Status of the remaining parotid duct and gland following superficial parotidectomy

The changes in Stensen’s duct and remaining parotid tissue following superficial parotidectomy have not been studied previously. The aim of this clinical case control study is to describe these changes using sialography and CT-sialography techniques. Fourteen superficial parotidectomy cases underwent parotid sialography bilaterally. CT sialography was also done. Stensen’s duct was patent in 11 cases (79%), and non-patent in three cases (21%). Its angle in relation to our reference line was 20° in operated cases versus 37° for the non-operated cases. Following superficial parotidectomy, the remaining parotid tissues usually remain functional and retain drainage through Stensen’s duct. Furthermore, superficial parotidectomy changes the direction of this duct. Parotid sialography and CT sialography can still be used to study the status of remaining parotid tissue following superficial parotidectomy. The post-surgical changes should be reviewed with care before interpreting these studies.     

Demonstration by western blotting of antiheart antibodies before and after cardiac transplantation

Western blotting has been used to detect antiheart antibodies in two groups of patients: two who required retransplantation for hyperacute rejection, and 22 consecutive patients, whose serum was tested at monthly intervals for three months following transplantation. Pretransplant and posttransplant serum samples were tested for IgM and IgG reactivity against the patients own heart and donor heart. In all patients the pretransplant lymphocytic crossmatch had been negative. In the two patients requiring retransplantation, both had multiple bands of strong IgM and IgG against their own heart prior to transplantation as well as antibodies against the donor heart. The study of 22 consecutive patients revealed that (1) the presence of strong antibody prior to transplantation is associated with unusually severe or frequent rejection episodes, (2) 20/22 patients made antiheart antibody following transplantation, but in 12 patients it was IgM only, and (3) most of the antiheart antibodies made posttransplant were not specific for the donor heart. Comparison of Western blotting with immunofluorescent detection of antibodies on frozen sections revealed that the Western blotting procedure is more sensitive and results are easier to interpret.     

Molecular analysis of genetic changes in the origin and development of renal cell carcinoma.

Renal cell carcinoma has been characterized by an abnormality on the short arm of chromosome 3 which suggests the presence of a tumor suppressor gene at this location. In order to more precisely define the location of the renal cell carcinoma gene and to differentiate molecular changes occurring in early stages of renal neoplasia versus those occurring later in malignant progression, DNA from normal and tumor tissue from 60 patients with various stages of renal cell carcinoma was analyzed for loss of alleles at different chromosomal loci. In tumor tissue from 51 of 58 evaluable patients (88%) there was loss of heterozygosity at one or more of 10 loci tested on chromosome 3 independently of tumor stage. Analysis of the genotypes identified the distal portion of 3p bounded by D3S2 and D3S22 (3p21-26) as the region of the disease gene. In tumor tissue from patients with advanced renal cell carcinoma, we found loss of heterozygosity on chromosome 11p in 5 of 21 (24%), on chromosome 13 in 3 of 9 (33%), and on chromosome 17 in 2 of 19 (11%). We found no loss of heterozygosity at the loci on chromosomes 11, 13, or 17 in tumor tissue from patients with localized renal cell carcinoma (N = 5). These data suggest the existence of a tumor suppressor gene on chromosome 3p which may be essential to the genesis of sporadic renal cell carcinoma and that other tumor suppressor genes are associated with progression of this malignancy.     

Histological reactions to bites of Amblyomma variagatum and Rhipicephalus appendiculatus (Acari: Ixodidae) fed simultaneously on naive or sensitized rabbits

Histopathological studies on attachment sites of nymphs, 48 h after attachment on three groups of rabbits, have revealed differences that were related to the rabbits' previous tick experience. Feeding lesions caused by Amblyomma variegatum (F.) in tick-naive rabbits were extensive and the total number of inflammatory cells was about 10 times greater than that in the feeding lesions caused by Rhipicephalus appendiculatus Neumann fed simultaneously on contralateral ears. Rabbits that were previously sensitized either to A. variegatum or R. appendiculatus by repeated tick infestations showed epidermal vesiculation and significant mobilization of eosinophils at the homologous tick feeding sites, events that did not occur with tick-naive rabbits. The feeding of A. variegatum nymphs on rabbits sensitized to R. appendiculatus produced a similar type of intense reaction, but the cellular responses to R. appendiculatus in the skin of rabbits sensitized to the A. variegatum were negligible.     

Guillain-Barré syndrome associated with human immunodeficiency virus infection in Zimbabwe

We studied the clinical features and human immunodeficiency virus (HIV) serology of 32 consecutive adults with inflammatory demyelinating polyneuropathy (IDP) admitted to the teaching hospitals in Harare, Zimbabwe. Twenty-nine of the IDP patients had Guillain-Barré syndrome (GBS), and the other three had chronic IDP. Sixteen of 29 (55%) GBS patients were HIV-seropositive, a higher frequency of HIV infection than in blood donors drawn from the population served by these hospitals. All three chronic IDP patients were HIV-seronegative. In all HIV-seropositive patients, GBS was the initial illness that brought the patient to medical attention and led to the diagnosis of HIV infection. Compared with seronegative patients, the HIV-seropositive GBS patients were more likely to have generalized lymphadenopathy, CSF pleocytosis, coexistent CNS disturbance, and prior sexually transmitted disease. GBS in this region of Africa is frequently associated with HIV infection.     

