Category Archives: Gastroenterology

Pre-Crohn’s Disease Stool Promotes Colitis in Germ-Free Mice Puls One

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C Dang et al. Gastroenterology, 2026; 171, 489-503. Pre-Crohn’s Disease Stool From Discordant Siblings Promotes the Development of Colitis in Germ-Free Mice

Methods: This study was conducted as part of The GEM Project, a prospective cohort study of healthy first-degree relatives of CD patients. Germ-free mice were colonized with fecal samples from 12 pairs of discordant siblings, where one sibling later developed CD (pre-CD), and the other remained a healthy matched control (HMC). The microbiome collected wa ~2.6 years before CD diagnosis.

Key findings:

  • Mice receiving pre-CD stool exhibited increased weight loss, fecal lipocalin-2, and intestinal histologic damage compared with mice receiving HMC stool. Thus, mice colonized with stool from individuals who later developed Crohn’s disease showed significantly faster and more severe intestinal inflammation compared with mice colonized with stool from the siblings who remained healthy.
  • Fecal metabolomic analysis revealed differences in 40 metabolites between pre-CD and HMC colonized mice.

My take:

  1. Silly take: It’s a good idea not to eat someone else poop — it might make you sick!
  2. Serious take (borrowed in part from the authors): “The stool microbiome of individuals susceptible to CD is altered years before diagnosis, exhibiting greater inflammatory potential when transferred to susceptible mice.” These studies about the microbiome are remniscent of studies 15-20 years ago indicating that manipulation of the microbiome may play a role in the developement of obesity and Kwashiokor. (Related posts: Could antibiotics make you fat? gutsandgrowth, Microbiome and the risk of Kwashiokor | gutsandgrowth, Microbial transfer for metabolic syndrome? | gutsandgrowth)

Related article: M Xue, C McShane, J Kim et al. Gastroenterol 2026; 171: 641-655. Open access! β-Glucan and Inulin Estimated Intake Are Associated With Reduced Risk of Crohn’s Disease, Improved Gut Barrier and Systemic Inflammation Markers, and Multi-Omic Signatures in a High-Risk Cohort

Methods: The Genetic, Environmental, Microbial (GEM) Project prospectively followed asymptomatic first-degree relatives of individuals with CD. Habitual intake of total fiber and select fiber subtypes was estimated from baseline food frequency questionnaires and biologic samples were collected.

Key findings:

  • During a median follow-up of 8.5 years of 3314 first-degree relatives, 94 developed CD. Higher β-glucan (HR, 0.70) and inulin (HR, 0.68 intake were associated with lower CD risk.
  • Higher β-glucan and inulin intake were associated with lower lactulose–mannitol ratio, lower abundance of pathobionts (Ruminococcus torques and Lachnoclostridium), and lower concentrations of inflammation- and barrier-related proteins.
  • Increased β-glucan found in oats, barley and grains. Increased inulin found in garlic, onions, leeks and asparagus

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Icotrokinra for Patients with Ulcerative Colitis (ANTHEM-UC Phase 2 Trial)

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MT Abreu et al. N Engl J Med 2026;395:1495-1504. Phase 2 Trial of Icotrokinra for Patients with Ulcerative Colitis

Background: “Icotrokinra (JNJ-77242113) is a first-in-class targeted oral peptide that precisely blocks the interleukin-23 receptor. The development of oral peptide therapeutics has historically been limited by poor epithelial membrane permeability, susceptibility to enzymatic degradation in the gastrointestinal tract, and low intestinal absorption.7 The cyclic peptide technology used in icotrokinra enables high stability and epithelial permeability.7 These features, in combination with high selectivity and potent binding of the interleukin-23 receptor, result in an orally administered peptide that effectively inhibits the interleukin-23 pathway.8,9“

Methods: This was a “phase 2b, double-blind, randomized trial of oral icotrokinra, a peptide that blocks the interleukin-23 receptor, in adults with moderately to severely active ulcerative colitis. Participants were assigned to receive icotrokinra at a once-daily dose of 400 mg, 200 mg, or 100 mg or placebo. The primary end point was clinical response at week 12.” A total of 252 participants underwent randomization.

