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Traumatic injuries from jet ski-related accidents have increased in incidence over the past few decades. Anorectal injuries are uncommon but typically arise from high-speed jet ski accidents. We present a case of a severe anorectal injury from a fall off the back of an accelerating jet ski.

In a rodent colorectal cancer model, nonsteroidal antiinflammatory drugs reduce tumor mass by increasing the rate of tumor cell apoptosis and decreasing proliferation. We have examined β-catenin as a potential target for these agents in colorectal cancer. Carcinogen-treated rats were treated for 23 weeks with a range of nonsteroidal antiinflammatory drugs. Control animals received vehicle alone. Intracellular β-catenin was examined using immunohistochemistry. In tumors from untreated animals, staining was seen in the cytoplasm and nucleus (median 24% of nucleii). The frequency of nuclear β-catenin staining correlated directly with the volume of tumor and inversely with the rate of apoptosis. In tumors from treatment groups, the cytoplasmic staining for β-catenin was unchanged; however, nuclear staining was absent except in the celecoxib group, where it was reduced to a median of 14%. Colorectal tumors from animals treated with NSAIDs show reduced levels of nuclear β-catenin immunoreactivity.

The ability of 5-aminosalicylic acid and olsalazine to inhibit colonic aberrant crypts and tumors was investigated in 1,2-dimethylhydrazine-treated rats. The effect of these drugs on the rates of tumor apoptosis and proliferation was studied as potential mechanisms for their action. 5-Aminosalicylic acid reduced the number of aberrant crypt foci by over one third, while olsalazine had no effect on this parameter. However, both agents effectively reduced tumor number and load, increased the rate of tumor apoptosis, and reduced the rate of tumor cell proliferation. In conclusion, 5-aminosalicylic acid and olsalazine are both ultimately effective chemopreventive agents in this model; however, only 5-aminosalicylic acid inhibited the formation of aberrant crypt foci. The inhibitory effect of these agents in tumors is related to the inhibition of proliferation and the induction of apoptosis.

In attempts to uncover a relatively mild method for the oxidative degradation of humic substances, a humic and a fulvic acid were oxidized with peracetic acid at 40 °C for 8 days. The oxidation products were extracted into organic solvents, methylated, separated by column-, thin layer-, and preparative gas-chromatography, and identified by matching their mass and micro-i.r. spectra with those of authentic specimens.The major humic acid oxidation products were phenolic acids (isolated in fully methylated forms, 8.4%), benzenecarboxylic acids (as methyl esters, 16.0%), and aliphatic acids (as methyl esters, 3.4%). The fulvic acid yielded 11.5% phenolic compounds, 8.4% benzenecarboxylic acids (as methyl esters), and 2.6% aliphatic acids (as methyl esters). These data indicated a more phenolic character for the fulvic acid than for the humic acid. In addition, small amounts of 2-methyl-3,4-furandicarboxylic acid were tentatively identified as dimethyl esters among humic and fulvic acid oxidation products. As far as total yields of oxidation products were concerned, peracetic acid oxidation at 40 °C of untreated humic and fulvic acids compared favorably with permanganate oxidation of methylated humic materials at about 100 °C, but was more time consuming.The results of this and earlier oxidative degradation studies show that the oxidation of humic substances produces phenolic and benzenecarboxylic acids as major products in addition to smaller amounts of aliphatic dicarboxylic acids. Whether these products arise from more complex structures of lignin or microbial origin or whether they occur in the forms in which they were isolated but held together by hydrogen-bonding or Van der Waal's forces requires further investigation.

The colonic microcirculation may be expected to have a central role in the absorptive, secretory, and protective functions of the colon. To characterize the microvascular structure of the colon in rats and humans, microvascular casts were prepared and examined by scanning electron microscopy. Quantitative measures of the microvasculature were obtained from histological sections. The overall organization of microvessels was found to be similar in the rat and human colon. Capillaries in the colonic mucosa formed a honeycomb-like network around each of the mucosal glands. This capillary plexus was supplied by arterioles which divide into their capillary branches at the level of the submucosa. Mucosal capillaries drain into venules at the luminal surface of the mucosa. Venules then pass to submucosal veins without receiving further capillary branches. Examination of vascular casts also showed that in both the rat and the human colon, there was an increased density of subluminal capillaries in the cecum and proximal colon compared to that of the rest of the colon. This was supported by quantitative measures which indicated a significantly greater microvascular surface area in the rat cecum (24.1 mm2/mm3) compared to that of the midcolon (19.8 mm2/mm3) (P= 0.04) and the distal colon (19.1 mm2/mm3) (P= 0.03). Similarly in the human colon there was a significantly greater total microvascular volume in the proximal colon (13.4%) compared to that of the distal colon (7.7%) (P< 0.0005) and there was a significantly greater total microvascular surface area in the proximal colon (22.4 mm2/mm3) compared to that of the distal colon (17.5 mm2/mm3) (P= 0.032). This study details quantitative vascular data for the colon in rats and humans which has not previously been documented, despite its important role in the absorptive function of the colon and in many disease processes affecting the colon. These data provide the normal values with which pathological conditions of the colon which affect the vasculature can be compared.

