Next Article in Journal
Endoscopic and Hybrid Approaches for Gastric Subepithelial Tumors: Expanding the Frontiers of Minimally Invasive Therapy
Previous Article in Journal
The Role of Primary Care and Noninvasive Testing in the Early Diagnosis of Metabolic-Associated Steatotic Liver Disease (MASLD)
 
 
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Article

The Resistance to Traction Forces Differs Substantially Between Intestinal Parts, but Not Between In- and Outbred Strains of Mice

by
Berkan Ertim
1,
Ejder Akinci
1,
Maximiliane von Stumberg
1,
David Katzer
2,
Rainer Ganschow
2,
Tim O. Vilz
1,3 and
Christina Oetzmann von Sochaczewski
1,*
1
Chirurgische Klinik, Universitätsklinikum Bonn, 53127 Bonn, Germany
2
Klinik und Poliklinik für Allgemeine Pädiatrie, Universitätsklinikum Bonn, 53127 Bonn, Germany
3
Klinik für Allgemein- und Viszeralchirurgie, Campus Benjamin Franklin, Charité—Universitätsmedizin Berlin, 12203 Berlin, Germany
*
Author to whom correspondence should be addressed.
Gastroenterol. Insights 2026, 17(1), 12; https://doi.org/10.3390/gastroent17010012
Submission received: 10 December 2025 / Revised: 11 January 2026 / Accepted: 2 February 2026 / Published: 7 February 2026
(This article belongs to the Section Alimentary Tract)

Abstract

Background/Objectives: Anastomoses under tension are associated with anastomotic leaks and strictures. In experimental surgery, anastomoses are frequently tested for their resistance to traction forces, but without the surgically untouched organ as a comparator. We therefore investigated whether and to what extent the breaking forces along the gastrointestinal tract differed in the intact intestinal organs to provide some data for the comparison of anastomoses to it and guide sample size estimation in the mouse. Methods: We included 54 mice of the Crl:CD1(ICR) stock and, as a comparator, 10 mice of the C57Bl/6J and 10 mice of the C57Bl/6NCrl strain of both sexes. We determined breaking forces using a motorised test stand. Results were compared via estimated marginal means with a control of the false-discovery rate by the Benjamini–Hochberg procedure. Results: In all mice strains, the resistance to traction forces was in a descending manner: stomach (mean (µ) ≥ 1.87 Newtons, standard deviation (σ) ≤ 0.63) > rectum(µ > 1.31 Newtons, σ ≤ 0.63) > caecum (µ > 1.1 Newtons, σ ≤ 0.37) > colon(µ > 0.93 Newtons, σ ≤ 0.31) > duodenum (µ > 0.65 Newtons, σ ≤ 0.28) > jejunum (µ > 0.5 N, σ ≤ 0.16) > ileum (µ ≥ 0.43 Newtons, σ ≤ 0.13). The analysis of variance showed a statistically significant effect of the mouse strain on breaking forces (F(2,497) = 16.81, p < 0.001). This was also the case for the investigated organ (F(6,497) = 104.18, p < 0.001) and the interaction between strain and organ (F(12,497) = 2, p = 0.022), indicating a difference between strains. Only the stomachs differed between the included strains; the stomach of Crl:CD1(ICR) sustained −0.81 Newtons (t = −6.23, p < 0.001) compared to those of C57Bl/6J, and −0.37 Newtons (t = −2.88, p = 0.006) compared to those of C57Bl/6NCrl. Other statistically significant differences were absent. Conclusions: Differences in breaking forces between inbred strains and outbred stock were only present for the stomach. Our results may provide a first baseline of breaking force measurements for other studies investigating anastomoses and the respective sample size analyses.

1. Introduction

Anastomotic leaks and postoperative strictures following gastrointestinal surgery are frequently encountered in four to five percent of patients included in large (multi-) national studies [1,2]. The frequency of anastomotic leaks is associated with several patient-, institution-, and technique-related factors [3,4]. A systematic review identified up to 173 factors associated with anastomotic leaks in the gastrointestinal tract [5]. One of these factors is anastomosis under tension. In gastrointestinal surgery, the odds of anastomotic leakage are increased tenfold if tension occurs at the anastomosis [6]. A similar effect, with a sevenfold increase in the odds for anastomotic leaks after low anterior rectum resection, was also described [7]. Likewise, the stricture rate increased after ileo-anal pouch anastomosis if anastomotic tension was present [8]. However, due to surgical strategies to avoid excessive anastomotic tension [9,10,11], strictures are less of an issue in gastrointestinal surgery than in oesophageal surgery. Nonetheless, there is some evidence for the relevance of anastomotic tension in relation to anastomotic complications in gastrointestinal surgery [12].
In contrast, oesophageal surgery has focused on anastomoses under tension for a much longer time after oesophagectomy [13] and oesophageal atresia repair [14]. It was associated with anastomotic leaks after oesophagectomy for cancer in adults [15,16,17]. Anastomotic tension occurred if the gastric conduit was insufficiently mobilised, especially in cervical anastomoses, which may require duodenal mobilisation to avoid anastomotic tension [18]. Anastomosis under tension is an obstacle commonly encountered by paediatric surgeons in the corrective surgery of oesophageal atresia due to insufficient oesophageal length [19,20]. Besides anastomotic leaks, anastomotic tension often results in anastomotic strictures [21,22,23].
Experimental investigations have addressed anastomotic tension in a variety of ways. Earlier research focused on the durability of anastomoses in the canine intestine, tested via bursting pressures [24]. Due to the higher relevance of anastomotic tension, research has long focused on oesophago-oesophageal [25,26,27] and oesophago-gastric anastomoses [28,29,30]. Investigations of intestinal anastomoses were relevant to a lesser degree, usually with a focus on different anastomotic techniques [31,32,33,34,35,36]. The tissue properties of the intestine without anastomoses have scarcely been investigated so far; the effect of ethnicity prompted an investigation of the mechanical properties of the colon using both bursting pressures and tensile strength comparatively [37]. Characterisation of the human small intestine aimed to describe its biomechanical properties [38], but only one study investigated the whole human gastrointestinal tract with both bursting pressures and tensile strength [39]. For experimental animals, this information is even rarer, and to date, there is only one available study on canine [40] and one on porcine [41] gastrointestinal tracts.
Breaking force, compared to bursting pressure, offers the opportunity for a between-study comparison of results, which is not the case for bursting pressures [42]. For decades, breaking force has been, besides bursting pressure [24], the parameter of choice in the investigation of surgical biomechanics [43,44,45], which aims to test anastomoses [46] and compare devices and suturing materials [47] and different types of anastomoses [36]. Its use is not limited to the intestinal organs; it is widely used in orthopaedic surgery [48,49] and otorhinolaryngology [50] too.
A relevant comparator for suturing techniques is the native and surgically unchanged organ, which offers the opportunity to increase the internal validity of a study comparing anastomotic techniques [51]. Moreover, this is of relevance because some studies indicate that anastomoses may have a substantially lower durability than the intact organ [52,53]. Although mouse models are one of the standard models of basic research in surgery, studies with information on the intact organ as a comparator are not available.
Mouse models in particular have a role in these investigations due to their short generation time, widespread availability, and, compared to larger models, lower costs. These factors resulted in suggestions to use an incremental approach, testing materials, techniques, and treatments in mice first and then proceeding to larger animals before transferral to human care [54]. A systematic review identified the mouse as the favourite model for mimicking the colonic anastomoses of humans because the widely used rat model is rather resistant to intra-abdominal infections [55]. These anastomoses in mice are well-described in great detail [56] and the investigation of their breaking force is an established experimental procedure used to determine factors of clinical relevance [57,58]. We therefore aimed to provide insight into the resistance to traction forces of the murine gastrointestinal tract.

2. Materials and Methods

2.1. Mice and Husbandry

Mice (mus musculus) of the CD-1 outbred stock, strain code Crl:CD1(ICR), were supplied in-house by the Haus für experimentelle Therapie. For comparisons to inbred strains, we included mice of C57Bl/6J genetic background and mice of C57Bl/6NCrl genetic background. The comparison between outbred stock and inbred mice was planned because the choice of animal models based on tradition has been criticised [59]. This issue became more pertinent due to research demonstrating that inbred strains did not exhibit more variation than outbred stock [60]. These mice were also supplied from in-house colonies at the Haus für experimentelle Therapie at our institution. The husbandry practices for the animals followed standard guidelines, with regular checks by keepers and veterinarians as necessary. The mice were of specific pathogen status. Temperatures were kept constant at 22 °C with a relative humidity of 45% to 65%. The air was exchanged 15 times per hour. Mice were housed in groups of five at maximum in individually ventilated cages with a light intensity of 325 lux at the cage level and a background noise level of 70 decibels. The cages were enriched with dust-free pulped cotton fibre nestlets (Ancare, Bellmore, NY, USA) and additional material to play with, which were gnawing sticks (Bricks M, Tapvei, Paekna, Estonia). The enrichment was changed every week along with the bedding by exchanging the cages. Dark–light cycles of twelve hours were used with artificial lighting between 7 and 19 o’clock. Autoclaved drinking water was available ad libitum and the mice were fed regular pelleted chow ad libitum (Ssniff V1534-300, Ssniff Spezialdiäten, Soest, Germany) [61].

2.2. Experimental Approach

Mice were included in our experiments irrespective of sex by design because we determined that it would be unethical to kill mice specifically for our experiments. Instead, we opted for the use of mice that were not included in the experiments of other groups and were scheduled to be killed due to their non-use. This is part of our commitment to the 3R guidelines, as it contributes to the reduction in the use of mice because no mice were bred and subsequently killed solely for our experiments. Mice were killed in a type II long narcotic chamber (Tecniplast, Hohenpeißenberg, Germany) via gradually increasing carbon dioxide insufflation. We determined death by a loss of respiratory excursions and ensured it by cervical dislocation. We performed our experiments on multiple days with a different number of animals per day in order to increase the reproducibility of our experiments [62]. Our experiment began by opening the carcass as described elsewhere in detail [63]. In brief, the abdominal cavity was opened, and the rectum was transected as deeply as possible into the retropubic space. It was then retracted from the carcass by the dissection of mesenteric attachments. After the caecum was reached, the remaining mesenteric attachments of the small intestine were removed in order to linearize the gut until the stomach was reached. The whole organ package was then removed from the carcass by dissection of the stomach just below the gastro-oesophageal junction. Afterwards, representative specimens were cut out of the respective segments of the gastrointestinal tract and submitted to linearly increasing traction in order to determine the tensile force. As the small intestines of mice lack clear boundaries between the different sections of the small intestine [64], we chose a pragmatic approach to identify the sections: the duodenum was identified by a segment five centimetres aboral to the pylorus, the jejunum by ten centimetres aboral to the duodenojejunal flexure, and the ileum by a segment five centimetres oral to the ileocolic junction.
Our experimental setup was described in detail before [65,66]. In brief, the excised specimens were mounted on the motorised test stand (Sauter THM500N, Kern & Sohn, Balingen, Germany) and subjected to linearly increasing traction forces, increasing by 10 mm per minute until the tissue tore (Figure 1). This was registered as a loss of force by the tensiometer (FL100, Kern & Sohn, Balingen, Germany), and the maximum value was recorded as tensile force [67,68]. The lowest measurable increment of the tensiometer in our measurements was 0.05 Newtons. We used breaking forces because we did not aim to investigate the complete biomechanical properties of the murine intestine, but provide results that are comparable with different studies. The use of breaking force as an outcome parameter in studies such as ours allows the intended between-studies comparison [42]. All experiments were conducted within two hours after the animals’ demise in order to avoid structural post mortem changes [69,70].

