Assessing clinical pathological characteristics and gene expression patterns associated with hepatoid adenocarcinoma of the stomach.

OBJECTIVE: The objective of this study is to assess the clinical pathological attributes of Hepatoid Adenocarcinoma of the Stomach (HAS) and to delineate the differential diagnostic considerations about it. METHOD: The investigation involved analyzing 31 HAS cases using histomorphological assessment, immunohistochemical profiling, and relevant gene detection methodologies. RESULTS: Among the 31 HAS cases, 9 (29.0%) were of trabecular hepatoid adenocarcinoma of the stomach, 7 (22.6%) were of glandular hepatoid adenocarcinoma of the stomach, 4 (12.9%) were of nesting hepatoid adenocarcinoma of the stomach, 3 (9.7%) were of clear cell hepatoid adenocarcinoma of the stomach, and 8 (25.8%) were of diverse hepatoid adenocarcinoma of the stomach. Of these 31 cases, 24 were male, accounting for 77.4% of the cases. Serum alpha-fetoprotein (AFP) levels were notably elevated, with radioimmunoassay results reaching 1240 ng/ml; 28 out of 31 cases had AFP levels below 25 µg/l, accounting for 90.3%. Related genes: HER2 protein indicated positive expression on the cell membrane in 35.5% (11/31) of the cases; HER2 gene amplification detected by the FISH technique was 12.9% (4/31). Tumoral stromal lymphocytes exhibited a PD-1 positive expression rate of 58.1% (18/31). In gastric cancer tissues, the PD-L1 positive rate was 45.1% (14/31). CONCLUSION: HAS represents a distinctive subtype of gastric cancer with a propensity for mimicking other forms of tumors, underscoring the significance of discerning its unique histopathological attributes for accurate differential diagnosis and tailored therapeutic interventions.

Histopathological staging of atrophic lesions of gastric mucosa.

Objective: To study the histopathological staging of atrophic lesions of the gastric mucosa. Methods: Histology and immunohistochemistry were used to closely examine 2144 specimens of atrophic gastric mucosa that were taken from endoscopic biopsies. Results: When the gastric mucosa epithelium is affected by infection, chemical stimulation, immune factors, genetic factors, and other factors, it may cause an atrophy of gastric mucosa epithelium and a decrease in the number of glands, intestinal metaplasia, hyperplasia of smooth muscle fibers, and atrophy of stem cells in the proliferative zone. In this study, we characterized the above lesions as atrophic lesions of the gastric mucosa. Based on the morphological and histological characteristics of the lesion, as well as the law of cell proliferation and transformation during its occurrence and development, we propose five stages. We also noted the onset age, gender correlation, and histopathological characteristics of each stage of gastric mucosal atrophies. Conclusion: Understanding the pathological staging of gastric mucosal atrophy is essential for treating patients correctly and keeping track of changes in malignant cells. It is also very important in preventing the initiation of gastric cancer or from getting worse.

Histopathological staging and differential diagnosis of marginal zone lymphoma of gastric mucosa-associated lymphoid tissue.

The purpose of this study was to explore the histopathological staging and differential diagnosis of marginal zone lymphoma in gastric mucosa-associated lymphoid tissue (MALT lymphoma). We performed detailed histomorphology and immunohistochemistry investigations as well as genetic testing on endoscopic biopsy and endoscopic mucosal resection specimens from 18 patients with gastric MALT lymphoma. We found that gastric MALT lymphoma typically begins as a small, isolated area outside the lymphoid follicular mantle zone or proliferates in a multifocal, patchy manner, gradually spreads to the interfollicular zone, forming diffuse proliferation, invades the gastric mucosal glands, and infiltrates or proliferates into the center of peripheral reactive lymphoid follicles. Abnormally proliferating lymphocytes invade the surrounding lymphoid follicles, resulting in damage, atrophy, and disappearance of their normal follicles as well as of the gastric mucosa glands, forming diffuse proliferation. Redifferentiation and proliferation lead to the transformation of lymphocytes; that is, MALT transitions into highly invasive lymphoma. Based on our findings in this study, we propose the following five stages in the process of development and progression of gastric MALT lymphoma: the stage of cell proliferation outside the lymphoid follicular mantle zone; the stage of heterogeneous proliferative lymphoepithelial lesion; the stage of reactive lymphoid follicular implantation; the stage of lymphoid follicular clonal proliferation; and the stage of MALT transforming into highly invasive lymphoma. We examined the differential diagnosis of histopathological features at each stage. The clinicopathological staging of gastric MALT lymphoma can help clinicians provide accurate treatment and track malignant cell transformation, thus playing a significant role in controlling its development and progression.

