Anatomical considerations of selective pudendal neurectomy

The pudendal nerve was examined in 100 cadavers of both sexes. Because of the variable number of trunks of the pudendal nerve, 5 types were distinguished: one-trunked; two-trunked, rectopudendal; two-trunked, pudendo-penile (or-clitoridal); three-trunked, recto-perineo-penile (or-clitoridal); four-trunked, recto-perineo-perineopenile (or-clitoridal). The authors' suggestions make it possible to perform selective pudendectomy, consisting in denervation of the sphincter urethrae muscle by neurectomy of the perineal branches of the pudendal nerve.     

Effects of prolonged administration of neurotensin, arginine-vasopressin, NPY, and bombesin on blood TSH, T3 and T4 levels in the rat

Adult female rats were i.p. infused (Alzet osmotic minipumps) with neurotensin (NT, 2 micrograms/rat/day for 7 days), arginine-vasopressin (AVP, 2 micrograms/rat/day for 8 days), bombesin (BM, 0.75 microgram/rat/day for 7 days) or injected with neuropeptide Y (NPY, 0.5 microgram/rat twice a day for 4 days). NT infusion increased absolute and relative thyroid gland weight and decreased serum T4 level, while serum TSH and T3 levels remained unchanged. AVP treatment increased thyroid gland weight and serum TSH and T4 levels and a similar effect was induced by prolonged BM infusion. On the other hand, NPY administration had no effect either on thyroid gland weight or on serum TSH, T4 and T3 levels. Results of the present study thus clearly demonstrate a potent stimulatory action of AVP and BM on thyroid gland function and suggest that this effect is mediated by the pituitary gland. On the contrary, prolonged NT infusion decrease serum T4 level while NPY had no effect on thyroid gland function.     

Inhibition of Expression of Hypoxia-inducible Factor-1α mRNA by Nitric Oxide in Hypoxic Pulmonary Hypertension Rats

Hypoxiaisadirectfactorcausinghypoxicpul monaryhypertension (HPH) .hypoxiainduciblefac tor 1α (HIF 1α)isfoundtobethemostcrucialfactorsofarwhichmediatesthecellularresponsetohypoxi a[1] .OurpreviousstudyrevealedthatoverexpressionofHIF 1andendothelin 1(ET 1…     

A tumor-targeted and conditionally replicating oncolytic adenovirus vector expressing TRAIL for treatment of liver metastases.

We have constructed a new capsid-modified adenovirus (Ad) vector that specifically replicates in tumor cells and expresses TNF-related apoptosis-inducing ligand (TRAIL). The Ad capsid contains short-shafted fibers derived from Ad serotype 35, which allow for efficient infection of malignant tumor cells, and largely avoids innate toxicity after intravenous application. Replication-dependent homologous recombination in Ad genomes was used to achieve tumor-specific expression of Ad E1a (to mediate viral replication) and TRAIL (to mediate apoptosis and enhance release of progeny virus from infected cells). We demonstrated that our oncolytic vector (Ad5/35.IR-E1A/TRAIL) induced apoptosis in human tumor cell lines derived from colorectal, lung, prostate, and liver cancer. Both in vitro and in vivo tumor models showed efficient intratumoral spread of this vector. In a model for metastatic colon cancer, tail vein infusion of Ad5/35.IR-E1A/TRAIL resulted in elimination of preestablished liver metastases. Intravenous injection of this vector caused a transient elevation of serum glutamic pyruvic transaminase in tumor-bearing mice, which we attributed to factors released from apoptotic tumor cells. Liver histology analyzed at day 14 after virus injection did not show signs of hepatocellular damage. This new oncolytic vector represents a potentially efficient means for gene therapy of metastatic cancer.     

Myoepitheliomas of the soft palate: helical CT findings in two patients.

We describe the enhancement patterns of myoepithelioma in two patients with a soft palate mass. In the first case, helical CT revealed a faintly enhancing mass. Histologically, the tumor was composed of plasmacytoid cells in a background of rich myxoid stroma. Immunostaining for CD34 showed scanty blood vessels. In the second case, helical CT revealed an intensely enhancing mass. Histologically, the mass was a cellular tumor with fibrous stroma. Immunostaining for CD34 also showed frequent blood vessels.     

Obesity in youth and middle age and risk of colorectal cancer in men

To investigate an association between colon cancer and obesity during early adulthood—a potentially important period in the etiology of this disease—the authors assembled, by computer linkage, a population-based historical cohort of 52,539 men born between 1913 and 1927 residing in Hawaii (USA), for whom weight and height had been recorded in 1942–43 and 1972. Linkage of this cohort to the Hawaii Tumor Registry resulted in the identification of 737 incident cases of colorectal cancer for 1972–86. An average of 3.8 cancer-free controls were matched to each case on month and year of birth and ethnicity of the parents. A case-control analysis in each anatomic subsite of the large bowel revealed that both early and middle-age body mass increased the risk of sigmoid cancer in men in a dose-dependent fashion. The odds ratios (OR) for sigmoid cancer for the highest compared with the lowest tertiles of Quetelet index were: 2.1 (95 percent confidence interval [CI]=1.4–3.2) and 1.7 (CI=1.1–2.5), at ages 15–29 and in prediagnostic years, respectively. These associations were additive and idependent of socioeconomic status. Men who were above the median Quetelet index in 1942 and 1972 had an OR of 2.7 (CI=1.8–4.0), compared with those who were below the median in both periods. This study provides further evidence for an association of obesity with colon cancer in men and suggests that this association is limited to the sigmoid colon and may be related to both early and late events of colon carcinogenesis.The authors are with the Epidemiology Program, Cancer Research Center of Hawaii, University of Hawaii. Address correspondence to Dr Le Marchand, Epidemiology Program, Cancer Research Center of Hawaii, 1236 Lauhala Street, Suite 407, Honolulu, HI 96813, USA. This work was supported in part by Public Health Service grant 5-R29-CA44503 and contract NO1-CN-55424 from the National Cancer Institute, National Institutes of Health, Department of Health and Human Services.