Spontaneous flexor tendon rupture due to an insufficiency fracture of the hamate hook in a patient with systemic lupus erythematosus: A case report

Introduction: Spontaneous flexor tendon rupture is usually caused by trauma, systemic diseases, or carpal bone and joint disorders. Here we report a case of spontaneous flexor tendon rupture occurring in a systemic lupus erythematosus (SLE) patient following nonunion of the hamate hook after an insufficiency fracture, and which was also associated with tendon degeneration caused by SLE. Case presentation: A 57-year-old woman was diagnosed with SLE 22 years ago and being treated with oral prednisolone. She became unable to flex her left little finger without any history of trauma or sporting activity. CT showed nonunion of the hamate hook. MRI showed rupture of the flexor digitorum profundus tendon of the little finger. We performed tendon transfer and excision of the hamate hook. She recovered active flexion of the little finger at 4 months postoperatively with full satisfaction. Discussion: There was no history of trauma that could have caused nonunion of the hamate hook. We considered that the insufficiency fracture of the hamate hook occurred as a result of osteoporosis caused by SLE and long-term steroid use. Nonunion of the hamate hook caused mechanical attrition of the tendons, and in combination with the tendon degeneration caused by SLE, further resulted in rupture of the flexor tendon. Conclusion: When we encounter a case of spontaneous flexor tendon rupture in a patient with systemic disease such as SLE or long-term steroid use, attention should be paid to the state of the carpal bones and joints as they sometimes accompany unexpected causes

Deactivation of external acid sites of H-mordenite by modification with lanthanide oxides for the isopropylation of biphenyl and the cracking of 1,3,5-triisopropylbenzene and cumene

The modification of H-mordenite (MOR) with lanthanide oxides La O , CeO , Pr O , Sm O , Dy O , and Yb O was examined for the deactivation of external acid sites and confirmed in the cracking of 1,3,5-triisopropylbenzene (TIPB) and cumene (IPB) and in the isopropylation of biphenyl (BP). The cracking of TIPB, which cannot enter the pores of MOR, shows that external acid sites were effectively deactivated by the modification of MOR with the lanthanide oxides in small amounts. Only the cracking of IPB over CeO -modified MOR exhibited excellent catalytic activities, even at a 30 wt % metal loading, whereas the activities of other lanthanide oxide-modified MORs rapidly decreased as the loadings were increased because pore entrances became choked. The isomerization of 4,4'-diisopropylbiphenyl (4,4'-DIPB) during the isopropylation of BP at high temperatures such as 300 °C was also effectively prevented by the modification of MOR with the lanthanide oxides. Particularly, CeO -modified MOR remained highly active even at a 30 wt % loading. Other lanthanide oxides can deactivate the isomerization of 4,4'-DIPB at 5-10 wt % loadings without significant loss of the activities at 300 °C, while the activity was rapidly lost as the loading amount was increased. The physicochemical properties of lanthanide oxide-modified MORs indicate that the lanthanide oxides modify the surface properties of MOR. The amounts of N , o-xylene, and NH adsorbed on MORs mostly remained high after CeO modification; however, they rapidly decreased when loadings of the other oxides increased. These results show that CeO remains the open pores at high loadings; however, the other oxides reduce the size of pore entrances as the loading is increased

Treadmill Running in Established Phase Arthritis Inhibits Joint Destruction in Rat Rheumatoid Arthritis Models

Exercise therapy inhibits joint destruction by suppressing pro-inflammatory cytokines. The efficacy of pharmacotherapy for rheumatoid arthritis differs depending on the phase of the disease, but that of exercise therapy for each phase is unknown. We assessed the differences in the efficacy of treadmill running on rheumatoid arthritis at various phases, using rat rheumatoid arthritis models. Rats with collagen-induced arthritis were used as rheumatoid arthritis models, and the phase after immunization was divided as pre-arthritis and established phases. Histologically, the groups with forced treadmill running in the established phase had significantly inhibited joint destruction compared with the other groups. The group with forced treadmill running in only the established phase had significantly better bone morphometry and reduced expression of connexin 43 and tumor necrosis factor α in the synovial membranes compared with the no treadmill group. Furthermore, few cells were positive for cathepsin K immunostaining in the groups with forced treadmill running in the established phase. Our results suggest that the efficacy of exercise therapy may differ depending on rheumatoid arthritis disease activity. Active exercise during phases of decreased disease activity may effectively inhibit arthritis and joint destruction

Deactivation of External Acid Sites of H‑Mordenite by Modification with Lanthanide Oxides for the Isopropylation of Biphenyl and the Cracking of 1,3,5-Triisopropylbenzene and Cumene

The modification of H-mordenite (MOR) with lanthanide oxides La₂O₃, CeO₂, Pr₂O₃, Sm₂O₃, Dy₂O₃, and Yb₂O₃ was examined for the deactivation of external acid sites and confirmed in the cracking of 1,3,5-triisopropylbenzene (TIPB) and cumene (IPB) and in the isopropylation of biphenyl (BP). The cracking of TIPB, which cannot enter the pores of MOR, shows that external acid sites were effectively deactivated by the modification of MOR with the lanthanide oxides in small amounts. Only the cracking of IPB over CeO₂-modified MOR exhibited excellent catalytic activities, even at a 30 wt % metal loading, whereas the activities of other lanthanide oxide-modified MORs rapidly decreased as the loadings were increased because pore entrances became choked. The isomerization of 4,4′-diisopropylbiphenyl (4,4′-DIPB) during the isopropylation of BP at high temperatures such as 300 °C was also effectively prevented by the modification of MOR with the lanthanide oxides. Particularly, CeO₂-modified MOR remained highly active even at a 30 wt % loading. Other lanthanide oxides can deactivate the isomerization of 4,4′-DIPB at 5–10 wt % loadings without significant loss of the activities at 300 °C, while the activity was rapidly lost as the loading amount was increased. The physicochemical properties of lanthanide oxide-modified MORs indicate that the lanthanide oxides modify the surface properties of MOR. The amounts of N₂, <i>o</i>-xylene, and NH₃ adsorbed on MORs mostly remained high after CeO₂ modification; however, they rapidly decreased when loadings of the other oxides increased. These results show that CeO₂ remains the open pores at high loadings; however, the other oxides reduce the size of pore entrances as the loading is increased