Spermatogenesis is a multiple-staged continuous progress of cellular differentiation. It has been reported that some cell surface glycoconjugates are modified during the early steps of spermatogenesis, and influence the differentiation of spermatogenic cells [26] . As ninecarbon sugars commonly found in many glycoproteins of spermatogenic cells, sialic acids represent a target for cell surface modification, that is, removal of 9-O-acetyl esters by enzymes such as Lse. Modification of sialic acids may result in alteration in cell-cell communication, that is, Sertoli cells and germ cells interaction, thereby influencing the differentiation of spermatogenic cells. Thus, future studies on the presently identified H-Lse may provide insight into molecular mechanisms underlying testicular development and/or germ cell differentiation during spermatogenesis in humans. The role of mast cells in the pathogenesis of pain in chronic pancreatitis BACKGROUND: The biological basis of pain in chronic pancreatitis is poorly understood. Mast cells have been implicated in the pathogenesis of pain in other conditions. We hypothesized that mast cells play a role in the pain of chronic pancreatitis. We examined the association of pain with mast cells in autopsy specimens of patients with painful chronic pancreatitis. We explored our hypothesis further using an experimental model of trinitrobenzene sulfonic acid (TNBS) -induced chronic pancreatitis in both wild type (WT) and mast cell deficient mice (MCDM). METHODS: Archival tissues with histological diagnoses of chronic pancreatitis were identified and clinical records reviewed for presence or absence of reported pain in humans. Mast cells were counted. The presence of pain was assessed using von Frey Filaments (VFF) to measure abdominal withdrawal responses in both WT and MCDM mice with and without chronic pancreatitis. RESULTS: Humans with painful chronic pancreatitis demonstrated a 3.5-fold increase in pancreatic mast cells as compared with those with painless chronic pancreatitis. WT mice with chronic pancreatitis were significantly more sensitive as assessed by VFF pain testing of the abdomen when compared with MCDM. CONCLUSION: Humans with painful chronic pancreatitis have an increased number of pancreatic mast cells as compared with those with painless chronic pancreatitis. MCDM are less sensitive to mechanical stimulation of the abdomen after induction of chronic pancreatitis as compared with WT. Mast cells may play an important role in the pathogenesis of pain in chronic pancreatitis. Although pain is the presenting symptom of most patients with chronic pancreatitis, its neurobiological basis remains poorly understood [1] . In the past, investigators have focused on the role of anatomical abnormalities such as a strictured pancreatic duct or narrowed intraparenchymal ducts. However, mechanical decompression techniques such as endoscopic stent placement or even surgical pancreatojejunostomy frequently do not provide a permanent solution to the pain [1] . More recently, investigators have begun focusing on the role of neurotransmitters and neurotrophins such as substance P and nerve growth factor with known or suspected roles in nociceptive signaling and/or sensitization and have reported an increased expression of several of them in the pancreas of patients with painful chronic pancreatitis [2] . Mast cells are also increased in both acute and chronic pancreatitis [3, 4] but their role in the generation of pain in pancreatitis has not been investigated.