Key findings:

  • All the doses of icotrokinra were superior to placebo with respect to a clinical response at week 12, which occurred in 63% of the participants in the 400-mg group, 58% in the 200-mg group, and 55% in the 100-mg group, as compared with 27% in the placebo group (P<0.001)
  • The percentage of participants with clinical remission at week 12 was also significantly higher in the 400-mg group than in the placebo group (30% vs. 11%, P=0.006), as were…the percentage of participants with endoscopic improvement (37% vs. 14%, P=0.002)
Clinical response was defined as a decrease from baseline in the modified Mayo score by at least 30% and at least 2 points, with either a decrease of at least 1 point from baseline in the rectal bleeding
subscore or a rectal bleeding subscore of 0 or 1
Clinical remission was defined by a stool frequency subscore of 0 or 1,
a rectal bleeding subscore of 0, and an endoscopic subscore of 0 or 1.
Symptomatic remission was defined by a stool frequency subscore of 0 or 1
and a rectal bleeding subscore of 0
Endoscopic improvement was defined by an endoscopic subscore of 0 or 1.

Discussion:

  • “The benefits of treatment with once-daily icotrokinra appeared to be generally sustained or improved through week 28 for all outcomes and doses tested.”
  • “Although all the tested doses of icotrokinra appeared to attenuate systemic inflammation, the 400-mg and 200-mg doses appeared to result in greater reduction of the inflammatory burden than the 100-mg dose.”
  • “The incidence of adverse events with icotrokinra was similar to that with placebo, and no dose–response relationship for adverse events was observed. Among the 212 participants treated with icotrokinra in this trial, no deaths, serious infections, or adverse events of special interest were reported through 28 weeks of treatment.”

My take: This is an important study indicating that an oral IL-23 can be effective for ulcerative colitis which is not surprising based on its previous effectiveness with plaque psoriasis, another immune-mediated disease. It would be helpful to determine the efficacy of this oral agent compared to the IV/SC IL-23 biologic medications (eg. risankizumab, guselkumab, and mirikizumab).

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AFFIRM Study: Subcutaneous Induction-Maintenance Data for Risankizumab

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Charlie Lees is a Professor of Gastroenterology, University of Edinburgh.

From Charlie Lees on X (10/14/26):

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Diet Based on Confocal Laser Endomicroscopy Did Not Improve Irritable Bowel Syndrome Symptoms: A Randomized Controlled Crossover Trial

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L Balsiger et al. Gastroenterology, 2026. Individualized Targeted Exclusion Diet Based on Confocal Laser Endomicroscopy Does Not Improve Irritable Bowel Syndrome Symptoms: A Randomized Controlled Crossover Trial

While foods often trigger IBS symptoms, there has not been a simple way to identify these foods with objective testing. Previous small studies have indicated that confocal laser endomicroscopy has the potential to identify these triggers (See prior post: Is There a Way to Prove Which Dietary Factors Trigger Irritable Bowel Syndrome?).

“The advent of confocal laser endomicroscopy (CLE) has enabled in vivo real-time visualization of the gastrointestinal mucosa.9 Using this approach, researchers have demonstrated acute food-induced mucosal alterations in the duodenum of patients with IBS.10,11 …The reliable identification of foods responsible for symptoms in individual patients with IBS is of great interest. Not only would it streamline the current trial-and-error approach, but it could also potentially avoid overly restrictive dietary patterns, which potentially can lead to avoidant restrictive food intake disorder.”

Methods: “This was a double-blind, controlled, crossover study in patients with IBS. After CLE, patients excluded up to 2 foods that did (= real diet) and up to 2 foods that did not (= sham diet) cause alterations in a randomized order. Diets were followed for 4 weeks each. Clinical response was defined as improving ≥50 points on the IBS Symptom Severity Score. Healthy controls underwent the same CLE protocol as patients with IBS.” 31 patients (median age 33 years) completed both phases of dietary interventions.

