Biomedical subjects

H Jiang

Publications and source records attributed to H Jiang.

At least 613 records · Page 34Linked to original sources

PubMed1992

Induction of tissue transglutaminase and apoptosis by retinoic acid in the limb bud.

Mesenchymal cells in the limb buds of midgestation mouse embryos suffer prominent cell death upon exposure to retinoic acid (RA), an event likely associated with the micromelic and phocomelic anomalies of the resultant fetuses. It has been suggested, but not yet shown, that cells die by an active process termed apoptosis rather than by necrotic cytolysis. In certain cell types, investigators have previously observed a specific and early effect of RA on transcriptional activation of the gene for tissue transglutaminase (tTG), an enzyme suspected to play a role in apoptosis. We report here a distinct but transient increase in tTG activity which accompanied the initiation of cell death in the mesenchymal cells located in the central core of RA-treated limb buds. We also ascertained microscopically that the cytological appearance of the affected cells was consistent with a characterization of the process of cell death as apoptosis.

Abnormalities, Drug-Induced↗

PubMed1992

Cellular mechanisms: induction of heart allograft survival in rats by 15-deoxyspergualin.

Survival of ACI rat heart grafts in Lewis rat (LEW) recipients treated with a short course of 15-deoxyspergualin (DSG), in a dose of 5 mg/kg daily beginning from day 4 of grafting, was markedly prolonged, with a mean survival time of 29.8 +/- 3.0 days. On day 20 after grafting, the cellular mechanism of inducing allograft survival after DSG treatment was analyzed by testing the activation of spleen cells in several assay systems. The results indicate that spleen cells from DSG-treated rats with surviving heart allografts show almost no proliferative response against donor strain stimulator cells in the mixed lymphocyte reaction (MLR) as compared with controls. Their cytotoxic activity was lower than that of spleen cells from rats with heart allograft rejection towards donor strain target cells. Adding various concentrations of spleen cells from DSG-treated LEW rats with surviving ACI heart allografts to the MLR when the responder cells from normal LEW rats were exposed to irradiated ACI or Wistar (third party) stimulator cells revealed a strong suppression, in a cell-dose-dependent manner. Moreover, the transfer of 2.0 x 10(8) spleen cells from DSG-treated LEW rats with surviving ACI heart allografts to an irradiated grafted host did not prolong the survival either of the ACI heart grafts or of the third party Wistar heart grafts. These results suggest that the proliferative response and cytotoxic activity are lowered and suppressor cells are induced by treatment with DSG, in rats with surviving allografts.

Animals↗

PubMed1992

Control of humoral and cellular immunity-mediated accelerated heart allograft rejection in sensitized rats by low dose FK 506 and splenectomy.

UNLABELLED: ACI heart grafts are rejected, at an accelerated pace, in Lewis (LEW) rats sensitized by donor-type blood admixed with immunoadjuvant (adjuvant complete Freund, ACF) 7 days earlier. In an in vitro study, the anti-ACI cytotoxic antibody titers in the serum increased from 1:4 in nonsensitized rats to 1:128 in sensitized rats; the spontaneous blastogenesis in spleen cells was higher in sensitized rats than in nonsensitized rats; spleen cells from sensitized rats showed a strong proliferative response against donor strain stimulator cells compared with the control; the cytotoxic T cell activity of spleen cells from sensitized rats was higher than that of spleen cells from nonsensitized rats. Treatment with low dose FK 506 in combination with splenectomy (Spx) synergistically prolonged the heart allograft survival in this sensitized rat model. IN CONCLUSION: (1) Both humoral and cellular responses against the donor antigen appear in the serum and in the spleen of rats sensitized by donor-type blood admixed with immunoadjuvant ACF. (2) A low dose of FK 506 together with Spx appears to control this sensitization through different mechanisms, resulting in a prolongation of heart allograft survival.

Animals↗

PubMed1992

Nonspecific hemolytic effector of activated macrophages as activation marker of allograft rejection.

