Kallikrein has been localized in rodent kidney and salivary glands by means of an immunoglobulin-enzyme bridge technique. In sections of kidney, anti-kallikrein antibodies bound to the apical region of certain distal tubule segments in the cortex, to reabsorption droplets of proximal convoluted tubules, and to certain duct segments in the papilla. In salivary glands of both male and female rats and mice, and apical rim of most striated duct cells of submandibular, parotid and sublingual glands and granular tubules of submandibular glands exhibited immunoreactivity. Granular intercalated duct cells in female submandibular glands also displayed immunostaining for kallikrein. Phenylephrine administration resulted in loss of immunoreactive granules from the granular convoluted tubule cells of male mouse submandibular gland. This response was paralleled by a biochemically demonstrable decrease in kallikrein-like tosylarginine methyl ester (TAME) esterase activity.
Standardizing total mesorectal excision (TME) has been a topic of interest since 1979 when Professor Richard J. Heald first described TME and a new approach to rectal cancer. The procedure is optimized only if every one of the relevant factors is tackled with precise attention to detail, so that the preoperative, operative, and postoperative practice is standardized completely. The same concept of TME standardization applies today regardless of technique chosen, that is, open laparoscopic, single-incision laparoscopic surgery, or robotic. This article reviews the relevant operative factors in performing a quality TME, looking at both the oncologic and nononcologic advantages and disadvantages. It supports TME as the standard of care in obtaining a negative circumferential margin for mid and lower-third rectal cancers, and discusses the role of tumor-specific mesorectal excision for upper-third rectal cancers. It discusses the new options and challenges each operative technique holds, and identifies the same standardized principles each must obey to provide the highest quality of oncologic resection. The operative documentation of these critical features from diagnostic workup to pathological reporting is also emphasized.
Paradoxical puborectalis contraction (PPC) and increased perineal descent (IPD) are subclasses of obstructive defecation. Often these conditions coexist, which can make the evaluation, workup, and treatment difficult. After a thorough history and examination, workup begins with utilization of proven diagnostic modalities such as cinedefecography and anal manometry. Advancements in technology have increased the surgeon's diagnostic armamentarium. Biofeedback and pelvic floor therapy have proven efficacy for both conditions as first-line treatment. In circumstances where PPC is refractory to biofeedback therapy, botulinum toxin injection is recommended. Historically, pelvic floor repair has been met with suboptimal results. In IPD, surgical therapy now is directed toward the potentially attendant abnormalities such as rectoanal intussusception and rectal prolapse. When these associated abnormalities are not present, an ostomy should be considered in patients with IPD as well as medically refractory PPC.
182 Background: Exosomes play pivotal roles in cancer progression, metastasis and chemoresistance. CD63 and CD9 are widely accepted exosomal markers. Their pattern of expression and prognostic significance in patients with RSCC and LSCC is unknown. This study explored CD63 and CD9 expression and prognostic significance in patients with RSCC and LSCC using immunohistochemistry (IHC). Methods: Between 2015 and 2018, 63 patients underwent surgical resection of colon cancer for whom we had available tissues for CD63 and CD9 IHC staining. Two pathologists independently scored the CD63 and CD9 expression in the tumor and adjacent normal mucosa (ANM). Staining intensity was graded 1-3 and staining percentage was estimated in 10% increments. Mean Quick-score (Q-score) (intensity X percentage of staining) was calculated. Results: RSCC and LSCC represented 52% and 48% of the patients respectively. The ANM and Tumor CD63 Q-scores were 225 vs 191 (p = 0.009) in RSCC and 224 vs 154 (p = 0.0001) in LSCC, respectively. The ANM and Tumor CD9 Q-scores were 134 vs 152 (p = 0.142) in RSCC and 135 vs 154 (p = 0.137) in LSCC, respectively. In patients with RSCC and LSCC, the mean Tumor CD63 Q-score was 191 vs 154 (p = 0.024), while the mean ANM CD63 Q-score was 225 vs 224 (p = 0.920). The mean Tumor CD9 Q-score was 152 and 154 (p = 0.883), and the mean ANM CD9 Q-score was 134 vs 135 (p = 0.926). In our cohort, there was no difference in progression free survival (PFS) between patients with RSCC and LSCC (p = 0.2349). In all patients, there was no difference in PFS in patients with CD63 expression < 100 and ≥100 (p = 0.8284). Among patients with RSCC, there was a significantly lower PFS in patients with CD63 expression < 100 vs. ≥100 (p = 0.0259). However, among patients with LSCC, there was no difference in PFS in patients with CD63 expression < 100 vs. ≥100 (p = 0.3494). Conclusions: To our knowledge, this is the first study to show a difference in exosomal marker (CD63) expression pattern and its prognostic significance in patients with RSCC and LSCC. There was a significant positive correlation between progression free survival in patients with RSCC and higher exosomal expression.
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