Spinal Cord Stimulation: A Comparison of Efficacy versus Other Novel Treatments for Refractory Angina Pectoris

Abstract: Recently much attention has been directed toward novel treatment alternatives for refractory angina pectoris. Refractory angina is persistent stable class III or IV angina despite maximally tolerated medical treatment in patients with end-stage coronary artery disease. Transmyocardial laser revascularization (TMLR), gene therapy, intermittent urokinase therapy, enhanced external balloon counterpulsation, and spinal cord stimulation have all been employed to treat refractory angina pectoris. TMLR and gene therapy are invasive open-chest procedures that have yielded controversial results. Intermittent urokinase and enhanced external balloon counterpulsation studies have limited follow-up times and require multiple clinic visits for treatment. Spinal cord stimulation has a proven short- and long-term efficacy and cost-effectiveness in the treatment of refractory angina. When compared to coronary artery bypass grafting (CABG), it has been shown to decrease the frequency of anginal attacks and consumption of short-acting nitrates to the same extent in refractory angina. Spinal cord stimulation's safety profile has also been well established and it can be used concurrently with cardiac pacemakers or MRI systems, provided the proper precautions are taken. Since spinal cord stimulation is a minimally invasive procedure with a favorable efficacy and safety profile, it should be considered as a valid treatment alternative after medical management has failed in refractory angina prior to implementing invasive modalities such as TMLR or gene therapy.     

Disruption of Tsc2 in pancreatic beta cells induces beta cell mass expansion and improved glucose tolerance in a TORC1-dependent manner

Regulation of pancreatic beta cell mass and function is a major determinant for the development of diabetes. Growth factors and nutrients are important regulators of beta cell mass and function. The signaling pathways by which these growth signals modulate these processes have not been completely elucidated. Tsc2 is an attractive candidate to modulate these processes, because it is a converging point for growth factor and nutrient signals. In these experiments, we generated mice with conditional deletion of Tsc2 in beta cells (betaTsc2(-/-)). These mice exhibited decreased glucose levels and hyperinsulinemia in the fasting and fed state. Improved glucose tolerance in these mice was observed as early as 4 weeks of age and was still present in 52-week-old mice. Deletion of Tsc2 in beta cells induced expansion of beta cell mass by increased proliferation and cell size. Rapamycin treatment reversed the metabolic changes in betaTsc2(-/-) mice by induction of insulin resistance and reduction of beta cell mass. The reduction of beta cell mass in betaTsc2(-/-) mice by inhibition of the mTOR/Raptor (TORC1) complex with rapamycin treatment suggests that TORC1 mediates proliferative and growth signals induced by deletion of Tsc2 in beta cells. These studies uncover a critical role for the Tsc2/mTOR pathway in regulation of beta cell mass and carbohydrate metabolism in vivo.     

Genetic analysis of mitochondrial complex II subunits SDHD, SDHB and SDHC in paraganglioma and phaeochromocytoma susceptibility

BACKGROUND: Germline mutations in three subunits of mitochondrial complex II (SDHB, SDHC and SDHD) may be associated with susceptibility to phaeochromocytoma (PC) and/or head and neck paraganglioma (HNPGL). METHODS: To further define the role of SDH subunit mutations in these disorders, we analysed a series of 22 probands with PC and evidence of genetic susceptibility (seven with familial PC only, one with familial PC and HNPGL, 10 sporadic cases with multiple PC and four cases of isolated paediatric onset PC) for germline SDHB, SDHC and SDHD mutations. In addition, we analysed 34 cases of HNPGL (30 isolated cases with single tumours, three isolated cases with multiple tumours and one familial case with multiple tumours) for somatic and germline mutations in SDHB, SDHC and SDHD. RESULTS: We identified four germline mutations (three SDHB and one SDHD, three novel) in the 22 PC probands. Combining these results with our previous series, we have detected germline SDHB or SDHD mutations in 2/12 (17%) of familial PC only kindreds, 4/5 (80%) of familial PC and HNPGL cases, 1/10 of sporadic multiple PC cases and 2/4 (50%) of paediatric PCs. No somatic mutations were detected in the HNPGL tumours, but four cases with multiple HNPGL had the common P81L germline SDHD mutation. Intriguingly a silent SNP (c.204C > T) in SDHD was significantly more common in HNPGL cases (6/34) than in controls (1/100, P = 0.0011). Combining our results with those from two other large studies in which both SDHB and SDHD have been analysed, SDHB mutations were most commonly associated with phaeochromocytoma susceptibility and SDHD with the development of HNPGL (P = 0.025). However, germline SDHB and SDHD mutations demonstrate considerable phenotypic variability and genotype-phenotype correlations are complex. CONCLUSION: The significantly lower frequency (P = 0.028) of germline SDH subunit mutations in familial PC only cases compared to those with familial PC and HNPGL suggests that further PC susceptibility gene(s) remain to be identified.