Key findings:

  • Clinical response rates were not different between real and sham diet (42% vs 36%; odds ratio, 1.33; P = .6). Symptoms improved both on the real and the sham diet (−30 vs −20; P = .7). 
  • In 15 healthy volunteers, altered mucosa was visualized in 100% of the examinations either at baseline (13%) or after food administration.

My take: CLE-based tailored diet was not beneficial compared to a sham diet. In addition, CLE changes were present in all of the healthy volunteers indicating that altered mucosa is a nonspecific reaction rather than pathognomonic IBS reaction. Thus, there remains no proven way to identify trigger foods in IBS. Exclusion diets can improve symptoms but require careful monitoring.

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Phase 3 Trial: Fecal Microbiota Transplantation Fails in IBS

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PH Johnsen et al. The Lancet, 2026 (published online September 24, 2026) https://doi.org/10.1016/S0140-6736(26)01424-8 Faecal microbiota transplantation in irritable bowel syndrome (REFIT2): a randomised, double-blind, placebo-controlled, phase 3 trial

Methods: This was a randomised, double-blind, multicentre study at five hospitals in Norway. Participants (median age 36 years, 65% women) were randomly assigned 2:1 to faecal microbiota transplantation (FMT) with faeces samples from either healthy donors (intervention, n=298) or the participants themselves (placebo group, n=150). All participants had baseline screening including prior colonoscopy. At baseline, the intervention group had 38% receiving a low FODMAP diet compared to 39% in the placebo group. There was also a similar degree of IBS severity: 93% and 96% had moderate-to-severe IBS, respectively. Each participant received one retention enema (60 g faeces); in the intervention group, the enema consisted of faeces from one of three donors.

Key findings:

  • 119 (40%) participants in the donor FMT group and 57 (38%) in the placebo group showed an improvement of at least 75 points on the IBS-SSS at 90 days after treatment.
  • The proportion of participants with adverse events was similar in the two study groups; however, the six serious adverse events all occurred in the donor FMT group; these included diverticulitis, cholecystitis, escalation of psychiatric condition, and appendicitis.
  • At 90 days after treatment, recipients of donor faecal microbiota transplantation showed a significant change in relative microbial abundance compared with baseline, and both relative microbial abundance and alpha diversity were significantly different in the intervention and placebo groups.
Treatment success at 90 days and 365 days follow-up. Treatment success defined as a 75-point drop in IBS-SSS score compared with baseline. IBS-SSS=Irritable Bowel Syndrome-Severity Scoring System.

Discussion points:

  • “Some earlier trials have reported clinical benefits of faecal microbiota transplantation in IBS; however, many studies have been limited by small sample sizes, single-donor designs, and less stringent endpoint definitions or did not allow for a robust assessment of donor-dependent effects… Although the gut microbiota might still contribute to IBS pathophysiology,
    these findings indicate that non-specific microbiota replacement strategies are unlikely to provide consistent therapeutic benefit.”
  • “The strengths of the current trial were the large sample size, rigorous design with double-blinding, random assignment of participants by donor, and multicentre recruitment.”
  • Limitations: “The reliance on patient-reported outcome measures is an inherent limitation in IBS trials, as few objective measures are available to assess clinical effects.”

My take (borrowed from the authors): “This phase 3 trial did not show any clinical benefit of
faecal microbiota transplantation for treating patients with moderate or severe IBS.”

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Evaluating Anti-TNF Withdrawal Success in UC Remission (BIOSTOP Study)

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IP Berset et al. Journal of Crohn’s and Colitis, 2026; 20: jjag110. Anti-TNF withdrawal or long-term treatment in ulcerative colitis (BIOSTOP): a multicentre open label, randomized controlled trial 

Methods: “In this prospective, multicentre, randomized, controlled, open-label non-inferiority study, patients in deep clinical, biochemical and endoscopic remission were randomized 1:1 to anti-TNF withdrawal or maintenance treatment. Primary endpoint was endoscopically confirmed remission (Mayo Endoscopic Score 0 or 1) after two years, including UC flares treated with anti-TNF, or non-biologic agents.” This study analyzed 163 adult UC patients (2017-2021, median age 45 years). 29% of patients in the withdrawal group were receiving azathioprine.

