幽门螺杆菌感染对胃酸及胃液氨浓度的影响

目的 :探讨幽门螺杆菌 (Hp)感染对胃酸分泌及氨浓度的影响以及十二指肠 (DU)的关系。方法 :对DU患者 ,Hp根治前后的胃液pH ,空腹胃酸及氨浓度之间的关系进行研究。结果 :Hp阳性的UC患者其空腹胃酸、氨浓度显著高于正常对照组 (P <0 0 5 ) ,而根除Hp后 ,空腹胃酸显著下降 ,接近正常水平 (P >0 0 5 ) ,氨浓度明显下降。结论 :Hp感染使DU患者胃酸分泌增多 ,二者之间的相互作用在DU的发病中占有重要地位。     

奥美拉唑与呋喃唑酮及阿莫西林联用治疗幽门螺杆菌阳性十二指肠肠溃疡的疗效观察

目的：观察奥美拉联用呋喃唑酮及阿莫西林治疗幽门螺杆菌(Hp)阳性十二指肠溃疡的临床疗效。方法：对45例经胃镜活检证实的Hp阳性十二指肠溃疡应用奥美拉唑20mg Bid 呋喃唑酮0．2g Bid 阿莫西林1．0g Bid,疗程1w。结果：45例病例中,42例愈合,40例根除,7d疼痛缓解率为87％。结论：呋喃唑酮三联疗法能有效地根除Hp,且不良反应少,疗效高,病人依从性好,价格适中,是较理想的方案,值得进一步尝试。     

The role of luminal factors in the recovery of gastric function and behavioral changes after chronic Helicobacter pylori infection

The role of chronic infections, such as Helicobacter pylori (Hp), to produce sustained changes in host physiology remains controversial. In this study, we investigate whether the antigenic or bacterial content of the gut, after Hp eradication, influences the changes in gut function induced by chronic Hp infection. Mice were infected with Hp for 4 mo and then treated with antibiotics or placebo for 2 wk. Gastric emptying was measured using videofluoroscopy, feeding behavior using a 24-h feeding system, and intestinal permeability using an isolated jejunal segment arterially perfused with an artificial oxygen carrier, hemoglobin vesicles. Immune responses were assessed by CD3(+) cell counts and anti-Hp antibodies using ELISA. To determine the role of luminal factors in host physiology posteradication, groups of mice received the probiotics containing Lactobacillus rhamnosus R0011 and L. helveticus R0052 or placebo for 2 wk or crude Hp antigen weekly for 2 mo. Chronic Hp infection was associated with delayed gastric emptying, increased intestinal permeability, and increased gastric CD3(+) cell counts. Hp-induced altered feeding patterns did not reverse after eradication. Probiotics accelerated the recovery of paracellular permeability and delayed gastric emptying, improved the CD3(+) cell counts, and normalized altered feeding patterns posteradication. Hp antigen resulted in increased anti-Hp antibodies and increased CD3(+) cell counts in the stomach and delayed recovery of gastric function. Our results suggest that the bacterial content of the gut, as well as the presence of relevant antigens, influences the rate of recovery of host pathophysiology induced by chronic Hp infection. These changes do not seem to occur in association with modulation of intestinal permeability.     

Genetic factors in the development of gastric precancerous lesions--a role of Helicobacter pylori ?

Helicobacter pylori is believed to predispose to gastric cancer by inducing gastric precancerous alterations. There is a well known predisposition to gastric cancer and the risk of developing it is greater in relatives of patients with familial cases of this malignancy. The aim of this study was to determine the prevalence of gastric precancerous lesions (atrophy and intestinal metaplasia) and their association with Hp infection in first-degree relatives in patients with noncardia gastric cancer. METHODS: Hp status and gastric histology assessed by upper gastrointestinal endoscopy, biopsies from the antral and body region, the rapid urease test and staining for Hp, inflammation, activity, atrophy and intestinal metaplasia (prevalence and grading) were studied in 108 first-degree relatives of patients with noncardia gastric cancer and compared with 73 controls with mild non-ulcer dyspepsia who had no cancer relatives and were examined in the same way. RESULTS: subjects with and without cancer relatives had a similar prevalence of Hp infection (49 vs. 47%). Endoscopy revealed a few asymptomatic duodenal ulcers and small hiatus hernias in Hp positive subjects of both groups. Hp positive relatives of gastric cancer had a markedly higher prevalence of atrophy than those with Hp negativity without cancer relatives (29 vs. 9%) and those with Hp negativity and cancer relatives (29 vs. 3%. Prevalence of intestinal metaplasia was also higher in those with Hp positivity and cancer relatives than in those without cancer relatives (15 vs. 5% and was not present in Hp negative subjects with cancer relatives. Inflammation and activity showed similar scores in subjects with and without cancer relatives with higher scores in both Hp positive groups. The prevalence of precancerous lesions in the relatives of gastric cancer was nearly always confined to those with Hp positivity. One year after eradication the prevalence of atrophy in cancer relatives decreased from 29 to 14%; prevalence of intestinal metaplasia remained without substantial changes. Scores for inflammation and activity were also lower after eradication. CONCLUSIONS: First-degree relatives of patients with gastric cancer have an increased prevalence of gastric precancerous abnormalities which are strongly confined to those with Hp infection. Eradication of Hp in these subjects with cancer relatives reduces the prevalence of precancerous lesions (atrophy) and grades of inflammation and activity. In view of these results, eradication of Hp should be offered to such subjects.     