Histopathological features of glandular atrophy of the lamina propria of the gastric mucosa during its occurrence and development.

OBJECTIVE: To explore the histopathological features of glandular atrophy of the lamina propria of gastric mucosa during its occurrence and development. METHOD: We performed detailed histological observation and immunohistochemical examination on the endoscopic biopsy and ESD endoscopic resection specimens of 896 patients with glandular atrophy of the lamina propria of gastric mucosa. The EnVision two-step method was used for immunohistochemical staining, and the slices were incubated with primary antibody CK7, CK20, villin, CDX2, MUC5AC, MUC6, p53 and ki-67. Hematoxylin staining was performed and observed under the microscope and statistically analyzed. RESULTS: In the initial stage of glandular atrophy of the lamina propria, the proliferation area of the deep gastric pits, and the isthmus and neck of the gastric glands are characterized by roughly normal structure of the glandular structure, increased mesenchyme, and widened space between glands. Subsequently, the gland becomes smaller in volume and less in number, especially at the base, in the gastric glandular part of the gastric unit. The disease at this stage has higher incidence, and occurs more often in the elderly who account for 64.0% (573/896) of our study group. The disease in this stage may exhibit some lesions that are physiologic (age-related degeneration) while others are pathological. Therefore, this condition is called simple glandular atrophy of the lamina propria of the gastric mucosa. When the gastric mucosal epithelium is subjected to infection or repeated infections, chemical stimuli, immune factors, and genetic factors, it can lead to the proliferation and transformation of stem cells in the proliferation area of the deep gastric pits, and the isthmus and neck of the gastric glands, forming single ducts, multiple ducts, or a proliferation of patchy cells. Then, atypical hyperplasia (intraepithelial neoplasia) presents, finally leading to gastric adenocarcinoma. CONCLUSION: Understanding the histopathological characteristics of glandular atrophy of the lamina propria of gastric mucosa is of great significance in controlling the occurrence and development of gastric cancer.

Clinicopathological features and differential diagnosis of gastric pleomorphic giant cell carcinoma.

The aim of this study was to investigate the clinicopathological features and differential diagnosis of gastric pleomorphic giant cell carcinoma. Histopathology, immunohistochemistry, and human epidermal growth factor receptor 2 (HER2) gene testing were conducted for seven cases of gastric pleomorphic giant cell carcinoma. In histomorphological terms, all seven cases involved pleomorphic giant cell carcinoma, accounting for more than 10% of the entire tumor, with pleomorphic spindle cells and giant cells mixed with various histomorphological structures of adenocarcinoma with high, intermediate, and low differentiation. There was large heterogeneity in the HER2 protein expression and HER2 gene amplification in the gastric pleomorphic giant cell carcinoma, and both levels of HER2 were focal in three cases, accounting for 42.9% (3/7). The mismatch repair gene proteins MLH1, MSH2, PMS2, and MSH6 were positive. Routine immunohistochemical markers, i.e., pan-cytokeratin, epithelial membrane antigen, villin, caudal-type homeobox 2, E-cadherin, and p53, were positive in the gastric pleomorphic giant cell carcinoma, while vimentin, calponin, smooth muscle actin, nestin, S-100, cluster of differentiation (CD) 99, desmin, and CD34 were focally expressed in both the spindle and the giant cells, with Ki-67-positive cells accounting for 70-80%. Gastric pleomorphic giant cell carcinoma presents multiple histomorphological features and is easily confused with various tumors. Clarifying the histopathological features of this type of tumor is important for differential diagnosis and precise treatment.

Advances in Cas12a-Based Amplification-Free Nucleic Acid Detection.