Inclusioin criteria:

  • Clinical remission defined as six-point Mayo score≤1
  • Endoscopic remission defined as Mayo endoscopic score (MES) 0 or 1
  • Biochemical remission defined as two consecutive fecal (f-) calprotectin tests<200µg/g
  • Minimum one year of first-line anti-TNF treatment (94% of withdrawal group had rec’d anti-TNF therapy for at least two years)

Key findings:

  • Eighty percent (66/82) of anti-TNF withdrawal group and 96% (78/81) of maintenance patients were in endoscopic remission after 2 years
  • UC flares occurred in 52% (45/86) of withdrawal and 12% (10/86) of maintenance patients
  • Anti-TNF retreatment was successful in 74% (20/27) in the intervention group
  • 48% of anti-TNF withdrawal patients remained in steroid-free remission
  • There were no significant predictors for successful anti-TNF withdrawal
  • Serious adverse events:
    • In the withdrawal group: colectomy (n=1), and hospitalizaiton for flare-up (n=2)
    • In the control group: hospitalization for infection (n=2), and cancer (n=1) which was successfully treated and included anti-TNF discontinuation

The authors conclude that “withdrawal of anti-TNF treatment should be restricted to selected, well-informed and highly motivated patients.”

My take: This two-year randomized study showed that among patients in deep remission, almost half who stopped anti-TNF treatment continued with a steroid-free clinical remission after two years; however, there were no factors which identified those who were able to successfully withdraw from anti-TNF therapy. The results may overestimate the success rate of anti-TNF withdrawal as ~30% of patients were receiving azathioprine. In pediatrics, expert advice has favored continuation of advance therapies when patients are in remission.

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Expert Practice Recommendations for C difficile Infection in Adults

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M Fischer et al. Clin Gastroenterol Hepatol 2026; 24: 2359-2369. AGA Clinical Practice Update on Management of Clostridioides difficile Infection in Adults: Expert Review

This article provides 14 “Best Practice Advice” statements. Since this is geared to adults, some are not applicable for the pediatric age group. I have highlighted five of them:

  • #4: Fidaxomicin (200 mg twice daily oral for 10 days) is a narrower spectrum agent, and given lower recurrence rates, is favored as first-line therapy for nonfulminant C difficile infection. However, given practical considerations, vancomycin (125 mg 4 times daily oral for 10 days) is also acceptable therapy. Metronidazole should not be used outside of fulminant disease.
  • #6: Following treatment of C difficile infection, clinicians should not perform routine test of cure. Stool testing should only be performed for persistent worsening of diarrheal symptoms.
  • #9: Prolonged, low dose, suppressive vancomycin regimen (125 mg daily) for secondary prophylaxis may be considered in patients with multiple recurrent episodes who are not candidates for fecal microbiota-based therapies due to ongoing comorbidities, limited life expectancy, or ongoing/frequent systemic antibiotics or who have failed multiple courses of fecal microbiota-based therapy.
  • #10: Fulminant C difficile infection should be managed by a multidisciplinary team (gastroenterology/infectious disease, surgery, medicine/critical care) and treated with high-dose vancomycin 500 mg every 6 hours (oral or enteral), with metronidazole 500 mg intravenously every 8 hours, and if ileus is present, rectal vancomycin 500 mg every 6 hours should be added.
  • #12: Use of vancomycin is not advised during systemic antibiotic administration to prevent C difficile infection. Probiotics are not advised to prevent an initial or recurrent C difficile infection. To promote restoration of healthy gut microbiota, patients should be instructed to consume a healthy diet including a variety of fruits and vegetables, rich in both soluble and insoluble fiber. ” Although some guidelines suggest OVP in high-risk patients, these recommendations were conditional and based on low-quality evidence.20“
Some of the advice from Table 1 on household prevention of CDI

For recurrent CDI, “experts recommend treating a first recurrence with an agent different from that used initially.” One option discussed by authors and in the treatment algorithms (Figure 2) includes use of a vancomycin taper. After a course of vancomycin 125 mg QID x 14 days, a typical taper would be BID x 14 days, then daily x 14 days, then every 3rd day x 14 days. An alternative is a fidaxomicin EXTEND (200 mg BID days 1-5, then every other day, days 7-25 days.