四联疗法和序贯疗法治疗服用非甾体类消炎药人群幽门螺杆菌感染的临 床对照研究

目的:对比四联疗法和序贯疗法对根除服用非甾体类消炎药(NSAID)人群幽门螺杆菌(Hp),改善其消化道不良症状及促进消化性溃疡愈合的临床效果。方法:对有消化不良症状的服用非甾体类消炎药物患者行胃镜检查、快速尿激酶及13C呼气试验检查,将155例幽门螺杆菌阳性合并有慢性胃炎或消化性溃疡患者作为研究对象,随机分为两组,A组采用四联疗法,B组采用序贯疗法。A组予雷贝拉唑+克拉霉素+阿莫西林+枸橼酸铋钾治疗10天;B组前5天予雷贝拉唑+阿莫西林,后5天予雷贝拉唑+克拉霉素+甲硝唑。治疗结束后,予雷贝拉唑和胃黏膜保护剂治疗8周。停药4周后,复查胃镜、13C呼气试验,观察和比较两组Hp根除率、消化不良症状缓解率及溃疡愈合率。结果:A、B两组Hp根除率分别为(ITT分析:86.7%和81.9%;PP分析:87.8%和84.3%);症状缓解率为(81.9%对79.2%);胃溃疡愈合率为(68.8%对66.7%),十二指肠球部溃疡的愈合率为(68.2%对70.0%),两组患者间Hp根除率、症状缓解率及溃疡愈合率比较均未见明显统计学差异(P>0.05)。四联疗法组和序贯疗法组不良反应的发生率分别为4.9%和4.3%。两组比较无明显差异(P>0.05)。结论:四联疗法和序贯疗法对长期服用非甾体类消炎药物人群的Hp根除疗效、消化不良症状的缓解及促进溃疡愈合的治疗作用均无明显差异。     

幽门螺杆菌在慢性阻塞性肺疾病发生及 发展过程中的作用

目的研究幽门螺杆菌(Helicobacter pylori,H.pylori)在慢性阻塞性肺疾病(COPD)发生及发展过程中的作用。方法对85例COPD患者(COPD组)和85例体检健康者(对照组)进行血清抗H.pylori抗体(抗Hp-IgG)检测,比较两组的抗Hp-IgG水平及H.pylori阳性率。全部COPD患者均行肺功能和免疫功能检查,分析抗Hp-IgG水平与COPD严重程度的相关性,比较合并H.pylori感染与无H.pylori感染COPD患者之间,以及合并H.pylori感染COPD患者根除H.pylori前后免疫功能的差异。结果 COPD组血清抗Hp-IgG水平和H.pylori阳性率均明显高于对照组(P0.05),FEV1%预计值与血清抗Hp-IgG水平呈负相关(P0.05)。与无H.pylori感染的COPD患者相比,合并H.pylori感染的COPD患者外周血CD_3~+和CD_4~+T细胞含量、CD_4~+/CD_8~+比值、血清免疫球蛋白(IgA、IgG、IgM)水平均明显较低(P0.05),经H.pylori根除治疗后各指标水平明显升高(P0.05)。结论 H.pylori感染可导致宿主免疫功能紊乱,可能因此促进了COPD的发生和发展。根除H.pylori可明显改善合并H.pylori感染COPD患者的免疫功能,有利于患者恢复。     