In biomedicine, rapid and sensitive nucleic acid detection technology plays an important role in the early detection of infectious diseases. However, most traditional nucleic acid detection methods require the amplification of nucleic acids, resulting in problems such as long detection time, complex operation, and false-positive results. In recent years, clustered regularly interspaced short palindromic repeats (CRISPR) systems have been widely used in nucleic acid detection, especially the CRISPR-Cas12a system, which can trans cleave single-stranded DNA and can realize the detection of DNA targets. But, amplification of nucleic acids is still required to further improve detection sensitivity, which makes Cas12a-based amplification-free nucleic acid detection methods a great challenge. This article reviews the recent progress of Cas12a-based amplification-free detection methods for nucleic acids. These detection methods apply electrochemical detection methods, fluorescence detection methods, noble metal nanomaterial detection methods, and lateral flow assay. Under various optimization strategies, unamplified nucleic acids have the same sensitivity as amplified nucleic acids. At the same time, the article discusses the advantages and disadvantages of each method and further discusses the current challenges such as off-target effects and the ability to achieve high-throughput detection. Amplification-free nucleic acid detection technology based on CRISPR-Cas12a has great potential in the biomedical field.

Early onset, development and histological features of gastric signet-ring cell carcinoma.

Objective: To explore the early onset, development and histological features of gastric signet-ring cell carcinoma (SRCC). Methods: Three hundred and sixty-two patients with differentiated adenocarcinoma with signet-ring cells were enrolled. Histomorphological and immunohistochemical features and patterns of the specimens were observed in detail. Results: Infection of the gastric mucosa, especially by Helicobacter pylori, can cause massive cell proliferation and transformation in the deep gastric foveola, the isthmus of the gastric gland, and the proliferative zone of the upper neck of the gland. Signet-ring-like heterocysts monoclonally proliferated after the redifferentiation and reproliferation, extending horizontally along the gastric foveola. Gastric foveolar-type SRCC grew infiltratively into the lamina propria of the mucosa and the submucosa, signet-ring cells could differentiate into undifferentiated adenocarcinoma with signet-ring cell differentiation, mucinous adenocarcinoma with signet-ring cell differentiation, gastric adenocarcinoma with signet-ring cell differentiation, and fundus gland adenocarcinoma with signet-ring cell differentiation. Conclusion: Early SRCC developed from the proliferative zones of the fundus of the gastric foveola and the neck of the gastric gland, growing horizontally along the gastric foveola. It developed into gastric adenocarcinoma with signet-ring cell differentiation after reproliferation and retransformation in the mucosa.

The occurrence, progression and development of four types of gastric mucosal atrophic lesions and their histopathological characteristics.

OBJECTIVE: To investigate the occurrence and development of gastric mucosal atrophic lesions and their histopathological characteristics. METHODS: Histopathological diagnosis and immunohistochemical staining using the EnVision two-step method were conducted on 1969 gastric mucosal atrophic lesions obtained from gastroscopic biopsy specimens. A total of 48-month three-stage endoscopic biopsy follow-ups were performed. RESULTS: When the gastric mucosal epithelium was affected by infection, chemical irritation, or immune or genetic factors, the gastric mucosal epithelium glands atrophied, the mucosa became thinner, the number of glands decreased, the intestinal epithelium progressed to metaplasia and smooth muscle fibre became hyperplasia. Such changes may lead to the proliferation and dysplasia of epithelial cells of the gastric mucosa and neoplastic hyperplasia in nature; this is referred to as gastric mucosal atrophic lesions in this study. According to this definition, the present study divided gastric mucosal atrophy into four types: (1) glandular atrophy of the lamina propria; (2) compensatory proliferative atrophy; (3) intestinal metaplasia atrophy; and (4) smooth muscle proliferative atrophy. The incidence rates of the above were 40.1% (789/1969), 14.3% (281/1969), 27.8% (547/1969) and 17.9% (352/1969), respectively. One- to 4-year follow-ups found that the changes were not significant and that the percentages of patients with disease exacerbation were 85.7% (1688/1969) and 9.8% (192/1969). The percentages of patients who developed low-grade intraepithelial neoplasia and high-grade intraepithelial neoplasia were 2.8% (55/1969) and 1.1% (21/1969), respectively; 0.7% (13/1969) of patients developed intramucosal cancer. CONCLUSION: Gastric mucosal atrophic lesions and histopathological staging are based on the morphological characteristics of gastric mucosal atrophy and the hypothesis of malignant transformation of cells during the occurrence and development of mucosal atrophy. Mastering pathological staging is beneficial to clinicians for enacting precise treatment and is important for reducing the incidence of gastric cancer.