2.3. Power Analysis

Due to the lack of available data on the murine intestine, a formal a priori power analysis was limited to using data from mongrel dogs provided by Ogurtan and co-workers [40]. Using G*Power 3.1.9.2. [71], with a one-way analysis of variance for the results of tensile strengths of duodenum, jejunum, ileum, and colon, we calculated an effect size of f = 2.58 using the highest standard deviation from the duodenum of 0.63. This resulted in a sample size of 12 animals, which would be sufficient to confirm the result of Ogurtan et al. with α = 0.005 [72] and β = 0.1, resulting in a statistical power of 90%. In the power analysis using existing data from Ogurtan et al. [40], we included only the intestine because the tensile strength of the stomach and rectum was much higher in their experiment and would have distorted the power calculation. In order to correct for publication bias [73], we used the BUCSS package (version 1.2.1) [74], which calculated 13 measurements in 4 groups. In order to correct for the uncertainty associated with a different animal species, mice versus mongrel dogs, we opted for at least 40 measurements per group. During the conduction of our experiments, additional data from Kratz et al. [41] on porcine intestines were published. Using their data for a formal power analysis with G*Power 3.1.9.2., with the parameters described above, resulted in an effect size of f = 0.47, which then resulted in a necessary sample size of n = 20 per group for the 6 intestinal segments: duodenum, jejunum, ileum, caecum, colon, and rectum. This confirms our initial cautious sample size calculation with the correction factor to account for uncertainty.

2.4. Statistical Analysis

Statistical analysis was conducted using GraphPad Prism 8 and R (version 4.3.3) [75]. The normality of the distribution of the included variables was checked via the Kolmogorov–Smirnov test, supported by the visual analysis of QQ-plots [76,77,78]. The homogeneity of variances was evaluated using Bartlett’s test [65]. In order to demonstrate the distribution of force measurements, violin plots depicting individual force measurements as well as the median and the interquartile range were provided. For comparison between the mouse strains and the intestinal segments within the mouse strains and between them, we created a factorial model using the afex package (version 1.0-1) and analysed it via a type III analysis of variance [79]. The measurements were compared via an estimated marginal means model using the emmeans package (version 1.7.1-1) [80,81]. We corrected for multiple comparisons using the Benjamini–Hochberg procedure [82,83,84]. Raw data for the numeric analyses are available via Zenodo.

2.5. Ethical Approval

The use of the mice was exempt from ethical approval by the Landesamt für Natur, Umwelt und Verbraucherschutz Nordrhein-Westfalen (LANUV). National regulations and the directive 2010/63/EU apply only to living animals, whereas our animals were provided dead, as they had been sourced from conservation colonies. German law for the protection of animals exempts all experiments in which laboratory animals are sacrificed to obtain isolated organs from approval by the relevant state authority (exact citation: section seven, subsection two, sentence three of the German law for the protection of animals [German legal citation: “Paragraph sieben, Absatz zwei, Satz drei des Tierschutzgesetzes”]) [85,86].

3. Results

We included 54 mice—53 females and 1 male—of Crl:CD1(ICR) stock, as well as 10 mice of C57Bl/6J background—six males and four females—and 10 mice of the C57Bl/6NCrl background—six males and four females. The mean age of the Crl:CD1(ICR) mice was 112 days (standard deviation 44) and their mean body weight was 39 g (standard deviation 6.8). The mean age of the C57Bl/6J mice was 268 days (standard deviation 73) and their mean body weight was 33 g (standard deviation 2.7). For the C57Bl/6NCrl mice, their mean age was 127 days (standard deviation 12) and their mean body weight was 27 g (standard deviation 2.9).

3.1. Breaking Forces of the Organs of the Gastrointestinal Tract in In- and Outbred Mice

The stomachs of the Crl:CD1(ICR) group sustained traction forces of 1.86 Newtons (standard deviation 0.62) compared to 2.67 Newtons (standard deviation 0.52) in C57Bl/6J mice and 2.23 Newtons (standard deviation 0.43) in C57Bl/6NCrl mice (Figure 2).
The breaking force of the duodenum of Crl:CD1(ICR) mice was 0.65 Newtons (standard deviation 0.28), while the duodenum of C57Bl/6J had a breaking force of 0.84 Newtons (standard deviation 0.28) and that of C57Bl/6NCrl mice had a breaking force of 0.67 Newtons (standard deviation 0.15) (Figure 3).
The jejuna of Crl:CD1(ICR) mice sustained traction forces of 0.53 Newtons (standard deviation 0.19), whereas the jejuna of C57Bl/6J mice had a breaking force of 0.8 Newtons (standard deviation 0.15) and the jejuna of C57Bl/6NCrl mice sustained traction forces of 0.59 Newtons (standard deviation 0.07) (Figure 4).
The ilea of Crl:CD1(ICR) mice had a breaking force of 0.45 Newtons (standard deviation 0.16), the ilea of C57Bl/6J mice sustained traction forces of 0.6 Newtons (standard deviation 0.17), and the ilea of C57Bl6/N mice had a breaking force of 0.47 Newtons (standard deviation 0.06) (Figure 5).
The breaking force of the caeca of Crl:CD1(ICR) mice was 1.11 Newtons (standard deviation 0.37), whereas the caeca of C57Bl/6J mice sustained traction forces of 1.36 Newtons (standard deviation 0.26) and the caeca of C57Bl/6NCrl mice withstood traction forces of 1.27 Newtons (standard deviation 0.15) (Figure 6).
The maximum of sustained traction forces of the colons of Crl:CD1(ICR) mice was 0.96 Newtons (standard deviation 0.33), while it was 1.06 Newtons (standard deviation 0.15) in C57Bl/6J mice and 0.97 Newtons (standard deviation 0.16) in C57Bl/6NCrl mice (Figure 7).
The breaking force of the rectums of Crl:CD1(ICR) mice was 1.31 Newtons (standard deviation 0.64), while it was 1.53 Newtons (standard deviation 0.4) in C57Bl/6J mice and 1.36 Newtons (standard deviation 0.21) in C57Bl/6NCrl mice (Figure 8).
As expected, the variability in breaking forces varies between in- and outbred strains and is consistently smaller in inbred strains despite their smaller sample size in our study. The one male mouse in the Crl:CD1(ICR) group did not yield an extreme measurement in breaking force, except for in the case of the jejunum (Supplementary Figure S1).

3.2. Comparison of Breaking Forces Within and Between the Different Mouse Strains

The factorial analysis of variance showed a statistically significant effect of the mouse strain on breaking forces (F(2,497) = 16.81, p < 0.001). This was also the case for the investigated organ (F(6,497) = 104.18, p < 0.001) and the interaction between strain and organ (F(12,497) = 2, p = 0.022), indicating a difference between strains.
We therefore contrasted organs first within the same mouse strain using estimated marginal means. For Crl:CD1(ICR) mice, almost all organs differed in breaking force except for the pair of duodenum and jejunum, as well as ileum and jejunum (Table 1).
The pairwise contrasts of the breaking forces of the organ of the gastrointestinal tract in C57Bl/6J mice showed a different pattern than in the outbred mice of the Crl:CD1(ICR) background. We could not show differences between the duodenum and jejunum, duodenum and ileum, duodenum and colon, jejunum and ileum, jejunum and colon, caecum and colon, and caecum and rectum (Table 2).
In C57Bl/6NCrl mice, the pairwise contrasts were similar to those of the C57Bl/6J mice. We could not show differences between the duodenum and jejunum, duodenum and ileum, duodenum and colon, jejunum and ileum, caecum and colon, and caecum and rectum (Table 3).
In the comparison of mean breaking forces between strains, differences only occurred between the stomachs. The stomachs of Crl:CD1(ICR) mice sustained −0.81 Newtons (t = −6.23, p < 0.001) compared to those of C57Bl/6J and −0.37 Newtons (t = −2.88, p = 0.006) compared to those of C57Bl/6NCrl. The comparison of the mean breaking forces of the stomachs of C57Bl/6J and C57Bl/6NCrl showed that those of C57Bl/6J mice sustained traction forces 0.44 Newtons higher (t = 2.58, p = 0.01) than the stomachs of C57Bl/6NCrl (Table 4). All other between-strain comparisons did not show statistically significant differences (Table 4).
In order to make the comparisons between and within strains and the respective organs of the gastrointestinal tract more accessible, we constructed a figure to allow the comparison of this information in parallel, but with less accuracy, as differences have to be determined graphically (Figure 9).