Duodenal ulcer relapse is not always associated with recurrence of H. pylori infection: a prospective three-year follow-up study

Background. Long-term data concerning the reappearance of Helicobacter pylori infection and duodenal ulcer (DU) recurrence after successful eradication are still few and conflicting. Inadequate histological assessment or use of indirect tests for the determination of H. pylori and bias in the selection of patients to be controlled can influence reported results. The aim of this study was to determine the rate of recurrence of H. pylori infection and ulcer relapse in a population of cured DU patients followed up for 3 years irrespective of their symptomatology. Methods. Between 1992 and 1994, 126 patients with DU disease were treated with double or triple therapy. Patients using nonsteroidal antiinflammatory drugs or aspirin or receiving maintenance antisecretory therapy were excluded. H. pylori infection was assessed by three bioptic tests from both the antrum and the body (culture, urease, histopathological examination). After 2 months from cessation of treatment, DU had healed and H. pylori infection was cured in 102 of 126 patients (81%). These patients were endoscopically followed up after 1 and 3 years, respectively, and were advised to contact us at symptom recurrence. At 1 and 3 years, we studied 95 (93.2%) and 79 (77.4%) patients, respectively, of the 102 who were cured. The other patients were untraceable or refused endoscopy because they were asymptomatic. Results. After 1 year, no patient had H. pylori recurrence, whereas three patients had a relapse of DU without evidence of infection. After 3 years, recurrence of H. pylori occurred in six patients (annual rate, 2.5%), DU relapsed in five H. pylori–positive patients (6.3%) and in two H. pylori–negative patients (annual rate, 1.9%). Fasting gastrin and acid secretion values studied in all relapsed patients were within the normal range except for one H. pylori–positive patient. Conclusions. Recurrence of H. pylori infection is very low where treatment is effective, but a DU relapse, not related to acid hypersecretion, can occur in a small percentage of cured patients.     

影响幽门螺杆菌根除疗效相关因素

幽门螺杆菌（Hp）是慢性活动性胃炎和消化性溃疡的主要病因,并与胃癌、MALT淋巴瘤的发生密切相关,其根除治疗在临床上具有重要的意义。大量研究显示Hp的根除疗效在下降,本文就有关影响Hp根除疗效的相关因素做一简要概述。     

Helicobacter pylori and its eradication in rosacea.

Rosacea is a common condition of unknown etiology usually accompanied by gastrointestinal symptoms and favorably responding to the treatment with antibiotics. This study was designed to examine the prevalence of gastric Helicobacter pylori (Hp) infection verified by 13C-UTB-test, CLO, Hp culture and serology (IgG) in patients with rosacea. Gastroduodenoscopy was combined with pentagastrin secretory test and antral and fundic biopsy samples were taken for histological evaluation (the Sydney system). Blood samples were also taken for the determination of plasma gastrin using RIA and plasma interleukin (IL)-8 and tumor necrosis factor alpha (TNFalpha) using ELISA. This study was performed in 60 patients, 31-72 year old, with visible papules and pustules associated with erythema and flushing on the face and on 60 age- and gender-matched patients without any skin diseases but with similar as in rosacea gastrointestinal symptoms but without endoscopic changes in gastroduodenal mucosa (non-ulcer dyspepsia - NUD). The Hp prevalence in rosacea patients was about 88 % as compared to 65% in control NUD patients. Among rosacea patients, 67% were cytotoxin associated gene A (CagA) positive, while in NUD patients only 32% were CagA positive. Rosacea patients showed gastritis with activity of about 2.1 in antrum and 0.9 in the corpus of the stomach while those with NUD only mild gastritis with activity of approximately 1.0) confined to the antrum only. Following initial examination, typical 1 wk anti-Hp therapy including omeprazole (20 mg bd.), clarithromycin (500 mg bd.) and metronidazol (500 mg bd.) was carried out. After eradication, 51 out of 53 treated rosacea patients became Hp negative. Within 2-4 weeks, the symptoms of rosacea disappeared in 51 patients, markedly declined in 1 and remained unchanged in 1 other subject. A dramatic reduction in activity of gastritis (to 0.3 in antrum and to 0.1 in corpus) was observed. Basal plasma gastrin decreased from 48 +/- 5 pM before to 17+/-3 pM after eradication, while pentagastrin-induced maximal (MAO) declined, respectively, from about 16.6 +/- 4.2 to 8.5 +/- 1.8 mmol/h. Plasma TNFalpha and IL-8 were reduced after the therapy by 72% and 65%, respectively. We conclude that: 1) Rosacea is a disorder with various gastrointestinal symptoms closely related to gastritis, especially involving the antrum mucosa, with Hp expressing cagA in the majority of cases and elevated plasma levels of TNFalpha and IL-8; 2) The eradication of Hp leads to a dramatic improvement of symptoms of rosacea and reduction in related gastrointestinal symptoms, gastritis, hypergastrinemia and gastric acid secretion; and 3) Rosacea could be considered as one of the major extragastric symptoms of Hp infection probably mediated by Hp-related cytotoxins and cytokines.     