The significance of the microlymphangiogenesis, microangiogenesis, and combined detection of programmed cell death-1 protein (PD-1)/ki67 in gastric cancer tissues.

PURPOSE: To investigate the relationship between the microlymphangiogenesis, microangiogenesis, and combined detection of the programmed cell death-1 protein (PD-1)/ki67 in patients with gastric cancer as well as the disease prognosis. METHODS: Immunohistochemistry was used to detect the microlymphatic density (MLD) and microvessel density (MVD) in the central and peripheral zones in 92 cases of gastric cancer, along with the number of PD-1- and ki67-positive tumor cells. RESULTS: The central zone of the gastric cancer tissue contained fewer atretic cord-like lymphatic vessels than the peripheral zone, while the peripheral zone contained an increased number of lymphatic vessels compared with the central zone. In most cases, the lumen was also dilated. Compared with the MLD in the peripheral zone, the MLD in central zone was significantly decreased. Compared with the number of PD-1-positive cells in the peripheral zone, the number of PD-1-positive cells in the central zone was significantly decreased, and compared with the number of ki67-positive cells in the peripheral zone. The differences in the microlymphangiogenesis, microangiogenesis, and the number of PD-1- and ki67-positive cells among the different histological types were not statistically significant. The microlymphangiogenesis, microangiogenesis, and PD-1- and ki67-positive cells were significantly decreased in the gastric cancer tissues from the patients in stages T1 and T2 compared with the gastric cancer tissues from the patients in stages T3 and T4. CONCLUSIONS: The detection of the MLD and MVD as well as the positive expression of PD-1 and ki67 in gastric cancer tissue are important reference indicators for judging the prognosis of gastric cancer.

Computer analysis of abnormal proliferation and transformation cells in gastric mucosa and its clinical significance.

To investigate the image computer analysis of abnormally proliferating transformed cells of gastric mucosa and its clinical significance. The pathological pictures of gastric adenomatous polyp cells, abnormally proliferating altered cells, and tubular adenocarcinoma cells in the stomach mucosa were assessed by image computer method on a total of 96 gastroscopic biopsy and ESD resection specimens. The data of cytoplasmic area, nuclear area, nuclear-cytoplasmic ratio, nuclear factor and N-heterotypic index of gastric adenomatous polyps, abnormal proliferative transformation and gastric intramucosal tubular adenocarcinoma were collected, and the mean, standard deviation and variance were calculated respectively. Standard Error, Maximum, Minimum Parameters and Statistical Structure. There were substantial discrepancies between gastric mucosal gastric adenomatous polyp cells and gastric mucosal abnormally proliferating transformed cells, according to the five data in the abnormal cells in the stomach mucosal proliferation area (p < 0.01); There was no significant difference between cells (p > 0.05). Computer analysis of cell images can provide quantitative values for the pathological diagnosis of gastric adenomatous polyp cells, abnormally proliferating transformed cells and tubular adenocarcinoma cells in the gastric mucosa, especially the degree of atypical proliferation. The monitoring of abnormally proliferated and transformed cells in gastric mucosa is of great significance for clinicians to accurately treat and track cell transformation, and to control the occurrence and development of gastric adenocarcinoma.

Histopathological Features of Helicobacter pylori Infection in Gastric Mucosa.

Objective: To investigate the histopathological characteristics of Helicobacter pylori (Hp) infection in the gastric mucosa in the process from occurrence to intraepithelial neoplasia. Methods: Specimens obtained from the endoscopic biopsy and endoscopic submucosal dissection of 2457 cases of gastric Hp infection were observed and assessed in detail using histology and immunohistochemistry techniques. The condition was divided according to the histopathological characteristics of gastric mucosal damage caused by Hp infection. The histopathological characteristics and immunophenotype of each stage were subsequently elucidated. Results: Helicobacter pylori is initially implanted in the mucus layer covered by the epithelium on the surface of the gastric mucosa. It then selectively adheres to the cytoplasm of the surface mucus cells, which makes the oval and spherical particles containing mucus that is wrapped by the bounded membrane in the cytoplasm on the nucleus of the surface mucus cells disappear, while the cytoplasm undergoes spiderweb-like vacuolar degeneration. This leads to the proliferation and transformation of the surface mucous cells before developing into intraepithelial neoplasia. In the process of histomorphology, mucosal ulcers, mucosal lymphoid tissue proliferation, gland atrophy, intestinal epithelial metaplasia, mucosa-associated lymphoid tissue lymphoma, and adenocarcinoma may occur. In this study, the condition was divided into five stages according to the histopathological characteristics of gastric mucosal damage caused by Hp infection, as well as the degree of gastric mucosal damage and involvement depth as follows: the mucus infection stage, the surface epithelial cell infection stage, the lamina propria lesion stage, the mucosal atrophy stage, and the intraepithelial neoplasia stage. Conclusion: Understanding the histopathological characteristics of gastric Hp infection in terms of its occurrence and development into intraepithelial neoplasia is conducive to the precise treatment and tracking of malignant cell transformation, and is of great significance in controlling the occurrence and development of gastric cancer.