4. Discussion

Anastomotic leaks and postoperative strictures are frequently encountered after gastrointestinal surgery [1,2]. Among the risk factors for anastomotic leaks in the gastrointestinal tract is anastomotic tension [7,8], which increased the odds for anastomotic leakage up to ten times compared to patients without anastomotic tension [6]. This demonstrates the deleterious effect anastomotic tension exerts. Although there are surgical options available to reduce anastomotic tension [9,10,11], it cannot be avoided in all situations. Animal models showed that anastomotic tension also causes postoperative strictures, inflammation, and impaired function of the gastrointestinal tract [87,88,89]. Increasing anastomotic tension was associated with anastomotic leaks in only one study [90], but it had not been experimentally assessed except for that single study [90].
Traditionally, it had been assumed that anastomotic tension is a relevant factor in the development of anastomotic leaks because experimentally induced increased anastomotic tension resulted in impaired blood flow. This occurred in the intestines [31,91] and in the oesophagus [92,93], but not consistently in the latter [94]. Moreover, tension impaired smooth muscle function in vitro, but this has been investigated only for oesophageal smooth muscles [95]. Therefore, some voices in the literature assumed that these traditional risk factors could be of lesser relevance compared to atypical factors [96]. Although anastomoses were commonly evaluated using bursting pressures and breaking forces [35,36,51,97,98,99,100], since both methods were first described [101,102], anastomoses under tension have only been investigated once [90].
Our study provides the first systematic assessment of the tensile force of the murine gastrointestinal tract. Thus far, the breaking forces of the gastrointestinal tract have been scarcely assessed, and such information is only available for dogs [40] and swine [41]. This is surprising because breaking forces are frequently used to evaluate anastomoses in the gastrointestinal tract; oesophageal [27,52], jejunal [103], ileal [104,105], colonic [33,105], and rectal anastomoses were tested using breaking forces [106,107]. Measuring breaking forces offers the opportunity to compare the measurements between studies, whereas this is impossible for burst pressure measurements [42]. The differences between burst pressures and breaking forces, exemplified by the lack of even a correlation between them in colonic anastomoses [108], indicate that they also measure different tissue properties of the intestine.
Moreover, the comparison to the surgically untouched organ offers the opportunity to have an internal control and thus increases the internal validity when comparing anastomoses [41,51]. For burst pressure measurements, this approach is unsuitable [109]. Our study, as others conducted before in dogs [40] and swine [41], showed that the breaking forces differed between the different parts of the intestine.
With regard to breaking force, our study demonstrates a different pattern of breaking forces compared to dogs and swine. In dogs, the duodenum sustained higher traction forces than the colon and the rectum, whereas the jejunum and ileum had the lowest breaking forces [40]. The pattern was substantially different in swine, in which the caecum sustained the highest traction force, followed by the ileum and the rectum, whereas the colon had a breaking force that was even lower than that of the jejunum and ileum [41]. In our murine study, the pattern was again different from that of other species. The stomach sustained the highest traction forces, followed by the rectum, the caecum, the colon, and the small bowel. These differences highlight the issue of a lack of transferability between species, which also indicates that sample size estimation cannot be directly based on measurements in other species.
Besides the anatomic localisation, the histologic composition, like the collagen and elastin content and their directional alignment [110,111,112,113], influences the biomechanical behaviour of intestinal organs. Similar influences are exerted by the morphometric parameters, for example, the wall thickness and diameter [114,115,116], which are also not addressed in our study. However, we did not investigate these parameters in our study and therefore, their discussion is beyond the scope of our study. This is also the case for more advanced biomechanical analyses, such as the determination of stress and strain.
We opted to investigate breaking forces and not tensile strength, as the latter would have required an exact assessment of the thickness of the specimen’s bowel wall. Specimen thickness influences the measurements and could result in altered results if misrepresented [114,117]. Biomechanical tissue characterisation studies use a rectangular specimen of the intestinal wall to control specimen thickness. Thereby, they provide exact measurements of specimen deformation [115,118,119]. Using that approach would not mimic the clinical situation that we aimed to provide comparators for. During the construction of anastomoses, the bowel thickness cannot be changed. Therefore, using area-normalised stress would not have been possible because the area would have to be measured continuously at every point of the bowel as a hollow organ during the increase in the axial tension. Such an experimental setup has not been described in the literature so far.
Interestingly, our study showed that besides the stomach, there were no differences in breaking forces between inbred strains and outbred stocks. Outbred stocks are used in experiments involving rats, whereas in mice, the inbred C57Bl and BALB/c strains are favoured [59,120]. There is no particular reason for this; it is just what has historically been common practice in research [59]. In line with the recent focus on variability being necessary for reproducibility and generalisability in experimental research [121], the aspect of stock and strain choice came back onto the table. In several areas of experimental research, there were no substantial differences between outbred stocks and inbred strains, although the contrary was expected [122,123,124,125]. Subsequently, a meta-analysis has shown that variability does not differ between in- and outbred mice [60]. Our finding is therefore not surprising with regard to the absence of differences along the gastrointestinal tract. It is, however, unclear why the breaking forces of the stomachs differed. Although substantial differences in the biomechanical behaviour of human and porcine stomachs have been demonstrated [126,127], this does not explain the differences noted in our study between in- and outbred strains and even between substrains. A systematic review identified the stomach to be an under-researched organ of the gastrointestinal tract with regard to its biomechanical properties, so the literature on it is rather scarce compared to that on the oesophagus or the small intestine [128]. In addition, our study only assessed simple breaking force and did not investigate structural aspects, and can therefore not offer explanations.
A limitation of our study is the use of different species—dogs [40] and swine [41]—for the power analysis. Biomechanical results differ between species, which can easily be exemplified by the different effect sizes calculated from dogs, f = 2.58, compared to those from swine, with just f = 0.47. However, we had to use these results for the power analysis because no others were available in the literature that could guide our sample size calculation. Of course, we could have used scientific judgement but this seemed less reliable to us compared to using published data from other species.
Another limitation of our study is the distribution of sexes among the mice from the Crl:CD1(ICR) stock. We did not impose sex restrictions in order to avoid the sex bias described in several research areas [129]. Therefore, we included both sexes, following recommendations [130]. Due to the inclusion of animals scheduled for killing anyway, as they were not required in other experiments, we avoided killing mice exclusively for study. However, we ended up with an almost exclusive sample of females in the Crl:CD1(ICR) group, but we attached more importance to ethical obligations in using experimental animals in our exploratory study. In contrast, the sex distribution in the C57Bl/6J and C57Bl/6NCrl groups was rather balanced. Sex might be a covariate in the assessment of breaking force, although there are currently no data on that matter because it has not been investigated before in mice or other species. In our study, the breaking forces of the different bowel segments varied compared to the measurements from females; while it was the highest measurement in the jejunum, the breaking forces were rather low in the stomach and the duodenum. Therefore, it is unlikely to have substantially influenced the data of the cohort. When sex was assessed as a covariate, it did not show statistically significant differences [131], but this data is only available for humans for suture pullout force. In contrast, investigations of the colon in humans showed a small effect for female sex, whose resistance to traction forces is higher than in males [132]. Nonetheless, due to the lack of data on this matter, it has to be assumed that there might be some influence and therefore it reduces the external validity of our cohort.
The external validity of our study is further limited by the inclusion of mice not only irrespective of their sex, but also of their weight and age. In 1992, Christensen and co-workers described in a comparison of 4-, 14-, and 27-month-old rats that the maximum load of the colon increased from young to middle-aged rats and then decreased in old rats [133]. In rats, the small intestine also showed an increase in stiffness that was age-dependent [134]. Age was also a modifying factor in the investigation of the mechanical properties of the colon in humans, but with a rather small effect [132]. Nevertheless, this indicates that some age-dependent effects are likely to be present and could have modified our results, although we did not account for this factor in our experimental design. As mice grow throughout their life, their body weight also increases in parallel [135,136]. This indicates that body weight might be, as age, an influencing factor that we did not address in the design of our study.

5. Conclusions

Our study demonstrates that differences in the breaking forces of intestinal organs were only present between the stomachs of inbred strains and outbred stocks. Between these mice, the breaking forces of the bowel sections did not differ. Within the different strains and stocks, the breaking forces were the highest in the stomach, followed by the large bowel segments and the small bowel segments.
While our study may aid in sample size calculations of further research, additional studies should investigate the influence of age, body weight, and sex, which were insufficiently covered in our study. It does, however, provide the initial data that justifies the killing of mice selected for sex, age, and body weight to increase the precision of the measurements.

Supplementary Materials

The following supporting information can be downloaded at https://www.mdpi.com/article/10.3390/gastroent17010012/s1: Figure S1: Individual measurements of the breaking forces separated by sex of the Crl:CD1(ICR) mice.

Author Contributions

Conceptualization, B.E. and C.O.v.S.; methodology, B.E. and D.K.; formal analysis, B.E. and C.O.v.S.; investigation, B.E., E.A., M.v.S., and C.O.v.S.; resources, D.K., R.G., and C.O.v.S.; data curation, B.E., E.A., M.v.S., and C.O.v.S.; writing—original draft preparation, B.E. and C.O.v.S.; writing—review and editing, E.A., M.v.S., D.K., R.G., and T.O.V.; visualisation, B.E., E.A. and M.v.S.; supervision, R.G. and T.O.V.; project administration, T.O.V. and C.O.v.S.; funding acquisition, T.O.V. All authors have read and agreed to the published version of the manuscript.

Funding

This research was funded intramurally by BONNFOR, grant number O-112.0068.1.

Institutional Review Board Statement

Ethical review and approval were waived for this study by law due to it not being applicable in our jurisdiction for studies using organs from animals sacrificed for scientific purposes: https://www.gesetze-im-internet.de/tierschg/__7.html (accessed on 29 October 2025). Exact citation: “Nicht als Tierversuch gilt 1. das Töten eines Tieres, soweit das Töten ausschließlich dazu erfolgt, die Organe oder Gewebe des Tieres zu wissenschaftlichen Zwecken zu verwenden […]” [61].

Informed Consent Statement

Not applicable.

Data Availability Statement

Raw data of our study are freely available from Zenodo (https://zenodo.org/records/17873133 (accessed on 1st February 2026).

Acknowledgments

We thank the technical staff of the Haus für Experimentelle Therapie, Universitätsklinikum Bonn, Germany, in particular Stephanie Oppitz and Alexander Tews, for their support for our study.

Conflicts of Interest

The authors declare no conflicts of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