Minor differences in body condition and immune status between avian influenza virus-infected and noninfected mallards: a sign of coevolution?

Wildlife pathogens can alter host fitness. Low pathogenic avian influenza virus (LPAIV) infection is thought to have negligible impacts on wild birds; however, effects of infection in free‐living birds are largely unstudied. We investigated the extent to which LPAIV infection and shedding were associated with body condition and immune status in free‐living mallards (Anas platyrhynchos), a partially migratory key LPAIV host species. We sampled mallards throughout the species' annual autumn LPAIV infection peak, and we classified individuals according to age, sex, and migratory strategy (based on stable hydrogen isotope analysis) when analyzing data on body mass and five indices of immune status. Body mass was similar for LPAIV‐infected and noninfected birds. The degree of virus shedding from the cloaca and oropharynx was not associated with body mass. LPAIV infection and shedding were not associated with natural antibody (NAbs) and complement titers (first lines of defense against infections), concentrations of the acute phase protein haptoglobin (Hp), ratios of heterophils to lymphocytes (H:L ratio), and avian influenza virus (AIV)‐specific antibody concentrations. NAbs titers were higher in LPAIV‐infected males and local (i.e., short distance) migrants than in infected females and distant (i.e., long distance) migrants. Hp concentrations were higher in LPAIV‐infected juveniles and females compared to infected adults and males. NAbs, complement, and Hp levels were lower in LPAIV‐infected mallards in early autumn. Our study demonstrates weak associations between infection with and shedding of LPAIV and the body condition and immune status of free‐living mallards. These results may support the role of mallards as asymptomatic carriers of LPAIV and raise questions about possible coevolution between virus and host.     

幽门螺杆菌感染与胃癌相关性的研究进展

胃癌(gastric cancer)是人类最常见的恶性肿瘤之一,是全球性的医疗难题,其病因尚未完全明确。自20世纪80年代初两位澳大利亚科学家Marshall和Warren首先从胃黏膜中分离出幽门螺杆菌(helicobacter pylori,Hp)至今,Hp与胃癌的关系为人们所关注。经过多年的研究,人们逐渐接受了Hp感染为胃癌发生发展的重要因素,大多数学者认为根除Hp治疗可以降低胃癌发生的风险。然而,近年来随着研究的不断深入,一些研究报道根除Hp治疗并不能预防胃癌的发生发展,也不能降低胃癌的发生率。胃癌的发病机制错综复杂,Hp感染作为单一致病因素如何引起胃癌的发生目前尚未阐述清楚。本文旨在对Hp感染与胃癌相关性的研究进展做一综述。     

Oxidative damage of the gastric mucosa in Helicobacter pylori positive chronic atrophic and nonatrophic gastritis, before and after eradication

Background. Helicobacter pylori is the main cause of gastritis and a primary carcinogen. The aim of this study was to assess oxidative damage in mucosal compartments of gastric mucosa in H. pylori positive and negative atrophic and nonatrophic gastritis. Materials and methods. Five groups of 10 patients each were identified according to H. pylori positive or negative chronic atrophic (Hp‐CAG and CAG, respectively) and nonatrophic gastritis (Hp‐CG and CG, respectively), and H. pylori negative normal mucosa (controls). Oxidative damage was evaluated by nitrotyrosine immunohistochemistry in the whole mucosa and in each compartment at baseline and at 2 and 12 months after eradication. Types of intestinal metaplasia were classified by histochemistry. Results. Total nitrotyrosine levels appeared significantly higher in H. pylori positive than in negative patients, and in Hp‐CAG than in Hp‐CG (p < .001); no differences were found between H. pylori negative gastritis and normal mucosa. Nitrotyrosine were found in foveolae and intestinal metaplasia only in Hp‐CAG. At 12 months after H. pylori eradication, total nitrotyrosine levels showed a trend toward a decrease in Hp‐CG and decreased significantly in Hp‐CAG (p = .002), disappearing from the foveolae (p = .002), but remaining unchanged in intestinal metaplasia. Type I and II of intestinal metaplasia were present with the same prevalence in Hp‐CAG and CAG, and did not change after H. pylori eradication. Conclusions. Oxidative damage of the gastric mucosa increases from Hp‐CG to Hp‐CAG, involving the foveolae and intestinal metaplasia. H. pylori eradication induces a complete healing of foveolae but not of intestinal metaplasia, reducing the overall oxidative damage in the mucosa.     

