by log-rank test). The hazard of dying was significant for the XRCC1 399 AA genotype (HR = 3.04, 95%CI: 1.393–6.670, P = 0.005). Higher tumour stage also came out as significant predictors of patient death. Conclusions These findings suggest that genetic polymorphisms in the DNA repair genes may modulate overall lung cancer susceptibility and that pathological stage and XRCC1 Arg399Gln independently predicted overall survival among Indian lung cancer patients.     

Subcutaneous adipose 11 beta-hydroxysteroid dehydrogenase type 1 activity and messenger ribonucleic acid levels are associated with adiposity and insulinemia in Pima Indians and Caucasians

Metabolic effects of cortisol may be critically modulated by glucocorticoid metabolism in tissues. Specifically, active cortisol is regenerated from inactive cortisone by the enzyme 11 beta-hydroxysteroid dehydrogenase type 1 (11-HSD1) in adipose and liver. We examined activity and mRNA levels of 11-HSD1 and tissue cortisol and cortisone levels in sc adipose tissue biopsies from 12 Caucasian (7 males and 5 females) and 19 Pima Indian (10 males and 9 females) nondiabetic subjects aged 28 +/- 7.6 yr (mean +/- SD; range, 18-45). Adipose 11-HSD1 activity and mRNA levels were highly correlated (r = 0.51, P = 0.003). Adipose 11-HSD1 activity was positively related to measures of total (body mass index, percentage body fat) and central (waist circumference) adiposity (P < 0.05 for all) and fasting glucose (r = 0.43, P = 0.02), insulin (r = 0.60, P = 0.0005), and insulin resistance by the homeostasis model (r = 0.70, P < 0.0001) but did not differ between sexes or ethnic groups. Intra-adipose cortisol was positively associated with fasting insulin (r = 0.37, P = 0.04) but was not significantly correlated with 11-HSD1 mRNA or activity or with other metabolic variables. In this cross-sectional study, higher adipose 11-HSD1 activity is associated with features of the metabolic syndrome. Our data support the hypothesis that increased regeneration of cortisol in adipose tissue influences metabolic sequelae of human obesity.     

Argyrophilic nucleolar organizer regions in the evaluation of tumour progression in the oral mucosa: correlation with tissue pathology

The present study has analysed the numbers of argyrophilic nucleolar organizer regions (AgNOR) in normal tissues and in premalignant and malignant lesions of the oral mucosa in order to assess their potential as a biological marker for tumour progression. On comparison of AgNOR numbers in different lesions, carcinomas showed the highest number (4.65±0.98) compared to leukoplakias (2.38±0.47) and normal tissues (1.53±0.39). Spindle cell carcinomas and poorly differentiated squamous cell carcinomas had higher AgNOR counts than well-differentiated carcinomas. In various clinically different types of oral leukoplakia, the lowest AgNOR counts were observed in homogenous leukoplakia and the highest in speckled leukoplakia. No significant difference in AgNOR number was observed between non-dysplastic and dysplastic leukoplakia, although a significant difference was evident between dysplastic leukoplakia and normal oral mucosa. Correlating the AgNOR count and tumour progression, a significantly high positive correlation coefficient (r=0.7969,P=0.0000) was observed.     

Combined gene therapy and ionizing radiation is a novel approach to treat human esophageal adenocarcinoma

Background The ability to infect tumor cells limits the antitumor effects of gene therapy. The addition of radiotherapy to treatment with Ad.Egr.TNF.11D, a replication-deficient adenovirus containing a radiation-inducible promoter, early growth response-1, and the tumor necrosis factor-α (TNFα) complementary DNA may enhance the therapeutic ratio. Methods Seg-1 human esophageal adenocarcinoma cells were treated with Ad.Egr.TNF.11D with or without radiation. TNFα levels were quantified with enzyme-linked immunosorbent assay. Athymic nude mice bearing Seg-1 tumors were randomized to buffer, ionizing radiation, Ad.Egr.TNF.11D, and combination therapy. Tumor growth delay was used to compare treatment regimens. TNFα levels were measured in tumor homogenates and plasma. Results Seg-1 cells treated with Ad.Egr.TNF-11D and ionizing radiation demonstrated increased TNFα levels at 72 hours compared with cells exposed to vector alone (124±0 pg/mL vs. 31.11±22 pg/mL;P=.008). In vivo, Ad.Egr.TNF.11D-treated tumors expressed low TNFα levels (151.5 ±107.11 pg/mg protein) compared with tumors receiving combined treatment (793.92±489.13 pg/mg protein;P=.067). Increased TNFα levels were associated with increased tumor growth delay after combined treatment (P<.05). Conclusions Radiotherapy enables focal stimulation of TNFα expression in Ad.Egr.TNF.11D-infected cells and thus improves local tumor control.