References

  1. Hamel, J.; Alves, A.; Beyer-Bergot, L.; Zerbib, P.; Bridoux, V.; Manceau, G.; Panis, Y.; Buscail, E.; Khaoudy, I.; Gaillard, M.; et al. Stenosis of the Colorectal Anastomosis after Surgery for Diverticulitis: A National Retrospective Cohort Study. Color. Dis. 2024, 26, 1437–1446. [Google Scholar] [CrossRef] [PubMed]
  2. Wells, C.I.; Baraza, W.; O’Grady, G.; Bissett, I.P. ‘Failure to Rescue’ from Anastomotic Leak Following Colorectal Cancer Resection: An Observational Study from a Binational Registry. Color. Dis. 2025, 27, e70262. [Google Scholar] [CrossRef] [PubMed]
  3. Rencuzogullari, A.; Benlice, C.; Valente, M.; Abbas, M.A.; Remzi, F.H.; Gorgun, E. Predictors of Anastomotic Leak in Elderly Patients After Colectomy: Nomogram-Based Assessment from the American College of Surgeons National Surgical Quality Program Procedure-Targeted Cohort. Dis. Colon. Rectum 2017, 60, 527–536. [Google Scholar] [CrossRef] [PubMed]
  4. Moojen, T.B.; Vlug, M.S.; Visser, E.; Reijntjes, M.A.; Lange, J.F.M.; Bislenghi, G.; Carvello, M.; Warusavitarne, J.; Hompes, R.; Stassen, L.P.S.; et al. Anastomotic Leakage after Ileoanal Pouch Surgery: Risk Factors and Salvage Rate. BJS Open 2025, 9, zraf110. [Google Scholar] [CrossRef]
  5. Bao, X.; Yi, K.; Cheng, J.; Shen, Y.; Cao, S.; Hu, B.; Wang, X.; Su, P.; Li, Y.; Xu, Q.; et al. Risk and Protective Factors for Postoperative Anastomotic Leakage in Esophageal and Gastrointestinal Surgery: An Umbrella Review of Meta-Analyses and Systematic Reviews. Int. J. Surg. 2025, 112, 1722–1736. [Google Scholar] [CrossRef]
  6. Morse, B.C.; Simpson, J.P.; Jones, Y.R.; Johnson, B.L.; Knott, B.M.; Kotrady, J.A. Determination of Independent Predictive Factors for Anastomotic Leak: Analysis of 682 Intestinal Anastomoses. Am. J. Surg. 2013, 206, 950–956. [Google Scholar] [CrossRef]
  7. Ito, R.; Matsubara, H.; Shimizu, R.; Maehata, T.; Miura, Y.; Uji, M.; Mokuno, Y. Anastomotic Tension “Bridging”: A Risk Factor for Anastomotic Leakage Following Low Anterior Resection. Surg. Endosc. 2024, 38, 4916–4925. [Google Scholar] [CrossRef]
  8. Wu, X.-R.; Kirat, H.T.; Xhaja, X.; Hammel, J.P.; Kiran, R.P.; Church, J.M. The Impact of Mesenteric Tension on Pouch Outcome and Quality of Life in Patients Undergoing Restorative Proctocolectomy. Color. Dis. 2014, 16, 986–994. [Google Scholar] [CrossRef]
  9. Man, J.; Hrabe, J. Anastomotic Technique—How to Optimize Success and Minimize Leak Rates. Clin. Colon. Rectal Surg. 2021, 34, 371–378. [Google Scholar] [CrossRef]
  10. Vargas, H.D. Gaining Mesenteric Length Following Colorectal Resection: Essential Maneuvers to Avoid Anastomotic Tension. Clin. Colon. Rectal Surg. 2023, 36, 37–46. [Google Scholar] [CrossRef]
  11. Dalmau, M.; Marti-Gallostra, M.; Pellino, G.; Espin-Basany, E.; Armengol, M. The Colon Does Not Reach! A Technical Note with Tricks to Avoid Colorectal Anastomoses under Tension. Color. Dis. 2024, 26, 564–569. [Google Scholar] [CrossRef] [PubMed]
  12. Khalid, M.U.; Ali, D.; Wu, J.Y.; Lee, H.; Khan, A. Impact and Measurement of Mechanical Tension in Bowel Anastomosis: A Scoping Review of the Current Literature. J. Surg. Res. 2025, 308, 161–173. [Google Scholar] [CrossRef] [PubMed]
  13. Herron, R.; Abbas, G. Techniques of Esophageal Anastomoses for Esophagectomy. Surg. Clin. North. Am. 2021, 101, 511–524. [Google Scholar] [CrossRef] [PubMed]
  14. Chen, H.; Chen, Z.-X.; Shi, G.-Q. Risk Factors and Prevention and Treatment Methods of Anastomotic Stricture after Esophageal Atresia Repair: A Literature Review. Pediatr. Surg. Int. 2025, 41, 99. [Google Scholar] [CrossRef]
  15. Hermreck, A.S.; Crawlord, D.G. The Esophageal Anastomotic Leak. Am. J. Surg. 1976, 132, 794–798. [Google Scholar] [CrossRef]
  16. Mahoney, J.L.; Condon, R.E. Adenocarcinoma of the Esophagus. Ann. Surg. 1987, 205, 557–562. [Google Scholar] [CrossRef]
  17. Kitayama, J.; Kaisaki, S.; Ishigami, H.; Hidemura, A.; Nagawa, H. Angleplasty in Gastric Tube Reconstruction after Esophagectomy. Dis. Esophagus 2009, 22, 418–421. [Google Scholar] [CrossRef]
  18. Hölscher, A.H.; Vallböhmer, D.; Brabender, J. The Prevention and Management of Perioperative Complications. Best. Pract. Res. Clin. Gastroenterol. 2006, 20, 907–923. [Google Scholar] [CrossRef]
  19. Schneider, A.; Blanc, S.; Bonnard, A.; Khen-Dunlop, N.; Auber, F.; Breton, A.; Podevin, G.; Sfeir, R.; Fouquet, V.; Jacquier, C.; et al. Results from the French National Esophageal Atresia Register: One-Year Outcome. Orphanet J. Rare Dis. 2014, 9, 206. [Google Scholar] [CrossRef]
  20. Aumar, M.; Sfeir, R.; Pierache, A.; Turck, D.; Gottrand, F. Predictors of Anastomotic Strictures Following Œsophageal Atresia Repair. Arch. Dis. Child. Fetal Neonatal Ed. 2022, 107, 545–550. [Google Scholar] [CrossRef]
  21. Serhal, L.; Gottrand, F.; Sfeir, R.; Guimber, D.; Devos, P.; Bonnevalle, M.; Storme, L.; Turck, D.; Michaud, L. Anastomotic Stricture after Surgical Repair of Esophageal Atresia: Frequency, Risk Factors, and Efficacy of Esophageal Bougie Dilatations. J. Pediatr. Surg. 2010, 45, 1459–1462. [Google Scholar] [CrossRef]
  22. Donoso, F.; Lilja, H. Risk Factors for Anastomotic Strictures after Esophageal Atresia Repair: Prophylactic Proton Pump Inhibitors Do Not Reduce the Incidence of Strictures. Eur. J. Pediatr. Surg. 2016, 27, 50–55. [Google Scholar] [CrossRef]
  23. Campos, J.; Tan Tanny, S.P.; Kuyruk, S.; Sekaran, P.; Hawley, A.; Brooks, J.-A.; Bekhit, E.; Hutson, J.M.; Crameri, J.; McLeod, E.; et al. The Burden of Esophageal Dilatations Following Repair of Esophageal Atresia. J. Pediatr. Surg. 2020, 55, 2329–2334. [Google Scholar] [CrossRef] [PubMed]
  24. Nelsen, T.S. Dynamic Aspects of Small Intestinal Rupture with Special Consideration of Anastomotic Strength. Arch. Surg. 1966, 93, 309. [Google Scholar] [CrossRef] [PubMed]
  25. Postlethwait, R.W.; Weinberg, M.; Jenkins, L.B.; Brockington, W.S. Mechanical Strength of Esophageal Anastomoses. Ann. Surg. 1951, 133, 472–476. [Google Scholar] [CrossRef] [PubMed]
  26. Livaditis, A.; Okmian, L.; Björck, G.; Ivemark, B. Esophageal Suture Anastomosis: An Experimental Study in Piglets. Scand. J. Thorac. Cardiovasc. Surg. 1969, 3, 163–173. [Google Scholar] [CrossRef]
  27. Cui, Y.; Urschel, J.D. Comparison of Anastomotic Suturing Techniques in the Rat Esophagus. J. Cardiovasc. Surg. 1999, 40, 613–614. [Google Scholar]
  28. Cui, Y.; Urschel, J.D. Esophagogastric Anastomotic Wound Healing in Rats. Dis. Esophagus 1999, 12, 149–151. [Google Scholar] [CrossRef]
  29. Drescher, D.G.; Vogt, J.; Gabriel, M.; Baumgart, J.; Schimanski, C.C.; Lang, H.; Gockel, I. Model of Wound Healing for Esophagogastric Anastomoses in Rats. Eur. Surg. Res. 2012, 48, 194–199. [Google Scholar] [CrossRef]
  30. Landes, L.C.; Drescher, D.; Tagkalos, E.; Grimminger, P.P.; Thieme, R.; Jansen-Winkeln, B.; Lang, H.; Gockel, I. Upregulation of VEGFR1 in a Rat Model of Esophagogastric Anastomotic Healing. Acta Chir. Belg. 2018, 118, 161–166. [Google Scholar] [CrossRef]
  31. Chung, R.S. Blood Flow in Colonic Anastomoses. Effect of Stapling and Suturing. Ann. Surg. 1987, 206, 335–339. [Google Scholar] [CrossRef] [PubMed]
  32. Wojtyczka, A.; Górka, Z.; Bierzynska-Macyszyn, G.; Rümenapf, G.; Jonderko, K.; Schwille, P.O. Gastrectomy in the Rat Using Two Modifications of Esophagojejunal Anastomosis. Eur. Surg. Res. 1999, 31, 497–507. [Google Scholar] [CrossRef] [PubMed]
  33. Ekmektzoglou, K.A.; Xanthos, T.; Dontas, I.A.; Zografos, G.C.; Giannopoulos, P.; Pantopoulou, A.; Papanicolopulos, S.A.; Kourkoulis, S.K.; Perrea, D.N. A Research Model of Measuring the Tensile Strength of Colonic Anastomosis in Wistar Rats. Scand. J. Lab. Anim. Sci. 2008, 35, 313–320. [Google Scholar]
  34. Holzner, P.; Kulemann, B.; Seifert, G.; Glatz, T.; Chikhladze, S.; Höppner, J.; Hopt, U.; Timme, S.; Bronsert, P.; Sick, O.; et al. Double 90 Degrees Counterrotated End-to-End-Anastomosis: An Experimental Study of an Intestinal Anastomosis Technique. Eur. J. Pediatr. Surg. 2015, 25, 269–276. [Google Scholar] [CrossRef] [PubMed]
  35. Khoorjestan, S.M.; Rouhi, G.; Toolabi, K. Experimental Investigations on Intestinal Anastomosis—A Comparison between Automatic and Hand Suturing Techniques. J. Mech. Med. Biol. 2016, 16, 1650056. [Google Scholar] [CrossRef]
  36. Khoorjestan, S.M.; Rouhi, G.; Toolabi, K. An Investigation of the Effects of Suture Patterns on Mechanical Strength of Intestinal Anastomosis: An Experimental Study. Biomed. Eng./Biomed. Tech. 2017, 62, 429–437. [Google Scholar] [CrossRef]
  37. Watters, D.A.; Smith, A.N.; Eastwood, M.A.; Anderson, K.C.; Elton, R.A.; Mugerwa, J.W. Mechanical Properties of the Colon: Comparison of the Features of the African and European Colon in Vitro. Gut 1985, 26, 384–392. [Google Scholar] [CrossRef]
  38. Bourgouin, S.; Bège, T.; Masson, C.; Arnoux, P.-J.; Mancini, J.; Garcia, S.; Brunet, C.; Berdah, S.V. Biomechanical Characterisation of Fresh and Cadaverous Human Small Intestine: Applications for Abdominal Trauma. Med. Biol. Eng. Comput. 2012, 50, 1279–1288. [Google Scholar] [CrossRef]
  39. Egorov, V.I.; Schastlivtsev, I.V.; Prut, E.V.; Baranov, A.O.; Turusov, R.A. Mechanical Properties of the Human Gastrointestinal Tract. J. Biomech. 2002, 35, 1417–1425. [Google Scholar] [CrossRef]
  40. Ogurtan, Z.; Gezici, M.; Kul, M.; Ceylan, C.; Alkan, F. Compararative Study of Bursting and Tensile Strengths of Digestive Tract in the Dog. Application to Esophago-Intestinal Sutures. Rev. Méd. Vet. 2001, 152, 491–494. [Google Scholar]
  41. Kratz, T.; Dauvergne, J.; Kronberg, A.-S.; Katzer, D.; Ganschow, R.; Bernhardt, M.; Westeppe, S.; Bierbach, B.; Strohm, J.; Oetzmann Von Sochaczewski, C. Not all Porcine Intestinal Segments are Equal in Terms of Breaking Force, but None were Associated to Allometric Parameters. Gastroenterol. Insights 2023, 14, 475–490. [Google Scholar] [CrossRef]
  42. Hendriks, T.; Mastboom, W.J.B. Healing of Experimental Intestinal Anastomoses: Parameters for Repair. Dis. Colon. Rectum 1990, 33, 891–901. [Google Scholar] [CrossRef]
  43. Tera, H.; Aberg, C. Tissue Holding Power to a Single Suture in Different Parts of the Alimentary Tract. Acta Chir. Scand. 1976, 142, 343–348. [Google Scholar] [PubMed]
