Purpose: This narrative review elucidates the complex pathogenesis, key risk factors, and effective management strategies for postoperative delayed gastric emptying (DGE) following distal gastrectomy with D2 lymphadenectomy, a definitive procedure for middle and lower gastric cancer. It also explores opportunities for improved prevention and innovative treatment options. Current concept: DGE significantly disrupts gastric motility and presents with symptoms such as early satiety, postprandial fullness, nausea, vomiting, and gastric atony. Although rarely fatal, DGE hampers oral intake, prolongs hospital stays, and diminishes quality of life. Current evidence indicates that DGE is a multifactorial disorder resulting from an interplay of vagal nerve disruption, damage to smooth muscle and interstitial cells of Cajal, imbalances in gastrointestinal hormones, and postoperative gut microbiome dysbiosis. Patient-specific factors, including advanced age, poor nutritional status, diabetes, and preoperative pyloric obstruction, along with surgical factors (most notably Billroth II reconstruction), further increase the risk of DGE. Management involves dietary modifications, prokinetic agents (such as metoclopramide and selective 5-HT4 agonists like prucalopride), and gastric decompression. Conclusion DGE is a challenging complication following gastrectomy that demands a deeper understanding of its underlying mechanisms to improve patient outcomes. Emerging therapies, including microbiota modulation and advanced pharmacological agents, offer promising new treatment avenues.

Purpose: This narrative review elucidates the complex pathogenesis, key risk factors, and effective management strategies for postoperative delayed gastric emptying (DGE) following distal gastrectomy with D2 lymphadenectomy, a definitive procedure for middle and lower gastric cancer. It also explores opportunities for improved prevention and innovative treatment options. Current concept: DGE significantly disrupts gastric motility and presents with symptoms such as early satiety, postprandial fullness, nausea, vomiting, and gastric atony. Although rarely fatal, DGE hampers oral intake, prolongs hospital stays, and diminishes quality of life. Current evidence indicates that DGE is a multifactorial disorder resulting from an interplay of vagal nerve disruption, damage to smooth muscle and interstitial cells of Cajal, imbalances in gastrointestinal hormones, and postoperative gut microbiome dysbiosis. Patient-specific factors, including advanced age, poor nutritional status, diabetes, and preoperative pyloric obstruction, along with surgical factors (most notably Billroth II reconstruction), further increase the risk of DGE. Management involves dietary modifications, prokinetic agents (such as metoclopramide and selective 5-HT4 agonists like prucalopride), and gastric decompression. Conclusion DGE is a challenging complication following gastrectomy that demands a deeper understanding of its underlying mechanisms to improve patient outcomes. Emerging therapies, including microbiota modulation and advanced pharmacological agents, offer promising new treatment avenues.

Purpose: This narrative review elucidates the complex pathogenesis, key risk factors, and effective management strategies for postoperative delayed gastric emptying (DGE) following distal gastrectomy with D2 lymphadenectomy, a definitive procedure for middle and lower gastric cancer. It also explores opportunities for improved prevention and innovative treatment options. Current concept: DGE significantly disrupts gastric motility and presents with symptoms such as early satiety, postprandial fullness, nausea, vomiting, and gastric atony. Although rarely fatal, DGE hampers oral intake, prolongs hospital stays, and diminishes quality of life. Current evidence indicates that DGE is a multifactorial disorder resulting from an interplay of vagal nerve disruption, damage to smooth muscle and interstitial cells of Cajal, imbalances in gastrointestinal hormones, and postoperative gut microbiome dysbiosis. Patient-specific factors, including advanced age, poor nutritional status, diabetes, and preoperative pyloric obstruction, along with surgical factors (most notably Billroth II reconstruction), further increase the risk of DGE. Management involves dietary modifications, prokinetic agents (such as metoclopramide and selective 5-HT4 agonists like prucalopride), and gastric decompression. Conclusion DGE is a challenging complication following gastrectomy that demands a deeper understanding of its underlying mechanisms to improve patient outcomes. Emerging therapies, including microbiota modulation and advanced pharmacological agents, offer promising new treatment avenues.

Purpose: This narrative review elucidates the complex pathogenesis, key risk factors, and effective management strategies for postoperative delayed gastric emptying (DGE) following distal gastrectomy with D2 lymphadenectomy, a definitive procedure for middle and lower gastric cancer. It also explores opportunities for improved prevention and innovative treatment options. Current concept: DGE significantly disrupts gastric motility and presents with symptoms such as early satiety, postprandial fullness, nausea, vomiting, and gastric atony. Although rarely fatal, DGE hampers oral intake, prolongs hospital stays, and diminishes quality of life. Current evidence indicates that DGE is a multifactorial disorder resulting from an interplay of vagal nerve disruption, damage to smooth muscle and interstitial cells of Cajal, imbalances in gastrointestinal hormones, and postoperative gut microbiome dysbiosis. Patient-specific factors, including advanced age, poor nutritional status, diabetes, and preoperative pyloric obstruction, along with surgical factors (most notably Billroth II reconstruction), further increase the risk of DGE. Management involves dietary modifications, prokinetic agents (such as metoclopramide and selective 5-HT4 agonists like prucalopride), and gastric decompression. Conclusion DGE is a challenging complication following gastrectomy that demands a deeper understanding of its underlying mechanisms to improve patient outcomes. Emerging therapies, including microbiota modulation and advanced pharmacological agents, offer promising new treatment avenues.