The aim was to assess a nonspecific hemolytic effector of activated monocytes/macrophages, designated spontaneous plaque-forming cell (SPFC), as an activation marker in allograft rejection. An in vitro study on the immunologic characteristics of SPFC monocytes in man and an in vivo study in Lewis rats as to the monitoring of SPFC generation of allograft infiltrating cells with or without immunosuppression were conducted. Hemolysis of SPFC was mediated by CR3 adhesion molecules, detected by Mo-1 and OKM10 monoclonal antibodies. Hemolysis of SPFC was nonspecific, and nonrosette-forming T cells with autologous erythrocytes (non-ARFC-T) acted as suppressor T cells inhibiting SPFC-hemolysis against autologous erythrocytes. A 6-day course of immunosuppression with a daily dose of cyclosporin A (CyA) 10 mg/kg and of FK506 1 mg/kg suppressed the SPFC generation to the level of syngeneic control. In contrast, peak SPFC generation coincided with rejection, and the degree of SPFC generation reflected the grade of histoincompatibility. The present findings suggested that SPFC-activated monocytes/macrophages may be one of the activation markers in allograft rejection and lead to a new concept of graft rejection and self or nonself discrimination mediated by nonspecific, hemolytic SPFC effectors and suppressor T cells inhibiting autoreactivity.

Animals↗

PubMed1992

In vivo and in vitro mechanisms of cardiac allograft acceptance in the rat after short treatment with 15-deoxyspergualin.

15-Deoxyspergualin (DSG) has been reported to be a useful immunosuppressive agent already used to inhibit acute rejection in clinical transplantation. In the present study, the survival of heart allograft in rats after a short course of DSG treatment and the mechanisms underlying DSG-induced heart allograft acceptance were studied. Male LEW rats were used as recipients. Male ACI and Wistar rats were used as donors and third-party donors, respectively. Survival of ACI heart grafts in LEW recipients treated with a short course of DSG starting on day 4 after grafting was markedly prolonged, with a mean survival time of 16.6 +/- 5.8 days and 29.8 +/- 3.0 days at doses of 2.5 mg/kg per day and 5 mg/kg per day, respectively. On day 20 after grafting, the mechanism of inducing allograft survival after DSG treatment at a dose of 5 mg/kg per day was analyzed by testing the activation of spleen cells or serum in several assay systems. Spleen cells from DSG-treated rats with surviving heart allografts showed almost no proliferative response against donor strain stimulator cells compared with controls. The cytotoxic activity towards donor strain target cells of spleen cells from DSG-treated rats with surviving heart allografts was lower than that of spleen cells from rats with rejected heart allografts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Modulation of the antigenic phenotype of human breast carcinoma cells by modifiers of protein kinase C activity and recombinant human interferons.

In the present study we have analyzed the effect of a synthetic protein kinase C (PKC) activator 3-(N-acetylamino)-5-(N-decyl-N-methylamino)-benzyl alcohol (ADMB) and the natural PKC-activating tumor-promoting agents 12-O-tetradecanoylphorbol 13-acetate (TPA) and mezerein on the antigenic phenotype of T47D human breast carcinoma cells. All three agents increased the surface expression of the tumor-associated antigen BCA 225 and various cellular antigens, including HLA class II antigens, intercellular adhesion molecule 1 (ICAM-1) and c-erbB-2. Expression of the same antigens was also upregulated to various extents in T47D cells by recombinant fibroblast (IFN beta) and immune (IFN gamma) interferon. Shedding of BCA 225 from T47D cells was induced by TPA, mezerein, IFN beta and IFN gamma, whereas ADMB did not display this activity. The ability of ADMB, TPA and mezerein to modulate the antigenic phenotype of T47D cells appears to involve a PKC-mediated pathway, since the PKC inhibitor, H-7, eliminates antigenic modulation. In contrast, the ability of IFN beta and IFN gamma to enhance the synthesis, expression and shedding of BCA 225, as well as to enhance HLA class II antigens, c-erbB-2 and ICAM-1 expression, was either unchanged or modestly reduced by simultaneous exposure to H-7. Analysis of steady-state mRNA levels for HLA class I antigens, HLA class II-DR beta antigen, ICAM-1 and c-erbB-2 indicated that the ability of H-7 to inhibit expression of these antigens in TPA-, mezerein- and ADMB-treated cells was not a consequence of a reduction in the steady-state levels of mRNAs for these antigens. The results of the present investigation indicate that the biochemical pathways mediating enhanced antigenic expression in T47D cells induced by TPA, mezerein and the synthetic PKC activator ADMB are different from those induced by recombinant interferons. Furthermore, up-regulation of antigenic expression in T47D cells can occur by a PKC-dependent or a PKC-independent pathway.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1992

Staurosporine, a potent protein kinase C inhibitor, augments phorbol ester-caused ornithine decarboxylase induction in mouse epidermis.

