A surgical activity model of laparoscopic cholecystectomy for co-operation with collaborative robots.

BACKGROUND: Laparoscopic cholecystectomy is a very frequent surgical procedure. However, in an ageing society, less surgical staff will need to perform surgery on patients. Collaborative surgical robots (cobots) could address surgical staff shortages and workload. To achieve context-awareness for surgeon-robot collaboration, the intraoperative action workflow recognition is a key challenge. METHODS: A surgical process model was developed for intraoperative surgical activities including actor, instrument, action and target in laparoscopic cholecystectomy (excluding camera guidance). These activities, as well as instrument presence and surgical phases were annotated in videos of laparoscopic cholecystectomy performed on human patients (n = 10) and on explanted porcine livers (n = 10). The machine learning algorithm Distilled-Swin was trained on our own annotated dataset and the CholecT45 dataset. The validation of the model was conducted using a fivefold cross-validation approach. RESULTS: In total, 22,351 activities were annotated with a cumulative duration of 24.9 h of video segments. The machine learning algorithm trained and validated on our own dataset scored a mean average precision (mAP) of 25.7% and a top K = 5 accuracy of 85.3%. With training and validation on our dataset and CholecT45, the algorithm scored a mAP of 37.9%. CONCLUSIONS: An activity model was developed and applied for the fine-granular annotation of laparoscopic cholecystectomies in two surgical settings. A machine recognition algorithm trained on our own annotated dataset and CholecT45 achieved a higher performance than training only on CholecT45 and can recognize frequently occurring activities well, but not infrequent activities. The analysis of an annotated dataset allowed for the quantification of the potential of collaborative surgical robots to address the workload of surgical staff. If collaborative surgical robots could grasp and hold tissue, up to 83.5% of the assistant's tissue interacting tasks (i.e. excluding camera guidance) could be performed by robots.

Positive selection of type 2 diabetes genotypes - the glycaemic threshold hypothesis.

The high prevalence of deleterious polygenic type 2 diabetes (T2D) is a paradox requiring explanation beyond food excess, inactivity and the obesity resulting from positive energy balance. Historically, hunting-foraging and later agrarian communities often manifested a converse negative energy balance due to nutritional deficit and/or high physical energy demand - both potentially resulting in hypoglycaemia. Since hypoglycaemia impairs both reproductive fitness and cognitive function, it is proposed that that by expressing resistance to hypoglycaemia, T2D phenotypes were subject to positive selection. The insulin resistance present in often-associated atherosclerotic cardiovascular disease, metabolic syndrome and polycystic ovarian disease may also explain their frequent coexistence and current prevalence.

Transdisciplinary translational science and the case of preterm birth.

Medical researchers have called for new forms of translational science that can solve complex medical problems. Mainstream science has made complementary calls for heterogeneous teams of collaborators who conduct transdisciplinary research so as to solve complex social problems. Is transdisciplinary translational science what the medical community needs? What challenges must the medical community overcome to successfully implement this new form of translational science? This article makes several contributions. First, it clarifies the concept of transdisciplinary research and distinguishes it from other forms of collaboration. Second, it presents an example of a complex medical problem and a concrete effort to solve it through transdisciplinary collaboration: for example, the problem of preterm birth and the March of Dimes effort to form a transdisciplinary research center that synthesizes knowledge on it. The presentation of this example grounds discussion on new medical research models and reveals potential means by which they can be judged and evaluated. Third, this article identifies the challenges to forming transdisciplines and the practices that overcome them. Departments, universities and disciplines tend to form intellectual silos and adopt reductionist approaches. Forming a more integrated (or 'constructionist'), problem-based science reflective of transdisciplinary research requires the adoption of novel practices to overcome these obstacles.

The effects of weightlessness on the human organism and mammalian cells.

It has always been a desire of mankind to conquest Space. A major step in realizing this dream was the completion of the International Space Station (ISS). Living there for several months confirmed early observations of short-term spaceflights that a loss of gravity affects the health of astronauts. Space medicine tries to understand the mechanism of microgravity-induced health problems and to conceive potent countermeasures. There are four different aspects which make space medicine appealing: i) finding better strategies for adapting astronauts to weightlessness; ii) identification of microgravity-induced diseases (e.g. osteoporosis, muscle atrophy, cardiac problems and others); iii) defining new therapies to conquer these diseases which will benefit astronauts as well as people on Earth in the end; and iv) on top of that, unveiling the mechanisms of weightlessness-dependent molecular and cellular changes is a requirement for improving space medicine. In mammalian cells, microgravity induces apoptosis and alters the cytoskeleton and affects signal transduction pathways, cell differentiation, growth, proliferation, migration and adhesion. This review focused on gravi-sensitive signal transduction elements and pathways as well as molecular mechanisms in human cells, aiming to understand the cellular changes in altered gravity. Moreover, the latest information on how these changes lead to clinically relevant health problems and current strategies of countermeasures are reviewed.

The front end test stand high performance H- ion source at Rutherford Appleton Laboratory.

The aim of the front end test stand (FETS) project is to demonstrate that chopped low energy beams of high quality can be produced. FETS consists of a 60 mA Penning Surface Plasma Ion Source, a three solenoid low energy beam transport, a 3 MeV radio frequency quadrupole, a chopper, and a comprehensive suite of diagnostics. This paper details the design and initial performance of the ion source and the laser profile measurement system. Beam current, profile, and emittance measurements are shown for different operating conditions.

