In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

[EX Q]: Context: Benign esophageal strictures are frequently encountered pathologies occurring due to various reasons. Repeated dilatations may be needed, particularly in resistant strictures. This study aimed to evaluate patients who underwent repeated dilatations in our clinic due to resistant esophageal strictures.', 'Sixteen patients who underwent multiple dilatations in our clinic with the diagnosis of resistant benign esophageal stricture between 2007 and 2014 were studied for age, sex, etiology, symptoms, complications, number of dilatations, and intervals between dilatations. Under general anesthesia, all patients underwent dilatation with Savary-Gilliard bougie dilators with the help of rigid esophagoscopy.', 'In 10 of the patients, stenosis was cervical, and in others it was in the thoracic esophagus. The mean dilatation performance was 4.4 (range: 3-12). In 9 patients, dilatations were performed when the patients presented with the complaint of dysphagia. Following the initial dilatation performed for dysphagia, 7 patients underwent endoscopy and dilatation 3-5 times with 1-week intervals without waiting for the development of dysphagia symptoms. These patients developed no complications, and no stenting was needed. In 5 patients, restenosis developed despite multiple dilatations, and esophageal stent placement was performed.\Question: Is recurrent dilatation in resistant benign esophageal strictures : timing significant?
[EX A]: Dilatations performed at frequent intervals without waiting for the symptoms of dysphagia can contribute to safer and more effective results in resistant benign esophageal strictures.

[EX Q]: Context: The proteasome is the proteolytically active core of the ubiquitin-proteasome system, which regulates vital processes and which can cause various diseases when it malfunctions. Therefore, the proteasome has become an attractive target for pharmaceutical interventions. Inhibition of the cardiac proteasome by specific proteasome inhibitors has been shown to attenuate cardiac hypertrophy and ischaemia reperfusion injury of the heart. We have resolved the cardiac proteasome into its subtypes and have addressed the key question of how proteasome inhibitors affect single cardiac proteasomal subtypes.', 'The 20S proteasome from rat heart was dissected into three different subpopulations (groups I-III), each comprising 4-7 different subtypes. The major group (group II) comprises standard proteasome subtypes; the two minor subpopulations (groups I and III) contain intermediate proteasome subtypes. All subtypes exhibit chymotrypsin-, trypsin-, and caspase-like activity but to different degrees. We have tested the effect of two common proteasome inhibitors on the chymotrypsin-like activity of all subtypes: 20-30 nmol/L MG132 caused 50% inhibition of all subtypes from groups I and II, whereas 100 nmol/L was necessary to affect group III subtypes to the same extent. However, another inhibitor, bortezomib (VELCADE), already used clinically, inhibited 50% of the activity of group III proteasome subtypes even below 20 nmol/L, a concentration showing almost no effect on group I and II proteasome subtypes. The caspase-like activity of group II proteasome subtypes was not affected by MG132 and was inhibited by bortezomib only at concentrations above 100 nmol/L.\Question: Do multiple cardiac proteasome subtypes differ in their susceptibility to proteasome inhibitors?
[EX A]: These data show that different inhibitors have differential inhibitory effects on the various cardiac proteasome subtypes. Different cardiac subtypes are inhibited by the same dose of proteasome inhibitor to a different extent.

[EX Q]: Context: Acute rejection is the major risk factor for the development of subsequent chronic allograft nephropathy (CAN), which is the primary reason for late allograft loss in kidney transplantation. Platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta) are the main mitogens mediating mesenchymal cell proliferation. Their early post-transplant induction may start cascades leading to the development of CAN. An immunosuppressive drug, FK778, inhibits de novo pyrimidine biosynthesis and several receptor tyrosine kinases (RTKs). Here we investigated its effects on acute and chronic rejection as well as post-transplant PDGF and TGF-beta expression in combination therapy with calcineurin inhibitors (CNIs).', 'Kidney transplantations were performed from DA to WF rats. Syngenic DA-DA grafts were used as controls. Allografts were immunosuppressed with a combination of FK778 (10 mg/kg/day p.o.) and CsA (1.5 mg/kg/day s.c.) or tacrolimus (Tac) (1.5 mg/kg/day p.o.). Grafts were harvested 5 and 90 days after transplantation for histology and immunohistochemistry (PDGF-A, PDGF-B, PDGFR-alpha, PDGFR-beta, TGF-beta, TGF-betaR). The dose response of FK778 on acute rejection was studied with monotherapy of 5, 10 and 20 mg/kg/day. Chronic changes were scored according to the Chronic Allograft Damage Index (CADI).', 'FK778 ameliorated the early post-transplant inflammatory response dose dependently. Additive effects were seen with FK778 and CNIs. Significantly lower CADI scores were seen in combination therapy of FK778 and CNIs compared with CNI monotherapies. FK778 also significantly reduced both early and late PDGF and TGF-beta expression when combined with CNIs.\Question: Does fK778 ameliorate post-transplant expression of fibrogenic growth factors and development of chronic rejection changes in rat kidney allografts?
[EX A]:
These results indicate that FK778 could prevent the development of CAN and be a promising therapy also in clinical kidney transplantation.