A single topical application of 12-O-tetradecanoylphorbol-13-acetate (TPA) to mouse skin caused an induction of epidermal ornithine decarboxylase (ODC) activity. When mice were topically pretreated with staurosporine, a most potent protein kinase C inhibitor, 6-84 h prior to TPA treatment, TPA-caused ODC induction was markedly enhanced. The enhancement of TPA-caused ODC induction by staurosporine was most pronounced when the time interval between staurosporine and TPA treatment was 36 h. Staurosporine elicited this enhancing effect in a dose-related manner. Staurosporine by itself also induced epidermal ODC activity. But the activity induced was very slight and would not directly contribute to the enhancing effect of this compound. Although staurosporine markedly augmented TPA-caused ODC induction, staurosporine-caused ODC induction was not augmented by this compound. Other protein kinase C inhibitors, such as 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine, sphingosine and palmitoylcarnitine did not mimic the enhancing effect of staurosporine. These results indicate that the enhancement of ODC induction by staurosporine is specific for the induction caused by TPA and that this enhancing effect is not related to the protein kinase C inhibitory action of staurosporine. TPA-caused epidermal ODC induction was inhibited by indomethacin, and this inhibition was reversed by prostaglandin E2 (PGE2). Staurosporine-caused ODC induction was also inhibited by indomethacin but the inhibition was not reversed by PGE2, indicating that the mechanism of staurosporine-caused ODC induction is different from that of TPA.

Administration, Topical↗

PubMed1992

Involvement of prostaglandin E2 in ornithine decarboxylase induction by a tumor-promoting agent, 7-bromomethylbenz[a]anthracene, in mouse epidermis.

A single topical application of 7-bromomethyl-benz[a]anthracene (BrMBA; 200 nmol) to mouse skin induced epidermal ornithine decarboxylase (ODC) activity. A topical application of indomethacin (1.2 mumol), a cyclooxygenase inhibitor, 10 min before BrMBA application markedly inhibited BrMBA-caused ODC induction. Concurrent application of prostaglandin E2 (PGE2; 0.1-1.5 mumol) reversed the inhibitory effect of indomethacin. Without indomethacin, PGE2 suppressed BrMBA-caused ODC induction. The results indicate that PGE2 has dual actions on the BrMBA-caused ODC induction, i.e. PGE2 plays an essential role in ODC induction caused by BrMBA, whereas exogenous PGE2 rather suppressed BrMBA-caused ODC induction.

Animals↗

PubMed1992

The in vitro immunosuppressive effect of deoxymethylspergualin in man as compared with FK506 and cyclosporine.

The effect of deoxymethylspergualin (MeDSG) on in vitro human lymphocyte response was assessed in comparison with FK506 and cyclosporine. Peripheral blood mononuclear cells from normal human volunteers were used for assay of mixed lymphocyte reaction, cell mediated lympholysis, and blastogenesis by PHA, IL-2, and OKT3. MeDSG suppressed only allogeneic stimulation (MLR and CML) and IL-2-induced blastogenesis, not PHA- or OKT3-induced blastogenesis, although the other immunosuppressive agents showed some suppressive effect for all assays. A kinetic study of MLR showed that the suppressive activity did not decrease even when MeDSG was added at day 3 or day 4. The other agents, however, showed a weak suppressive effect when added at a later phase of MLR.

Cyclosporine↗

PubMed1992

Modulation of the antigenic phenotype of human melanoma cells by differentiation-inducing and growth-suppressing agents.

