Dataset of night-time emissions of the Earth in the near UV range (290-430 nm), with 6.3 km resolution in the latitude range -51.6

The data presented in this article are related to the research paper entitled "Observation of night-time emissions of the Earth in the near UV range from the International Space Station with the Mini-EUSO detector" (Remote Sensing of Environment, Volume 284, January 2023, 113336, https://doi.org/10.1016/j.rse.2022.113336). The data have been acquired with the Mini-EUSO detector, an UV telescope operating in the range 290-430 nm and located inside the International Space Station. The detector was launched in August 2019, and it has started operations from the nadir-facing UV-transparent window in the Russian Zvezda module in October 2019. The data presented here refer to 32 sessions acquired between 2019-11-19 and 2021-05-06. The instrument consists of a Fresnel-lens optical system and a focal surface composed of 36 multi-anode photomultiplier tubes, each with 64 channels, for a total of 2304 channels with single photon counting sensitivity. The telescope, with a square field-of-view of 44°, has a spatial resolution on the Earth surface of 6.3 km and saves triggered transient phenomena with a temporal resolution of 2.5 µs and 320 µs. The telescope also operates in continuous acquisition at a 40.96 ms scale. In this article, large-area night-time UV maps obtained processing the 40.96 ms data, taking averages over regions of some specific geographical areas (e.g., Europe, North America) and over the entire globe, are presented. Data are binned into 0.1° × 0.1° or 0.05° × 0.05° cells (depending on the scale of the map) over the Earth's surface. Raw data are made available in the form of tables (latitude, longitude, counts) and .kmz files (containing the .png images). These are - to the best of our knowledge - the highest sensitivity data in this wavelength range and can be of use to various disciplines.

Randomised clinical trial: efficacy and safety of vonoprazan vs. lansoprazole in patients with gastric or duodenal ulcers - results from two phase 3, non-inferiority randomised controlled trials.

BACKGROUND: Vonoprazan is a new potassium-competitive acid blocker for treatment of acid-related diseases. AIM: To conduct two randomised-controlled trials, to evaluate the non-inferiority of vonoprazan vs. lansoprazole, a proton pump inhibitor, for treatment of gastric ulcer (GU) or duodenal ulcer (DU). METHODS: Patients aged ≥20 years with ≥1 endoscopically-confirmed GU or DU (≥5 mm white coating) were randomised 1:1 using double-dummy blinding to receive lansoprazole (30 mg) or vonoprazan (20 mg) for 8 (GU study) or 6 (DU study) weeks. The primary endpoint was the proportion of patients with endoscopically confirmed healed GU or DU. RESULTS: For GU, 93.5% (216/231) of vonoprazan-treated patients and 93.8% (211/225) of lansoprazole-treated patients achieved healed GU; non-inferiority of vonoprazan to lansoprazole was confirmed [difference = -0.3% (95% CI -4.750, 4.208); P = 0.0011]. For DU, 95.5% (170/178) of vonoprazan-treated patients and 98.3% (177/180) of lansoprazole-treated patients achieved healed DU; non-inferiority to lansoprazole was not confirmed [difference = -2.8% (95% CI -6.400, 0.745); P = 0.0654]. The incidences of treatment-emergent adverse events were slightly lower for GU and slightly higher for DU with vonoprazan than with lansoprazole. There was one death (subarachnoid haemorrhage) in the vonoprazan group (DU). The possibility of a relationship between this unexpected patient death and the study drug could not be ruled out. In both studies, increases in serum gastrin levels were greater in vonoprazan-treated vs. lansoprazole-treated patients; levels returned to baseline after treatment in both groups. CONCLUSIONS: Vonoprazan 20 mg has a similar tolerability profile to lansoprazole 30 mg and is non-inferior with respect to GU healing and has similar efficacy for DU healing.

Sensitivity of biopsy site in evaluating regression of gastric atrophy after Helicobacter pylori eradication treatment.