Exendin-4 alleviates ß-Amyloid peptide toxicity via DAF-16 in a Caenorhabditis elegans model of Alzheimer's disease.

Epidemiological analyses indicate that type 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer's disease (AD). They share common pathophysiological mechanisms. Thus, it has been increasingly suggested that several anti-T2DM drugs may have therapeutic potential in AD. Exendin-4, as a glucagon-like peptide-1 (GLP-1) receptor agonist, is an approved drug used to treat T2DM. In this research, the neuroprotective effect of Exendin-4 was investigated for the first time using transgenic Caenorhabditis elegans. Our results demonstrated that Exendin-4 attenuated the amyloid-ß (1-42) (Aß1-42) toxicity via multiple mechanisms, such as depressing its expression on protein and mRNA and reducing Aß (1-42) accumulation. Exendin-4 at 0.5 mg/ml had been shown to extend life by 34.39% in CL4176 and delay the onset of paralysis in CL4176 and CL2006 which were increased by 8.18 and 8.02%, respectively. With the treatment of Exendin-4, the nuclear translocation of DAF-16 in the transgenic nematode TJ356 was enhanced. Superoxide dismutase-3 (SOD-3), as a downstream target gene regulated by DAF-16, was upregulated on mRNA level and activity. The reactive oxygen species (ROS) level was decreased. In contrast, we observed that the ability of Exendin-4 to regulate SOD was decreased in CL4176 worms with the DAF-16 gene silenced. The activity of SOD and the mRNA level of sod-3 were downregulated by 30.45 and 43.13%, respectively. Taken together, Exendin-4 attenuated Aß (1-42) toxicity in the C. elegans model of AD via decreasing the expression and the accumulation of Aß (1-42). Exendin-4 exhibited the ability of antioxidant stress through DAF-16. With continuous research, Exendin-4 would become a potential therapeutic strategy for treating AD.

The Histopathological Types and Distribution Characteristics of Gastric Mixed Tumors.

Objective: The present study aimed to investigate the histopathological types and distribution characteristics of gastric mixed tumors. Methods: Detailed histological observations, together with related immunohistochemical and genetic tests, were analyzed on 960 surgically resected samples in 6 hospitals with gastric mixed tumors from May 2017 to May 2021 in this retrospective study. Results: Epithelial-derived tumors accounted for 80.10% (769/960) of the gastric mixed tumor samples studied, and tumors of different tissue origins accounting for 10.83% (104/960), mesenchymal-derived tumors accounting for 6.25% (60/960), neuroendocrine tumors accounting for 2.40% (23/960), and lymphoma accounting for 0.42% (4/960). The histological types of gastric mixed tumors identified as most commonly were epithelial originated, followed by mixed tumors of different tissue originated, then mixed neuroendocrine, lymphoma, and mesenchymal originated in sequence. The histological number of gastric mixed tumors was ≤ 3 in 83.23% (799/960) of cases and > 4 in 16.77% (161/960) of cases. The mixed histological patterns of gastric mixed tumors were divided into three types: those with tumor cells interspersed with each other, those with incomplete fibrous tissue separation, and those without fibrous tissue separation. The gene target characteristics of gastric mixed tumors were the existence of multi-gene mutation, including human epidermalgrowth factor receptor-2 (HER2) gene amplification, key result areas (K-ras) and platelet-derived growth factor receptor alpha (PDGFRA). Conclusion: Gastric mixed tumors should be adequately sampled, each piece of tissue should be involved in the morphological proportional division of the tumor, and any independent histological component should be written into the pathological examination report.

