HistoryRectoanal intussusception (RI), also known as internal intussusception, occult rectal prolapse, intrarectal prolapse, and internal procidentia, is a telescoping of the rectal wall during fecal evacuation. 1 Allingham, in the late 1800s, first described what we label today as rectoanal intussusception as the third variety of procidentia recti in which "the upper part of the rectum descends through the lower part, but does not appear outside the anus." 2,3 He diagnosed this with physical exam and symptoms included "obstinate constipation unrelieved by purgatives; a sensation of burning and fullness in the bowel attended with tenesmus, straining, and difficulty in defecation with occasional discharges of blood and mucus." He postulated that the intussusception was caused by a redundant sigmoid or rectal mesentery. Treatment options at that time included cauterizing portions of the intussusception or a sort of rectopexy via a left lower quadrant incision in which a silk suture is passed through the mesentery and secured it to the abdominal wall. 3 Since its first description, advances have been made in the diagnosis and treatment of rectal intussusception. However, there are many unanswered questions and the best treatment option remains unclear. EtiologyThe pathophysiology and etiology of RI is not well elucidated. Existing theories of etiology fall along two general lines of thought: RI is a dynamic anomaly which may progress to rectal prolapse; or RI is secondary to other abnormalities of pelvic floor function. 1,2 Loose fixation of the rectum to the sacrum or connective tissue disorders may contribute to RI. 4 It is hypothesized that symptoms of obstructed defecation due to RI occur owing to the circular infolding of the rectal wall with subsequent occlusion of the rectal lumen.Several studies have examined whether RI progresses to rectal prolapse. Wijffels et al found a positive correlation between grade of prolapse and age, supporting this postulation. 5 However, other studies do not support this hypothesis. Choi et al found that only 1 in 26 patients treated with dietary therapy or biofeedback for large RI ( 10 mm) developed fullthickness rectal prolapse during 45 months of follow-up (range: 12-118 months). 1 Similarly, Mellgren et al studied 38 patients with rectal intussusception on defecography who were treated nonsurgically, and found that only 2 developed rectal prolapse during the follow-up period. 6 A much larger study of 1,014 women with fecal incontinence and/or obstructive defecation found that of the 26 patients with initial rectorectal intussusception, 1 progressed to external rectal AbstractRectoanal intussusception is an invagination of the rectal wall into the lumen of the rectum. Patients may present with constipation, incomplete evacuation, incontinence, or may be asymptomatic. Defecography has been the gold standard for detection. Magnetic resonance imaging defecography and dynamic anal endosonography are alternatives to conventional defecography. However, both methods are not as sens...

A congenic model of SHR was developed by mating HT female SHR (Aoki‐Okamoto strain) with NT, male Brown Norway rats (Charles River Labs, Inc.). HT female offspring then were backcrossed with the original Brown Norway male for 6 generations (F6). F6 HT and NT congenic female rats then were inter‐bred with HT and NT F6 male rats. Salt appetite related to hypertension was evaluated to determine whether HT rats (129.0 ± 5.2 mmHg) have altered sodium (Na+) intake sensitivity compared to NT controls (100.7 ± 6.2 mmHg). Rats were housed in metabolic pens and were allowed distilled water and Na+ free chow. Rats titrated Na+intake by drinking 0.9% saline (5 days), 2.0% hypertonic saline (5 days) and 0.9% saline (5 days) during the 15 day protocol. In days 1–5, Na+ intake averaged 1.98 ± 0.55 mMol in NT and 1.46 ± 0.82 mMol in HT rats (p ≥ 0.05). After offering 2.0% saline, NT rats decreased Na+ intake but that of HT rats remained unchanged. Both NT and HT rats increased water intake during 2.0% saline with that of NT rats exceeding HT rats despite NT rats decreasing Na+ intake. Both HT and NT rats had similar urinary protein excretions indicating normal kidney function in both groups. These data indicate that HT SHR/BN congenic rats have reduced sensitivity to orally ingested NaCl. This reduced sensitivity may cause HT congenic SHR to increase long term NaCl intake and predispose them to hypertension in adulthood.

STARD5 belongs to the START protein superfamily of lipid transport proteins and functions in intracellular non‐vesicular cholesterol transport. The kidney is a major site of expression and we reported STARD5 expression to be localized to the renal proximal tubules and increased in diabetic mouse kidney. The goal for this study was to characterize the HKC‐8 human proximal tubule kidney cells for STARD5 regulation by high glucose, endoplasmic reticulum (ER) stress, and oxysterols. Cells were treated with low (5 mM) or high (25 mM) glucose for 24 hr – 7 days and mRNA levels were measured by RT‐qPCR. STARD5 expression was decreased 50% under high glucose conditions, consistent with a decrease in ER stress as measured by decreased GRP78 mRNA levels. Oxysterols, ligands for the LXR nuclear receptor, had no effect on STARD5 expression but induced ABCA1 promoter activity and mRNA levels. Thus, HKC‐8 cells have an intact LXR response and express ABCA1. Tunicamycin‐induced ER stress increased STARD5 expression and enhanced cholesterol efflux from the cells but had no effect on ABCA1 mRNA levels. Our results suggest that high glucose conditions do not directly stimulate STARD5 expression or ER stress in HKC‐8 cells. Induction of ER stress, on the other hand, enhances cholesterol efflux, as well as STARD5 expression. A direct role for STARD5 in cholesterol efflux is currently under investigation.