My take: This is a useful reminder of current best practices for C diff infection (in adults). Updated guidelines in pediatrics would be helpful.

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Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician. Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure. This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

PODIUM Study: Jak Inhibitors and Ustekinumab Outperformed Vedolizumab as a 2nd Line Agent for Ulcerative Colitis

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G Privitera et al. Clin Gastroenterol Hepatl 2026; 24: 2539-2550. Open Access! Ustekinumab and Janus Kinase Inhibitors Outperform Vedolizumab as Second-Line Therapy in Anti-Tumor Necrosis Factor-Experienced Patients With Ulcerative Colitis

Before reading this article, I had to research why it was called “The Podium Study.” The research directly stacks three competing second-line classes of advanced therapies against each other: vedolizumab, ustekinumab, and JAK inhibitors; this is similar to a sports podium (1st, 2nd, and 3rd place), as the ultimate clinical goal of the study was to “rank” which medication performed best in terms of efficacy and safety after a patient fails anti-TNFα therapy. Of historical interest, there was an older, unrelated PODIUM trial, which stood for Pentasa Once Daily in Ulcerative Colitis for Maintenance of Remission.

Methods: In this retrospective, multicenter European study, there were 596 patients were included (301 vedolizumab, 149 ustekinumab, 146 JAKi) with a mean age of 43.9 ± 15.5 years.  JAKi included 114 with tofacitinib, 28 with upadacitinib, and 5 with filgotinib. Achievement of biochemical steroid-free clinical remission (SFCR) within 12 months was identified by having SFCR associated with biomarker normalization: FCP <250 μg/g or CRP <5 mg/L—if discordant, FCP was considered the reference biomarker.

Key findings:

  • Compared with vedolizumab, both ustekinumab and JAKi showed significantly higher probability of steroid-free clinical remission (SFCR) (aHR, 1.54 and aHR, 1.66, respectively) and biochemical SFCR (aHR, 2.26 and 3.37, respectively) at 12 months
  • The crude incidence rate of SFCR at 12 months was 65.3% for vedolizumab, 87.0% for ustekinumab, and 80.2% for JAKi.
  • From a safety standpoint, JAKi were associated with an approximately 4-fold increase in the incidence rate of treatment-related AEs—primarily infections—compared with both vedolizumab and ustekinumab.

Discussion Points:

“Optimal sequencing in UC after anti-TNF-α exposure remains an open issue, as direct comparisons are scarce. Overall, our findings are consistent with the network meta-analysis by Lasa et al, which reported superior efficacy of JAKi and ustekinumab compared with vedolizumab in inducing clinical remission and endoscopic improvement in anti-TNF-α-experienced patients.14 However, these conclusions derive from indirect comparisons across heterogeneous randomized trials.”

My take: Vedolizumab is a good choice as a 1st line agent for ulcerative colitis but has a lower success rate as a 2nd line agent. Also, this study likely underestimates the potential effectiveness of JAKi as most individuals received tofacitinib rather than upadacitinib.

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Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician.  Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

AI for Capsule Endoscopy:

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D Fan et al. Clin Gastroenterol Hepatol 2026; 24: 2571-2583. Open Access! INTELCAPE: A Deep Learning-Powered System for Automated, High-Accuracy Crohn’s Disease Diagnosis via Capsule Endoscopy

Methods: In this retrospective, multi-center study with data from 2 Chinese hospitals, the authors developed artificial intelligence, INTELCAPE, for a multi-task deep learning system, to perform small-intestine segmentation, lesion detection, and CD diagnosis from full (capsule endoscopy) CE videos.