BACKGROUND: Helicobacter pylori infection is a major cause of the progress of gastric glandular atrophy, a high-risk background factor in the development of gastric cancer. Regression of gastric atrophy is critical to prevention of cancer by H. pylori eradication treatment. However, it is controversial whether gastric atrophy regresses after H. pylori eradication. AIM: To determine the most sensitive and appropriate biopsy site for evaluation of regression of atrophy after treatment. SUBJECTS AND METHODS: Thirty-eight patients who showed regression of gastric atrophy in histology after treatment were investigated. Four biopsy specimens from the lesser and greater curvatures in the antrum and corpus were evaluated before and after treatment according to the Updated Sydney System. RESULTS: Regression of atrophy after treatment was seen in 30 of 38 biopsy specimens from the lesser curvature of the corpus (79%), and this site was most sensitive. Odds ratio of this site to the others was 8.28. Regression of atrophy in this site was observed at 12.2 months in the younger patients and 15.9 months in the elder patients. CONCLUSION: Biopsy sampling from the lesser curvature of the corpus is the most sensitive and appropriate for evaluation of regression of gastric atrophy after H. pylori eradication treatment.

Ten-year prospective follow-up study on the relationship between Helicobacter pylori infection and progression of atrophic gastritis, particularly assessed by endoscopic findings.

AIM: To ascertain the progression of atrophic gastritis due to Helicobacter pylori infection, we conducted a 10-year prospective follow-up study with annual endoscopy of the stomach. METHODS: Prospective endoscopic observation was started in 53 subjects in 1989 and 1990 after informed consent was obtained. The progression of atrophic gastritis was evaluated mainly by the endoscopic pattern of atrophy. Histological assessment was performed on biopsy specimens taken from the lesser curvature of the lower corpus. By 2000, 43 patients (20 males, 23 females, mean age 56.7 years at entry) had completed at least 10 years of endoscopic follow-up. RESULTS: Eight H. pylori-negative patients with normal fundic mucosa showed no change endoscopically or histologically. In 35 H. pylori-positive patients, the progression of histological atrophy was observed in 46% and intestinal metaplasia was observed in 49%. Fifteen of 35 H. pylori-positive cases exhibited a cephaloid shift of the endoscopic atrophic border. The cephaloid shift of the atrophic area occured suddenly. The cumulative progression rate of atrophic patterns was 6% after 2 years, 22% after 4 years, 34% after 6 years and 43% after 10 years. These atrophic changes were related to neutrophil infiltration. CONCLUSION: The progression of atrophic gastritis is a result of chronic active gastritis caused by H. pylori infection.

Winter seasonality and rotavirus diarrhoea in adults.

We investigated the aetiological role of group A rotavirus in adults with acute diarrhoea in a 4-year prospective study. Of 683 patients with acute diarrhoea, 97 (14%) shed rotavirus as a sole agent, whereas six (5%) of 115 patients without diarrhoea shed rotavirus. Half of patients with rotavirus diarrhoea required admission to hospital. Unlike rotavirus diarrhoea in children, the occurrence of rotavirus-positive cases did not show a significant winter seasonality. Rotavirus infection should be included in the differential diagnosis of diarrhoeal diseases in adults.

[Clinicopathologic study on chronic pancreatitis with diffuse irregular narrowing of the main pancreatic duct].

We studied the clinicopathologic features of 13 cases of chronic pancreatitis with diffuse irregular narrowing of the main pancreatic duct (MPD). It occurs frequently in relatively elder men. Diffuse irregular narrowing of the MPD and stenosis of the common bile duct on ERCP, and swelling of the pancreas on US/CT were detected in all cases. An autoimmune mechanism might be involved in the etiology at least in 5 patients with hypergammaglobulinemia and positive autoantibodies. Surgical therapy was performed in 8 patients and 3 patients were treated with steroids. No patients showed recurrence of pancreatitis. Histologic findings were characterized by diffuse lymphoplasmacytic infiltration with marked interstitial fibrosis in the pancreas, obliterated phlebitis of the pancreatic veins. Similar inflammatory process involved the bile duct and the gallbladder. These histologic findings were similar to those of multifocal fibrosclerosis. Chronic pancreatitis with diffuse irregular narrowing of the MPD is overlapped with autoimmune pancreatitis in many cases, but may be a variant of multifocal fibrosclerosis involving the pancreas in some cases.

[Intestinal metaplasia and Helicobacter pylori infection, their relationship and effects of eradication therapy].

Intestinal metaplasia is characterized by Goblet cells and Peneth cells in histological examination. It is frequently observed in gastric mucosa with atrophic gastritis and easily diagnosed using Methylene blue stain in endoscopy. Intestinal metaplasia is seemed to occur during the progression of atrophic gastritis. From our prospective endoscopic follow-up study over 8 years, progression of intestinal metaplasia in gastric body is observed in 44.4% out of 27 H. pylori positive patients. Progression of atrophy is also observed in 37.0% of cases. Development of intestinal metaplasia is also assured in other clinical investigations and experimental studies using Mongolian Gerbils. However, reversibility of intestinal metaplasia after H. pylori eradication is under discussion still now. In our study, we can not observe the regression of intestinal metaplasia even 2 years after successful H. pylori eradication.