Studies of experimental tumors in rodents indicate that there are morphological abnormalities of the tumor microcirculation compared to normal tissues. The aim of this study was to examine the structure of the microvasculature in benign and malignant colonic tumors in humans using microvascular casting techniques. There were 15 adenocarcinomas, four benign sporadic adenomas, and three specimens from patients with familial adenomatous polyposis (FAP). A cast of the microvessels of these tumors was prepared by intraarterial administration of acrylic resin (Mercox) and the cast examined by scanning electron microscopy. Quantitative measures of the microvasculature were obtained from histological sections using stereological techniques in four carcinomas, two sporadic adenomas, and 12 adenomas from patients with FAP. Vascular casts of benign colonic adenomas showed that the microvasculature had a similar organization to normal colon. However, capillaries and venules were elongated and had increased diameters compared to normal. In adenomas greater than 3 mm in diameter, there was an increased density of microvessels in the spaces between tumor cells. Vascular casts of colonic carcinomas were characterized by a disorganized structure and increased density of microvessels. The organization of microvessels within carcinomas had a similar overall pattern to normal colon. However, the increased number and density of microvessels resulted in formation of nodular clusters of capillaries, formation of “sheets” of frequently anastomosing capillaries, or almost complete packing of the interstitial spaces of the tumor by capillaries in places. Most capillaries had a long and tortuous course and numerous capillary sprouts were identified. Tumor microvessels had greater mean diameters than normal. Extravasation of resin from microvessels in carcinomas was frequently seen. The vascular volume of carcinomas (23.1%±12.2), sporadic adenomas (16.3%±3.4), and adenomas >3 mm diameter in patients with FAP (17.7%±3.0) were significantly greater than in normal colon (11.0%±4.2). This study indicates that there is an increased vascular density in benign and malignant tumors of the colon compared to normal colon. The presence of profusely anastomotic microvessels and frequent capillary sprouts is evidence of active neovascularization and suggests control of tumor growth could be achieved by modifiers of angiogenesis.

• Sulindac (cis-5-fluoro-2-methyl-1-[p-(methylsulfinyl) benzylidene] indene-3-acetic acid), an inhibitor of prostaglandin synthesis, has been reported to cause regression of colon polyps in patients with familial polyposis coli and Gardner's syndrome. We examined the effect of sulindac on the growth of primary colon carcinomas in rats. Colon tumors were induced in 18 rats by repeated subcutaneous administration of dimethylhydrazine. The site and diameter of each tumor were measured via laparotomy and colonoscopy. Rats were randomized to receive either sulindac (10 mg/kg) twice daily or vehicle (0.5% methylcellulose). After 4 weeks of treatment, the site and size of tumors in the colon were again recorded. In eight rats receiving sulindac, no new tumors were identified, while in 10 control rats, 13 additional tumors were found after treatment. There was a significantly greater increase in size of the tumors in the control group (56.4 mm for 26 tumors) compared with the rats receiving sulindac (9.3 mm for 14 tumors). We report that sulindac inhibits the rate of development and the rate of growth of colon tumors in the rat.(Arch Surg. 1991;126:1094-1096)

Several observational studies suggest that bariatric surgery leading to sustained weight loss confers substantial benefit on obese individuals with type 2 diabetes, but no randomized controlled trials have been reported. This unblinded randomized controlled trial enrolled 60 obese persons 20 to 60 years of age who had a body mass index above 30 but less than 40. Type 2 diabetes had been clearly documented within the past 2 years. Thirty patients were randomly assigned to undergo laparoscopic adjustable gastric banding, while 30 others received conventional treatment for diabetes focusing on weight loss through lifestyle changes. Remission of diabetes was defined as a fasting glucose level below 126 mg/dL and a glycated hemoglobin (HbA1c) value below 6.2% without glycemic medication.