Structural definition on the surface of Helicobacter pylori type IV secretion apparatus

Genetic and functional studies have indicated that the type IV secretion system (TFSS) of Helicobacter pylori forms a secretion complex in the cell envelope that protrudes towards the outside in order to inject CagA protein into gastric epithelial cells. However, the proposed structural model is based on partial amino acid homology with the components of the Agrobacterium tumefaciens TFSS. Therefore, we undertook the identification of the structural features of the TFSS exposed on the surface of H. pylori and found that filamentous structures present on the bacterial surface are related to the secretion apparatus. Using immunofluorescence microscopy with antibodies directed to tyrosine-phosphorylated CagA (pY-CagA) and Hp0532 (VirB7) in the infection assay, pY-CagA signals were detected just below the host cell-attached bacteria, where Hp0532 (VirB7) signals were detected as co-localized, suggesting that the CagA injected into the host cell through the TFSS apparatus is still mostly confined to the areas just below the attached bacteria after being phosphorylated. Furthermore, the filamentous structures on bacterium were found to be associated with Hp0532 (VirB7) or Hp0528 (VirB9), the major components of TFSS, by immunogold electron microscopy. These results strongly suggest that the H. pylori TFSS apparatus is a filamentous macromolecular structure protruding from the bacterial envelope.     

Interaction of Helicobacter pylori Infection and Nonsteroidal Anti‐Inflammatory Drugs in Gastric and Duodenal Ulcers

Background: Gastric (GU) and duodenal ulcers (DU) are in most instances either induced by Helicobacter pylori infection or by nonsteroidal anti‐inflammatory drugs (NSAIDs). Whether eradication of H. pylori is beneficial in NSAID users for preventing NSAID induced GU and DU has been the focus of different studies. Materials and Methods: Mechanisms shared by both H. pylori and NSAIDs for the induction of GU and DU were reviewed and randomized controlled trials on H. pylori eradication for prevention and healing of GU and DU in patients requiring NSAID therapy were identified by a PubMed search. Results: Key factors in the induction of GU and DU for both H. pylori and NSAIDs are a decrease in pH, imbalance between apoptosis and proliferation, reduction in mucosal blood flow, and recruitment of polymorphonucleates in distinct compartments. For primary ulcer prevention, H. pylori eradication before starting an NSAID therapy reduces the risk of NSAID induced GU and virtually abolishes the risk of DU. H. pylori eradication alone is not sufficient for secondary prevention of NSAID induced GU and DU. H. pylori infection appears to further increase the protective effects of proton‐pump inhibitors (PPI) to reduce the risk of ulcer relapse. H. pylori eradication does not influence the healing of both GU and DU if NSAID intake is discontinued. Conclusions: Duodenal ulcer is more closely related to H. pylori infection than GU in NSAID users. H. pylori eradication is recommended for primary prevention of GU and DU in patients requiring NSAID therapy. PPI therapy is mandatory for secondary prevention of gastroduodenal ulcers, and appears to further reduce the risk of ulcer relapse in the presence of H. pylori.     

益生菌抑制幽门螺杆菌的作用机制及研究进展

幽门螺杆菌在胃部疾病的发病过程中起着重要作用,是导致胃炎、胃溃疡,甚至胃癌的关键因素之一。随着胃部疾病患者幽门螺杆菌阳性检出率的不断升高,人们对于胃病和幽门螺杆菌的相关性研究也有了一定进展。如今,对于幽门螺杆菌阳性患者根除治疗的必要性,以及抗生素治疗耐药性等问题已引起广泛关注。在这种情况下,益生菌作为相对安全的天然微生物,在抑制幽门螺杆菌并促进胃部健康的益生功能方面具有重要的研究潜力。本综述对幽门螺杆菌的致病机理、不同基因分型的致病程度等方面进行了总结,并对益生菌抑制幽门螺杆菌的机制进行了探讨。建议在治疗幽门螺杆菌感染时,应与常规的治疗手段结合应用,不仅会增加幽门螺杆菌的根除率,还能减少治疗相关的副作用。     

One year follow-up of patients after successful helicobacter pylori eradication therapy.