Primary sclerosing cholangitis complicated with idiopathic thrombocytopenic purpura.

We present a 66-year-old woman with primary sclerosing cholangitis (PSC) complicated with idiopathic thrombocytopenic purpura (ITP). Both PSC and ITP are considered to reflect an immunological disturbance. However, their coexistence is very rare and to the best of our knowledge this is only the second reported case. In Japan, PSC patients are rarely treated with liver transplantation. Fortunately, the present patient underwent successful hepatic transplantation from a brain-dead donor and simultaneous splenectomy. This case emphasizes the importance of liver transplantation as an effective treatment for primary sclerosing cholangitis.

Peptic ulcer recurrence during maintenance therapy with H2-receptor antagonist following first-line therapy with proton pump inhibitor.

We investigated the peptic ulcer recurrence rates during maintenance therapy with H2-receptor antagonists (H2RAs) following first-line therapy with a proton pump inhibitor (PPI). Patients with gastric ulcer (GU) or duodenal ulcer (DU) were enrolled in this study; 583 eligible patients (GU, 325; DU, 258) were administered lansoprazole (30 mg/day for 8 weeks for GU, and the same dosage for 6 weeks for DU) as first-line therapy, and a half dose of H2RA as maintenance therapy for 12 months. Endoscopic photographs were taken before administration and after 8 (GU) and 6 (DU) weeks of lansoprazole administration. Ulcer stage was evaluated using the classification of Sakita and Miwa. Endoscopic examinations were performed 6 months or 12 months after the start of maintenance therapy or when a recurrence was suspected because of the appearance of subjective symptoms. The healing rates for GU and DU patients after completion of lansoprazole therapy were 79% in both groups, while the S2-stage healing rates were 18% and 31%, respectively. At 1 year after the start of maintenance therapy, the recurrence rates were 25% for GU and 39% for DU patients. In DU patients, the recurrence rates from S1-stage and S2-stage were 49% and 20%, respectively (P = 0.004), but no significant difference was found between these rates in GU patients. The recurrence rates in H. pylori-positive patients before lansoprazole administration were 27% for GU and 43% for DU patients. We concluded that the maintenance therapy with a half-dose of H2RA following PPI therapy was insufficient to prevent recurrences of GU and DU.

The role of juxtapapillary duodenal diverticulum in the formation of gallbladder stones.

BACKGROUND/AIMS: Juxtapapillary diverticula (JPD) are considered to be associated with choledocholithiasis but not with cholecystolithiasis. However, there have been few comparative studies on the relationship between JPD and cholecystolithiasis under strict matching for sex and age. METHODOLOGY: Among 4542 consecutive ERCPs at Tokyo Metropolitan Komagome Hospital, 549 patients who were 63 years of age or older were enrolled in this study and were matched for sex and age. They were divided into two groups: with and without JPD. Firstly, the frequency of cholecystolithiasis was compared between the two groups. Next, we recruited 83 patients whose JPD size could be measured by the ERCP films and investigated the relationship between JPD size and gallstones. RESULTS: We found no correlation between JPD and the overall frequency of cholecystolithiasis. However, an analysis of 83 patients with measurable JPD revealed that the size of JPD was closely linked to the occurrence of cholecystolithiasis. The JPD size was statistically larger in patients with cholecystolithiasis than those without. Moreover, when the mean diameter of JPD was 20 mm or more, the incidence of cholecystolithiasis rose up to 73.3%, which was significantly greater compared to the incidence in patients without JPD (p< 0.05). CONCLUSION: A larger JPD may play a role in the formation of gallbladder stones.

Preliminary study on a novel quadruple eradication therapy with a mucoprotective drug, sofalcone, for Helicobacter pylori infection.

