Use of the free prefabricated temporoparietal fascia-chondro-cutaneous flap nourished by only arterial inflow: an arterial flap

Summary Pedicled temporoparietal fascial flaps have been used extensively in head and neck reconstruction for many years. Also, the fascia has been grafted, and the skin graft transformed into a vascularized pedicled flap (prefabricated temporoparietal fasciocutaneous flap). On the other hand, some authors have used free temporoparietal fascial flaps for defects that require to be filled in lower and upper extremity wounds. In this case, a free prefabricated temporoparietal fascio-chondro-cutaneous flap having only an arterial inflow was used in eyelid reconstruction.Presented at the 14th Congress of Turkish Plastic and Reconstructive Surgery, Ankara, Turkey, October 1992     

Thymidylate synthase activity,folates, and glutathione system in head and neck carcinoma and adjacent tissues

Background. Head and neck squamous cell carcinomas (HNSCC) present variable aggressiveness and chemosensitivity. Because the glutathione (GSH) system and thymidylate synthase (TS) are involved in the resistance to the main drugs used in HNSCC (cisplatin and 5-FU), we studied these systems in tumors and normal mucosae. Methods. Tumor samples and normal adjacent mucosae were collected from 37 untreated HNSCC patients. GSH and glutathione S-transferase (GST) activity were assayed by spectrophotometry, whereas TS activity and folates were determined by radioassays. Results. Mean GSH levels were higher in tumors (15.2 ± 8.2 nmol/mg protein) than in mucosae (8.3 ± 4.1 nmol/mg protein) (p = 0.005, paired t test). GST activity was also higher in tumors (394 ± 194 nmol/min/mg protein) than in mucosae (261 ± 132 nmol/min/mg protein) (p = 0.0003). TS activity was markedly higher in tumors (9.2 ± 21.5 pmol/min/mg protein) compared to that of mucosae (0.9 ± 1.2 pmol/min/mg protein) (p = 0.0001). Folate levels in tumors and mucosae were similar (1.2 ± 1.1 and 0.8 ± 0.9 pmol/mg protein, respectively; p = 0.1, NS). In relation to clinical stage and tumor size, a statistical difference was found in GSH and GST values between tumors and mucosae for stage IV and T3/T4. The increase in tumor TS compared to that of mucosae was significant for all clinical stages, tumor sizes, and nodal involvement. Conclusions. These data enhance our understanding of the enzymatic systems involved in cisplatin and 5-fluorouracil (5-FU) resistance in HNSCC and normal mucosae and may help to elucidate tumor behavior and interpatient differences in drug sensitivity. © 1994 John Wiley & Sons, Inc.     

Long-term risk of second malignant neoplasm after a cancer in childhood

The risk of subsequent second malignant neoplasm was studied in a cohort of 634 patients, treated for a childhood cancer at the Gustave Roussy Institute between 1942 and 1969, and in complete remission five years after diagnosis. The most frequent types of first primary cancers (FPC) were Wilms' tumours (28% of the children), neuroblastomas (16%), lymphomas (12%) and soft tissue sarcomas (11%). Median follow-up duration after FPC was 19 years. Thirty-two patients (obs = 32) developed a total of 35 second cancers. Bone, thyroid, connective tissues and skin were the most frequent types of second cancer, with six patients for each type. The average annual incidence of second cancer was 0.36%. The average annual incidence for the periods 5-9, 10-14, 15-19, 20-24 and 25+ years after FPC was respectively 0.16%, 0.34%, 0.36%, 0.71% and 1.18%. The cumulative incidence of second cancer for the periods 5-20, 5-25 and 5-30 years after FPC was, respectively, 4.3% (95% CI: 2.8-6.6%), 7.8% (95% CI: 5.1-11.8%) and 13.0% (95% CI: 8.2-20.0%). The expected number of cancers in the cohort, computed from Danish cancer incidence data, was exp = 2.2. When compared to this expected number, the average annual excess incidence of second cancer, defined as obs-exp divided by the number of person years of observation, was 0.33%. This rose from 0.15% for the period 5-9 years after FPC to 1.09% for the period beginning 25 years after FPC. The standardised incidence ratio of second cancer (i.e. obs/exp) was 15 (95% CI: 10-21), and was fairly constant in the period extending from 15 to 20 years after FPC diagnosis. Obs/exp was equal to 25 for the patients who had had chemotherapy and equal to 9 for those who had not. Cyclophosphamide seemed less carcinogenic than the other alkylating agents. Obs/exp was similar for the patients who had received radiotherapy and for those who had not. The risk of cancer increased with age in the reference population and increased faster in the cohort, because the standardised incidence ratio is constant over a long period.     

