Towards Runtime Verification of Programmable Switches

Is it possible to patch software bugs in P4 programs without human involvement? We show that this is partially possible in many cases due to advances in software testing and the structure of P4 programs. Our insight is that runtime verification can detect bugs, even those that are not detected at compile-time, with machine learning-guided fuzzing. This enables a more automated and real-time localization of bugs in P4 programs using software testing techniques like Tarantula. Once the bug in a P4 program is localized, the faulty code can be patched due to the programmable nature of P4. In addition, platform-dependent bugs can be detected. From P4_14 to P4_16 (latest version), our observation is that as the programmable blocks increase, the patchability of P4 programs increases accordingly. To this end, we design, develop, and evaluate P6 that (a) detects, (b) localizes, and (c) patches bugs in P4 programs with minimal human interaction. P6 tests P4 switch non-intrusively, i.e., requires no modification to the P4 program for detecting and localizing bugs. We used a P6 prototype to detect and patch seven existing bugs in eight publicly available P4 application programs deployed on two different switch platforms: behavioral model (bmv2) and Tofino. Our evaluation shows that P6 significantly outperforms bug detection baselines while generating fewer packets and patches bugs in P4 programs such as switch.p4 without triggering any regressions

Chronic Pancreatitis and Systemic Inflammatory Response Syndrome Prevent Impact of Chemotherapy with Gemcitabine in a Genetically Engineered Mouse Model of Pancreatic Cancer

BACKGROUND AND AIMS: BACKGROUND AND AIMSGemcitabine is the standard therapy for patients with pancreatic cancer with metastatic disease. Patients with metastatic pancreatic cancer presenting with increased values of C-reactive protein do not respond to gemcitabine. So far, no studies have evaluated the correlation between chronic pancreatitis, systemic inflammatory response syndrome, and the loss of chemotherapeutic benefit. METHODS: Pdx-1-Cre;LSL-KrasG12D/+;LSL-Trp53R172H/+ mice were assigned into four groups: 1) Sixteen animals received a daily intraperitoneal injection of caerulein from their ninth week of life on. 2) Sixteen mice were additionally given gemcitabine. 3) Twelve animals received gemcitabine only. 4) Saline-treated control group. Furthermore, human Paca44 pancreatic ductal adenocarcinoma cells were seeded and cultured in 0.5% FBS containing growth medium plus/minus 1 μM gemcitabine plus/minus recombinant human interleukin (IL)-6. RESULTS: Induced systemic inflammatory response syndrome and a mild chronic pancreatitis diminished the beneficial effects of gemcitabine upon median overall survival. In median, the monogemcitabine group survived 191 days, whereas the caerulein-mono group survived 114, the control group 121, and the caerulein gemcitabine group 127 days (P < .05). In vitro, the induction of STAT3 phosphorylation by recombinant human IL-6 promoted pancreatic ductal adenocarcinoma cell survival during gemcitabine treatment. CONCLUSION: We could demonstrate for the first time that an improvement in median overall survival with gemcitabine is significantly abolished by a persistent mild chronic pancreatitis and a systemic inflammatory response syndrome. In particular, the inflammation biomarkers C-reactive protein, IL-6, and IL-1α could indicate the prognostic benefit of gemcitabine chemotherapy and should now be tested in prospective patient-controlled trials