Tumor cells often display alterations in their normal program of cellular differentiation. A promising approach for the treatment of cancer involves the induction of terminal differentiation and a loss of proliferative capacity in cancer cells. In human melanoma cells, the combination of mezerein (MEZ) and fibroblast interferon (IFN-beta), results in a rapid and irreversible suppression of cell growth with a concomitant increase in the synthesis of melanin. The induction of terminal differentiation is associated with alterations in the expression of several cellular genes, including fibronectin, ISG-15 and ISG-54, and changes in the expression of specific cell surface antigens, including intercellular adhesion molecule-1 (ICAM-1) and HLA Class I antigens. In the HO-1 human melanoma cell line, induction of terminal differentiation by MEZ plus IFN-beta results in an induction and/or increased expression of ICAM-1, HLA Class I antigens and HLA Class II antigens. IFN-beta and MEZ alone can modulate expression of these antigens to a lower extent than does the combination of compounds. Induction of terminal differentiation and the irreversible suppression of cell growth is not a prerequisite for antigenic modulation in HO-1 cells. This is indicated by the inability of immune interferon (IFN-gamma), a strong inducer of ICAM-1, HLA Class I antigens and HLA Class II antigens synthesis, or the combination of IFN-beta plus IFN-gamma which synergistically but reversibly suppresses HO-1 growth, to induce melanin synthesis or terminal differentiation in HO-1 cells.(ABSTRACT TRUNCATED AT 250 WORDS)

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1992

Cross-activation: overriding cAMP/cGMP selectivities of protein kinases in tissues.

cAMP- and cGMP-dependent protein kinases are homologous proteins and are predicted to exhibit very similar three-dimensional structures. Their cyclic nucleotide binding domains share a high degree of amino acid sequence identity. cAMP- and cGMP-dependent protein kinases are activated relatively specifically by cAMP and cGMP, respectively; and a single alanine-threonine difference between cAMP- and cGMP-binding domains partially accounts for this specificity. Thus, it would be expected that cAMP and cGMP mediate separate physiological effects. However, owing in part to the lack of absolute specificity of either enzyme and to the relatively high level of cAMP or cGMP in certain tissues, it is also possible that either cyclic nucleotide could cross-activate the other kinase. Increases in either cAMP or cGMP cause pig coronary artery relaxation. However, only cGMP-dependent protein kinase specific cyclic nucleotide analogues are very effective in causing relaxation, and cAMP elevation in arteries treated with isoproterenol or forskolin activates cGMP-dependent protein kinase, in addition to cAMP-dependent protein kinase. Conversely, increases in either cAMP or cGMP cause Cl- secretion in T-84 colon carcinoma cells, and the cGMP level in T-84 cells can be elevated sufficiently by bacterial enterotoxin to activate cAMP-dependent protein kinase. These results imply specific regulation of cAMP- and cGMP-dependent protein kinases by the respective cyclic nucleotides, but either cyclic nucleotide is able to cross-activate the other kinase in certain tissues.

Animals↗

PubMed1992

The biophysics and biochemistry of smooth muscle contraction.

In this review the biophysics and biochemistry of smooth muscle contraction are dealt with. We describe a new model for the study of bronchial smooth muscle, which facilitates study of cellular contractile mechanisms. A new concept emerging is that study of steady-state mechanical parameters such as maximal isometric force (Po) velocity is inadequate because two types of crossbridges (normally cycling (NBR) and latch) seem to be sequentially active during smooth muscle contraction. Thus quick-release techniques are required to characterize the force-velocity properties of the two types of bridges. Pathophysiological processes that affect the muscle's shortening ability seem to affect the early NBRs only. With respect to maximal shortening capacity of the smooth muscle, the role of loading is very important. The differences between isotonic, elastic, and viscous loading are considerable. Ultimately, the time course and magnitude of loading should exactly resemble that operative in vivo. Once again, it is the characteristic of loading in the early phase of contraction that is crucial, as most of the shortening in smooth muscle occurs early in the contraction. While the maximum force developed by smooth muscle per unit cross-sectional area is the same as for striated muscle, the velocity is 50 times less. The properties of the series and parallel elastic elements of smooth muscle are described. The latter, when in compression mode, acts as an internal resistance to shortening and probably limits it. Isotonic relaxation has therefore not been studied in smooth muscle. We have developed a shortening parameter that is independent of the load on the muscle and of the initial length of the muscle's contractile element. We report the novel observation that isotonically relaxing smooth muscle reactivates itself, resulting in terminal slowing of the relaxation process. With respect to the biochemistry of smooth muscle contraction, contractile (actin isoforms, myosin heavy and light chains and their isoforms), regulatory (calmodulin-4 Ca2+, myosin light chain kinase, myosin light chain and its phosphorylation, tropomyosin, caldesmon, and calponin), and cytoskeletal (chiefly desmin and vimentin) proteins are discussed. While the kinase activates the contractile system, caldesmon and calponin modulate the activity downward. The cytoskeletal proteins desmin, vimentin, and alpha-actinin could constitute the muscle cell's internal resistor.