To assess the effects of the mucoprotective drug sofalcone, which has direct and indirect effects on Helicobacter pylori in vitro, the eradication rate, adverse effects, and the quality of healing peptic ulcers were evaluated. Each study patient was given 500 mg t.i.d. amoxicillin and 200 mg t.i.d. clarithromycin. In addition, three different treatment regimens were compared: a standard dose (20 mg q.d.) of the proton pump inhibitor omeprazole (OAC), a double dose (20 mg b.i.d.) of omeprazole (Ox2AC), and a standard dose of omeprazole and a standard dose (100 mg t.i.d.) of sofalcone (OACS). Thirty-one H. pylori-positive patients were treated with OAC, 37 with Ox2AC, and 41 with OACS therapy. With an intention-to-treat analysis, the eradication rates were 74.2% for OAC, 86.2% for Ox2AC, and 85.0% for OACS therapy. The incidence of side effects was 9.6% for patients given OAC therapy, 86.5% for Ox2AC, and only 7.5% for OACS-treated patients, which was significantly lower than the incidence in the Ox2AC group. High-quality peptic ulcer scars were observed after eradication therapy which included solfacone. Although it is necessary to conduct a randomized double-blind study to obtain definitive conclusions, our results indicate that this novel quadruple eradication therapy with solfacone is an efficacious regimen with a high eradication rate and positive effects on ulcer healing, combined with a low incidence of adverse events.

Nontoxic embolic liquids for treatment of arteriovenous malformations.

Interventional radiology is becoming one of the standard treatments of arteriovenous malformation (AVM). Cyanoacrylate derivatives and polymer solutions are widely used to occlude the AVM nidus by their injection through a catheter, but they are far from satisfactory embolic liquids. For instance, cyanoacrylate derivatives sometimes glue the catheter to the artery, resulting in serious complications; in addition, the organic solvents used to dissolve polymers cause damage to the surrounding brain tissue of the AVM. Therefore, we attempted to develop embolic liquids by dissolving poly(2-hydroxyethyl methacrylate-co-methyl methacrylate) in Iopamiron with an addition of a small amount of ethyl alcohol. This new embolic liquid is not cytotoxic and is easily injected into the AVM through a thin, long catheter to effectively occlude the AVM.

Relationship between progression of gastric mucosal atrophy and Helicobacter pylori infection: retrospective long-term endoscopic follow-up study.

A retrospective long-term endoscopic follow-up study was designed to examine atrophic changes in the gastric mucosa over time in Helicobacter pylori-positive patients. Over a period of 8-17 years (mean, 13.4 years) 22 subjects (5 men, 17 women, mean age, 55 years) without localized gastroduodenal lesions underwent serial endoscopic examinations and serological and microbiological assessments of H. pylori infection. The extent of atrophic mucosa in the gastric body was expressed using the Kimura-Takemoto classification of atrophic pattern. Atrophic patterns were unchanged over time in 7 H. pylori-seronegative and culture-negative subjects with normal stomach, and in 1 seropositive and culture-negative subject with severe atrophy. Seven of 10 H. pylori culture-positive subjects not including three with the O-3 pattern, i.e., open type atrophic pattern, exhibited a cephalad shift of atrophic pattern. The cumulative progression rates of atrophy in the culture-positive subjects excluding O-3 subjects, were 10% after 2 years, 20% after 4 years, 50% after 6 years, and 70% after 8 years. The increases in the extent of the atrophic area were discontinuous, in terms of age, in the H. pylori-positive individuals and occasionally advanced rapidly within periods of several years with no relation to age.

Linkage map of Syrian hamster with restriction landmark genomic scanning.

We have constructed the linkage map with precise genetic analysis of the Syrian hamster, Mesocricetus auratus, according to the restriction landmark genomic scanning (RLGS) spot mapping method. Although only 3.2-6.6% of the total RLGS spots between the two strains, ACN and BIO 14.6, showed genetic variance, 572 loci were found to be polymorphic. Out of 569 RLGS loci and 3 other loci, 531 were mapped with the backcross (ACN x BIO 14.6) F1 x BIO 14.6. The cumulative map was 1111.6 cM, indicating that the spots/loci are located throughout the genome at 1.94 cM intervals on average. Thus, RLGS provides us with a rapid tool to construct the genetic map of any species, even if it has less genetic variation.

Preliminary clinical study on gastric ulcer scars and ulcer relapses after Helicobacter pylori eradication therapy.