  44. Graffner, H.; Andersson, L.; Löwenhielm, P.; Walther, B. The Healing Process of Anastomoses of the Colon: A Comparative Study Using Single, Double-Layer, or Stapled Anastomosis. Dis. Colon Rectum 1984, 27, 767–771. [Google Scholar] [CrossRef] [PubMed]
  45. Walther, B.; Löwenhielm, P.; Strand, S.E.; Ståhlberg, F.; Uvelius, B.; Oscarson, J.; Evander, A. Healing of Esophagojejunal Anastomoses after Experimental Total Gastrectomy. A Comparative Study Using Manually Sutured or Stapled Anastomoses. Ann. Surg. 1986, 203, 439–446. [Google Scholar] [CrossRef] [PubMed]
  46. Waninger, J.; Kauffmann, G.W.; Shah, I.A.; Farthmann, E.H. Influence of the Distance between Interrupted Sutures and the Tension of Sutures on the Healing of Experimental Colonic Anastomoses. Am. J. Surg. 1992, 163, 319–323. [Google Scholar] [CrossRef]
  47. Jansson, O.K.; Zilling, T.L.; Walther, B.S. Healing of Colonic Anastomoses: Comparative Experimental Study of Glued, Manually Sutured, and Stapled Anastomoses. Dis. Colon. Rectum 1991, 34, 557–562. [Google Scholar] [CrossRef]
  48. Schädel-Höpfner, M.; Windolf, J.; Lögters, T.T.; Hakimi, M.; Celik, I. Flexor Tendon Repair Using a New Suture Technique: A Comparative In Vitro Biomechanical Study. Eur. J. Trauma. Emerg. Surg. 2011, 37, 79–84. [Google Scholar] [CrossRef]
  49. Andrzejewski, T.; Czarnecki, P.; Dąbrowski, M.; Spławski, R.; Rogala, P.; Romanowski, L. Biomechanical Properties of Alternative Suture Technique for Flexor Tendon Repair. Acta Bioeng. Biomech. 2017, 19, 167–172. [Google Scholar] [CrossRef]
  50. Behrend, M.; Kluge, E.; Schüttler, W.; Klempnauer, J. Breaking Strength of Native and Sutured Trachea. An Experimental Study on Sheep Trachea. Eur. Surg. Res. 2001, 33, 255–263. [Google Scholar] [CrossRef]
  51. Oetzmann von Sochaczewski, C.; Tagkalos, E.; Lindner, A.; Lang, H.; Heimann, A.; Schröder, A.; Grimminger, P.P.; Muensterer, O.J. Esophageal Biomechanics Revisited: A Tale of Tenacity, Anastomoses, and Suture Bite Lengths in Swine. Ann. Thorac. Surg. 2019, 107, 1670–1677. [Google Scholar] [CrossRef] [PubMed]
  52. Tagkalos, E.; Lindner, A.; Gruber, G.; Lang, H.; Heimann, A.; Grimminger, P.P.; Muensterer, O.J.; Oetzmann von Sochaczewski, C. Using Simple Interrupted Suture Anastomoses May Impair Translatability of Experimental Rodent Oesophageal Surgery. Acta Chir. Belg. 2020, 120, 310–314. [Google Scholar] [CrossRef] [PubMed]
  53. Varga, A.; Matrai, A.A.; Fazekas, L.A.; Al-Khafaji, M.Q.M.; Vanyolos, E.; Deak, A.; Szentkereszty, Z.; Peto, K.; Nemeth, N. Changes in Microcirculation of Small Intestine End-to-End Anastomoses in an Experimental Model. Microvasc. Res. 2024, 156, 104731. [Google Scholar] [CrossRef] [PubMed]
  54. Kapoor, H.; Lohani, K.R.; Lee, T.H.; Agrawal, D.K.; Mittal, S.K. Animal Models of Barrett’s Esophagus and Esophageal Adenocarcinoma-Past, Present, and Future: Animal Models of Barrett’s Carcinogenesis. Clin. Transl. Sci. 2015, 8, 841–847. [Google Scholar] [CrossRef]
  55. Pommergaard, H.C.; Rosenberg, J.; Schumacher-Petersen, C.; Achiam, M.P. Choosing the Best Animal Species to Mimic Clinical Colon Anastomotic Leakage in Humans: A Qualitative Systematic Review. Eur. Surg. Res. 2011, 47, 173–181. [Google Scholar] [CrossRef]
  56. McCarthy, C.K.; McGaha, P.K.; Rozich, N.S.; Yokell, N.A.; Lees, J.S.; Berry, W.L. Creation of Colonic Anastomosis in Mice. JoVE 2019, e58742. [Google Scholar] [CrossRef]
  57. Ågren, M.S.; Andersen, L.; Heegaard, A.M.; Jorgensen, L.N. Effect of Parenteral Zinc Sulfate on Colon Anastomosis Repair in the Rat. Int. J. Color. Dis. 2008, 23, 857–861. [Google Scholar] [CrossRef]
  58. Pommergaard, H.-C.; Achiam, M.P.; Burcharth, J.; Rosenberg, J. Impaired Blood Supply in the Colonic Anastomosis in Mice Compromises Healing. Int. Surg. 2015, 100, 70–76. [Google Scholar] [CrossRef]
  59. Festing, M.F.W. Evidence Should Trump Intuition by Preferring Inbred Strains to Outbred Stocks in Preclinical Research. ILAR J. 2014, 55, 399–404. [Google Scholar] [CrossRef]
  60. Tuttle, A.H.; Philip, V.M.; Chesler, E.J.; Mogil, J.S. Comparing Phenotypic Variation between Inbred and Outbred Mice. Nat. Methods 2018, 15, 994–996. [Google Scholar] [CrossRef]
  61. Von Stumberg, M.; Akinci, E.; Ertim, B.; Oetzmann Von Sochaczewski, C. Shortcoming of the Mouse Model of Postoperative Ileus: Small Intestinal Lengths Have Similar Variations in In- and Outbred Mice and Cannot Be Predicted by Allometric Parameters. Biomedicines 2025, 13, 2948. [Google Scholar] [CrossRef]
  62. Von Kortzfleisch, V.T.; Karp, N.A.; Palme, R.; Kaiser, S.; Sachser, N.; Richter, S.H. Improving Reproducibility in Animal Research by Splitting the Study Population into Several ‘Mini-Experiments’. Sci. Rep. 2020, 10, 16579. [Google Scholar] [CrossRef] [PubMed]
  63. Treuting, P.M.; Snyder, J.M. Mouse Necropsy. CP Mouse Biol. 2015, 5, 223–233. [Google Scholar] [CrossRef] [PubMed]
  64. Block, C.L.; Childers, L.; Cortez, A.L.; Sakers, K.; Lewis, T.R.; Levic, D.S.; Frazer, L.C.; Jania, C.M.; Arshavsky, V.Y.; Good, M.; et al. The Mouse Neonatal Small Intestine Is Regionally Specialized for Protein Absorption and Transepithelial Transport. Development 2025, 152, dev205127. [Google Scholar] [CrossRef] [PubMed]
  65. Oetzmann von Sochaczewski, C.; Tagkalos, E.; Lindner, A.; Lang, H.; Heimann, A.; Muensterer, O.J. Technical Aspects in Esophageal Lengthening: An Investigation of Traction Procedures and Suturing Techniques in Swine. Eur. J. Pediatr. Surg. 2019, 29, 481–484. [Google Scholar] [CrossRef]
  66. Oetzmann von Sochaczewski, C.; Tagkalos, E.; Lindner, A.; Lang, H.; Heimann, A.; Muensterer, O.J. A Continuous Suture Anastomosis Outperforms a Simple Interrupted Suture Anastomosis in Esophageal Elongation. Eur. J. Pediatr. Surg. 2021, 31, 177–181. [Google Scholar] [CrossRef]
  67. Oetzmann von Sochaczewski, C.; Tagkalos, E.; Lindner, A.; Baumgart, N.; Gruber, G.; Baumgart, J.; Lang, H.; Heimann, A.; Muensterer, O.J. Bodyweight, Not Age, Determines Oesophageal Length and Breaking Strength in Rats. J. Pediatr. Surg. 2019, 54, 297–302. [Google Scholar] [CrossRef]
  68. Ginghina, R.C.; Kronberg, A.-S.; Dauvergne, J.; Kratz, T.; Katzer, D.; Ganschow, R.; Bernhardt, M.; Westeppe, S.; Vilz, T.O.; Bierbach, B.; et al. Anatomical Parameters Do Not Determine Linear Breaking Strength or Dimensions of the Porcine Biliary System. Bull. Natl. Res. Cent. 2024, 48, 94. [Google Scholar] [CrossRef]
  69. Bhattarai, A.; May, C.A.; Staat, M.; Kowalczyk, W.; Tran, T.N. Layer-Specific Damage Modeling of Porcine Large Intestine under Biaxial Tension. Bioengineering 2022, 9, 528. [Google Scholar] [CrossRef]
  70. Saxena, A.K.; Biro, E.; Sommer, G.; Holzapfel, G.A. Esophagus Stretch Tests: Biomechanics for Tissue Engineering and Possible Implications on the Outcome of Esophageal Atresia Repairs Performed under Excessive Tension. Esophagus 2021, 18, 346–352. [Google Scholar] [CrossRef]
  71. Faul, F.; Erdfelder, E.; Lang, A.-G.; Buchner, A. G*Power 3: A Flexible Statistical Power Analysis Program for the Social, Behavioral, and Biomedical Sciences. Bev. Res. Method. 2007, 39, 175–191. [Google Scholar] [CrossRef] [PubMed]
  72. Benjamin, D.J.; Berger, J.O.; Johannesson, M.; Nosek, B.A.; Wagenmakers, E.-J.; Berk, R.; Bollen, K.A.; Brembs, B.; Brown, L.; Camerer, C.; et al. Redefine Statistical Significance. Nat. Hum. Behav. 2017, 2, 6–10. [Google Scholar] [CrossRef] [PubMed]
  73. Anderson, S.F.; Kelley, K.; Maxwell, S.E. Sample-Size Planning for More Accurate Statistical Power: A Method Adjusting Sample Effect Sizes for Publication Bias and Uncertainty. Psychol. Sci. 2017, 28, 1547–1562. [Google Scholar] [CrossRef] [PubMed]
  74. Anderson, S.F.; Kelley, K. BUCSS: Bias and Uncertainty Corrected Sample Size; The Comprehensive R Archive Network, CRAN: Vienna, Austria, 2020. [Google Scholar]
  75. R Core Team. R: A Language and Environment for Statistical Computing; R Foundation for Statistical Computing: Vienna, Austria, 2019. [Google Scholar]
  76. Heydweiller, A.; Kurz, R.; Schröder, A.; Oetzmann von Sochaczewski, C. Inguinal Hernia Repair in Inpatient Children: A Nationwide Analysis of German Administrative Data. BMC Surg. 2021, 21, 372. [Google Scholar] [CrossRef]
  77. Oetzmann von Sochaczewski, C.; Gödeke, J. Pilonidal Sinus Disease on the Rise: A One-Third Incidence Increase in Inpatients in 13 Years with Substantial Regional Variation in Germany. Int. J. Colorectal Dis. 2021, 36, 2135–2145. [Google Scholar] [CrossRef]
  78. Heydweiller, A.; Oetzmann von Sochaczewski, C. The Epidemiology of Funnel Chest Repairs in Germany: Monitoring the Success of Nuss’ Procedure. Cardiothorac. Surg. 2022, 30, 17. [Google Scholar] [CrossRef]
  79. Singmann, H.; Bolker, B.; Westfall, J.; Aust, F.; Ben-Shachar, M.S.; Højsgaard, S.; Fox, J.; Lawrence, M.A.; Mertens, U.; Love, J.; et al. Afex: Analysis of Factorial Experiments; The Comprehensive R Archive Network, CRAN: Vienna, Austria, 2021. [Google Scholar]
  80. Lenth, R.V.; Buerkner, P.; Herve, M.; Love, J.; Miguez, F.; Riebl, H.; Singmann, H. Emmeans: Estimated Marginal Means, Aka Least-Squares Means; The Comprehensive R Archive Network, CRAN: Vienna, Austria, 2021. [Google Scholar]
  81. Oetzmann von Sochaczewski, C.; Riedesel, A.; Lindner, A.; Heimann, A.; Schröder, A.; Muensterer, O.J. A Novel Piglet Model of Esophageal Stricture Following Variable Segmental Esophageal Resection and Re-anastomosis. Anim. Models Exp. Med. 2024, 7, 936–943. [Google Scholar] [CrossRef]
  82. Oetzmann von Sochaczewski, C.; Muensterer, O.J. Pediatric Surgical Research Output in Germany in the Last 30 Years—An Assessment and International Comparison of Three Dedicated Paediatric Surgical Journals. Front. Pediatr. 2020, 8, 152. [Google Scholar] [CrossRef]
  83. Oetzmann von Sochaczewski, C.; Deigendesch, N.; Lindner, A.; Baumgart, J.; Schröder, A.; Heimann, A.; Muensterer, O.J. Comparing Aachen Minipigs and Pietrain Piglets as Models of Experimental Pediatric Urology to Human Reference Data. Eur. Surg. Res. 2020, 61, 95–100. [Google Scholar] [CrossRef]
  84. Baumgart, J.; Deigendesch, N.; Lindner, A.; Muensterer, O.J.; Schröder, A.; Heimann, A.; Oetzmann von Sochaczewski, C. Using Multidimensional Scaling in Model Choice for Congenital Oesophageal Atresia: Similarity Analysis of Human Autopsy Organ Weights with Those from a Comparative Assessment of Aachen Minipig and Pietrain Piglets. Lab. Anim. 2020, 54, 576–587. [Google Scholar] [CrossRef]
