The effect of capsaicin (10–80 mg/kg sc) on reflex activity of the urinary bladder was examined in anesthetized normal as well as anesthetized and awake chronic spinal cord-injured (SCI) cats. In normal cats, capsaicin elicited a transient increase in the frequency of isovolumetric bladder contractions and reduced the volume threshold for inducing micturition, but did not depress the amplitude of bladder contractions or the reflex firing on bladder nerves. In anesthetized SCI cats, capsaicin depressed reflex bladder activity and firing on bladder nerves. In awake SCI cats, capsaicin initially decreased the volume threshold for inducing micturition; however, after a delay of 3–6 h the volume threshold increased and intravesical voiding pressure decreased. This effect persisted for 4–12 days. It is concluded that capsaicin-sensitive C fiber bladder afferents are not involved in initiating reflex micturition in normal cats, but play an essential role in triggering automatic micturition in chronic SCI cats. The results are consistent with the clinical data indicating that C fiber bladder afferents contribute to bladder hyperactivity and incontinence in patients with neurogenic bladder dysfunction.

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One hundred dry skulls of adult Chinese of both sexes were studied. They were homogeneous in the form of maxillary arch and having full eruption of the upper third molar, without missing teeth and malposition of teeth. Our findings revealed that the mean distance from the center of the greater palatine foramen (GPF) to the midsagittal plane of the hard palate was 16.00 mm, and to the posterior border of the hard palate, 4.11 mm. The location of the GPF related to the maxillary molars was expressed as percentage in 5 relations. We found that the most common location of the GPF was between the maxillary second and third molars (relation III: 48%) and less common was lingual to the maxillary third molar (relation IV: 33.5%). The usually accepted description of the GPF location was lingual to the second molar (relation II), but in our study this relative position occurred in only 17% of the skulls. The long axis of the greater palatine canal directing to the GPF in the oral cavity was found to be directed anteriorly in 181 openings (90.5%) of the 200 GPF, and only 19 openings (9.5%) directed vertically. The bilateral symmetry of GPF on both sides of each skull was remarkable. The discrepancy of our observations on the Chinese skulls from those on other ethnic groups was discussed. Our findings suggest, therefore, the existence of an ethnic variation and the necessity of a more accurate method of locating the GPF in clinical practice.

Hypertrophic scarring is related to persistent activation of transforming growth factor-β (TGF-β)/Smad signaling. In the TGF-β/Smad signaling cascade, the TGF-β type I receptor (TGFBRI) phosphorylates Smad proteins to induce fibroblast proliferation and extracellular matrix deposition. In this study, we inhibited TGFBRI gene expression via TGFBRI small interfering RNA (siRNA) to reduce fibroblast proliferation and extracellular matrix deposition. Our results demonstrate that downregulating TGFBRI expression in cultured human hypertrophic scar fibroblasts significantly suppressed cell proliferation and reduced type I collagen, type III collagen, fibronectin, and connective tissue growth factor (CTGF) mRNA, and type I collagen and fibronectin protein expression. In addition, we applied TGFBRI siRNA to wound granulation tissue in a rabbit model of hypertrophic scarring. Downregulating TGFBRI expression reduced wound scarring, the extracellular matrix deposition of scar tissue, and decreased CTGF and α-smooth muscle actin mRNA expression in vivo. These results suggest that TGFBRI siRNA could be applied clinically to prevent hypertrophic scarring.

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