To determine the effect of Helicobacter pylori eradication on the healing of gastric ulcers, endoscopic examinations of gastric ulcer scars and ulcer relapse after eradication therapies or antisecretory therapy were carried out in 24 H. pylori-positive patients with recurrent gastric ulcers located in the gastric angle. Sixteen patients were initially treated with 2-week triple eradication therapy. Subsequently, seven of eight noneradicated cases were retreated with triple therapy, which included metronidazole. Eight patients received antisecretory monotherapy. Endoscopic examinations were performed at 4 weeks and 6 months after the treatments. Gastric ulcer scars were classified endoscopically into three types: Sa, a central depression surrounded by a coarse pattern: Sb, a coarse regenerated pattern; and Sc, a fine pattern indicating matured scar of high quality. Transformations of the scar patterns and ulcer relapse were assessed in 19 patients who showed an ulcer scar at 4 weeks after initial therapy. Thirteen cases in which H. pylori was successfully eradicated, either after initial or re-eradication therapies, mainly showed Sc scars and had no ulcer relapse. Sa scar was mainly observed during H. pylori-positive conditions. Transformation from the Sa to the Sc was observed after successful re-eradication. Ulcer relapses occurred in three patients who showed Sa scar after antisecretory therapy. Although a random study would be needed to obtain a definite conclusion, we suspect that the H. pylori-negative condition after eradication therapies may result in good ulcer healing and may subsequently reduce ulcer relapse.

Quantitative analysis of striped coat-color patterns in Large White-->Duroc chimeric pigs with special reference to the genetic control mechanisms of the dominant black-eyed white phenotype.

Coat colors of four chimeric pigs produced by the microinjection of dissociated blastomeres of (Landrace x Large White) blastocysts to the blastocyst cavity of Duroc x Duroc) blastocysts (Kashiwazaki et al., 1992) exhibited characteristic horizontal stripe-patterns. We carried out quantitative analysis of those patterns in order to derive information concerning the genetic regulatory mechanisms of the dominant black-eyed white phenotypes in the pig. In the four chimeras, the theoretical mean widths of the single-clone stripe calculated from the estimated widths of minimal recognizable stripe (MRS) (Tachi, 1988) were 2.1 +/- 0.1, 2.23 +/- 0.15, 1.89 +/- 0.06, and 1.93 +/- 0.28 cm respectively. The estimated number of single-clone stripes in the thoracico-lumbar region of those animals were 42.3, 40.7, 46.3, 44.2, and about twice the mean number of vertebrae in the same region (Duroc, 20 or 21; Large White 21 or 22). Furthermore, the mean length of thoracico-lumbar vertebrae in two of the chimeric pigs, as measured on X-ray radiographs, was approximately twice the mean single-clone stripe width. It was concluded that the stripe-patterns of the chimeric pigs probably represented the dermatome patterns of epidermis; and in the pig, a single somite was likely to be derived from the clones of two primordial cells, as originally proposed by Gearhart & Mintz (1972) in the mouse. It was suggested, furthermore, that in the Large White-->Duroc chimeric pigs, melanocytes that migrated into the region of skin formed by a Large White dermatome could not survive, thus creating a clearly demarcated white stripe. Possible involvement of KL or c-kit in the dominant black-eyed white phenotype of the pig is discussed.

Distribution of inflammation and atrophy in the stomach of Helicobacter pylori-positive and -negative patients with chronic gastritis.

OBJECTIVES: To investigate the extent of inflammation and atrophy in the stomach of Helicobacter pylori-positive and -negative patients with chronic gastritis. METHODS: Endoscopy with biopsies from the lesser curvatures of the antrum, angulus, middle body, and the greater curvature of the middle body of the stomach was performed in 59 patients with histologically confirmed chronic gastritis. The extent of atrophic gastritis was assessed endoscopically as well histologically. H. pylori status was assessed by histology as well as enzyme-linked immunosorbent assay. The histological severity of chronic and acute inflammation, glandular atrophy, and intestinal metaplasia was assessed according to the Sydney system. RESULTS: In H. pylori-positive patients, H. pylori was evenly distributed throughout the stomach when the extent of atrophic gastritis was limited to the antrum and the lesser curvature of the body, but disappeared from the antrum of patients with more extensive atrophic gastritis. The severity of acute and chronic inflammation at the greater curvature of the body increased with the extension of atrophic gastritis. In H. pylori-negative patients, the severity of chronic inflammation at the greater curvature of the body was significantly higher in patients with extensive atrophic gastritis than in those with a lesser extent of atrophic gastritis. CONCLUSION: At the greater curvature of the body, the development of atrophy is closely associated with the increase in the severity of inflammation, which is more marked in H. pylori-positive patients.