The <Emphasis Type="Italic">Arg</Emphasis>194<Emphasis Type="Italic">Trp</Emphasis> polymorphism in DNA repair gene XRCC1 and the risk for sporadic late-onset Alzheimer's disease

Abstract Alzheimer's disease (AD) is defined pathologically by the presence of β-amyloid plaques, neurofibrillary tangles and extensive neuronal loss. Evidence indicates that increased DNA damage may contribute to neuronal loss in AD. Recently, it has been shown that in AD neurons have a reduced capacity for some types of DNA repair. Polymorphisms in DNA repair genes may be associated with differences in repair efficiency of DNA damage. Variants of several DNA repair genes, including the base excision repair gene XRCC1, have been described previously. We hypothesised that Arg194Trp polymorphism of XRCC1 gene may contribute to genetic susceptibility for AD. In order to test this hypothesis, we investigated Arg194Trp polymorphism at the XRCC1 gene in the DNA samples of 98 patients with AD and 95 healthy subjects. The frequency of the Trp allele was more pronounced among cases (11.2%) compared with controls (5.8%). On combining the homozygous and heterozygous variants of each codon, the variants seemed to be at twofold risk of AD, although the risk estimates were not statistically significant (OR=1.95, 95% CI 0.88–4.34, p=0.09). In addition, the 194Trp allele revealed a borderline significance (OR=2.05, 95% CI 0.96–4.37, p=0.056). According to our results, it may be speculated that the polymorphic variants of XRCC1 codon 194 have a role in the development of AD.     

Extending the capability paradigm to address the complexity of disability

Amartya Sen looks at people's well-being in terms of functioning and freedom, rather than in terms of the amount of goods or services consumed. The capability approach, developed by Sen, deals with what people are able to achieve by using these commodities. Concerning disability, he wrote: “We must take note that a disabled person may not be able to do the many things that an able-bodied individual can, with the same bundle of commodities” [Sen, A. K. (1985). Commodities and capabilities. Oxford: Oxford University Press [1999], p. 7]. The capability approach makes it possible to analyse the economic situation of people with disabilities in a different way. What becomes important is their functioning, i.e. what they are able to achieve within a given context. In fact, the capability set includes not only what a person is effectively able to achieve, but also the potential functionings that he/she can choose. This expresses the degree of freedom that a person with disability benefits from in a given environment. The challenge is therefore to reduce the constraints that the environment adds to a person's impairment in order to expand their capability set and to allow them to live a life which they value. This paper reviews the paradigms that address disability and the ways of assessing a person's capability set within this framework. Achieved functionings are easily measured through cross-sectional surveys, using counterfactual analysis to compare the situations of disabled and non-disabled people. This was done in 2005 in Afghanistan when a national disability survey was carried out on a random sample of households. Measuring detailed capabilities, especially their freedom dimension, is quite complex and requires identifying people's potential choices in an ever-changing environment. This implies a need to extend the philosophical framework and to adopt appropriate statistical methodologies.     

Human papillomavirus and HIV coinfection and the risk of neoplasias of the lower genital tract: a review of recent developments

ONE OF THE RISK FACTORS FOR HUMAN PAPILLOMAVIRUS (HPV) INFECTION and subsequent lower genital tract neoplasias and cancers is impaired cell-mediated immunity. HIV-positive women with severe immunosuppression are 5 times more likely than HIV-negative women to have lower genital tract neoplasias. A corresponding increase in the risk of invasive vulvar and anal cancers, but not of cervical cancer, has also been observed among HIV-positive women. Treatment failure and recurrence of neoplasia occur much more frequently among HIV-positive than among HIV-negative women. In this review, we discuss recent advances in the understanding of the relation between HIV and HPV coinfection and the development of lower genital tract neoplasias and cancers in women. In addition, we present strategies for monitoring and treating noninvasive and invasive neoplasias of the lower genital tract in HIV-positive women.