Low Spigelian hernia in a 6-year-old boy presenting as an incarcerated inguinal hernia: a case report

<p>Abstract</p> <p>Introduction</p> <p>Lower Spigelian hernia is a very rare entity. The clinical findings are similar to those of inguinal hernias and in many cases may be misdiagnosed. In the literature, only a few references to this entity have been reported in children. To the best of our knowledge, this is the first case report of a lower Spigelian hernia in a child who presented with an acute painful scrotum.</p> <p>Case presentation</p> <p>We discuss the case of a 6-year-old Greek boy who presented to our emergency department complaining of severe pain in the left inguinal area and scrotum. The acute painful swelling started suddenly, without any obvious cause. The initial diagnosis was incarcerated inguinal hernia which was reduced with difficulty. Five days later, the patient still experienced mild pain during palpation and he was operated on. During the operation, a large lower Spigelian hernia was revealed and reconstructed.</p> <p>Conclusion</p> <p>Although Spigelian hernias are rare in children and difficult to diagnose, physicians should be aware of them and include them in the differential diagnosis.</p

ER stress and the unfolded protein response in intestinal inflammation

Although there have been advances in our understanding of carcinogenesis and development of new treatments, cancer remains a common cause of death. Many regulatory pathways are incompletely understood in cancer development and progression, with a prime example being those related to the endoplasmic reticulum (ER). The pathological sequelae that arise from disruption of ER homeostasis are not well defined. The ER is an organelle that is responsible for secretory protein biosynthesis and the quality control of protein folding. The ER triggers an unfolded protein response (UPR) when misfolded proteins accumulate, and while the UPR acts to restore protein folding and ER homeostasis, this response can work as a switch to determine the death or survival of cells. The treatment of cancer with agents that target the UPR has shown promising outcomes. The UPR has wide crosstalk with other signaling pathways. Multi-targeted cancer therapies which target the intersections within signaling networks have shown synergistic tumoricidal effects. In the present review, the basic cellular and signaling pathways of the ER and UPR are introduced; then the crosstalk between the ER and other signaling pathways is summarized; and ultimately, the evidence that the UPR is a potential target for cancer therapy is discussed. Regulation of the UPR downstream signaling is a common therapeutic target for different tumor types. Tumoricidal effects achieved from modulating the UPR downstream signaling could be enhanced by phosphodiesterase 5 (PDE5) inhibitors. Largely untapped by Western medicine for cancer therapies are Chinese herbal medicines. This review explores and discusses the value of some Chinese herbal extracts as PDE5 inhibitors

Intestinal myofibroblasts: targets for stem cell therapy

The subepithelial intestinal myofibroblast is an important cell orchestrating many diverse functions in the intestine and is involved in growth and repair, tumorigenesis, inflammation, and fibrosis. The myofibroblast is but one of several α-smooth muscle actin-positive (α-SMA+) mesenchymal cells present within the intestinal lamina propria, including vascular pericytes, bone marrow-derived stem cells (mesenchymal stem cells or hematopoietic stem cells), muscularis mucosae, and the lymphatic pericytes (colon) and organized smooth muscle (small intestine) associated with the lymphatic lacteals. These other mesenchymal cells perform many of the functions previously attributed to subepithelial myofibroblasts. This review discusses the definition of a myofibroblast and reconsiders whether the α-SMA+ subepithelial cells in the intestine are myofibroblasts or other types of mesenchymal cells, i.e., pericytes. Current information about specific, or not so specific, molecular markers of lamina propria mesenchymal cells is reviewed, as well as the origins of intestinal myofibroblasts and pericytes in the intestinal lamina propria and their replenishment after injury. Current concepts and research on stem cell therapy for intestinal inflammation are summarized. Information about the stem cell origin of intestinal stromal cells may inform future stem cell therapies to treat human inflammatory bowel disease (IBD)

Should We Be Concerned About Jejunoileal Atresia During Repair of Duodenal Atresia?

Introduction: During repair for duodenal atresia, it has been emphasized that inspection of the small bowel to identify a second atresia is required. The laparoscopic approach for repair of duodenal atresia has been criticized for its limitation to perform this step. Given that duodenal atresia and jejunoileal atresias do not share common embryologic origins, we question the validity of this concern. Therefore, we conducted a multicenter retrospective review of duodenal atresia patients to quantify the incidence of jejunoileal atresia in this population.Methods: After institutional review board approval (IRB #07-12-187X), a retrospective review was conducted on all patients who have undergone duodenal atresia repair at seven institutions over the past 7-12 years. Demographics and the presence or absence of a jejunoileal atresia were recorded.Results: Four hundred eight patients with duodenal atresia were identified. The mean gestaational age was 36.3 ± 2.9 weeks, and the mean weight was 2.5 ± 0.8 kg. Mean age at operation was 19 days (range, 1-1314). There was a 28% incidence of trisomy 21. Two patients (0.5%) were identified as having a second intestinal atresia, and both were type IIIb. One patient was diagnosed at the time of duodenal atresia repair; the other was a delayed diagnosis. Both patients did well after repair.Conclusions: In this, the largest series of duodenal atresia patients compiled to date, the rate of a concomitant jejunoileal atresia is less than 1%. This low incidence is not high enough to mandate extensive inspection of the entire bowel in these patients, and a second atresia should not be a concern during laparoscopic repair of duodenal atresia