  85. Nuber, M.; Lindner, A.; Baumgart, J.; Baumgart, N.; Heimann, A.; Schröder, A.; Muensterer, O.J.; Oetzmann von Sochaczewski, C. Sex Represents a Relevant Interaction in Sprague–Dawley Rats: The Example of Oesophageal Length*. All Life 2020, 13, 448–455. [Google Scholar] [CrossRef]
  86. Lindner, A.; Tagkalos, E.; Heimann, A.; Nuber, M.; Baumgart, J.; Baumgart, N.; Muensterer, O.J.; Oetzmann von Sochaczewski, C. Tracheal Bifurcation Located at Proximal Third of Oesophageal Length in Sprague Dawley Rats of All Ages. Scand. J. Lab. Anim. Sci. 2020, 46, 25–30. [Google Scholar]
  87. Montedonico, S.; Diez-Pardo, J.A.; Possögel, A.K.; Tovar, J.A. Effects of Esophageal Shortening on the Gastroesophageal Barrier: An Experimental Study on the Causes of Reflux in Esophageal Atresia. J. Pediatr. Surg. 1999, 34, 300–303. [Google Scholar] [CrossRef] [PubMed]
  88. Morozov, D.; Morozova, O.; Severgina, L.; Mokrushina, O.; Marchuk, T.; Budnik, I.; Özbey, H.; Morozov, D. Effects of Extensive Mobilization and Tension Anastomosis in Anorectal Reconstruction (Experimental Study). Pediatr. Surg. Int. 2022, 39, 10. [Google Scholar] [CrossRef]
  89. Zhang, M.; Ma, J.; Shi, A.; Gong, R.; Zhao, X.; Zhong, Q.; Shen, L.; Lyu, Y.; Yan, X. Effect of Tissue Tension on Magnetic Compression Anastomosis of Digestive Tract. Sci. Rep. 2024, 14, 14265. [Google Scholar] [CrossRef]
  90. Cui, Y.; Chen, H. The Effect of Tension on Esophagogastric Anastomotic Wound Healing in Rats. J. Cardiovasc. Surg. 2003, 44, 775–778. [Google Scholar]
  91. Shikata, J.; Shida, T. Effects of Tension on Local Blood Flow in Experimental Intestinal Anastomoses. J. Surg. Res. 1986, 40, 105–111. [Google Scholar] [CrossRef]
  92. Fujiwara, H.; Kuga, T.; Esato, K. High Submucosal Blood Flow and Low Anastomotic Tension Prevent Anastomotic Leakage in Rabbits. Surg. Today 1997, 27, 924–929. [Google Scholar] [CrossRef]
  93. Mun, S.-P.; Kim, S.-H.; Song, C.-H.; Min, Y.-D. The Effect of Anchoring Suture on the Anastomotic Blood Flow in a Rat Model of Human Esophagojejunostomy. J. Surg. Res. 2006, 134, 163–167. [Google Scholar] [CrossRef]
  94. Oetzmann von Sochaczewski, C.; Heimann, A.; Linder, A.; Kempski, O.; Muensterer, O.J. Esophageal Blood Flow May Not Be Directly Influenced by Anastomotic Tension: An Exploratory Laser Doppler Study in Swine. Eur. J. Pediatr. Surg. 2019, 29, 516–520. [Google Scholar] [CrossRef]
  95. Soyer, T.; Kalkışım, S.; Yalcin, S.; Müderrisoğlu, A.; Taş, S.T.; Tanyel, F.C.; Ertunç, M.; Sara, Y. The Effects of Acute Tension Increase on Rat Esophageal Muscle Contractions: An in Vitro Study. J. Pediatr. Surg. 2015, 50, 1691–1694. [Google Scholar] [CrossRef] [PubMed]
  96. Lam, A.; Fleischer, B.; Alverdy, J. The Biology of Anastomotic Healing—The Unknown Overwhelms the Known. J. Gastrointest. Surg. 2020, 24, 2160–2166. [Google Scholar] [CrossRef] [PubMed]
  97. Ikeuchi, D.; Onodera, H.; Aung, T.; Kan, S.; Kawamoto, K.; Imamura, M.; Maetani, S. Correlation of Tensile Strength with Bursting Pressure in the Evaluation of Intestinal Anastomosis. Digest Surg. 1999, 16, 478–485. [Google Scholar] [CrossRef] [PubMed]
  98. Muensterer, O.J.; Sterlin, A.; Oetzmann von Sochaczewski, C.; Lindner, A.; Heimann, A.; Balus, A.; Dickmann, J.; Nuber, M.; Patel, V.H.; Manfredi, M.A.; et al. An Experimental Study on Magnetic Esophageal Compression Anastomosis in Piglets. J. Pediatr. Surg. 2020, 55, 425–432. [Google Scholar] [CrossRef]
  99. Fahmy, Y.; Trabia, M.; Ward, B.; Gallup, L.; Elks, W. Ex Vivo and Simulation Comparison of Leakage in End-to-End Versus End-to-Side Anastomosed Porcine Large Intestine. Bioengineering 2025, 12, 676. [Google Scholar] [CrossRef]
  100. Pantelis, D.; Beissel, A.; Kahl, P.; Vilz, T.O.; Stoffels, B.; Wehner, S.; Kalff, J.C. Colonic Anastomotic Healing in the Context of Altered Macrophage Function and Endotoxemia. Int. J. Colorectal Dis. 2011, 26, 737–746. [Google Scholar] [CrossRef]
  101. Chlumsky, V. Experimentelle Untersuchungen Über Die Verschiedenen Methoden Der Darmvereinigung. Bruns Beitr. Klin. Chir. 1899, 25, 539–600. [Google Scholar]
  102. Howes, E.L.; Sooy, J.W.; Harvey, S.C. The Healing of Wounds as Determined by Their Tensile Strength. JAMA 1929, 92, 42–45. [Google Scholar] [CrossRef]
  103. Rimereit, J.E.; Lindgren, C.G.W.; Nerup, N.; Madsen, G.I.; Le, D.Q.S.; Möller, S.; Qvist, N.; Ellebaek, M.B. Incorporating a Poly-ε-Caprolactone Scaffold in a Stapled Small Intestinal Anastomosis with Induced Ischemia Significantly Increased Anastomotic Tensile Strength. An Experimental Study in Pigs. Scand. J. Gastroenterol. 2025, 60, 54–61. [Google Scholar] [CrossRef]
  104. Holland-Cunz, S.; Chmelnik, M.; Roll, M.; Günther, P.; Schäfer, K.-H. The Clipped Intestinal Non-Perforating Anastomosis of Small Bowel: A New Technique. Pediatr. Surg. Int. 2006, 23, 87–93. [Google Scholar] [CrossRef]
  105. Willems, M.C.M.; Van Der Vliet, J.A.; De Man, B.M.; Van Der Laak, J.A.W.M.; Lomme, R.M.L.M.; Hendriks, T. Persistent Effects of Everolimus on Strength of Experimental Wounds in Intestine and Fascia. Wound Repair. Regen. 2010, 18, 98–104. [Google Scholar] [CrossRef] [PubMed]
  106. Castilho, T.J.C.D.; Almeida, G.H.D.R.D.; Mello, E.V.D.S.L.; Campos, A.C.L. Effect of Supplementation with Probiotics on Clonic Anastomoses in Rats: Morphological and Tensiometric Study. Arq. Bras. Cir. Dig. 2021, 33, e1550. [Google Scholar] [CrossRef] [PubMed]
  107. Petersen, L.L.K.; Dursun, M.D.; Madsen, G.; Le, D.Q.S.; Möller, S.; Qvist, N.; Ellebæk, M.B. Poly-ϵ-Caprolactone Scaffold as Staple-Line Reinforcement of Rectal Anastomosis: An Experimental Piglet Study. BMC Gastroenterol. 2024, 24, 112. [Google Scholar] [CrossRef] [PubMed]
  108. Durães, L.D.C.; Durães, E.F.R.; Lobato, L.F.D.C.; Oliveira, P.G.D.; Sousa, J.B.D. Correlation between Bursting Pressure and Breaking Strength in Colonic Anastomosis. Acta Cir. Bras. 2013, 28, 447–452. [Google Scholar] [CrossRef]
  109. Juo, Y.-Y.; Dutson, E. Comment on: Improving the Side-to-Side Stapled Anastomosis: Comparison of Staplers for Robust Crotch Formation. Surg. Obes. Relat. Dis. 2018, 14, 21–22. [Google Scholar] [CrossRef]
  110. Stavropoulou, E.A.; Dafalias, Y.F.; Sokolis, D.P. Biomechanical and Histological Characteristics of Passive Esophagus: Experimental Investigation and Comparative Constitutive Modeling. J. Biomech. 2009, 42, 2654–2663. [Google Scholar] [CrossRef]
  111. Stavropoulou, E.A.; Dafalias, Y.F.; Sokolis, D.P. Biomechanical Behavior and Histological Organization of the Three-Layered Passive Esophagus as a Function of Topography. Proc. Inst. Mech. Eng. H. 2012, 226, 477–490. [Google Scholar] [CrossRef]
  112. Siri, S.; Maier, F.; Chen, L.; Santos, S.; Pierce, D.M.; Feng, B. Differential Biomechanical Properties of Mouse Distal Colon and Rectum Innervated by the Splanchnic and Pelvic Afferents. Am. J. Physiol. Gastrointest. Liver Physiol. 2019, 316, G473–G481. [Google Scholar] [CrossRef]
  113. Siri, S.; Zhao, Y.; Maier, F.; Pierce, D.M.; Feng, B. The Macro- and Micro-Mechanics of the Colon and Rectum I: Experimental Evidence. Bioengineering 2020, 7, 130. [Google Scholar] [CrossRef]
  114. Hosseini, H.S.; Dunn, J.C.Y. Biomechanical Force Prediction for Lengthening of Small Intestine during Distraction Enterogenesis. Bioengineering 2020, 7, 140. [Google Scholar] [CrossRef]
  115. Dou, Y.; Fan, Y.; Zhao, J.; Gregersen, H. Longitudinal Residual Strain and Stress-Strain Relationship in Rat Small Intestine. BioMed Eng. OnLine 2006, 5, 37. [Google Scholar] [CrossRef] [PubMed]
  116. Sokolis, D.P. Strain-Energy Function and Three-Dimensional Stress Distribution in Esophageal Biomechanics. J. Biomech. 2010, 43, 2753–2764. [Google Scholar] [CrossRef] [PubMed]
  117. Bonaldi, L.; Berardo, A.; Pirri, C.; Stecco, C.; Carniel, E.L.; Fontanella, C.G. Mechanical Characterization of Human Fascia Lata: Uniaxial Tensile Tests from Fresh-Frozen Cadaver Samples and Constitutive Modelling. Bioengineering 2023, 10, 226. [Google Scholar] [CrossRef] [PubMed]
  118. Yang, W.; Fung, T.C.; Chian, K.S.; Chong, C.K. Directional, Regional, and Layer Variations of Mechanical Properties of Esophageal Tissue and Its Interpretation Using a Structure-Based Constitutive Model. J. Biomech. Eng. 2006, 128, 409. [Google Scholar] [CrossRef]
  119. Jia, Z.G.; Li, W.; Zhou, Z.R. Mechanical Characterization of Stomach Tissue under Uniaxial Tensile Action. J. Biomech. 2015, 48, 651–658. [Google Scholar] [CrossRef]
  120. Standley, A.; Xie, J.; Lau, A.W.; Grote, L.; Gifford, A.J. Working with Miraculous Mice: Mus musculus as a Model Organism. Curr. Protoc. 2024, 4, e70021. [Google Scholar] [CrossRef]
  121. Usui, T.; Macleod, M.R.; McCann, S.K.; Senior, A.M.; Nakagawa, S. Meta-Analysis of Variation Suggests That Embracing Variability Improves Both Replicability and Generalizability in Preclinical Research. PLoS Biol. 2021, 19, e3001009. [Google Scholar] [CrossRef]
  122. Jensen, V.S.; Porsgaard, T.; Lykkesfeldt, J.; Hvid, H. Rodent Model Choice Has Major Impact on Variability of Standard Preclinical Readouts Associated with Diabetes and Obesity Research. Am. J. Transl. Res. 2016, 8, 3574–3584. [Google Scholar]
  123. Scholz, J.; LaLiberté, C.; Van Eede, M.; Lerch, J.P.; Henkelman, M. Variability of Brain Anatomy for Three Common Mouse Strains. NeuroImage 2016, 142, 656–662. [Google Scholar] [CrossRef]
  124. Hsieh, L.S.; Wen, J.H.; Miyares, L.; Lombroso, P.J.; Bordey, A. Outbred CD1 Mice Are as Suitable as Inbred C57BL/6J Mice in Performing Social Tasks. Neurosci. Lett. 2017, 637, 142–147. [Google Scholar] [CrossRef]
  125. Pohorec, V.; Križančić Bombek, L.; Skelin Klemen, M.; Dolenšek, J.; Stožer, A. Glucose-Stimulated Calcium Dynamics in Beta Cells from Male C57BL/6J, C57BL/6N, and NMRI Mice: A Comparison of Activation, Activity, and Deactivation Properties in Tissue Slices. Front. Endocrinol. 2022, 13, 867663. [Google Scholar] [CrossRef] [PubMed]
  126. Friis, S.J.; Hansen, T.S.; Poulsen, M.; Gregersen, H.; Brüel, A.; Vinge Nygaard, J. Biomechanical Properties of the Stomach: A Comprehensive Comparative Analysis of Human and Porcine Gastric Tissue. J. Mech. Behav. Biomed. Mater. 2023, 138, 105614. [Google Scholar] [CrossRef] [PubMed]