Animals↗

PubMed1992

Normalization of contractile parameters in canine airway smooth muscle: morphological and biochemical.

Asthma research has recently highlighted the importance of correctly normalizing force development for purposes of comparing stiffness properties of smooth muscle between different airways, between airways at different stages of maturity, and between airways from different animal species. This problem does not exist in striated muscle where the entire tissue consists almost entirely of muscle and where cross bridges cycle at the same rate throughout a contraction when load correlation is made. In the bronchus, cross-sectional area of true muscle may constitute only 20-30% of the total tissue cross section, and load-independent cycling rate varies fourfold during the course of a contraction because of the occurrence of normally cycling and latch bridges. These features are responsible for the difficulty in force normalization in smooth muscle. Our studies indicate that normalization with respect to true muscle cell cross-sectional area (derived by quantitative morphometry of appropriate tissue transverse sections) is the most valid. This is only so, however, when it has been proved that the actomyosin content per unit weight of the different muscle tissues is the same.

Animals↗

PubMed1992

Isotonic relaxation of sensitized bronchial smooth muscle.

Although the mechanisms underlying asthma are not clear, we have demonstrated that in dogs antigen sensitization results in alterations of contractile properties, such as greater early maximum shortening velocity and capacity of bronchial smooth muscle. These changes could account for the hyperresponsiveness reported in asthma. The failure of the muscle to relax could be another important factor responsible for maintaining high airway resistance. This, a relatively less-studied area, requires study. In the current study, we therefore developed an index of isotonic relaxation, T1/2,CE (half-time for relaxation which is independent of muscle load and initial contractile element length) for evaluation of the relaxation process. Because the maximum shortening velocity at 2 s but not at 10 s was greater in sensitized bronchial smooth muscle (SBSM) than that in controls studies of relaxation were also undertaken at these two times. The mean half-relaxation time indicated by T1/2,CE showed no difference between sensitized and control muscles after 10 s of stimulation (8.38 +/- 0.92 s vs. 7.78 +/- 0.93, means +/- SE); however, it was prolonged significantly in SBSM stimulated only for 1 s (12.74 +/- 2.5 s, mean +/- SE) compared with the control (6.98 +/- 1.01). Unexpectedly, we found that during the late phase of isotonic relaxation, both groups showed spontaneous increase in zero load shortening velocity, which is an index of cross-bridge cycling rate.2

Animals↗

PubMed1992

Bronchial smooth muscle mechanics of a canine model of allergic airway hyperresponsiveness.

Although we have reported that tracheal smooth muscle from sensitized dogs shows altered mechanical properties, we did not know, because of technical difficulties with the preparation, whether similar changes occur in the properties of sensitized central bronchial smooth muscle (BSM), the site at which the acute asthmatic response is believed to develop. We have now succeeded in developing a cartilage-free BSM preparation that retains optimal mechanical properties. Such strips were obtained from mongrel dogs that had been sensitized to ragweed pollen. Controls were littermates injected with adjuvant alone. Length-tension relationships were obtained for both control and sensitized BSM strips (CBSM and SBSM, respectively). The maximal active stresses were the same (P greater than 0.05) when normalized to muscle fraction in total tissue cross-sectional area [6.2 +/- 0.6 x 10(4) and 5.9 +/- 0.6 x 10(4) (SE) for SBSM and CBSM, respectively]. This suggests that optimal tension is an insensitive indicator of bronchial hyperresponsiveness and that isotonic studies might be more revealing. The maximal shortening velocity (Vo) for SBSM at 2 s [0.35 +/- 0.017 (SE) lo/s, where lo signifies optimal muscle length], in the course of a 10-s contraction, was significantly greater (P less than 0.05) than Vo measured for CBSM (0.27 +/- 0.015 lo/s). However, Vo did not differ at the 8-s point of contraction. The sensitized group demonstrated a statistically significantly greater maximal shortening capacity (0.67 +/- 0.04 lo) than the control group (0.51 +/- 0.04 lo). At 2 s of contraction, 80% of maximal SBSM shortening had been completed and was significantly greater than for CBSM.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Ragweed sensitization-induced increase of myosin light chain kinase content in canine airway smooth muscle.