How Does Helicobacter pylori Infection Cause Gastric Mucosal Atrophy.

Objective: To investigate the occurrence and development of gastric mucosal atrophy due to Helicobacter pylori (Hp) infection and the accompanying histomorphological features. Methods: Detailed histological observations and immunohistochemical examinations were conducted via 197 endoscopic biopsies and endoscopic submucosal dissection specimens of gastric mucosal atrophic lesions with gastric Hp infection. Detailed observation was made of columnar cells in the proliferative region of the deep gastric pit and the isthmus of the gastric gland, as well as the upper part of the glandular cervix. Results: The infection of the gastric mucosa by Hp firstly led to the proliferative disorder of stem cells in the normal proliferative region of the gastric mucosa. This caused substantial propagation of cells in the proliferative region of the deep gastric pit and the isthmus of the gastric gland, as well as the upper part of the glandular cervix, as a means to replenish the damaged surface mucus cells. However, the propagation of stem cells in the proliferative region was insufficient for downward migration, and the normal physiological process of differentiation into fundic/pyloric gland cells was disrupted, resulting in glandular atrophy of the intrinsic layer of the gastric mucosa. Persistent Hp infection and disruption of stem cell proliferation in the proliferative region subsequently resulted in extensive segmental hyperplasia of the gastric mucosa and glandular atrophy of the lamina propria. Conclusion: The occurrence, development, and histomorphological features of gastric mucosal atrophy due to gastric Hp infection provide a reliable pathological basis for precise treatment by clinicians and are of great significance for controlling the development of gastric cancer.

Research on the Histological Features and Pathological Types of Gastric Adenocarcinoma With Mucinous Differentiation.

Objective: To discuss the histological features, pathological types, and prognosis of gastric adenocarcinoma with mucinous differentiation. Methods: Specimens of 189 cases of gastric adenocarcinoma with mucinous differentiation were collected for detailed histomorphology, immunohistochemistry, fluorescence in situ hybridization, and follow-up. Results: In accordance with the morphological and histological structural features of the cancer cells as well as the area ratio of the mucus, gastric adenocarcinoma with mucinous differentiation was divided into four types, namely pure mucinous carcinoma, intraductal papillary mucinous carcinoma, signet ring cell type mucinous carcinoma, and mixed cell type mucinous carcinoma. Based on the macroscopic types according to Bormann's classification, pure mucinous carcinoma was mostly Type I, intraductal papillary mucinous carcinoma was mostly Type II, signet ring cell type mucinous carcinoma was mostly Type IV, and mixed cell type mucinous carcinoma was mostly Type III. The 5-year survival rate was 69.2, 64.2, 0, and 31.5%, respectively. There was a statistical difference in the lymph node metastasis rate and survival rate of the four carcinoma types. The invasion features of pure mucinous carcinoma entailed penetrating corrosively in a push-in form, without blood vessel or lymphatic metastasis and with few lymphocytes and lymphatic nodules in the marginal area. Thus, there was little lymph node metastasis and invasion of nerves. The HER2 protein expression rate was 40.2% (76/189), the HER2 gene amplification detected by FISH technology was 16.9% (32/189). Conclusion: The independent histological type, four subtypes, and histopathological classification of gastric mucinous adenocarcinoma are important for the prognosis evaluation and precise treatment of this disease.

Follow-up analysis and histopathological study of gastric mucosa in patients with Helicobacter pylori infection.

OBJECTIVE: To investigate the histomorphological characteristics of the gastric mucosa and the prognosis in patients with Helicobacter pylori infection. METHODS: Progressive damage to the gastric mucosa was examined by immunohistochemistry in 2294 patients with H. pylori infection and follow-up information was analyzed. RESULTS: H. pylori initially colonized the mucus layer covered by the gastric mucosa epithelium, then selectively adhered to and destroyed the surface mucus cells causing intra-gastric and extra-gastric lesions. Gastric mucosal damage induced by H. pylori was divided into five stages according to the depth of H. pylori invasion and degree of lesion deterioration: mucilaginous, surface mucocellular, lamina propria lesion, mucosal atrophy, and intraepithelial neoplasia stages. Morphological follow-up analysis revealed no significant difference in 6-month curative effects between stage I and stage II, but significant differences were found between stages II and III, stages III and IV, and between stages IV and stage V, respectively. CONCLUSIONS: This novel staging strategy may be a valuable tool for diagnosing and predicting the results of gastric mucosal damage induced by H. pylori infection.