  127. Li, F.; Liu, J.; Liu, X.; Wu, Y.; Qian, L.; Huang, W.; Li, Y. Comparison of the Biomechanical Properties between Healthy and Whole Human and Porcine Stomachs. Bioengineering 2024, 11, 233. [Google Scholar] [CrossRef] [PubMed]
  128. Durcan, C.; Hossain, M.; Chagnon, G.; Perić, D.; Girard, E. Mechanical Experimentation of the Gastrointestinal Tract: A Systematic Review. Biomech. Model. Mechanobiol. 2024, 23, 23–59. [Google Scholar] [CrossRef]
  129. Flórez-Vargas, O.; Brass, A.; Karystianis, G.; Bramhall, M.; Stevens, R.; Cruickshank, S.; Nenadic, G. Bias in the Reporting of Sex and Age in Biomedical Research on Mouse Models. eLife 2016, 5, e13615. [Google Scholar] [CrossRef]
  130. Karp, N.A.; Reavey, N. Sex Bias in Preclinical Research and an Exploration of How to Change the Status Quo. Br. J. Pharmacol. 2019, 176, 4107–4118. [Google Scholar] [CrossRef]
  131. Gong, A.T.; Yau, S.-W.O.; Erickson, H.B.; Toepfer, R.J.; Zhang, J.; Deschmidt, A.M.; Parsey, C.J.; Norfleet, J.E.; Sweet, R.M. Characterizing the Suture Pullout Force for Human Small Bowel. J. Biomech. Eng. 2024, 146, 014502. [Google Scholar] [CrossRef]
  132. Massalou, D.; Masson, C.; Afquir, S.; Baqué, P.; Arnoux, P.-J.; Bège, T. Influence of Gender, Age, Shelf-Life, and Conservation Method on the Biomechanical Behavior of Colon Tissue under Dynamic Solicitation. Clin. Biomech. 2019, 65, 34–40. [Google Scholar] [CrossRef]
  133. Christensen, H.; Andreassen, T.T.; Oxlund, H. Age-Related Alterations in the Strength and Collagen Content of Left Colon in Rats. Int. J. Colorect Dis. 1992, 7, 85–88. [Google Scholar] [CrossRef]
  134. Zhao, J.; Gregersen, H. Morphometric and Biomechanical Remodeling of the Small Intestine during Aging in Rats. J. Biomech. 2015, 48, 4271–4278. [Google Scholar] [CrossRef]
  135. Eisen, E.J.; Lang, B.J.; Legates, J.E. Comparison of Growth Functions within and between Lines of Mice Selected for Large and Small Body Weight. Theoret Appl. Genet. 1969, 39, 251–260. [Google Scholar] [CrossRef]
  136. Eisen, E.J. Results of Growth Curve Analyses in Mice and Rats. J. Anim. Sci. 1976, 42, 1008–1023. [Google Scholar] [CrossRef]
Figure 1. A detailed view of the murine stomach inside the motorised test stand at the beginning of the traction experiment.
Figure 1. A detailed view of the murine stomach inside the motorised test stand at the beginning of the traction experiment.
Gastroent 17 00012 g001
Figure 2. Violin plot of sustained traction forces of the stomachs of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Figure 2. Violin plot of sustained traction forces of the stomachs of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Gastroent 17 00012 g002
Figure 3. Violin plot of sustained traction forces of the duodena of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Figure 3. Violin plot of sustained traction forces of the duodena of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Gastroent 17 00012 g003
Figure 4. Violin plot of sustained traction forces of the jejuna of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Figure 4. Violin plot of sustained traction forces of the jejuna of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Gastroent 17 00012 g004
Figure 5. Violin plot of sustained traction forces of the ilea of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Figure 5. Violin plot of sustained traction forces of the ilea of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Gastroent 17 00012 g005
Figure 6. Violin plot of sustained traction forces of the caeca of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Figure 6. Violin plot of sustained traction forces of the caeca of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Gastroent 17 00012 g006
Figure 7. Violin plot of sustained traction forces of the colons of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Figure 7. Violin plot of sustained traction forces of the colons of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Gastroent 17 00012 g007
Figure 8. Violin plot of sustained traction forces of the rectums of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Figure 8. Violin plot of sustained traction forces of the rectums of 54 Crl:CD1(ICR), 10 C57Bl/6J, and 10 C57Bl/6NCrl mice. The dashed line represents the median and the dotted lines the interquartile range.
Gastroent 17 00012 g008
Figure 9. Depiction of the estimated marginal means of the breaking forces in Newtons of the organs of the gastrointestinal tract of all three included mouse strains: Crl:CD1(ICR) [n = 54], C57Bl/6J [n = 10], and C57Bl/6NCrl [n = 10]. The point indicates the mean breaking force. The shadowed green rectangle indicates the 95% confidence interval of the mean breaking force. The arrows indicate if there are measurements smaller or larger than the respective measurement.
Figure 9. Depiction of the estimated marginal means of the breaking forces in Newtons of the organs of the gastrointestinal tract of all three included mouse strains: Crl:CD1(ICR) [n = 54], C57Bl/6J [n = 10], and C57Bl/6NCrl [n = 10]. The point indicates the mean breaking force. The shadowed green rectangle indicates the 95% confidence interval of the mean breaking force. The arrows indicate if there are measurements smaller or larger than the respective measurement.
Gastroent 17 00012 g009
Table 1. Pairwise contrasts of the breaking forces of the gastrointestinal tracts of 54 Crl:CD1(ICR) mice. ∆ represents the mean difference in breaking forces in Newtons. p-values are corrected for multiple testing using the Benjamini–Hochberg procedure.
Table 1. Pairwise contrasts of the breaking forces of the gastrointestinal tracts of 54 Crl:CD1(ICR) mice. ∆ represents the mean difference in breaking forces in Newtons. p-values are corrected for multiple testing using the Benjamini–Hochberg procedure.
Contrast∆ [Newton]t-Ratiop-Value
Stomach–Duodenum1.2116.66<0.001
Stomach–Jejunum1.3318.33<0.001
Stomach–Ileum1.419.32<0.001
Stomach–Caecum0.7410.25<0.001
Stomach–Colon0.8912.32<0.001
Stomach–Rectum0.547.49<0.001
Duodenum–Jejunum0.121.660.102
Duodenum–Ileum0.192.660.009
Duodenum–Caecum−0.47−6.41<0.001
Duodenum–Colon−0.32−4.35<0.001
Duodenum–Rectum−0.67−9.17<0.001
Jejunum–Ileum0.0710.32
Jejunum–Caecum−0.59−8.08<0.001
Jejunum–Colon−0.446.01<0.001
Jejunum–Rectum−0.79−10.84<0.001
Ileum–Caecum−0.66−9.07<0.001
Ileum–Colon−0.51−7.01<0.001
Ileum–Rectum−0.86−11.83<0.001
Caecum–Colon0.152.070.043
Caecum–Rectum−0.2−2.760.008
Colon–Rectum−0.35−4.82<0.001
Table 2. Pairwise contrasts of the breaking forces of the gastrointestinal tracts of 10 C57Bl/6J mice. ∆ represents the mean difference in breaking forces in Newtons. p-values are corrected for multiple testing using the Benjamini–Hochberg procedure.
Table 2. Pairwise contrasts of the breaking forces of the gastrointestinal tracts of 10 C57Bl/6J mice. ∆ represents the mean difference in breaking forces in Newtons. p-values are corrected for multiple testing using the Benjamini–Hochberg procedure.
Contrast∆ [Newton]t-Ratiop-Value
Stomach–Duodenum1.83−10.85<0.001
Stomach–Jejunum1.87−11.09<0.001
Stomach–Ileum2.0712.28<0.001
Stomach–Caecum1.317.77<0.001
Stomach–Colon1.619.55<0.001
Stomach–Rectum1.146.73<0.001
Duodenum–Jejunum0.040.240.813
Duodenum–Ileum0.241.420.192
Duodenum–Caecum−0.52−3.080.004
Duodenum–Colon−0.22−1.310.225
Duodenum–Rectum−0.7−4.12<0.001
Jejunum–Ileum0.21.190.261
Jejunum–Caecum−0.56−3.320.002
Jejunum–Colon−0.26−1.540.162
Jejunum–Rectum−0.74−4.36<0.001
Ileum–Caecum−0.76−4.51<0.001
Ileum–Colon−0.46−2.730.01
Ileum–Rectum−0.94−5.55<0.001
Caecum–Colon0.31.780.106
Caecum–Rectum−0.18−1.040.315
Colon–Rectum−0.48−2.820.008
Table 3. Pairwise contrasts of the breaking forces of the gastrointestinal tracts of 10 C57Bl/6NCrl mice. ∆ represent the mean difference in breaking forces in Newtons. p-values are corrected for multiple testing using the Benjamini–Hochberg procedure.
Table 3. Pairwise contrasts of the breaking forces of the gastrointestinal tracts of 10 C57Bl/6NCrl mice. ∆ represent the mean difference in breaking forces in Newtons. p-values are corrected for multiple testing using the Benjamini–Hochberg procedure.
Contrast∆ [Newton]t-Ratiop-Value
Stomach–Duodenum1.559.16<0.001
Stomach–Jejunum1.659.76<0.001
Stomach–Ileum1.7710.47<0.001
Stomach–Caecum0.975.72<0.001
Stomach–Colon1.277.5<0.001
Stomach–Rectum0.885.19<0.001
Duodenum–Jejunum0.10.590.581
Duodenum–Ileum0.221.310.225
Duodenum–Caecum−0.58−3.440.001
Duodenum–Colon−0.28−1.660.12
Duodenum–Rectum−0.67−3.97<0.001
Jejunum–Ileum0.120.710.572
Jejunum–Caecum−0.68−4.03<0.001
Jejunum–Colon−0.38−2.250.035
Jejunum–Rectum−0.77−4.57<0.001
Ileum–Caecum−0.8−4.75<0.001
Ileum–Colon−0.5−2.970.005
Ileum–Rectum−0.89−5.28<0.001
Caecum–Colon0.31.780.1
Caecum–Rectum−0.09−0.530.594
Colon–Rectum−0.39−2.310.032
Table 4. Pairwise contrasts of the breaking forces of the gastrointestinal organs between the included mouse strains: Crl:CD1(ICR) [n = 54], C57Bl/6J [n = 10], and C57Bl/6NCrl [n = 10]. ∆ represents the mean difference in breaking forces in Newtons. p-values are corrected for multiple testing using the Benjamini–Hochberg procedure.
Table 4. Pairwise contrasts of the breaking forces of the gastrointestinal organs between the included mouse strains: Crl:CD1(ICR) [n = 54], C57Bl/6J [n = 10], and C57Bl/6NCrl [n = 10]. ∆ represents the mean difference in breaking forces in Newtons. p-values are corrected for multiple testing using the Benjamini–Hochberg procedure.
Contrast∆ [Newton]t-Ratiop-Value
Stomach
Crl:CD1(ICR)–C57Bl/6J−0.81−6.23<0.001
Crl:CD1(ICR)–C57Bl/6NCrl−0.37−2.880.006
C57Bl/6J–C57Bl/6NCrl0.442.580.01
Duodenum
Crl:CD1(ICR)–C57Bl/6J−0.19−1.440.448
Crl:CD1(ICR)–C57Bl/6NCrl−0.04−0.290.773
C57Bl/6J–C57Bl/6NCrl0.150.890.561
Jejunum
Crl:CD1(ICR)–C57Bl/6J−0.27−2.070.118
Crl:CD1(ICR)–C57Bl/6NCrl−0.06−0.450.654
C57Bl/6J–C57Bl/6NCrl0.211.250.32
Ileum
Crl:CD1(ICR)–C57Bl/6J−0.14−1.080.662
Crl:CD1(ICR)–C57Bl/6NCrl−0.01−0.080.936
C57Bl/6J–C57Bl/6NCrl0.130.770.662
Caecum
Crl:CD1(ICR)–C57Bl/6J−0.24−1.870.188
Crl:CD1(ICR)–C57Bl/6NCrl−0.15−1.170.363
C57Bl/6J–C57Bl/6NCrl0.090.530.594
Colon
Crl:CD1(ICR)–C57Bl/6J−0.09−0.710.891
Crl:CD1(ICR)–C57Bl/6NCrl00.020.988
C57Bl/6J–C57Bl/6NCrl0.090.530.891
Rectum
Crl:CD1(ICR)–C57Bl/6J−0.22−1.670.285
Crl:CD1(ICR)–C57Bl/6NCrl−0.04−0.320.746
C57Bl/6J–C57Bl/6NCrl0.181.040.5
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