Previous studies have identified changes of mechanical properties of airway smooth muscle (ASM) from a canine model of atopic airway hyperreactivity. These changes, including increased maximum shortening capacity (delta Lmax) and early shortening velocity (Vo), may be responsible for the airway hyperresponsiveness in asthma. We have suggested that these changes may be due to increased actomyosin ATPase activity, controlled via phosphorylation of the 20 kD myosin light chain (MLC20) by MLC kinase (MLCK). Therefore, ATPase activity, MLC20 phosphorylation, and MLCK content and activity were assessed in tracheal and bronchial smooth muscles (TSM and BSM) of ragweed pollen-sensitized dogs (S) and their littermate controls (C). Specific ATPase activities from STSM and SBSM were significantly higher than their control counterparts (CTSM, CBSM). Phosphorylation of MLC20 in STSM was greater both at rest and during electrical stimulation due to the increased amount of MLCK in STSM and SBSM by 30 and 25%, respectively. MLCK activity was also increased significantly in STSM and SBSM (from 46.99 +/- 8.33 and 42.85 +/- 5.92 to 91.9 +/- 6.43 and 64.12 +/- 7.88 32P mmol/mg fresh tissue weight/min respectively [mean +/- SEM]). When normalized to the amount of MLCK in the tissue, however, specific MLCK activity in STSM and SBSM was similar to that in controls. It is unlikely that myosin phosphatase plays any role in the changes of MLC20 phosphorylation in sensitized animals. Peptide mapping showed no visible change in primary structure of MLCK in STSM and SBSM compared with those of controls. We report that ASM actomyosin ATPase activity is increased in STSM and SBSM. The increased ATPase activity is the result of increased MLC20 phosphorylation, the latter likely resulting from the increased MLCK content, which may account for the hyperresponsiveness found in ASM from these animals.

Allergens↗

PubMed1992

[The experience of administration of 15-deoxyspergualin on rejection in kidney transplant recipients].

We report here the favorable results of clinical application of 15-deoxyspergualin (DSG) as a rescue therapy for rejection episodes in kidney transplant recipients. DSG was discovered in Japan and was proved to be a novel immunosuppressant in various animal transplantation models. The immunosuppressive mechanism of DSG is unclear yet, but its point of action is supposed to be in the early immuno response to allogeneic stimulation without the regulation of cytokine production. We performed the administration of DSG in fifteen patients, who had rejection episodes, with a dosage of 3 mg/kg/day or 5 mg/kg/day for five days by drip infusion. In the group of recipients who had rejection episodes within six months after kidney transplantation, DSG proved effective on six out of seven acute rejection episodes and induced favorable remission. And in the group of recipients who had rejection episodes after six months since kidney transplantation, DSG proved effective on all of ten rejection episodes. There was not a difference of effectiveness in respect to the dosage of DSG. The side effect of DSG treatment was mainly leukopenia but in most cases these leukopenia was remitted just under careful observation. Some patients complained the sense of abdominal discomfort. But so far, we did not encounter serious or critical side effects and complications during all the time of progression. Another benefit was that DSG was able to reverse the rejection episode even in the patient who had already treated with anti lymphocyte globulin and/or anti CD3 monoclonal antibody OKT3. We concluded that the administration of DSG as a rescue therapy was not accompanied by the serious side effects and was most effective against acute rejection after kidney transplantation.

Adult↗

PubMed1992

[Microneurovascular free abductor hallucis muscle transplantation for resuscitation of facial paralysis in one stage].

After study of local anatomy in fresh cadaver the authors carried out free abductor hallucis muscle transplantation successfully in three patients with facial paralysis. In one patient the plantaris medialis vessels were anastomosed to the contralateral facial vessels and the plantaris medialis nerve was anastomosed to buccal branch of the contralateral facial nerve. In two patients the plantaris medialis vessels were anastomosed to the ipsilateral facial vessels and the plantaris medialis nerve was anastomosed to the myloidens branch from ipsilateral trigeminal nerve. The authors described the local anatomy and operative methods in details. The advantages of this operative method were also discussed.

Adolescent↗