Purpose: This narrative review elucidates the complex pathogenesis, key risk factors, and effective management strategies for postoperative delayed gastric emptying (DGE) following distal gastrectomy with D2 lymphadenectomy, a definitive procedure for middle and lower gastric cancer. It also explores opportunities for improved prevention and innovative treatment options. Current concept: DGE significantly disrupts gastric motility and presents with symptoms such as early satiety, postprandial fullness, nausea, vomiting, and gastric atony. Although rarely fatal, DGE hampers oral intake, prolongs hospital stays, and diminishes quality of life. Current evidence indicates that DGE is a multifactorial disorder resulting from an interplay of vagal nerve disruption, damage to smooth muscle and interstitial cells of Cajal, imbalances in gastrointestinal hormones, and postoperative gut microbiome dysbiosis. Patient-specific factors, including advanced age, poor nutritional status, diabetes, and preoperative pyloric obstruction, along with surgical factors (most notably Billroth II reconstruction), further increase the risk of DGE. Management involves dietary modifications, prokinetic agents (such as metoclopramide and selective 5-HT4 agonists like prucalopride), and gastric decompression. Conclusion DGE is a challenging complication following gastrectomy that demands a deeper understanding of its underlying mechanisms to improve patient outcomes. Emerging therapies, including microbiota modulation and advanced pharmacological agents, offer promising new treatment avenues.

BACKGROUND: Hypoxic pulmonary vasoconstriction (HPV) is unique to pulmonary circulation. Recent hypotheses have emerged indicating that O2 levels per se can regulate ion channel activity. The modulation of both cation channels differs according to the conduit or resistance pulmonary vessel type. However, it is not yet studied that the cation channel blocker has the same effect in an animal experimental model, which can exclude several factors that may influence on HPV. The purpose of the present study was, therefore, to determine the effect of nonspecific cation blocker, Gadolinium, on HPV in a rabbit model of isolated lung perfusion. METHODS: In adult white rabbits (n = 6), lungs were isolated and perfused with the constant pulmonary perfusate flow. Acid-base status and electrolytes of perfusate also constantly maintained. Thirty minutes after, baseline hypoxic pulmonary vasoconstriction (HPV) was measured as the difference of pulmonary artery pressure between a period of 21% normoxic gas inhalation and that of 3% hypoxic gas inhalation. After another thirty minutes, Gadolinium 50microgram were mixed to the perfusate, and then HPV were measured three times. After then Gadolinium 100, 200, 400microgram were mixed to the perfusate and HPV were measured. RESULTS: Gadolinium decreased the HPV response according to the dose. The ED50 of the response was 143microgram/100 ml. CONCLUSIONS: The regulation of HPV is based on the cation channel in the isolated rabbit lung.
Adult ; Animal Experimentation ; Electrolytes ; Gadolinium* ; Humans ; Inhalation ; Ion Channels ; Lung* ; Perfusion ; Pulmonary Artery ; Pulmonary Circulation ; Rabbits ; Vasoconstriction*

PURPOSE: The aim of this study was to evaluate the preoperative and postoperative nutritional statuses of patients with gastric cancer and to investigate the nutritional factors that are correlated with perioperative complications. MATERIALS AND METHODS: From January 2008 to Jun 2008, 669 patients who underwent curative gastrectomy were enrolled in a retrospective study. To evaluate the changes of their nutritional status preoperatively and postoperatively, we measured the total lymphocyte count, the serum albumin, the body weight change and the BMI. The nutritional factors correlated with short-term postoperative complications were analyzed. RESULTS: The total lymphocyte count and serum albumin decreased from the first preoperative day to the 5th day after operation, but they tended to increase and approach the normal range 6 months after operation. The only factor correlated with the short-term postoperative complications (defined as the ones that occurred for 30 days) was the serum albumin checked on the 5th day after operation. CONCLUSION: Low serum albumin on the 5th day after operation was correlated with postoperative short-term complications. Serum albumin can be the preoperative statistical parameter that can predict the occurrence of postoperative complications.
Body Weight Changes ; Gastrectomy ; Humans ; Lymphocyte Count ; Nutrition Assessment ; Nutritional Status ; Postoperative Complications ; Reference Values ; Retrospective Studies ; Serum Albumin ; Stomach Neoplasms