Ertim, B.; Akinci, E.; von Stumberg, M.; Katzer, D.; Ganschow, R.; Vilz, T.O.; Oetzmann von Sochaczewski, C. The Resistance to Traction Forces Differs Substantially Between Intestinal Parts, but Not Between In- and Outbred Strains of Mice. Gastroenterol. Insights 2026, 17, 12. https://doi.org/10.3390/gastroent17010012

AMA Style

Ertim B, Akinci E, von Stumberg M, Katzer D, Ganschow R, Vilz TO, Oetzmann von Sochaczewski C. The Resistance to Traction Forces Differs Substantially Between Intestinal Parts, but Not Between In- and Outbred Strains of Mice. Gastroenterology Insights. 2026; 17(1):12. https://doi.org/10.3390/gastroent17010012

Chicago/Turabian Style

Ertim, Berkan, Ejder Akinci, Maximiliane von Stumberg, David Katzer, Rainer Ganschow, Tim O. Vilz, and Christina Oetzmann von Sochaczewski. 2026. "The Resistance to Traction Forces Differs Substantially Between Intestinal Parts, but Not Between In- and Outbred Strains of Mice" Gastroenterology Insights 17, no. 1: 12. https://doi.org/10.3390/gastroent17010012

APA Style

Ertim, B., Akinci, E., von Stumberg, M., Katzer, D., Ganschow, R., Vilz, T. O., & Oetzmann von Sochaczewski, C. (2026). The Resistance to Traction Forces Differs Substantially Between Intestinal Parts, but Not Between In- and Outbred Strains of Mice. Gastroenterology Insights, 17(1), 12. https://doi.org/10.3390/gastroent17010012

Article Metrics

Back to TopTop