Clinicopathological features of gastric inflammatory myofibroblastic tumor: Report of five cases.

The present study reported on the histomorphological observations and immunohistochemical features of five cases of gastric inflammatory myofibroblastic tumor (IMT). Loosely arranged fat fusiform myofibroblast-fibroblasts and diffusely or patchily distributed inflammatory cells, which formed a diverse morphological structure, were observed. In the mucous vascular structure, mucoid or collagenous areas, fibromatosis- or scar-like lesions were generally <10 mm in size and both had diffuse or patchy plasma cells, lymphocytes and other inflammatory-cell infiltration backgrounds. The immunophenotype was vimentin- and smooth muscle actin-positive with pan-cytokeratin, desmin and calponin expression and CD34-positive foci; furthermore, three cases were positive for anaplastic lymphoma kinase expression. Gastric IMT is rare, with unique histopathological changes and corrosion-like invasion of the smooth muscle of the stomach wall, blood vessels, nerves and adipose tissue. It should be differentiated from a variety of spindle cell tumor types and tumor-like lesions.

GhUBX controlling helical growth results in production of stronger cotton fiber.

Cotton fiber is an excellent model for studying plant cell elongation and cell wall biogenesis as well because they are highly polarized and use conserved polarized diffuse growth mechanism. Fiber strength is an important trait among cotton fiber qualities due to ongoing changes in spinning technology. However, the molecular mechanism of fiber strength forming is obscure. Through map-based cloning, we identified the fiber strength gene GhUBX. Increasing its expression, the fiber strength of the transgenic cotton was significantly enhanced compared to the receptor W0 and the helices number of the transgenic fiber was remarkably increased. Additionally, we proved that GhUBX regulates the fiber helical growth by degrading the GhSPL1 via the ubiquitin 26S-proteasome pathway. Taken together, we revealed the internal relationship between fiber helices and fiber stronger. It will be useful for improving the fiber quality in cotton breeding and illustrating the molecular mechanism for plant twisted growth.

Histopathological classification and follow-up analysis of chronic atrophic gastritis.

BACKGROUND: The pathological diagnosis and follow-up analysis of gastric mucosal biopsy have been paid much attention, and some scholars have proposed the pathological diagnosis of 12 kinds of lesions and accompanying pathological diagnosis, which is of great significance for the treatment of precision gastric diseases, the improvement of the early diagnosis rate of gastric cancer, and the reduction of missed diagnosis rate and misdiagnosis rate. AIM: To perform a histopathological classification and follow-up analysis of chronic atrophic gastritis (CAG). METHODS: A total of 2248 CAG tissue samples were collected, and data of their clinical characteristics were also gathered. Based on these samples, the expression levels of Mucin 1 (MUC1), MUC2, MUC5AC, and MUC6 in CAG tissue were tested by immunohistochemical assay. Moreover, we followed these patients for up to four years. The difference between different stages of gastroscopic biopsy was observed. RESULTS: Through observation, it is believed that CAG should be divided into four types, simple type, hyperplasia type, intestinal metaplasia (IM) type, and intraepithelial neoplasia (IEN) type. Simple CAG accounted for 9.1% (205/2248), which was more common in elderly people over 60 years old. The main change was that the lamina propria glands were reduced in size and number. Hyperplastic CAG accounted for 29.1% (654/2248), mostly occurring between 40 and 60 years old. The main change was that the lamina propria glands were atrophy accompanied by glandular hyperplasia and slight expansion of the glands. IM CAG accounted for 50.4% (1132/2248), most of which increased with age, and were more common in those over 50 years. The atrophy of the lamina propria glands was accompanied by significant IM, and the mucus containing sialic acid or sulfate was distinguished according to the nature of the mucus. The IEN type CAG accounted for 11.4% (257/2248), which developed from the previous types, with severe gland atrophy and reduced mucus secretion, and is an important precancerous lesion. CONCLUSION: The histological typing of CAG is convenient to understand the property of lesion, determine the follow-up time, and guide the clinical treatment.