Carcinoid tumors are 15 times more common in patients with Crohn's disease.

BACKGROUND: The coexistence of intestinal neoplasms with Crohn's disease (CD) has been reported, but the evidence of an increased risk of carcinoid tumor with Crohn's disease has been mixed. We present 4 patients with CD with associated carcinoid tumor. METHODS: The charts of 111 patients with CD who had undergone resection between June 2001 and March 2005 were reviewed. The number of incidental carcinoid tumors in patients who underwent an appendectomy was used as a control. RESULTS: Four cases of carcinoid tumor discovered in patients at resection for CD were identified. None had metastatic disease or carcinoid syndrome. These included 1 cecal (1 mm), 2 appendiceal (3 and 7 mm), and 1 transverse colon (7 mm) carcinoid tumors. None of the carcinoid tumors were identified in regions of active Crohn's disease. The incidence of carcinoid tumor in patients with Crohn's disease was 4 of 111 (3.6%). In comparison, 3 of 1199 patients (0.25%) who had appendectomies were identified as having appendiceal carcinoid tumor. Crohn's disease was associated with an increased incidence of carcinoid tumor; OR 14.9 (95% CI 2.5-102.5), P<0.0001. CONCLUSIONS: There was a significantly increased incidence of carcinoid tumor in our Crohn's patients compared to the control patients. None of the carcinoid tumors developed in areas of Crohn's disease. This suggests that the development of carcinoid tumors may be secondary to distant proinflammatory mediators, rather than a local inflammatory effect from adjacent Crohn's disease. Patients with CD may be at increased risk of developing a carcinoid tumor.

SSRIs & the risk of abnormal bleeding.

Considerable research is needed to fully understand the interactions of SSRIs and hematological functioning. Adequate studies of platelet function in patients taking SSRIs are lacking. The risk of bleeding with SSRI treatment appears to be low, and the occurrence of bleeding is usually minor when it does occur. However, the risk does exist and must be considered in any patient taking SSRIs who develops abnormal bleeding or bruising not otherwise explained by an appropriate assessment to determine the etiology. Routine monitoring of patients taking SSRIs should probably include questions about bruising or bleeding, particularly in patients with blood dyscrasias and in older patients taking medications that affect platelet function. Caution should be exercised before starting patients with preexisting bleeding risks on SSRIs, including patients taking NSAIDs, aspirin, or other drugs that may impair coagulation.

Stroke injury in rats causes an increase in activin A gene expression which is unaffected by oestradiol treatment.

Activins are members of the transforming growth factor-beta superfamily that exert neurotrophic and neuroprotective effects on various neuronal populations. To determine the possible function of activin in stroke injury, we assessed which components of the activin signalling pathway were modulated in response to middle cerebral artery occlusion (MCAO). Furthermore, because oestradiol replacement protects against MCAO-induced cell death, we explored whether oestradiol replacement influences activin gene expression. Female Sprague-Dawley rats underwent permanent MCAO and the expression of activins and their corresponding receptors was determined by semiquantitative reverse transcriptase-polymerase chain reaction at 24 h after onset of ischaemia. We observed up-regulation of activin betaA and activin type I receptor A mRNA in response to injury. Dual-label immunocytochemistry followed by confocal z-stack analysis showed that the activin A expressing cells comprised neurones. Next, we monitored the time course of activin betaA mRNA expression in oestradiol- or vehicle-treated rats at 4, 8, 16 and 24 h after MCAO via in situ hybridisation. Starting at 4 h after injury, activin betaA mRNA was up-regulated in cortical and striatal areas in the ipsilateral hemisphere. Activin betaA mRNA levels in the cortex increased dramatically with time and were highest at 24 h after the insult, and oestradiol replacement did not influence this increase.

Estrogen therapy: does it help or hurt the adult and aging brain? Insights derived from animal models.

Hormone therapy and estrogen therapy in postmenopausal women have been thought to ameliorate cognitive dysfunction and decrease the risk and/or progress of neurodegenerative conditions such as Alzheimer's disease and stroke. Furthermore, estrogens have been shown to exert neuroprotective actions in a variety of in vitro and in vivo models of brain injury. However, the findings of the Women's Health Initiative have made us re-evaluate these assumptions. Our laboratory has shown that physiological levels of estradiol attenuate ischemic brain injury in young and middle-aged female rats. We have begun to probe the cellular and molecular mechanisms that underlie these novel non-reproductive actions of this steroid. Our findings demonstrate that in both young and aging rats, treatment with physiological concentrations of estradiol decreases ischemic injury by almost 50%, compared with oil-treated controls. Additionally, our data suggest that estradiol acts by altering the expression of genes that suppress apoptosis and enhance survival in the penumbral region of the infarct. These observations demonstrate that estrogen therapy protects against stroke-related injury in young and aging female rats and strongly suggest that middle-aged animals remain responsive to the protective actions of estradiol. Furthermore, they suggest that estrogen therapy protects against cell death by influencing the expression of genes that suppress apoptotic cell death pathways.