Key findings:

  • “INTELCAPE achieved state-of-the-art performance across all tasks.”
  • “For lesion detection, it achieved area under the curve values of 0.993 (Cohort 1) and 0.980 (Cohort 2), with 99.33% classification accuracy, which was comparable to that of specialists (97.83%) but superior to that of residents (91.05%; P < .001).”
  • “For CD diagnosis, INTELCAPE demonstrated robust generalizability, achieving area under the curve values of 0.982 (Cohort 1) and 0.984 (Cohort 2) with 90% diagnostic accuracy, comparable to that of specialists (93.33%) but 10-fold faster (P < .001).”
  • “INTELCAPE improved doctors’ diagnostic accuracy (76.7%–94.8%; P < .001), while reducing their interpretation time (67.9–22.5 minutes; P < .001).”

Discussion Points:

  • “CE generates thousands of images per examination, imposing a substantial analytical burden on clinicians. Manual analysis is labor-intensive and prone to human error, increasing the risk of missed lesions, particularly those with subtle appearances.”
  • “Real-world clinical workflows will require prospective validation on “all-comers” populations, robust handling of poor-quality videos, and device-specific fine-tuning.”

My take: Capsule endoscopy appears to be an ideal target for AI assistance. It has the potential to improve accuracy, reduce time, and augment the performance of less experienced clinicians.

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Flawed Dual Therapy Study of Vedolizumab and Upadacitinib

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J Yao et al. Clinical Gastroenterology and Hepatology, 2026. Combined Upadacitinib and Vedolizumab as 8-Week Induction Therapy for Moderate-to-Severe Ulcerative Colitis: A Multicenter, Randomized Controlled Trial

Many patients do not respond to current advanced therapies which have prompted evaluation of dual therapy regimens. In this randomized open-label trial, the authors compared upadacitinib-vedolizumab dual therapy against vedolizumab monotherapy (40 combination, 73 monotherapy) for moderate-to-severe ulcerative colitis. Upadacitinib was dosed at 45 mg per day.

Key findings:

  • Endoscopic remission at week 8 was achieved by 37.5% in the dual therapy group compared to 15.1% with vedolizumab monotherapy (adjusted odds ratio, 3.34, 1.34–8.58; P = .010)
  • Clinical remission (65.0% vs 35.6%; P = .002) was significantly higher with combination therapy.
  • Adverse event rates were comparable (7.5% vs 6.8%), with no serious adverse events.

It is great to see more dual therapy data . While I am a little reluctant to criticize this study, as I think this type or research is both important and difficult, this trial has a couple problems. First of all, vedolizumab monotherapy may take twice as long to become effective; as such, the results at week 8 in isolation provoke more questions than answers. In addition, at this time point, it is not clear if combination therapy would be more effective than upadacitinib monotherapy.

In their discussion, the authors state that “the 65.0% clinical remission rate at week 8 substantially exceeds rates reported in pivotal induction trials for either upadacitinib (up to 34%11,25) or vedolizumab (approximately 17%24) as monotherapy….. The absence of a upadacitinib monotherapy arm precludes formal assessment of synergy; however, the observed combination endoscopic remission rate (37.5%) exceeds published upadacitinib monotherapy rates for Mayo score = 0 (approximately 14%–18%),11 suggesting a benefit beyond that of upadacitinib monotherapy alone.” However, in a study (RS Dalal et al. Clin Gastroenterol Hepatol 2024; 22: 666-668) comparing monotherapy with upadacitinib versus ustekinumab, upadacitinib had a steroid-free clinical remission rate of 62.1 %, and an endoscopic remission 37.5%. These results are nearly identical to the results of the combination therapy group.

My take: This study shows that upadacitinib works quicker than vedolizumab for moderate-to severe UC. It does not prove that upadacitinib in combination with vedolizumab is more effective than upadacitinib monotherapy.

The anticipated followup data at 1 year will be helpful to determine whether the combination with vedolizumab impacts long-term effectiveness of upadacitinib monotherapy. It is unfortunate that an upadacitinib monotherapy arm was not included in this study.

Another useful study would be whether patients who respond to upadacitinib as an induction combination therapy with vedolizumab could transition to vedolizumab monotherapy. This would leverage upadacitinib’s rapid onset and if effective, allow long-term treatment with vedolizumab which is considered to have the most favorable long-term safety data.

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