PURPOSE: The aim of this study was to analyze the trend of the literature reported in the Journal of Korean Gastric Cancer Association (JKGCA) and the Journal of Korean Surgical Society (JKSS) in order to suggest new directions for the future studies on gastric cancer. MATERIALS AND METHODS: The papers published in the Journal of Korean Gastric Cancer Association (JKGCA) and the Journal of Korean Surgical Society (JKSS) between 2001 and 2008 were compared and summarized in terms of the following categories, retrospective study, prospective study, case report, biomolecular study, genetic study, tumor marker study, review article, and report. RESULTS: For recent 8 years, while the number of review articles in JKSS had initially increased, gradually fallen down and recently increased again, only a few (only 6 publications) in JKGCA have been published. The number of case reports in JKSS has gradually increased and fallen down. On the other hand, a few of case reports (1~3 publications) has been annually published in JKSS. Uniquely, reports were published only in JKGCA with the noticeable increase during the period from 2004 to 2005. For retrospective studies, in JKGCA the number started off very high and decreased, and finally increased again (U-shaped), whereas it had a bell-shaped trend in JKSS. The number of prospective studies in JKGCA had a bell-shaped trend, but the one in JKSS continued to decrease. Few papers of molecular biologic study, tumor marker study and genetic study had been published in both journals. CONCLUSION: We concluded that the transition from retrospective studies to prospective studies as well as a comprehensive multi-disciplinary team management of a clinical research would represent a desirable strategy in gastric cancer research.
Hand ; Korea ; Stomach Neoplasms

RAS guanyl-releasing protein 3 (RasGRP3), a member of the Ras subfamily of GTPases, functions as a guanosine triphosphate (GTP)/guanosine diphosphate (GDP)-regulated switch that cycles between inactive GDP- and active GTP-bound states during signal transduction. Various growth factors enhance hepatocellular carcinoma (HCC) proliferation via activation of the Ras/Raf-1/ extracellular signal-regulated kinase (ERK) pathway, which depends on RasGRP3 activation. We investigated the relationship between polymorphisms in RasGRP3 and progression of hepatitis B virus (HBV)-infected HCC in a Korean population. Nineteen RasGRP3 SNPs were genotyped in 206 patients with chronic liver disease (CLD) and 86 patients with HCC. Our results revealed that the T allele of the rs7597095 SNP and the C allele of the rs7592762 SNP increased susceptibility to HCC (OR=1.55, p=0.04 and OR=1.81~2.61, p=0.01~0.03, respectively). Moreover, patients who possessed the haplotype (ht) 1 ( A-T-C-G) or diplotype (dt) 1 ( ht1/ht1) variations had increased susceptibility to HCC (OR=1.79 ~2.78, p=0.01~0.03). In addition, we identified an association between haplotype1 (ht1) and the age of HCC onset; the age of HCC onset are earlier in ht1 +/+ than ht1 +/- or ht1 -/- (HR=0.42~0.66, p=0.006~0.015). Thus, our data suggest that RasGRP3 SNPs are significantly associated with an increased risk of developing HCC.
Alleles ; Carcinoma, Hepatocellular ; GTP Phosphohydrolases ; Guanosine Triphosphate ; Haplotypes ; Hepatitis B virus ; Humans ; Intercellular Signaling Peptides and Proteins ; Liver ; Liver Diseases ; Phospholipase C gamma ; Phosphotransferases ; Polymorphism, Single Nucleotide ; Polyphosphates ; Signal Transduction

To investigate the neuroprotective effects of bovine colostrums (BC), we evaluate the ability of consuming BC after focal brain ischemia/reperfusion injury rat model to reduce serum cytokine levels and infarct volume, and improve neurological outcome. Sprague-Dawley rats were randomly divided into 4 groups; one sham operation and three experimental groups. In the experimental groups, MCA occlusion (2 h) and subsequent reperfusion (O/R) were induced with regional cerebral blood flow monitoring. One hour after MCAO/R and once daily during the experiment, the experimental group received BC while the other groups received 0.9% saline or low fat milk (LFM) orally. Seven days later, serum pro-inflammatory cytokine (IL-1beta, IL-6, and TNF-alpha) and anti-inflammatory cytokine (IL-10) levels were assessed. Also, the infarct volume was assessed by using a computerized image analysis system. Behavioral function was also assessed using a modified neurologic severity score and corner turn test during the experiment. Rats receiving BC after focal brain I/R showed a significant reduction (-26%/-22%) in infarct volume compared to LFM/saline rats, respectively (P < 0.05). Serum IL-1beta, IL-6, and TNF-alpha levels were decreased significantly in rats receiving BC compared to LFM/saline rats (P < 0.05). In behavioral tests, daily BC intake showed consistent and significant improvement of neurological deficits for 7 days after MCAO/R. BC ingestion after focal brain ischemia/reperfusion injury may prevent brain injury by reducing serum pro-inflammatory cytokine levels and brain infarct volume in a rat model.
Animals ; Brain ; Brain Injuries ; Colostrum ; Cytokines ; Eating ; Interleukin-6 ; Milk ; Neuroprotective Agents ; Rats ; Rats, Sprague-Dawley ; Reperfusion ; Salicylamides ; Tumor Necrosis Factor-alpha