The aim of this study was to investigate the Helicobacter pylori (Hp) status of patients who underwent successful eradication therapy 1 year prior to the study and to evaluate their current symptoms. METHODS: all of the patients were initially evaluated by oesophago-gastro-bulboscopy and the Hp status was determined by at least two different methods [rapid urease test, histology or urea breath test (UBT)]. The Hp infection was treated with a 1-week triple therapy protocol, and the UBT was repeated 4-6 weeks later. We invited back 110 patients who had negative post-eradication UBT results 12+/-3 months prior to the study period. UBT was repeated and a questionnaire was completed about the previous and present complaints and medication. RESULTS: 80 of the 110 patients (73%) came back for the follow-up. Twenty five patients had peptic ulcer disease, 36 patients had gastritis or duodenitis without erosive lesions, and 19 patients had erosive form of gastritis or duodenitis initially. All of the patients except one in the erosive gastritis group had negative control UBT 1 year after the eradication, which means 1.25% recurrence rate within 1 year. The eradication therapy completely revealed the symptoms of 16 patients in the ulcer group (64%), 13 patients in the gastroduodenitis group (36%, P=0.03 vs. ulcer patients), 10 patients with erosive gastroduodenitis (52%), but this was only temporary. One year after the eradication therapy seven of the ulcer patients (28%), 11 patients with gastroduodenitis (31%) and seven patients with erosive gastroduodenitis (37%) were symptom-free. Most of the patients had epigastric pain (44%), heartburn (43%) and/or abdominal distension (33%). Nine ulcer patients (36%), 10 patients with gastroduodenitis (28%) and five patients with erosive gastroduodenitis (26%) were taking H(2)-blockers regularly. CONCLUSION: the 1-month post-eradication UBT was probable true negative in all of the evaluated cases, since 79 patients (98.75%) were also negative after 1 year. The Hp recurrence rate is very low (1.25%) in a 1-year period. The symptoms were relieved shortly after eradication therapy in the majority of patients with ulcer disease or erosive lesions. However, significantly smaller portion of the patients with gastroduodenitis became symptom-free. Only about one third of the treated patients remained symptom-free 1 year after the eradication.     

Isolation and identification of nine sulfated glycosphingolipids containing two unique sulfated gangliosides from the African green monkey kidney cells, Verots S3, and their possible metabolic pathways

Verots S3 cells derived from the African green monkey kidney were revealed to contain nine types of sulfoglycolipids by incorporating [35S]sulfate. These sulfated glycolipids were separated by DEAE-Sephadex column chromatography and preparative thin-layer chromatography (TLC). The major sulfoglycolipids were characterized using TLC, gas-liquid chromatography (GLC), mass spectrometry, solvolysis, TLC immunostaining, and nuclear magnetic resonance spectra as follows: V1, SM4s (GalCer I3-sulfate); V2, SM3 (LacCer II3-sulfate); V3, SM2a (Gg3Cer II3-sulfate); V4, globopentaosyl ceramide sulfate (Gb5Cer V3-sulfate); V5, (Gg4Cer II3-sulfate, IV3-NeuAc); V6, SB1a (Gg4Cer II3, IV3-bis-sulfate); and V8, (Gg4Cer II3-NeuAc, IV3-sulfate). Both V5 and V8 were sulfated gangliosides comprising both N-acetyl neuraminic acid and sulfate, and this was the first report on V8. A minor component V7 was identified as SM1a (Gg4Cer II3-sulfate) based on its behavior in TLC, GLC, and liquid secondary ion mass spectroscopy. It was postulated that this substance was a precursor of V6 (SB1a) and V5 (Gg4Cer II3-sulfate, IV3-NeuAc), and to date, its presence has not been demonstrated in nature. Another minor component V9 was identified as glucosyl ceramide sulfate based on its migration in TLC and GLC. This renal cell line was shown to be an excellent model for studying the metabolism and function of sulfoglycolipids.